views updated May 17 2018



The term activity, in regards to hyperactivity, generally refers to movement, particularly gross motor movement. Individuals activity levels are variable and are affected by development, daily cycles, environmental demands, and internal states. After taking into account these factors, an individual may be considered hyperactive if his or her activity level is excessive compared to others. Since activity level, like height or weight, is continuous and can be characterized by a bell curve, hyperactivity is a term generally used to indicate those individuals on the high end of this continuum. Hypoactivity signifies those individuals on the low end of this continuum. Significant hyperactivity may impair an individuals ability to function across academic, occupational, social, and familial domains.

Multiple medical and psychological disorders are characterized by symptoms of hyperactivity. Perhaps the disorder that is most closely tied to hyperactivity is attention deficit hyperactivity disorder (ADHD). Hyperactivity, combined with impulsive symptoms, is one of the core behavioral symptom domains identified by current diagnostic nosology; inattention represents the other behavioral symptom domain. Most pediatric patients diagnosed with ADHD have hyperactive symptoms. Hyperactive symptoms of ADHD include fidgeting or squirming in ones seat, difficulty remaining seated, running about or climbing excessively, difficulty engaging in leisure activities quietly, acting as if driven by a motor, and talking excessively. As exhibited by the patient with ADHD, these behaviors are purposeless. Patients are judged to have these symptoms if they exhibit these behaviors excessively compared to individuals of the same sex and age under similar circumstances.

The hyperactivity observed in patients with ADHD is generally not episodic. Several other disorders/diseases are defined by hyperactivity that is episodic or appears as discrete behavioral events. For example, Huntingtons disease is a neurodegenerative disease that affects cognition, memory, and mood. The hallmark of this disease is hyper-activity consisting of rapid, jerky motions with no clear purpose. Similarly, tic disorders (e.g., Tourettes disorder) are characterized by repeated and involuntary bodily movements or uncontrollable vocal sounds.

Across disorders with hyperactive features, the neurological causes of hyperactivity appear to be related to the brains motor circuitry or dopaminergic abnormalities. The human brain has numerous functional regions, most of which are interconnected to constitute neural circuits. One neural circuit primarily involved in motor activity begins in the cerebral cortex, connects to basal ganglia, which connect to the thalamus, and finally loops to the motor cortex. Within this circuit, there are minicircuits with substantia nigra and the subthalamic nucleus. Further, there are both direct and indirect pathways that project through this circuitry. Irrespective of subcircuitry and pathways, the basal ganglia (i.e., caudate, putamen, and globus pallidus) exert a modulating effect on this neural circuit and thus affect the behavioral manifestation of movement. The basal ganglia are primarily innervated with dopaminergic neurons. Concordantly, ADHD, tic disorders, and Huntingtons disease have all been associated either morphometric abnormalities (i.e., usually reductions) or dopaminergic abnormalities in basal ganglia regions.

Hyperactivity as manifested in disorders with episodic hyperactive symptoms, such as Huntingtons or Tourettes, can often be assessed through observation. The mere presence of tics or choreiform movements may be considered pathological. Even at low frequencies, these abnormal episodic movements are usually indicative of disease presence. The hyperactivity associated with ADHD is less well defined. Because ADHD-related hyperactivity occurs along a continuum, the assessment of presence or absence of this hyperactivity relies heavily on clinical judgment of what is a clinically significant level of hyperactive behavior. Using all available information, a clinician must decide whether the hyperactive behavior exhibited by a patient falls outside the realm of normal behavior. Commonly utilized tools for helping to make this determination are parent and teacher rating scales for pediatric patients and self-and other-report rating scales for adult patients. Several rating scales exist for assessing ADHD behaviors, including the Vanderbilt Rating Scales, the DuPaul ADHD Rating Scale, and the Connerss Rating Scales. Ratings are scored according to several empirically derived factors. Most scales have a factor measuring hyperactivity. An individuals scores on the hyperactivity factors can be compared to derived age and sex norms to determine the severity of hyperactive behavior.

