This article revisits the neuropathological history of attention deficit and related behavioral problems in children, and focuses on the important contribution of EEG findings to both the classification and treatment of these disorders. Recent topographic quantitative EEG methods have disclosed several distinct patterns of abnormality in children diagnosed as ADD, and have provided improved guidelines for pharmacological treatment. Additionally, advances in EEG technology have given rise to a promising new alternative behavioral treatment for ADD called neurofeedback. Quantitative EEG assessment is considered essential in relation to this treatment approach as well. Objective findings and theoretical models relevant to both modalities of treatment are reviewed.
The idea that some type of brain disturbance could be responsible for abnormalities in attention and hyperactivity in children actually arose from pathological findings and physiological theories related to an epidemic that spread through the city of Vienna in the early years of the 20th century. An infection of the brain, which was called "Encephalitis Lethargica", left a strange disruption of behavior in its victims. A Viennese physician named von Economo (1918) distinguished himself by his classic study of the brain damage that this disorder inflicted on patients who succumbed to its lethal impact. He identified two symptomatic patterns associated with two different areas of inflammatory injury to the rostral brain stem and hypothalamus. In one of these patterns patients were inattentive and lethargic, often becoming comatose; in the other, they showed the opposite behavior, being unable to fall asleep and displaying impulsive and often uncontrolled physical behavior. Von Economo concluded that the two pa rts of the brain affected were interactive, and collectively responsible for the coordinated regulation of mental and physical arousal.
Drawing upon these observations, neurologists who later encountered a nonlethal pattern of mental lethargy combined with motor hyperactivity in children proposed that elements of this same regulatory system were damaged in some complex way by infection or birth trauma. Since these cases were clearly less serious than the encephalitis of von Economo's time, they used terms such as "Minimal Brain Damage" and "Childhood Behavior Disorder" to describe a syndrome that included hyperactive behavior, short attention span, frequent mood shifts, and various minor perceptual disturbances. The concept of a physiological +disturbance was reinforced almost at the outset by the discovery of a high incidence of unusually slow EEG brain wave patterns in these children (Lindsley & Cutts, 1940; Solomon, Bradley & Jasper, 1938). In fact, this finding originally suggested that these children were under-aroused, and contributed to the initial exploration of stimulants and other centrally acting medications as a therapy (Lindsley & Henry, 1942; Walker & Kirkpatrick, 1947).
By mid-century, however, the lack of evidence for gross neurological damage or deficits associated with this syndrome led to a change in accepted terminology, and adoption of the new label "Minimal Cerebral Dysfunction" (MCD). EEG studies during this period also found that a high percentage of children with a diagnosis of MCD showed diffuse abnormal EEG slow activity (Capute, Niedermeyer, & Richardson, 1968; Klinkerfuss, Lange, Weinberg, & O'Leary, 1965; Small, Milstein, & Jay, 1978). Although this term became widely accepted by the professional community, it was clear to many that the syndrome was poorly defined and that its symptoms were seen often in combination with other behavioral and functional disturbances. Additionally, since stimulant medications were in common use by this time, it was essential to distinguish an attention/hyperactivity disorder from others that might be adversely affected by these drugs.