Drug Types

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There are many ways to classify drugs, depending on the purposes for the classification. For example, a classification can be based on the chemical properties of drugs and may actually disregard the effects the drugs have on the body, or it may be based on legal principles, such as legal versus illegal, or prescription versus over-the-counter (prescription not needed). For purposes of discussion and teaching, the various drugs that are used and abused by humans for nonmedical purposes are usually grouped into several major categories, each based on their pharmacological actions and their subjective effects. Although the mechanisms of action may vary among drugs within a single category, the general subjective effects of the drugs are similar.

The major categories include: (1) ethanol (Alcohol); (2) Nicotine and tobacco: (3) central nervous system depressants (Barbiturates, Benzodiazepines); (4) central nervous system stimulants (Amphetamines, Cocaine); (5) cannabinoids; (6) Opiods (Morphine, Heroin, Methadone); (7) psychedelics (lsd, Mescaline);(8) Inhalants (glue, nitrous oxide);(9) arylcyclohexylamines (pcp). Some categorizers might put cocaine and the amphetamines into separate categories and group alcohol and the central nervous system depressants together. Some might have a separate category for Caffeine; others, one for "Designer Drugs" (such a Smdma), and refer to them as entactogens. There might also be a miscellaneous category, where drugs such as Betel Nut, Kava-Kava, or Nutmeg would be included.

Drugs from the various categories are described below in terms of their pharmacology, abuse, Dependence, and Withdrawal as well as their toxicity. The legal and readily available drugs (alcohol and tobacco) are described first because the worldwide use and abuse of these drugs is far more widespread than all the other categories of abused drugs combined. The ill health associated with the ongoing use of alcohol and tobacco has become a far-reaching problemnot only because of the vast numbers of people who suffer and die each year from the toxic effects of these drugs but also because of the financial drain in terms of employee absenteeism as well as the staggering increases in annual health-care costs. Prescription drugs are covered next, since more prescriptions are written for diazepam (Valium) and the related benzodazepines each year than for any other drug.

The illegal drugs are then discussed. Although the illicit use of heroin, cocaine, and other drugs remains a major social, legal, financial and health problem in the United States today, the proportion of the population physically dependent on these drugs is actually relatively low when compared to the legal drugs listed above. Finally, it is important to take into consideration the fact that individuals often do not restrict their drug use only to drugs within a single category. Alcoholics typically smoke cigarettes and often use benzodiazepines as well. Heroin users also smoke and may consume alcohol and other sedatives, as well as Cannabis and stimulants in some instances. Multiple-drug use is, therefore, a relatively common occurrence for those using legal and/or illegal drugs.


Although alcohol (ethyl alcohol, called ethanol) has been in use since prehistory and worldwide throughout recorded history, it is generally accepted that its therapeutic value is extremely limited and that chronic Alcoholism is a major social and medical problem. Perhaps 65 percent of all adults in the United States use alcohol occasionally. Hundreds of thousands of individuals suffer and die each year, however, from complications associated with chronic alcoholismand tens of thousands of innocent individuals are injured or killed each year in alcohol-related traffic Accidents. Therefore, alcoholism is a far-reaching problem, affecting the lives of individuals who consume ethanol as well as those who do not. Although alcohol is considered by many people to be a stimulant drug because it typically releases an individual's latent behavioral inhibitions (i.e., through disinhibition), alcohol actually produces a powerful primary and continuous depression of the central nervous system similar to that seen with general anesthetics. In general, the effects of alcohol on the central nervous system are proportional to the blood concentrations of the drug. Initially, Memory and the ability to concentrate decrease, and mood swings become more evident. As the intoxication increases, so does the impairment of nervous function until a condition of general anesthesia is reached ("passing out" or "sleeping it off"). There is little margin of safety, however; between an anesthetic close of ethanol and severe respiratory depression (unconsciousness or coma).

