Cerebral Lesions with Shortened Silent Period after Transcranial Magnetic Stimulation in Stroke.
- Author:
Tae Hwan PARK
1
;
Hyung Kun OH
;
Jong Won PARK
;
Oh Sang KWON
Author Information
1. Department of Neurology, College of Medicine, Chung-ang University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Silent period;
Stroke;
Transcranial magnetic stimulation
- MeSH:
Caudate Nucleus;
Head;
Humans;
Motor Cortex;
Muscles;
Putamen;
Stroke*;
Thalamus;
Transcranial Magnetic Stimulation*
- From:Journal of the Korean Neurological Association
2000;18(5):529-534
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: A silent period (SP), recorded with transcranial magnetic stimulation (TMS) reflects the cortical inhibition of the central motor pathway. In most previous reports involving unilateral cerebral lesions, prolonged cortical SPs recorded with TMS on the affected side compared with SPs on the contralateral hemisphere were observed. However, in only a few studies, a shortened SP has been observed. In the present study, we assumed a shortened SP mechanism in the association with stoke. METHODS: We studied cortical SPs of both first dorsal interossei muscles evoked by TMS in 21 normal subjects and 13 patients with single focal cerebral lesions (lacunar infarct or small hemorrhage). We divided lesions into two groups with prolonged and shortened SP. Interside differences of SP recorded in both groups were compared with that of normal subjects. RESULTS: Shortened SP was observed in 3 thalamic, 3 motor cortical, and 1 caudate nucleus head lesions. Four thalamic and 2 putamenal lesions showed prolonged SP. In patients with thalamic lesions, SPs were shortened in ventrolateral thalamic lesions and prolonged in dorsomedial lesions. Interside differences of both the shortened and prolonged groups were 85.8+/-47.6 msec, and 99.3+/-49.7 msec, respectively (normal control, 7.3+/-5.9 msec). CONCLUSIONS: These results suggest that shortened SP is related to anatomical sites of lesions including motor cortex, caudate nucleus, and ventrolateral thalamus. Divergent results obtained from thalamic lesions also suggest that the thalamocortical pathway plays a significant role in cortical SP induced by TMS.
