Schizophrenia is believed to involve altered activation of dopamine receptors, and support for this hypothesis comes from the antipsychotic effect of antagonists of the dopamine D2 receptor (D2R). D2R is expressed most highly in the striatum, but most of the recent positron emission tomography (PET) studies have failed to show any change in D2R densities in the striatum of schizophrenics, raising the possibility that other receptors may also be involved. In particular, the dopamine D1 receptor (D1R), which is highly expressed in the prefrontal cortex, has been implicated in the control of working memory, and working memory dysfunction is a prominent feature of schizophrenia. We have therefore used PET to examine the distribution of D1R and D2R in brains of drug-naive or drug-free schizophrenic patients. Although no differences were observed in the striatum relative to control subjects, binding of radioligand to D1R was reduced in the prefrontal cortex of schizophrenics. This reduction was related to the severity of the negative symptoms (for instance, emotional withdrawal) and to poor performance in the Wisconsin Card Sorting Test. We propose that dysfunction of D1R signalling in the prefrontal cortex may contribute to the negative symptoms and cognitive deficits seen in schizophrenia.

Spontaneous dehiscence of the superior semicircular canal (SSC) in the middle cranial fossa is rare and may cause clinical problems. This dehiscence was investigated in cadaveric and dried temporal bone specimens. One cadaveric specimen showed a spontaneous defect: the dehiscence was a symmetrical, elongated ellipse with smooth margins. Four of 244 dry bone specimens showed bony defects in the roof of the SSC, however, only one specimen was thought to have a spontaneous defect. Based on computer-simulation models, we hypothesized that spontaneous defects of the SSC may arise during the fetal period. Although rare, this defect may cause problems in middle cranial fossa surgery and may relate to certain vertiginous disorders.

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