General considerations underlying the study of mental disorders are discussed in the articles under this heading. Concepts of direct relevance are also discussed in Anxiety; Defense mechanisms; Stress. General categories of mental disorders are reviewed in the articles Neurosis; Psychosis; specific disorders are discussed in Character disorders; Depressive disorders; Hysteria; Obsessive-compulsive disorders; Paranoid reactions; Phobias; Psychopathic personality;; Psychosomatic illness; Schizophrenia. Methods of assessing mental disorders are discussed in Electroencephalography; Interviewing, article onpersonality appraisal; Personality measurement; Projective methods. The treatment of mental disorders is discussed under Clinical psychology; Counseling psychology; Interviewing, article ontherapeutic interviewing; Mental disorders, treatment of; Psychiatry; Psychoanalysis. Social problems that can be considered as aspects of mental disorders are discussed in Drinking and alcoholism; Drugs; Sexual behavior, articles onhomosexualityandsexual deviation; Suicide.
I. GENETIC ASPECTSEliot Slater
II. ORGANIC ASPECTSJoseph M. Wepman in.
III. BIOLOGICAL ASPECTSJoel Elkes
IV. EPIDEMIOLOGYErnest Gruenberg
V. CHILDHOOD MENTAL DISORDERSBritton K. Ruebush
VI. EXPERIMENTAL STUDYGeorge Talland
People who are related to one another by blood tend to resemble one another in, among other things, their mental make-up and their liability to mental illness. Both genetic and environmental factors may play a part in this resemblance. The most widely accepted view of the nature of the interaction between heredity and environment has been called the diathesis–stress theory (Rosenthal 1963). In its application to mental illness this view suggests that the susceptibility to mental illness, insofar as it is genetically based, varies along a continuum ranging from high to low extremes, most people clustering about an average of moderate susceptibility. Environmental stresses, also, vary from severe to slight. Accordingly, when a mental breakdown occurs, a combination of both factors is involved; thus, we should expect a high rate of breakdown among normal individuals subjected to severe stress, and a high rate also among very susceptible people placed under even mild stress. Such a quantitative relationship has been shown to hold in fact, e.g., in the neurotic illnesses of combat troops (Symonds 1943). Whether psychotic illnesses follow the same general law is a matter more difficult to decide.
Personality deviations and neurotic illness
An important part of the work in the field of personality deviations and neurotic illness has been studies of twins. One-egg, or monozygotic (MZ), twins, whose entire genetic equipment is identical, are of the same sex and are very much alike in physical characteristics. Twoegg, or dizygotic (DZ), twins ordinarily resemble each other no more than any pair of brothers or sisters and are as likely to be of opposite sexes as of the same sex. As a rule only the same-sexed DZ twin pairs are taken by investigators for comparison with MZ pairs. Twin pairs are said to be concordant when it is found that the twin of a proband (index case) with a particular deviation also shows the same anomaly. Concordance rates are usually given as percentages. Genetic hypotheses lead one to suppose that concordance rates should be much higher in MZ than in DZ pairs and that variability within MZ pairs should be smaller than within DZ pairs. Table 1 lists the percentage of concordances found for a variety of conditions, in which the statistics are based on at least thirty pairs.
Criminality and delinquency. Much effort has been put into the investigation of criminality and behavior disorder. The results of Rosanoff in juvenile delinquency are noteworthy (Rosanoff et al. 1934; 1941). There are high rates of concordance both in MZ and in DZ twin pairs, and little difference between them. This suggests that the similarity in the twins’ behavior is due to common factors in their environment. It is at least possible that each of the twins constitutes part of the stress factor for his twin partner. The same suggestion arises from the observations of behavior disorder and neurotic traits in school children. Shields found that in these children the degree of neurotic reaction was more noticeably related to environmental factors than genetic constitution; the hereditary factor showed itself in the type of reaction (1954). [SeeCriminology; Delinquency;SychopathicPersonality.]
Adult neuroses. Concordance rates are lower in neurotic adults, both in the MZ and in the DZ pairs. The greatly increased variability within both kinds of pairs can be put down to the much wider range of experience, and wider variety of stresses, to which adults are subjected.
Male homosexuality. At the opposite extreme are Kallmann’s findings of 100 per cent concordance in MZ pairs, as against 12 per cent concordance in DZ pairs, for male homosexuality. This would suggest that in these cases the genetic factors account for the greater part of the variance. Some caution in interpretation is needed, however. The importance that the genetic contribution acquires here may be due to the fact that there was a pre-dominance of the more constitutional type of homo-sexual in the sample studied by Kallmann and his team. [SeeSexual Behavior, articles onSexual Deviationand Homosexuality.]
Studies of relatives
Attempts to estimate the importance of hereditary factors in causing neurotic illness have been made by investigating the frequency of such illnesses among the relatives of neurotic patients. Findings have varied greatly from observer to observer. One of the early workers, Brown (1942), started by investigating the first-degree relatives of patients who had been diagnosed as suffering from obsessional neurosis, anxiety neurosis, and hysteria, as well as those of a control group. Among the relatives of all groups he found individuals suffering from obsessional neurosis, anxiety neurosis, and hysteria, as well as from other personality deviations of a kind not easily named and classified. There were three significant findings: the relatives of the control group had much less psychiatric abnormality than the relatives of any of the other three groups; all three diagnoses were represented among the relatives of
|Table 1 – Concordance rates for personality deviation and behavior disorders in monozygotic and same-sexed dizygotic twin|
|PER CENT OF CONCORDANCE|
|Deviation||Number of pairs||Investigator(s)||MZ||DZ|
|source: shilds & slater 1960,p. 327,table 8.6|
|Male homosexuality||63||Kallmann 1952||100||12|
|Adult crime||216||Lange 1929; Rosanoff et al. 1934; Kranz 1936;|
Stumpfl 1936; Borgstroem 1939
|Juvenile delinquency||67||Rosanoff et al. 1934; 1941||85||75|
|Childhood behavior disorder||107||Rosanoff et al. 1934; 1941||87||43|
|Behavior disorder or marked neurotic traits|
in school children
|Neurosis, psychopathic personality||37||Slater 1953||25||14|
|Alcoholic addiction||82||Kaij 1960||65||30|
all three patient groups; among those relatives who were classifiable under the three named diagnoses, it was found that there was a tendency for them to be in the same diagnostic category as the related patient. For example, of the nine obsessional relatives discovered, seven were related to the obsessional patients. This finding suggests a certain degree of specificity, which is best seen in the investigations which have been made on the relatives of obsessional patients (Luxenburger 1930; Lewis 1936; Rüdin 1953). Among the 100 parents of 50 obsessional patients Lewis found that 37 showed pronounced obsessional traits in one form or another; 21 per cent of the 206 siblings also showed obsessional traits. [SeeObsessive–Compulsive Disorders.]
At the opposite pole are the findings in the relatives of patients diagnosed as suffering from “hysteria.” The best family study was made by Ljungberg (1957), who found that among the fathers, brothers, and sons of hysterics, 2 per cent, 3 per cent, and 5 per cent respectively were themselves hysterics; and among the mothers, sisters, and daughters, 7 per cent, 6 per cent, and 7 per cent respectively. His observations also suggested that hysterical symptoms were not necessarily associated with hysterical personalities, and of the 363 hysterics whose personality structures were analyzed, 55 per cent were found to be nondeviant.
Similar conclusions were reached by the writer (Slater 1961) from a study of 24 pairs of twins, 12 MZ and 12 DZ, in which the proband had been diagnosed as suffering from hysteria. In none of these pairs was there a co-twin who had ever been diagnosed as suffering from hysteria, though abnormalities of personality and psychiatric illness were common. Among the relatives of these pairs the incidence of hysteria was even lower than in Ljungberg’s material, and the anomalies found to be most noticeably in excess were manic–depressive and endogenous affective psychoses. [SeeHysteria.]
It seems probable that environmental factors are more important than genetic ones in determining whether or not a man breaks down with a neurotic illness. But it would seem that genetic factors influence the predisposition to such breakdown, help to determine whether the personality is a stable one, and, in the event of breakdown, have a large effect on the type of symptoms which are likely to be shown.
The risk of affective psychoses in the first-degree relatives of manic–depressive patients is shown in
|Table 2 – Per cent of manic–depressiv disorders among|
relatives of manic–depressive patients
|Investigator||NUMBER OF PROBANDS||NATURE OF RELATIONSHIP|
|Röll and Entres 1936||83||13.0||10.7|
Table 2. It will be seen that there is much variation in the data reported by different observers. Nevertheless, these risk figures are all very much higher than would be expected of a sample taken from the general population, in which the incidence level is probably of the order of 0.4 per cent.
Approximately 15 per cent of the first-degree relatives of manic–depressives may themselves have affective disorders of the same generic group.
One explanation suggests that there is a single dominant autosomal gene which predisposes a spontaneous variation in mood. Most people with such a tendency are likely to remain healthy throughout their lives, though their cyclothymic temperament may be clearly recognizable both to themselves and to their families. If such cyclothymic individuals are subjected to stresses, the spontaneous swing of mood into depression or elation may go so far and last so long that medical treatment becomes necessary; and then the patient may be stigmatized as a “manic–depressive.” The genetic hypothesis proposes, in fact, to account for only a part of the causation. Environmental factors and threshold effects must also be playing a part. The theory requires that 50 per cent of the first-degree relatives of manic–depressives should be gene carriers; if only 15 per cent of the relatives show themselves as such, this can be put down to low penetrance of the gene. [SeeDepressive Disorders.]
A single-gene hypothesis, however, is not the only possibility; polygenic inheritance is an alternative explanation. Edwards (1960; 1963) has drawn attention to the fact that, in the case of common conditions, it is not easy to distinguish between the expected consequences of a single gene with diminished penetrance and of multifactorial inheritance with a threshold effect. Assuming that the predisposition to a condition, such as schizophrenia or diabetes, is quantitatively graded, with a normal distribution, Edwards suggests that when p = the frequency of the disorder, the incidence of the disorder in the first- degree relatives of persons suffering from the disorder will be approximately . If the frequency of manic–depressive illness in the general population is approximately 0.004, then the frequency of manic–depressive illness in the first-degree relatives of manic–depressives should be about 6 per cent to 7 per cent. The observations are about double that figure, but it is not possible to say that observation and expectation, on the multifactorial hypothesis, are irreconcilable.
Extensive investigations of the hereditary factor in schizophrenia have been made by Kallmann and his associates in the New York State Psychiatric Institute and Hospital (Columbia University). A synopsis of the results obtained is given in Table 3. These risk figures should be compared with the estimated risk of schizophrenia for a member of the general population of 0.9 per cent. Environmental effects show up: association with a schizophrenic proband in the same home virtually doubles the risk of schizophrenia for step-sibs and spouses; and there is a greater risk for the non-separated MZ co-twin of a schizophrenic than for an MZ co-twin who has lived apart from the pro-band for five years or more. However, the table also shows the risk of schizophrenia running up steeply with increasingly close degrees of blood relationship. In view of these figures it is difficult and, the writer feels, unrealistic to dispute the conclusion that genetic factors play a significant role in the causation of schizophrenia.
The risk figures published by Kallmann are some-what higher than those obtained by other workers but are in the main reconcilable with them. The writer, for instance (Slater 1953), found a risk of
|Table 3 – Per cent of risk of schizophrenia among rela tives of schizophrenics|
|Nature of relationship||Per cent risk|
|Source: Adapted from Kallmann 1950.|
|Not related by blood, step-sibs||1.8|
|Not related by blood, spouses||2.1|
|Nephews and nieces||3.9|
|DZ co-twins of same sex||17.6|
|Children with one schizophrenic parent||16.4|
|Children with two schizophrenic parents||68.1|
|MZ co-twins living apart for at least 5 years||77.6|
|MZ co-twins not so separated||91.5|
76 per cent for the MZ co-twin and 14 per cent for the DZ co-twin, in a sample of 41 MZ and 115 DZ pairs. However, it is noteworthy that Essen-Moller (1941) in Sweden found larger differences within MZ pairs than were found by other workers, and investigations in Norway and Finland show tendencies in the same direction. Thus Kringlen (1966) collected 50 MZ and 94 same-sexed pairs, with concordance rates of 38 per cent and 14 per cent; and Tienari (1963) found that none of the 16 male MZ pairs he studied were concordant. It is possible that what is diagnosed as schizophrenia in Scandinavia is not quite the same as schizophrenia in Germany, Britain, the United States, and Japan. That there may be peculiar features about the gene distributions in northern lands is also suggested by the work of Böök (1953). In a remote part of Sweden north of the Arctic circle, in a population of farmers and lumbermen, he found a high incidence of schizophrenia, in a predominantly cata-tonic form; the incidence of schizophrenia in the relatives of probands, however, was also high, suggesting an intermediate gene with 20 per cent penetrance in the heterozygote. The possible prevalence of different genetic predisposing factors for schizophrenia in different parts of the world is a possibility which deserves investigation.
The findings of Tienari, by themselves, are anomalous and should not be taken as throwing doubt on the results obtained by others; they should be considered in relation to those of other observers, summarized in Table 4. In this table the figures relating to schizophrenia are derived from work in Germany, the United States, Sweden, and England. To these should be added the results obtained by the Japanese workers Kurihara (1959) and Inouye (1961). Inouye found concordance for schizophrenia in 60 per cent of 55 MZ pairs and in 12 per cent (two pairs) of the DZ pairs. Kurihara also found that 29 of 45 MZ pairs were concordant for schizophrenic symptomatology, but none of the 9 DZ pairs were.
The twin work on schizophrenia has been analyzed and discussed critically by Rosenthal in a number of papers (1962 a; 1962 b; 1963). He concludes that concordance rates have been artificially inflated by the sampling methods employed. Cases have been largely taken from standing populations and include an unrepresentative proportion of severe cases; if genetic factors are connected with reduced chances of remission (which has yet to be shown), this sampling would obviously bias the results. Clearly, sampling from consecutive admissions, or better still from birth registers, would be an improvement. Rosenthal criticizes standards
|Table 4 – Concordance rates for mental disorders in same-sexed dizygotic and monozygotic twins|
|Type of disorder||Number of|
|PER CENT OF CONCORDANCE||Relative increase*|
|* The relative increase in concordance associated with identity of genetical constitution, between theoretical limits of 1 and 0: (MZ – DZ)/(100 – DZ).|
|Source: Adapted from Essen-Möller 1963.|
|Child and juvenile||5||209||87||53||.73|
of diagnosis, both of zygosity and clinical classification, and considers that these diagnoses should be made independently of one another by different observers. Not all recorded work is equally open to such criticism; it is, for instance, a considerable safeguard to publish protocols in full, as the writer did, to make them available to rediagnosis by the reader. [SeeSchizophrenia.]
Rosenthal classifies the etiological theories of schizophrenia into (1) monogenic–biochemical, (2) diathesis–stress, and (3) life-experience theories, his own views inclining to a theory of the second type. This is no place for the discussion of the difficult problems involved, but the writer inclines to a theory of the first type. It can be shown (Slater 1958) that a monogenic theory fits fairly well with the empirically obtained figures for the frequency of schizophrenia in the siblings of schizophrenics, in the children of one schizophrenic parent, and in the children of parents both of whom had schizophrenic illnesses. These data can be reconciled with a gene of inter-mediate type, manifesting itself in all homozygotes but in only 26 per cent of heterozygotes; all but 3 per cent of schizophrenics would be heterozygous for the gene. This hypothesis clearly involves a massive environmental contribution in the causation of manifest illness and therefore differs from theories of type (2) only in supposing that the element of specificity in determining the type of psychosis is provided by the genetic constitution. One may expect that decisive support or refutation of type (1) theories will depend on biochemical investigations.
Presenile and senile dementias
Inheritance in Huntington’s chorea is dependent on an autosomal dominant gene. Its incidence in the sexes is about equal. The age of onset, according to Panse (1942), extends from early childhood to the late sixties, with a mean at age 36; Wendt and his colleagues estimate the mean age of onset at 44 (1960). These estimates mean that most of the children of gene carriers are born before the parent has developed the disease. Elimination of the pathogenic gene by processes of natural selection is, accordingly, very slow. The disease is slowly progressive and fatal, with a mean duration of 13 years (Wendt et al. 1960).
Unusual forms of presenile dementia are Pick’s disease and Alzheimer’s disease; both have a genetic basis. Compared with Huntington’s chorea, they occur later in life, with a mean age of onset of 55, and with about seven years as the mean duration. Although the conditions are distinct pathologically, they are often difficult to distinguish clinically. According to Sjölgren (Sjögren et al. 1952), the genetic factor in Pick’s disease is most probably a dominant major gene, its manifestation subject to modifying genes; in Alzheimer’s disease Sj6ögren thinks multifactorial inheritance more probable.
The problem of genetic determination in senile dementia is even more difficult. The most generally accepted opinion in the past has been that senile dementia is but one aspect of senescence and that specific genetic causation is improbable. However, this established viewpoint has been challenged by the work of Larsson, Sjögren, and Jacobson (1963). In a large study in Stockholm they found that se-nile dementia was not correlated with senescence. The relatives of patients suffering from senile dementia were not more than normally subject to other conditions, although their risk of senile dementia itself was increased; no instances of Pick’s or Alzheimer’s disease were found among them. There did not appear to be special factors for longevity whose presence or absence was connected with senile dementia. No evidence could be found of environmental factors of a sociomedical kind playing a part in determining the onset of senile dementia. Furthermore, there was no secular change in the incidence of the disease. Particularly in favor of an explanation in terms of a single gene rather than multifactorial inheritance were the variations in geographical distribution and the absence of intermediate states between senile dementia and normal aging in the siblings and children of the probands. [SeeAging.]
The morbidity risk for senile dementia was found to be greatly increased among the relatives of the patients. These researchers consider that the best working hypothesis for the explanation of their findings is that of an autosomal major domi- nant gene. This gene would be subject to diminished penetrance, the manifestation rate increasing with age. Only a minority even of the gene carriers would ever develop senile dementia; and since the calculated gene frequency was 0.12, the great bulk of the population would be immune.
Banse, J. 1929 Zum Problem der Erbprognosebestim-mung: Die Erkrankungsaussichten der Vettern und Basen von Manisch–Depressiven. Zeitschrift fur die gesamte Neurologic und Psychiatric 119:576–612.
Böök, J. A. 1953 A Genetic and Neuropsychiatric Investigation of a North-Swedish Population: I. Psychoses. Acta genetica et statistica medico. (Basel) 4:1–100.
Borgstroem, C. A. 1939 Eirie Serie von kriminellen Zwillingen. Archiv für Rassen- und Gesellschaftsbiologie 33:334–343.
Brown, Felix W. 1942 Heredity in the Psychoneuroses.Royal Society of Medicine, Proceedings 35:785–790.
Edwards, J. H. 1960 The Simulation of Mendelism. Acta genetica et statistica medica (Basel) 10:63–70.
Edwards, J. H. 1963 The Genetic Basis of Common Disease. American Journal of Medicine 34:627–638.
Essen-möller, Erik 1941 Psychiatrische Untersuchungen an einer Serie von Zwillingen. Acta psychiatrica et neurologica scandinavica Supplement 23.
Essen-möller, Erik 1963 Twin Research and Psychiatry. Acta psychiatrica scandinavica 39, fasc. 1:65–77.
Fonseca, Antonio F. Da 1959 Andlise heredo–clinic a das perturbações afectivas: Estudo de 60 pares de gémeos a seus consanguíneos. Universidad de Porto (Portugal): Faculdade de Medicina.
Inouye, Eiji 1961 Similarity and Dissimilarity of Schizophrenia in Twins. Volume 1, pages 524–530 in World Congress of Psychiatry, Third, Montreal, Proceedings. Univ. of Toronto Press.
Kaij, Lennart 1960 Alcoholism in Twins: Studies on the Etiology and Sequels of Abuse of Alcohol. Stock-holm: Almqvist & Wiksell.
Kallmann, Franz J. 1950 The Genetics of Psychoses:An Analysis of 1,232 Twin Index Families. American Journal of Human Genetics 2:385–390.
Kallmann, Franz J. 1952 Comparative Twin Studies on the Genetic Aspects of Male Homosexuality. Journal of Nervous and Mental Disease 115:283–298.
Kranz, Heinrich 1936 Lebensschicksale krimineller Zivillinge. Berlin: Springer.
Kringlen, Einar 1966 Schizophrenia in Twins: An Epidemiological–Clinical Study. Psychiatry 29:172–184.
Kurihara, M. 1959 A Study of Schizophrenia by Twin Method. Psychiatria et neurologia japonica (Seishin shinkeigaku zasshi) 61:1721–1741. → Text in Japanese; title and summary in English.
Lange, Johannes (1929) 1931 Crime as Destiny: A Study of Criminal Twins. London: Allen & Unwin. → First published as Verbrechen als Schicksal.
Larsson, Tage; Sjögren, Torsten; and Jacobson, George1963 Senile Dementia: A Clinical Sociomedical and Genetic Study. Copenhagen: Munsgaard.
Lewis, Aubrey 1936 Problems of Obsessional Illness.Royal Society of Medicine, Proceedings 29:325–336.
Ljungberg, L. 1957 Hysteria: A Clinical, Prognostic and Genetic Study. Acta psychiatrica et neurologica scandinavica Supplement 112.
Luxenburger, H. 1930 Psychiatrisch–neurologische Zwillingspathologie. Zeitschrift für die gesamte Neurologic und sychiatric 56:145–180.
Panse, Friedrich 1942 Die Erbchorea: Eine klinischgenetische Studie. Leipzig: Thieme.
Roll, A.; and Entres, J. L. 1936 Zum Problem der Erbprognosebestimmung: Die Erkrankungsaussichten der NefFen und Nichten von Manisch–Depressiven. Zeitschrift fiir die gesamte Neurologic und Psychiatric 156:169–202.
Rosanoff, Aaron J.; Handy, L. M.; and Plesset, I. R.1941 The Etiology of Child Behavior Difficulties, Juvenile Delinquency and Adult Criminality, With Special Reference to Their Occurrence in Twins. Sacramento: California State Printing Office.
Rosanoff, Aaron J.; Handy, L. M.; and Rosanoff, I. A.1934 Criminality and Delinquency in Twins. Journal of Criminal Law and Criminology 24:923–934.
Rosenthal, David 1962a Familial Concordance by Sex With Respect to Schizophrenia. Psychological Bulletin 59:401–421.
Rosenthal, David 1962b Problems of Sampling and Diagnosis in the Major Twin Studies of Schizophrenia. Journal of Psychiatric Research 1:16–34.
Rosenthal, David (editor) 1963 The Genain Quadrup-lets: A Case Study and Theoretical Analysis of Heredity and Environment in Schizophrenia. New York: Basic Books.
Rüdin, Edith 1953 Ein Beitrag zur Frage der Zwangskrankheit, insbesondere ihrer hereditären Beziehungen. Archiv für Psychiatric und Nervenkrankheiten 191: 14–54.
Shields, James 1954 Personality Differences and Neurotic Traits in Normal Twin Schoolchildren: A Study in Psychiatric Genetics. Eugenics Review 45:213–245.
Shields, James; and Slater, Eliot (1960) 1961 Heredity and Psychological Abnormality. Pages 298–343 in Hans J. Eysenck (editor), Handbook of Abnormal Psychology: An Experimental Approach. New York: Basic Books.
Sjogren, Torsten 1948 Genetic–Statistical and Psychiatric Investigations of a West Swedish Population. Acta psychiatrica et neurologica scandinavica Supplement 52.
Sjögren, Torsten; Sjögren, Hakon; and Lindgren, AkeG. H. 1952 Morbus Alzheimer and Morbus Pick: A Genetic, Clinical and Patho-anatomical Study. Acta psychiatrica et neurologica scandinavica Supplement82.
Slater, Eliot 1938 Zur Erbpathologie des manisch–depressiven Irreseins: Die Eltern und Kinder von Manisch–Depressiven. Zeitschrift für die gesamte Neurologic und Psychiatric 163:1–47.
Slater, Eliot 1953 Psychotic and Neurotic Illnesses in Twins. Medical Research Council Special Report No. 278. London: H.M. Stationery Office.
Slater, Eliot 1958 The Monogenic Theory of Schizophrenia. Acta genetica et statistica medica (Basel) 8:50–56.
Slater, Eliot 1961 The Thirty-fifth Maudsley Lecture:Hysteria 311. Journal of Mental Science 107:359–381.
Stenstedt, Ake 1952 A Study in Manic–Depressive Psychosis. Acta psychiairica et neurologica scandinavica Supplement 79.
Stromgren, Erik 1938 Beiträge zur psychiatrischen Erblehre. Acta psychiatrica et neurologica scandinavica Supplement 19.
Stumpfl, Friedrich 1936 Die Urspriinge des Verbrechens dargestellt am Lebenslauf von Zwillingen. Leipzig: Thieme.
Symonds, C. P. 1943 The Human Response to Flying Stress. British Medical Journal : 703–706, 740–744. → Lecture 1: “Neurosis in Flying Personnel.” Lecture 2: “The Foundations of Confidence.”.
Tienari, P. 1963 Psychiatric Illnesses in Identical Twins. Acta psychiatrica scandinavica 39 (Supplement 171). → The entire issue is devoted to Tienari’s study.
Wendt, G. G.; Landzettel, I.; and SOLTH, K. 1960 Krankheitsdauer und Lebenserwartung bei der Huntingtonschen Chorea. Archiv för Psychiatric und Nervenkrankheiten 201:298–312.
Traditionally, description of the organic syndromes, in relation to their effect upon the central nervous system and behavior generally, has included such generalizing conditions as cerebral arteriosclerosis, acute and chronic alcoholism, pre-senile and senile conditions, degenerative neural diseases, and developmental mental deficiencies, as well as conditions producing more focal disorders such as head injuries, brain tumor extirpations, and cerebrovascular accidents (the boxer who is punch-drunk or the stroke patient).
The trend in recent literature, however, confirms what is a notably progressive shift in emphasis away from strictly clinical or case description, as exemplified by texts in psychiatry and neurology, toward more varied studies, which consider psycho-diagnostic and psycholinguistic phenomena in the context of clinical observations.
With these important changes in the study of organic pathology has also come a voluminous growth in the literature. Within this literature (see Wepman 1961) can be found the continuing traditional interest of the neurologist and psychiatrist, as seen, for example, in the recently published American Handbook of Psychiatry (Arieti 1959). However, the great breadth of the field can be noted in the work of experimental psychologists using both animal and human subjects; in the recent neurophysiologic research on such central nervous system areas as the reticular formation, the limbic lobes, and the association tracts; in the dramatic electrode stimulation studies of cortical reactions carried on during neurosurgery; in the elaboration of new psychodiagnostic signs by psychometric researchers; and in the growing group of neurophysiological theories related to brain function. Additional examples, from the more applied fields, are rehabilitation for brain-impaired persons and the not inconsiderable addition of research on language disabilities.
As can be seen, the literature of neuropsychology is rich and varied. Within it, the reader will find, however, that there are more unknowns than knowns,, more questions than answers, more theories than facts. While a great deal has been written about the behavior of the brain-impaired, very few facts have been demonstrated. For example, it is generally accepted that in thought, emotional control, and intellection, the role of the central nervous system is crucial. Yet the precise manner in which the nervous system and the human brain work to fulfill this function is undetermined and vague. A leading neurophysiologist once described the human brain as a “black box” that must function in certain well-prescribed ways in order to produce all that it does in human behavior but unfortunately is not available for viewing.
Nevertheless, the great concentration of attention by so many trained observers, the extensive studies of clinical cases, the host of theories, the wide and growing application of differential diagnostic techniques, and the increasing activities of both language therapists and psychotherapists treating patients suffering from brain impairment have all produced a considerable body of knowledge available for better understanding of organic mental disorders. The following is an attempt to de-scribe some of the more prominent behavioral phenomena commonly associated with neural impairment and includes major sources of data and references in order to facilitate and encourage further investigation by the reader.
Common behavioral manifestations
Alteration in thought, personality changes, and changes in language comprehension and usage take on many forms following cortical insult. By and large, however, most investigators agree that individual patterns of behavior in the brain-impaired differ from those of the unimpaired more in degree than in type. Table 1 presents the reader with a list of the most common indications of brain impairment.
While space limitations preclude extensive comment on the relative merit of individual signs of organicity as indicators of organic psychopathology, some generalizations about them are warranted. Many of these signs appear as the result of a dis-ordering process producing abnormal behavior; others are the product of the retained ability to function of what is left of the nervous system; and
|Table 1—Behavioral symptoms of the brain-impaired|
|Memory loss (especially immediate memory)||poor attention and concentration||Aphasia|
|Reduced association of ideas||Memory loss||Agnosia|
|Perseveration of thought and language||Abstract—concrete imbalance||Apraxia|
|Feelings of inadequacy||Poor ability to organize and preplan||Dysarthria|
|Egocentricity||Difficulty in forming generalizations|
|Hyperirritability||Inability to categorize|
|Overfatiguability||Lowered general intelligence|
|Catastrophic overreaction||Perplexity (questioning one’s own ability)|
Lack of spontaneity
|Psychological impotence (recognition of errors|
without the obility to alter to responses
|Fluctuating ability||Specific modality disabilities in learning|
|Situational or fixed anxiety||Body-image distortion|
Spiral afterimage reactions
Delayed response patterns
still others derive from the altered self-concept of the people involved (their reactions to their impairment). At any rate, these signs, while not necessarily pathognomonic of the brain-injured, are rather useful indicators of the likelihood that a cortical impairment has occurred. Research comparing known brain-impaired subjects with normal individuals and subjects with thought disorders (for example, schizophrenics) has consistently shown that pathological conditions, while frequently unlike normal states, are most often like each other (Chapman 1960). In fact, the argument has been advanced that the very presence of so many so-called organic signs in schizophrenia may indicate that this psychiatric condition is indeed an organic psychosis. Thus, behavioral symptoms can be viewed as frequently occurring telltale indicators of pathology but cannot themselves be viewed as differentially diagnostic signs of organic pathology.
It should also be pointed out that most of the signs used as organic indicators have not been found by research studies to occur in every organic condition. In part this is true, the present writer feels, because few of the studies have been really comparable. Research populations differ in so many ways (for example, age of subjects and location and extent of lesion or impairment) that the signs said to be associated with brain pathology in one study may be completely lacking in an equally well attested study of another group of brain-injured patients. A final source of inconsistency is related to subjects with a known brain injury but who differ in behavior from other such subjects even though neuropathies may be alike, the location of damage is thought to be the same, and the amount or size of the lesion is thought to be roughly equal. The generalization must be made, therefore, that brain-impaired patients differ from one another not only in the size and location of their structural defect but also in the behavioral aftereffects of similar neurological impairment.
Certain commonalities do exist, however, and it is to these that students of brain pathology turn in attempting to gain a greater understanding of cortical function and dysfunction. The remainder of this article will be concerned with a more particular discussion of the behavioral signs appearing in Table 1 in relation to organic disorder, with emphasis upon the literature and major sources of data. Shortage of space unfortunately limits consideration to only the most prominent and generally elicited signs appearing in each of the three categories arbitrarily designated as clinically observed behavior, psychodiagnostically elicited behavior, and psycholinguistic disturbance patterns.
Clinically observed behavior
Many of the signs enumerated in the category of clinically observed behavior can be related to certain basic processes that seem to underlie the signs themselves.
Lack of control over behavior. Most notable among these processes is the concept of “control.” Since the central nervous system is generally considered a major determinant in the control of behavior as the individual seeks to adapt to his environment, loss of memory and similar behavior may be best understood, in this context, as a loss of selective control over recall of events from the past. Further, memory loss in organic conditions is said to be most severe in the area of recall of very recent events, for example, when the individual must select (control) the appropriate impressions from a variety of recent ones. Related to the recall aspect of memory loss is the loss of capacity to attend, concentrate, or exert simple control over one’s ideas.
Impulsiveness, emotionality, and rigidity. Similarly, many clinicians have observed that the brain-impaired are often impulsive and emotionally labile. They react catastrophically to noncatastrophic events, or they become easily frustrated. At the other extreme, the brain-impaired often display tendencies toward rigidity or repetition in thought and language, find it difficult to shift from one idea to another, and are frequently inflexible in behavior. In each case then, these signs point to the patient’s inability to regulate his behavior in a flexible fashion. Lack of adequate inhibition and sufficient control brings about these overt behavioral patterns, which have been termed symptoms of brain damage. With adequate control, the unimpaired behave with intent, behave appropriately, and be-have purposively. The impaired, having lost control, show abnormalities of behavior in all three areas. (Note: The writer feels it is unnecessary to discuss clinically observed symptoms more extensively here, as they are generally self-explanatory; however, more detailed consideration may be found in the references cited in the bibliography.)
Psychodiagnostically elicited symptoms. The loss of perceptual ability is a basic process that frequently affects the brain-impaired. This loss of function is especially noticeable in the capacity to learn through specific sense modalities. Consequently, it is most often described in relation to problems of children with known neurological deficiencies. But it seems equally true in all adults with brain damage, where perceptual deficiencies have been noted as being modality-bound rather than generalized. Auditory perception, for example, may be affected by brain impairment or by failure of certain portions of the nervous system to develop, while other perceptual abilities may remain intact (Wepman 1960). Some children, it has been noted, fail to develop language at the time expected of them (that is, by two or three years of age). This is not because of any lack of general intelligence or because of deafness or emotional instability but rather because they are unable to learn in situations that involve the auditory pathway. Other children, who do speak adequately, have been observed having difficulty in learning to read at the expected age. Again, this may be caused by no other reason than their inability to use the visual modality in learning, and this despite the measurable adequacy of their visual acuity. [SeeHearing; Vision.]
These auditory and visual agnosias in children are paralleled by similar disturbances of transmission of input stimuli following cortical insult in adults. Perceptual learning disability along specific modality lines has become the center of attention for many students of behavior in brain-impaired children and adults.
As Table 1 implies, many signs of organic brain impairment can be elicited by psychometric and projective assessment. In some instances these are found to duplicate the clinically observed signs. But in others, they are observed only when the subject is under the stress and scrutiny of formal testing.
Verbal and nonverbal functioning. The use of psychological tests as a means of isolating behavioral indicators of brain impairment continues to be a source of considerable research. Babcock (1941) noted in her studies of the brain-injured that certain intellectual faculties seem better retained after trauma than others. She then proposed to study subjects and evaluate their product in terms of these better retained areas (verbal behavior) as compared with the abilities that are less well retained (visually stimulated abstraction ability). A similar differentiation was used in the Shipley-Hartford Scale (Shipley 1940) and the Hunt-Minnesota Test for Brain Impairment (Hunt 1943). Some support for this notion also seemed to follow from the characteristics of the tests used. Vocabulary retention, or verbal ability, as measured by most tests, is statistically well equated with general intelligence, is known to have a high test-retest reliability, and is generally a stable measure. In contrast, the tasks of visual abstraction are less stable, have less reliability over time, and are therefore more likely to be susceptible to change as a result of organic conditions affecting the nervous system.
Wechsler followed the concept of retained as op-posed to sensitive functions, not in a comparison of verbal versus nonverbal behavior, but in empirically determined responses to various subtests in his intelligence scale. From the results of his studies of an aging population, he devised a deteri-oration index (1955). By and large, this approach has fallen into disfavor among psychologists, however, since confirming research for the deficiencies found by the original author has been lacking (Kass 1949). Those who argue against the use of the verbal versus the nonverbal differential, or, as the believers in perceptual disabilities put it, “the differential between aurally stimulated verbal behavior and visually stimulated nonverbal behavior,” seem to this writer to be correct in their conclusion—but for the wrong reasons. In none of the research reported on the many indexes of deterioration was any attempt made to isolate the location of the organic condition, even to the rather loose degree of determining the hemisphere affected. Yet many language studies (Wepman 1951; Ettlinger et al. 1956) and the work of such researchers as Reitan and Reed (1962), Milner (1954), Bauer and Wepman (1955), and others have reported each of the two hemispheres differentially responsible for various intellectual tasks. [SeeIntelligence AND Intelligence Testing.]
In conclusion, therefore, it would be expected that the verbal-nonverbal paradigm would be successful. When damage has occurred to the left brain (the apparent site of integrations necessary for verbal behavior) it would seem that subjects should do less well with verbal than with nonverbal material. When, on the other hand, notable damage occurs in the right hemisphere, which, according to many studies, is the locus of control and integration for nonverbal thought, the expectancy would then be that nonverbal material would pre-sent greater difficulty. To the degree that such a distinction can be made in psychological tests—and it can be in many of them—the tendency for the effects of brain damage to be depicted seems high. Re-examining known organically impaired subjects from this viewpoint shows this differentiation to be a meaningful one. The degree to which this approach can be used in differential diagnosis where brain damage is suspected but not certain, however, still needs research verification.