In chronic (long-term) alcoholism, brain damage, memory loss, sleep disturbances, psychoses, and increased seizure susceptibility often occur. Chronic alcoholism is also one of the major causes of cardiomyopathy (heart disease) in the United States due to ethanol-induced, irreversible damage to the heart muscle. Ethanol also stimulates the secretion of gastric acid in the stomach and can contribute to the production of ulcers of the stomach and gastrointestinal system. One of the primary metabolic products of ethanol is acetaldehyde. In chronic alcoholism, acetaldehyde can accumulate in the liver, resulting in hepatitis and cirrhosis of the liver. Finally, the long-term use of alcohol can result in a state of Physical Dependence. With relatively low levels of dependence, withdrawal from alcohol may be associated with rather minor problems such as Sleep disturbances, Anxiety, weakness, and mild tremors. In more severe dependence, the alcohol withdrawal syndrome includes more pronounced tremors, seizures, and Delirium, as well as a number of other physiological and psychological effects. In some cases, this withdrawal can be life-threatening.

Since alcohol has Cross-Tolerance with other central nervous system (CNS) depressants (i.e., ethanol shares many of the same biological effects as other CNS depressants), benzodiazepines or barbiturates can be substituted for ethanol to successfully decrease the severity of the alcohol withdrawal syndrome. Longer-acting benzodiazepines and related drugs can be used as an ethanol substitute, and the dose of the benzodiazepine can then be gradually reduced over time to attenuate or prevent the occurrence of convulsions and other potentially life-threatening toxic reactions generally associated with alcohol withdrawal.

As outlined above, the chronic use of ethanol can result in a wide range of toxic effects on a variety of organ systems; however, the mechanisms through which ethanol produces its varied effects are not clearly understood. The anesthetic or central nervous system depressant effects may result, in part, from general changes in the function of ion channels that occur when ethanol dissolves in lipid (fat) membranes. Other research suggests that alcohol may interact with specific receptorsbinding sites associated with the inhibitory Neurotransmitter Gamma-Aminobutyric Acid (GABA), in a manner somewhat analogous to other central nervous system depressants (e.g., benzodiazepines or barbiturates). Since an ethanol Receptor site has not yet been conclusively identified, specific receptor Ago-Nists and Antagonists are not yet available for the treatment of ethanol intoxication, Withdrawal, and abstinence. The drug Disulfiram (Antabuse) is sometimes used in the treatment of chronic Alcoholism, although it does not cure alcoholism. Rather, disulfiram interacts with ethanol to alter the intermediate metabolism of ethanol, resulting in a five- to tenfold increase in plasma acetaldehyde concentrations. Those who drink while on disulfiram experience the acetaldehyde syndromevasodilatation, headache, difficulty breathing, nausea, vomiting, sweating, faintness, weakness, anti vertigo. Taking the drug helps persuade alcoholics to remain abstinent, since they realize that they cannot drink ethanol for at least three or four days without provoking ill-effects.


Tobacco was first introduced to Europe by the crews that accompanied Columbus to the New World, and by the middle of the nineteenth century, tobacco use had become widespread. By the 1990s, almost 30 percent of the adults in the United States were still regular tobacco smokers. This relatively high use of tobacco continues despite the growing warnings that are based on a wealth of scientific evidence linking cigarette smoking to numerous life-threatening health disorders, including lung Cancer and heart disease. The constituents of tobacco smoke that most likely contribute to these health problems include carbon monoxide, Nicotine, and "tar." However, nicotine also appears to be the primary component of tobacco smoke that promotes smoking. In regular cigarette smokers, nicotine facilitates memory, reduces aggression, and decreases weight gain. Each of these effects could, by itself, provide a rationale for continued tobacco use since most individuals find increased alertness and memory, decreased irritability, and decreased weight gain to be somewhat pleasant or desirable; however, these effects may actually be secondary to the primary reinforcing effects of nicotine itself. Nicotine is self-administered by laboratory animals, and in laboratory settings, smokers report that the intravenous injection of nicotine produces a pleasant feeling on its own. It is of interest to note, however, that nicotine is aversive to nonsmokers, often resulting in dizziness, nausea, and vomiting. Tolerance rapidly develops to these unpleasant effects in tobacco smokers, however.

