ABSTRACT

Accepting a biological basis for schizophrenia still leaves an explanatory gap: it is not readily apparent how an abnormality in brain structure or function might become translated into the many and varied symptoms of the disorder, most if not all of which are quite different from the usual signs of brain disease, not to mention being prone to erratic fluctuations in a way not at all reminiscent of neurological disorders. The usual way of bridging this gap has been to postulate an intervening variable in the shape of a neurochemical disturbance. Such a disorder could easily be the expression of a genetic fault, such as one affecting the regulation of a neurotransmitter; and it is not difficult to imagine it in turn giving rise to a derangement of brain function, of a rather subtle kind, resulting in disorders that are primarily in the realm of thinking, feeling and perception. Nor is a neurochemical disturbance completely incompatible with structural brain abnormality – for example, insidiously evolving damage in certain key areas might trigger off pathological fluctuations in neurotransmitter levels.