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Current concepts of hyperkinetic and attention deficit disorder have several historical roots (Rutter, 1982; Schachar, 1986; Weiss & Hechtman, 1986). However, much of the earlier literature was based on the notion that the disorder was synonymous with "minimal brain dysfunction" or MBD (Wender, 1971; Clements, 1966). This idea derived from the writings of Strauss and his colleagues (Strauss & Lehtinen, 1947) regarding behavioral syndromes supposedly due to brain damage in mildly mentally handicapped individuals; from the studies of Pasamanick and his colleagues (Pasamanick & Knobloch, 1966) linking a "continuum of reproductive casualty" with hyperactive behaviour; and most of all from Bradley's (1937) discovery of the therapeutic effect of amphetamines in the treatment of behavioral and educational problems. Much of the argument in favor of the concept of "minimal brain dysfunction" was based on circular reasoning of various types and it has not stood the test of time (Rutter, 1983). The hypothesis of a single characteristic MBD syndrome that takes the form of hyperactivity no longer warrants serious scientific consideration.

Because the diagnostic term 'MBD' continues to be used by some clinicians and a few researchers, it is perhaps important to make explicit what is, and is not, being rejected. There is, of course, no doubt that there can be substantial brain disease or damage without this being evident in abnormalities on the clinical neurological examination (Rutter, 1983; Rutter, Chadwick & Schachar, 1983). It cannot therefore be doubted that some psychiatric syndromes for which there is no clinical evidence of neurological disorder at present will ultimately turn out to have a basis in organic brain pathology. As our understanding of brain function improves and as our tools to investigate brain malfunction develop so the range of psychiatric disorders known to have an organic basis is likely to increase (Rutter, 1986). It also cannot be doubted that child psychiatric disorder has important associations with neurodevelopmental immaturities, so-called "neurological soft signs" (Shaffer et al., 1983), and with developmental delays in functions such as language (Howlin & Rutter, 1987). In these instances the conceptual difficulty stems from the uncertainty as to what the "soft signs" or developmental delays reflect (Shafer et al., 1983; 1986). As such, they cannot be taken as unambiguous indicators of organic brain dysfunction, although sometimes this will be the case. A further difficulty, moreover, with respect to consideration of hyperkinetic or attention deficit syndromes, is that the neurodevelopmental associations are by no means confined to this type of behavioral problem. Thus, Shaffer and his colleagues (1985) found that neurological soft signs were most strongly associated with anxiety disorders in adolescence. Accordingly, one of the key features of the MBD concept that must be rejected is the idea that brain damage or dysfunction gives rise to a uniform behavioral picture. It does not (Rutter, 1981). Indeed, the presence of brain damage or dysfunction is associated with an increase in the risk for a wide range of psychiatric disorders of which attention deficit disorders are by no means the most prominent. . . 

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