Diminished pain perception in schizophrenia

Abstract

In their Case Report (March 6, p 864), Hiroshi Murakami and colleagues describe administration of quetiapine to a patient with diabetes mellitus. I would like to ask why they did so, given that quetiapine has been contraindicated for diabetes mellitus in Japan since 2004, when a death occurred due to its side-eff ect of exacerbating diabetes mellitus. Additionally, Murakami and colleagues insist that the hypoalgesia of their schizophrenic patient with diabetes mellitus, who had neither abdominal pain nor guarding despite severe bacterial panperitonitis, was attributable to hypoperception related to schizophrenia, and that such fi ndings were unlikely to have resulted from diabetic neuropathy because there were no signs of obvious peripheral neuropathy. However, impaired pain perception cannot explain the lack of abdominal guarding, which is a type of visceral–somatic spinal refl ex. Because perception is an executive function controlled in the cerebral cortex, no matter how much pain perception is aff ected, the spinal refl ex ought to be preserved. Therefore, peripheral neuropathy is more likely than hypoperception to be the explanation for both hypoalgesia and the disappearance of abdominal guarding. Furthermore, I wonder whether Murakami and colleagues considered the possibility that inappropriate use of quetiapine exacerbated diabetic neuropathy via aggravation of diabetes mellitus? Although they saw no signs of obvious peripheral neuro pathy, neuropathy can occur in parts of the body other than those examined—eg, visceral autonomic neurons—and damage to aff erent visceral nerves might eliminate guarding and produce hypoalgesia. We physicians have an obligation to provide unbiased care for patients with schizophrenia, and not attribute inexplicable physical symptoms to their psychotic disorder.