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disinhibition
In psychology, disinhibition is a lack of restraint manifested in disregard for social conventions, impulsivity, and poor risk assessment. Disinhibition affects motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms similar to the diagnostic criteria for mania. Hypersexuality, hyperphagia, and aggressive outbursts are indicative of disinhibited instinctual drives.
==Clinical concept==
According to Grafman et al. (1) “disinhibition” is a lack of restraint manifested in several ways, affecting motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms e.g. impulsivity, disregard for others and social norms, aggressive outbursts, misconduct and oppositional behaviors, disinhibited instinctual drives including risk taking behaviors and hypersexuality. Disinhibition is a common symptom following brain injury, or lesions, particularly to the frontal lobe and primarily to the orbitofrontal cortex. 〔Starkstein SE, Robinson RG. Mechanism of disinhibition after brain lesions. J Nerv Ment Dis. 1997 Feb;185(2):108-14.〕 The neuropsychiatric sequelae follow brain injuries could include diffuse cognitive impairment, with more prominent deficits in the rate of information processing, attention, memory, cognitive flexibility, and problem solving. Prominent impulsivity, affective instability, and disinhibition are seen frequently, secondary to injury to frontal, temporal, and limbic areas. In association with the typical cognitive deficits, these sequelae characterize the frequently noted "personality changes" in TBI (Traumatic Brain Injury) patients. Disinhibition syndromes, in brain injuries and insults including brain tumors, strokes and epilepsy range from mildly inappropriate social behavior, lack of control over one’s behaviour to the full-blown mania, depend on the lesions to specific brain regions. Several studies in brain traumas and insults have demonstrated significant associations between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices, affecting visuospatial functions, somatosensation, and spatial memory, motoric, instinctive, affective, and intellectual behaviors. 〔 Starkstein SE, Robinson RG. Mechanism of disinhibition after brain lesions. J Nerv Ment Dis. 1997 Feb;185(2):108-14. 〕
Disinhibition syndromes have also been reported with mania-like manifestations in old age with lesions to the orbito-frontal and basotemporal cortex involving limbic and frontal connections (orbitofrontal circuit), especially in the right hemisphere. 〔Shulman KI. Disinhibition syndromes, secondary mania and bipolar disorder in old age. J Affect Disord. 1997 Dec;46(3):175-82.〕 Behavioral disinhibition as a result of damage to frontal lobe could be seen as a result of consumption of alcohol and central nervous system depressants drugs, e.g. benzodiazepines that disinhibit the frontal cortex from self-regulation and control. 〔 Silveri MM, Rogowska J, McCaffrey A, Yurgelun-Todd DA. Adolescents at risk for alcohol abuse demonstrate altered frontal lobe activation during Stroop performance. Alcohol Clin Exp Res. 2011 Feb;35(2):218-28. 〕 〔 Cservenka A, Herting MM, Nagel BJ. Atypical frontal lobe activity during verbal working memory in youth with a family history of alcoholism. Drug Alcohol Depend. 2012 Jun 1;123(1-3):98-104. 〕 It has also been argued that ADHD, hyperactive/impulsive subtype have a general behavioural disinhibition beyond impulsivity and many morbidities or complications of ADHD, e.g. conduct disorder, anti-social personality disorder. substance abuse and risk taking behaviours are all consequences of untreated behavioural disinhibition.〔Showraki, Mostafa:”ADHD:Revisited”, Kindle Books, Amazon. 2013.〕
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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