Introduction

The last few years have witnessed a major paradigm shift in the understanding of basal ganglia function. In line with this has been an increasing appreciation of both the centrality of psychomotor deficits in melancholia and the striking clinical parallels between melancholia and certain basal ganglia disorders. In view of these developments, a more considered appraisal of the role of the basal ganglia and their frontal connections in the pathogenesis of melancholia has become possible (Krishnan 1993b; Austin and Mitchell 1995).

There is now a large body of work focussing on the presence of depression in a number of neurological disorders, particularly those affecting striatal and frontal structures (see Starkstein and Robinson 1993 for review). Because of the historical dichotomy between psychiatric and neurological disorders, few have explored the possibility that melancholia may be a neurological disorder in its own right, and that the mechanisms leading to the motor, cognitive and mood changes in certain neurological disorders may also be involved in creating a similar, albeit characteristically individual, combination of such features in melancholia.

As noted in previous chapters, amongst a number of statistical attempts to separate melancholic and non-melancholic depression, some factor analytic studies have demonstrated that psychomotor retardation may be one of the best discriminators of these two syndromes (Nelson and Charney 1981), a finding extended by our development of the core measure and study of its properties.