Introduction

Schizophrenia provides a compelling challenge to neurobehavioral approaches to understanding mental disease. The neurobehavioral approach attempts to identify the central nervous system (CNS) substrates of a variety of psychiatric/ behavioral disorders. There is an underlying CNS dysfunction in most schizophrenic individuals. However, the nature of this CNS dysfunction is not well understood. Genetic factors have been implicated in the etiology of schizophrenia (Gottesman & Shields, 1982). The efficacy of neuroleptic drugs in reducing positive symptoms of schizophrenia suggests that, in some schizophrenic patients, there may be a “neurochemical” lesion involving (at least indirectly) certain aspects of the dopamine system. Anatomical changes have been demonstrated in schizophrenic patients with both computer tomography and magnetic resonance imaging (MRI). One of the most replicated findings in schizophrenia research is that the third and fourth ventricles are enlarged in many schizophrenic patients (Nasrallah, 1990). Histological studies of the fine structure of schizophrenic brains have detected subtle cytoarchitectural anomalies, including loss or disarray of hippocampal tissue (Kovelman & Scheibel, 1986). Positron emission tomography studies indicate relative hypometabolism in a variety of brain structures, including the frontal lobes (Buchsbaum et al., 1990). There is clearly no dearth of putative CNS abnormalities in schizophrenic patients. The number and sheer diversity of these abnormalities have resulted in a situation where, while there is general agreement that many schizophrenic individuals have some form of CNS dysfunction, the specific nature of that dysfunction has yet to be detailed. Thus, the major challenge to a neurobehavioral approach to schizophrenia is to elucidate the nature of the CNS impairments underlying this disorder.