The qualitative approach for the delineation of personality disorganization, using projective tests as the source of data, has proven of value in the hands of many psychologists (Aita et al. 1947; Baker 1956; Hughes 1948; Piotrowski 1937). Un-fortunately, most of the results reported are the subjective interpretations of individual examiners and are barely or not at all confirmed in replicated studies. Where such studies have been attempted, few of the signs found diagnostic by one examiner have been elicited by others. For the purposes of demonstrating some of the psychodynamic processes affected in many brain-injured subjects, however, the different projective techniques have proven of considerable value. Yet even here it seems important to point out the individual variability in behavioral reactions. Since brain-injured subjects differ so markedly, for example, in their responses to their traumas, or with respect to their self-conceptions, it has been found to be of little value to look for commonality of reaction in personality change.
Abstract and concrete functioning. Goldstein, perhaps more than any other student of brain dis-orders, has postulated both specific disabilities and changes in basic attitudes and thought processes as a result of organic conditions. He pointed out that “. . . even in cases of circumscribed cortical damage, the disturbances are scarcely ever confined to a single field of performance. In such intricate syndromes, we deal not only with a simple combination of disparate disturbances but also with more or less unitary, basic change that affects different fields homologously and expresses itself through different symptoms . . .” ( 1939, pp. 15-16).
Of all the symptomatology noted in the study of the organic psychopathologies, none has had greater impact or perhaps stirred greater controversy than Goldstein’s concept of the shift from the abstractive to the concrete mode of thought (Goldstein & Scheerer 1941). With his co-workers, he postulated both theory and methods for determining the loss of categorical, abstracting behavior. The concept, by and large, has received greater acceptance than the methods. Today almost every clinician studying the behavior of the brain-impaired patient concedes the correctness of Goldstein’s observation that organic brain disease impairs abstract functioning. The many Goldstein tests, however, have been less successfully used by other examiners.
Changes in intellectual performance. Finally, some attention should be directed toward the concept of changes in general intellectual level as a consequence of brain impairment. Essentially, there are two types of change that have been widely noted. In some patients, over-all intellectual level seems grossly affected, as in conditions that to a certain degree affect the nervous system in its entirety. A good example is the deterioration that accompanies progressive cerebral disease and that is demonstrated by progressive generalized intellectual decline. In other patients, the condition is localized and affects intellectual ability within fairly circumscribed areas. It can be shown in most cases of brain disorder that one or the other of these two forms of intellectual loss occurs. In certain types of localized damage that affect only specific functions, as in the limited agnosias and apraxias affecting language, it may be held that no intellectual loss need be predicated. However, even here a loss must be considered to occur, since the deficiency in those functions immediately affected makes adaptation to the environment more difficult and more circumscribed. Thus, even very minor brain damage that functionally affects only the capacity to read or write and that might not affect the individual’s capacity to think or perform on intelligence tests would still have its deleterious effect upon the totality of behavior and, consequently, upon intelligence. It would make the patient a less efficient organism and would thus make adaptation to life a more complex task for him.
Generalized deterioration, whether progressive or not, rarely permits alterations in behavior through therapy and rehabilitation. On the other hand, focalized injuries that produce limitations of intellectual ability can frequently be offset by proper training and therapeutic rehabilitation (Harlow 1953).
Organic language disturbances
Language function and dysfunction have also become the focus of attention of many researchers in recent years. Loss of the ability to comprehend and use language has an extensive literature of its own. Aphasia, a loss of ability to utilize verbal symbols, is a relatively common aftereffect of brain damage, especially when that damage affects the left cortical hemisphere. There have been widely different approaches to the study of the language syndromes. Schuell and Jenkins (1959) have postulated that language is a unitary process that may be lost in varying degrees. They have concluded from their studies that the language deficit may be measured along a continuum of severity of dysfunction. This would include difficulties with a variety of individual tasks, such as the abilities to speak, read, and write. Wepman and Jones (1961), on the other hand, contend that language is divisible into a series of different linguistic processes and that each process may be differentially affected. Five types of symbolic loss of language—five types of aphasia—have been described in this research: global, jargon, pragmatic, semantic, and syntactic.
Partial support for this viewpoint is seen in the insightful work of Jakobson (Jakobson & Halle 1956), who related certain observed aphasic disturbances, noted above as semantic and syntactic aphasia, to two basic linguistic processes. He pointed out that there are two basic types of aphasia, differentiated according to whether the deficiency is in the selection and substitution of words or in their combination and contexture.
Further support for this linguistic differentiation also comes from other sources. The research of Goodglass and his co-workers on agrammatism and paragrammatism (Goodglass & Hunt 1958; Good-glass & Mayer 1958) confirmed the Jakobson distinction. The work of Luriia (1947; 1958) in the Soviet Union goes far beyond the linguistic approach, identifying the process changes with neural constructs and specific localization of damage. Also included in his work is a description of five very similar types of language disturbance (1958).
The conception of aphasia as representing disorders along a continuum of severity and the psycholinguistic classification of aphasic types as discussed above are fairly recent developments. In contrast, traditional neurological literature treats language disturbances as receptive or expressive disorders, closely related to specific neurological substrata. Indeed, a fair proportion of the literature on the whole field of brain damage is given over to discussions of the question of localization of function in the nervous system. Harlow’s review of literature dealing with the higher functions of the nervous system (1953) is devoted solely to the difference of opinion concerning localization. Discussing Hebb’s brilliant Organization of Behavior (1949), the Hixon Symposium on Cerebral Mechanisms in Behavior (Jeffress 1951), and Fulton’s Functional Localization in Relation to Frontal Lobotomy (1949), as well as research devoted to specific architectonic divisions of the cortex, Harlow concludes in part that “the data would appear to be almost overwhelmingly opposed to any theory of cortical localization of intellectual function which is anatomically precise or temporarily static” (1953, p. 512). Writers in the field vary from a position of extreme belief in punctate localization to the opposite view of equipotentiality or mass action. Somewhere between these two polar view-points rest the opinions of most present-day exponents of the role of the cortex in relation to behavior.
Recent reports of psychodiagnosticians studying the behavior of patients with known brain damage give some credence to a gross type of localization. Reitan and his co-workers (Reitan & Reed 1962), as mentioned earlier, have been able to show that subjects with left brain damage, when tested by such scaled instruments as the Wechsler Adult Intelligence Scale, show a greater deficit in performing verbal tasks, and less deficit, if any, in performing nonverbal tasks. The opposite findings were reported on patients with known right brain damage; that is, they did better on verbal tasks than on nonverbal ones. This general finding bears out what has previously been said about language disorders following brain injury; that is, symbolic verbal behavior is found to be disturbed only in left brain-injured subjects (Wepman 1951).
It is the viewpoint of most students of brain function that while there is a type of localization of function within the nervous system, the end product, which is an individual’s behavior, is the result not of the functioning of any localized section or subsection but of the integrated nervous system as a whole. For example, Penfield and Rasmussen (1950), by their ingenious placement of electrodes during neurosurgery, have demonstrated that while aphasic arrest does occur more frequently when Broca’s area (the third prefrental convolution of the left cortex) is stimulated electrically, a similar arrest of language occurs when widely scattered areas of the parietal and even the temporal lobes are stimulated. From such studies it would appear that while a high concentration of cells in Broca’s area may be responsible for a type of word-finding ability, other areas subserve the same function but in a less concentrated way. Behavior, it is held, is a far too complex process to be conceptualized as the product of any localized area of the brain. It is much more reasonably thought of as the integration of perceptual, conceptual, mnemonic, and motor processes—with factors of motivation, emotion, and the processes of feedback playing their various roles.
Organic mental disorders can thus be best described as the results of a variety of conditions—disease processes, traumas, agenesis, deteriorations, etc. These conditions in turn produce alterations in the consequent behavioral patterns of the brain-impaired. Certain specific signs of alteration are more commonly seen in the behavior of the impaired than in the unimpaired. These signs are recognizably not pathognomonic of the neural dis-order. Yet, by their consistency of occurrence, the are often the best indicators available of brain damage in those in whom pathological behavior is noted. Many of these indications are admittedly seen only clinically and rarely verified by research. Others are elicited through more organized and scientific psychological and linguistic studies.
Joseph M. Wepman
[Other relevant material may be found in Language, article on Speech Pathology; Nervous System; Schizophrenia.]
aita, John A.; Reitan, Ralph M.; and Ruth, Jane M. 1947 Rorschach’s Test as a Diagnostic Aid in Brain Injury. American Journal of Psychiatry 103:770-779.
Arieti, Silvano (editor) 1959 American Handbook of Psychiatry. 2 vols. New York: Basic Books.
Babcock, Harriet 1941 The Level-efficiency Theory of Intelligence. Journal of Psychology 11:261-270.
Baker, Gertrude 1956 Diagnosis of Organic Brain Damage in the Adult. Pages 318-428 in Bruno Klopfer (editor), Developments in the Rorschach Technique. Volume 2: Fields of Application. New York: World Book.
baue,R Robert; and Wepman, Joseph M. 1955 Lateralization of Cerebral Functions. Journal of Speech and Hearing Disorders 20:171-177.
Chapman, Loren J. 1960 Confusion of Figurative and Literal Usages of Words by Schizophrenics and Brain Damaged Patients. Journal of Abnormal and Social Psychology 60:412-416.
Ettlinger, George; Jackson, C. V.; and ZANGWILL, O. L. 1956 Cerebral Dominance in Sinistrals. Brain 79: 569-588.
Fulton, John F. 1949 Functional Localization in Relation to Frontal Lobotomy. New York: Oxford Univ. Press.
Goldstein, Kurt  1939 The Organism. New York: American Book. → First published in German.
Goldstein, Kurt; and Scheerer, Martin 1941 Abstract and Concrete Behavior: An Experimental Study With Special Tests. Psychological Monographs 53, no. 2.
Goodglass, H.; and Hunt, J. 1958 Grammatical Complexity and Aphasic Speech. Word 14:197-207.
Goodglass, H.; and Mayer, J. 1958 Agrammatism in Aphasia. Journal of Speech and Hearing Disorders 23:99-111.
Halstead, Ward C. 1947 Brain and Intelligence. Univ. of Chicago Press.
Harlow, Harry 1953 Higher Functions of the Nervous System. Annual Review of Physiology 15:493-514.
Hebb, Donald O. 1949 The Organization of Behavior. New York: Wiley.
Hughes, Robert M. 1948 Rorschach Signs for the Diagnosis of Organic Pathology. Rorschach Research Exchange 12:165-167. → Now called Journal of Projective Techniques.
Hunt, Howard F. 1943 A Practical Clinical Test for Organic Brain Damage. Journal of Applied Psychology 27:375-386.
Jakobson, Roman; and Halle, Morris 1956 Fundamentals of Language. The Hague: Mouton.
Jeffress, LLOYD A. (editor) 1951 Cerebral Mechanisms in Behavior: The Hixon Symposium. New York: Wiley. KASS, WALTER 1949 Wechsler’s Mental Deterioration Index in the Diagnosis of Organic Brain Disease. Kansas Academy of Science, Transactions 52:66-70.
Lashley, Karl S. 1929 Brain Mechanisms and Intelligence: A Quantitative Study of Injuries to the Brain. Univ. of Chicago Press.
Luriia, Aleksandr R. 1947 Travmaticheskaia afaziia (Traumatic Aphasia). Moscow: Academy of Medical Science.
Luriia, Aleksandr R. 1958 Brain Disorders and Language Analysis. Language and Speech 1:14-34.
Milner, Brenda 1954 Intellectual Functions of the Temporal Lobes. Psychological Bulletin 51:42-62.
Penfield, Wilder; and Rasmussen, Theodore 1950 The Cerebral Cortex of Man. New York: Macmillan.
Piotrowski, Zygmunt A. 1937 The Rorschach Ink Blot Method in Organic Disturbances of the Central Nervous System. Journal of Nervous and Mental Diseases 86:525-537.
R,eitan, Ralph M.; and Reed, HMER B. 1962 Consistencies in Wechsler-Bellevue Mean Values in Brain- damaged Groups. Perceptual and Motor Skills 15:119-121.
Schuell, Hildred; and Jenkins, J. J. 1959 The Nature of Language Deficit in Aphasia. Psychological Review 66:45-67.
Shipley, Walter C. 1940 A Self-administering Scale for Measuring Intellectual Impairment and Deterioration. Journal of Psychology 9:371-377.
Teuber, Hans L. 1950 Neuropsychology. Pages 30-52 in Recent Advances in Diagnostic Psychological Testing. Springfield, 111.: Thomas.
Wechsler, David 1955 Wechsler Adult Intelligence Scale (WAIS). New York: Psychological Corp.
Wepman, Joseph M. 1951 Recovery From Aphasia. New York: Ronald Press.
Wepman, Joseph M. 1960 Auditory Discrimination, Speech and Reading. Elementary School Journal 60: 325-333.
Wepman, Joseph M. 1961 A Selected Bibliography on
Brain Impairment, Aphasia, and Organic Psycho-diagnosis. Chicago: Language Research Associates.→ Lists over a thousand items collected from 220 recent American journals and books.
Wepman, J. M.; and JONES, L. V. 1961 The Language Modalities Test for Aphasia. Chicago: Education-Industry Service.
In 1884 the founding father of neurochemistry,J. W. L. Thudichum, wrote:
Many forms of insanity are unquestionably the external manifestations of the effects upon the brain substance of poisons fermented within the body, [in the same way that] mental aberrations accompanying chronic alcoholic intoxication are the accumulated effects of a relatively simple poison fermented out of the body. These poisons we shall, I have no doubt, be able to isolate after we know the normal chemistry to its uttermost detail. And then will come in their turn the crowning discoveries to which all our efforts must ultimately be directed, namely, the discoveries of the antidotes to the poisons, and to the fermenting causes and processes which produce them. (1884, p. xiii)
Thudichum anticipated trends which we would regard as very modern in our day. Two premises are explicitly stated. An aberrant biological product (or “a product fermented in the body”) leads to aberrant behavior; and knowledge of normal chemistry “to the uttermost detail” is an essential prerequisite to the isolation of such a product. Thudichum’s own crowning achievement was an analysis of the brain in terms of its chemical building blocks, the so-called lipoproteins, which are complexes formed between fatty bodies (lipids) and proteins. This work still stands as a classic.
Yet this approach—what one might call a clock-work approach—reflects the hopes and limitations of an age. In the Victorian era, governed by the meter rule, the clock, and the kilogram, an under-standing of the chemical machinery was regarded as a reasonable basis for the understanding of mental disorder and thus, by inference, of mental order. Attitudes have great viability; similar approaches (with somewhat better reason) are with us to this day. They aim at an understanding of the chemistry of the strange detector we carry in our skull. But of environment, forever playing upon this detector, and so often disrupting and distorting it, chemistry will tell us nothing. Nor can chemistry, in its old and classic form, tell us much of how environment is transcribed and coded by nervous tissue.
Yet in man the brain in some strange way internalizes and stores environment; it models it in sight and sound and uses these models as predictors; it transmits information from generation to generation by a symbolic (nongenetic) process, which is a radically new departure in evolution. Neurochemistry thus poses problems very different from those posed by classical chemistry or even by modern physical chemistry. It demands a revision of attitudes, and perhaps like no other field in biology is forcing a confrontation of biological process with the emerging concepts of system theory. In short, any attempt at understanding the brain as a chemically mediated organ of information forces an en-counter between somatic transaction and symbolic process. This field one can, justifiably, term psychobiology.
Principles of regional brain organization
We may be a long way from understanding the nature of the chemical control processes which enable the brain to function as an integrating, “feeling,” information-storing, predicting, and computing organ, but we have also come some way since Thudichum. Thudichum’s analysis involved the analysis of the brain as a single organ. However, the brain, unlike the liver, is not a homogeneous organ; and in terms of anatomical arrangement, cell population, and chemistry it shows a regional economy which reflects the course of its own evolution. The distinctive attribute of the human and primate brain is the size and structure of its cortex. Its0 contribution to the analysis of secondary signaling (that is, symbolic) systems has been extensively studied by the Pavlovian school. Yet work since the 1940s has also emphasized the role of some developmentally older subcortical centers buried deep in the brain and the relationship of these structures to the cerebral cortex. The brain centers in question are the hypothalamus, the reticular activating system, the rhinencephalic (“smell brain”) formation (also known as the limbic system), and the caudate and lentiform masses (the corpus striatum). Each of these systems has received its share of extensive review; and accumulated experience, using a variety of techniques with each, has steadily emphasized three separate, though related, trends. The first is the discrete neuroanatomic and cellular suborganization of these systems; the second, the interconnectedness between the systems themselves and between the systems and relatively distant elements at high cortical and spinal levels; and the third, the reciprocal, complementary, yet mutually exclusive relationship which some patterns represented in these systems bear to each other. These findings are relevant when considered in relation to the regional chemistry of these structures. [SeeNervous system, article onstructure and function of the brain.]
There is little doubt of the anatomical heterogeneity and cytological differentiation of the hypothalamus, where small areas measuring hardly more than a few millimeters in diameter control the central representation of the autonomic nervous system and the appetitive drive systems (fight, flight, hunger, thirst, sex). Similarly, more recent studies have emphasized the remarkable anatomical and cytoarchitectonic differentiation within the reticular activating system, governing wakefulness, sleep, and focused attention. Elements in the structure of the limbic system have similar differentiation. Each of these systems thus encompasses a mosaic of subsystems which in a manner only poorly understood at present are fitted into one another. This understanding, however, is being steadily enhanced by mounting knowledge of the anatomical connections and electrophysiological properties. These connections are in both directions between the hypothalamus and the reticular formation, the limbic system and the hypothalamus, and between these structures and the cortex. [SeeAttention; Sleep.]
The term “limbic system midbrain circuit” is entirely apt (Nauta 1958). In a way still poorly understood, the limbic system would appear to be an intermediate between discrete analysis of diverse signals at high levels and the discharge of a limited genetically coded stereotyped response known as “affective” behavior. It appears to participate in and to modulate both.
There is a tremendous convergence of information in this area. There are structural counterparts of this convergence; in the olfactory bulb, for example (which in man can be regarded as a homologue of the hippocampus), the messages of about 50 million receptors are reduced to 150 thousand in mitral cells and finally reach the brain through the axons of a mere 45,000 pyramidal cells. These cells and their branchings thus have the structural features which make for an extraordinary funneling and filtering of information (Green 1964). It is, incidentally, in these areas too that a rich, tessellated, terrazzo-like apposition of shared membranes, a virtual mosaic, is found. These junctional areas are also highly localized electrical generators.
It is usually found convenient to speak of the reticular formation and the hippocampal amygdaloid cell assemblies as areas that control sleep, wakefulness, and the states between wakefulness and sleep. Yet there is evidence that these areas are pre-eminent in their relation to patterns of emotional expression of autonomic functioning and, also, that interference in these areas may be important for the process of “recall” and possibly for the process of registering the memory trace. Seen dimly, then, and in broadest silhouette, the functions covered by the terms “consciousness,” “affect,” and at any rate “recall” thus appear to be subserved by congruent or at least intimately connected systems (Elkes 1966). That we are “aware,” that we are “responsive,” that we are “appropriate,” that we can plan a piece of behavior and be sequent rather than random, confused, and “in-con-sequent” in its execution may well be due to some elements and processes vested by evolution in these remarkable cell groups. Somehow, they appear to have the ability to build short-term representational systems of temporarily related events and to use them in the construction of appropriate responses. These models, these tiny maps in time, may be intercellular or cellular; at this stage we do not know.
We may thus regard the brain as a mosaic of what have appropriately been called “biased homeostats” (Pribram & Kruger 1954). The bias, handled by genetically coded “Yes-No” drive systems, keeps changing constantly in the light of ongoing events. To allow adequate comparison of events, slow-fading traces must be available to set up such transient comparisons. It is possible that the so-called after discharges (slow-fading electrical discharges) for which the cells—particularly of the hippocampus—are noteworthy provide a medium for the establishment of such traces. In a manner which is only just beginning to be understood, the coincident is detected and the concurrent arranged into an appropriate action that is consequent. Whereas internal perception and comparison may be multiple, action and preparation for action are essentially serial: it requires a rigorous regulation of construction of events at the time; it demands apprehension of the redundant and, above all, a selective inhibition of those elements which are judged irrelevant; a construction of subsets which carry meaning by ignoring but also can carry coded traces of what they ignore. Inhibition is thus the agent of structure in the central nervous system. This is borne out by all that we know of reciprocal inhibition in the spinal cord and all that is being learned of the organization of sensory processes. All evidence coming from visual, auditory, and the somatosensory fields points to the operation of highly patterned inhibitory processes reciprocating with the excitation. Delay of the immediate response—that is, the reduction of the immediate reactivity—is merely the giant child of inhibition, a vast and pervasive function woven by evolution into the nervous tissue as a device for judging rele-vance and for structuring time. Time, indeed, would appear to be the main axis around which the nervous system constructs its model of reality. It does so by judging what is relevant in time and “banking” what is irrelevant. The higher nervous system is remarkable for its ability to ignore; accurate adaptive performance is attained by ignoring all that is adjudged irrelevant.
Somehow, then, in such transactions the simultaneous has to be changed to the successive, and global or random apprehension likewise has to be transformed into rank-ordered sequential responses. It has been observed by Pribram and Kruger (1954) that it may be the role of the limbic system to provide the context in which drive stimuli are reinforcing and then to reverse the context–content relationship between the drive stimuli and reinforcing events. Thus affective connotation becomes a label and a gating device. Affect gates the emergence of memory traces into preconscious knowing and conscious action. The events and the internal representation may be highly varied and complex; the affective response patterns, however, are finite. Seen very broadly, the anatomy of the neuraxes reflects these requirements. For we are dealing here with two great vertical systems and one, so to speak, horizontal system.
First, there is the so-called specific afferent–efferent system which in particular preserves in-formation coming from receptors in a point-to-point representation; second, there is the core of the mid-line structures comprising the massive facilitatory and inhibitory structures and characterized by a great variety of cells which serve as a mixing pool for each sense modality. Connected with both systems are the elements of the limbic system in which the indications for somewhat longer traces of activity (the so-called “after discharges”) are located and which makes this information available for reference, for comparison, and for labeling. It is possible that the caudate and the striatal nuclei may have somewhat similar properties. In man the vast neocortical mantle provides a tremendous reservoir of cells for the storage of recorded traces of events and for their use in the shaping of new events, either symbolic or actual, i.e., those expressed in action. It is also well to recall that wherever we look in the central nervous system, extracellular space is scarce; nonneuronal (so-called) glial structures and membranes predominate. In fact (although this may prove to be an extravagant generalization), we may look upon the central nervous tissue as an array of growing, polymerizing protein fibers and a mosaic of lipid-protein membranes.
Studies have shown the power, the growth, and the specificity of connection formation in the peripheral nervous system. There is also evidence of the presence of nerve growth factors promoting the growth of nerve fibers (Levi-Montalcini & Angeletti 1961). It would seem that, scaled down and com-pressed to an enormously faster time scale, we may be dealing in the central nervous system with the growth and evolution of macromolecular forms, which by their interaction determine what we know as symbolic form. The junctional sites between cells, and particularly the enormous and highly ordered membranes existing in the central nervous system, may play a part in the initial construction of trace models capable of acting as recognizers, and hence as organizers and ultimately as decision points—organizers, that is, of coincidences, of sequences of pattern, that is, patterns in time. [SeeTime, article onpsychological aspects.]
Central neurohumoral substances
It may very well be asked why one should emphasize structural features in the context of a statement on the biological background of mental disorder. The partial answer is that the anatomical and functional attributes have some suggestive chemical correlates. For it is precisely in the areas just mentioned (the hypothalamus, the midline gray area, and elements of the limbic system, the amygdala, the hippocampus, the reticular activating system, and certain layers of the cortex) that one repeatedly encounters a number of small molecules which appear to have evolved for a role in the organization of control systems in the central nervous system. These molecules are acetylcholine, and possibly other choline esters; gamma amino-butyric acid, a derivative of glutamic acid; hista-mine, also found in the skin and released in injury of all tissues; catecholamines such as dopamine, norepinephrine, and epinephrine, mediators of sympathetic system responses at peripheral effector sites; and indoles such as serotonin. All these molecules show a regional gradient in their distribution. Histamine, for example, is found principally in the midline diencephalic structures; norepinephrine is present in the hypothalamus and in the periventricular gray matter; serotonin is present in both diencephalic and limbic structures. Two further features should be emphasized concerning these substances. First, they are representative members of families of compounds. As chemical mapping proceeds, related members of these various sub-groups, their precursors, and their products are identified. Second, the metabolic pathways of each of these compounds—within and without the brain—are steadily being defined more clearly. New and elegant techniques are capable of demonstrating these materials in situ in the brain. These studies show that the intercellular and pericellular economies of these substances are organized very precisely. The molecules are transported into cells or their precursors by the energy-yielding system; once synthesized, they are transported and packaged into granular particles or “vesicles” inside cells; they are carefully stored in equilibrium at these sites and are released in response to electrical stimulation by mechanisms still poorly understood. Moreover, all work so far on how the psychoactive drugs act—be they tranquilizers, stimulants, or the so-called hallucinogenic compounds—suggests that all substances interfere in varying ways and to varying degrees with the uptake, storage, and re-lease of the catecholamines (such as epinephrine and dopamine), indolic substances (such as serotonin), and possibly histamine in the areas that have been mentioned. The precise action profiles of these drugs are different, and it is upon such subtle differences in action that variation in therapeutic effect may well depend.
This, then, puts an end to the simple “clock model” of an earlier day. For we are not only dealing with families of compounds, but we are also considering multiple binding sites of organelles exquisitely sensitive to local subcellular conditions. The uneven distribution of these chemicals at neuronal decision points, the trigger (or selective suppressor) function of certain elements, and the anatomically imposed economy in terms of convergence and occlusion all suggest that we are dealing with transaction sites at highly localized subcellular levels which need not necessarily be reflected in gross over-all shifts. These sites are evidently un-evenly distributed in nonhomogeneous cell populations. Their state at any one time depends exquisitely upon the short-term history of preceding or coincidental events. It is impossible to think in terms of a mechanistic spatial localization, i.e., in terms of points. Rather, one is forced to think in terms of convergence, coincidence, stochastic processes, and probabilities of interaction in time. It was earlier suggested that inhibition is the agent of structure in the nervous system and that the silence in the central nervous system is, so to speak, informed silence. The chemical computer we carry in our skulls apparently writes its chemical text of experience in proteins; and some small molecules appear to play a key part in the transcription or readout. Much work on the biology of mental dis-order centers on the identification of the normal molecules mentioned above and of their deviant metabolites.
Chemical aspects of mental development
Chemical factors certainly operate in the development of the nervous system. Some of these are general; others are more special. Of the general factors, oxygen supply is one and hormones are another. Cerebral ischemia, i.e., restriction of blood supply, even for a short time in the developing animal, causes marked forms of mental deficiency. Yet in the adult animal, oxygen supply and fuel consumption are not necessarily related to mental functioning: they may be, but they need not be. A major advance in methodology (Kety & Schmidt 1948) has made it possible to make exact measurements of blood flow, oxygen consumption, and glucose consumption in the conscious human brain, in a variety of functional states in the normal brain and in various forms of mental disorder. These studies have shown quite clearly that in normal man the major substrate for oxidation is glucose and that the rate of energy utilization of the human brain is on the order of a mere 20 watts—eloquent testimony to the efficiency and miniaturization of the brain–computer, weighing about three pounds.
These same studies also showed that general anesthesia reduces cerebral oxygen consumption to about 40 per cent; in contrast, normal sleep did not show such reduced oxygen consumption. Similarly, in studies of schizophrenia and of the effects of LSD-25 and other hallucinogenic drugs there were no changes in over-all total oxygen consumption. First and last, the brain is an organ of information. To be sure, energy is needed to keep the living computer going, to synthesize the building blocks, particularly proteins and lipoproteins essential for its development. However, information storage and retrieval are evidently low-energy processes.
Another equally general factor concerned in intellectual development and mental functioning is presented by a number of hormones, of which thyroxin can serve as a useful example. Hypothyroidism due to an iodine deficiency leads to a mental deficiency syndrome known as cretinism. Hyperthyroidism (an excess of thyroxin) leads to striking hyperirritability and various signs of over-activity of the autonomic nervous system. There is much experimental evidence (Sokoloff & Kaufman 1959) that thyroxin may exert its action on the brain through influencing protein synthesis. It is relevant that although thyroxin does not stimulate protein synthesis in the mature brain, it does significantly do so in the newborn brain. The main structural defect in experimentally induced cretinism (produced by thyroid deficiency) is a deficiency in the proliferation of fine nerve fibrils (dendrites) in the immature cerebral cortex. Here again, a structural feature stresses the importance of connectivity between neurones (the so-called neuropile) rather than mere number of cells.
The pathology of phenylpyruvic oligophrenia (phenylketonuria, PKU) may serve as a useful example of the way in which a specific and genetically determined metabolic error—a so-called biochemical lesion—may profoundly affect the development of higher nervous function. In 1934 A. Z. Foiling observed in the course of an investigation of mentally defective children that some of them excreted phenylpyruvic acid in the urine and that there appeared to be a relation between the anomaly and the imbecility. This was the first demonstration of a metabolic error definitely associated with a form of mental defect and also with physical characteristics (blond hair and blue eyes). In phenylketonuria the subject is unable to oxidize a normally occurring essential amino acid (phenylalanine) to tyrosine at a normal rate. Because of this inability, phenylalanine accumulates in the tissues, rises in the blood stream, and spills over in the urine. This error also mobilizes other metabolic routes which normally play little part in the metabolism of these amino acids. In 1953 it was definitely shown that enzymic extracts prepared from the livers of phenylketonuric patients failed to further the oxidation of phenylalanine to tyro-sine (Jervis 1953; Wallace, Moldave & Meister 1957). Extracts of normal livers do so quite readily. Furthermore, the use of radioactively labeled phenylalanine showed that the phenylketonuric can convert this phenylalanine to tyrosine at only a fraction of the normal rate. The most striking result of this deficient oxidation mechanism is the appearance in the urine of phenylpyruvic acid, a compound which is readily detected through the greenish color it acquires when it reacts with ferric chloride. This provides a ready screening test for the deficiency in the newborn. The striking decreased pigmentation seen in phenylketonuria—blue eyes and blond hair—may be due to the de-creased formation of melanin pigment, through inhibition of an enzyme known as tyrosinase. The abnormal metabolites of phenylalanine also apparently interfere with the synthesis of catecholamines important for brain functions. This may account for the lowered level of epinephrine and norepinephrine in the plasma of the phenylketonuric. Whether excess of phenylalanine or one of its breakdown products or an interference with some of the biosynthetic processes of catecholamines accounts for the mental defect remains uncertain. However, the concept opens up an inviting area for producing experimental phenylketonuria in the laboratory by means of “loading” the system with phenylalanine and also suggests a way of treating or preventing the disorder by withdrawing the offending amino acid from the diet.
The first attempt to relieve phenylketonuria by such dietary means followed only four years after the discovery of the syndrome (Penrose & Quastel 1937). A new approach to the problem was introduced in 1951, when, for the first time in the field of mental deficiency, diets specifically low in one amino acid (namely, phenylalanine) were introduced (Woolf & Vulliamy 1951). The so-called synthetic phenylalanine-low diets have now been used with varying success in a number of studies. They result in a sharp lowering of urinary phenylpyruvic acid and plasma phenylalanine. The patients so treated show a striking reduction in seizures and spasticity and increased responsiveness in motor development. There is also a darkening of the hair. Reversal to full phenylalanine natural diet leads to relapse. It has also become unambiguously clear that treatment must be introduced as early as possible and that improvement falls off sharply if this regimen is introduced beyond the stage of infancy. The developing nervous system is a vulnerable one. [SeeMental retardation.]
These studies are mentioned because in a sense they represent a prototype of approach which is now being applied, with some modest success, in other studies of the biological basis of mental disorder. The steps are as follows: An empirical finding—a deviant metabolite in urine—leads to a suspicion of a metabolic defect. The natural history of the disorder suggests a genetic basis for this defect. A biochemical lesion—a specific biochemical defect—is defined. Since the metabolic pathways are interrelated, this single defect leads to consequences only indirectly related to the primary defect, yet very pertinent to the total pathology. The correction of the defect by reducing the metabolic load forms the basis of therapy. An animal model for this disorder is developed, and, finally, the fit of the model in terms of detection and prevention is tested.
However, there is still a large no man’s land between evidence and inference. The effects of the deviant metabolites on the development of the nervous system, and particularly those areas concerned with perception, coordination, control of motor activity, and maturation of intellectual function, remain largely unknown.
The facts cited above point to the complexity of the field of disorder when it is seen in terms of available biochemical facts and biochemical hypotheses alone. These complexities are compounded many times over in an attempt to relate known biochemical facts to the group of disorders known as the schizophrenias. It is by now generally accepted that we may be dealing, in this group, with a number of very different disorders, sharing a general symptomatology but quite possibly in need of a radical regrouping. The role of genetic factors is reviewed elsewhere [seeMental disorders, article ongenetic aspects]. Careful genetic psychosocial studies of twins, on a national and international scale, are now proceeding, and such studies (particularly of families in which twins are discordant for schizophrenia) may contribute some of the facts which are needed to separate, on a conceptual basis, nature from nurture. Equally, careful longitudinal studies—prospective rather than retrospective—are needed (starting, preferably, in early infancy) to establish the role of genetic “givens” in the autonomic reactivity patterns which have been claimed to be deviant among schizophrenics. These suggest an instability of hormonal control and diminished compensatory physiological responses: peripheral vasoconstriction, capillary abnormalities in the nail bed, and abnormal pupil responses have been implicated as such signals. Yet the one measure which reliably distinguishes schizophrenic populations from normal is their state of readiness in the face of oncoming stimuli (Rodnick & Shakow 1940). This anticipatory set or “set index” suggests that in schizophrenia one may be dealing with a disorder of the attention process. How much this disorder represents the collusion between a genetically determined instability in homeostatic control and a defensive homeostatic withdrawal from stressful stimulus situations and thus, ultimately, a learned pattern of adaptation (enhanced, for example, by the double message structure found in schizophrenogenic families) still remains a matter of conjecture. [SeeAttention; Reaction time; Schizophrenia; Stress.]
Nor does the difficulty of relating biochemical varibles to clinical states end there. Even when the data are from the observation of schizophrenics in a hospital ward, there are a number of sources of errors which have seriously affected investigation (Kety 1959). These include long hospitalization, diet (including dietary iodine and protein deficiency), various therapeutic maneuvers (including medication), and the actual circumstances—stressful or otherwise—accompanying the drawing of the biochemical sample. Also, as in all other fields of psychobiology, subjective bias has cast a pall over many painstaking studies. All these reservations notwithstanding, there are, however, some findings largely attributable to the striking advances in present-day methodology. These advances are essentially three in number. First, the refinement of protein fractionation procedures (derived from the needs of blood transfusion and of plasma substitutes); second, the advance of microfluorometric techniques for the detection of very small quantities of catecholamines, indole derivatives, and their metabolites; and third, the development of radioactive tracer techniques and particularly the advent of the liquid scintillation counter, which makes it possible to follow a particular compound through a metabolic maze. As always, it is a moot question whether technical methods or intuitive insights are the more powerful propellants of science. Evidently, in our age they are inextricably connected.
In 1957 it was first reported that a serum fraction obtained from schizophrenic patients, when injected into carefully selected nonschizophrenic prisoner volunteers, led to the development of symptoms of thought disorder, autism, depersonalization, paranoid ideas, hallucinations, and catatonic stupor which were likened to schizophrenia (Heath et al. 1958). Attempts to replicate this finding by injection of material prepared according to similar instructions, however, were not successful (see Conference on Neuropharmacology 1959). This finding, however, seems to this writer less pertinent than the various lines of investigation which were stimulated by the finding. A number of groups have now independently obtained evidence which suggests at least the possibility that an abnormal protein may be present to a greater extent in the blood of schizophrenics than in normals and that this substance may be capable of producing behavioral metabolic changes in some animal tests. There is also evidence that there is an antigenic abnormality in the pooled serum of chronically ill schizophrenic patients (Haddad & Rabe 1963) and that plasma from schizophrenic patients affects learning and retention of learning in the rat (Bishop 1963). Similarly, serum of schizophrenic patients has been shown to affect cortical (electrically evoked) responses of animals (German 1963). However, it is of more than suggestive significance that in these various studies plasma derived from normal individuals put under stress produced somewhat similar responses. It is therefore possible that one may be dealing here with a small molecular constituent liberated during stress and attached to one of the plasma fractions; the constituent may not be a unique characteristic of schizophrenia.
Another approach to the problem is the characterization of various serum protein fractions, rather than total proteins, in terms of electrophoretic and immunochemical properties. There is evidence from double-blind studies that there may be abnormal protein fractions in a considerable proportion of schizophrenic patients (Fessel & Grunbaum 1961).
