Attempts at a theoretical classification have been made. The first in the modern era was Crow's Type I and Type II distinction, (1D although it echoes older notions of 'process'—chronic and deteriorating versus 'reactive' (relapsing and remitting) typologies. The innovation was to link the distinction with proposed differences in dopamine receptor hyperactivity (Type I), associated with positive symptoms and good response to dopamine antagonist drugs, and on the other hand, to neurological damage (Type II) as evidenced by ventricular enlargement on CT brain scans, associated with chronicity, poor premorbid functioning and poor response to treatment.

Building on this was the 'aetiological classification' proposed by Murray et al.{l3 which contrasted cases with a presumed genetic aetiology and those who had other putative risk factors such as early brain damage (see Chapter4.3.i5.!). Although these attempts have served as useful stimuli for research, they have not been found to aid clinical decision-making. In fact the search for 'biological markers' which might validate diagnostic distinctions has yet to yield conclusive positive results. For example, the presence of ventricular enlargement or cortical thinning, as detected using CT and now magnetic resonance imaging ( MRI), is a case in point. Meta-analyses have confirmed that indices of 'cerebral atrophy' are strongly associated with schizophrenia but the effect sizes are small (approximately 10 per cent).(!.3> Hence, there is substantial overlap between normal controls and schizophrenia cases.

Positive family history remains an important finding in the psychiatric history of an individual patient. Although none of the diagnostic criteria permits the influence of family history, in clinical settings, 'odd' or withdrawn behaviour takes on a very different meaning if seen in the first-degree relative of someone with a firm schizophrenia diagnosis.

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