Mechanism of disinhibition after brain lesions.

Disinhibition syndromes, ranging from mildly inappropriate social behavior to full blown mania, may result from lesions to specific brain areas. Several studies in patients with closed head injuries, brain tumors, stroke lesions, and focal epilepsy have demonstrated a significant association between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices of the right hemisphere. Based on the phylogenetic origin of these cortical areas and their main connections with dorsal regions related to visuospatial functions, somatosensation, and spatial memory, the orbitofrontal and basotemporal cortices may selectively inhibit or release motor, instinctive, affective, and intellectual behaviors elaborated in the dorsal cortex. Thus, dysfunction of these heteromodal ventral brain areas may result in disinhibited behaviors.

[1]  Sheilagh Hodgins,et al.  Ventral frontal deficits in psychopathy: Neuropsychological test findings , 1995, Neuropsychologia.

[2]  M. Buchsbaum,et al.  Selective reductions in prefrontal glucose metabolism in murderers , 1994, Biological Psychiatry.

[3]  R. Robinson,et al.  Specificity of changes in cerebral blood flow in patients with frontal lobe dementia. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[4]  A. Damasio,et al.  The return of Phineas Gage: clues about the brain from the skull of a famous patient. , 1994, Science.

[5]  S. Arndt,et al.  Secondary mania following traumatic brain injury. , 1993, The American journal of psychiatry.

[6]  H N Wagner,et al.  Mania after brain injury: Neuroradiological and metabolic findings , 1990, Annals of neurology.

[7]  D. Neary.  Dementia of Frontal Lobe Type , 1990, Journal of the American Geriatrics Society.

[8]  R. Robinson,et al.  Behavioral abnormalities induced by frontal cortical and nucleus accumbens lesions , 1988, Brain Research.

[9]  R. Robinson.  American Handbook of Psychiatry, 2nd ed., vol. VIII: Biological Psychiatry , 1988 .

[10]  R. Robinson,et al.  Mechanisms of Mania after Brain Injury: 12 Case Reports and Review of the Literature , 1988, The Journal of nervous and mental disease.

[11]  J. Sackellares,et al.  Right Hemisphere Partial Complex Seizures: Mania, Hallucinations, and Speech Disturbances During Ictal Events , 1988, Epilepsia.

[12]  R. Robinson,et al.  Comparison of mania and depression after brain injury: causal factors. , 1988, The American journal of psychiatry.

[13]  E. Edmunds,et al.  Hypomania Following Complex Partial Seizures , 1988, British Journal of Psychiatry.

[14]  G. Pearlson,et al.  Mania after brain injury. A controlled study of causative factors. , 1987, Archives of neurology.

[15]  R. Robinson.  Differential behavioral and biochemical effects of right and left hemispheric cerebral infarction in the rat. , 1979, Science.

[16]  G. Klerman,et al.  Secondary mania: manic syndromes associated with antecedent physical illness or drugs. , 1978, Archives of general psychiatry.

[17]  F. Sanides.  COMPARATIVE ARCHITECTONICS OF THE NEOCORTEX OF MAMMALS AND THEIR EVOLUTIONARY INTERPRETATION * , 1969 .

[18]  H. Klüver,et al.  PRELIMINARY ANALYSIS OF FUNCTIONS OF THE TEMPORAL LOBES IN MONKEYS , 1939 .

[19]  M. Jastrowitz,et al.  Beiträge zur Localisation im Grosshirn und über deren praktische Verwerthung1) , 1888 .

[20]  R. Robinson,et al.  SPECT findings in patients with primary mania. , 1993, The Journal of neuropsychiatry and clinical neurosciences.

[21]  M. Ichise,et al.  Violent visual hallucinations and aggression in frontal lobe dysfunction: clinical manifestations of deep orbitofrontal foci. , 1992, The Journal of neuropsychiatry and clinical neurosciences.

[22]  J. Tonkonogy.  Violence and temporal lobe lesion: head CT and MRI data. , 1991, The Journal of neuropsychiatry and clinical neurosciences.

[23]  J. Haxby,et al.  Cerebral metabolic and cognitive studies in dementia with frontal lobe behavioral features. , 1990, Journal of psychiatric research.

[24]  M. Drake.  Episodic depression and hypomania with temporal EEG paroxysms. , 1988, Psychosomatics.

[25]  H. D. Steklis,et al.  A neural substrate for affiliative behavior in nonhuman primates. , 1976, Brain, behavior and evolution.