Comparisons of Clinical Efficacy

Abstract

This paper does not attempt to review the whole topic of clinical efficacy but will consider general concepts, particularly in the light of the advent of the serotonin (5-HT) uptake inhibitors (SSRIs).The aetiology of depression is complex. In most cases there is some form of predisposition based on problematical family dynamics, disordered family communication and/or genetic factors; each may be present to a variable extent. On top of this predisposition, some form of stimulus - ‘stress’, an external problem, loss of control, a physical disorder, adverse life circumstances - appears to affect those who are already primed. There are a variety of possible outcomes from this combination of predisposition and stimuli: low mood, depression in the full syndromic sense, and depression with biological features. It seems likely that, particularly with severe depressions (the major syndromic forms and those with biological features), there are neuroendocrine and neurochemical changes to mediate the effects of stress into those of the clinical symptoms and signs. It has been hypothesised that stressors induce adaptive neurochemical changes, failure of which may engender behavioural disturbances (Anisman & Zacharko, 1992). However, there are also many individuals who may not undergo this process, but who probably have some cognitive or learned change leading to dysphoria; this aspect needs to be considered carefully in relation to efficacy.