Binder Devin K, Lyon Russ, Manley Geoffrey T
Department of Neurological Surgery, M779 Moffitt Hospital, Box 0112, University of California-San Francisco, San Francisco, CA 94143-0112, USA.
Neurosurgery. 2004 Apr;54(4):999-1002; discussion 1002-3. doi: 10.1227/01.neu.0000115674.15497.09.
Compression of the cerebral peduncle against the tentorial incisura contralateral to a supratentorial mass lesion, the so-called Kernohan-Woltman notch phenomenon, can be an important cause of false localizing motor signs. Here, we demonstrate a case in which clinical, radiological, and electrophysiological findings were used together to define this syndrome.
A 21-year-old man sustained a left temporal depressed cranial fracture from a motor vehicle accident. Serial computed tomographic examinations demonstrated no evolution of hematomas or contusions, and he was managed nonsurgically with ventriculostomy for intracranial pressure control. Throughout his course in the neurosurgical intensive care unit, he displayed persistent left hemiparesis.
Further radiological and electrophysiological studies were undertaken in an attempt to explain his left hemiparesis. Brain magnetic resonance imaging demonstrated T2 prolongation in the central portion of the right cerebral peduncle extending to the right internal capsule. Electrophysiological studies using transcranial electrical motor evoked potentials revealed both a marked increase in voltage threshold, as well as a reduction in the complexity of the motor evoked potential waveform on the hemiparetic left side. This contrasted to significantly lower voltage threshold as well as a highly complex motor evoked potential waveform recorded on the relatively intact contralateral side.
This is the first time that clinical, radiological, and electrophysiological findings have been correlated in a case of Kernohan's notch syndrome. Compression of the contralateral cerebral peduncle against the tentorial incisura can lead to damage and ipsilateral hemiparesis. The anatomic extent of the lesion can be defined by magnetic resonance imaging and the physiological extent by electrophysiological techniques.
大脑脚被幕切迹对侧的幕上占位性病变压迫，即所谓的克诺汉-沃尔特曼切迹现象，可能是假定位运动体征的重要原因。在此，我们展示了一个通过综合临床、影像学和电生理检查结果来明确该综合征的病例。
一名21岁男性因机动车事故导致左颞部颅骨凹陷性骨折。系列计算机断层扫描检查显示血肿或挫伤无进展，遂对其进行非手术治疗，通过脑室造瘘术控制颅内压。在神经外科重症监护病房的整个病程中，他一直存在持续性左侧偏瘫。
为解释其左侧偏瘫，进一步进行了影像学和电生理研究。脑磁共振成像显示右侧大脑脚中部至右侧内囊T2信号延长。经颅电运动诱发电位的电生理研究显示，偏瘫的左侧电压阈值显著升高，且运动诱发电位波形的复杂性降低。这与相对完整的对侧记录到的电压阈值明显较低以及高度复杂的运动诱发电位波形形成对比。
这是首次在克诺汉切迹综合征病例中对临床、影像学和电生理检查结果进行相关性分析。对侧大脑脚被幕切迹压迫可导致损伤及同侧偏瘫。病变的解剖范围可通过磁共振成像确定，生理范围可通过电生理技术确定。