Although nicotine obviously binds to nicotinic receptors associated with the neurotransmitter Acetylcholine, there is evidence that the reinforcing or rewarding properties of nicotine may result from an activation of ascending limbic neurons, which release the neurotransmitter Dopamine (i.e., the mesocorticolimbic dopaminergic system). Interestingly, this same system has been implicated in the reinforcing properties of a variety of drugs, including stimulants and opiates. As stated above, tobacco smoking has been associated with a wide variety of serious health effects, including cancer and heart disease; however, the chances of developing them decrease once smoking is terminated. Although some of the smoking-induced damage is irreversible, the incidence rates for cancer and heart disease gradually become more similar between smokers and nonsmokers the longer the smoker refrains from smoking. However, withdrawal from tobacco smoking results in a withdrawal syndrome that varies in intensity from individual to individual and often leads to a relapse of smoking. This syndrome consists of cravings for tobacco, irritability, weight gain, difficulty concentrating, drowsiness, and sleep disturbances. The recent introduction of nicotine-containing chewing gum and transdermal patches have significantly helped to facilitate abstinence from smoking in a number of individuals by delivering nicotine through a relatively less toxic route of administration.


In general, the incidence and prevalence of the nonmedical use of central nervous system depressants (approximately 6 to 8% of young adults) exceeds that of the opioids. These drugs include the barbiturates, benzodiazepines, and related drugs. The shorter-acting barbiturates, such as pentobarbital ("yellow jackets") or Secobarbital ("red devils"), are usually preferred to the longer-acting drugs such as phenobarbital. Nonbarbiturates such as Meprobamate, Glutethamide, methyprylon, Methaqualone (Quaalude) and some of the shorter-acting benzodiazepines are also abused. Presumably, the quicker the onset of action for a particular central nervous system depressant, the better the "high."

There is no general rule that can be used to predict the pattern of use of a central nervous system depressant for a given individual. Often there is a fine line between appropriate therapy for insomnia or Anxiety and drug dependence. Some individuals exhibit cyclic patterns of use with gross intoxication for a few days interspersed with periods of abstinence. Other barbiturate or benzodiazepine users maintain a chronic low level of intoxication without observable signs of impairment because of the development of tolerance to many of the actions of these drugs. When higher doses are used, however, the intoxication may resemble alcohol intoxication, with slurred speech, difficulty thinking, memory impairment, sluggish behavior, and emotional instability. Withdrawal from chronic barbiturate or benzodiazepine use can also be manifested to varying degrees. In the mildest form, the individual may only experience mild anxiety or insomnia. With greater degrees of physical dependence, tremors and weakness may also be included. In severe withdrawal, delirium and tonic-clonic (epileptic) seizures may also be present. This severe withdrawal syndrome can be life-threatening. The degree of severity of the withdrawal syndrome appears to be related to the pharmacokinetics of the drug used. Shorter-acting benzodiazepines and barbiturates produce much more severe cases of withdrawal than do the longer-acting drugs. Therefore, in the case of severe withdrawal symptoms associated with the chronic use of a short-acting drug, a longer-acting drug should be substituted. The dose of this drug can be gradually decreased so that the individual experiences a much milder and less threatening withdrawal.

Receptor-binding sites for benzodiazepines and barbiturates are part of a macromolecular complex associated with chloride ion channels and the inhibitory neurotransmitter GABA. The interaction of these drugs with their distinct binding sites results in a facilitation of GABAergic neurotransmission, producing an inhibitory effect on neuronal impulse flow in the central nervous system.


Central nervous system stimulants include caffeine, cocaine, and amphetamine, although the use and abuse of amphetamines and cocaine represent a much greater health risk, with deviation from social norms.


Perhaps 80 percent of the world's population ingests caffeine in the form of Tea, Coffee, Cola-flavored drinks, and Chocolate. In the central nervous system, caffeine decreases drowsiness and fatigue and produces a more rapid and clearer flow of thought. With higher doses, however, nervousness, restlessness, insomnia, and tremors may result. Cardiac and gastrointestinal disturbances may also be observed. Tolerance typically develops to the anxiety and dysphoria experienced by some individuals. Some degree of Physi-Cal Dependence has, however, been associated with the chronic consumption of caffeine. The most characteristic symptom of caffeine withdrawal is a long throbbing headache, although fatigue, lethargy, and some degree of anxiety are also common. In general, the long-term consequences of chronic caffeine consumption are relatively minor.