A cognate approach to the above are the findings of another group (Frohman et al. 1960), who re-ported that when red blood cells of chickens are incubated with plasma or plasma fractions of some schizophrenic patients, there is an increase, compared with normal controls, of the lactate–pyruvate ratio. This finding, however, still awaits full confirmation, for the difference (in the lactate–pyruvate ratio) is seen only when the subjects have been engaged in moderate exercise before the blood samples are drawn. It may be that these serum factors, while responsive to stress in normals, may be greatly increased in schizophrenics subjected to stress. The serum factor apparently influences the stability of the red cell membrane, the rupture of which may alone account for the changes in the lactate–pyruvate ratio.
Broadly, then, the conclusion at this stage is that there is evidence of a plasma protein abnormality in schizophrenia capable of producing measurable behavioral, immunological, electrophysiological, and biochemical responses in suitable test preparations; and that this abnormal constituent may in fact contain a small molecular substance released by, or related to, physiological stress.
There are, however, a number of other small molecules which are increasingly being implicated in the search for a biochemical factor (the so-called psychotoxic factor) in schizophrenia. As early as 1952 Osmond and Smythies pointed out that there is a close chemical similarity between the drug mescaline, derived from a Mexican cactus plant, and epinephrine and its precursor dopamine, both of which are usually found in the brain. Mescaline is a methylated derivative of dopamine. The mental changes produced by mescaline bear some re-semblance to those seen in schizophrenia. The same paper concluded that “it is extremely probable that the final stage in the biogenesis of epinephrine is a transmethylation of norepinephrine, the methyl groups arising from methionine or choline” (a well-known methyl donor). It is just possible that a defective transmethylation of norepinephrine might lead to methylation of one or both of its hydroxyl groups instead of its amino group. This defective methylation could thus give rise to a mescaline-like toxic substance—Thudichum’s “internally fermented psychotoxic.” There is no denying the attractiveness of this hypothesis, for it relates the metabolism of epinephrine, a hormone liberated during stress, to the pathology of a condition in which stress tolerance and responsiveness to stress are markedly altered or reduced.
This suggestion that there may, in schizophrenia, be a disturbance of the transmethylation process is supported by the fact that a number of drugs (such as dimethyltryptamine, DMT) producing pro-found mental changes in man are in fact methylated congeners of normal body metabolites. On the basis of such findings it was indeed suggested by Hoffer and his colleagues (1957) that substances which would compete for methyl groups and act as methyl acceptors could competitively inhibit the abnormal process. The vitamins niacin and niacinamide are such substances, and some beneficial results following the administration of large doses of these vitamins in schizophrenia have been reported (Hoffer et al. 1957). These findings still await confirmation. A more direct approach to the problem was to administer large doses of L-methionine, a powerful methylating agent, and a number of other amino acids to chronic schizophrenic patients (Pollin et al. 1961). The changes seen in some patients following the administration of this material were striking; there was a brief and sharp intensification of the psychotic symptoms. This finding has since been confirmed by three other groups and suggests that methylation of aromatic compounds may indeed lead to substances which greatly affect brain function. another piece of evidence along the same line is the reported occurrence in the urine of schizophrenic patients of a substance 3-4-dimethoxy-phenyl-ethylamine (Friedhoff & Van Winkle 1962), suggested in 1952 by Osmond and Smythies as possibly an abnormally methylated and toxic metabolite. This compound is indeed the dimethyl derivative of dopamine, the precursor of epinephrine, and in structure is closely related to mescaline (the trimethyl derivative of this substance).
It is only fair to say, however, that the finding of this compound in urine is still subject to confirmation. The presence of the compound may be related to dietary factors and there is, so far, only preliminary evidence that the substance identified in the urine is indeed produced in the body. Once again, then, one can but say that we are at the beginning; yet the pieces are showing some fit.
The relation of the midbrain structures and certain elements of the limbic system to the regulation of the visceromotor and affective states has already been mentioned. It is also clear that catecholamines and indoles play a dominant role in these highly specialized and all-pervasive regulatory centers.
The past few years have seen increasing evidence to suggest a possible link between affective disorders (i.e., depression or elation of mood) and changes in the metabolism of catecholamines in the central nervous system. Most of the evidence so far is inferential, yet the advent of pharmacological agents which strikingly affect mood by interfering with the storage, release, and disposition of catecholamines in the central nervous system and at peripheral sites has added an important segment to the body of evidence. [SeeDepressive disorders.]
Quite early it was reported, in a carefully controlled metabolic study, that clinical manifestations of periodic catatonic excitement and stupor were correlated with a change in the nitrogenous constituents of the urine (Gjessing 1938; Gjessing et al. 1958). Longitudinal studies have shown that the urinary excretion of nor epinephrine is increased in the manic phase and decreased in the retarded depression phase in manic–depressive (“cyclic”) patients (Ström-Olsen & Weil-Malherbe 1958). Yet urinary epinephrine represents only a small fraction of the total metabolites of epinephrine. However, it is now possible to study and identify most other breakdown products of epinephrine and to draw up a full balance sheet of catecholamine metabolites in man. Such studies of urinary metabolites in depressed patients and normal controls suggest as a reasonable hypothesis that “some, if not all, depressions are associated with an absolute or relative deficiency of catecholamines ... at functionally important receptor sites in the brain” (Schildkraut 1965, p. 509).
The major inferential evidence so far derives not from physiological studies in the natural un-treated states but from the results of pharmacological intervention. In this respect, three groups of drugs are of particular import, namely, reserpine (a major tranquilizer exerting its effect by depleting serotonin and norepinephrine sites in the brain and peripheral sites); the monoamine oxidase inhibitors, which are powerful antidepressants and inhibit the destruction of naturally occurring amines (epinephrine, serotonin, and the like) by oxidation; and various imipramine-like compounds which, in a way not yet clearly understood, interfere with the local economy of catecholamines at intracerebral sites. Reserpine has been found to induce severe depression in patients, yet whether reserpine-induced depression is a valid pharmacological model of the naturally occurring clinical state remains to be seen. In animals, reserpine induces sedation, which is associated with a decrease in the brain levels of norepinephrine, dopamine, and serotonin. The level of sedation correlates well with the depletion of catecholamines in the brain and, furthermore, shows a rise in level of catecholamines with a return of normal motor behavior. Furthermore, the administration of dihydroxy-phenylalanine and dopamine promptly reverses the reserpine-induced sedation in animals and restores normal behavior and norepinephrine level, A while an administration of the corresponding serotonin precursor (5-hydroxy-tryptophan) does not. In man, dopamine has been reported to counteract the sedating effect of reserpine. Thus catecholamine depletion (i.e., depletion of dopamine, epinephrine, and norepinephrine) may be of major importance in reserpine-induced sedation in animals; reserpine-induced depression in man may possibly have a similar basis.
The gross picture is reversed for the antidepressive agents. Administration of monoamine oxidase inhibitors, such as iproniazid, and other clinically effective antidepressives both produced behavioral excitation in animals and correlated well with elevated levels of brain norepinephrine. The behavioral stimulation is less related to an elevation of brain serotonin. The mood-elevating properties of amphetamine (benzedrine) are well known. It may be that amphetamine acts by releasing active norepinephrine from its anchoring sites. Furthermore, the “rebound” effect following amphetamine intoxication (which shows clinically in depression) is reflected in a temporary depletion of norepinephrine stores available for continued release. Imipramine, another antidepressant, does not inhibit the enzymes involved in metabolic reactivation of norepinephrine and may interfere with the uptake of norepinephrine into peripheral tissue. There is also some evidence that imipramine inhibits norepinephrine uptake in the brain.
These findings are indicative of the kind of sub-cellular organization that one is compelled to consider. Little is known as yet of the physiological (rather than pharmacological) factors which govern the storage and release of substances at these subcellular sites. One would naturally suspect ionic shifts, although evidence in this respect so far is very circumstantial. The metallic ion lithium is used in the treatment of manic behavior. Evidence of the role of hormones in these transactions is also at present hardly more than suggestive. There is, however, a respectable body of evidence recently reviewed (Ramey & Goldstein 1957) which indicates a close physiological interaction between the adrenocortical steroids and the catecholamines. The two groups of stress hormones would seem to operate physiologically as one functional unit, the steroids maintaining the integrity and responsiveness of tissues in the process of reacting to norepinephrine. Indeed, many actions of epinephrine, norepinephrine, and dopamine are not elicitable in the absence of steroids. Equally, and perhaps more significantly, many actions attributable to the steroids may in fact be more accurately ascribed to the catecholamines. There is some clinical data available on the relation of plasma hydrocortisone levels to mood. There is, for example, a significant linear relationship between an increase in anxiety, anger, and plasma hydrocortisone levels; moreover, and perhaps less expected, severe depression is accompanied by elevated plasma hydrocortisone levels; and deeply retarded underactive patients show hormone levels higher than those of less depressed groups. Depression would thus appear to be an active stress response; the retarded tearless state, the final phase of an active, adaptive process. This phase is largely inhibitory, in contrast with the excitatory component commonly seen in the so-called agitated depressive syndromes. It would be idle to speculate at present on the possible effects of various degrees of adrenocortical mobilization on the binding and releasing of epinephrine and norepinephrine in trigger areas of the brain. It may even be that the reverse is true and that the differential proportion of amines in the brain may affect the degreeof adrenocortical mobilization.
In closing, however, it would be safe to surmise that affective behavioral responses may have pecu-liar chemical topology in some nodal areas of the brain and that some small molecules, particularly catecholamines and indoles, may by virtue of differential storage, release, and disposition determine the particular pattern of response which is selected by the organism in the light of adaptive need. The affective responses are very simple and are relatively stereotyped. The symbols which produce them are infinitely more complex. We do not know what factors go into determining the responsiveness of the affective apparatus during an early developmental period, i.e., how much depends on certain genetic “givens” (enzyme proteins); how much is learned (incorporated into the plastic biological system during an early developmental period). Yet even in this area there is some suggestive evidence. For example, animals reared in isolation show a different pattern in the metabolism of actively labeled dopamine from animals which are forced to interact (Welch & Welch 1965).
Could, one might ask, the coldness and unresponsiveness of the sociopath have a biochemical basis? Could such an understanding yield, in time, appropriate additive therapies? Could learning be modified by chemical means, even in the adult? Could the affective disorders yield to specific chemo-therapy? Is there a rational basis for a so-called biological theory of the schizophrenias? More important, could the slowly evolving principles of psychobiology be applied equally to states of mental well-being and ill-being? We know little about the physiology of these states, yet it is clear that whatever direction neurobiology takes, it cannot go it alone. It deals with the machinery and not with information; information is symbolic and social. Whatever hopes there may be for the brain sciences, they remain inseparable from education and social change. Human development, human learning, human communication, human social-field dependence remain the heart of the study of mental health. In these, the neurobiologist must take his modest place.
[Directly related are the entries Drinking and al-coholism, article onpsychological aspects; Drugs, articles onpsychopharmacologyanddrug addiction: organic and psychological aspects; Evolution, article onevolution and behavior; Genetics, article ongenetics and behavior; Learning, article onneurophysiological aspects; Mental disorders, treatment of, article onsomatic treatment. Other relevant material may be found in Anxiety; Depressive disorders; Drives, article onphysiological drives; Emotion; Homeostasis; Infancy, article onthe effects of early experience; Mental retardation; Nervous system; Schizophrenia; Senses; Stress.]
Bishop, M. P. 1963 Effects of Plasma From Schizo-phrenic Subjects Upon Learning and Retention in the Rat. Pages 77–91 in Robert G. Heath (editor), Serological Fractions in Schizophrenia: A Research Symposium. New York: Harper.
Conference on Neuropharmacology, Fourth, September 25–27, 1957, Princeton, N.J. 1959 Neuropharmacology: Transactions. Edited by Harold A. Abramson. New York: Josiah Macy, Jr. Foundation.
Elkes, J. 1966 Psychoactive Drugs: Some Problems and Approaches. Pages 4–21 in P. Solomon (editor), Psychiatric Drugs. New York: Grune.
Fessel, W. J.; and Grunbaum, B. W. 1961 Electrophoretic and Analytical Ultra-centrifuge Studies in Sera of Psychotic Patients: Elevation of Gamma Globulins and Macroglobulins, and Splitting of Alpha Globulins. Annals of Internal Medicine 54:1134–1145.
FØlling, A. 1934 Excretion of Phenylpyruvic Acid in Urine as Metabolic Anomaly in Connection With Imbecility. Nordisk medicinsk tidskrift (Stockholm) 8:1054–1059.
Friedhoff, A. J.; and Van Winkle, E. 1962 The Characteristics of an Amine Found in the Urine of Schizophrenic Patients. Journal of Nervous and Mental Disease 135:550–555.
Frohman, Charles E. et al. 1960 Further Evidence of a Plasma Factor in Schizophrenia. A.M.A. Archives of General Psychiatry 2:263–267.
German, G. A. 1963 Effects of Serum From Schizophrenics on Evoked Cortical Potentials in the Rat. British Journal of Psychiatry 109:616–623.
Gjessing, L.; Bernhardsen, A.; and FrØshaug, H. 1958 Investigation of Amino Acids in a Periodic Catatonic Patient. Journal of Mental Science 104:188–200.
Gjessing, R. 1938 Disturbances of Somatic Functions in Catatonia With a Periodic Course, and Their Compensation. Journal of Mental Science 84:608–621.
Green, J. D. 1964 The Hippocampus. Physiological Re-views 44:561–608.
Haddad, R. K.; and Rabe, Ausma 1963 An Antigenic Abnormality in the Serum of Chronically 111 Schizophrenic Patients. Pages 151–157 in Robert G. Heath (editor), Serological Fractions in Schizophrenia: A Research Symposium. New York: Harper.
Heath, R. G. et al. 1958 Behavioral Changes in Non-psychotic Volunteers Following the Administration of Taraxein, the Substance Obtained From Serum of Schizophrenic Patients. American Journal of Psychiatry 114:919–920.
Hoffer, A. et al. 1957 Treatment of Schizophrenia With Nicotinic Acid and Nicotinamide. Journal of Clinical and Experimental Psychopathology 18:131–158.
Jervis, G. A. 1953 Phenylpyruvic Oligophrenia Deficiency of Phenylalanine-oxidizing System. Society for Experimental Biology and Medicine, Proceedings 82: 514–515.
Kety, Seymour S. 1959 Biochemical Theories of Schizophrenia. Science New Series 129:1528–1532, 1590–1596.
Kety, Seymour S. 1960 Measurement of Local Blood Flow by the Exchange of an Inert, Diffusable Substance. Volume 8, pages 228–236 in Methods in Medical Research. Edited by H. D. Bruner. Chicago: Year Book Publishers.
Kety, Seymour S.; and Schmidt, C. F. 1948 Nitrous Oxide Method for the Quantitative Determination of Cerebral Blood Flow in Man: Theory, Procedure and Normal Values. Journal of Clinical Investigation 27: 476–483.
Levi-Montalcini, Rita; and Angeletti, Pietro U. 1961 Biological Properties of a Nerve-growth Promoting Protein and Its Antiserum. Pages 362–377 in International Neurochemical Symposium, Fourth, Varenna, Italy, 1960, Regional Neurochemistry; the Regional Chemistry, Physiology, and Pharmacology of the Nervous System: Proceedings. Edited by Seymour S. Kety and Joel Elkes. New York: Pergamon.
Nauta, W. J. 1958 Hippocampal Projections and Related Neural Pathways to the Mid-brain in the Cat. Brain 81:319–340.
Osmond, H.; and Smythies, J. 1952 Schizophrenia: A New Approach. Journal of Mental Science 98:309–315.
Penrose, Lionel; and Quastel, Juada H. 1937 Metabolic Studies in Phenylketonuria. Biochemical Journal 31:266–274.
Persky, H. et al. 1958 Relation of Emotional Responses and Changes in Plasma Hydrocortisone Level After Stressful Interview. A.M.A. Archives of Neurology and Psychiatry 79:434–447.
Pollin, William; Cardon, Philippe V. JR.; and Kety, Seymour S. 1961 Effects of Amino Acid Feedings in Schizophrenic Patients Treated With Iproniazid. Science New Series 133:104–105.
Pribram, K. H.; and Kruger, L. 1954 Functions of the “Olfactory Brain.” New York Academy of Sciences, Annals 58:109–138.
Ramey, E. R.; and Goldstein, M. S. 1957 The Adrenal Cortex and the Sympathetic Nervous System. Physiological Reviews 37:155–195.
Rodnick, E. H.; and Shakow, D. 1940 Set in the Schizophrenic as Measured by Composite Reaction Time Index. American Journal of Psychiatry 97:214–225.
Schildkraut, Joseph J. 1965 The Catecholamine Hypothesis of Affective Disorders: A Review of Supporting Evidence. American Journal of Psychiatry 122: 509–522.
Sokoloff, Louis; and Kaufman, Seymour 1959 Effects of Thyroxine on Amino Acid Incorporation Into Protein. Science New Series 129:569–570.
Ström-Olsen, R.; and Weil-Malherbe, H. 1958 Humoral Changes in Manic–Depressive Psychosis With Particular Reference to the Excretion of Catechol Amines in Urine. Journal of Mental Science 104: 696–704.
Thudichum, John W. L. 1884 A Treatise on the Chemical Constitution of the Brain. London: Ballière.
Wallace, H. W.; Moldave, K.; and Meister, A. 1957 Studies on Conversion of Phenylalanine to Tyrosine in Phenylpyruvic Oligophrenia. Society for Experimental Biology and Medicine, Proceedings 94:632–633.
Welch, Bruce L.; and Welch, Ann Marie 1965 An Effect of Aggregation Upon the Metabolism of Dopamine-1-H3. Pages 201–206 in Symposium on Binding Sites of Brain Biogenic Amines, Galesburg, III., 1963, Biogenic Amines. Progress in Brain Research, Vol. 8. Amsterdam: Elsevier.
Woolf, L. I.; and Vulliamy, D. G. 1951 Phenylketonuria With Study of Effect Upon It of Glutamic Acid. Archives of Disease in Childhood 26:487–494.
“Epidemiology” refers to the science which studies “the mass phenomena of disease” (Greenwood 1935) by determining the distribution of conditions or diseases and the factors which determine these distributions (Lilienfeld 1959); that is, it is “the study of the distribution and determinants of disease prevalence in man” (MacMahon et al. 1960). The analysis that epidemiology makes of these findings results in a “medical ecology” (Gordon 1952). Epidemiology relates observed distributions of disorders to the environments in which people live—the physical, biological, and social environments.
“Mental disorder” is used in this article to refer to the full range of psychic conditions identified by psychiatrists or competent social authorities as abnormal or needing improvement. This is a broader range than would be used in planning or conducting any single inquiry but permits consideration, where necessary, of studies of delinquency, criminality, military desertion, and group fads (such as fish swallowing), as well as any conventional psychiatric diagnostic category or an individual symptom or special syndrome recognized in psychiatry.
Uses of epidemiology
Seven uses of epidemiology can be distinguished (Morris 1957): (1) knowledge regarding historical trends helps to distinguish disorders that are on the increase from those that are disappearing; (2) community diagnosis of the size, location, and distribution of a condition aids in planning health programs for the community; (3) from accumulated records of the ages at which individuals contract a disease, individual risks can be calculated (a basic tool in calculating insurance premiums), and knowledge of contingency risks aids in estimating the effects of host factors in determining the distribution of cases; (4) knowledge of the attributes of cases not in treatment enlarges the clinical picture by making our concept of a disorder less dependent on the clinician’s limited perspective on cases; (5) occasionally, new syndromes are identified because clinically dissimilar cases are found to arise from a particular common background or because clinically similar cases are found to arise in two or more distinct sets of circumstances; (6) the working of health services can be studied in terms of their successes and failures, their selection of cases for treatment, and their deleterious effects on the people they seek to serve; and (7) in the search for causes of disorders, data on the factors associated with the distribution of a disorder supplement laboratory and clinical data in the elucidation of causal mechanisms—at times the crucial breakthrough in our understanding of the way in which a condition is caused is made by epidemiological inquiry (this occurred with cholera, pellagra, and lung cancer).
Historical trends are important but difficult to study. The Group for the Advancement of Psychiatry reviewed psychiatric knowledge recently (1961). The use of old data gathered for another purpose is sometimes tried. It is difficult to identify two groups at two different points in time which can be considered different time samples of the same population. If the questions are asked broadly enough and if the population being considered has some sort of continuing dimensions, an approximation of trends can sometimes be established. Two studies are noteworthy because they are particularly well done.
Goldhamer and Marshall (1949), in a superb study of the admission of psychotics to mental hospitals in Massachusetts during a hundred-year period, found evidence to contradict the widely held view that schizophrenia is becoming more common. In spite of the work’s excellence, the implications of the findings remain uncertain, mainly because the data depend entirely on records of cases admitted to mental hospitals and because the population “sample” was taken from an area (Massachusetts) that was the first in North America to be industrialized and was subject to gross emigration and immigration during the time period observed.
With the hope of showing that an inverse relationship between intelligence and fertility was leading to a decrement in the national average intelligence quotient (IQ), a survey of Scottish intelligence tested “all” 11-year-olds on one day in 1930 and repeated almost the same procedure on one day in 1949. The findings were negative, according to the publications (Scottish Council for Research in Education 1953), but reinterpretation of the differences between the methods used in the two surveys suggests that the prevalence of very low scores among Scottish 11-year-olds may actually have decreased (Gruenberg 1964).
Many studies of particular communities have been carried out for diagnostic purposes; some outstanding examples are mentioned later in this article, in the section on case-finding methods. Since community diagnosis, by its nature, is done for a particular community, it is no more reasonable to borrow the diagnosis of one community and apply it to another than to borrow a neighbor’s X ray because he had a similar cough. The general picture will be more or less the same, but the details which differentiate one community from the other may be crucial. Techniques for making rapid and relevant surveys of communities to aid mental health planning are sadly lacking. A few demographic facts are often used (as in the American Psychiatric Association’s consultations) to infer what the findings would be.
From the health service’s point of view, enumeration of cases that do not distinguish preventable or curable conditions from nonpreventable or noncurable cases are of little value. One learns only that the problem is small, big, very big, or enormous, depending on how one defines the problem. The American Public Health Association’s Mental Disorders (1962) is a milestone because it indicates the conditions for which it is currently important to be able to enumerate cases. As the technology of treatment and prevention grows, this list will grow. This analysis also indicates that the social-breakdown syndrome is important in evaluating the benefits of a comprehensive community mental health service (e.g., Gruenberg 1966). Similarly, future studies for community diagnosis, as well as for analysis of health services, will require techniques for counting cases of conditions for which something can be done.
The calculation of individual risks
The risk of a child’s being Mongoloid is dependent on its mother’s age at the time of birth, but not its father’s (Penrose 1949). If a woman has German measles while pregnant, there is an increased risk of her child’s being brain-damaged; this increased risk is highest if the infection occurs during the third month of pregnancy (Hill et al. 1958). If a young child is removed from his parental home for months, there is an increased risk of nightmares, bed-wetting, and some other neurotic symptoms; if the mother leaves the child’s home for several months, the increased risk is much less or non-existent (Douglas & Blomfield 1958, pp. 112-113).
Calculating individual risks is frequently helpful; it should not be confused with measuring the incidence of a condition (number of new cases arising during a unit of time in a defined population, divided by the number of people in the defined population), or with measuring the prevalence (number of cases present at one point in time in a defined population, divided by the number of persons in that population at that point in time).
Enlarging the clinical picture
The clinical picture of a condition is almost automatically enlarged by follow-up studies. Follow-up studies of persons identified at about the age of 12 or 13 as mentally retarded are needed now because many cross-sectional prevalence studies have shown an age distribution of cases indicating a rapid fall in prevalence after age 14 that is incompatible with the definition of the condition, which includes the concept of a fixed, permanent state. [See Mental Retardation.]
The Medical Research Council Unit for Research on the Epidemiology of Psychiatric Illness provides psychiatric care in a general hospital ward in Edinburgh to which are routinely brought, regardless of severity, all self-poisoning cases in the city of Edinburgh. This comprehensive experience has made the clinicians aware of self-poisoning cases with intent at self-destruction by people who do not exhibit evidence of any psychiatric disorder; they find that the severity of need for psychiatric attention has no relation to the probability that the self-poisoning would lead to death. Thus, looking at all cases of self-poisoning is beginning to provide a different picture of the range of clinical findings.
The study of population distributions of cases resulted in separating typhus (“jail fever”) from typhoid (water- and food-borne). Psychiatry has not made progress this way. Yet, certain diagnostic categories have been set up in terms of the age or personal characteristics or situations of the cases (e.g., involutional melancholia, combat fatigue, dementia praecox, senile dementia); such a classification short-circuits epidemiological inquiry. The course of disorders has been a key criterion in characterizing manicdepressive psychoses, dementia praecox, and mental retardation. Patients discourteous enough to violate the rules have simply had their diagnoses changed. Such practices hinder progress. ’Puerperal psychoses’ have been in and out of fashion, but pregnancy has not yet been shown to be associated with psychoses (Pugh et al. 1963). Involutional melancholia is confined to certain age levels and is out of favor at present. These illustrations indicate the special problems of classification in psychiatry, where entities like the Ganser syndrome in prisoners and combat fatigue in soldiers gain currency in each generation.
The social-breakdown syndrome is a new sociogenic entity. Its identification arose from observations that can be loosely termed clinical epidemiology (Pickles 1939). A community served by a single mental hospital that undergoes radical reform of patient care and breaks down barriers between hospital and community services stops producing new cases of severely deteriorated, helpless, vegetating individuals. Similar reforms elsewhere lead to similar observations.
As a result of these observations, clinicians with a broad (population) perspective change their views of the disorders. Disturbances in capacities to fill social roles come to be seen as extrinsic to the mental disorders of the patients and of secondary importance in comparison with the society’s customs and attitudes regarding mental disorders which result in rejections and degrading behavior toward the ill. This sequence of observations leads to a reformulation of clinical syndromes that puts together manifestations previously thought to be due to several different disorders and that attributes these manifestations to a series of particular social events likely to occur in the presence of any of these disorders.
Like any other conclusion derived from unsystematic observations, it may gain currency because it fits the prevailing preconceptions of many people, without being further established. Unless systematic evidence is obtained, its validity remains untested.
The new sociogenic social-breakdown syndrome is best examined as a promising hypothesis. In order to test the sociogenic hypothesis, the syndrome must be defined operationally and case-finding techniques developed. These must be kept separate from the specification of the social conditions suspected of favoring the syndrome’s appearance. Recent investigations have shown that these are soluble problems and confirm the hypothesis in large part; further investigation will also make clearer which mental disorders make people particularly susceptible to the noxious social forces [Gruenberg 1966; see also Psychiatry,article on Social psychiatry].
Working of health services
Much of the data gathered on the distribution of mental disorders can be studied to help us understand how hospitals and clinics work. This can be a productive approach to data gathered for other uses. When a population is surveyed for cases similar to those that have gone to a hospital, many unhospitalized cases are found. This suggests that social forces control ad-missions; if so, these social forces may account partly, or entirely, for variations in admission rates. This proved to be a productive hypothesis in studying the distribution of admissions for the elderly (Mental Health Research Unit 1959-1960) and could be used to interpret many findings (e.g., Faris and Dunham 1939; Goldhamer and Marshall 1949). Readmission rates can also be looked at this way. Freeman and Simmons (1963) found that the types of homes to which mental hospitals released patients did not affect the probability of return to the hospitals; from this they concluded that reasons for rehospitalization are unrelated to the social environment. However, the same data can be approached by starting with the assumption that a hospital staff releases only certain patients and, in deciding which to release, takes the family situation into account; if this is true, the data can be used to argue that the observed lack of difference only shows that the various staffs are equally competent in evaluating the suitability of different types of homes for their patients.
Thus, the plan to see whether variations in home living arrangements affect the probability of rehospitalization by studying a cohort of patients released from hospitals to varying home situations is irrelevant to the question. The plan is suitable for an evaluation of the hospitals’ release policies with regard to different types of home situations. Obviously, volunteer subjects cannot be assumed to be randomly selected subjects; it is just as important—but sometimes more difficult—to perceive that subjects have been selected by someone else or by some agency. It is necessary to realize that when a bureaucracy selects subjects, the data reflect the behavior of the bureaucracy. The same principle applies to analysis of first mental-hospital admission rates.
The most important studies of health services are those which are carried out in the form of a preventive trial when the health services seek to prevent a particular disorder. The population given the service is selected so that there is a comparable control population to whom service is not given (Pasamanick et al. 1964). The study then becomes a crucial experiment for the health service; it can also be a crucial experiment, if all goes well, for testing an etiological hypothesis. The preventive trial is often thought to represent the last stage of inquiry and to be justified only when much other evidence has been accumulated. But when the preventive procedure advocated is believed to be harmless and generally thought to be desirable and when its supply cannot satisfy all demands, the preventive trial is justified even if prior evidence is very weak. It is wrong to assume that preventive trials are inherently more expensive, more dangerous, or more difficult than passive studies; such research can be easier and cheaper. However, creating the opportunity for preventive trials and ascertaining that the design of the study is being adhered to throughout pose difficult problems.
The search for causes
Each use described above generates data with implications for causes. Outstanding today are the efforts to identify the mechanisms which lead to what Pasamanick has called the “continuity of fetal damage,” ranging from death to mild brain damage followed by reading disabilities, impulsive behavior disorders, and other syndromes. Fetal damage has been linked to rubella, to the effects of poverty, and to early complications of pregnancy. Several lines of evidence suggest its linkage to very mild or moderate malnutrition of the mother during the first few months of gestation (MacMahon & Sowa 1961).
The hypothesis of schizophrenogenic mothering is being pursued (Lidz & Fleck 1960). Current work is clarifying the nature of the hypothesis and may do more [see Schizophrenia].
Maternal deprivation, as Bowlby (Bowlby et al. 1956) named a hypothetically pathogenic experience, has been investigated a number of times (e.g., Douglas & Blomfield 1958). These studies, like those of Pasamanick, not only look for causes but relate dissimilar clinical syndromes to one set of causes. Many investigations are required before the relationships become clarified and before the credibility of the hypothesis can be appraised. Bowlby’s own study has weakened the initial hypothesis. Hunt (1965) has recently pointed to some further weaknesses in the hypothesis [see Infancy,article on THE Effects of Early Experience].
Down’s syndrome (Mongolism, trisomy-21) is not only a major cause of serious mental handicap, but the new and growing knowledge regarding the associated chromosomal abnormality supports the notion that some particular cause or group of causes must be at work and that other chromosomal abnormalities may have the same causes. It is complicated to investigate these conditions, and social phenomena have not yet been implicated.
Too often efforts to find the determinants of the distribution of a mental disorder are launched as one-shot investigations, without the researchers’ knowing what the distribution of cases is. This procedure assumes that if the distribution is found to be that predicted in the hypothesis, then the hypothesis has been proved, and if not, then it has been disproved. Such a course is not absolutely doomed to failure, but it is not likely to lead to the gathering of data that can rule out alternative explanations of the observed distributions.
Tools and techniques
Hospital and state school records, clinic outpatient records, records of private practitioners, and key-informant methods have all been used repeatedly in case finding.
Hospital records have been used to study firstadmission rates in relation to various hypotheses. Faris and Dunham (1939) pioneered the analysis of first-admission rates in terms of the modern social ecology of a city. Using the census-tract classification of Chicago, based on the University of Chicago sociology department’s methods of characterizing urban land use, they allocated the first admissions to mental hospitals to the census tract of origin. They predicted correctly the now wellestablished fact that the first-admission rates for schizophrenia are highest in the central, deteriorated section of the city and decline with the distance of neighborhoods from the center. This was a startlingly successful fusion of Durkheim’s ideas, urban sociology, and a hypothesis about the social origins of schizophrenic syndromes. Even more startling were the failure of manic-depressive psychoses to fall into such a pattern and the existence of a different pattern for organic psychoses. These different patterns tend to confirm the importance of the psychiatric diagnosis in spite of the skepticism of many psychiatrists regarding the objective nature of their diagnoses.
These findings have been confirmed in other cities. A literature has developed seeking to account for the high first-admission rates of schizophrenics from the city’s center. The straightforward notion that the depersonalized, socially isolated part of the city favored the development of schizophrenic disorders has not been universally accepted. Attempts to demonstrate that the disproportionate concentration of schizophrenic cases coming to hospitals from the central part of the city is due to consequences of schizophrenic disorders rather than the pathogenic nature of these neighborhoods can be thought of as studies of the “drift hypothesis.” This states that schizophrenics tend to drift into the rooming-house areas of cities at a higher rate than do other people, producing the concentration of cases found there.
Sanua (1963) points to the main studies of this hypothesis and to the conflicting evidence, citing Morrison’s (1959) finding that patients had a lower social-class status than their fathers, whose social-class distribution was similar to that of the general population. The inference that schizophrenia causes downward social mobility does not necessarily follow from this observation; since occupational levels tend to rise with age, schizophrenics may accumulate in lower occupational categories because they fail to climb the occupational ladder as fast as other young people.
If downward mobility (or failure to rise with one’s generation) is really at the root of the phenomenon, then the etiological theory advanced by Faris and Dunham does not hold. Their observations would remain, however, and require explanation.
A more recent study, Social Class and Mental Illness, by Hollingshead and Redlich (1958), found that in New Haven the prevalence of treated cases was related to social class. The authors asserted that their data show a gradient of prevalence rates which falls from a high rate in the lowest social class to a low rate in the upper social classes. Miller and Mishler (1959), however, state (correctly, I believe) that the New Haven data show only a very high rate for the lowest social class and that the observed figures in other classes do not demonstrate a gradient of rates.
The difficulties of interpreting such studies are compounded by the reliance of the studies on clinical records of cases in treatment and by the social factors affecting hospital-utilization patterns. To obviate the weaknesses of relying solely on clinical records, a method centering on a structured household-interview questionnaire derived in part from the Cornell neuropsychiatric inventory has been developed; this method has not yet been systematically calibrated (Macmillan 1959), but it holds out a promising potential. Its first important use for case finding on a large scale was by Stouffer (Stouffer et al. 1949) in World War II. It was one of the methods used in the first large-scale metropolitan survey, the Midtown Manhattan Study (Langner & Michael 1963).
One population of over two thousand has been personally interviewed by psychiatrists at both the beginning and the end of a decade (Essen-Moller 1956). Participant-observers with a psychiatric background have been useful (e.g., Eaton 1955).
Finding cases of severe deterioration (severe social-breakdown syndrome) has been carried out by means of a semistructured interview by specially trained public health nurses, psychiatric social workers, and graduate behavioral-science students. Another method involves interviewers’ filling out structured questionnaires—together with answers to open-ended questions—after they have been trained to complete the protocols following open-ended interviews; these protocols are then evaluated by psychiatrists, who categorize the individuals (Mental Health Research Unit 1959-1960). A method similar in principle was used in the following years in the age groups under 60 in Stirling County and in midtown Manhattan (A. Leighton 1959; Hughes et al. 1960; D. Leigh ton et al. 1963; Langner & Michael 1963).
Cases derived from nonmedical-service-agency records were identified by Lemkau and associates (1941-1942) in the Eastern Health District in Baltimore and in the survey of the mentally retarded in Onondaga County, New York State, by the Mental Health Research Unit staff, under the direction of the program director (Goodman et al. 1956). All of these are useful devices. In practice all are complicated to use and none are easily applied with precision and accuracy. None of them have been adequately calibrated against a standardized ultimate criterion. Such a criterion requires a set of explicit objective criteria for identifying a case, a standardized method of observation, and an estimate of observer variability (Cochrane et al. 1951).
The methods of household sampling of populations, highly developed by social scientists, have been used in a number of studies; their most extensive use currently is in the continuous National Health Survey (U.S. National Health Survey 1958).
The use of statistical techniques in planning and interpreting studies has developed to a very high level, borrowing from general statistical theory, agricultural research, genetic research, social science, and economics. Epidemiologic inquiries have contributed devices for age standardization and for adjustment of data, which have in turn been used by those fields (Hill 1937).
The study of case aggregations in neighborhoods, households, and families has developed a whole series of techniques. Some of these depend on the concept of primary-case (or proband) rates and secondary-case rates. In the study of mental dis-orders this has been most frequently associated with genetic hypotheses, and in these instances the concept of lifelong expectation of manifesting the disorder has been developed. In this field the formulas of Wilhelm Weinberg and the mathematician G. H. Hardy (1908) and of Stern (1943) are particularly appropriate. They depend, however, on estimates of differential death and migration rates, whose validity is hard to judge from existing data. The study of familial and household aggregations is not confined to genetic hypotheses, however, as is shown in a review of the literature (Gruenberg 1950) and by Bleuler’s review of studies on schizophrenia (1955); a review of the knowledge regarding group disorders brings together concepts from psychiatry, social psychiatry, and social psychology (Gruenberg 1957).
