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Although the disorder may best be conceptualized in terms of both the severity and the pervasiveness of inattention and hyperactivity, it is not easy to reach a unified definition. This is partly reflected in differences between the two commonly used diagnostic schemes: DSM-III and ICD-9 (Ninth Revision of the World Health Organization's International Classification of Disease) and partly in the cross-cultural differences in diagnostic practice as discussed by Eric Taylor. Both Rutter and Taylor, as well as Sergeant and van der Meere, and Sally and Bennett Shaywitz, argue that the formulation of the diagnostic schemes need to be reconsidered. Such nosological problems hamper, of course, basic research on the extrapolation and evaluation of animal models which, in general, may be of vital importance for the advancement of medical knowledge and clinical therapy.
Rutter discusses in great detail why the MBD concept should be abandoned. His point is partly that brain damage does not give rise to a uniform behavioral picture and that there is no strong association between the diagnosis of MBD and generalized hyperkinesis. It is important to notice that this is not the same as saying that the disorder might not have an organic basis, or bases. Although computer tomographic (CT) brain scans of ADD children do not show any pathology ( Shaywitz, Shaywitz, Byrne, Cohen & Rothman, 1983), considerable evidence support the hypothesis put forth by Wender in 1971 that central catecholaminergic mechanisms may play a role in the genesis of ADD. For example, urinary MHPG, a noradrenaline metabolite, is reduced in ADD children ( Shaywitz & Shaywitz; Shekim, DeKirmenjian & Chapel, 1977; Yu-cull & Yu-feng, 1984). . .
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