The problems associated with chronic cocaine and amphetamine use and withdrawal are much more serious than those associated with caffeine. By the mid-1980s, more than 20 million people had used cocaine in the United States. With the recent introduction of cocaine in the free alkaloid base (" Freebase" or "Crack") form, there has been a significant increase in cocaine-related medical, economic, social, and legal problems. In the free-base form, cocaine can be smoked, resulting in blood levels and brain concentrations of the drug that compare to those observed when the drug is injected intravenously. In non-user subjects in a laboratory setting, the administration of cocaine or amphetamine produces an elevation of mood, an increase in energy and alertness, and a decrease in fatigue and boredom. In some individuals, however, anxiety, irritability, and insomnia may be observed.

In nonlaboratory settings, heavy users of cocaine often take the drug in bouts or binges, only stopping when their supply runs out or they collapse from exhaustion. Immediately following the intravenous administration or inhalation of cocaine, the individual experiences an intense pleasurable sensation known as a "rush" or "flash," followed by euphoria. Cocaine rapidly penetrates into the brain to produce these effects, but then is rapidly redistributed to other tissues. In many cases, the intense pleasure followed by the rapid decline in the cocaine-induced elevation of mood is sufficient for the individual to begin to immediately seek out and use more of the drug to prolong these pleasurable effects. Following the intranasal administration of cocaine, the pleasure is less intense and the decline in brain concentrations of the drug progresses much more slowly, so that the craving for more of the drug is less pronounced. Cocaine and amphetamine appear to produce their reinforcing or pleasurable effects through interactions with the neurotransmitter dopamine, especially in limbic and cortical regions of the brain (i.e., within the mesocorticolimbic dopaminergic system). Both cocaine and amphetamine block the reabsorption of dopamine into the Neurons, where it was released, thereby prolonging the action of dopamine in the synapsethe space between nerve cells. Amphetamine can also cause the direct release of dopamine from nerve cells and can inhibit the metabolism of the neurotransmitter. It is important to note, however, that every drug that augments the action of dopamine does not produce pleasurable or rewarding subjective effects.

The toxicity associated with cocaine or amphetamine use can be quite severe; it is often unrelated to the duration of use or to preexisting medical conditions in the individual. This potential for serious toxic side effects is amplified by the fact that tolerance usually develops to the subjective feelings of the cocaine-induced rush and euphoria, but not to some of the other central nervous system effects of the drug (especially seizure susceptibility). Some of the more minor toxic reactions include dizziness, confusion, nausea, headache, sweating, and mild tremors. These symptoms are experienced by virtually all cocaine and amphetamine users to some degree, as a result of stimulation of the sympathetic nervous system. More serious reactions are also frequently observed. These serious toxic effects can include irregular heartbeats, convulsions and seizures, heart attacks, liver failure, kidney failure, heart failure, respiratory depression, stroke, coma, and death. The effects on the heart and cardiovascular system can sometimes be treated with alpha and beta noradrenergic-receptor antagonists or calcium channel blockers, although even prompt medical attention is not always successful. The convulsions can sometimes be controlled with diazepam (Valium); ventilation (oxygen) may be required for the respiratory depression. In addition to the effects described above for cocaine, amphetamine has been reported to produce direct and irreversible neuronal damage to dopaminergic neurons. A similar effect for cocaine has not yet been identified.

Psychiatric abnormalities resulting from chronic central nervous system stimulant abuse can include anxiety, Depression, Hallucinations, and, in some cases, a paranoid psychosis that is virtually indistinguishable from a paranoid Schizophrenic psychosis. A withdrawal syndrome is also observed following the abrupt cessation of chronic cocaine or amphetamine use. This syndrome begins with exhaustion during the "crash" phase and is followed by prolonged periods of anxiety, depression, anhedonia (loss of pleasure), hyperphagia (gluttony), and high craving for the drug. This craving may persist for several weeks, depending on the individual. The administration of dopaminergic agonists or tricyclic Antidepressants may have some utility in decreasing the severity of the withdrawal symptoms.