Populations have commonly been characterized by age and sex and time ever since the Hippocratic writings on times, places, and persons. Variations in incidence and prevalence rates by age and sex are frequently interpreted as though age and sex were causative factors. Generally they are not mechanisms by which disorders are produced but convenient ways of classifying populations which develop disorders at different rates. The suspected mechanisms which are distributed according to age and sex also need to be looked into, as was done recently by Langner and Michael (1963). Categorizing the population according to previous illnesses is a frequent but not highly standardized procedure. Except for body typing, the categorizing of populations according to physical characteristics has not been used in inquiries regarding mental disorders. Studies attempting to link genetic characteristics to certain disorders have focused on blood types. It is to be expected that in the next decade other physical characteristics will prove relevant to mental disorder epidemiology. Categorizing populations by their social characteristics is almost standard nowadays in epidemiological inquiry in all fields. The social environment has usually been regarded as important by epidemiologists, and this recognition has been increased greatly by advances in methods of characterizing socioeconomic status and other social variables. The complexity of socio-economic classifications in a rapidly changing society has made this type of categorizing hard to standardize; attention will probably become more focused on specific characteristics of individuals, some of which are incorporated into indices of socioeconomic status. One study showed that hospital-admission rates for elderly persons were un-related to economic levels of neighborhoods but were closely related to the frequency of multiple-family dwellings in neighborhoods; yet no correlations with socioeconomic status (a composite index) could be found [see Gruenberg 1953; see also Aging].
The conduct of studies
The list of references makes it clear that contributions to the epidemiology of mental disorder have been made by workers with various professional backgrounds; there is no reason to expect this to be altered in the future. Technical expertness in such work does not develop from any one course of professional training but is acquired by experience in conducting and interpreting the findings of investigations. Too many investigations have been conducted with the hope of testing a hypothesis about the determinants of the distribution of a disorder in a single investigation. The opportunity for refining a hypothesis and going back with experienced investigators to the same population rarely occurs. But such steps can be expected to yield larger returns in knowledge than a proliferation of single investigations. These defects in the social organization of research are being rectified by the creation of permanent laboratories for conducting investigations.
The first such laboratory was created at Syracuse, New York, in 1950, on a pilot basis, by the New York State Department of Mental Hygiene and was made permanent in 1955. Since then the Medical Research Council of Great Britain has created one in the University of Edinburgh department of psychiatry; the Danish government has set up one at Aarhus; and the Swedish government, one at Lund. The U.S. National Institute of Mental Health finances one at the Columbia University department of psychiatry.
These improvements in social support should lead to a more rapid exploitation of advances as they are made and thus should speed up the acquisition of knowledge. But it is to be expected that a larger number of contributions to our understanding of mental-disorder epidemiology will continue to come from workers who are not labeled epidemiologists and who will in many instances not regard their work as particularly relevant to mental health. The epidemiologist will continue to be interested in getting answers to his questions and will, hopefully, judge new contributions on their merits rather than on their author’s school of thought or previous conditions of servitude (i.e., degree sequences).
In the context of this encyclopedia it may be well to point out that all disorders, whatever the causes, have distributions that reflect social factors. This universal proposition follows from the simple fact that all classes of causes have such social distributions.
For example, Goldberger (1964) showed that pellagra is due to a nutritional deficiency by studying its incidence in different social groups in southern mill towns. MacMahon and Roller (1957) showed that the higher leukemia death rate among whites, as compared to nonwhites, may well be due to more exposure to diagnostic radiation among Jews (who apparently use medical specialists at a higher rate). Gelfand and his associates (1957) showed that naturally acquired immunity to polio viruses occurs at early ages most frequently in low-income groups. Book (1961) reviewed accumulations of genes in particular linguistic and social groupings.
Roueche (1954) describes how poisons can spread through socially isolated parts of a population.
Sometimes the social forces are considered the main factors (as in “diseases of poverty” and in “diseases of affluence,” such as coronary heart disease) and sometimes the intermediate variables that help unravel the chain (as in pellagra). But in understanding every distribution of disorders, knowledge of social forces plays some role.
[Directly related are the entries Epidemiologyand Public HEALTH. Other relevant material may be found in Population; Psychiatry; Sample SURVEYS.]
American Public Health Association, Technical Development Board, Program Area Committee ON Mental Health 1962 Mental Disorders: A Guide to Control Methods. New York: The Association.
Bleuler, M. 1955 Research and Changes in Concepts in the Study of Schizophrenia: 1941-1950. Isaac Ray Medical Library, Bulletin : 1-132.
Böök, Jan A. 1961 Genetical Etiology in Mental Illness. Pages 14-45 in Milbank Memorial Fund, Causes of Mental Disorders: A Review of Epidemiological knowledge, 1959. New York: The Fund.
Bowlby, John et al. 1956 The Effects of Mother-Child Separation: A Follow-up Study. British Journal of Medical Psychology 29:211-247.
Cochrane, A. L.; Chapman, P. J.; and Oldham, P. D. 1951 Observers’ Errors in Taking Medical Histories. Lancet 1B:1007-1009.
Douglas, James W. B.; and Blomfield, J. M. 1958 Children Under Five. London: Allen & Unwin.
Eaton, Joseph W. 1955 Culture and Mental Disorders: A Comparative Study of the Hutterites and Other Populations. Glencoe, III.: Free Press.
Essen-möller, Erik 1956 Individual Traits and Morbidity in a Swedish Rural Population. Acta psychiatrica et neurologica scandinavica Supplement 100.
Faris, ROBERT E. L.; and Dunham, H. Warren (1939) 1960 Mental Disorders in Urban Areas: An Ecological Study of Schizophrenia and Other Psychoses. New York: Hafner.
Freeman, Howard E.; and Simmons, Ozzie G. 1963 The Mental Patient Comes Home. New York and London: Wiley.
Gelfand, Henry M. et al. 1957 Studies on the Development of Natural Immunity to Poliomyelitis in Louisiana. American Journal of Hygiene 65:367-385.
Goldberger, Joseph 1964 Goldberger on Pellagra. Edited by Milton Terris. Baton Rouge: Louisiana State Univ. Press. → Reprint of 17 papers.
Goldhamer, Herbert; and Marshall, Andrew W. (1949) 1953 Psychosis and Civilization. Glencoe, III.: Free Press.→ First published as The Frequency of Mental Disease: Long-term Trends and Present Status.
Goodman, M. B. et al. 1956 A Prevalence Study of Mental Retardation in a Metropolitan Area. American Journal of Public Health. 46:702-707.
Gordon, John E. 1952 The Twentieth Century—Yesterday, Today, and Tomorrow (1920- ). Pages 114-167 in Franklin H. Top (editor), The History of American Epidemiology. St. Louis, Mo.: Mosby.
Greenwood, Major 1935 Epidemic and Crowd Diseases. London: Williams & Norgate.
Group FOR THE Advancement of Psychiatry, Committee ON Preventive Psychiatry 1961 Problems of Estimating Changes in Frequency of Mental Disorders. New York: The Group.
Gruenberg, Ernest M. 1950 Review of Available Material on Patterns of Occurrence of Mental Disorders: Major Disorders. Pages 176-196 in Milbank Memorial Fund, Epidemiology of Mental Disorder. New York: The Fund.
Gruenberg, Ernest M. 1953 Community Conditions and Psychoses of the Elderly. American Journal of Psychiatry 110:888-896.
Gruenberg, Ernest M. 1957 Socially Shared Psycho-pathology. Pages 201-229 in Alexander H. Leighton, John A. Clausen, and Robert N. Wilson (editors), Explorations in Social Psychiatry. New York: Basic Books.
Gruenberg, E,rnest M. 1964 Epidemiology. Pages 259-306 in Harvey A. Stevens and Rick Heber (editors), Mental Retardation. Univ. of Chicago Press.
Gruenberg, Ernest M. (editor) 1966 Evaluating the Effectiveness of Mental Health Services. Milbank Memorial Fund Quarterly 44, no. 1, part 2.
Hardy, G. H. 1908 Mendelian Proportions in a Mixed Population. Science 28:49-50.
Hill, A. Bradford (1937) 1961 Principles of Medical Statistics. 7th ed. London: Lancet.
Hill, A. Bradford et al. 1958 Virus Diseases in Pregnancy and Congenital Defects. British Journal of Preventive and Social Medicine 12:1-7.
Hollingshead, August B.; and Redlich, Frederick C. 1958 Social Class and Mental Illness: A Community Study. New York: Wiley.
Hughes, Charles et al. 1960 People of Cove and Woodlot: Communities From the Viewpoint of Social Psychiatry. The Stirling County Study of Psychiatric Disorder and Sociocultural Environment, Vol. 2. New York: Basic Books.
Hnt, J. McV. 1965 Traditional Personality Theory in the Light of Recent Evidence. American Scientist 53: 80-96.
Langner, Thomas S.; and Michael, Stanley T. 1963 Life Stress and Mental Health. Volume 2 of The Mid-town Manhattan Study. New York: Free Press.
Leighton, Alexander H. 1959 My Name Is Legion: Foundations for a Theory of Man in Relation to Culture. The Stirling County Study of Psychiatric Disorder and Sociocultural Environment, Vol. 1. New York: Basic Books.
Leighton, Dorothea et al. 1963 The Character of Danger. The Stirling County Study of Psychiatric Disorder and Sociocultural Environment, Vol. 3. New York: Basic Books.
Lemkau, Paul; Tietze, Christopher; and Cooper, Marcia 1941-1942 Mental-hygiene Problems in an Urban District. Mental Hygiene 25:624-646; 26:100-119, 275-288.
Lidz, Theodore; and Fleck, Stephen 1960 Schizophrenia, and Human Integration, and the Role of the Mental disorders: Childhood Mental Disorders Family. Pages 323-345 in Don D. Jackson (editor), The Etiology of Schizophrenia. New York: Basic Books.
Lilienfeld, Abraham M. 1959 A Methodological Problem in Testing a Recessive Genetic Hypothesis in Human Disease. American Journal of Public Health 49: 199-204.
Macmahon, Brian; and Roller, Ernest K. 1957 Ethnic Differences in the Incidence of Leukemia. Blood: The Journal of Hematology 12:1-10.
Macmahon, Brian; Pugh, Thomas F.; and IPSEN, Johannes 1960 Epidemiologic Methods. Boston: Little.
Macmahon, Brian; and Sowa, James M. 1961 Physical Damage to the Fetus. Pages 51-110 in Milbank Memorial Fund, Causes of Mental Disorders: A Review of Epidemiological Knowledge, 1959. New York: The Fund.
Macmillan, Allister M. 1959 A Survey Technique for Estimating the Prevalence of Psychoneurotic and Related Types of Disorders in Communities. Pages 203-218 in American Psychiatric Association, Epidemiology of Mental Disorder. Washington: The Association.
Mental Health Research Unit, New York State Department of Mental Hygiene, Syracuse, NEW’ YORK 1959-1960 A Mental Health Survey of Older People. Parts 1-3. Psychiatric Quarterly Supplement 33:45-99, 252-300; 34:34-75.
Miller, S. M.; and Mishler, E. G. 1959 Social Class, Mental Illness, and American Psychiatry: An Exposi-tory Review. Milbank Memorial Fund Quarterly 37: 174-199.
Morris, Jeremy N. (1957)1965 Uses of Epidemiology. 2d ed. Baltimore: Williams & Wilkins.
Morrison, S. L. 1959 Principles and Methods of Epidemiological Research and Their Application to Psychiatric Illness. Journal of Mental Science 105: 999-1011.
Pasamanick, Benjamin et al. 1964 Home vs. Hospital Care for Schizophrenics. Journal of the American Medical Association 187:177-181.
Penrose, Lionel S. (1949) 1963 The Biology of Mental Defect. 3d ed. London: Sidgwick & Jackson. Pickles, William N. 1939 Epidemiology in Country Practice. Bristol (England): Wright; Baltimore: Williams & Wilkins.
Pugh, Thomas F. et al. 1963 Rates of Mental Disease Related to Childbearing. New England Journal of Medicine 268:1224-1228.
Roueche, Berton 1954 Eleven Blue Men. Boston: Little. Sanua, Victor D. 1963 The Etiology and Epidemiology of Mental Illness and Problems of Methodology, With Special Emphasis on Schizophrenia. Mental Hygiene 47:607-621.
Scottish Council FOR Research IN Education, Mental Survey Committee 1953 Social Implications of the 1947 Scottish Mental Survey. Univ. of London Press.
Stern, Curt 1943 The Hardy-Weinberg Law. Science 97:137-138.
Stouffer, Samuel A. et al. 1949 The American Soldier. Studies in Social Psychology in World War II. Vols. 1 and 2. Princeton Univ. Press.→ Volume 1: Adjustment During Army Life. Volume 2: Combat and Its Aftermath.
U.S. National Health Survey 1958 Health Statistics, Series A. Volume I. Washington: Government Printing Office.
Early conceptions of mental disorders in children are reflected in several clinical papers on child-rearing practices from the sixteenth, seventeenth, and eighteenth centuries (see Kessen 1965). These precursors of present ideas about causality failed to receive widespread acceptance and scientific interest, however, until recently. Even Kraepelin’s influential Psychiatric, first published in 1893, did not discuss mental disorders in children in any of its many editions. Scientific interest in deviant mental processes in children has flowered in the twentieth century, stimulated in large part by theories of mental functioning advanced by Freud, Piaget, Watson, and others which emphasized developmental and dynamic factors as well as notions of environment causality and learning. Further, interest in mental disorders in children has increased with the resurgence of scientific interest in children’s behavior in general in the twentieth century, particularly since the late 1940s.
Resources for the diagnosis and treatment of mental disorders in children have multiplied in the United States and in Europe since the 1950s. In the United States, the establishment of the National Institute of Mental Health and the National Institute of Child Health and Development and the allocation of federal funds for the development of plans for organizing and providing comprehensive mental health services in local communities have stimulated the growth of relevant programs of service, professional training, and research. A federally supported conference of professional organizations and interested agencies was held in 1964 to insure and to plan for the provision of diagnosis and treatment of mental disorders in children under federally sponsored community health programs (American Psychiatric Association 1964).
Definition, predisposition, precipitation
The definition of disorders of mental functioning in children varies depending upon one’s conception of mental functioning in general. Most professionals—including psychologists, psychiatrists, and social workers—with special training in the diagnosis and treatment of mental disorders in children currently emphasize a multidimensional approach. This approach encompasses psychosomatic considerations; developmental capacities and vulnerabilities; constitutional and genetic factors; the internal personality system, including cognitive, perceptual, and affective mechanisms and the fluidity and plasticity of the child’s personality characteristics; and psychosocial considerations, including parent—child relationships, family interactions, and sociocultural influences. This approach also stresses the need to assess and capitalize upon the healthy and adaptive facets of the child’s personality.
A conceptual framework which encompasses all of the above aspects of the child’s functioning inclusively and systematically has not been developed. However, the Committee on Child Psychiatry of the Group for the Advancement of Psychiatry has prepared (in unpublished form) what appears to be the best available approximation of such a framework (Committee on Child Psychiatry 1965). The present discussion of mental disorders in children leans heavily upon its work.
Mental disorder can be defined as a failure in the child’s attempt to maintain an adaptive equilibrium between physiological, psychological, and interpersonal systems; there is a close relationship between physical and psychological factors. In the child with certain constitutional or experiential predispositions, disordered mental functioning may be precipitated and sustained by physical, psychological, or social stimuli.
Biochemical stimuli or stressful insufficiencies of chemical substances may disrupt the child’s physiological equilibrium as well as associated perceptual, cognitive, and emotional systems. In addition, the child’s restitutive efforts involve an interaction between physiological, psychological, and social systems.
Stimuli of a psychological nature may also precipitate mental disorder. Such stimuli include conscious or unconscious thoughts and feelings which arouse anxiety in the child because of their association with stressful past or present experiences. They involve the cognitive system in that they are represented in symbolic form in memory and thinking, and the perceptual apparatus. Thoughts, memories, and feelings triggered by anxiety-arousing psychological stimuli lead to the child’s employment of psychological defenses or compensating behaviors as he seeks to avoid a breakdown in adaptation or equilibrium.
Stressful social stimuli in the child’s environment may also precipitate disorder. Such stimuli include the loss, or threat of loss, of close interpersonal relationships and the frustration of basic needs resulting from disturbances in relationships within the family.
The nature and severity of the mental disorder precipitated by physical, psychological, or social stimuli, or of interactions among them, is contingent upon the stressfulness of the stimuli as well as upon genetic and constitutional factors (for example, temperament, body build), previous experience, and the developmental level of the child. Stressful stimuli initially disruptive of one of these systems may, and often do, have repercussions in other systems. Thus mental disorders in children may be precipitated by disruptions of a physical, social, or psychological nature, but the child’s defensive efforts or attempts at restoration of ego functions or compensatory behavior almost always involve all three systems. For example, a stressful thought or fantasy may lead to emotional conflict which triggers “signal anxiety.” This signal, warning of possible breakdown in adaptation or mental equilibrium, leads to the establishment of psycho-logical defenses or adaptive interpersonal behaviors. If emotional conflict and anxiety are severe or become chronic, physiological concomitants may develop. Such physiological symptoms are reversible if the underlying emotional conflicts are resolved; chronic unresolved conflict and anxiety may lead, however, to serious strain and even breakdown of weakened physiological systems or organs. [SeeAnxiety; Conflict, article on Psychological Aspects; Stress.]
In the first several months of life the immaturity of the physical and mental systems results in the infant’s responding in a global manner to lack of gratification of his needs or to stressful stimuli. The very young infant shows little differentiation of emotional response; he tends to respond to stressful stimuli with general symptoms of distress (for example, crying, global motor activity). However, there is increasing evidence of systematic individual differences in response even at this early level of development (Murphy 1962). Individual differences in stress thresholds, modes of expressing distress, and secondary reactions to distress—including the number of organ systems involved and the intensity of their involvement—may be prognostic in infants of a predisposition to mental disorder in later childhood (Korner 1964).
In children predisposed by stressful experiences and by personality structure, continued emotional conflict may lead to the chronic use of psychological defenses and maladaptive social behaviors known as symptoms of mental disorder. Particular constellations of such symptoms define the different types of mental disorder in children. In general, these clusters of clinical symptoms can be assigned to one of three general divisions: psychoneuroses, personality or character disorders, or psychoses.
Some of the physical or psychological symptoms in each cluster may result from the child’s attempt to maintain equilibrium or adaptation in the face of current stressful events or to compensate for the disturbance, to make restitution, or to obtain gratification of physical, psychological, or interpersonal needs. Other symptoms in each clinical picture may define the new equilibrium resulting from the child’s adaptive and compensating efforts. They may include partial restriction or malfunctioning of perceptual, cognitive, social, or physiological functions, rigid reliance upon defense mechanisms such as repression and denial, or a more severe breakdown in adaptive efforts.
Anna Freud (1965), Erik Erikson (1950), and many others have emphasized that in addition to the physical and personality characteristics and the experiences of the child, it is important to consider both his developmental level and “lines” or continuities of development. Thus, the notion of a state of psychological equilibrium in the child is only a relative one, with such states stable and definable only at cross-sectional points in time during his growth. These “states” interact systematically, and lines of development such as that from “dependency to emotional self-reliance and adult object relationships” may be observed (A. Freud 1965).
Interpersonal or psychological events may have stressful effects upon a relatively immature mental apparatus, whereas the same stimuli may be handled without disruptive anxiety by an older child or adult. In addition, the child may defend against anxiety resulting from such stimuli through regression to a more immature level of adaptation. Or, such stimuli may reinforce fixations of personality development which partially preclude further development in one or more areas of functioning (for example, learning). Thus the child’s developmental level partially determines his capacities and modes of coping with potentially stressful stimuli of a physical, social, or psychological nature and partially determines the type and severity of mental disorder. For example, certain intrauterine viral infections during early pregnancy are more likely to produce congenital anomalies than such infections occurring later in gestation. In addition, a prolonged lack of adequate mothering is particularly damaging to infants in the second half of the first year. The research of Spitz (1946), Bowlby (1960 a; 1960 b), Provence and Lipton (1962), Piaget (Flavell 1963), Escalona and Heider (1959), and Heider (1960), as well as recent animal research by ethologists (Ostow 1959), suggests that serious and perhaps irreversible defects in social and intellectual development may follow if the child fails to receive sufficient interpersonal or perceptual stimulation during appropriate developmental phases, including those of early infancy. Such defects may predispose the child to one or another type of mental disorder, but knowledge of the specific nature of such relationships depends upon future research. [SeeInfancy, article on The Effects Of Early Experience.]
Freud’s concept of emotional conflict as amplified by Anna Freud, Hartmann, Erikson, and others is central in contemporary theories of mental disorder in children, particularly with respect to the development of psychoneuroses. As the infant or preschool child develops relationships with people and as his mental functions become more complex, he may show a variety of reactive disturbances in behavior, such as temper tantrums, aggressive behavior, and crying. These disturbances are reactive to environmental stress, primarily conflicts with parents over the control (socialization) of basic sexual and aggressive drives, and are the early precursors of internalized emotional conflict. In the early years, these disturbances are generally transient and reversible in response to positive changes in the environment, although as a result of continued disturbances in parent–child relationships, they may become chronic and fixed. Reactive disorders are also seen in the older child; the symptoms may include anxiety, unrealistic fears, shyness, feelings of inadequacy or loneliness, disturbances in attentional processes and learning, and inappropriate social behavior.
If the child’s emotional conflicts are especially anxiety-arousing and unresolved, they later lose their conscious nature and are repressed and internalized. The conflicts are then inaccessible to further attempts at resolution, including new efforts made possible by the development of more powerful and complex cognitive and other ego functions: the capacities for greater independence in the gratification of needs, a longer attention span, improved reality testing, increased ability to think abstractly as well as concretely, and further differentiation and integration of perceptual and motor functions—together with further differentiation of the emotions, more effective repression of anxiety and other affects, and the internalization and symbolic representation of conflict. Because of their relative inaccessibility to conscious problem-solving efforts, emotional conflicts in the child may become self-perpetuating and lead to the establishment of chronically maladaptive behavior learned in early periods of development.
Depending upon his experiences and his own developmental capacities, however, the child may instead resolve conflicts established earlier, or a new conflict facing him in a crisis situation, and thereby achieve a higher level of differentiation and structure of personality. If such resolution and mastery is prevented, temporary regression, long-term arrest in cognitive or emotional function and development, or decompensation or adaptive failure may occur. Thus, unconscious conflicts, with associated alternating experiences of anxiety and employment of maladaptive psychological defenses, may become firmly established components of the personality, leading to structural rigidity and brittleness and presenting the model of psychoneurosis in the child.
A variety of symptoms and patterns of symptoms may be observed in the psychoneurotic mental disorders of children. These symptomatic reactions to neurotic conflict may fluctuate and change with changes in development and socialization. The psychoneuroses are not characterized by extreme personality disorganization and grossly distorted reality testing. Although psychoneurotic symptoms of internalized emotional conflict may be observed in children as young as three or four years, fully structured neurotic disorders are not ordinarily seen in children until the early school-age period. The typical childhood neurosis develops in a youngster who has already evolved a conscience or superego, who has achieved an internalization of conflict and the use of a variety of defense mechanisms, including repression of affects from consciousness, and who manifests symptoms symbolically relevant to the underlying conflicts. Several relatively independent types of psychoneurotic disturbances in children have been defined, including anxiety, phobic, conversion, dissociative, obsessive-compulsive, and depressive disorders. Detailed descriptions of these disorders are discussed elsewhere [seeAnxiety; Depressive Disorders; Obsessive-Compulsive Disorders; Phobias; see alsoCommittee on Child Psychiatry 1965].
The well-known cases of “Frankie” (Bornstein 1949) and “Little Hans” (Freud 1909) are illustrative of the phobic type of neurotic disorder in which the defense mechanism of displacement is prominent. Here the child unconsciously displaces the meaning or content of the underlying emotional conflict onto an object or situation in his environment which is symbolically relevant. The fears derived from the internalized conflict are experienced in a distorted and irrational manner. The child avoids stimuli which reactivate or intensify his displaced conflict, and he often projects his sexual, hostile, and other unacceptable feelings onto the external feared objects such as animals, dirt, elevators, or situations such as school. Mild and transient fears, fearful reactions to stressful experiences (reactive disorders), and common developmental crises involving separation anxiety in children should be carefully distinguished from phobic psychoneurotic disorders, with their internalized and structured nature. [SeeDefense Mechanisms.]
Remission of symptomatic behaviors without treament may be observed in some of the milder psychoneurotic disorders as the child masters the developmental tasks and crises of later stages (Nagera 1966). However, such disorders ordinarily require psychotherapeutic intervention with the child and his family. The prognosis for response to treatment is good. Treatment requires assessment of the balance of external and internal forces involved in the disorder (Haworth 1964). Depending upon the balance of such forces, therapeutic intervention may be made primarily through manipulation of the environment, or the therapist may focus upon achieving intrapsychic changes in the child and other family members, leading to the resolution of interpersonal conflict, the relieving of neurotic symptoms, the promoting of further development in the mental apparatus, and the learning of more adequate social responses and modes of coping with stressful stimuli (Kessler 1966).
The personality disorders differ from psychoneurotic disorders in children in the following ways. In personality disorders, chronic (fixed) pathological trends and traits are prominent, and they are ego-syntonic—that is, they are not perceived by the child as anxiety-arousing or as a source of distress. Most of the personality disorders in children appear to involve strong fixations and/or disturbances in earlier psychological and psychosexual development, related to crises and conflicts involving wishes for dependency and autonomy, the handling of sexual and aggressive impulses and behaviors, and sex role identification. The types of personality disorder which have been defined (Committee on Child Psychiatry 1965) include the anxious personality, compulsive personality, hysterical personality, overly dependent personality, oppositional personality, overly inhibited personality, overly independent personality, isolated personality, distrustful personality, personality with discharge disorder (impulse-ridden or neurotic types), and sociosyntonic personality disorder.
Discharge disorders. The discharge-disorder category includes many children who are classified in other systems as delinquent, acting-out, psychopathic, or sociopathic. Children in this general category tend to act out directly their feelings and impulses in an antisocial and often highly destructive manner. Two subcategories have been defined which distinguish between an impulse-ridden group and a group in whose discharge disorder neurotic conflict plays an important role. There is a central tendency in both of these subgroups to discharge rather than delay or inhibit antisocial impulses, but the sources of the tendency to discharge differ. The child with an impulse-ridden personality shows low frustration tolerance and difficulty in controlling or channeling sexual and aggressive impulses; his interpersonal relationships tend to be shallow, he experiences little anxiety or guilt, and there is considerable deficiency in conscience development and in the development of flexible and complex defense mechanisms. He tends to have a history of extreme emotional deprivation. The neurotic personality disorder subgroup, on the other hand, has achieved a more complex level of personality development. The child in this subgroup has developed the capacity to internalize conflict, and his antisocial behavior tends to be reactive to such conflicts and to have unconscious symbolic significance to such conflicts. These children experience some anxiety and guilt, and their interpersonal relationships, while ambivalent, are warmer and more meaningful than those of children with impulse-ridden personality [seeDelinquency, article on Psychological Aspects; Psychopathic Personality].
Developmental deviations. It is important to distinguish between the diagnoses of psychoneurosis and personality disorder, and developmental deviations. Some behaviors (for example, sexual deviations), often part of a neurotic and personality disorder, may also be related primarily to delay, acceleration, or unevenness in development and should be classified as developmental deviations rather than as neuroses or personality disorders.
Psychotic mental disorders in children are characterized by marked and pervasive deviations from mental functioning normal for the child’s age. In general, these disorders usually include chronic and severe impairment or deterioration of emotional relationships, preoccupation with inanimate objects, failure to develop speech or loss of speech for purposes of communication, bizarre behavior and unusual motility patterns, extreme mood swings and intensity of affective experience and expression (as in sudden temper outbursts, panic, etc.), and failure to develop or loss of a sense of individual identity. There are generally severe disturbances in perceptual and cognitive development and functioning, but with onset in later childhood certain areas of intellectual functioning and achievement may be adequate or better. Some of the symptoms seen in childhood psychosis—such as some of the disorders in thinking, affect, perception, motility, speech, object relations, and reality testing—represent efforts at restitution or compensation for the psychotic process.
Autism and symbiotic psychosis. Childhood psychoses do not tend to crystallize into as many varieties or subtypes as is the case with adult psychoses (Kessler 1966). Two major subtypes have been defined in early childhood: infantile autism and symbiotic or interactional psychotic disorder. Age of onset in infantile autism is the first few months of life as the infant fails to develop a normal emotional attachment to a mother figure. He remains emotionally aloof, speech development is delayed or absent, feeding and sleeping problems and stereotyped motor and motility patterns are prominent, and the child responds to relatively slight changes in his environment with intense outbursts of anger or anxiety. Some intellectual functions are intact, but their use is impaired by the defective reality testing and lack of communication.
Age of onset of symbiotic psychosis is after the first year or two of life. The child develops a normal emotional attachment to his mother but fails to achieve separation and individuation. Intense and prolonged dependency upon the mother (or between mother and child) is prominent in the early history. The disorder is usually precipitated by some real or fantasied threat to the mother—child relationship. Symptoms include marked and severe separation anxiety, clinging (sometimes indiscriminately), regression (for example, giving up speech, loss of bowel control), gradual withdrawal from object relations, autistic behavior, and distortions in perceptual and cognitive functioning.
Childhood schizophrenia. Childhood schizophrenia or “schizophreniform” psychotic disorder occurs in middle childhood—ages 6 through 12 or 13. The disorder may be of gradual or relatively acute onset. Where onset of the disorder is gradual, the development of neurotic symptoms is followed by regression to use of the primitive defenses of marked denial and projection. Low frustration tolerance, hypochondriacal tendencies, and inappropriate outbursts of temper or panic are often observed, and these are followed by withdrawal, increasing involvement in private fantasy, emotional aloofness, disorders in thinking and perception, autistic behavior, and a breakdown in reality testing (e.g., Goldfarb 1961). The prognosis is more favorable if the psychosis is an acute reaction to a developmental crisis. Few adultlike hallucinations are experienced by psychotic children until ages 9 or 10 at least. However, bizarre motor behavior (for example, whirling), self-mutilation and suicidal attempts, and inappropriate mood swings are seen with some frequency in these cases. Occasionally, some of the symptoms more characteristic of adult psychoses are seen in children. These include ideas of reference, somatic delusions, catatonic behavior, and paranoia. [SeeSchizophrenia.]
In diagnosing neurosis, personality disorder, or psychosis in children, the healthy, positive responses and capacities as well as psychopathological trends should be assessed, along with the positive and negative physical, social, and psychological determinants of the child’s behavior (A. Freud 1965).
Current views of the diagnosis and treatment of mental disorders in children stress the importance of parent—child relationships, family processes, and sociocultural influences, while remaining cognizant of contributing and predisposing genetic and constitutional factors.
Disturbances in parent–child relationships have been implicated in a variety of children’s mental disorders, including unusual fluctuations in mood, psychoneuroses, certain psychotic disorders, and “antisocial” personality disorders, as well as disorders in which both physical and psychological functions are disturbed, such as marasmus or failure to thrive in infants, ulcerative colitis, asthma, and disturbances in perceptual, cognitive, and sensory–motor functions related to structural changes in the central nervous system.
The connection between type of mental disorder and specific characteristics of parent—child relationships is complex and not clearly understood. Research on certain personality factors characteristic of parents of psychotic and neurotic children (such as that of Sarason et al. 1960) shows that parents of children with high anxiety differ in certain personality traits from parents of children with low anxiety, and the “superego lacunae” shown by Johnson and Szurek (1952) in the parents of some kinds of antisocial children indicate the probability of some specificity in the relationship between parent–child interaction variables and type and severity of mental disorder.
In addition to the quality of the parent–child relationship, other family variables may predispose and contribute to the development of mental disorders in children (e.g., Ross 1964). For example, loss of a family member, lack of family cohesiveness, distorted and neurotic communication patterns, deviant role functions, conflicting value orientations, or poor integration with the community may serve as stressful stimuli which upset the functioning of the family and lead to a reactive disorder, developmental deviation, neuroses, personality disorder, or psychoses in the child.
One of the characteristics of the healthy family is the capacity to respond adaptively to crisis. Serious illness, economic losses, death of a parent, removal to a new community, and other such stressful events tend to be disruptive of family equilibrium and established modes of functioning and relating. Such disruptions may be temporary and through mastery lead to a higher level of functioning, or they may continue and result in family disintegration or pathology in one or more family members.
There is some indication of a specific relationship between type of family disruption and type of mental disorder in the child. For example, certain types of delinquent acting-out tend to occur in families with little cohesiveness and faulty disciplinary practices (e.g., Bandura & Walters 1959; McCord et al. 1961). Certain patterns seem characteristic in families of children suffering from schizophrenia or certain types of autism (e.g., Lidz & Fleck 1960). However, as is the case with other variables which have been implicated to some degree in mental disorders of children, the establishment of clear-cut relations between family variables and individual child disorders depends upon further research.
Sociocultural variables have also been implicated in the etiology of children’s mental disorders. Variations in child-rearing practices and attitudes have been noted in different ethnic and social-class groups and cultures, as have incidence and type of disorder and attitudes and responses to treatment (e.g., Whiting 1963; Clinard 1957). However, the social and psychological mechanisms mediating the relationship between sociocultural variables and mental disorder are still poorly understood. Potentially stressful events for families and individuals include movement from rural to urban areas; shifts in socioeconomic conditions and traditional customs, attitudes, and interpersonal functions; and the acculturation of primitive or previously relatively isolated cultures. Children who experience such events without adequate preparation are particularly vulnerable to mental disorder (Kessler 1966).
The economic, religious, and educational status of the family also seems related to the manner in which the other family members react to mental disorder in a child, just as stereotypes of these groups tend to affect the treatment plans and services offered by agencies and clinicians.
BRITTON K. RUEBUSH
[Directly related are the entries Mental Retardation; Psychiatry,article on Child Psychiatry.Other relevant material may be found in Developmental Psychology; Infancy.]
American Psychiatric Association 1964 Planning Psychiatric Services for Children in the Community Mental Health Program. Washington: The Association.
Bandura, Albert; and Walters, Richard H. 1959 Adolescent Aggression. New York: Ronald Press.
Bornstein, Berta 1949 The Analysis of a Phobic Child: Some Problems of Theory and Technique in Child Analysis. Psychoanalytic Study of the Child 3/4:181-226.
Bowlby, John 1960 a Separation Anxiety. International Journal of Psycho-analysis 41:89-113.
Bowlby, John 1960 b Grief and Mourning in Infancy and Early Childhood. Psychoanalytic Study of the Child 15:9-52.
Chess, Stella 1959 An Introduction to Child Psychiatry. New York: Grune.
Clinard, Marshall B. (1957) 1963 Sociology of Deviant Behavior. Rev. ed. New York: Holt.
Committee On Child Psychiatry, Group For The Advancement Of Psychiatry 1965 A Proposed Classification of Psychological Disorders in Childhood. Unpublished manuscript.
Cramer, Joseph B. 1959 Common Neuroses of Childhood. Volume 1, pages 797-815 in American Handbook of Psychiatry. Edited by Silvano Arieti. New York: Basic Books.
Erikson, Erik H. (1950) 1964 Childhood and Society. 2d ed., rev. & enl. New York: Norton.
Escalona, Sibylle; and Heider, Grace 1959 Prediction and Outcome. New York: Basic Books.
Flavell, John H. 1963 The Developmental Psychology of Jean Piaget. Princeton, N.J.: Van Nostrand.
Freud, Anna 1965 Normality and Pathology in Childhood: Assessment of Development. New York: International Universities Press.
Freud, Sigmund (1909) 1955 Analysis of a Phobia in a Five-year-old Boy. Volume 10, pages 3-149 in Sigmund Freud, The Standard Edition of the Complete Psychological Works of Sigmund Freud. London: Hogarth; New York: Macmillan. → First published in German.
Goldfarb, William 1961 Childhood Schizophrenia. Cambridge, Mass.: Harvard Univ. Press.
Haworth, Mary R. (editor) 1964 Child Psychotherapy: Practice and Theory. New York: Basic Books.
Ehider, Grace 1960 Vulnerability in Infants. Menninger Clinic, Bulletin 24:104-114.
Johnson, Adelaide M.; and SZUREK, S. A. 1952 The Genesis of Antisocial Acting Out in Children and Adults. Psychoanalytic Quarterly 21:323-343.
Kessen, William 1965 The Child. New York: Wiley. Kessler, Jane W. 1966 Psychopathology of Childhood. Englewood Cliffs, N.J.: Prentice-Hall.
Korner, Anneliese F. 1964 Some Hypotheses Regarding the Significance of Individual Differences at Birth for Later Development. Psychoanalytic Study of the Child 19:58-72.
Lidz, Theodore; and Fleck, Stephen 1960 Schizophrenia, Human Integration, and the Role of the Family. Pages 323-345 in Don Jackson (editor), The Etiology of Schizophrenia. New York: Basic Books.
Mccord, William; Mccord, Joan; and Howard, Alan 1961 Familial Correlates of Aggression in Nondelinquent Male Children. Journal of Abnormal and Social Psychology 62:79-93.
