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Letters to the editor

According to the classification of chronic pain published by the International Association for the Study of Pain (IASP) (1) and a recent editorial in Br Med J (2), central pain is a pain state seen in primary lesions of the central nervous system (e.g. thalamic syndrome, post-stroke pain). The disease entities (phantom/stump pain and post-herpetic neuralgia) included in the trial of Panerai et al. should therefore not be designated as central pain. In line with this classification, it is assumed that the pain after amputation, as well as in post-herpetic neuralgia and other peripheral neuropathies, may come from spontaneous nerve impulses generated in diseased peripheral nociceptive nerves (3-6). The authors state that the efficacy of tricyclic antidepressant in central pain have never been examined. This might be true for central pain as defined by the IASP classification, but several controlled studies have been published on antidepressants in post-herpetic neuralgia (7-8), diabetic neuropathy (10-12) and in mononeuropathies of traumatic, surgical or infectious origin (13). Clomipramine inhibits serotoninreuptake and posses several postsynaptic blocking effects (14). However, its major metabolite desmethylclomipramine, often being present with higher blood levels than the parent compound, is a combined noradrenaline and serotonin reuptake inhibitor. Therefore, the benefits of clomipramine cannot unequivocally be attributed to the serotonergic effect. The importance of serotonergic andnoradrenergicmechanisms ofantidepressants in post-herpetic and diabetic neuropathy (9, 15, 16) is not finally settled, and it may turn out that both mechanisms are needed for an optimal effect. In my opinion VAS data should not be analysed by parametric statistics. Although such data at first glance appears to be interval data, it cannot be taken for granted that the “steps” on these scales are equal throughout their range. The suggestions that the action by antidepressants in these pain conditions is not mediated by the antidepressive effect has also been suggested in earlier publications, both due to the fast onset of action, and the finding of lower effective plasma drug levels in neuropathy than in depression (10, 15, 17). Furthermore, some previous studies that included rating of depressive symptoms, are in line with this suggestion (12, 15). 1990: 82: 34-38). Monitoring of plasma drug levels in controlled trials can serve several purposes. The investigators can confirm that the coding has been done correctly and can check patient compliance. Finally, interesting hypotheses concerning drug level-effect relations can often be generated (10, 12, 15). Besides these points, I think this is a further contribution to the evidence of the efficacy of antidepressants in different pain conditions, and an important hint about the possible role of different receptor interactions, which may in the future lead to the introduction of effective and well-tolerated drugs for these pain conditions.