Marijuana is probably still the most commonly used illicit drug in the United States, with about 55 percent of young adults reporting some experience with the drug during their lifetimes. The active ingredient in Marijuana is delta9-Tetrahy-Drocannabinol (Δ9-THC), which exerts its most prominent effects on the central nervous system and the cardiovascular system. A marijuana cigarette that contains approximately 2 percent of the active ingredient can produce an increase in feelings of well-being, euphoria, and relaxation when smoked; however, short-term memory can be impaired as is the ability to carry out goal-directed behavior. The ability to drive or operate machinery is similarly impaired, often much longer than the persistence of subjective effects. With higher doses, paranoia, hallucinations, and anxiety or panic may be manifested.

Chronic marijuana users sometimes exhibit what is called the Amotivational Syndromewhich consists of apathy, impairment of judgment, and a loss of interest in personal appearance and the pursuit of conventional goals. However, it is not clear whether this syndrome results from the use of marijuana alone or from other factors. Although this is seldom severe, Δ9-THC also produces a dose-related increase in heart rate. Tolerance does develop to the effects of marijuana, and in some countries, regular users of Hashish (a concentrated resin containing increased amounts of Δ9-THC) consume quantities of the drug that would be toxic to most marijuana users in the United States. The withdrawal associated with the cessation of marijuana smoking is relatively mildconsisting of irritability, restlessness, nervousness, insomnia, weight loss, chills, and increased body temperature.


The use of opioids in the United States is much less prevalent than reported for the other drugs discussed above. For example, as of the 1990s, less than 0.5 percent of young adults have reported trying heroin at some time during their lives. There are three basic patterns of opioid use and dependence in the United States. The first group constitutes the smallest percentage of opioid usersthose who initially began using morphinelike drugs medically, for the relief of Pain. The second group began using illegal drugs through experimentation and then progressed to chronic use and dependence. The third group represents physically addicted individuals who eventually switched to oral Methadone, obtained through organized treatment centers. Interestingly, the incidence of opioid addiction is greater among physicians, nurses, and related health-care professionals (who have access to these drugs) than in any group with a comparable educational background. In many instances (but not all), those addicted either to heroin (usually purchased illegally on the street) or to methadone (usually from treatment centers) are able to hold jobs and raise a family. Opioids reduce pain, aggression, and sexual drives, so the use of these drugs is unlikely to induce crime. Those who cannot afford opioids, those who like the "drug life," and those who are unable or unwilling to hold a job, resort to crime to support their drug habits.

Opioid drugs produce their pharmacological effects by binding to opiate Receptors. The euphoria associated with the use of opioids results from interactions of these drugs with the mu-opiate receptor, possibly resulting in the stimulation of mesocorticolimbic dopaminergic neuronal activity. The rapid intravenous injection of morphine (or heroin, which is converted to morphine once it enters the brain) results in a warm flushing of the skin and sensations in the lower abdomen that are often described as being similar in intensity and quality to sexual orgasm. This initial rush ("kick" or "thrill") lasts for about 45 seconds and is followed by a highdescribed as a state of dreamy indifference. Depending on the individual and the social circumstances, good health and productive work are not incompatible with the regular use of opioids. Tolerance can develop to the Analgesic, respiratory depressant, sedative, and reinforcing properties of opioids, but the degree and extent of tolerance depends largely on the pattern of use. Desired analgesia can often be maintained through the intermittent use of morphine. Tolerance develops more rapidly with more continuous opioid administration.