Murphy, Lois 1962 The Widening World of Childhood: Paths Toward Mastery. New York: Basic Books.
Nagera, H. 1966 Early Childhood Disturbances, the Infantile Neurosis, and the Adult Disturbances. New York: International Universities Press.
Ostow, Mortimer 1959 The Biological Basis of Human Behavior. Volume 1, pages 58-87 in Silvano Arieti (editor), American Handbook of Psychiatry. New York: Basic Books.
Provence, Sally; and Lipton, Rose 1962 Infants in Institutions. New York: International Universities Press.
Ross, Alan O. 1964 The Exceptional Child in the Family. New York: Grune.
Sarason, Seymour et al. 1960 Anxiety in Elementary School Children. New York: Wiley.
Spitz, Rene 1946 Anaclitic Depression. Psychoanalytic Study of the Child 2:313-342.
Whiting, Beatrice B. (editor) 1963 Six Cultures: Studies of Child Rearing. New York: Wiley.
Mental disorders vastly extend the normal range and variety of human behavior available for psychological study. They present familiar patterns in exaggerated form or in unusual combinations, in-completely developed, or disorganized. Although these derangements are often accompanied by seemingly arbitrary and unique manifestations, there is enough regularity in them to allow for prediction from one occasion to another and for generalization within groups of persons. Experiments help to determine lawful relations in this area, as they do in other fields.
Since mental derangements are often accompanied by considerable discomfort or distress, they call first for caretaking and administrative action which, if feasible, includes treatment and rehabilitation. In addition, mental disorders provide a source of information about the mechanisms of normal, as well as impaired, function. We are apt to take for granted our ability to execute the many intricate operations necessary for the coordinated and complete performance of even quite simple movements and mental processes. Only when these operations break down, become inefficient, or fail to develop do we recognize the contribution of one or another mechanism to normal functioning. Any systematic examination of mental disorders involves the identification of the mechanisms or processes that are damaged in function. From this follows the determination of their part, typically in interaction with other mechanisms or processes, in the behavior disorder or symptoms. Such an analysis, often performed implicitly and schematically, constitutes the diagnosis. When it is explicit and precise, when it allows for prediction (i.e., prognosis) and is followed up by observations on the patient’s progress, it can contribute to knowledge of mental function in general, as well as of psychopathology in particular.
Experimental techniques are better suited to the study of disorders in cognitive and motor function than to the study of disorders in emotions, but, with some ingenuity, these techniques have been made to serve in the exploration of affective and motivational anomalies as well. Experiments can serve to test a specific hypothesis or merely to verify the fact that some type of behavior does occur. More particularly, they are employed to determine the conditions under which such behavior occurs and the factors that influence its magnitude or frequency. Experimental techniques have been used not only to explore phenomena relevant to mental disorders but also to bring about such derangements (by drugs, fatigue, etc.) and to treat others that have emerged in the course of development or as a result of accident.
Thus, experimentation is appropriate at every stage of the evolution and remission of mental disorders. Its special virtue lies in its capacity to refine clinical observations, to evalute their accuracy and delineate the boundaries of their validity, and to sort out the several sources that contribute to the effects under investigation. An experiment may be necessary, for example in diagnosis, to decide whether a patient’s sensory or motor function has been completely lost or is available in extreme emergencies, as happens with hysterical conversion symptoms. Experimental procedures are also widely used to determine the extent of an incapacity. These may include procedures such as perimetry of visual fields and determination of dark adaptation, or performance tasks, such as memorizing pairs of nonsense words and sorting designs.
Psychological tests used in diagnosis also have their origin in experimental procedure and retain some of its features—the objective tests more so than the projective. For example, certain aspects of the test situation are always standardized, e.g., the content and phrasing of the questions, the instructions given, the perceptual information presented, the method of recording the patient’s responses, the format of the protocol taken for the record. In other respects clinical tests may not satisfy the requirements of control and reproducibility that distinguish the experimental from other methods of observation. Also, clinical test scores are evaluated against pre-established population norms, an advantage over the experimental method in determining the baseline and the extent of the deviation, that may have significance for psychopathology. In standardized tests, however, a significant clue could be missed if it emerges, not against the background of average performance, but in the unique pattern of the particular patient’s function and dysfunction. Here the flexibility of the experimental method, its resources of manipulation and control, and, above all, its rationale of specifying functions by operations offer the investigator a considerable gain. [SeePersonality measurement; Projective methods.]
Although this article is concerned with the psychological study of mental disorders, it should be remembered that these disorders furnish subjects for experimental investigation by other disciplines, e.g., pathology, biochemistry, and neurophysiology. Even within psychology, the spectrum of experimental techniques and problem areas covers a wide range, from physiology to the social sciences. Experiments in autonomic and endocrine function, for instance, belong within its boundaries and have been of especial interest to students of unconscious psychic processes. At the other end, experiments in role playing, in group processes, and in the restructuring of social systems, such as hospital wards, have been undertaken jointly or alternately by psychologists and social scientists. The middle ground is marked by experiments in psychophysical measurement and perceptual judgment, by the several conditioning techniques, and by the immense variety of performance tasks—from simple motor responses to the solution of syllogistic problems, from the retention of nonsense syllables over a few minutes to the enduring acquisition of a new skill. [SeePsychiatry, article onsocial psychiatry.]
As in other areas of research, in the study of mental disorders the experimental approach implies that as many as possible of the conditions that bear upon the subject under investigation are held constant, while the others are controlled by the design of the research. Only a few, and preferably only one, of the conditions is allowed to vary, and that one is varied systematically, so that its effect on the outcome can be evaluated, whenever possible in some quantified terms. The purpose of an experiment is not just to discover whether an anticipated result can be discerned but also to give an estimate of its magnitude and of the probability that it could be reproduced under similar circumstances.
In this methodological sense, “experiment” means something very different from the improvised trial or casual exploration to which the name is also applied. Ventures of that type are not unknown in the study of mental disorders, especially in the study of treatment and rehabilitation programs. They may be successful and even valuable in suggesting hypotheses or in demolishing an established misconception, but they are not experiments in the sense that their results can be attributed to a specific variable in the total situation. Certain guesses at the hidden meaning of a patient’s obscure statement are experimental in this improvisational sense. Even though they may solve a riddle, there is no certainty that they hold the only solution or, indeed, that the riddle has been posed. Like other intuitive observations, such stabs at interpretation or intervention can supply hypotheses for subsequent testing.
The experimental method was introduced into the study of mental disorders soon after it appeared in general psychology. Kraepelin, the great system builder in clinical psychiatry, had worked with Wundt, and in due course he founded an experimental psychological laboratory at his research institute in Munich. Its program was out-lined as far back as 1894, while Kraepelin was in Heidelberg, and appeared in print as the first in a series of reports under the title Psychologische Arheiten (Kraepelin 1896). Periodic publications on research conducted by Kraepelin himself, and, under Kraepelin’s editorship, on work done by his associates and students, followed during the first quarter of the twentieth century and constitute a record of eight volumes [seeKraepelin]. Kraepelin credited Gabriele Buccola, an Italian, with the first psychophysical experiments on patients with mental disorders and also noted the beginnings of such research in Russia and the United States. Another neuropsychiatrist whose prolific experimental activity started before the turn of the century was Paul Ranschburg, a Hungarian, most noted for his research in memory disturbances. By 1902 Ranschburg had established a permanent laboratory in Budapest, with government support, for the study of abnormal mental function.
In America, Shepard Ivory Franz set up the first laboratory dedicated to the experimental study of behavior in mental patients, at the McLean Hospital in Belmont, Massachusetts, in 1904. The apparatus came from Leipzig, and Franz’s first experiments were concerned with the association areas in the brain, aphasia, memory defects, and especially with the physiology of manic–depressive psychosis. Psychological research was typically introduced into mental hospitals via physiology, with experiments on fatigue, speed of reaction, and time judgment. Significantly, Franz’s laboratory was established for research in pathological physiology. When in 1907 he transferred his activities to the Government Hospital for the Insane in Washington, D.C., F. L. Wells succeeded him at McLean, heading a laboratory in pathological psychology. Wells was indeed less interested than Franz in cerebral localization, and his work in clinical psychology is best remembered for experiments in reaction time, the design of psychometric tests, and the pioneer use of psychogalvanic measurement.
Kraepelin’s experimental program encompassed all the principal approaches to mental disorders. He studied normal function, in order to establish baselines, isolate distinct mental processes, and perfect techniques for their measurement. The same processes were also investigated in patients with various mental diseases and with mental disturbances brought on by drugs, fatigue, or sleep deprivation. The ultimate goal was to gain a clearer understanding of mental illness in order to determine its etiology and render its treatment more effective and more amenable to evaluation. Kraepelin’s methodological goals have proved understandably uncongenial to the currently dominant school of psychiatry. One clue to his unpopularity is his definition of psychology as a branch of physiology, i.e., physiology of the mind. It is a definition that today few, even among his admirers, would accept, although the concepts underlying it inspired his research. The definition implied that mental function can be measured; that deranged mental function differs from the normal in some quantifiable properties; that operations allowing for the exact assessment of the speed, the regularity, or the frequency of certain incidents in performance can serve as diagnostic and prognostic devices.
This view entailed neither an atomistic model of personality nor a denial of psychogenic etiology. Kraepelin unequivocally declared that the physician concerned with mental disorders aims at forming a total picture of his patient and that the vast majority of these disorders originate from inside—genetic disposition being one of the prime determining factors. Experimental psychologists of the present day, while paying homage to his pioneer work, nonetheless adopt a critical attitude toward Kraepelin’s contribution, for two reasons. One is the structuralist theory he inherited from Wundt, which has proved to be of limited value—especially Wundt’s concept of apperception, which played an important part in the theory of Kraepelin’s school. Second, Kraepelin himself and several of his associates—although not all, Ernst Grünthal being a notable exception—worked with extremely small samples of subjects. Typically, the investigator himself, not only dubiously representative of the general population but also far from naive in regard to the anticipated effects of the experimental treatment, was the only subject. Kraepelin and an associate’s report of impaired performance attributed to a daily dose of alcohol no larger than two quarts of beer is the envy of later experimentalists who, like the author, have been unsuccessful in demonstrating impairment with much larger doses of alcohol [seeDrinking and alcoholism, article onpsychological aspects].
Theory and operationalism
While the program expounded by Kraepelin has been adapted by experimentalists to other psychological theories and to the requirements of representative sampling and stricter control, laboratory research on problems related to mental disorders has branched in other directions as well. Hughlings Jackson’s hierarchic model of dissolution of function (1884) has stimulated innumerable experiments, especially with neurological patients, and Pavlov’s theory of conditioning has been applied to mental disorders of every kind. Whether tied to a theoretical position or concerned only with the problem in hand, experimental studies of neurological patients have enriched, refined, and at times corrected our notions about sensory and motor function and higher mental processes. Since the purpose of most investigators has been to isolate the damaged function from those that remain intact or to arrive at a differential determination of deficit, the general approach to neurological disorders has been operational. The experimenter defines the function that seems impaired, selects operations that involve the function, and sets the patient experimental tasks that test these operations.
As a rule, the more closely defined these operations, the more informative they are to the investigator. This scale of value may, however, be reversed by his commitment to a theory couched in such global constructs that each and any derangement in function serves as an illustration of the general principle. A classical instance of that view, advanced by a clinician who was also a notable experimenter, is Goldstein’s principle of abstraction. Goldstein conceived of abstraction as a composite function, central to which is the ability to categorize concrete instances. Its impairment is cited to account for disorders in speech and in thought, for the psychopathology associated with lesions in diverse areas of the brain, and for disorders that occur without known cerebral damage, such as schizophrenia. [SeeGoldstein.]
Werner’s developmental principle was another such general concept, which inspired experimental attacks on mental derangements as diverse as aphasia, the psychoses, and mental deficiency. Implicit in Werner’s principle is the notion that seemingly instantaneous events in perception and thought in fact evolve by steps over a microscopic time scale. The evolution of these processes is usually too rapid to be open to inspection, but with appropriate experimental techniques it can be demonstrated in some instances of disturbed mental function. This was done, for example, by Klaus Conrad, a clinical psychiatrist and ingenious experimenter, who derived quite specific neuropsychological formulations from the broad and formal gestalt laws of integration and differentiation.
In the aphasias, amnesias, and other cognitive derangements, experiments with the tachistoscope and memory drum (laboratory instruments for the regular, and very short, presentation of visual displays) merely extended the routine neurological examination and psychological testing. Students of the psychoses and psychoneuroses, on the other hand, could not always admit the relevance of experimental techniques. The psychoanalytic school, which in one version or another has undoubtedly been the most influential force in psychiatry and its ancillary professions in the United States, relies on analogy rather than on operational constructs. This applies even more emphatically to the existentialist and other metaphysical doctrines of psychiatry. In these theories explanation is more often by retrodiction than by prediction; the antecedent events are reconstructed without an exact weighting of the factors that contributed to the outcome or an analysis of their interaction. [SeePsychology, article onexistential psychology.]
To be sure, certain key concepts in psychoanalytic theory, such as conflict, have been subjected to laboratory experiments. The effects of stress interviews, frustration, pain, and vexation have been studied with human subjects, but for obvious reasons the threat to health and human dignity had to be well below the level at which lasting mental disorders are likely to develop. Most of the laboratory studies, therefore, have been done with infrahuman species. A powerful stimulus to such studies was the almost undivided sway of learning theory in American experimental psychology following the behaviorist revolution. If mental disorders, or so many of them, are not diseases but, rather, clusters of maladaptive habits and drives, persistently faulty perceptions or thoughts, and stunted social skills, then the laws of learning and conditioning may explain the emergence of symptoms and lead to successful methods of treatment. Attempts to reconcile the clinical formulations of Freud with an experimentally based academic theory appealed strongly to Hull and his school, whose learning theory shared with psycho-analysis a hedonic principle of motivation. It is, perhaps, disappointing that experiments concerning the development of defense mechanisms have been largely equivocal (see Sears 1943; Miller 1944), although this is hardly surprising in view of the fact that most of them employed rats for subjects. [SeeConflict, article onpsychological aspects; Learning theory; Stress; and the biography ofHull.]
While there is unquestionable elegance in the graphic representation of gradients and the equilibrium point between a rat’s approach to food and avoidance of shock and there is quite live evidence of regression, fixation, and other maladaptive habits in the experimentally induced neuroses of cats, dogs, pigs, and sheep trapped in a physical or psychological harness (Liddell 1944), the leap from the laboratory to the human family setting is still a long one. It has been quite spectacularly shortened by Harlow’s experiments with monkeys (1958; 1962). The affectionate display directed by infant monkeys toward their surrogate mothers—cloth dummies—was not only comparable with their responses to the natural mothers but also uncannily reminiscent of the behavior of human infants. Since these observations were made in a laboratory, several influences on the growth of affectional responses could be controlled and systematically varied. Furthermore, the situation seemed more likely to produce a lasting mental disturbance similar to those that afflict man than did the traditional procedure of inducing experimental neurosis in social isolation. As the monkeys grew up, some of them indeed developed marked personality disorders. Rather surprisingly, however, this outcome could not be traced to the artificial surroundings of the laboratory or to the substitution of a cloth dummy for the mother or, indeed, to her replacement by surrogates who rejected the clinging infant with a violent mechanical thrust or a concentrated blast of air. The infant experience that seemed chiefly to account for the adult monkey’s psychopathology was deprivation of contact with other infants. [SeeAffection; Infancy.]
Mental disorders and brain function
The problems of generalizing from infrahuman animals to man will be briefly considered below. At this juncture another problem demands attention: the relationship of mental disorders to disturbed brain function. The conception that behavior disorders develop as a result of infantile deprivation or other stressful life experiences makes no explicit assumptions about alterations in the organism by which such effects could be mediated over time. It is, of course, tacitly assumed that learning, whether it results in greater efficiency or is maladaptive, involves some enduring organic changes, more particularly in the central nervous system. What these changes are is unknown, partly because of the inadequacy of current neurological techniques and partly because of the inadequacy of neuropsychological concepts. These two factors are as closely related as are technology and theory in other domains.
After many false attributions and an occasional correct guess in past centuries, it is now pretty universally agreed that the organ of the mind is the brain. The traditional metaphysical controversies about the relationship of body and mind have not been so completely resolved. They may be dismissed as irrelevant to the problem of mental disorders, but there survives a prejudice from the days when body and mind were regarded as two distinct substances, coordinate but not coequal in value or power. In the chain of being, man occupied a position intermediate between that of inanimate matter and the soulless animals, with whom he shared the bodily attributes, and that of the several classes of spiritual beings, whom he resembled by virtue of his mental faculties. His mind received credit for very extensive powers over the body, while control in the reverse direction was thought to be more limited in scope and also to be a likely avenue to sin. Moral judgments have changed, but clinicians are still apt to regard brain damage as but one of several causes of mental disorder and quite readily attribute disturbances in visible and tangible behavior to psychic processes that, at least by implication, take place outside the bodily dimensions.
The implication is made by the rough division between organic and functional disorders that has been established in the usage of psychiatrists and neurologists, as well as of clinical psychologists. “Organic” refers to brain damage, and that term is understood to stand for such structural impairment of brain tissue as can be observed directly or by means of currently available neurological techniques, e.g., electroencephalography, pneumography, angiography, etc. “Functional,” by elimination, does not refer to organic or brain function. A classificatory principle as incompatible with present-day scientific notions as this is can be defended only on pragmatic grounds. It may, indeed, help with the prescription of treatment, but it introduces an unnecessary division into the research on mental disorders.
Localization of brain function. On the one hand, investigations of patients with brain lesions tend to be focused exclusively on the topographical localization of the damaged function. Preoccupation with specialized centers or areas discourages the search for functional systems in the brain or, for that matter, in behavior and experience. On the other hand, psychological concepts have been derived without reference to systems and processes within the organism, and it is hardly astonishing that they do not always fit exactly the neurologist’s model. Derangement of function, especially when it can be determined independently by neurological techniques and by experimental studies of behavior, furnishes the most revealing clues about mechanisms and systems common to neurology and psychology. The concepts and patterns that will be meaningful in both disciplines need not correspond to those presently current in either. For example, if future research confirms the author’s experimental and clinical observations about the close association of an extremely severe memory disorder with a general lack of spontaneity in the patient’s behavior—although no comparable deficit in reasoning or intelligence is found—these two seemingly unrelated psychological functions could be properly subsumed under a common concept. Moreover, if evidence accumulates that this combined deficit occurs with lesions in a certain fairly well defined subcortical system of the brain, such a concept should be meaningful in the language of neural as well as of behavioral processes.
Although the accomplishment of experimental studies aimed at this objective is but modest to date, the advance has been considerable (a good share of that achievement being the result of investigations of disordered mental function; see Boring 1929; Flugel 1933; Hebb 1949; 1958) since G. Spurzheim, who ranks next to Franz Joseph Gall as the founder of phrenology, drew his spuriously detailed map of some thirty-odd brain areas that subserved as many mental faculties, with mirrorlike duplication in the two hemispheres. More reliable evidence for the functional subdivision of the brain came first from Paul Broca’s clinical observations and shortly afterward from Luigi Rolando’s experiments with electrical stimulation. Pierre Flourens, another pioneer in experimental research in this area, however, arrived at different conclusions in his studies using the extirpation technique. Phrenology survives today in the mosaic theory of the brain. An opposite point of view was forcefully advanced by Goldstein, whose concept of abstraction has already been mentioned, and, for a while, by Lashley, who derived the laws of mass action and equipotentiality from ablation experiments. These laws imply that the size, rather than the site, of brain damage determines the disturbance in behavior and that—outside the sensory and motor areas—any part of the cortex can potentially subserve any learned behavior. [SeeBroca; Flourens; Gall; Lashley.]
Laboratory studies of human patients have led to formulations intermediate between the two poles. Teuber, who conducted extensive and carefully de-signed experiments on a group of patients with combat injuries, the majority with gunshot wounds in the brain, demonstrated that these lesions result in both specific and general impairment of perceptual function (Teuber & Liebert 1958). Halstead reached a somewhat different, intermediate position, from studies of patients with lesions in the various lobes of the cortex (1947). Statistical analysis of his experimental results showed that no intellectual function is uniquely dependent on a single region of the brain but that these areas differ in their importance for one or another function.
Experimental techniques have been extensively used to test hypotheses about cerebral dominance and the division of function between the hemispheres. In this context one again meets spokesmen of extreme as well as intermediate positions. At one pole is the opinion that man has two brains, that one hemisphere all but completely duplicates the function of the other. Indeed, experiments have repeatedly shown that the surgical removal of a diseased hemisphere or its decay through atrophy may cause little discernible loss of intellectual ability. Opponents of this view attribute a high degree of specialization to each half. Speech, for example, has been associated with the left hemisphere since Broca’s time, and, correspondingly, control over manipulative skills has been attributed to the right hemisphere. The proposition that cerebral dominance is thus manifested and that it is reversed in left-handed persons has been tested by many experimenters. Zangwill’s survey (1960) of these studies reached the conclusion that the speech area is not invariably contralateral to the dominant hand. Nor is representation exactly identical in the two hemispheres when (as, for example, in sensory function) the rule of contralaterality obtains, Semmes and her associates (1960) have demonstrated this for somatosensory function, while experiments determining the two-point discrimination and pressure thresholds were used in Teuber’s study of disabled veterans (Teuber & Liebert 1958).
Pathological damage to the brain that corresponds exactly to a functional impairment is the exception and so far has not been found typical of mental disorders. Lesions in the visual or auditory cortex offer the closest examples. Students of mental illness have been especially interested in the frontal lobe, which seems to play an important part in such emotional disturbances as depression and distress over pain. A functional severance of the prefrontal cortex from the central nervous system has been successfully applied in treating these complaints. Experimental studies, however, have been inconclusive in assigning a particular function or ability to the frontal lobe. Advocates of the mosaic theory of brain function have found more encouragement in the temporal lobe. Penfield, the neurosurgeon, exposed the temporal cortex in several patients while removing a focus of epileptic discharge (1954). Applying electric stimulation to clearly marked points, he was able to elicit repeatedly—although not always—the same sensation or evoke recall of the identical episode from the past. These recollections appeared to be as sensorially sharp as the original experience, even though the patient was fully aware of his immediate surroundings in the operating room. At first it seemed that the site where the organism stores its discrete memories had been discovered in the temporal lobe, and although later interpretations have been more cautious, they do not diminish the significance of these experimental findings, especially for the demonstration that experiences and memories are classified in the nervous system according to abstract principles.
This deeply hidden surface of the cortex and the adjacent subcortical regions are undoubtedly implicated in some of the processes of memory. Milner’s reports with Penfield (Milner & Penfield 1955) and with Scoville (Scoville & Milner 1957), as well as other investigators’ reports on patients who had lesions from surgery or disease in those areas, have noted grave defects in memory for recent events. Memory for remote events—like those which emerged under stimulation of the temporal cortex—is less consistently and less severely affected. Newer techniques in brain surgery, such as electrocoagulation, have widened the area of experimental investigation of neuropsychological processes. Experiments performed with chronically implanted electrodes allow for the simultaneous recording of neuroelectric activity at deep brain centers and of overt behavior, as well as for electric stimulation. The subject in such investigations, however, is always a sick person, whose function is often influenced by drugs as well as the disease. Alternatively, the subject of an investigation may be a healthy monkey or cat, animals whose brains as well as behavioral repertoire have a good deal in common with man, although not quite as much as would satisfy many students of mental disorders. [SeeNervous system, article onbrain stimulation.]
There are well-established anatomical differences between the brain of man and that of even the highest subhuman primate; there is also reason to believe that some structures or neurophysiological systems are identical but serve different functions at the two different phylogenetic levels. Whether the accomplishments of the rat or the ape in learning and problem solving furnish an informative analogy for man’s feats in forming unique memories and operating with symbols remains a debatable issue. Many experiments tracing the relationships between derangements in behavior and in the brain can be carried out only with human patients, because the psychological defect is entirely in the use of language. The variety of aphasias distinguished in clinical observation and confirmed by experimental tests are proof not so much of an ingenuity in classificatory exercises as of the scientific endeavor to expand our knowledge of significant lawful relationships. [SeeLanguage, article onspeech pathology; Perception, article onspeech perception.]
Kinsbourne and Warrington’s investigation of six patients with a reading disability (1962) is an example of the contribution experimental procedures can make in a clinical situation. These patients were right-handed, and they were known to have brain lesions in the right (i.e., minor) hemisphere. Paralexic errors, which their defects first seemed to exemplify, are regarded as aphasic in origin and are therefore attributed to damage in the dominant hemisphere. It appeared significant that the errors observed in these patients also differed from those commonly made in reading, in that they tended to occur with the first letters of a word. The investigators designed experiments to test the hypothesis that the reading errors arose from a perceptual derangement. By means of a tachistoscope, they exposed to the patients brief glimpses of whole and fragmented words and geometrical figures. It became apparent that the patients had an abnormal field of perception, in which fine discriminations were restricted to the right side, although gross operations, such as judging the length of words, were unaffected. Unaware of their disability, the patients attempted to complete what they could read of a word, always in a leftward direction. Experimental checks ruled out the possibility that the disability arose from faulty fixation or defective eye movements, and the investigators therefore attributed it to an abnormal distribution of visual attention—to an unconscious neglect of space. They also recognized that their findings may have implications for reading disabilities that originate from a failure to execute the normal operation of forward completion. [SeeReading disabilities; Vision, article oneye movements.]
Experiments following the trail between mental disturbances and cerebral dysfunction, in either direction, have the advantage of a clearly defined objective. The pursuit itself, however, may become exceedingly complex and involve—over and above the neurological and psychological considerations—such diverse disciplines as biochemistry, genetics, social science, and history (the patient’s life history, as well as the history of the disease process). These disciplines have indeed appeared more promising for research in schizophrenia than have the neural sciences. Experimental studies of schizophrenia in the biochemistry laboratory, although varied, allow for a broad, threefold classification. Their goal is (1) to determine the chemical causes of the mental disorder; or (2) to assess metabolic, and particularly endocrine, function in patients, at different stages of their illness, under induced stress, special experimental conditions, or in the standard hospital setting; or (3) to form a part of a pharmacological treatment program. These experiments often include investigations of physiological and/ or psychological function as well.
Experimental studies of schizophrenia, manic–depressive psychosis, and the neuroses are typically confined to the verification of clinical observations. The major exception to this trend has been research stimulated by theories that do not distinguish between functional disturbances attributed to brain damage and those due to psychological factors. Followers of Hughlings Jackson and Head, of Pavlov and the gestalt school, of Goldstein, Werner, and Schilder, have exerted an influence in that direction. More recently, models built around the activating properties of a subcortical neural system have served as a comprehensive conceptual frame work for disordered mental function.
Theories that transcend the boundaries of established brain damage and psychogenic dysfunction employ loose and not fully operational constructs. Goldstein’s principle of abstraction is an example, and, indeed, several experimenters have produced partial evidence against it. Some of these support Cameron’s proposition (1947) that distractibility is an important source of concrete thinking in schizophrenia and that in several instances of mental disorder abstraction is manifested but is masked by the use of inappropriate, overinclusive, bizarre concepts, especially when they concern the social context. Of course, the conclusions of these experiments are limited by the extent to which their operations represent abstractness and concreteness in thinking. Uncertainty and disagreement about adequate correspondence between behavior under laboratory control and hypothetical mechanisms or processes—in personality dynamics or neural function alike—present the most difficult problem to the experimental psychologist investigating mental disorders.
Experimental reports about the slow responses, sluggish work rate, and straying attention of depressed or schizophrenic patients are unlikely to arouse much controversy. In these instances, behavior observed in the laboratory does not conflict with clinical impressions, although inferences drawn from the two sets of data to underlying mechanisms may clash, whether they concern hypothetical psychic mechanisms, such as defenses against impulses, or hypothetical neural mechanisms, such as cortical arousal. Experimental techniques have also been used as a subsidiary procedure to clinical interviewing, e.g., the measuring of motor and autonomic responses in tests of word association or perception. If a patient seems to be unusually disturbed or ill at ease when discussing—or keeping silent about—certain topics, such suggestive impressions can be confirmed by the relatively exact measurement of his psychogalvanic response or hand movements. Evidence thus obtained may help in delineating and exploring his areas of conflict. This technique—popularly known as the lie detector—was systematically explored for the purpose of psychological research by Luriia in Moscow in the 1920s (1932). Other investigators, in the United States as well as in the Soviet Union, have further developed this technique, following clues from the patient’s autonomic and skeletal behavior and measuring the latency, rhythm, and amplitude of his responses in structured interviews or during his performance of an experimental task.
Laboratory techniques have also been used in the study of the regularity of grossly distorted perceptions in patients with mental disorders. Estimates of the patient’s body or of its parts; of the size and distance of objects, especially when the judgment involves the perceptual constancies; and of his dependence on external cues for accurate assessment of the vertical dimension have added to our knowledge of the effects of mental disease or of particular diagnostic types, but have neither promised nor succeeded in getting at the roots of these disorders.
Malmo and his associates (1951) have questioned the wisdom of resorting to tests of perception, and especially of concept formation, in order to establish characteristic differences between normal persons and neurotic or psychotic patients. In an experiment demanding difficult perceptual judgment under time pressure, it was demonstrated that groups representing these three classes barely differed in their accuracy. They did differ, though, in the regularity and duration of the motor response by which they indicated their judgment (this was simply pressing a button with the right thumb). They also differed in the frequency and magnitude of the synchronous response with the left hand and in the motor activity of their left hand between responses. The experimenters presented these results in support of the thesis that disproportionate motor disturbance is typical of patients with mental disorder under any stressful situation, and not only when the stress is specific to their emotional problem.
This line of reasoning is very congenial to Eysenck (1947; 1961), who has undertaken the most ambitious and extensive experimental research in mental disorders, with the purpose of establishing a reliable psychiatric nosology. Experimental studies have played an important part in this program and have contributed data to the factor analyses from which three personality dimensions were derived. One of these represents introversion–extroversion and accounts for certain individual differences in normal, healthy persons, as well as for the two types of disorders into which Eysenck groups the neuroses. The other dimensions represent the magnitude of a patient’s neurotic and psychotic disturbance. The three dimensions are orthogonal to each other (i.e., independent), so that the extent of a patient’s psychotic derangement is unrelated to the magnitude or type of his neurotic abnormality. Most of Eysenck’s earlier experiments demanded performance of some task, but more recently he has preferred laboratory methods that call for judgments on perceptual illusions or aftereffects. Some of these procedures, such as assessing the afterimage of a rotating spiral, have been widely used by clinical psychologists for diagnostic as well as research purposes.
Induction and treatment
Experimental techniques have also been used for the induction and treatment of mental disorders. While the development of a lasting experimental neurosis in an animal may be a perfectly justified venture, with human subjects the derangement of mental function can be considered only if it is a reversible process of short duration. Various psychotomimetic drugs have been used for this purpose, producing effects that have been reported as pleasant by some, disagreeable by others, and weird by most persons undergoing the experience. Perception and thought processes are distorted in fairly predictable fashion, but it remains a matter of debate whether the abnormal effects thus induced are the same as, similar to, or different in character from those of, for example, schizophrenia. Sleep deprivation, extreme fatigue, anoxia, starvation, heat and cold, excessive sensory stimulation (e.g., continuous noise) and its opposite, sensory and social isolation, have been among the experimental devices used to induce transitory mental disorders. [SeeDrugs; Perception, article onperceptual deprivation.]
The application of experimental techniques to the treatment of mental disorders has received its strongest impetus from theories of conditioning. The therapeutic goal is to retrain the patient by progressive weakening of the maladaptive habit or symptom or by reinforcement of an adaptive response. From isolated experiments with laboratory techniques to cure enuresis or hysterical tics or paralysis, or to reach autistic or mentally defective children, there has now developed a recognized practice of behavior therapy. Its methods—desensitization, satiation, counterconditioning, reciprocal inhibition, operant and avoidance conditioning—were formulated and first tested with animals. Now they are applied by clinicians, whose relationship to the patient may not be very different from the psychotherapist’s. Also, like the latter, the behavior therapist can combine psychological treatment with pharmacological treatment. [SeeLearning, articles Onclassical conditioning, instrumental learning, andavoidance learning; Learning theory; Mental disorders, treatment of, article Onbehavior therapy.]
Drug therapy and electroshock treatment have many of the features of a research experiment. The agents administered to bring about certain effects, i.e., improvement in the patient’s condition, are under control. The amount given, the duration of treatment, and the avenue by which the agent is administered can be varied, within limits, and the manifestation of side effects, as well as of the principal outcome, can be evaluated and related to the input variables. Opportunities to explore these relationships have been thoroughly exploited by experimenters. [SeeElectroconvulsive shock; Mental disorders, treatment of, article onsomatic treatment.]
The use of experiments in evaluating process and outcome in psychotherapy is far more limited. In individual and group therapy alike, too many of the relevant influences are outside the scope of controlled manipulation. Hypnotherapy offers more attractive possibilities; indeed, all research related to hypnosis seems to be relevant to an understanding of mental derangements and, in the light of Orne’s findings, to an accurate assessment of experimental findings in psychology. Orne’s experiments (1959) have shown that behavior under hypnosis depends very largely on the current notions about hypnotic effects and, also, that subjects volunteering for psychological experiments tend to have very definite ideas about how they are expected to behave in the laboratory, ideas which may exert a considerable influence on what they do or accomplish there. [SeeHypnosis.]
Experiments in human behavior, whether they reflect normal or disordered mental function, pose certain problems that are of little or no concern to experimenters in other biological sciences. The patient or control subject does not ever merely react to stimuli. The best the experimenter can achieve is to elicit, with his instructions and setting, an unprejudiced cooperation and to rely on observations that allow the least possible latitude for subjective interpretation. In the course of his work he may make new and significant clinical observations or discover lawful relationships that explain some phenomena of the mental disorders. His special contribution, however, is the testing of such observations and the definition of clinical terms by operations that are reproducible and open to inspection by all who will take the trouble to look.
[Directly related are the entries Experimental design; Psychoanalysis, article onexperimental studies. Other relevant material may be found in Anxiety; Depressivedisorders; Drugs; Fatigue; Mental disorders, treatment of; Nervous system; Schizophrenia; Sleep; Stress; and in the biographies of Goldstein; Kraepelin; Lashley.]
Boring, Edwin G. (1929) 1950 A History of Experimental Psychology. 2d ed. New York: Appleton. → See especially pages 50–60, “Phrenology and the Mind-Body Problem,” and pages 61–79, “Physiology of the Brain: 1800–1870.”
Cameron, Norman A. 1947 The Psychology of Behavior Disorders: A Biosocial Interpretation. Boston: Hough ton Mifflin.
Conrad, Klaus 1954 New Problems of Aphasia. Brain 77:491–509.
Conrad, Klaus 1960 Die Gestaltanalyse in der psychiatrischen Forschung. Nervenarzt 31:267–273.
Eysenck, Hans J. 1947 Dimensions of Personality. London: Routledge.
Eysenck, Hans J. (editor) 1961 Handbook of Abnormal Psychology. New York: Basic Books.
Flugel, John C. (1933) 1964 A Hundred Years of Psychology: 1833–1933. With an additional part, 1933–1963, by Donald J. West. New York: Basic Books.
Goldstein, Kurt (1934) 1939 The Organism: A Holistic Approach to Biology Derived From Pathological Data in Man. New York: American Book. → First published as Der Aufbau des Organismus.
Goldstein, Kurt 1942 Aftereffects of Brain Injuries in War, Their Evaluation and Treatment: The Application of Psychologic Methods in the Clinic. New York: Grune.
Halstead, Ward C. 1947 Brain and Intelligence. Univ. of Chicago Press.
Harlow, Harry F. 1958 The Nature of Love. American Psychologist 13:673–685.
Harlow, Harry F. 1962 The Heterosexual Aifectional System in Monkeys. American Psychologist 17:1–9.
Head, Henry et al. 1920 Studies in Neurology. 2 vols. London: Hodder & Stoughton. → Consists mainly of papers published in Brain between 1905 and 1918. See especially Volume 2, pages 533–800, “The Brain.”
Hebb, Donald O. 1949 The Organization of Behavior: A Neuropsychological Theory. New York: Wiley.
Hebb, Donald O. 1958 A Textbook of Psychology. Philadelphia & London: Saunders.
Jackson, J. Hughlings (1884) 1958 Evolution and Dissolution of the Nervous System. Volume 2, pages 45–75 in J. Hughlings Jackson, Selected Writings .... Edited by James Taylor. New York: Basic Books. → First published in 1884 in Lancet.
King, Henry E. 1954 Psychomotor Aspects of Mental Disease. Cambridge, Mass.: Harvard Univ. Press.
Kinsbourne, M.; and Warringtqn, Elizabeth K. 1962 A Variety of Reading Disability Associated With Right Hemisphere Lesions. Journal of Neurology, Neurosurgery, and Psychiatry 25:339–344.
