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(Stroke. 2004;35:2484.)
© 2004 American Heart Association, Inc.

Original Contributions

Motor Cortex Excitability After Cerebellar Infarction

From the Department of Neurology (J.L., O.T., T.B., C.W.), and the Department of Neuroradiology (T.K.), University Hospital Eppendorf, Hamburg, Germany; and the General Hospital Altona (F.P.), Hamburg, Germany.

Correspondence to Dr Joachim Liepert, Department of Neurology, University Hospital Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany. E-mail liepert{at}uke.uni-hamburg.de

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.

Conclusion— 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.

Key Words: cerebral infarction • cerebellar disease • electromagnetics • superior cerebral arteries

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