The abrupt discontinuation of opioid use can lead to a withdrawal syndrome that varies in degree and severity depending on the individual as well as the particular opioid used. Watery eyes (lacrimation), a runny nose (rhinorrhea), yawning and sweating occur within twelve hours from the last dose of the opioid. As the syndrome progresses, dilated pupils, anorexia, gooseflesh ("cold turkey"), restlessness, irritability, and tremor can develop. As the syndrome intensifies, weakness and depression are pronounced, and nausea, vomiting, diarrhea, and intestinal spasms are common. Muscle cramps and spasms, including involuntary kicking movements ("kicking the habit"), are also characteristic of opioid withdrawal; however, seizures do not occur and the withdrawal syndrome is rarely life-threatening. Without treatment, the morphine-induced withdrawal syndrome usually runs its course within seven to ten days. Opiate-receptor antagonists (e.g., Naloxone) are contraindicated in opioid withdrawal, since these drugs can precipitate a more severe withdrawal on their own. Rather, longer-acting, less potent, opiate-receptor agonists such as methadone are more commonly prescribed. The symptoms associated with methadone withdrawal are milder, although more protracted, than those observed with morphine or heroin. Therefore, methadone therapy can be gradually discontinued in some heroin-dependent individuals. If the patient is unwilling or unable to withdraw from methadone, the individual can be maintained on methadone indefinitely.


Psychedelics include drugs related to the indolealkylamines, such as lysergic acid diethylamide (LSD), Psilocybin, psilocin, Dimethyltryptamine (DMT) and diethyltryptamine (DET), to the phenylethylamines, such as mescaline, or to the phenylisopropylamines, such as 2, 5-dimethoxy-4-methylamphetamine (dom or "STP") as well as 3, 4-methylene-dioxyamphetamine (mda) and 3, 4-methylene-dioxymethamphetamine (mdma or "ecstasy"). The feature that distinguishes these psychedelic agents from other classes of drugs is their capacity to reliably induce states of altered perception, thought, and feeling. There is a heightened awareness of sensory input accompanied by an enhanced sense of clarity, but a diminished control over what is experienced. The effects of LSD and related psychedelic drugs appear to be mediated through a subclass of receptors associated with the inhibitory neurotransmitter serotonin (i.e., serotonin 5HT2 receptors). Immediately after the administration of LSD, somatic symptoms such as dizziness, weakness and nausea are present, although euphoric effects usually predominate. Within two to three hours, visual perceptions become distorted; colors are heard and sounds may be seen. Vivid visual hallucinations are also often present. Many times this loss of control is disconcerting to the individual, resulting in the need for structurein the form of experienced companions during the "trip." The entire syndrome begins to clear after about twelve hours.

Little evidence exists for long-term changes in personality, beliefs, values, or behavior produced by the drug. Tolerance rapidly develops to the behavioral effects of LSD after three or four daily doses of the drug. In general, however, the psychedelic drugs do not give rise to patterns of continued use over extended periods. The use of these drugs is generally restricted to the occasional trip. Withdrawal phenomena are not observed after the abrupt discontinuation of LSD-like drugs, and deaths directly related to the pharmacological effects of LSD are unreported in humanshowever, fatal Accidents and Suicides have occurred during periods of LSD intoxication.


The intoxicating and euphorigenic properties of nitrous oxide and ethyl ether were well known even before their potential as anesthetics was recognized. Physicians, nurses and other health-care professionals have been known to inhale anesthetic gases even though they have access to a wide variety of other drugs. Adolescents with restricted access to alcohol often resort to "glue sniffing" or the inhalation of vapors from substances with marked toxicity, such as gasoline, paint thinners, or other industrial solvents. The alkyl nitrites (butyl, isobutyl, and amyl) have been used as aphrodisiacs, since the inhalation of these agents is suggested to intensify and prolong orgasm. At least 12 percent of young adults have reported some experience with inhalantshowever, fatal toxic reactions (usually due to cardiac arrhythmias) are often associated with the inhalation of many of these drugs. Inhalation from a plastic bag can result in hypoxia (too little oxygen) as well as an extremely high concentration of vapor. Fluorinated hydrocarbons can produce cardiac arrhythmias and ischemia (localized anemia). Chlorinated solvents depress heart muscle (myocardial) contractility. Ketones can produce pulmonary (lung) hypertension. Neurological impairment can also occur with a variety of solvents.


