Mechanism of disinhibition after brain lesions

J Nerv Ment Dis. 1997 Feb;185(2):108-14. doi: 10.1097/00005053-199702000-00007.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adult
  • Animals
  • Bipolar Disorder / diagnosis
  • Bipolar Disorder / physiopathology
  • Bipolar Disorder / psychology
  • Brain Diseases / diagnosis
  • Brain Diseases / physiopathology*
  • Brain Diseases / psychology
  • Brain Injuries / diagnosis
  • Brain Injuries / physiopathology*
  • Brain Injuries / psychology
  • Cerebral Cortex / physiopathology*
  • Female
  • Frontal Lobe / physiopathology
  • Functional Laterality / physiology
  • Humans
  • Inhibition, Psychological*
  • Male
  • Neural Pathways / physiopathology
  • Neurocognitive Disorders / diagnosis*
  • Neurocognitive Disorders / physiopathology
  • Neurocognitive Disorders / psychology
  • Risk Factors
  • Temporal Lobe / physiopathology