Kraepelin, E. 1896 Der psychologische Versuch in der Psychiatric. Volume 1, pages 1–91 in E. Kraepelin, Psychologishe Arbeiten. Leipzig: Englemann.
Krech, David 1962 Cortical Localization of Function. Pages 31–72 in Leo Postman (editor), Psychology in the Making. New York: Knopf.
Lashley, Karl S. 1929 Brain Mechanisms and Intelligence: A Quantitative Study of Injuries to the Brain. Univ. of Chicago Press.
Liddell, H. S. 1944 Conditioned Reflex Method and Experimental Neurosis. Volume 1, pages 389–412 in Joseph McV. Hunt (editor), Personality and the Behavior Disorders: A Handbook Based on Experimental and Clinical Research. New York: Ronald.
Luriia, Aleksandr R. 1932 The Nature of Human Conflicts; or, Emotion, Conflict and Will: An Objective Study of Disorganization and Control of Human Behaviour. New York: Liveright.
Magoun, Horace W. (1958) 1963 The Waking Brain. 2d ed. Springfield, Ill.: Thomas.
Malmo, Robert B. et al. 1951 Motor Control in Psychiatric Patients Under Experimental Stress. Journal of Abnormal and Social Psychology 46:539–547.
Miller, Neal E. 1944 Experimental Studies of Conflict. Volume 1, pages 431–465 in Joseph McV. Hunt (editor), Personality and the Behavior Disorders: A Handbook Based on Experimental and Clinical Research. New York: Ronald.
Milne, Brenda; and Penfield, Wilder 1955 The Effect of Hippocampal Lesions on Recent Memory. American Neurological Association, Transactions 80: 42–48.
Orne, Martin T. 1959 The Nature of Hypnosis: Artifact and Essence. Journal of Abnormal and Social Psychology 58:277–299.
Osgood, Charles E. (1953) 1959 Method and Theory in Experimental Psychology. New York: Oxford Univ. Press.
Penfield, Wilder 1954 Studies of the Cerebral Cortex of Man: A Review and an Interpretation. Pages 284–309 in Council for International Organizations of Medical Sciences, Brain Mechanisms and Consciousness. Edited by J. F. Delafresnaye. Oxford: Blackwell.
Ranschburg, Paul 1939 Les bases somatiques de la mémoire. Pages 513–531 in Centenaire de Th. Ribot: Jubilé de la psychologic scientifique francaise, 1839–1939. Agen (France): Imprimerie Moderne.
Schilder, Paul 1942 Mind: Perception and Thought in Their Constructive Aspects. New York: Columbia Univ. Press.
Scoville, William B.; and Milner, Brenda 1957 Loss of Recent Memory After Bilateral Hippocampal Lesion. Journal of Neurology, Neurosurgery, and Psychiatry 20:11–21.
Sears, Robert R. 1943 Survey of Objective Studies of Psychoanalytic Concepts. Bulletin No. 51. New York: Social Science Research Council.
Semmes, Josephine et al. 1960 Somatosensory Changes After Penetrating Brain Wounds in Man. Cambridge, Mass.: Harvard Univ. Press.
Talland, George A. 1965 Deranged Memory. New York: Academic Press.
Teuber, Hans L. 1964 The Riddle of Frontal-lobe Function in Man. Pages 410–444 in Symposium on the Frontal Granular Cortex and Behavior, Pennsylvania State University, 1962, The Frontal Granular Cortex and Behavior. Edited by J. M. Warren and K. Akert. New York: McGraw-Hill.
Teuber, Hans L.; and Liebert, Robert S. 1958 Specific and General Effects of Brain Injury in Man. Archives of Neurology and Psychiatry 80:403–407.
Weisenburg, Theodore; and McBride, Katharine 1935 Aphasia: A Clinical and Psychological Study. New York: Commonwealth Fund.
Werner, Heinz (1926) 1957 Comparative Psychology of Mental Development. Rev. ed. New York: International Universities Press. → First published in German.
Zangwill, O. L. 1960 Cerebral Dominance and Its Relation to Psychological Function. Edinburgh: Oliver & Boyd.
"Mental Disorders." International Encyclopedia of the Social Sciences. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/social-sciences/applied-and-social-sciences-magazines/mental-disorders
"Mental Disorders." International Encyclopedia of the Social Sciences. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/social-sciences/applied-and-social-sciences-magazines/mental-disorders
MENTAL ILLNESS The Seventeenth through the Nineteenth Centuries
The history of mental illness in the United States reflects the ever-changing landscape of mental disorders and the medical specialties responsible for their management and treatment. Mental illness (psychiatric disorders) is a nebulous term that has evolved over time. Insanity, lunacy, madness, mental illness, derangement, or unreason are among the many labels used to describe those individuals who, for various reasons, are psychologically unable to successfully function in society and require some form of intervention or treatment. The underlying causality for mental illness may be either physical (as in senile dementia), psychological (as in depression), or a combination of both. Since the middle of the nineteenth century, medical science has revolutionized treatment for numerous medical conditions, including mental illness. Many conditions previously believed to be psychological have been determined to be organic and removed from psychiatric nomenclature (conditions caused by vitamin deficiency, for example). Other conditions, such as schizophrenia and bipolar disorders, are the subject of dispute as to whether or not they are organic or psychological. Consequently, psychiatric nosology (the use of diagnostic categories) has remained fluid, as has the reported incidence of mental illness, ranging from approximately 3 percent of the population for psychotic disorders to 50 percent of the population for depression. Treatment approaches have been fluid as well, ranging from the exclusively physical to the exclusively psychological. Most mental health professionals advocate a combination of physical (psychotropic medications) and psychological (counseling) for most forms of mental disturbance.
Attitudes toward, and treatment for, the mentally ill in the United States accompanied the colonists from Europe, particularly England. By the beginning of the colonial period in America, the mad in Europe were confined to a variety of facilities called workhouses or houses of correction, along with other deviant groups. Treatment for the mad was predicated on the belief that mental illness was either the result of some mysterious physical malady or punishment for sin. What constituted treatment was extreme: bleeding, cathartics, emetics, hot and cold showers, whipping, and chaining. The history of the insane in colonial America followed a similar pattern: the mad were confined together with other deviant groups, either at home or in institutions. However, "home confinement" meant detention within the community, which led to rigorous settlement laws for newcomers, intended to prevent economic dependency on the community. If the new settler or visitor could not satisfy the settlement laws, they were "warned out" or asked to leave the settlement. Thus many of the mentally afflicted, the poor, the disabled, and petty criminals were forced to wander from township to township, occasionally housed overnight in the town jail and then forced to leave the community. As population increased and communities became more urban, hospitals were established at Philadelphia (1751) and New York (1773) that accepted both the physically and the mentally ill. However, treatment for the mentally disturbed was unchanged. Benjamin Rush, the "father of American psychiatry" and a medical practitioner at the Pennsylvania Hospital, advocated the same "heroic" treatment procedures as had his predecessors.
The emergence of a radically different approach at the Retreat in York, England (founded in 1792; first patients in 1796), established by William Tuke, ushered in a new era in the management of the mad. Similar developments had been taking place about the same time in Paris, initiated by Philippe Pinel, who unchained the mad and imposed a more humanitarian treatment regimen. Labeled moral therapy, the new form of treatment for the mad became the dominant approach for more than one hundred years. Moral therapy, or moral management, included removing the mad from their environment and secluding them in facilities exclusively for them, providing a structured daily schedule and work therapy, and confronting
their "inappropriate" behavior for the purposes of reducing or eliminating such behavior. The goal of moral therapy was to restore the individual's sanity and to return the patient to society as a fully functioning, productive member of society through order, regularity, and discipline. Concurrently, the punitive treatments of the past were abolished. The introduction of moral therapy or management fostered a new optimism regarding treatment for the mad. Based on the new confidence, there followed an intense period of asylum building. Initially the new asylums were privately sponsored (corporate facilities), such as the one at the Charlestown branch of the Massachusetts General Hospital (1818; later renamed the McLean Asylum), the Bloomingdale Asylum (1821), and the Connecticut Retreat for the Insane (1824; later renamed the Hartford Retreat), but in short order, state governments began erecting public asylums. Although the first state asylum exclusively for the insane had been completed at Williamsburg, Virginia, in 1773, it remained a unique facility until 1824, when other states began to assume responsibility for the care and treatment of the insane. Between 1825 and 1865, fifty-three insane asylums were constructed, bringing the total in the United States to sixty-two. One individual, Dorothea Dix (1802– 1887), had a significant influence on asylum construction. After a visit in 1841 to a local Massachusetts jail, where she observed the deplorable conditions for the insane inmates, Dix began a forty-year campaign to reform conditions for the mad. She appealed to various individuals and government bodies with remarkable success. Dorothea Dix has been credited with the erection of thirty-two asylums, including Dorothea Dix Hospital in Raleigh, North Carolina (first patients in 1856). As state asylums were erected, they incorporated moral therapy as their treatment model, with unfortunate consequences. Whereas private, or corporate, asylums could limit patient population, public institutions could not. Populations in public facilities increased beyond the ability of the staff to realistically implement moral management. Consequently, public asylums became severely overcrowded and reduced to merely custodial institutions, a circumstance that was perpetuated well into the twentieth century.
The Association of Medical Superintendents of American Institutions for the Insane (AMSAII), organized in 1844, could do nothing to prevent or ameliorate the worsening problem of overcrowding and reduced funding. The Association was not an organization with an agreed-upon body of knowledge and theories concerning the causes and treatment of the insane that sought to inform and shape social attitudes toward the mentally ill. To the contrary, asylum superintendents and the facilities they administered had been assigned a role to play regarding a specific deviant group. Therefore, ideas articulated by the superintendents regarding the causes and treatment of mental illness were consistent with society's attitudes toward the asylum population. They were, first and foremost, agents of society and, second, physicians to the mad. Accordingly, there was a general consensus among the superintendents that most forms of madness were the consequence of some kind of physical trauma. Hallucinations, delusions, or disorders of the cognitive mind where observable aberrant behaviors were involved were easy to classify as madness and attribute to a blow to the head, fever, chronic illness, or some other easily discernible cause.
The difficulty with this theory lay in socially deviant behaviors where there was no observable mental or physical cause. How to diagnose, or classify, those individuals who committed apparently senseless, socially unacceptable acts? Were the individuals criminal, insane, or both? The answer was "moral insanity, " an ambiguous label for various forms of social deviancy in the nineteenth century. The primary cause of "moral insanity" was a disordered society, the effect of urbanization and immigration. As a result, the asylum itself became the remedy for insanity and other forms of social deviancy. If insanity could not be "cured, " at least it was confined and segregated from the remainder of society, where the mad would remain until 1964. From the beginning of the Civil War to the turn of the century, asylums continued to experience worsening overcrowding, decline in quality and quantity of personnel, reduced budgets, and a myriad of other problems.
Following the Civil War, neurology began to emerge as a new medical specialty and as one of the two major critics of asylum superintendents and asylum conditions. While neurologists agreed with asylum superintendents that insanity was a disease of the brain and that the deplorable asylum conditions were due to budgetary issues, they were critical of the superintendents. Neurologists argued that the superintendents were no more than asylum administrators, certainly not physician-scientists concerned with clinical practice and medical research concerning the origins and treatment of aberrant mental conditions. The conflict between the two specialties culminated in 1894 when Silas Weir Mitchell addressed the American-Medico-Psychological Association (AMPA) (formerly the AMSAII; the new name was adopted in 1892). Mitchell declared that the asylum physicians were not collecting adequate case histories or mental status examinations, they were neglecting autopsy and laboratory work, and they were failing to properly care for their patients. Thereafter, the two medical specialties reached an accommodation that was perpetuated well into the twentieth century.
Allied with neurologists as the other significant critic of asylum management and inmate care were state boards of charities. Once state governments determined that asylum budgets were their single greatest expense, administrative and budgetary control of the asylums was transferred to the boards of charities. As a consequence, once again the mentally disordered were grouped together with other deviant groups, criminals, the indigent, and the disabled, as a function of centralizing and rationalizing public welfare.
Thus, by the end of the nineteenth century, treatment of the mentally ill in America had come full circle. Housed in separate facilities, the mad were once again the responsibility of a centralized agency, the public welfare departments of state governments. Moreover, the earlier optimism regarding moral management had been replaced by a renewed pessimism. By the end of the nineteenth century, the asylums had failed as a cure for madness. There was no recognized medical cure for madness; confinement had only removed the mad as a threat to social order ("out of sight, out of mind"). An impasse had been reached, with no effective treatment available; all that remained was the asylum.
The Twentieth Century
The origins of a new approach to mental disorders began in the decade preceding the turn of the century. The informal adoption of Emil Kraepelin's classification system by Adolf Meyer in 1896, accompanied by the new title for the official organization of asylum physicians (AMPA), signaled a change in the approach to the treatment of the mentally ill. Both developments suggested that the profession was moving toward a disease concept of mental illness, in keeping with growing influence of scientific medicine. However, the most significant catalyst for change was Sigmund Freud (1856–1939), the creator of psychoanalysis as a valid approach for the treatment of mental disorders. Freud's innovation was the development of a systematic psychology of the mind and techniques to access the unconscious. Introduced to the American medical community during the first decade of the twentieth century, psychoanalytic techniques fundamentally altered treatment of the mentally ill. Freud and Carl G. Jung, the most prominent of Freud's followers, visited the United States to give a series of lectures at Clark University in 1909. Jung was one of the first psychoanalysts to employ psychoanalytic techniques with severely disturbed (psychotic) individuals, particularly schizophrenics. Freud's techniques were readily adapted to "office practice, " whereas Jung's methods were particularly useful with more severely disturbed, hospitalized patients.
Psychoanalysis was modified and popularized by American physicians such as A. A. Brill, Freud's American translator; Adolf Meyer, the first director of the Henry Phipps Psychiatric Clinic (1913) at Johns Hopkins Medical Center; and William Alanson White, the superintendent (1903) of the federal psychiatric hospital, St. Elizabeth's, in Washington, D.C. From their respective positions, Meyer and White became two of the most influential members of the psychiatric specialty in America. Both men shaped the evolution of psychiatric concepts and training during the first half of the twentieth century. In their professional roles, Meyer and White supported a more general reform of treatment for the mentally ill, lending their support to the National Committee for Mental Hygiene, founded by Clifford Beers, a former mental patient, in 1909. The goals of the National Committee were to prevent mental illness and to improve institutional conditions for the mentally ill.
Meyer and White symbolized the revolution in psychiatry and, more generally, medicine at the beginning of the twentieth century. Medical science had a profound impact on psychiatry, as new developments in medicine altered treatment procedures for many psychiatric disorders, as it did for physical ailments. Physical and psychological medicine fused to become modern psychiatry, a legitimate, accepted medical science of the mind. In 1921, its professional organization adopted a new name, the American Psychiatric Association, changed the name of its professional journal to the American Journal of Psychiatry, and accepted Kraepelin's nosology as the standard nomenclature for classifying psychiatric disorders. In the decades that followed to the close of the twentieth century, there were three important developments: continuing developments in medicine that directly affected the treatment of mental illness; expanding government participation in funding and oversight of patient care; and a proliferation of psychotherapeutic "schools, " most a response to the growing popularity of psychoanalysis.
Medical discoveries continued to redefine diagnostic categories and influence treatment for mental disorders. Therapeutic procedures appeared to revert to the former "heroic" measures of the past with the application of Metrazol, insulin, and electric shock therapies between 1937 and 1940. All three induced severe convulsions in the subject, who was typically chronically psychotic, with questionable results and at some risk to the patient. More effective and benign treatment appeared in the early 1950s in the form of chemical compounds known today as tranquilizers or, more accurately, psychotropic medication. The continuing evolution and effectiveness of these drugs has had a profound effect on treatment for the mentally ill, enabling many hospitalized patients to return to home and work or precluding hospitalization in the first place. As more effective treatment regimens appeared and as a response to public demand, government took a more active role in allocating funds for research and the establishment of model programs for the mentally ill. In 1946, the National Mental Health Act provided for the establishment of the National Institute of Mental Health; in 1963, the National Community Mental Health Centers Act was passed, which effectively "deinstitutionalized" most chronically ill patients and brought to an end reliance on custodial care facilities for the most severely disturbed individuals. The legislation anticipated that most former chronic patients would be managed by medications provided through local community mental health centers, but these expectations were not realized. The unfortunate consequence of this legislation has been to create an indigent homeless population in larger municipalities that absorbs law enforcement, medical, and other community resources. Nonetheless, state and federal governments have assumed a seemingly limitless role regarding mental disorders and the mentally ill.
Perhaps even more startling than any other development regarding mental illness in the United States has been an explosion in the number of mental health professionals during the past one hundred years. From an extraordinarily small group of psychiatrists, 222 in 1900, the number and variety of mental health professionals has grown enormously. No longer is psychiatry the only discipline concerned with treatment of the mentally ill. By the end of the twentieth century there were more than thirty-two thousand psychiatrists, seventy thousand psychologists, and many hundreds of thousands practicing in related professions—psychiatric social workers, pastoral counselors, sex therapists, marriage counselors, and a myriad of other quasi-professional and lay practitioners. Moreover, the number of psychotherapeutic approaches grew to nearly three hundred competing therapies, including various forms of psychoanalysis, individual and group psychotherapy, marriage and family counseling, "primal scream" therapy, "est, " transactional analysis, Gestalt therapy, and so on. Public and private hospital expenditures surpassed $69 billion and continued to increase, while private out-patient expenditures were undetermined. A vast array of psychoactive medications became available, either over the counter or by prescription. What were once private, personal problems became the subject of radio and television talk shows and newspaper advice columns.
Mental illness in America was transformed during the twentieth century. The single therapeutic tool of the nineteenth century, the asylum, virtually disappeared. Once the stepchild of medicine, psychiatry became a recognized medical specialty, a requirement in most medical schools. Underlying causes for mental illnesses are now recognized as a combination of environment and biology. One constant remains: as the medical and natural sciences continue to make new discoveries, what constitutes mental illness continues to be redefined.
Grob, Gerald N. Mental Institutions in America, Social Policy to 1875. New York: Free Press, 1973.
———. Mental Illness and American Society, 1875–1940. Princeton, N.J.: Princeton University Press, 1983.
———. From Asylum to Community: Mental Health Policy in Modern America. Princeton, N.J.: Princeton University Press, 1991.
Hale, Nathan G. The Beginnings of Psychoanalysis in the United States, 1876–1917. New York: Oxford University Press, 1971.
———. The Rise and Crisis of Psychoanalysis in the United States: Freud and the Americans, 1917– 1985. New York: Oxford University Press, 1995.
Porter, Roy. The Greatest Benefit to Mankind: A Medical History of Humanity. Chapter XVI, "Psychiatry." New York: Norton, 1997.
Shorter, Edward. A History of Psychiatry: From the Era of the Asylum to the Age of Prozac. 2d ed. New York: Wiley, 1998.
"Mental Illness." Dictionary of American History. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/history/dictionaries-thesauruses-pictures-and-press-releases/mental-illness
"Mental Illness." Dictionary of American History. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/history/dictionaries-thesauruses-pictures-and-press-releases/mental-illness
Mental illness is a series of disorders and diseases that affect the intellectual, emotional, and psychological makeup of individuals. Causation is wide ranging (from organic and genetic maladies to environmental triggers; from poor nutrition and poverty to psychological trauma) but many times unknown. Because of the myriad of disorders under the label of mental illness, a generalized "cure" has not been developed. Measures to ameliorate the effects of the spectrum of disorders include therapy of various forms, counseling, and pharmacological interventions.
Mental illness does not exist in a social vacuum, independent of the context of time and place. Its assumed etiology (causes) and manifestations are reflections of the social setting in which it exists. The twentieth century saw a large increase in the number of individuals exhibiting symptoms of mental illness. Whether this resulted from better reporting methods, shifting levels of category description, or a generalized increase in the number of individuals afflicted is still open to debate. It is apparent, however, that children at the turn of the twenty-first century were suffering from an epidemic of mental illness. More children in the United States in 2003 suffered from psychiatric illness than from AIDS, leukemia, and diabetes combined. The solutions proposed to the problems caused by mental illness in children reflect the underlying assumptions of society. That these solutions have changed over time similarly reflect that American society itself has reshaped its intellectual presuppositions throughout history.
Religious Causes in Colonial America
Traditionally, emotional and psychological problems in children were viewed through the prism of religion. Children experiencing visions, hearing voices, or enduring seizures were seen as individuals touched by either God or Satan. Etiology was considered as otherworldly; therefore, alleviation of the disorder would come through supplication to the Deity. This was in the form of prayer, Scripture reading, and personal admission of sin and guilt.
The Salem, Massachusetts, witchcraft crisis of 1692 provides the most familiar example of how childhood mental illness was perceived and dealt with during the colonial American era. Dozens of young women were involved in a wide-ranging frenzy of accusations of witchcraft, punctuated by visions, spells, physical maladies, and the belief that Satan was actively working to control individuals in and around Salem Village. Historians have argued over the "actual" cause of these happenings, positing economic, cultural, psychological, and medical explanations. What is known, however, is that contemporaries had only one explanation–the young women participating in the naming of witches were not mentally ill in the modern sense of the term: they were victims in the ongoing battle between God and Satan for the souls of mankind. Cotton Mather, the influential Puritan clergyman, expressed this belief most clearly in his book Wonders of the Invisible World, published in 1692. Mather and other Puritan leaders saw young women, because of their age and dependent condition, as especially susceptible to the hallucinations and physical assaults caused by this cosmic battle. Prayer for the afflicted, as well as punishment for those bewitched by Satan himself, were seen as cures for the physical and mental ailments of the girls involved in the witchcraft hysteria.
Shift to Social Causes in the Eighteenth Century
By the eighteenth century, the hysterical outbursts associated with witchcraft and Satanic possession subsided, lending credence to the belief that social, rather than religious, causes led to the maladies. Incidences of childhood mental disorders were not as visible, or seemingly as prevalent, during this period. Childhood was viewed as a time of unrequited joy, when children did not face the problems and toil of adult life. Adults exhibiting overt signs of mental disorder were treated in differing ways depending on their class and status in society. Upper-class individuals who showed signs of mental problems were usually cared for within the family and labeled as strange or eccentric. Members of the lower class who gave signs of mental disorder often were not able to take care of themselves or their families and were "warned out" of communities or placed in poorhouses, with other undifferentiated categories of dependent individuals. Separate institutions for the mentally ill were developed in the late colonial or early national period throughout the United States and treated their patients (often called inmates) with a combination of primitive medical care (such as purging or bleeding), forced work to give the mind discipline, and moral care based on the treatment plans developed by the French physician Philippe Pinel (1745–1826). Few children, however, were admitted to these new institutions (often called asylums, as their founders saw them as refuges from the problems of an increasingly complex society). Children appeared more often as the victims of familial mental disorder, as wards forced to depend on private and religious philanthropies or the state to raise them.
Gendered Differentiation in the Nineteenth Century
The nineteenth century saw an increasingly gendered differentiation in the maladies that comprised the spectrum of mental disorder. The Industrial Revolution that swept over western Europe and the United States in the first half of the nineteenth century was both a cause and consequence of the emerging separation of the sexes by occupation and position. Dubbed the notion of "separate spheres," this vision of society was one in which men worked outside the home as providers and women ran the household as protectors of the domestic sphere. Changing perceptions of women's emotional, intellectual, and sexual makeup accompanied this paradigm shift. Seen as needing male protection to survive, women were classified into a larger category of dependent individuals, a category that also included children. By the middle of the nineteenth century, women and young girls were exhibiting a series of mental maladies that doctors and social critics tied to the specific problems of female anatomy and emotionalism. Running the emotional gamut from depressive melancholia to hyperemotional hysteria, these disorders could be acute or chronic, incapacitating or simply bothersome. Attempts at cures ranged from bed rest, asylum stays, and dietary changes to medical interventions such as water treatments and purgatives. Most regimens were not successful, but many women recovered to live what seemed to be "normal" lives.
These disorders were inordinately centered in young women of the upper and middle classes who were among the first of their sex to achieve higher levels of formal education, an education that may have been in strong conflict with the prevailing assumptions of female dependency. By the last quarter of the century, medical doctors had developed a name for these emotional illnesses–neurasthenia, or a weakness of the nervous system. Popularized by the American neurologist George Beard and the American physiologist S. Weir Mitchell, the term became a catchall category for the mental problems associated with feminized nervous energy. That young upper-class males also began to be diagnosed with the disease (for example, the American psychologist and philosopher William James was incapacitated for almost a year with nervous problems) led doctors to decry the feminization of American culture. A strident dose of "the strenuous life" was recommended to cure "weak" young males of this malady.
Neurasthenia was not seen as a problem among young people from the working class. The emotional problems these people exhibited were thought to arise from their inferior intellectual makeups or their genetic background. With the advent of massive streams of immigrants from southern and eastern Europe in the last twenty years of the nineteenth century, the composition of the American working class took on an increasingly foreign character. Medical doctors (almost exclusively from white American backgrounds) viewed foreigners as inferior and unable to handle the problems associated with complex modern societies. The lack of assimilation into mainstream American society, the petty crime that many young immigrant males seemingly engaged in, and the perceived inability of young immigrant women to rise to standards of appropriate feminine behavior all contributed to notions of immigrant inferiority. The increasingly foreign composition of state institutions for those with mental problems seemed to validate that belief. These mental problems among immigrants were not thought to be curable, as they were believed to be manifestations of inherited, and therefore, unchangeable traits.
Twentieth Century: Competition among Social, Psychological, and Medical Paradigms
By 1900, childhood and adolescence were clearly viewed as separate stages of life, with their own problems and possibilities. The development of separate public institutions designed around the needs of children became a key component of Progressive-era changes during the first two decades of the twentieth century. Historians debate whether juvenile courts and specialized facilities for young offenders that arose during this period were instruments of social reform or social control. What is not at issue, however, is the notion that children were to be treated differently because they had different needs and concerns. Because of this seminal shift, historian Theresa R. Richardson, following the lead of reformer Ellen Key, has called the twentieth century "TheCentury of the Child."
With this transition, doctors began to examine the issue of childhood diseases as a separate category of analysis. The mental disorders of children were not immune from this alteration. Simultaneously, the development of psychology as a discrete discipline saw the bifurcation of the understanding of what caused and what constituted mental disorders. The neurasthenic problems were increasingly viewed as emotional or intellectual problems, rather than somatic illnesses (those affecting the body). They could be cured or alleviated through therapy and counseling, not medical intervention. The more serious mental illnesses, often labeled around the catchall phrase of insanity, still remained the purview of medical doctors, who were marginalized as employees of large state institutions. Insanity appeared incurable, but by the 1920s and 1930s doctors experimented with such invasive techniques as electroshock therapy and lobotomy surgery with decidedly mixed results. Finally, problems that had been categorized as mental disorders, particularly those associated with young boys such as theft and truancy, were increasingly viewed as social, rather than medical, disorders. As such, they became issues for social workers and juvenilejustice officials, rather than psychologists or medical doctors.
The social, psychological, and medical paradigms competed for control over the issues of mental disorder in general, and childhood mental illness more specifically, throughout the twentieth century. By approximately 1975, the success of the medical model in establishing hegemony over the field of what became known as mental illness was a seminal moment. The medicalization of problems in adjusting to social situations led to a reliance on both over-the-counter and prescription pharmaceuticals to solve disorders previously assumed to be social in nature. New advances in genetics revealed the importance of biological characteristics in the development of such disorders as drug addiction and alcoholism. Finally, the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association drastically increased the type and number of mental disorders from 112 in the first edition, published in 1952, to 374 in the fourth edition, published in 1994. Many of these newly defined disorders deal specifically with mental illnesses of childhood. As the twenty-first century began, childhood mental illness was defined as a major social problem. Solutions and cures appeared difficult to come by, as contentious arguments continued over the efficacy of medical interventions and the true nature of childhood mental disorders.
Exacerbating the issues surrounding the medicalization of childhood mental disorders are concerns over both the increasing number of children exhibiting these illnesses and of the class, racial, and gendered nature of these problems. Whereas some disorders, such as conduct disorders and oppositional defiance, occur overwhelmingly in young males, others, especially eating disorders such as anorexia and bulimia, are mainly female in character. The epidemics of attention deficit hyperactivity disorder (ADHD) and autism similarly show significant male components, whereas anxiety disorders occur largely in females. Physicians and researchers search for stronger connections between genetics and disorders such as childhood schizophrenia, while rates of teen suicide continue to increase. Teen violence–despite high-profile cases such as the Columbine High School shootings in middle-class, white, suburban Littleton, Colorado, in 1999–is overwhelmingly centered in poor, minority, urban neighborhoods. Physicians report that minority youths receive approximately one-third the support given to white youths suffering from similar mental health problems. National Institutes of Health reports show that in 2001, one out of ten children and adolescents suffered from a mental disorder severe enough to cause some level of impairment, yet only about 20 percent of those affected received needed treatment. The issue of mental illness in children will remain a pervasive national concern to Americans well into the twenty-first century, as citizens debate the nature of these disorders and their relationship to broader social trends.
See also: Child Psychology.
Lutz, Tom. 1991. American Nervousness, 1903: An Anecdotal History. Ithaca, NY: Cornell University Press.
Safford, Philip L., and Elizabeth J. Safford. 1996. A History of Childhood and Disability. New York: Teachers College Press.
"Childhood Mental Health." Available from <www.childhooddisorders.com>.
"Mental Disorders in America." Available from <www.nimh.nih.gov/publicat/numbers.cfm>.
"Mental Illness." Encyclopedia of Children and Childhood in History and Society. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/children/encyclopedias-almanacs-transcripts-and-maps/mental-illness
"Mental Illness." Encyclopedia of Children and Childhood in History and Society. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/children/encyclopedias-almanacs-transcripts-and-maps/mental-illness
Mental illness is a global term for disorders of thought, mood, affect, and behavior that impair normal functioning, social relationships, and productivity. Worldwide, mental illnesses account for four of the ten leading causes of premature death or of disability in terms of lost years of healthy life. Major depression is the leading cause of disability worldwide, as measured by years of living with this disorder. Mental illnesses, including suicide, account for over 15 percent of disease burden, more than the burden from cancers, in established market economies such as the United States and Europe (National Institute of Mental Health 2006).
Mental illnesses such as schizophrenia and other psychotic disorders, mood disorders, anxiety disorders, and adjustment, identity, and personality disorders, are defined by discrete, clinically meaningful clusters of behavioral symptoms. The German psychiatrist Emil Kraepelin (1856–1926) was the first to develop a unified classification of the psychoses. His emphasis on precision and objective behavioral criteria greatly influenced the current diagnostic system, the American Psychiatric Association’s periodically updated and revised Diagnostic and Statistical Manual of Mental Disorders (DSM -IV-TR, 2000). The DSM codes are fully compatible with those in the mental disorders section of the World Health Organization’s International Classification of Diseases (ICD -10, 2005), with worldwide applicability. Patients are assessed on five axes:
Axis I—clinical disorders and other conditions that may be a focus of clinical attention;
Axis II—personality disorders and mental retardation;
Axis III—general medical conditions;
Axis IV—psychosocial and environmental problems; and
Axis V—global assessment of functioning.
Multiaxial assessment yields multiple domains of information that indicate possible comorbidities and permit comprehensive treatment planning.
Mental illnesses vary in severity, duration, and degree of incapacitation. Some specialists distinguish between acute reactive (brief nonrecurring) and chronic (long-term episodic) mental illness. The term chronic, disavowed by consumers (present and former psychiatric patients) as promoting hopelessness, has largely been replaced by “severe and persistent mental illness.” This description typically applies to persons with major Axis I disorders who manifest long-term disability.
Despite increasing evidence that most major mental illnesses appear to be biologically based, vulnerability and prognosis seem highly sensitive to the social environment. Epidemiologic studies indicate that major mental illnesses such as schizophrenia, depression, and bipolar or manic-depressive illness are found in all cultures throughout the world. However, there is considerable variability based on immigrant and socioeconomic status, and on urban versus rural living. Studies in Great Britain have found significantly higher prevalence rates for psychotic disorders in immigrants, city dwellers, and black and ethnic minority groups than in white British natives (Kirkbride et al. 2006). Incidence rates for schizophrenia drawn from 158 studies of 32 countries were significantly higher for males, migrants, city dwellers, and individuals born in the winter months (McGrath 2006), the latter presumably because of greater exposure of fetuses and neonates to viral insults to developing brain structures. Internationally, female gender and income inequality are major risk factors for depression (Patel 2001). World Health Organization studies indicate that although the diagnostic criteria for schizophrenia are applicable cross-culturally, prognosis and recovery rates are significantly better in the developing world than in Western industrialized nations (Jablensky et al. 1992)
Prolonged hospitalization for mental illness has long been on the decline in the industrialized world. Most mental disorders currently are treated on an outpatient basis, with various forms of individual, group, and family psychotherapy and in most cases, psychotropic medications. These include antipsychotic, antidepressant, antianxiety, and antiobsessional agents, as well as mood stabilizers and psychostimulants. More disabling disorders may require brief hospitalizations and rehabilitative interventions such as supported housing, supported employment, social-skills training, and combined mental health and substance abuse treatment. There is increasing demand for research-supported evidence-based treatments. Among these, psychotropic medications, cognitive and behavioral psychotherapies, family psychoeducation, and rehabilitative interventions have yielded the most empirical validation. However, studies also suggest that the patient-therapist relationship may be more salient than particular therapeutic models. Some mental health systems are promoting the involvement of consumers as service providers in rehabilitation and in peer counseling. Persons in recovery are able to share experiences and coping strategies, provide role models, and help reduce selfstigmatization.
The concept of mental illness as a biomedical condition distinct from social context has been subject to extensive criticism by social scientists and by some psychiatrists. Prominent writers such as Michel Foucault (1926–1984), R. D. Laing (1927–1989), and Thomas Szasz (b. 1920) have disputed the validity of a concept based on cultural definitions of normalcy and often mediated by social and economic concerns. Every culture has some concept of “madness,” defined as negatively perceived deviant behaviors that are distinguished from merely antisocial behaviors because they are incomprehensible within that cultural idiom. Despite transnational acceptance of ICD codes, the identification of a behavior or behavioral syndrome as denoting mental illness by ordinary citizens, as opposed to mental health professionals, is still to a considerable extent culture-bound. In certain individuals, religious delusions or hallucinations may be viewed as extraordinary gifts rather than symptoms. It is only when the symptoms impair role functioning and productivity that the person is labeled as mentally ill. Depression is sometimes manifested as somatization (diffuse bodily complaints) in some traditional cultures and is conceptualized by the sufferer as a physical rather than psychological condition. Stigmatization of mental illness is ubiquitous, yet research shows that social factors may affect perceptions of deviance and subsequent labeling and discrimination. In many cultures stigma seems to be related to chronic dysfunction and dependency, or to assumed threat, rather than to bizarre behaviors.
There is also a substantial literature on culture-bound syndromes—seemingly unique patterns of disordered or psychotic behaviors that are manifested only in particular cultural settings. Whether or not these are unique syndromes or variant forms of universal diagnostic categories, the behaviors are locally perceived as mental disturbances with specific names. The DSM -IV-TR lists twenty-five culture-bound syndromes found in various parts of the world, most of which appear as temporary delusional or dissociative states in which the person acts out in culturally aberrant and sometimes self-harmful ways. Some culture-bound syndromes appear as anxiety states with paranoid ideation about external malevolence or sorcery, or possession by spirits, accompanied by debilitating somatic symptoms. Still others are manifested as panic reactions, sexual fears, or paralyzing phobias. Most culture-bound syndromes are time-limited and do not seem to engender stigma. If they prove to be ongoing or potentially life-threatening, remedies are sought primarily in traditional healing rituals rather than in Western medicine.
Despite local variants, there is compelling evidence of universality and genetic predisposition in major Axis I and some Axis II disorders. The literature on schizophrenia also offers proliferating research findings from neuroradiology, neuropathology, neurochemistry, hematology, and psychopharmacology, indicating biological parameters of what was once considered a psychogenic or sociogenic disorder. Depression is associated with catecholamine deficits or excess, and hormonal imbalance. Obsessive-compulsive disorders have unique neurological substrates. Lesions in the orbitofrontal cortex have been linked to the impulsivity and affective instability of borderline personality disorder and other disorders of impulse control. Many mental illnesses show abnormalities in the serotonin neurotransmitter system. The permanent effects of these biological anomalies is still in question. There is increasing evidence of recovery from disorders that were once considered lifetime disabilities with a deteriorating course. Three major long-term outcome studies of formerly hospitalized persons with schizophrenia in Europe and the United States indicated a recovery or mild impairment rate ranging from 50 percent to 66 percent (Harding 1988). Representing a heterogeneous body of behavioral symptoms varying widely in severity and potential for remission, the term mental illness remains a concept in flux and the subject of ongoing research.
American Psychiatric Association. 2000. Diagnostic and Statistical Manual of Mental Disorders. 4th ed., text revision. Washington, DC: Author.
