TRANSCRANIAL MAGNETIC DOUBLE STIMULATION - METHODS AND CLINICAL-STUDIES

Citation
M. Vorgerd et al., TRANSCRANIAL MAGNETIC DOUBLE STIMULATION - METHODS AND CLINICAL-STUDIES, EEG-EMG, 27(2), 1996, pp. 85-91
Citations number
28
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00127590
Volume
27
Issue
2
Year of publication
1996
Pages
85 - 91
Database
ISI
SICI code
0012-7590(1996)27:2<85:TMDS-M>2.0.ZU;2-0
Abstract
Transcranial magnetic double stimulation of the motor cortex was perfo rmed with various intensities of both stimuli and at different interst imulus intervals. With conditioning stimulus 1.5-threshold and test st imulus near threshold, a suppression of the test response was found at interstimulus intervals between 50 and 200 ms (fig. 4), which was ind ependent of pre-innervation. This refractory period is most likely cau sed by inhibitory mechanisms within the motor cortex. We performed dou ble stimulation (conditioning stimulus = 1.5-threshold, test stimulus = threshold) at rest in a healthy control group (21 subjects, 14-79 ye ars, mean age 46 years) and in patients with stroke (11 patients, 30-8 2 years, mean age 71 years) and in patients with Huntington's disease (9 patients, 28-57 years, mean age 44 years). In the control group mea n refractory period by double stimulation was 162.2 +/- 23.1 ms and in traindividual side-to-side-difference of refractory period by double s timulation was 17.6 +/- 9.5 (tab. 1). In patients with stroke 8 of 11 patients had pathologically prolonged refractory period by double stim ulation, Mean refractory period by double stimulation on the clinicall y affected side was significantly prolonged compared with normal contr ols (250.9 ms +/- 52.5 ms, p < 0.001) (tab. 1). This indicates functio nal or structural lesions of the pyramidal neurons or increased inhibi tion of the corticospinal tract or both.In 7 out of 9 patients with Hu ntington's disease a pathological prolongation of refractory period by double stimulation was found and mean refractory period by double sti mulation was significantly prolonged compared with the control group ( 302.7 ms +/- 151.3 ms, p < 0.05) (tab. 1). This result is probably cau sed by an altered excitability of the corticomotoneuron system in the course of Huntington's disease.