Arylcyclohexylamines include phencyclidine (PCP or "angel dust") and related drugs that possess central nervous system stimulant, central nervous system depressant, hallucinogenic, and analgesic properties. These drugs (also known as dissociative anesthetics) are well absorbed following all routes of administration. With even small doses, intoxication is produced, with associated staggering gait, slurred speech, and numbness in the extremities. PCP users may also exhibit sweating, catatonia, and a blank stare as well as hostile and bizarre behavior. Amnesia during the intoxication may also occur. In higher doses, anesthesia, stupor, convulsions, and coma may appear. The typical high from a single dose can last four to six hours and is followed by a prolonged period of "coming down."

PCP and related compounds bind with high affinity to a number of distinct sites in the central nervous system, although it is not certain which site(s) is responsible for the primary pharmacological effects of these drugs. PCP binds to the sigma site, which also has a high affinity for some selected opioids, although the function of the sigma site is unknown. PCP blocks the cation channel (e.g., Ca2+) that is regulated by N-methyl-D-aspartate (NMDA), one type of receptor for excitatory amino acid neurotransmitters such as glutamate or aspartate. PCP also blocks the reabsorption of the neurotransmitter dopamine into the neurons, where it was released, resulting in a prolonged action of the neurotransmitter, especially within the mesocorticolimbic dopaminergic neuronal system.

There appears to be some degree of tolerance to the effects of PCP, and some chronic users of PCP complain of cravings and difficulties with recent memory, thinking, and speech after discontinuing the use of the drug. Personality changes can range from social withdrawal and isolation to severe anxiety, nervousness, and depression. Although the frequency is uncertain, deaths due to direct toxicity, violent behavior, and accidents have been reported following the use of PCP. PCP can also produce acute behavioral toxicityconsisting of intoxication, aggression, and confusion, as well as coma, convulsions, and psychoses. A PCP-induced psychosis can persist for several weeks following a single dose of the drug.

(See also: Addiction: Concepts and Definitions ; Complications ; Epidemiology of Drug Abuse ; National Household Survey on Drug Abuse ; Treatment )


Aniline, O., & Pitts, F. N., Jr. (1982). Phencyclidine (PCP): A review and perspectives. CRC Critical Review of Toxicology, 10, 145-177.

Benowitz, N. L. (1988). Pharmacologic aspects of cigarette smoking and nicotine addiction. New England Journal of Medicine, 319, 1318-1330.

Bloom, F. E. (1989). Neurobiology of alcohol action and alcoholism. Annual Review of Psychiatry, 8, 347-360.

Cloninger, C. R., Dunwiddie, S. H., & Reich, T. (1989). Epidemiology and genetics of alcoholism. Annual Review of Psychiatry, 8, 331-346.

Dewey, W. L. (1986). Cannabinoid pharmacology. Pharmacology Review, 38, 151-178.

Freedman, D. X. (1969). The psychopharmacology of hallucinogenic agents. Annual Review of Medicine, 20, 409-418.

Gawin, F. H., & Ellinwood, E. H., Jr. (1988). Cocaine and other stimulants: Actions, abuse, and treatment. New England Journal of Medicine, 318, 1173-1182.

Griffiths, R. R., & Woodson, P. P. (1988). Caffeine physical dependence: A review of human and laboratory animal studies. Psychopharmacology (Berlin) 94, 437-451.

Hollister, L. E. (1986). Health aspects of cannabis. Pharmacology Review, 38, 1-20.

Jaffe, J. H. (1990). Drug addiction and drug abuse. In A. G. Gilman et al. (Eds.), Goodman and Gilman's the pharmacological basis of therapeutics, 8th ed. New York: Pergamon.

Kranzler, H. R., & Orrok, B. (1989). The pharmacotherapy of alcoholism. Annual Review of Psychiatry, 8, 397-417.

Nutt, D., Adinoff, B., & Linnoila, M. (1989). Benzodiazepines in the treatment of alcoholism. Recent Developments in Alcohol, 7, 283-313.

Robinson, G. M., Sellers, E. M., & Janecek, E. (1981). Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique. Clinical and Pharmacological Therapeutics, 30, 71-76.

Woods, J. H., Katz, J. L., & Winger, G. (1987). Abuse liability of benzodiazepines. Pharmacology Review, 39, 251-419.

Nick E. Goeders