M
Mark Hallett
Researcher at National Institutes of Health
Publications - 1234
Citations - 136876
Mark Hallett is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transcranial magnetic stimulation & Motor cortex. The author has an hindex of 186, co-authored 1170 publications receiving 123741 citations. Previous affiliations of Mark Hallett include Government of the United States of America & Armed Forces Institute of Pathology.
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Journal ArticleDOI
Abnormal dorsal premotor-motor inhibition in writer's cramp.
Sarah Pirio Richardson,Sarah Pirio Richardson,Sandra Beck,Sandra Beck,Barbara Bliem,Mark Hallett +5 more
TL;DR: The results suggest that abnormal premotor–motor interactions may play a role in the pathophysiology of focal dystonia, and dPMI was not modulated by task in either group, but was constantly greater in the patients.
Journal Article
Physiology of negative myoclonus.
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Motor cortex excitability in patients with cerebellar degeneration
Joachim Liepert,Mark Hallett,Ali Samii,Daniele Oddo,Pablo Celnik,Leonardo G. Cohen,Eric M. Wassermann +6 more
TL;DR: M1 excitability prior to movement in an RT task increases abnormally early in cerebellar patients, may reflect compensation for deficient thalamocortical drive, and subthreshold transcranial magnetic stimulation can partially normalize the prolonged RT and abnormal excitability rise in patients.
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Etiological musculo-skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist
J.N.A.L. Leijnse,Mark Hallett +1 more
TL;DR: The case would demonstrate that task‐specific hand dystonias can arise as overcompensations for (peripheral) neuro‐musculoskeletal defects.
Journal ArticleDOI
Impaired long-term potentiation–like plasticity of the trigeminal blink reflex circuit in Parkinson's disease
Fortunato Battaglia,Maria Felice Ghilardi,Angelo Quartarone,Sergio Bagnato,Paolo Girlanda,Mark Hallett +5 more
TL;DR: It is concluded that nigrostriatal denervation disrupts LTP‐like plasticity in the trigeminal reflex circuit and reduces the facilitation of the R2 response after the induction protocol.