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DOI 10.1016/s1388-2457(03)00161-5

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2003

Long-latency motor evoked potentials in congenital hemiplegia.

Vandermeeren Y, Bastings E, Fadiga L, Olivier E

Сравнительное исследованиеСтатьяПеревод пока не подготовлен

Аннотация

OBJECTIVE

To investigate long-latency motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation in congenital hemiplegia (CH) and to seek for correlation with paretic hand movement deficits.

METHODS

MEPs were recorded from the first dorsal interosseous of both hands in 12 CH patients and 12 age-matched controls; dexterity and upper limb function were quantitatively assessed in both groups.

RESULTS

In CH patients, long-latency MEPs, occurring much later than the commonly reported MEPs, were frequently observed in the paretic and non-paretic hands. Four distinct groups of long-latency MEPs were found, each cluster being identified by its mean latency, namely 35, 85, 160 and 225 ms. The residual dexterity of the paretic hand was correlated with the presence of contralateral MEPs with a 20 and 225 ms latency and was negatively correlated with ipsilateral MEPs, irrespective of their latency. In controls, only few MEPs with a latency of 225 ms were found in 4 out of 12 subjects.

CONCLUSIONS

The pattern of MEPs found in CH patients differs dramatically from that reported in adult stroke patients, suggesting that long-latency MEPs are a rather distinctive consequence of early corticospinal lesions. The hypothesis that a given cluster of long-latency MEPs is mediated by a particular pathway appears very unlikely. Rather, we suggest that an exacerbation of cortical and/or spinal excitability is at the origin of these long-latency MEPs.

Для цитирования: Vandermeeren Y, Bastings E, Fadiga L, Olivier E. Long-latency motor evoked potentials in congenital hemiplegia.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2003. DOI: 10.1016/s1388-2457(03)00161-5.

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