Restuccia Domenico, Valeriani Massimiliano, Barba Carmen, Le Pera Domenica, Bentivoglio Annarita, Albanese Alberto, Rubino Marco, Tonali Pietro
Department of Neurology, Catholic University, Policlinico A. Gemelli, L.go A. Gemelli 8, 00168, Rome, Italy.
Clin Neurophysiol. 2003 Jan;114(1):120-9. doi: 10.1016/s1388-2457(02)00335-8.
To study whether sensorimotor cortical areas are involved in Essential Tremor (ET) generation.
It has been suggested that sensorimotor cortical areas can play a role in ET generation. Therefore, we studied median nerve somatosensory evoked potentials (SEPs) in 10 patients with definite ET.
To distinguish SEP changes due to hand movements from those specifically related to central mechanisms of tremor, SEPs were recorded at rest, during postural tremor and during active and passive movement of the hand. Moreover, we recorded SEPs from 5 volunteers who mimicked hand tremor. The traces were further submitted to dipolar source analysis.
Mimicked tremor in controls as well as active and passive hand movements in ET patients caused a marked attenuation of all scalp SEP components. These SEP changes can be explained by the interference between movement and somatosensory input ('gating' phenomenon). By contrast, SEPs during postural tremor in ET patients showed a reduction of N20, P22, N24 and P24 cortical SEP components, whereas the fronto-central N30 wave remained unaffected.
Our findings suggest that in ET patients the physiological interference between movement and somatosensory input to the cortex is not effective on the N30 response. This finding thus indicates that a dysfunction of the cortical generator of the N30 response may play a role in the pathogenesis of ET.
研究感觉运动皮层区域是否参与特发性震颤(ET)的产生。
有研究表明感觉运动皮层区域可能在ET的产生中起作用。因此,我们对10例确诊为ET的患者进行了正中神经体感诱发电位(SEP)研究。
为了区分因手部运动引起的SEP变化与震颤的中枢机制所特有的变化,我们在静息状态、姿势性震颤期间以及手部主动和被动运动期间记录SEP。此外,我们还记录了5名模拟手部震颤的志愿者的SEP。这些记录进一步进行偶极子源分析。
对照组的模拟震颤以及ET患者的手部主动和被动运动均导致所有头皮SEP成分明显衰减。这些SEP变化可以用运动和体感输入之间的干扰(“闸门”现象)来解释。相比之下,ET患者姿势性震颤期间的SEP显示N20、P22、N24和P24皮层SEP成分减少,而额中央N30波不受影响。
我们的研究结果表明,在ET患者中,运动与皮层体感输入之间的生理干扰对N30反应无效。这一发现表明,N30反应的皮层发生器功能障碍可能在ET的发病机制中起作用。