Literature DB >> 15502271

Lesion-induced and training-induced brain reorganization.

J Liepert1, F Hamzei, C Weiller.   

Abstract

INTRODUCTION: A stroke may modulate motor cortex excitability. We examined if distinct ischemic brain lesions are associated with a specific pattern of excitability changes. We also investigated the effects of a rehabilitative therapy on motor excitability.
METHODS: In stroke patients, the consequences of a) a lesion in the central somatosensory system, b) a cerebellar lesion and c) a two week period of Constraint-induced movement therapy (CIMT), on motor cortex excitability were studied. Transcranial magnetic stimulation techniques and functional magnetic resonance imaging (fMRI) were employed.
RESULTS: Patients with a lesion in the primary somatosensory cortex or in the ventroposterolateral nucleus of the thalamus had a decreased intracortical inhibition on the affected side. Patients with lesions in the territory of the superior cerebellar artery had a loss of intracortical facilitation and an increase of intracortical inhibition. Patients with cortical lesions undergoing CIMT had a loss of intracortical inhibition prior to therapy. After CIMT, changes of ICI were stronger in the lesioned than in the non-lesioned hemisphere but could result either in an increase of ICI or a reduction of ICI. In three patients fMRI results showed that cortical activation was less post CIMT as compared to pre-treatment activation. In parallel, ICI was reduced after treatment.
CONCLUSIONS: Our results suggest that, physiologically, central somatosensory influence on the motor cortex is inhibitory. In contrast, the cerebellum normally exerts a facilitatory influence on the motor cortex. CIMT induces changes of intracortical excitability mainly in the affected hemisphere.

Entities:  

Mesh:

Year:  2004        PMID: 15502271

Source DB:  PubMed          Journal:  Restor Neurol Neurosci        ISSN: 0922-6028            Impact factor:   2.406


  24 in total

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9.  Cortical overlap of joint representations contributes to the loss of independent joint control following stroke.

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