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Biological Aspects of Affective Illness: Are we Any Nearer?

THEORIES of affective illness have been dominated by the amine hypotheses. Initially 5HT was proposed since the concentration of this metabolite was found to be low in CSF in depressive illness. Subsequent studies showed that the concentration of this metabolite did not tend to change with recovery and was also low in hypomania. The biological evidence in man for the catecholamine hypothesis is negligible. Yet for all that the currently accepted mode of action of drugs used in the treatment of depression, potentiation of noradrenergic mechanisms, still attractively grace the theory. However, drugs used in the treatment of mania produce a blockade of central dopaminergic receptors. Animal experiments suggest that the dopaminergic system provides the master drive to which others such as hunger, thirst and possibly sex and exploration are secondary (Vallenstein et al., 1968). Crow (1973) has elaborated on this theme suggesting that the dopamine system subserves the driving force or 'incentive motivation' and that the noradrenergic system mediates 'reinforcement'. The possibility in man is that not only is the dopaminergic system concerned with biological drives but may propel him into his social contacts, exploration and integration. Mood may be the labelling process of experience. These two processes may be dissociated as envisaged by Kraepelin who in certain cases of manic depressive illness found changes in psychomotor activity to be out of phase with mood -and this would account for the 'mixed states' seen in bipolar affective illness. The use of Dopa in depressive illness (Goodwin et al., 1970) frequently led to hypomanic episodes which were characterised by increase in activity without a change in depression. Not only amine output in affective illness may be important but also change in receptor sensitivity. Again Dopa given to a group of severely disabled patients suffering from