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Titolo:
Basal ganglia motor function in relation to Hallervorden-Spatz syndrome
Autore:
Mink, JW;
Indirizzi:
Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Neurol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Anat, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 , Dept Anat, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Neurobiol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 t Neurobiol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pediat, St Louis, MO 63110 USA
Titolo Testata:
PEDIATRIC NEUROLOGY
fascicolo: 2, volume: 25, anno: 2001,
pagine: 112 - 117
SICI:
0887-8994(200108)25:2<112:BGMFIR>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRIMATE GLOBUS PALLIDUS; GABA-RELATED SUBSTANCES; SACCADIC EYE-MOVEMENTS; SUBTHALAMIC NUCLEUS; IMMUNOREACTIVE NEURONS; DOPAMINE-RECEPTORS; SQUIRREL-MONKEY; SYNAPTIC INPUT; AMINO-ACIDS; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Mink, JW Washington Univ, Sch Med, Dept Neurol, Box 8111,660 S Euclid Ave,St Louis, MO 63110 USA Washington Univ Box 8111,660 S Euclid Ave St Louis MO USA 63110 A
Citazione:
J.W. Mink, "Basal ganglia motor function in relation to Hallervorden-Spatz syndrome", PED NEUROL, 25(2), 2001, pp. 112-117

Abstract

Hallervorden-Spatz syndrome (HSS) is a degenerative neurologic disorder associated with progressive rigidity, dystonia, impaired voluntary movement, dysarthria, and mental deterioration. Pathologically, there is iron deposition in the basal ganglia, with destruction of basal ganglia output neurons. Recent advances in the understanding of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to specific clinical manifestations of HSS. Experimental lesions of the basal ganglia output nucleic cause involuntary muscle contractions, similar to contractions observed in dystonia. A model of selection and suppression of competing motor patterns by the basal ganglia is presented in relation to the manifestations of damage to basal ganglia output neurons. It is hypothesized that the dystonia and other motor abnormalities seen in HSS can be attributed to degeneration of basal ganglia output neurons. (C) 2001by Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 23:37:14