Other methods for assessing ADHD-related hyperactivity are the use of actometers and observation. Actometers are mechanical devices that can be worn on a patients limb or placed on a patients chair. The actometer is designed to measure movement. Actometers attached to the patients body can provide valuable information about cycles of movement throughout the day and night. Patient observation can be performed in a variety of formats. Most simply, a clinician can observe the ADHD patient during interviews or testing on the day of clinical evaluation. An alternative format is to have the patient engage in an analog task (e.g., perform an academic assignment) while an observer codes activity level using an observational coding system. One may increase the ecological validity of the observation procedure by observing the patient in his or her natural environment (e.g., school). Similarly, qualitative or quantitative methods could be utilized to describe the patients activity level.

Evidence-based treatment of ADHD-related hyper-activity can be classified into either of two treatment strategies: medication or behavioral treatment. The most frequently used class of medications that target hyperactive symptoms among patients with ADHD are the stimulants. Stimulant medications exert their effect by increasing levels of extracellular dopamine in the brain. Stimulants wield their effects quickly and effectively. Other medications, such as atomoxetine, bupropion, and tricyclic antidepressants, have also been shown to decrease hyperactivity levels in patients with ADHD. In addition, behavioral treatment has been shown to be an effective treatment for patients with ADHD. Behavioral treatments primarily consist of consequating a patients behavior with behavioral contingencies. Common behavioral techniques are token economies, response cost, or daily report cards. Behavioral therapy likely exerts its effect in children by increasing their awareness of their own mal-adaptive behavior by making environmental contingencies increasingly salient. Both medication and behavioral therapy have been shown to be effective treatments for improving hyperactivity symptoms in children with ADHD. However, medication does appear to have a more robust treatment effect when hyperactive symptomatology is used as the outcome measure.

SEE ALSO Attention Deficit Hyperactivity Disorder; Psychotherapy; Psychotropic Drugs


Barkley, Russell, and Charles Cunningham. 1979. The Effects of Methylphenidate on the Mother-Child Interactions of Hyperactive Children. Archives of General Psychiatry 36 (2): 201208.

MTA Cooperative Group. 1999. A 14-Month Randomized Clinical Trial of Treatment Strategies for Attention-Deficit/Hyperactivity Disorder. Archives of General Psychiatry 56 (12): 10731086.

Solanto, Mary. 2002. Dopamine Dysfunction in AD/HD: Integrating Clinical and Basic Neuroscience Research. Behavioural Brain Research 130: 6571.

Jeffery N. Epstein


views updated May 17 2018


The pinpointing and treatment of hyperactivity in children forms a fascinating link between medical research and popular attitudes about and settings for the child. Scattered indications of new concern about hyperactive behavior began to accumulate in the second half of the nineteenth century. Hyperactivity formed part of a new interest in identifying and segregating "backward" children in the early twentieth century, particularly in western Europe. Medical research on brain dysfunctions accelerated in the 1920s and 1930s, but there was continued dispute about whether some special condition of hyperactivity existed. Drug treatment, first introduced in 1937, became more common after 1957. But it was only after 1970 that identification of hyperactive children, under the designation attention deficit disorder (ADD), became widely accepted. Amid controversy, treatment programs gained ground steadily through the 1990s.

Historical Background

Children's hyperactivity, to the extent it existed, was simply a question of discipline until modern times and received no specific attention. Protestant clergymen and parents in the eighteenth and nineteenth centuries often resorted to physical discipline against children who could not sit still in long church services, but since this was seen as an expression of children's original sin and natural unruliness it did not come in for specific comment. We have no systematic indications of how what we would now call hyperactivity affected children's work performance.

