Some remarks on etiological aspects of early-onset schizophrenia

Abstract

Neurophysiological, neuropsychological, neuroanatomical, and neuroradiological findings in schizophrenic psychoses demonstrate that subcortical (e.g., mesolimbic and diencephalic regions) as well as neocortical structures (e.g., dorsolateral prefrontal cortex, superior temporal and inferior parietal cortices) are involved. Special significance is accorded to the neuroanatomical connection between limbic structures and the dorsolateral prefrontal cortex. Here myelinization begins relatively late in humans, during the second and third decade of life—a particularly vulnerable period for schizophrenic onset. The nature of prepsychotic behavioral abnormalities in patients with early-onset schizophrenia as well as the existence of typical cognitive dysfunctions preceding the manifestation of psychotic symptoms points to the importance of a dynamic imbalance of neocortical-subcortical interactions in the etiology of schizophrenia. Based on the crucial importance of the prefrontal-hippocampal circuitry a stimulus barrier model of schizophrenic psychoses is elaborated, which integrates recent neurobiological findings as well as results of research in modern developmental psychology. One of the implications of this model is the multidimensional treatment of schizophrenic patients.