The role of the cerebellum in the pathogenesis of cortical myoclonus
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The role of the cerebellum in the pathogenesis of cortical myoclonus. / Ganos, Christos; Kassavetis, Panagiotis; Erro, Roberto; Edwards, Mark J; Rothwell, John; Bhatia, Kailash P.
in: MOVEMENT DISORD, Jahrgang 29, Nr. 4, 01.04.2014, S. 437-43.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - The role of the cerebellum in the pathogenesis of cortical myoclonus
AU - Ganos, Christos
AU - Kassavetis, Panagiotis
AU - Erro, Roberto
AU - Edwards, Mark J
AU - Rothwell, John
AU - Bhatia, Kailash P
N1 - © 2014 International Parkinson and Movement Disorder Society.
PY - 2014/4/1
Y1 - 2014/4/1
N2 - The putative involvement of the cerebellum in the pathogenesis of cortical myoclonic syndromes has been long hypothesized, as neuropathological changes in patients with cortical myoclonus have most commonly been found in the cerebellum rather than in the suspected culprit, the primary somatosensory cortex. A model of increased cortical excitability due to loss of cerebellar inhibitory control via cerebello-thalamo-cortical connections has been proposed, but evidence remains equivocal. Here, we explore this hypothesis by examining syndromes that present with cortical myoclonus and ataxia. We first describe common clinical characteristics and underlying neuropathology. We critically view information on cerebellar physiology with regard to motorcortical output and compare findings between hypothesized and reported neurophysiological changes in conditions with cortical myoclonus and ataxia. We synthesize knowledge and focus on neurochemical changes in these conditions. Finally, we propose that the combination of alterations in inhibitory neurotransmission and the presence of cerebellar pathology are important elements in the pathogenesis of cortical myoclonus.
AB - The putative involvement of the cerebellum in the pathogenesis of cortical myoclonic syndromes has been long hypothesized, as neuropathological changes in patients with cortical myoclonus have most commonly been found in the cerebellum rather than in the suspected culprit, the primary somatosensory cortex. A model of increased cortical excitability due to loss of cerebellar inhibitory control via cerebello-thalamo-cortical connections has been proposed, but evidence remains equivocal. Here, we explore this hypothesis by examining syndromes that present with cortical myoclonus and ataxia. We first describe common clinical characteristics and underlying neuropathology. We critically view information on cerebellar physiology with regard to motorcortical output and compare findings between hypothesized and reported neurophysiological changes in conditions with cortical myoclonus and ataxia. We synthesize knowledge and focus on neurochemical changes in these conditions. Finally, we propose that the combination of alterations in inhibitory neurotransmission and the presence of cerebellar pathology are important elements in the pathogenesis of cortical myoclonus.
KW - Ataxia
KW - Cerebellum
KW - Cerebral Cortex
KW - Electroencephalography
KW - Humans
KW - Myoclonus
KW - Synaptic Transmission
U2 - 10.1002/mds.25867
DO - 10.1002/mds.25867
M3 - SCORING: Journal article
C2 - 24634361
VL - 29
SP - 437
EP - 443
JO - MOVEMENT DISORD
JF - MOVEMENT DISORD
SN - 0885-3185
IS - 4
ER -