S21-4. Neuropathological hypothesis of sleep dysfunction in Schizophrenia

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The purpose of this lecture is to review the polysomnographic non-rapid eye movement sleep abnormalities in schizophrenic patients and to present evidence for possible pathophysiologic mechanisms. Deficits of delta wave sleep are commonly reported sleep architecture abnormalities in schizophrenia. In the1960’s, Feinberg described this abnormality and about twenty years later, he first proposed that a decline in synaptic density resulting from abnormal reorganization of brain structure during early adolescence might cause the decline in delta wave amplitude and the onset of schizophrenia. Recent neuropathological studies of schizophrenia revealed that the dendritic spine density was particularly reduced in layer three of the neocortex. And excessive spine pruning is now considered a potential factor underlying reduced cortical gray matter volume in schizophrenia. Aberrant neuronal pruning is also believed to contribute to compromise the thalamocortical circuitry. Several recent studies have reported markedly reduced sleep spindle activity mediated by thalamocortical circuits in schizophrenia. Animal studies have reported sleep spindles have been linked to synaptic plasticity and memory consolidation. Thus, aberrant pruning can result in structural brain abnormalities and deficits of two distinct rhythms during sleep. Furthermore, each of these impairments appears to be associated with both cognitive deficits and symptoms of schizophrenia.