Influence of peripheral nerve stimulation on human motor cortical excitability in patients with ventrolateral thalamic lesion.

OBJECTIVE

To determine the peripheral afferent pathways that influence the activities of the motor cortex by examining the effects of peripheral nerve stimulation on motor cortical excitability.

PATIENTS AND

METHODS

We examined 12 healthy volunteers and 4 patients with localized brain lesions caused by cerebrovascular attack. Of the 4 patients, 1 patient had pontine infarction, including medial lemniscus, and severe sensory deficit and 3 had small localized lesions in the lateral part of the thalamus and neither sensory impairment nor abnormal N20 waves on somatosensory evoked potential recordings. Central motor tract excitability was examined by measuring a change in the motor evoked potential (MEP), using transcranial magnetic stimulation of the motor cortex after peripheral nerve stimulation at the wrist significantly increased MEP response in the controls at long conditioning-test intervals of 28 to 60 milliseconds, as well as at short intervals of 0 to 6 milliseconds. A late MEP potentiation was not observed on the affected side in all patients.

CONCLUSIONS

The loss of late MEP potentiation in patients with pontine and thalamic lesions indicates that this potentiation is caused by the alternation of the motor cortical excitability. Furthermore, the results in the patients with thalamic lesions suggest that the lateral nuclei of the thalamus, other than the ventral posterolateral nucleus and probably including the ventrolateral nucleus, have an important function in the processing of peripheral sensory input for tuning motor cortical excitability.