Frontal lobe dysfunctions in schizophrenia--II. Impairments of psychological and brain functions.
In Part I of this paper (Levin, 1984), it was proposed that the phenomena of eye movement impairments in schizophrenia are consistent with a dysfunction of frontal eye field mechanisms of ocular-motor control. In Part II, a frontal lobe dysfunction in schizophrenia is also proposed on the basis of clinical, psychological, neurochemical, and neuropathological grounds. There are striking similarities between the clinical frontal syndrome and negative symptom schizophrenia. Parallels between experimental studies of disturbances in attention and information processing, in humans and animals with frontal lobe lesions on the one hand, and in schizophrenics on the other, are noteworthy. The evidence for seemingly disparate dysfunctions in schizophrenia of eye movements, psychomotility, cognition, arousal, motivation and affect, is consistent with a disruption of frontal lobe mechanisms of stimulus-response and drive-response modulation. Studies on the neurochemistry and neuroanatomy of schizophrenia provide further evidence for a frontal lobe dysfunction in a subgroup of schizophrenic patients, particularly those with negative symptoms.
D001288:Attention; D001927:Brain Diseases / Q000503:physiopathology / Q000523:psychology; D002560:Cerebrovascular Circulation; D002755:Choice Behavior / Q000502:physiology; D005133:Eye Movements; D005625:Frontal Lobe / Q000503:physiopathology*; D006801:Humans; D009949:Orientation / Q000502:physiology; D011954:Receptors, Dopamine / Q000502:physiology; D012559:Schizophrenia / Q000503:physiopathology*; D013681:Tegmentum Mesencephali / Q000503:physiopathology
D011954:Receptors, Dopamine