The trait nature of dysthymia can be further observed in the fact that dysthymia often pursues an unrelenting course towards chronicity. (11) Thus, spontaneous recovery has been shown to occur in no more than 13 per cent of subjects in the community over 1 year.(58) In outpatient clinics, the outcome is somewhat better, but this is probably due to the treatment received and a longer follow-up.(11)


Most classes of antidepressants^5 6 ^l62,6. 6 65 and 66> have been shown to be effective in dysthymia in double-blind studies (Tab]e 3). The rationale for using classic antidepressants such as tricyclic compounds was the observation of shortened REM latency in dysthymic subjects in our sleep laboratory. (27) Irreversible monoamine oxidase inhibitors such as phenalzine were used because of the belief that non-classical depressions respond preferentially to this class of drugs; (61) the same can be said for the reversible inhibitors of type A monoamine oxidase.(66) Ritanserin(62) (now withdrawn because of cardiotoxicity) and amisulpride(65) were tried, because both compounds reverse 'negative' symptoms in schizophrenia and, by analogy, it was hypothesized that the low motivation and lethargy seen in some patients with dysthymia reflected a shared underlying dimensional transnosological pathology. The selective serotonin re-uptake inhibitors ( SSRIs) were used empirically/,6 ,64) because of good tolerance compared with the tricyclic antidepressants, and later it was suggested that improvement in dysthymia correlates with normalization of serotonergic indices.(67) The foregoing trials, conducted in different countries during the past 12 years represent the most eloquent evidence for the increasing worldwide acceptance of the concept of dysthymia as a clinically significant variant of affective disorder.

Table 3 Major controlled pharmacological trials in dysthymia worldwide

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