Harding, Courtenay M. 1988. Course Types in Schizophrenia: An Analysis of European and American Studies. Schizophrenia Bulletin 14: 633–643.
International Statistical Classification of Diseases. 2005. ICD -10-Classification of Mental and Behavioral Disorders and Related Health Problems. Geneva, Switzerland: World Health Organization.
Jablensky, Assen, Norman Sartorius, Georg Ernberg, et al. 1992. Schizophrenia; Manifestations, Incidence, and Course in Different Cultures: A World Health Organization 10-Country Study. Psychological Medicine Monograph Supplement 20: 1–97.
Kirkbride, James B., Paul Fearon, Craig Morgan, et al. 2006. Heterogeneity in Incidence Rates of Schizophrenia and Other Psychotic Syndromes: Findings from the 3-Center AESOP Study. Archives of General Psychiatry 63 (3): 250–258.
McGrath, John J. 2006. Variations in the Incidence of Schizophrenia: Data Versus Dogma. Schizophrenia Bulletin 32 (1): 195–197.
National Institute of Mental Health. 2006. The Impact of Mental Illness on Society. NIH publication no. 01-4586. http://www.nimh.nih.gov/publicat/burden.cfm.
Patel, Vikram. 2001. Cultural Factors and International Epidemiology. British Medical Bulletin 57 (1): 33–45.
Harriet P. Lefley
"Mental Illness." International Encyclopedia of the Social Sciences. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/social-sciences/applied-and-social-sciences-magazines/mental-illness
"Mental Illness." International Encyclopedia of the Social Sciences. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/social-sciences/applied-and-social-sciences-magazines/mental-illness
The term used to describe a disorder or condition that negatively affect cognition (thought), behavior, and/or affect (mood) to such a point where it causes a significant amount of distress and functional impairment for a prolonged period of time.
Mental illness is a serious public health problem. According to the World Health Organization and the Harvard School of Public Health, mental illness accounts for nearly 11 percent of total worldwide disease burden. (Disease burden is determined by the calculation of DALYs, or disability-adjusted life years. The DALY statistic measures lost years of healthy life from death or disability due to a disease.) In countries that are considered "established market economies" (i.e., United States, Great Britain), mental illness is second only to heart disease as the most disabling disease category. Unipolar major depression was determined to be the second leading source of disease burden (after ischemic heart disease) in established market economies, and the fourth leading cause of disease burden worldwide.
In its Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), a reference standard for mental health professionals, the American Psychiatric Association distinguishes 16 different subtypes (or categories) of mental illness. These include:
- Disorders usually first diagnosed in infancy childhood, or adolescence. These include learning and developmental disorders, mental retardation , and attention-deficit hyperactivity disorder.
- Delirium, dementia, amnestia, and other cognitive disorders. These include dementia related to Alzheimer's disease , head injury, and central nervous system infection; and substance-induced delirium.
- Mental disorders due to a general medical condition. Medical/mental conditions that are not classified in other areas of the DSM-IV are found in this category.
- Substance-related disorders. Disorders related to alcohol and drug use, abuse, dependence, and withdrawal are included in this category.
- Schizophrenia and other psychotic disorders. These include the schizoid disorders (schizophrenia , schizophreniform, and schizoaffective disorder), delusional disorder, and psychotic disorders.
- Mood disorders. Depressive disorders (major, dysthymic) and bipolar disorders are classified as mood disorders.
- Anxiety disorders. This classification includes panic disorder, agoraphobia, social phobia , obsessive-compulsive disorder , posttraumatic stress disorder, and generalized anxiety disorders, all disorders in which a certain situation or place triggers excessive fear and/or panic symptoms (i.e., dizziness, racing heart).
- Somatoform disorders. Somatoform disorders involve clinically significant physical symptoms that cannot be explained by a medical condition. Somatization disorder, conversion disorder, pain disorder, hypochondriasis, and body dysmorphic disorder.
- Factitious disorders. These are disorders in which the individual creates and complains of symptoms of a non-existent illness in order to assume the role of a patient (or sick role).
- Dissociative disorders. These disorders involve a change in memory , identity, and/or consciousness . They include dissociative amnesia , dissociative fugue , dissociative identity disorder , and depersonalization disorder.
- Sexual and gender identity disorders. Disorders of sexual desire, arousal, performance, and pain are included here, as is gender identity disorder. It should be noted that the inclusion of gender identity disorder as a mental illness in the DSM-IV has been a point of some contention among mental health professionals.
- Eating disorders. Anorexia and bulimia are both eating disorders.
- Sleep disorders. Insomnia, narcolepsy , hypersomnia, and parasomnias (nightmares and sleepwalking) are all considered sleep disorders.
- Impulse-control disorders not elsewhere classified. Includes kleptomania and pyromania.
- Adjustment disorders. Adjustment disorders involve an excessive emotional or behavioral reaction to a stressful event.
- Personality disorders. These are maladjustments of personality , including paranoid, schizoid, schizotypal, antisocial, borderline, histrionic, narcissistic, avoidant, dependent, and obsessive-compulsive personality disorder (not to be confused with the anxiety disorder OCD).
Causes and symptoms
The causes of mental illness are not completely understood, but organic, genetic (hereditary), familial, traumatic life events, and social factors all may play a part in triggering mental illness. Frequently, it is a combination and interrelationship of several of these factors. For example, schizophrenia is caused by genetically determined abnormalities in the structure and chemistry of the brain , but the course and severity of the disease can be influenced by social factors such as environmental stress and the absence of a family or peer support system.
In some cases, mental illness is primarily a byproduct of a disease or general medical condition. For example, central nervous system infections that can occur in advanced AIDS can cause dementia. Depending on their location and severity, neurological conditions such as traumatic brain injury, tumor, or infarct (areas of tissue death as a result of loss of blood supply) can also cause various symptoms of mental illness.
Individuals dealing with traumatic life events (e.g., death of a close friend, experiencing a natural disaster, witnessing a brutal crime) may experience psychological distress and difficulty dealing with day-today tasks. Because these mental health problems tend to be of a temporary nature, they aren't termed mental illness. It is important to remember that prompt and proper treatment of these issues in the form of counseling or other psychological interventions is critical, as they have the potential to progress into a long-term mental disorder or illness.
Diagnosis and treatment
Patients with symptoms of mental illness should undergo a thorough physical examination and patient history to rule out an organic or structural cause for the illness. If a neurological cause for the disorder is suspected, further diagnostic tests (e.g., CT scan, MRI, PET scan, neuropsychological assessments) are typically required. If a disorder with no organic cause is suspected, a psychologist or other mental healthcare professional will conduct a patient interview and administer one or more psychological assessments (also called clinical inventories, scales, or tests).
Counseling is typically a front-line treatment for mental illness. A number of counseling or talk therapy approaches exist, including psychotherapy , cognitive therapy , behavioral therapy, and group therapy . These are sometimes used in conjunction with alternative therapy approaches such as art or music therapy that use the creative process to promote patient self-discovery and awareness. A number of mental healthcare professionals are involved in the treatment of mental illness, including licensed counselors and therapists, social workers, nurses, psychologists, and psychiatrists.
Psychoactive medication is prescribed for symptom relief in patients with organic and non-organic mental illness. For mental illnesses that are considered biological in nature, such as bipolar disorder or schizophrenia, pharmaceutical therapy is considered a primary treatment approach. In other cases, such as in personality disorder or dissociative disorder, psychoactive medications are usually considered a secondary, or companion treatment to psychotherapy.
Many individuals suffering from mental illness choose to treat their illness through regular attendance in self-help groups , where they can seek advice and counsel from others in similar circumstances. Some of the most popular self-help organizations (i.e., Alcoholics Anonymous), are as, if not more, effective than traditional doctor/patient therapy for many individuals.
In some cases, effectively treating mental illness requires hospitalization of the patient. This hospitalization, also known as inpatient treatment, is usually employed in situations where a controlled therapeutic environment is critical for the patient's recovery (e.g., rehabilitation treatment for alcoholism or other drug addictions), or when there is a risk that the patient may harm himself (suicide) or others. One popular variation of the inpatient treatment program, known as milieu therapy, focuses on providing the patient with opportunities to gain self-confidence and interact with peers in a positive way. Activities that encourage self-discovery and empowerment such as art, music, dance, and writing are important components of this approach.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders 4th ed. Washington, DC: American Psychiatric Press, Inc., 1994.
World Health Organization, World Bank, and Harvard University. Murray CL, Lopez AD, eds. The Global Burden of Disease: A comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Cambridge, MA: Harvard University Press, 1996.
Satcher, David. Mental Health: A Report of the Surgeon General. Washington, DC: Government Printing Office, 1999. [available online at www.surgeongeneral.gov]
National Institute of Mental Health (NIMH). 6001 Executive Boulevard, Rm. 8184, MSC 9663, Bethesda, MD, USA. 20892-9663, fax: 301-443-4279, 301-443-4513. Email: firstname.lastname@example.org. http://www.nimh.nih.gov.
"Mental Illness." Gale Encyclopedia of Psychology. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/mental-illness
"Mental Illness." Gale Encyclopedia of Psychology. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/mental-illness
Historically, the medical concept of mental illness has its basis in lay judgements of mental states, which were embodied in notions such as insanity and lunacy–real madness–as well as in concepts such as ‘troubled in mind’, ‘mopish’, and ‘distracted’, which encompassed the less severe forms of psychological disturbance. Then as now these terms were applied to persons whose behaviour seemed in some way inexplicable or irrational. Deviant or delinquent it might be, but it could not be understood as readily as the usual forms of delinquency, often because it involved a rejection of what was highly valued in society. Present-day medical conceptions of mental illness are still intimately linked to lay judgements of what is rational, reasonable, and appropriate. However, psychiatry has embraced and transformed the everyday lexicons, classifying and listing a diverse set of mental illnesses. These range from conditions such as Alzheimer's disease, which are known to involve brain pathology, through the archetypical mental illnesses such as schizophrenia and manic depression (which belong to the group of psychoses), to conditions such as anxiety states, phobias, and obsessions (frequently termed neuroses), as well as to the so-called behaviour disorders such as alcoholism, anorexia nervosa, drug addiction, and sexual deviations.
Psychiatrists' lists of mental illnesses provide a formal specification of the boundaries of mental illness, however the boundaries are changing and contested. The distinction between mental illness and physical illness is itself highly problematic. It is most obviously made in terms of manifest pathology, but is often not clear-cut, with many illnesses having mental and physical symptoms; once we turn to causes the distinction is even more problematic and the idea of two mutually exclusive categories of illness soon founders. An identifiable mental pathology may well have physical causes, as in the case of Alzheimer's disease; equally, some physical pathologies such as ulcers have mental causes (as the concept of psychosomatic illnesses allows). Indeed, the interrelation of mental and physical has frequently been used to justify attempts to integrate mental health services with other health services. In practice, where the boundary is set between mental and physical illness is a matter of convention, and depends on ideas about causation as well as on the extent of the manifest mental and behavioural problems.
The boundary between mental illness and deviance (‘madness and badness’) is equally problematic, especially in relation to behaviour or personality disorders, where symptoms are very obviously behavioural. Analytically the distinction is one of referent: mental illness is a judgement of mind, deviance one of behaviour. However, since observations of behaviour are the basis for judgements of mind, in practice confusions and difficulties arise. Here, as on its other margins, changing conventions are involved in determining the boundaries between the two, as in the increasing tendency to see child abuse less as a form of deviance than as indicative of underlying mental pathology. Finally, there is the boundary between what is normal and abnormal mental functioning. Again this boundary is largely set by changing conventions, and as with other boundaries its location also varies from individual to individual, according to social background and circumstances.
Ideas about the causes of mental illness vary. Psychiatry, by virtue of medicine's emphasis on physical processes, has focused on physical causes and treatment and given them primacy, frequently and mistakenly seeing physical explanations as precluding the necessity for any examination of the place of psychological and social factors. In contrast, a number of sociologists and social theorists have made significant contributions to the understanding of the social causes of mental illnesses, as for example in the case of George Brown and Tirril Harris's work on depression, or feminist analyses of anorexia nervosa.
However, the sociological contribution to the understanding of mental illness also derives from the analysis of mental illness as a social construct. This construct, as is noted above, sets the boundaries of normal, acceptable mental functioning in different cultures and societies, and as such is part of the social regulation of human conduct. See also COMMUNITY CARE; SICK ROLE.
"mental illness." A Dictionary of Sociology. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/social-sciences/dictionaries-thesauruses-pictures-and-press-releases/mental-illness
"mental illness." A Dictionary of Sociology. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/social-sciences/dictionaries-thesauruses-pictures-and-press-releases/mental-illness
Mental, or psychological, illnesses and disorders occur in or relate to the mind. Mental disorders differ from physical (related to the body) disorders because there are usually no physical symptoms of a mental disorder (such as a broken arm or an upset stomach) for a doctor to observe. Mental disorders originate in the mind of an individual and display themselves outwardly through a person's behavior or emotions. When behavior or emotions are deemed "abnormal," a mental illness might be at the root of the problem.
In a world in which cultural and social differences are abundant, particularly as one moves from one country or region to another, it is very difficult to define what is "normal" behavior over what is "abnormal" behavior. However, abnormal behavior has come to be identified through the presence of different coexisting characteristics or conditions:
Infrequency is one facet of abnormal behavior; in other words, a behavior or characteristic exhibited or not exhibited by the majority of people determines normalcy. Another hallmark of abnormal behavior is whether or not the behavior violates social norms; this will differ from culture to culture and therefore allows for a range of differences in behavior. This can present difficulties in definition because while many criminals violate social norms, they are not always deemed to be mentally ill. Another way of identifying abnormal behavior is personal distress and the degree of an individual's suffering. For example, does a person's grief over something fall outside the scope of what is a "normal" level of grief or is it exceeding the average time it takes for an individual to recover from the grief?
Disability and dysfunction are also used to assess an individual's well-being. For example, someone with a great but irrational fear of something might not be able to participate in daily activities or may be experiencing a great deal of personal distress because of this fear. Finally, another factor in determining abnormality of behavior is whether someone's response to a situation is unexpected. For example, thirst is an expected response to not drinking enough fluids, but becoming emotionally distraught over thirst would not be an expected response.
This chapter describes a variety of major mental conditions and disorders. Some are deep-rooted mental illnesses, such as schizophrenia; others are more easily treatable, such as a learning disorder. Most mental disorders are treatable and, like many physical disorders, mental illness is not the result of something a person has or has not done to influence its development. Mental illness, like physical disease, can and does strike people from all walks of life. However, just as medical treatment for physical ailments has improved markedly over time, so has the diagnosis and treatment of mental illness.
The classification of abnormal behavior in childhood depends greatly on development in terms of what is and is not considered normal behavior for a child at a certain age. This often makes it difficult to diagnose certain disorders of childhood as children develop at different rates and only a qualified therapist can make the distinction between what is appropriate and inappropriate behavior. Also, childhood disorders can be a sensitive subject,
Mental Illness: Words to Know
- Adaptive behavior:
- Things a person does to adjust to new situations.
- An individual's emotional response and demeanor.
- Artificial attitudes or behaviors.
- The inability to experience pleasure.
- Antipsychotic drugs:
- Drugs that reduce psychotic behavior, often having negative long-term sideeffects.
- An abnormal and overwhelming sense of worry and fear that is often accompanied by physical reaction.
- Attention-Deficit/Hyperactivity Disorder (ADHD):
- A disorder that involves difficulty in concentrating and overall inattentiveness.
- A developmental disorder marked by the inability to relate socially to others and by severe withdrawal from reality. Language limitations and the extreme desire for things to remain the same are common symptoms.
- Existing, or occurring, at the same time.
- Habitual behaviors or mental acts an individual is driven to perform in order to reduce stress and anxiety brought on by obsessive thoughts.
- The relation of two or more things that is not naturally expected.
- False or irrational beliefs that an individual holds in spite of proof that his or her beliefs are untrue.
- A disorder marked by constant feelings of sadness, emptiness, and irritability as well as a lack of pleasure in activities.
- Down syndrome:
- A form of mental retardation due to an extra chromosome present at birth, often accompanied by physical characteristics, such as sloped eyes.
- The inability to function properly.
- A reading disorder that centers on difficulties with word recognition.
- Understanding of another's situation and feelings.
- The inability to control one's bladder while sleeping at night; bed-wetting.
- Something present in the genes that is inherited from a person's biological parents.
- The perception of things when they aren't really present.
- Marked by compassion or sympathy for other people or creatures.
- Intelligence quotient (IQ):
- A standardized measure of a person's mental ability as compared to those in his or her age group.
- To incorporate something into one's self.
- Lacking reason or understanding.
- Learning disorders:
- Developmental problems relating to speech, academic, or language skills that are not linked to a physical disorder or mental retardation.
- Repeating thoughts, impulses, or mental images that are irrational and which an individual cannot control.
- A form of an anxiety disorder that involves intense and illogical fear of an object or situation.
- Relating to the functions and activities of life on a biological level.
- Post-Traumatic Stress Disorder (PTSD):
- Reliving trauma and anxiety related to an event that occurred earlier.
- Ill feelings stemming from guilt over past actions.
- Residential treatment:
- Treatment that takes place in a facility in which patients reside.
- A person with extensive knowledge in a very specific area.
- A chronic psychological disorder marked by scattered, disorganized thoughts, confusion, and delusions.
- Social norms:
- Things that are standard practices for the larger part of society.
- Having origins from within the body, as opposed to the mind.
- Something (for example, an event) that causes stress.
- Taking one's own life.
- A quirk of behavior or speech that happens frequently.
- Tourette's Disorder:
- A disorder marked by the presence of multiple motor tics and at least one vocal tic, as well as compulsions and hyperactivity.
particularly learning disorders, as parents and children are afraid of the social stigma (shame) that often comes with a diagnosis. Children and adolescents strive for acceptance, and any indication of being different or being separated into "special" classes can have devastating effects on a child's self-esteem and the reaction of his or her peers to the situation.
The Diagnostic and Statistical Manual of Mental Disorders (DSM) and other sources categorize the following conditions as "Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence" or simply "Childhood Disorders"; technically, there isn't any difference between these disorders and other mental disorders except for the higher incidence of diagnosis in childhood rather than adulthood.
Attention-deficit/hyperactivity disorder (ADHD) is a disorder that involves difficulty in concentrating and overall inattentiveness. ADHD affects people of all ages but is usually diagnosed in childhood. This condition has received a great deal of attention in the media in the last ten to fifteen years, because there has been a marked increase in the number of diagnoses of this disorder by mental health practitioners in recent years. No longer seen just as a problem centering around hyperactivity, or excessive activity, the focus of ADHD is also on a child's difficulty in concentrating on tasks at hand. While most children have notoriously short spans of attention, children battling ADHD have increased difficulty controlling their level of activity and attention particularly in situations that call for maintaining a certain degree of composure, such as in the classroom or in public places like restaurants.
THE DSM, IV
Mental health care practitioners today rely heavily on the Diagnostic and Statistical Manual of Mental Disorders, IV (DSM, IV) to diagnose patients. Compiled and produced by the American Psychiatric Association, the DSM, IV is used by an array of individuals as well as by insurance companies. The DSM system of classification grew out of the International Statistical Classification of Diseases, Injuries, and Causes of Death or ICD, which was comprised of listings detailing all medical diseases and included abnormal behavior. The World Health Organization backed this system, but it was not widely accepted. In 1952, then, the first edition of the DSM was published, and it evolved into the comprehensive edition that it is today.
Controversy still exists around this volume, much of it based on the nature of categorizing mental illness in general. For example, the DSM, IV focuses largely on behavior while mental health researchers focus on psychological characteristics in assessing a condition. With each new edition of the DSM, efforts are being made to address all of these concerns; however, as society changes and new diagnoses are added, controversies will likely continue to arise.
The DSM, IV employs a multiaxial system of classification to rate an individual on five different levels. This is done to ensure that a wide array of possibilities and factors are considered when diagnosing a patient. Axis I includes all categories of mental disorders except personality disorders and mental retardation. These two categories comprise Axis II. Axis III covers medical conditions that are important to understanding a mental disorder, such as Alzheimer's disease. Axis IV includes problems or events that can affect the diagnosis, treatment, and outlook of a mental disorder (such as a death in the family, problems at work or school, and even issues such as living in an unsafe neighborhood). Axis V involves the use of the Global Assessment of
Functioning (GAF) Scale, which mental health professionals use to assess how well an individual is functioning on a scale of 1 to 100. When used together, these axes are designed to allow a comprehensive diagnosis that takes into consideration all aspects of an individual's life and personality in making a diagnosis and implementing a treatment plan.
ADHD makes it difficult for sufferers to sit still or even to stop talking. When they are called upon to be quiet and remain seated, they might squirm, fidget, tap their hands, swing their feet and legs, and make noise. The diagnosis is often difficult to make, as most children can be full of energy, particularly during times of play. However, children suffering from ADHD are disorganized, bossy and ill-mannered more often than the average child. Because of the increased prevalence of this diagnosis in recent years, there has
been the suggestion that children who are appropriately energetic, hard to handle, or suffering from a conduct disorder (see below) are being given a diagnosis of ADHD unnecessarily. This assessment, however, is difficult to quantify or prove. Furthermore, the Council on Scientific Affairs of the American Medical Association has investigated the issue and determined that while there isn't a concern for general overdiagnosis, some students belonging to minority groups are being diagnosed at a disproportionate rate.
SYMPTOMS. According to the DSM, IV some of the symptoms of ADHD include lack of attention to details; difficulty paying attention in school or at play; not paying attention when being spoken to; not following through on instructions or failure to finish things; disorganization, forgetfulness, losing or misplacing important things; fidgeting excessively; difficulty in playing quietly; excessive talking, difficulty in awaiting turn, and a tendency to interrupt others. In order to be diagnosed with ADHD, more than one of these symptoms must be present, and those symptoms must be creating a specific problem for the sufferer (lack of friends, poor performance in school, etc.).
CAUSES. Although there is no known single cause for ADHD, there are theories as to why certain children develop ADHD while others do not. Some experts propose that ADHD is inherited, while others have blamed the development of the disorder on environmental toxins, such as food additives or nicotine while a child is growing in the mother's womb. Psychological causes may include demanding, authoritative parenting that creates stress and triggers the development of ADHD.
TREATMENTS. ADHD has been treated effectively with certain drugs, including Ritalin, a stimulant that helps improve concentration, behavior, and directed activities. However, Ritalin's effectiveness has not been proven for the long term and some researchers have suggested that Ritalin actually hampers a child's creativity. Operant conditioning (see Chapter 15: Mental Health Therapies) has also been successful in helping those with ADHD. This therapy, which centers on rewarding good behavior, supports the belief that ADHD means that a child has a lack of basic skills to help him or her be effective, rather than the belief that a child simply has too much energy.
Although conduct disorders cover a wide array of "bad" behaviors, the underlying principle of the diagnosis is that an individual exhibits inappropriate behaviors that violate the basic rights of other people. These are behaviors that fall outside the scope of normal childhood pranks and mischief; rather, conduct disorder includes behavior that is often vicious, and sufferers typically display no remorse (regret or guilt for having done something wrong), something that links conduct disorder to antisocial personality disorder or psychopathy (see section on Personality Disorders below).
In addition to the dysfunctional behaviors they exhibit, people with conduct disorders do not possess a great deal of empathy (understanding of other people's feelings) for others. Sufferers may also mistakenly think others are behaving aggressively toward them when they are not. Although an individual might seem to have a tough exterior, that person may in fact have low self-esteem, another feature common to those with conduct disorder. Recklessness, angry outbursts, and the tendency to get easily frustrated are also common traits of this problem.
SYMPTOMS. The DSM, IV splits conduct disorder into four categories: aggression toward people and animals (bullying, fighting, use of weapons, physical cruelty to both, stealing, and forced sexual contact); destruction of property (setting fires and destroying property deliberately through another method); deceitfulness or theft (breaking and entering, lying, covert stealing[e.g., forging a check]); and serious violations of rules (staying out past curfew at a young age, running away from home, and cutting school).
CAUSES. Just as with ADHD, there is no known single cause for conduct disorders, but there are theories as to why certain children develop conduct disorders while others do not. One theory is that conduct disorder may be an inherited ailment. Another possibility is that there is a lack of moral awareness in the family of origin of a person suffering from conduct disorder. In general, children learn what is right and wrong and refrain from breaking the boundaries of decency because they have been taught that it is wrong to hurt others. If, for whatever reason, these lessons are not learned in the home, a conduct disorder, and even more ominous psychological problems could develop. Furthermore, a child may witness disordered conduct from his or her parents and learn aggressive, improper behavior. Other researchers have postulated that children prone to developing conduct disorder could have flawed thinking processes. That is, very aggressive children may perceive an otherwise harmless event (for instance, being last in a line) as a slight, place unusual importance on the event, and hold a grudge because of the occurrence.
TREATMENTS. The most successful treatments of conduct disorders involve treating not just the child (or adult) but rather those around him or her as well (family and, in some cases, friends). Cognitive therapy, a form of therapy in which a therapist helps a patient become aware of maladaptive thinking and flawed belief systems and helps change beliefs that can interfere with healthy living (see Chapter 15: Mental Health Therapies), may also improve behavior as can teaching children moral reasoning skills.
Oppositional Defiant Disorder
Children often disobey their parents or teachers, particularly when they are extremely young, as a way of asserting their independence. However, when a child consistently is disobedient, disrespectful, hostile, and defiant toward parents, teachers, and other figures of authority for a period of six months, the child might be diagnosed with oppositional defiant disorder (ODD), a disorder that is not uncommon. Stubbornness and an unwillingness to deal rationally with others when there is disagreement are also signs of ODD.
Because defiant behavior is common in the development in both very young children and teenagers, it is cautioned that mental health practitioners make this diagnosis very carefully. Interestingly, more boys tend to suffer from ODD than girls do in the years before puberty; however, when adolescence arrives, both girls and boys are diagnosed at about the same rate.
The presence of this disorder is marked by a frequent loss of temper, arguing with adults, behaving annoyingly on purpose, blaming others for errors, anger, resentment, and spitefulness or vindictiveness. To be properly diagnosed with ODD, several of these characteristics must be noted for an extended period of time and these behaviors must prevent the child from performing properly at school or relating to family and friends.
While ODD may share similarities with both ADHD and conduct disorder, there are differences. Conduct disorder usually manifests itself in physical violence while ODD usually does not. ODD differs from ADHD in that the bratty behavior seen in ODD seems to be conscious and planned while ADHD suffers seem unable to control their actions. Treatment for ODD often involves cognitive therapy and operant conditioning therapy featuring a system of rewards.
Learning disorders refer to developmental problems relating to speech, motor, and academic or language skills that are not linked to a physical disorder or mental retardation (see section below). The presence of a learning disability is not a reflection of how intelligent an individual is. In fact, people with learning disabilities are often of average or above-average intelligence, but there is a problem in development or processing that prevents that person from performing at proper levels. Most often, parents and teachers become aware of learning disorders through a child's results on standardized academic tests administered by the school. It is believed that learning disorders may be inherited, particularly dyslexia (see Reading Disorder below).
The treatment of learning disorders focuses on instruction in the area in which there are problems. The most effective programs are those that give children a chance to make small steps toward progress that can help restore self-esteem and confidence.
Learning disorders are broken down into three separate diagnoses: reading disorder, mathematics disorder, and disorder of written expression; there is also a generalized diagnosis (Learning disorder not otherwise specified) to address problems in all three areas or a combination of two areas.
READING DISORDER. A reading disorder is commonly known as dyslexia (pronounced dis-LEX-ee-a). Dyslexia comes from the Greek words "dys" (meaning poor or inadequate) and "lexis" (which refers to words or language). Dyslexia is a disorder that centers on difficulties with word recognition. Sufferers most often add, omit, or transpose (change the sequence of) letters in a word (for example, mistaking "sing" for "sign" or "left" for "felt"). All of these symptoms manifest themselves in problems with reading aloud, comprehending what is read, and spelling words correctly. Dyslexia can also affect mathematical skills, causing the person to add, omit, or transpose numbers.
MATHEMATICS DISORDER. While math can be difficult for many people, some children have difficulties that go beyond the normal scope. The problem can be as serious as someone being unable to recognize mathematical symbols and numbers to having difficulty following the proper steps in solving a mathematical equation. The degree of the difficulty is the key to making a diagnosis of mathematics disorder.
DISORDER OF WRITTEN EXPRESSION. This disorder centers on problems with writing skills. This, obviously, can affect many areas of academics, as can a reading disorder. Poor handwriting as well as difficulty with
punctuation, grammar, and spelling are common. While many young people may have difficulties with some or all of these things, what makes a diagnosis necessary is the degree to which the problem interferes with academic achievement.
Mental retardation is a condition of below-normal mental ability or intelligence due to disease, injury, or genetic defect. The average person has an intelligence quotient (IQ) between 70 and 130, with the majority of the population having IQs between 85 and 115. (IQ is the measure of one's intelligence as based on intelligence tests and the intelligence of the general population; see Chapter 11: Mental Health for more information on IQ.) Those suffering from some degree of mental retardation have IQs below 70 and as low as 20. Accompanying a low level of intelligence is trouble with adaptive behavior or functioning (skills such as dressing oneself, being socially responsive, understanding certain abstract concepts like time and money, etc.). These conditions are usually discovered prior to the age of eighteen.
CAUSES. Often, there is no identifiable biological cause for mental retardation, especially in the cases of mildly or moderately mentally retarded individuals.
However, in the cases of more severe mental retardation, genetic, or birth, defects—such as Down syndrome—can be the cause. Down syndrome usually causes people to have moderate to severe retardation. Furthermore, Down syndrome sufferers share certain physical characteristics that have become hallmarks of the disorder including oval, upward-slanting eyes; fine straight hair; and a stocky build and short stature. Other complications, including infectious diseases—such as encephalitis (swelling of the brain) and meningococcal meningitis (swelling of the lining around the brain or spinal cord)—can sometimes also cause mental retardation.
TREATMENTS. Treatment of mental retardation varies to the degree of retardation. Residential treatment, that is treatment in live-in residences, is very popular. Sometimes a patient will develop enough skills to move into a group home, which features a homey setting, living with patients at similar levels of functioning. Operant conditioning is often employed as well as certain cognitive therapies (see Chapter 15: Mental Health Therapies). Whatever the case, working with individuals to bring them to the highest level of functioning possible will benefit them; of course, compassion and protection are the key to helping these individuals lead comfortable, happy lives.
There are four major diagnoses relating directly to mental retardation:
MILD MENTAL RETARDATION. The IQ range for this diagnosis is between 50 and 55 to 70. Oftentimes, these individuals are not diagnosed as mentally retarded until later in their development because they are usually able to learn at a sixth-grade level. People who are mildly mentally retarded can usually hold jobs and often marry and successfully raise children. Approximately 85 percent of mentally retarded people have been diagnosed in this category.
MODERATE MENTAL RETARDATION. Ten percent of the mentally retarded are diagnosed with an IQ range of 35-40 to 50-55. Physical problems, including brain damage, are often present and tasks such as running or grasping things can be extremely difficult. Many people in this category live with their families or in supervised group homes with a great deal of success.
SEVERE MENTAL RETARDATION. Approximately three to four percent of individuals with mental retardation are at this level, with an IQ range of 20-25 to 35-40. Birth defects are often present and communication skills are limited. Although they may be able to do certain tasks under supervision, often they are unable to function independently in any capacity.
PROFOUND MENTAL RETARDATION. One to two percent of the mentally retarded have IQs falling below 20-25. These individuals require supervision for their entire lives. Because of physical deformities and other problems, people in this range often have a short life span.
LIFE GOES ON
Life Goes On, a television program popular in the late 1980s and early 1990s, featured a main character, Corky, who was mentally retarded as a result of Down syndrome. Corky attended a mainstream public high school and even went on to marry. The character of Corky was portrayed by actor Chris Burke (1965–), who has Down syndrome in real life.
Autism is a developmental disorder marked by the inability to relate socially to others and by severe withdrawal from reality. Language limitations and the extreme desire for things to remain constant are common traits of autism. Autistic children and adults seem to "look through" people and very often avoid eye contact. More often than not, they are unresponsive to touch and are unable to accept and display affection. An interest in ritual and repetitive body movements, such as rocking back and forth, and of repeating certain words or phrases, are also usually present. In many cases, speech is absent and, when it is present, autistic individuals are often unable to hold a conversation with others. In some cases, those with autism may form strong attachments to inanimate (nonliving) objects, such as keys or even a refrigerator.
Another aspect of autism is that while many suffering from the disorder are mentally retarded to some degree (approximately 80 percent), they also may display almost incredible skill in other areas, such as mathematics. This facet of autism has prompted the use of the term idiot savant. A savant is one with detailed knowledge in a specialized field, such as math or science. Some people suffering from autism may also have exceptional memories or have a profound physical grace. Others with autism may, however, exhibit awkward physical affectations and posture and may not possess any outstanding, savant-like abilities.
CAUSES. Autism was originally thought to be the result of emotionally distant parenting but this has not been proven. However, a specific biological cause also has not been found. Still, it is believed that autism has its origins in biology, and studies of twins have indicated that autism may be genetic. It is difficult to confirm this, however, because of the rarity of autism (two to five births in 10,000) and the fact that persons with autism rarely have children. Most of the symptoms of autism are usually present and a diagnosis made by the time a child reaches toddler age.
TREATMENT. Treatment for autism is not always effective. However, operant conditioning and modeling (see Chapter 15: Mental Health Therapies) have proven to be successful in enabling parents to, at the very least, bring their child into social situations without the child acting out. Some therapists have had success in using intense behavioral therapy as well.
In his book, The Man Who Mistook His Wife for a Hat, renowned neurologist Dr. Oliver Sacks (1933–) detailed an example of the savant qualities some autistic individuals have. While speaking with autistic twins at the hospital in which they lived, a box of matches fell on the floor. Moments later, both twins shrieked, "111." Dr. Sacks was confused until he painstakingly counted the matches to discover there were, indeed, 111. When he pressed the twins as to how they knew how many matches there were, they said that they simply "saw" the number and looked at him in bewilderment over the fact that he hadn't.
THE TEMPLE GRANDIN STORY
There are those with autism who have managed to become fully functional adults. One woman, Temple Grandin, Ph.D., was diagnosed with autism at the age of three. Her case has been documented by neurologist Dr. Oliver Sacks, and she has written two autobiographical books. Grandin managed to learn how to speak by age six and went on to earn her doctoral degree in animal science, to run her own business, and instruct courses at
Colorado State University. However, for all of her academic and professional achievements, she still remains in awe of people and human relations, calling herself an "observer" rather than a participant in the social realm of life. While she has managed to overcome many of the negative traits of autism, such as violent rages and acting out impulsively and seemingly without reason, she has been unable to bridge the gap between herself and others on an emotional level. Dr. Sacks noted that while Grandin is able to converse at length about intellectual matters, she lacks many standard social graces (manners).
Usually diagnosed before a person reaches the age of eighteen, the main feature of Tourette's disorder is the presence of multiple motor tics and at least one vocal tic (a tic is a quirk of behavior or speech that happens frequently). Examples of such tics include frequent eye blinking, throat clearing, sniffing, repeating words or sounds over and over, or coprolalia (repeatedly saying obscenities). Such symptoms must be exhibited for more than a year, without a lapse in symptoms exceeding three months in a row, and the condition must have a negative effect on one area of functioning (social, educational, professional, etc.). More common in males than females, the average onset age of Tourette's is seven.
SYMPTOMS. Symptoms accompanying Tourette's range from obsessions and compulsions (see section on Anxiety Disorders below), to hyperactivity, social discomfort, and depression. Social problems and depression may stem from embarrassment over a sufferer's inability to control his or her actions. Exaggerated behaviors not uncommon to Tourette's, such as head banging, knee bending, head jerking, and picking the skin, can cause injury and/or illness.
CAUSES. Tourette's disorder is genetic in origin. While not all individuals who inherit the predisposition toward Tourette's will develop the disorder, 70 percent of females and 99 percent of men carrying the genes will develop it.
TREATMENTS. Tourette's is often treated with prescription drugs, which can help to lessen the presence of tics and other symptoms.
Many people have heard another person stutter; what might strike many people is the number of individuals who have outgrown or overcome stuttering. Stuttering is a disturbance in verbal fluency of speech; for example, a stutterer might repeat whole words several times before being able to move on to the next word in the sentence ("I want to go-go-go-go to the movies."). Another sign may be a person's consistent difficulty in pronouncing certain consonants, or having long pauses between words in a sentence.
Stuttering is frustrating because, like Tourette's, it separates people from others by hampering easy communication. It can also affect learning, as a child may be embarrassed to ask or answer questions in class because of fear of classmates' teasing. Furthermore, stuttering can become worse when one is nervous, which can prevent a stutterer from answering difficult questions or doing any type of public speaking.
