Motor cortex excitability after cerebellar infarction.

Standard

Motor cortex excitability after cerebellar infarction. / Liepert, J; Kucinski, T; Tüscher, O; Pawlas, F; Bäumer, Tobias; Weiller, C.

In: STROKE, Vol. 35, No. 11, 11, 2004, p. 2484-2488.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Liepert, J, Kucinski, T, Tüscher, O, Pawlas, F, Bäumer, T & Weiller, C 2004, 'Motor cortex excitability after cerebellar infarction.', STROKE, vol. 35, no. 11, 11, pp. 2484-2488. <http://www.ncbi.nlm.nih.gov/pubmed/15375297?dopt=Citation>

APA

Liepert, J., Kucinski, T., Tüscher, O., Pawlas, F., Bäumer, T., & Weiller, C. (2004). Motor cortex excitability after cerebellar infarction. STROKE, 35(11), 2484-2488. [11]. http://www.ncbi.nlm.nih.gov/pubmed/15375297?dopt=Citation

Vancouver

Liepert J, Kucinski T, Tüscher O, Pawlas F, Bäumer T, Weiller C. Motor cortex excitability after cerebellar infarction. STROKE. 2004;35(11):2484-2488. 11.

Bibtex

@article{859190504e224a1d80c55e6c32df2697,
title = "Motor cortex excitability after cerebellar infarction.",
abstract = "BACKGROUND AND PURPOSE: The cerebellum has an influence on motor excitability. We investigated if the location of a cerebellar infarction was crucial for changes of motor cortex excitability and if the electrophysiological findings were correlated with motor performance. METHODS: Transcranial magnetic stimulation was applied to study intracortical inhibition (ICI), intracortical facilitation (ICF), motor thresholds, and corticospinal excitability. Dexterity as a measure of motor performance was tested with the Nine-Hole-Peg Test (9HPT). Ratios (affected/unaffected) were also calculated. RESULTS: ICI and ICF ratios were negatively correlated with 9HPT ratios in all patients (n=9). Compared with an age-matched control group, patients with lesions in the territory of the superior cerebellar artery (SCA) (n=3) or a lesion rostral of the dentate nucleus (n=1) had abnormally enhanced ICI and a loss of ICF (3 patients). Dexterity was impaired in all 4 patients. Motor excitability and motor performance normalized over the subsequent weeks. Patients with an infarct either in the territory of the anterior inferior cerebellar artery (n=2) or in the territory of the posterior inferior cerebellar artery (n=3) displayed motor excitability and motor performance within the normal range. CONCLUSIONS: The superior part of the cerebellum has a strong influence on motor cortex excitability. We suggest that the enhancement of motor inhibition and reduction of motor facilitation is mediated by an impairment of the deep cerebellar nuclei.",
author = "J Liepert and T Kucinski and O T{\"u}scher and F Pawlas and Tobias B{\"a}umer and C Weiller",
year = "2004",
language = "Deutsch",
volume = "35",
pages = "2484--2488",
journal = "STROKE",
issn = "0039-2499",
publisher = "Lippincott Williams and Wilkins",
number = "11",

}

RIS

TY - JOUR

T1 - Motor cortex excitability after cerebellar infarction.

AU - Liepert, J

AU - Kucinski, T

AU - Tüscher, O

AU - Pawlas, F

AU - Bäumer, Tobias

AU - Weiller, C

PY - 2004

Y1 - 2004

N2 - BACKGROUND AND PURPOSE: The cerebellum has an influence on motor excitability. We investigated if the location of a cerebellar infarction was crucial for changes of motor cortex excitability and if the electrophysiological findings were correlated with motor performance. METHODS: Transcranial magnetic stimulation was applied to study intracortical inhibition (ICI), intracortical facilitation (ICF), motor thresholds, and corticospinal excitability. Dexterity as a measure of motor performance was tested with the Nine-Hole-Peg Test (9HPT). Ratios (affected/unaffected) were also calculated. RESULTS: ICI and ICF ratios were negatively correlated with 9HPT ratios in all patients (n=9). Compared with an age-matched control group, patients with lesions in the territory of the superior cerebellar artery (SCA) (n=3) or a lesion rostral of the dentate nucleus (n=1) had abnormally enhanced ICI and a loss of ICF (3 patients). Dexterity was impaired in all 4 patients. Motor excitability and motor performance normalized over the subsequent weeks. Patients with an infarct either in the territory of the anterior inferior cerebellar artery (n=2) or in the territory of the posterior inferior cerebellar artery (n=3) displayed motor excitability and motor performance within the normal range. CONCLUSIONS: The superior part of the cerebellum has a strong influence on motor cortex excitability. We suggest that the enhancement of motor inhibition and reduction of motor facilitation is mediated by an impairment of the deep cerebellar nuclei.

AB - BACKGROUND AND PURPOSE: The cerebellum has an influence on motor excitability. We investigated if the location of a cerebellar infarction was crucial for changes of motor cortex excitability and if the electrophysiological findings were correlated with motor performance. METHODS: Transcranial magnetic stimulation was applied to study intracortical inhibition (ICI), intracortical facilitation (ICF), motor thresholds, and corticospinal excitability. Dexterity as a measure of motor performance was tested with the Nine-Hole-Peg Test (9HPT). Ratios (affected/unaffected) were also calculated. RESULTS: ICI and ICF ratios were negatively correlated with 9HPT ratios in all patients (n=9). Compared with an age-matched control group, patients with lesions in the territory of the superior cerebellar artery (SCA) (n=3) or a lesion rostral of the dentate nucleus (n=1) had abnormally enhanced ICI and a loss of ICF (3 patients). Dexterity was impaired in all 4 patients. Motor excitability and motor performance normalized over the subsequent weeks. Patients with an infarct either in the territory of the anterior inferior cerebellar artery (n=2) or in the territory of the posterior inferior cerebellar artery (n=3) displayed motor excitability and motor performance within the normal range. CONCLUSIONS: The superior part of the cerebellum has a strong influence on motor cortex excitability. We suggest that the enhancement of motor inhibition and reduction of motor facilitation is mediated by an impairment of the deep cerebellar nuclei.

M3 - SCORING: Zeitschriftenaufsatz

VL - 35

SP - 2484

EP - 2488

JO - STROKE

JF - STROKE

SN - 0039-2499

IS - 11

M1 - 11

ER -