Corticocortical connectivity, autonomous networks, and schizophrenia

Abstract

Dr. David hypothesizes that increased, not decreased, corticocortical connectivity causes schizophrenia. He cites studies suggesting excessive semantic priming and cross-hemispheric interference in this disorder to support his hypothesis. These findings, David suggests, reflect excessive transmission of information between neurons or within neural systems. However, considerable caution should be exercised in making neuroanatomic inferences on the basis of cognitive studies alone. There is an increasing consensus that information is represented by the brain as patterns of neural activation, where the same neuron or group of neurons participates in many different representations. Our simulations, which reflect this consensus, suggest that persistent or intrusive activation patterns do not emerge from too many neural connections, but from too few. This condition causes subgroups of neurons to disregard information processing by other neurons and to produce autonomously their own output, which interferes with the functioning of the system as a whole. Direct neuroanatomic or neurochemical studies of the cerebral cortex are needed to fully assess hypotheses regarding abnormal corticocortical connectivity in schizophrenia.