• Devin K Binder, Russ Lyon, and Geoffrey T Manley.
• Department of Neurological Surgery, M779 Moffitt Hospital, Box 0112, University of California-San Francisco, San Francisco, CA 94143-0112, USA. dbinder@itsa.ucsf.edu
• Neurosurgery. 2004 Apr 1; 54 (4): 999-1002; discussion 1002-3.

Objective And ImportanceCompression 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.Clinical PresentationA 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.InterventionFurther 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.ConclusionThis 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.

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