Attempts at a theoretical classification have been made. The first in the modern era was Crow’s Type I and Type II distinction,
(11) 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 Computerized Tomography (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.
(12) which contrasted cases with a presumed genetic aetiology and those who had other putative risk factors such as early brain damage (see
Chapter 4.3.6.1). Although these attempts have served as useful stimuli for research, they have not been found to aid clinical decision-making and in fact now appear to support a blurring of diagnostic boundaries rather than a sharpening or subdivision.
(13) In fact the search for ‘biological markers’ often called ‘endophenotypes’, which might validate diagnostic distinctions continues. Take for example, the presence of ventricular enlargement or cortical thinning, first detected using CT and now magnetic resonance imaging (
MRI). Meta-analyses have confirmed that indices of ‘cerebral atrophy’ are strongly associated with schizophrenia but the effect sizes are small.
(14) Medial temporal lobe structures are the region of most grey matter volume loss. However, there is substantial overlap between normal controls and schizophrenia cases and MRI cannot be considered a useful diagnostic test. A host of genetic markers have been identified in the last 5 years, each of small effect and some showing overlap between the major schizophrenic and affective syndromes.
(15)
