Abnormal Repetitive Behaviours: Shared Phenomenology and Pathophysiology

Autor/inn/en	Muehlmann, A. M.; Lewis, M. H.
Titel	Abnormal Repetitive Behaviours: Shared Phenomenology and Pathophysiology
Quelle	In: Journal of Intellectual Disability Research, 56 (2012) 5, S.427-440 (14 Seiten)Infoseite zur Zeitschrift PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	0964-2633
DOI	10.1111/j.1365-2788.2011.01519.x
Schlagwörter	Behavior Problems; Anxiety Disorders; Animals; Mental Retardation; Developmental Disabilities; Genetics; Phenomenology; Injuries; Self Destructive Behavior; Incidence; Neurology; Physiology; Neurological Impairments; Comorbidity; Pathology; Brain Hemisphere Functions + Suchen Sie Ihr Suchwort? Animal; Tier; Tiere; Geistige Behinderung; Entwicklungsstörung; Humangenetik; Phenomenological psychology; Phänomenologie; Psychologie; Self destrucive behaviour; Selbstzerstörung; Vorkommen; Neurologie; Physiologie; Neurodegenerative Erkrankung; Pathologie
Abstract	Background: Self-injurious behaviour (SIB) is a devastating problem observed in individuals with various neurodevelopmental disorders, including specific genetic syndromes as well as idiopathic intellectual and developmental disability. Although an increased prevalence of SIB has been documented in specific genetic mutations, little is known about the neurobiological basis of SIB. This makes vulnerability assessment and pharmacological treatment incredibly challenging. Method: Here we review evidence that SIB and other repetitive, invariant behaviours, such as stereotypy, compulsions and tics, share many phenotypic similarities, are often co-morbidly expressed and have common inducing conditions. This argues for shared or overlapping pathophysiology. As much more is known about the neurobiology of these related disorders, this should make the neurobiology of SIB a more tractable problem. Results: Stereotypy, compulsions and tics are diagnostic for disorders that have received focused neurobiological investigation (autism, obsessive compulsive disorder, Tourette syndrome, respectively). In addition, animal models of these repetitive behaviours have been well characterised. Collectively, these studies have found that cortical basal ganglia circuitry dysfunction mediates repetitive behaviour. Moreover, these studies provide more detailed information and potentially testable hypotheses about specific aspects of the circuitry that may be operative in SIB. Conclusions: We can use available information from clinical and animal models to make more precise hypotheses regarding the particular pathophysiology driving SIB. The results of testing such hypotheses should generate pharmacological strategies that may prove efficacious in reducing SIB. (As Provided).
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Erfasst von	ERIC (Education Resources Information Center), Washington, DC
Update	2017/4/10