WHEN A STUTTERER SINGS, HIS STUTTER EITHER IMPROVES MARKEDLY OR DISAPPEARS. THIS MAY HAVE TO DO WITH BREATHING, BEING RELAXED, AND A STUTTERER KNOWING EXACTLY WHAT HE IS GOING TO SAY (STUTTERERS OFTEN STUTTER LESS WHEN READING ALOUD).
Stuttering affects more males than females and usually is present at or around the age of five. It has been estimated in the DSM, IV that eighty percent of stutterers recover, with sixty percent overcoming their stutter through no apparent reason. Speech-language pathologists (see Chapter 7: Health Care Careers) perform therapy with stutterers to help them overcome the disorder.
Mood disorders cause a disturbance in mood (state of mind) and include depression and bipolar disorders. Mood disorders can be devastating as, depending on their severity, they can emotionally paralyze people, rendering them unable to work or attend classes or even enjoy the most basic things. Mood disorders can also disrupt appetite and sleep patterns and an individual's sense of well-being. It is not known why some people suffer from mood disorders while others do not.
For many children, nighttime enuresis, or bed-wetting, is an embarrassing and painful problem. The inability to control one's bladder while sleeping is stressful and, unfortunately, still something of a mystery. Enuresis will not be diagnosed until after a child is at least five years old (the age by which most children have been toilet-trained). At age five, the DSM estimates that approximately seven percent of boys and three percent of girls are enuretic. Furthermore, the majority of enuretics have always had problems with bladder control during the night (they are called primary enuretics); secondary enuretics, in the minority, were once able to control their bladders but have lost that ability.
A variety of factors have been blamed for bedwetting. There is a strong genetic link for bedwetting (if a parent wet the bed, the child is much more likely to do so). Certain medical conditions cause enuresis, such as urinary tract infections and kidney disease. Some psychoanalytic therapists have suggested that bed-wetting is an act that can indicate anger toward parents. Still other schools of therapists have proposed that children encounter enuresis when they have been toilet-trained at too early an age.
Whatever the cause, enuresis is treatable. Using principles of classical conditioning (see Chapter 15: Mental Health Therapies), Drs. O.H. Mowrer and W.M Mowrer developed the bell-and-pad apparatus, which involves a pad that, when moisture hits it, sounds a bell, waking the child and prompting him to go to the bathroom to finish urinating. Prescription medicine is also effective in ending episodes of bed-wetting but is only effective when it is being used; when enuretics stop taking the drugs, the bed-wetting returns. Many enuretics simply outgrow the problem as they approach puberty.
Major depression, the condition of feeling deep and constant sadness, is one of the most common mental disorders. It strikes almost one in five people at some point. More common in women than in men, depression tends to recur, making it a lifelong battle for some people. Depression, too, has become more common over the last few decades. This may be attributable to social changes that have occurred simultaneously (society moving at a faster pace, individuals bearing more stress as life becomes increasingly urbanized, and many institutions—church, family, cultural customs—that once acted as support systems no longer as common). It may also be that people are more aware of the symptoms of depression and are more willing to seek treatment than in the past.
SYMPTOMS. There are several possible symptoms of depression, whether it be a major depressive episode (which lasts approximately up to two weeks) or major depressive disorder (of longer duration and higher rate of return of the depression). Symptoms can include: constant feelings of sadness, emptiness, or irritability; a lack of pleasure in activities, even those that once brought enormous pleasure; a noticeable drop or increase in weight; the inability to sleep; extreme exhaustion; feelings of worthlessness; an inability to make decisions or concentrate on performing tasks; and thoughts of death and suicide. In order for a diagnosis of depression to be made, none of these symptoms can be caused by drugs or a medical disorder (there are separate categories of depression that are caused by illness or substance abuse) and a diagnosis should not be made if an individual is mourning the very recent loss of a loved one.
CAUSES. Many different theories account for the development of depression, depending upon the therapist's school of thought. Psychoanalysts (see Chapter 15: Mental Health Therapies) believe that the seeds of depression are sown in early childhood when something goes wrong with one stage of development or another. Cognitive therapists, such as Aaron Beck, believe that an individual battling depression has a faulty perception of the world, tending to view things negatively, and this impacts the person and his or her
reactions to different situations later in life, increasing susceptibility to developing depression. Behavioral therapists believe that depression may strike individuals who do not have strong social support and whose depression further deepens their isolation from others. There are also those who attribute depression to biological causes, including the possibility that it is inherited or caused by a chemical imbalance in the brain.
TREATMENTS. Depression has been treated with success with cognitive therapy and interpersonal therapy (a therapy that focuses on how a person interacts with others and which instructs him or her how to interact more
effectively). Drug therapies have also worked well in treating depression. Antidepressants, such as Tofranil and Elavil, as well as Prozac, have been effective in alleviating the symptoms of depression. Drug therapies are most beneficial when they are accompanied by sessions with a therapist who can help an individual better understand depression and how he or she is reacting to the medication.
Bipolar disorders are marked by extreme highs and extreme lows in mood. Similar to depression in that they include the occurrence of major depressive episodes, bipolar disorders are also accompanied by manic episodes or hypomanic episodes. A manic episode is when a person is in an intense emotional state of elation (extreme happiness) and overactivity in which he or she is abnormally energetic and talks in an almost stream-of-consciousness way, with ideas and grandiose plans being shared (however implausible they may seem). Examples of other symptoms of a manic episode include an inflated sense of self, a reduced need for sleep, and engaging in reckless activities (for example, irresponsible sexual behavior or excessive spending). A hypomanic episode is similar to a manic episode though not as extreme.
Bipolar I disorder is marked by manic episodes accompanied by major depressive episodes. Bipolar II disorder has major depressive episodes at its center which are accompanied by at least one hypomanic episode.
Bipolar depression also differs from major depression, which is also known as unipolar depression, in that it strikes males and females at the same rate. Typically, bipolar depression is treated with drugs and counseling. As with major depression, there exists a genetic correlation.
Psychotic disorders, including schizophrenia, center around psychoses, which refer to mental disorders that involve a dramatic impairment in thinking,
SUICIDE: A DEADLY SIDE-EFFECT OF DEPRESSION
Suicide is when a person takes his or her own life. Not all people who kill themselves do so solely because of depression. However, many depressed people entertain the thought of ending their lives, attempt to end their lives, or sadly, succeed in ending their lives. Often times, the first sign of a person's depression may be a suicide attempt.
According to the American Psychiatric Association, depression is very common among teenagers and young adults. Studies have shown that teens who are depressed, abusing substances, or acting out on violent feelings are all at high risk for suicide. In fact, among teens and young adults between the ages of 15 and 24, suicide is the third leading cause of death. It is estimated that 5,000 teens commit suicide each year.
Suicide prevention centers around the country offer twenty-four-hour assistance to people in despair and considering suicide. However, the most important mechanism in preventing suicide can usually come from the depressed or despondent person or the people around that individual. Watching for warning signs of depression or reckless behavior and helping someone get professional counseling is crucial in preventing this senseless act. These warning signs can include: sleep disturbances (sleeping too much or too little), a change in appetite and weight, feelings of restlessness, lack of concentration, withdrawal from friends and activities once considered fun, sudden mood swings, and feelings of guilt and hopelessness.
such that an individual is almost completely out of contact with reality. Most often this means that a person is experiencing hallucinations, or having delusions. Hallucinations are the perception of things that aren't present (seeing things, hearing things, etc.); delusions are false or irrational beliefs that an individual holds in spite of proof that those beliefs are untrue. It is these qualities that render psychotic disorders frightening and mysterious, especially for those afflicted by them.
Schizophrenia, perhaps the most severe psychotic disorder, is still not fully understood by the mental health community. When it strikes, more often than not, sufferers need to be on medication for the rest of their lives in order to keep the disorder under control. Furthermore, many schizophrenics are unable to resume normal lives; this tragedy is compounded by the fact that schizophrenia often develops when individuals are in their late teens through mid-thirties. This means that some persons could have been working toward building a full life only to find themselves in jeopardy of losing everything they have worked for.
SYMPTOMS. Symptoms of schizophrenia include having scattered, disorganized thoughts. People with schizophrenia will lose their train of thought when conversing with others, often bringing up completely different issues and causing others to become confused. Delusions are another symptom of schizophrenia. Delusions can include anything from a person's belief that others are plotting against him or her, or that a person's food is being poisoned because someone is trying to kill him or that another person can read his mind. Hallucinations often accompany delusions as well. Many times, schizophrenics hear strange voices inside their heads. Naturally, this is extremely disturbing and feeds a schizophrenic's fear.
Other symptoms include a lack of motivation to engage in normal daily activities, such as maintaining one's hygiene or doing chores. Also, although schizophrenics will tend to speak, they will have less to say; their conversations may be repetitive and nonsensical. The inability to experience pleasure, known as anhedonia, may also be present, as may problems with a person's affect (an individual's emotional response and demeanor); often times, a schizophrenic's affect may be flat (lacking in emotional response) or inappropriate (for example, laughing upon hearing that someone has died).
CAUSES. There is no single, definitive answer as to why some people develop schizophrenia. It is believed that it is genetic and that if a person has a schizophrenic relative in his or her family, there is an increased incidence of the person developing schizophrenia. Studies on families and twins have supported the genetic link, although the statistics are not very high, meaning that there may be schizophrenia in a family's gene pool, but the likelihood of someone developing it isn't all that great. Among twins with schizophrenia, the incidence of both having the disorder is quite high in identical twins (almost 44.30 percent according to one 1987 study); further, fraternal (nonidentical) twins also have an increased risk, although it's not as high as in identical twins.
It has also been suggested that chemical imbalances in the brain could account for the development of schizophrenia, something that certain researchers believe may also be inherited as well. Finally, psychological stress has been identified as being a possible cause.
TREATMENTS. Schizophrenia is almost always treated with antipsychotic drugs, such as Thorazine, which reduce psychotic symptoms, particularly because hallucinations and delusions can cause schizophrenics to engage in behaviors that make them a risk to themselves and even others around them. Medication is usually successful in suppressing symptoms but, alone, it is not enough. Therapy is a necessary ingredient in treatment to help the individuals accept and cope with their situations and understand the importance of continuing to take medication even if they feel "cured." Therapy can also be useful in helping a schizophrenic's family understand the patient's plight and contribute to helping manage and maintain a person's plan of care.
Anxiety, the unpleasant feeling of fear and apprehension, is something that most people experience at one point or another in their lives. People have anxious feelings about taking tests, speaking in public, interacting with the opposite sex, making new friends and acquaintances, traveling to strange places, or personal situations (for example, money, job, family, etc.). Anxiety of this nature is completely normal, as long it does not prevent people from going ahead and doing these activities anyway, facing their minor fears or worries and moving forward.
Sometimes, though, some people find that they are paralyzed by their anxiety about a situation or a thing and cannot act. Instead of doing what they know they should, they retreat and avoid the situation entirely. This might not seem too harmful if it is a case of a person being afraid, for example, of tigers. As long as he or she doesn't live in an area populated by such animals, the situation might never present a problem. However, what happens if individuals have extreme anxiety in social situations to the point that they avoid interacting with others entirely? Or, what if people are so afraid of germs that they cannot stop compulsively cleaning themselves to the point that they are unable to engage in normal activities for fear of contamination? It is at this point that individuals must seek professional help in order to conquer their fears so that they can live normal, full lives.
Phobia is a form of an anxiety disorder that involves intense and illogical fear of an object or situation. Usually, the individual is aware that the fear is out of proportion to the danger of the thing they fear. In other words, someone being afraid of skydiving or rock climbing wouldn't have a phobia; both of these activities carry high risks for injury or death. However, someone who has never had a negative experience with a dog but is afraid of dogs has a phobia. And, even allowing for the fact that a person has had a negative experience with the thing or situation feared, the presence of a phobia is indicated if the level of fear is out of proportion with the threat the situation or object presents.
The most common phobia is agoraphobia, the fear of public places. This is a phobia that can impair a person's ability to connect with others, to attend
school, and to hold a job. People with severe agoraphobia will not only avoid crowds and busy places, some may refuse to leave their homes entirely. Other common phobias include the fear of heights, called acrophobia, and claustrophobia, which is the fear of closed spaces (such as elevators or overly crowded rooms that leave little personal space).
TREATMENTS. Treatments for phobias usually involve confronting the fear in some way. Behavioral therapists (see Chapter 15: Mental Health Therapies) may use a variety of techniques that involve visualization or actual contact with the object or situation around which the phobia centers. The thinking behind this, for certain schools of therapies, is that it will desensitize the phobic to the phobia. For example, flooding, a behavioral technique, involves exposing a phobic person to the cause of the phobia in an extreme way; however, this can cause the phobic serious initial discomfort, at the very least, and many therapists shy away from therapies that could potentially traumatize a patient.
Operant conditioning is also used in similar ways. Cognitive therapists will work with phobics using cognitive therapies alone (without some type of exposure to the source of the phobia), but this is usually effective only in the case of social phobics. Furthermore, social phobics have responded well to behavioral techniques that involve acquiring better social skills so that they feel more comfortable in social situations. Drugs have also been used to lessen a phobic's anxiety but drugs only mask the fear and will not solve the problem in the long term.
WHAT ARE YOU AFRAID OF?
For every fear, it seems there is a phobia. Listed below are just some phobias, from the common to the plain weird.
|Ailurophobia||The fear of cats|
|Bibliophobia||The fear of books|
|Coulrophobia||The fear of clowns|
|Didaskaleinophobia||The fear of going to school|
|Entomophobia||The fear of insects|
|Glossophobia||The fear of speaking|
|Heliophobia||The fear of the sun|
|Ichthyophobia||The fear of fish|
|Lachanophobia||The fear of vegetables|
|Myctophobia||The fear of darkness|
|Nosocomephobia||The fear of hospitals|
|Ophidiaphobia||The fear of snakes|
|Pantophobia||The fear of everything|
|Rupophobia||The fear of dirt|
|Sophophobia||The fear of learning|
|Triskadekaphobia||The fear of the number 13|
|Urophobia||The fear of urine or urinating|
|Xenophobia||The fear of strangers or foreigners|
|Zoophobia||The fear of animals|
Panic Attacks and Disorder
A panic attack can accompany several different anxiety disorders, so in and of itself, a panic attack is not a separate disorder. Essentially, a panic attack is a short period involving intense feelings of fear or discomfort along with several telltale symptoms. These symptoms include an irregular or accelerated heart rate or a pounding of the heart; sweating, discomfort or pain in the chest; a feeling of choking or not being able to breathe properly; trembling, feelings of detachment, of things being "unreal," and/or of impending doom. People experiencing panic attacks have described feeling as though they would lose control completely or were about to have a heart attack or stroke.
Panic attacks can be caused by certain situations, such as being in a strange place, or while a person is relaxing or even sleeping. If panic attacks continue to occur when there is no apparent stressor (stress-inducing event), an individual might be diagnosed with having panic disorder. Panic disorder is a reasonably common ailment, affecting two percent of men and five percent of women. It may begin in adolescence and the disorder is inherited. Biological theories as to the disorder's origin have been put forth as have theories that suggest that panic disorders and agoraphobia are solely psychological in origin. Furthermore, one set of researchers has even suggested that the agoraphobia that so often coexists with panic disorders isn't really a fear of public places but rather a fear of losing control and having a panic attack in a public place.
Certain drugs, such as antidepressants, have been used to treat people with panic disorder and agoraphobia with some success; however, the drugs are merely a temporary measure as people's symptoms will return when they stop taking the drugs. A better approach in terms of a cure might be methods used by cognitive and behavioral therapists, which have proven to help lessen the severity of the disorder.
Obsessive-compulsive disorder (OCD) involves obsessions (repeating thoughts, impulses, or mental images that are irrational and which an individual cannot control) and compulsions (habitual behaviors or mental acts an individual is driven to perform in order to reduce stress and anxiety brought on by obsessive thoughts or because individuals believe those behaviors or acts will prevent a certain calamity from occurring [for example, believing that a certain behavior will prevent a car accident]). While almost every person may have behavioral quirks or strong preferences (cracking one's knuckles, or wanting things to be kept neat), obsessions and compulsions are different in that they prevent people from living normal lives because they take up an inordinate amount of time.
Obsessions can include thoughts ranging from a person constantly thinking about becoming "contaminated" with germs and avoiding shaking hands with others because of that fear, to a person being convinced that he has left his front door unlocked. The compulsions accompanying these obsessions can include things such as someone repeatedly washing hands for fear of germs, or checking repeatedly (sometimes a certain number—for instance, three times) to see if they have indeed locked the front door. Unlike preferences, a compulsion is something that is viewed as not being part of someone's personality but rather irrational behavior that a person is unable to stop. Due to the nature of this disorder, it can separate people from others, rendering afflicted individuals unable to participate in everyday activities because their obsessions and compulsions prevent them from doing so.
CAUSES. There are many theories surrounding the development of OCD. Behavioral and cognitive therapists believe that the behaviors and thinking related to OCD are learned and reinforced. For example, a person may have the irrational belief that she has not locked her door; by going back to check whether or not it is indeed locked, she is able to relieve the stress that is related to her worries. Some therapists have also pointed to the fact that a lot of the problem stems from the fact that those suffering from OCD simply cannot remember whether or not they did something. There can also be organic (relating to the body) causes for OCD, such as head injuries and brain tumors as well as chemical imbalances in the brain.
TREATMENTS. Treating OCD is not an easy task. One of the most successful therapies involves placing a person in a situation that usually triggers his anxiety, but the patient is not allowed to engage in the compulsive behavior that is the typical response. The idea is that eventually the stress from not performing the compulsive behavior will lessen over time to the point where the person no longer feels compelled to do it.
Prescription drugs have also proven successful in reducing a person's obsessive thoughts and compulsive behaviors; this approach will not necessarily resolve the problem entirely but will free a person to live a normal life while confronting the issues appropriately through therapy.
Post-Traumatic Stress Disorder
Every day, people experience traumatic events, anything from being in a car accident to being robbed or even witnessing such an event happening to someone else. While people may survive these events (which involve intense fear and a feeling of helplessness), and their physical wounds may heal, they can still carry emotional scars. When an individual experiences emotional aftereffects from a traumatic event days, months, or even years after the actual event, this is known as post-traumatic stress disorder (the prefix "post" means after or later). Many of these individuals, even much later, will relive the event, become extremely upset and/or have nightmares about the event. They will also try to avoid things that remind them of the trauma. Finally, they may also be plagued by sleep disruptions, have difficulty concentrating, and startle easily and dramatically.
Post-traumatic stress disorder received a great deal of attention in the years following the Vietnam War (1954–75), as it had after World Wars I (1914–17) and II (1939–45), the Korean Conflict (1950–53) and, in fact, even after earlier conflicts such as the American Civil War (1861–65), because of the emotional scars that those who had served in a war often seemed
to display. In fact, PTSD was originally called "shell shock" (in reference to the ammunition used during times of war). It is now known that those who have witnessed or participated in any type of traumatic event—such as being involved in the search-and-rescue or recovery missions for the victims of plane crashes in which hundreds of people perish—are now known to be potential sufferers from PTSD. What is mysterious about PTSD is why it affects only certain people and not all of those experiencing similar events or even the same event.
TREATMENTS. Great strides have been made in treating PTSD through group therapy. Talking in a group to others who have experienced similar events and have been suffering from them continuously can be very helpful because patients can feel that they are not alone in their feelings and that there are people who understand the intensity of their traumatic experience. Most therapies, in groups or single client therapy, usually will involve confronting the event in some way. Stress management and medication have also been used with some success.
People who have lived through traumatic events should be encouraged to seek at least brief therapy to ensure that PTSD won't develop years later.
OTHER TYPES OF MENTAL DISORDERS
There are a number of other mental or psychological disorders that afflict millions of people each day. These can range from disorders most often appearing in old age, such as Alzheimer's disease, to gender-identity disorders, in which people wish to be members of the opposite sex. Eating disorders are also a common mental illness. [For more information on eating disorders, see Chapter 13: Eating Disorders.]
What follows is a small sampling of other common psychological disorders.
Sometimes people will complain of pain or discomfort that lingers but, when these individuals seek medical treatment, doctors can find no physical cause for the symptoms. When this persists, and the pain and discomfort prevent a person from participating in day-to-day life, a mental health professional may diagnose that person with pain disorder, which is just one of several somatoform disorders. Somatoform disorders are psychological disorders that manifest themselves physically without the presence of a true physical ailment.
Somatoform disorders can include conversion disorders, which can result in sudden loss of vision (once called hysterical blindness) or paralysis. People have also been known to lose their senses of hearing and smell as well. Another somatoform disorder is body dysmorphic disorder (BDD). While many people would like to change something about themselves (such as being more muscular, having smaller ears, having straight or curly hair, being taller or shorter, etc.), people with BDD grossly exaggerate what they perceive to be flaws with themselves and spend hours obsessing about these so-called flaws. Some BDD sufferers even take measures to act upon their impulses by picking at their skin (if they think they have too many blemishes) or getting plastic surgery unnecessarily.
As with many other mental disorders, there is no single theory that can account for why certain people develop somatoform disorders while others do not. Oftentimes, a person will recover suddenly from the problem while others require therapy. Behavior therapists will use techniques that center around making it appealing for a person to abandon his or her symptoms. Other therapists have used techniques similar to those used on people with phobias, wherein the patient will be exposed to the cause of the stress in order to diminish its effect.
When someone dissociates, it means that a certain behavior or part of the personality becomes removed from the rest of his or her consciousness. This can be something as harmless as becoming preoccupied while listening to a song on a portable stereo while walking and then not remembering which route was taken upon arriving at a destination. However, dissociation can also be a very serious problem and several disorders are attached to this phenomenon.
BARON VON MUNCHAUSEN AND MENTAL ILLNESS
Baron Von Munchausen was an eighteenth-century German huntsman and soldier known for telling greatly exaggerated tales about his exploits. Because of his reputation and the publication of tales based on his anecdotes (written by Rudolph Erich Raspe), the name Munchausen is now associated with exaggeration. So it came to be that when people faked symptoms of illnesses or parents faked the illnesses of their children, those disorders were named the Munchausen syndrome and Munchausen-by-proxy syndrome, respectively.
Although Munchausen syndrome and Munchausen-by-proxy syndrome are still recognizable names and in use, the proper clinical terms for these somatoform disorders are malingering (in the case of an individual who fakes illness in order to avoid doing something or to receive attention) and factitious disorder (in which a parent or guardian lies about a child's medical history and current condition in order to make others believe the child is ill). Both syndromes go beyond fibbing; they are serious psychological disorders, and both have consequences that affect others.
In the case of malingering (or Munchausen syndrome), a healthy individual is wasting the time of medical professionals and perhaps even taking up valuable bed space in a hospital. Factitious disorder (or Munchausen-by-proxy syndrome) can threaten the life of an otherwise healthy child because the disturbed caretaker may even go so far as to injure the child or taint blood or urine specimens to sustain the illusion of illness. Most often, sufferers from factitious disorder do what they do based on a warped need for attention from others and the desire for an abnormally intense and dependent relationship with the child.
DISSOCIATIVE AMNESIA. Dissociative amnesia, which occurs when a person cannot remember personal information, such as where a person has been, who a person is, or even entire conversations. Often this is prompted by a stressful event, such as abuse, a traumatic experience similar to those detailed in the section on PTSD, or the death of a loved one. Memory loss is the primary symptom of this disorder, which is more common among young adults.
DISSOCIATIVE FUGUE. Dissociative fugue (pronounced fyoog) is a particularly disturbing mental phenomenon as it involves one or more instances of a person leaving their normal, everyday life for a period of time and taking up a new life, with no recollection of their former life. Like dissociative amnesia, fugues are often triggered by traumatic events and are often fueled by unfulfilled wishes. An individual in the midst of a fugue will often leave home, abandoning all aspects of his or her life, and assume a new identity in another place. A fugue can last hours or days or longer.
DISSOCIATIVE IDENTITY DISORDER. Dissociative identity disorder, or DID (formerly known as multiple personality disorder, or MPD), involves an individual having two or more identities or personalities that are in control of an individual's behaviors and thoughts at different times. A controversial diagnosis (as it violates the basic belief that only one person can inhabit a body), people diagnosed with DID will often have a variety of personalities that are very different from one another and that may be in opposition to one another. For example, one personality may require an individual to wear glasses in order to see clearly, while another personality will not wear glasses. Or one personality may be left-handed whereas the other(s) are right-handed. DID usually begins in childhood and is often the result of severe trauma or an individual's repressing, or keeping back, strong feelings and desires.
Because of the association of the concept of repression (holding back painful memories) with dissociative disorders, psychoanalytic therapists seem to have good success in treating these disorders (for an explanation of the principles of psychoanalysis, see Chapter 15: Mental Health Therapies). Hypnosis may be also be used by psychoanalysts to help uncover forgotten memories in order to get to the root of why individuals disconnect from themselves.
People have different personalities (one's behavioral and emotional traits). Many people, however, share a type of personality, which means they have certain tendencies. For example, an individual who is sensitive to criticism might have an avoidant personality type. This is perfectly acceptable unless that person's behavior is extreme, thereby presenting problems in personal relationships and the ability to function in society. If one avoids people in social and work-related situations out of fear of being criticized or rejected; shies away from getting close to other people for fear of being made fun of; has low self-esteem; and is painfully shy and standoffish, that person might have an avoidant personality disorder. In other words, the difference between a personality type and a personality disorder is that the disorder separates people from others and the separation can prevent them from being happy and successful.
There is a wide range of personality disorders. There is the histrionic personality disorder, in which an individual needs to be the center of attention; behaves inappropriately (making sexual comments, for example); wears revealing clothes; is overly dramatic; is easily influenced by other people or events; and exaggerates how emotionally close one actually is to another person.
Dependent personality disorder is marked by an overwhelming need for advice and reassurance from others; being unable to disagree with others for fear he or she will no longer be liked; having a lack of initiative and self-direction; and showing an unusual need for close relationships along with a fear of being alone.
MENTAL ILLNESS IN THE MOVIES
Over the years, a great number of films have presented audiences with characters struggling with a mental illness. Sometimes, filmmakers are able to humanize the face of mental illness and demystify it by showing everyday people triumphing over a disorder. Other times, filmmakers have reached into the darkest depths of the human psyche and created terrifying characters with mental problems so severe that the individuals are a threat to others and themselves. The following films include characters with varying degrees and types of mental illness:
Benny and Joon
Desperately Seeking Susan
Good Will Hunting
I Never Promised You a Rose Garden
One Flew over the Cuckoo's Nest
Silence of the Lambs
Splendor in the Grass
The Glass Menagerie
The Other Sister
The Prince of Tides
The Three Faces of Eve
What's Eating Gilbert Grape?
Other personality disorders include the paranoid personality disorder (which involves constant distrust and suspicion of other people; thinks others are "out to get them."). There is also the schizoid personality disorder (in which people are removed from social contact with others and have problems experiencing and expressing emotion). Another is the borderline personality disorder (wherein an individual is unstable in relationships with others, has poor self-image and extremist thinking, and is very impulsive). Lastly, there is the narcissistic personality disorder (wherein an individual is overly conceited, having an abnormal need for admiration and lack of empathy for others).
Personality disorders are treated differently, depending upon which type of disorder is present. The difficulty lies in the fact that personality disorders carry risks with them that can affect treatment and a person's personal safety. For instance, people with severe personality disorders often engage in high-risk behavior, such as excessive drinking or taking illegal drugs. Furthermore, they are particularly vulnerable to psychiatric breakdowns, are less likely to take medications prescribed to them in the proper manner, and have a hard time taking responsibility for their behavior or trusting their mental health care provider.
FOR MORE INFORMATION
Cush, Cathie. Depression (Teen Hot Line). Raintree/Steck Vaughn, 1994.
Friedland, Bruce. Personality Disorders (Psychological Disorders and Their Treatment). Chelsea House, 1991.
Ingersoll, Barbara D. Distant Drums, Different Drummers: A Guide for Young People with ADHD. Cape Publications, 1995.
Klebanoff, Susan and Ellen Luborsky. Ups and Downs: How to Beat the Blues and Teen Depression. New York: Price Stern Sloan, Inc. 1999.
Levine, Mel, Melvin D. Levine, and Ann Jennings. Keeping a Head in School: A Student's Book About Learning Abilities and Learning Disorders. Educator's Publishing Service, Inc., 1991.
Roleff, Tamara L., ed. Suicide: Opposing Viewpoints. Greenhaven Press, 1997.
Sebastian, Richard. Solomon H. Snyder and Dale C. Garell, eds. Compulsive Behavior (Encylopedia of Health Series: Psychological Disorders and Their Treatment). Chelsea House, 1993.
American Psychiatric Association. [Online] http://www.psych.org (Accessed July 28, 1999).
American Psychological Association. [Online] http://www.apa.org/ (Accessed July 28, 1999).
Yellow Ribbon Suicide Prevention Program. [Online] http://www.yellowribbon.org (Accessed July 28, 1999).
"Mental Illness." UXL Complete Health Resource. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/medicine/news-wires-white-papers-and-books/mental-illness
"Mental Illness." UXL Complete Health Resource. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/medicine/news-wires-white-papers-and-books/mental-illness
Mental disorders cover a wide range of conditions that lead to abnormalities of thought, feeling, and behavior. These abnormalities cause distress or impair a persons ability to function.
for searching the Internet and other reference sources
A man in a tattered coat stands on the street corner, yelling at no one in particular. Although the man appears to think that he is arguing logically, his words are jumbled together and make little sense.
In a nearby apartment, a young woman cannot sleep until she is sure that her kitchen stove is turned off. She leaves her bed, checks the stove, and then returns to bed. But can she be sure? Once more, she goes to check the stove, a process she will repeat many times throughout the night.
In a suburban home, an 11-year-old boy wakes in a panic. He dashes to his parents’ bedroom to make sure that they are safe, gripped by fear that they have been in mortal danger while he slept.
What do these three people have in common? While their thoughts, feelings, and behaviors are very different, each has a mental disorder that requires careful diagnosis and can be helped with proper treatment.
- means related to the way a person thinks and feels.
- means related to the way a person acts.
from disorders first diagnosed during childhood or adolescence, such as the separation anxiety experienced by the 11-year-old above, to disorders often associated with old age or with medical illnesses, including Alzheimer’s disease*, AIDS*, Huntington’s disease*, and strokes*.
- *Alzheimer’s disease
- leads to changes in personality and to a gradually worsening loss of mental abilities, including memory judgment and abstract thinking.
- (acquired immune deficiency syndrome) is a viral infection that can lead to damage in many parts of the body including the brain and nervous system.
- *Huntington’s disease
- is a genetic condition that leads to involuntary twitching or jerking of the muscles in the face, arms, and legs along with a gradual loss of mental abilities.
- are events that occur when a blood vessel bringing oxygen and nutrients to the brain bursts or becomes clogged by a blood clot or other particle. As a result nerve cells in the affected area of the brain cannot function properly.
Many mental disorders have been found to stem from changes in the structure or function of the brain. Some disorders also may be related to drug or alcohol abuse. Although the exact cause of most mental disorders is not known, some of these conditions tend to run in families, indicating that inherited or genetic factors may play a role.
Among the more common mental disorders are schizophrenia, depressive disorders, anxiety disorders, eating disorders, and sleep disorders. Phobias, such as claustrophobia (fear of closed spaces) and social phobias (fear of embarrassment in social situations), also are classified as mental disorders.
Psychologists and psychiatrists use many different terms to describe mental disorders and their symptoms:
- Anxiety disorders (ang-ZY-e-tee dis-OR-derz) are mental disorders characterized by extreme, unpleasant, and unwanted feelings of apprehension or fear, sometimes accompanied by physical symptoms.
- Delirium (de-LEER-e-um) is a mental state in which a person suddenly becomes confused and disoriented, perhaps not knowing what day it is or not recognizing a friend. It often accompanies a physical illness and usually goes away when the illness gets better.
- Delusions are false beliefs that a person clings to, despite their lack of basis in reality. For example, delusion of grandeur refers to the false belief that a person has great importance, power, wealth, intelligence, or ability.
- Dementia (de-MEN-sha) is a gradually worsening loss of mental abilities, including memory, judgment, and abstract thinking. It is more common in older people.
- Depressive disorders (de-PRES-iv dis-OR-derz) are mental disorders associated with feelings of sadness, hopelessness, and loss of self-esteem and enjoyment. Significant levels of depression impair a person’s feelings, thoughts, and behaviors.
- Eating disorders are mental disorders that lead people to starve themselves or to eat huge amounts of food.
- Hallucinations are false perceptions by the senses. People hear voices, see visions, or sense things that are not really there.
- Mental retardation is a condition present since childhood in which the person has significantly below-average intelligence. These individuals may be limited in their ability to learn, work, communicate with others, care for themselves, and live independently.
- Neurosis (noo-RO-sis) is a broad term covering many mental disorders that are long-lasting or recurring. People who have a neurosis remain in touch with reality, unlike those who have a psychosis. But the anxiety, depression, and distress common to neurosis can interfere with the quality of life.
- Obsessive-compulsive disorder (ob-SES-iv-kom-PUL-siv dis-OR-der) is a mental disorder that causes people to feel trapped by distressing or senseless thoughts and to feel as if they have to repeat actions.
- Phobias (FO-be-as) are mental disorders that lead to a lasting, intense, irrational fear of a particular object, activity, or situation.
- Post-traumatic stress disorder (post-traw-MAT-ik STRESS dis-OR-der) is a mental disorder that interferes with everyday living and occurs in people who survive a life-threatening event, such as school violence, car accidents, natural disasters (earthquakes, hurricanes, floods), or military combat.
- Psychosis (sy-KO-sis) is a broad term covering severe mental disorders that make a person unable to recognize reality, relate to other people, or function in daily life. A disorder like depression could be considered a neurosis or a psychosis depending on how severe it is.
- Schizophrenia (skitz-so-FRE-ne-a) is a form of psychosis that causes people to have hallucinations, delusions, and other confusing thoughts that distort their view of reality.
- Separation anxiety (sep-a-RAY-shun ang-ZY-e-tee) is a mental disorder in which children worry excessively about leaving their homes, parents, or caregivers.
- Sleep disorders are long-lasting disturbances of sleep. Some sleep disorders have mainly psychological causes, while others have mainly physical causes.
Diagnosis of mental disorders requires careful evaluation by a qualified physician or mental health professional. A variety of tests are used. The physician may assess how severe a person’s symptoms are, how long the symptoms have lasted, the person’s prior mental and medical history, whether the disorder has a medical basis, and whether the disorder is caused by alcohol or another drug.
Treatment depends on the specific disorder and may include psychotherapy* for the individual or for the family. Often a combination of psychotherapy and medication is prescribed.
- is treatment for a mental disorder that usually involves talking with a trained therapist to undercover the roots of a person’s behavior or to learn new ways of thinking or behaving.
Attention Deficit Hyperactivity Disorder
Post-Traumatic Stress Disorder
U.S. National Institute of Mental Health, 6001 Executive Boulevard, Room 8184, MSC 9663, Bethesda, MD 20892-9663. NIMH is the government institute that oversees research on mental disorders and provides information for professionals and the public.
American Psychological Asssociation, 750 First Street NE, Washington, DC 20002-4242. The American Psychological Association publishes books, brochures, and fact sheets about mental health, mental disorders, and psychotherapy. It provides referrals to local psychologists, and its website includes a KidsPsych feature.
American Psychiatric Association, 1400 K Street NW, Washington, DC 20005. The American Psychiatric Association publishes the Diagnostic and Statistical Manual of Mental Disorders for doctors, and the Let’s Talk Facts About pamphlet series for the public. Its website also posts a Psychiatric Medications fact sheet.
National Alliance for the Mentally 111, 200 North Glebe Road, Suite 1015, Arlington, VA 22203-3754. A self-help organization for people with serious mental illness, their families, and their friends.
National Mental Health Association, 1021 Prince Street, Alexandria, VA 22314-2971. A national organization that offers information to the public about various mental disorders and mental health.
"Mental Disorders." Complete Human Diseases and Conditions. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/mental-disorders
"Mental Disorders." Complete Human Diseases and Conditions. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/mental-disorders
"mental handicap." World Encyclopedia. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/environment/encyclopedias-almanacs-transcripts-and-maps/mental-handicap
"mental handicap." World Encyclopedia. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/environment/encyclopedias-almanacs-transcripts-and-maps/mental-handicap
"mental disorders." The Columbia Encyclopedia, 6th ed.. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/reference/encyclopedias-almanacs-transcripts-and-maps/mental-disorders
"mental disorders." The Columbia Encyclopedia, 6th ed.. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/reference/encyclopedias-almanacs-transcripts-and-maps/mental-disorders
"mental handicap." A Dictionary of Nursing. . Encyclopedia.com. (June 28, 2017). http://www.encyclopedia.com/caregiving/dictionaries-thesauruses-pictures-and-press-releases/mental-handicap
"mental handicap." A Dictionary of Nursing. . Retrieved June 28, 2017 from Encyclopedia.com: http://www.encyclopedia.com/caregiving/dictionaries-thesauruses-pictures-and-press-releases/mental-handicap