Published Online
on November 3, 2005

A more recent version of this article appeared on December 1, 2005

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Submitted on May 22, 2005
Revised on September 3, 2005
Accepted on September 16, 2005

Motor Strokes. The Lesion Location Determines Motor Excitability Changes

Joachim Liepert MD^*; Cordula Restemeyer MD; Thomas Kucinski MD; Simone Zittel MD; and Cornelius Weiller MD

From the Departments of Neurology (J.L., C.R., S.Z.) and Neuroradiology (T.K.), University Medical Center Eppendorf, Hamburg, and Department of Neurology (C.W.), University Hospital, Freiburg, Germany.

^* To whom correspondence should be addressed. E-mail: liepert{at}uke.uni-hamburg.de.

Background and Purpose--The purpose of this research was to investigate the impact of lesion location on motor excitability and motor performance.

Methods--We studied patients with pure motor strokes in 4 different brain areas: motor cortex lesions (n=7), striatocapsular lesions (n=13), lacunar lesions of the internal capsule (n=13), and paramedian pontine lesions (n=10). Motor performance tests included the 9-hole-peg test and grip strength recordings. Motor excitability was determined by transcranial magnetic stimulation. Motor thresholds, stimulus-response curves, silent periods, motor cortical inhibition, and facilitation were investigated.

Results--The 4 groups were clinically similar but showed major differences in motor excitability. Only motor cortex lesions had a loss of intracortical inhibition in the affected hemisphere. In the internal capsule lesion group and the pontine lesion group, stimulus-response curves were depressed on the affected side. All of the subcortical lesions showed a prolongation of the silent period in the paretic side. Motor thresholds were predominantly elevated in the lesioned hemisphere of patients with internal capsule or pontine lesions. Motor performance was correlated with silent period duration in internal capsule lesions and with motor thresholds in internal capsule and pontine lesions.

Conclusions--Motor cortex lesions exhibited deficient inhibitory properties. In contrast, subcortical lesions displayed an enhancement of inhibition. Internal capsule and pontine lesions affecting the corticospinal tract on different levels particularly impaired neuronal recruitment. Our results suggest that the lesion location determines a specific pattern of motor excitability changes.

Key words: cerebral infarction • electromagnetics • evoked potentials, motor

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