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OADES, R. D.,
Attention deficit disorder and
hyperkinetic syndrome: Biological perspectives.
In, Attention deficit disorder and hyperkinetic syndrome, eds,
T. Sagvolden and T. Archer, Lawrence Erlbaum, New York, pp. 353-368. (pdf
file)
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 oif 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 andsocial 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 (3).
(1) . Oades,
Daniels & Rascher (1998) : Oades
(2000)
(2) . Oades,
1985
(3) . Oades,
1987
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