Our findings support an association between inflammation and TNFalpha in particular and severe depression, and suggest that ECT may down-regulate this immune activation.

Epidemiological findings indicate a connection between depressive symptoms and changes in status of the immune system in depressed patients. This raises the possibility of causative connections. Theories on mechanisms for interactions between immune and affective systems -directly and via endocrine system -are evolving. Such hypothesized causative connections are supported by several findings. First, in depressed patients changes in the status of the immune system in vivo and ex vivo are seen. Also, depressive symptoms are seen in patients with altered immune status (physiologically, pathologically or chemically induced). Knowledge in this field may have implications regarding psychiatric follow up of physically ill people suffering from diseases caused by an altered immune system (long lasting infections, autoimmune diseases, hypersensitivity disorders) as well as disorders for which treatment and prognoses depends on the immune system (infections, cancer). Similarly, medical treatment of depressed patients may be adjusted by more specific knowledge about the interaction between neuroimmunology and depression. Important findings and the present knowledge and theories are reviewed.

The isozyme debrisoquine hydroxylase (CYP2D6) is central for the elimination of neuroleptic drugs. The capacity to hydroxylate debrisoquine is currently examined by genotyping of the isozyme. Approximately 7% of Europeans have a reduced capacity to hydroxylate debrisoquine, and they are de®ned as poor metabolizers. Two studies of small samples of well-de®ned patients with schizophrenia have shown that 6 . 5±6 . 6% were poor metabolizers, which is close to the rate in psychic normals. We found a total rate of 3 . 9% of poor metabolizers in a big sample (N 509) of patients with schizophrenia. The rate in the Danish subsample (N 221) was 4 . 5%, and in the Norwegian subsample (N 288) the rate was 3 . 5%. Our results indicate that the true rate of poor metabolizers among patient's with schizophrenia is still to be determined. #

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