The condition, biological indicators and animal models of the symptoms and the disorder are briefly reviewed. Condition: No single symptom is indispensable to diagnosis. But measures of the condition include motor activity, attention, motivation and psychostimulant responsiveness. Caveat: In the study of the condition, measuring biological correlates of unusual function may prove useful for management of the condition, but could mislead in the search for causes. Biological indicators: Investigation of attention-related function and associated regional cerebral activity would be improved by the careful application of the results of neuropsychological and psychophysiological study. A more extensive use of within subject protocols would greatly assist interpretation of the relevance of physiological states and the contribution of activity in different transmitter systems. Why are MHPG levels low, and lower in stimulant responders: HVA/MHPG ratios high in responders and nonresponders alike? However, the author sees the paradox to lie less with the induced (sic) metabolic changes as with the inability to mimic the changes with other catecholaminergic agents. Attention is drawn to the trophic effects of the monoamines. Attention is also drawn to the colocalisation of neuropeptide Y in NA neurons and the possibility that alterations in this relationship could underlie other ADHD characteristics such as thirst (1). Models: Symptom-models attempt to investigate the determinants a single feature of the illness. Examples have been recent demonstrations that where NA activity is low or depleted selective attention may be impaired (e.g. latent inhibition). An interesting observation here is that where NA activity is low, learning in a variety of situations occurs at normal rates to a modest criterion, but then slows severely before eventually reaching good stringent criteria. It is suggested that this is consistent with an NA role in "tuning" (2). Discussion of the various roles of DA must make mention of the specific improvement seen after amphetamine treatment in those children who only achieve a low response criterion: in contrast in animals amphetamine promotes the impulsive response lowering beta-criterion. The resolution of the enigma may well lie in a better understanding of the interactions of the mesolimbic with the mesocortical DA system. Mesocortical activity can suppress mesolimbic activity, impairment of frontal function releases the mesolimbic system - a change that can be countered by psychostimulant treatment. Disorder-models are concerned with mimicking a whole cluster of symptoms if not the syndrome itself. Claims of the usefulness of depleting catecholamines with 6-hydroxydopamine (on the one hand) and modifying the environment in which young animals are brought up (rich and social contexts for development) are elaborated elsewhere in this book. The similarity of some of the features of hypertensive patients and those of youngsters with ADHD initiates interest in the "spontaneously hypertensive rat" (SHR). Encouraging the use of the SHR as a model are similarities in the DA and NA activity and reactivity. Further, there are similarities in between the responses of the SHR and children on learning schedules requiring the delay of response, - the delay of gratification that is characteristic of many ADHD children, and leads to impulsive responding in the SHR. Lastly one should not overlook the possible lessons to be learned in the comparative approach, - namely to look at syndromes with more or fewer comorbid symptoms such as Tourette, Conduct-Disorder, Autism, Lesch.Nyhan and Phenylketonuria