A German children's book in the 1850s offered a character, "Fidgety Phil," who was the characteristic hyperactive child, unable to sit still. By this point stricter manners for children included explicit injunctions about body control, which would implicitly single out children who had difficulties in this area. More regular schooling also created problems for hyperactive children. Still, a truly troubled child could still be pulled out of school and either sent directly to work or (in wealthy families) given private tutoring.

More extensive school requirements plus new medical research capabilities opened a new chapter in the identification of hyperactive children around 1900, particularly in England and Germany. Generally such children fell into a larger category of backward or mentally deficient children who could not perform well on standardized tests and/or who caused persistent behavior problems in school. Some of these children were placed in special schools or classes, where different kinds of instruction, focusing on specific tasks, could lead to improvements in learning capacity. By the 1920s experts began to realize that hyperactive children were often quite intelligent, and inclusion into a generic backward category began to diminish.

Research continued on brain dysfunction of children with hyperactive behavior problems, with increasing interest in the United States. A study by Charles Bradley in 1937 introduced the first possibility of medication, using Benzedrine. Widespread identification of a hyperactivity problem was still limited by a belief that a certain amount of unruliness in children was natural, that schools themselves were part of the problem, and that it was up to parents to figure out how to keep their children in hand.

Research, Diagnosis, and Treatment since 1957

Several developments, including the introduction of new psychostimulant medication, particularly the drug Ritalin in 1957, began to accelerate attention to and concern about hyperactivity. Fewer children were now encouraged to drop out before completing secondary school. With more mothers working, parental availability to help with hyperactive children declined; indeed parental interest in finding assistance intensified. With more children in day care facilities by the 1960s, opportunities to identify problems of hyperactivity at a younger age expanded. Increasing school integration in the United States exposed teachers to categories of children they might more readily define as behavior problems. Finally, teachers themselves faced new constraints in physically disciplining children, which put aggressive restlessness in a new light.

These various developments, along with effective medication, prompted a steady growth in the numbers of behaviors that were regarded as symptoms of attention deficit disorderbehaviors that in earlier decades might often have been regarded as normal. There were cautions: some observers worried about unduly frequent use of medicines that could have adverse side effects or induce dependency; some studies suggested that minority children were particularly likely to be cited as needing medication, with teachers using this option as a means of facilitating classroom control.

But acceptance of hyperactivity as a disease category gained ground steadily, and some schools required drug treatments for certain children as a condition of entry. Estimates in 1980 that 3 percent of all children suffered from ADD grew to 5 percent a decade later. Production of Ritalin soared 500 percent between 1990 and 1996. Popularizations of the ADD concept bolstered many parents, who could now point to a problem of brain function for behaviors that used to be blamed on poor home discipline. Supplementary measures, including therapy, special diets, and adult support groups, were deployed against hyperactivity, but medication continued to command the greatest attention.


Armstrong, Thomas. 1996. "ADD: Does it Really Exist?" Phi Delta Kappan (February): 424428.

Charles, Alan F. 1971. "The Case of Ritalin." New Republic (October): 1719.

Fowler, Mary. 1994. NICHCY Briefing Paper: Attention Deficit/Hyperactivity Disorder. Washington, DC: Government Printing Office, 1-S.

Smelter, Richard W., et al. 1996. "Is Attention Deficit Disorder Becoming a Desired Diagnosis?" Phi Delta Kappan (February): 2932.

Swanson, James. 1995. "More Frequent Diagnosis of Attention Deficit-Hyperactivity Disorder." New England Journal of Medicine 33: 944.

Peter N. Stearns


views updated May 18 2018

hy·per·ac·tive / ˌhīpərˈaktiv/ • adj. abnormally or extremely active: a hyperactive pituitary gland. ∎  (of a child) showing constantly active and sometimes disruptive behavior.DERIVATIVES: hy·per·ac·tiv·i·ty / -ˌakˈtivitē/ n.


views updated May 21 2018

hyperactivity (hy-per-ak-tiv-iti) n. see hyperkinesia.