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(Stroke. 2000;31:1766.)
© 2000 American Heart Association, Inc.

Case Reports

Facial Palsy in Cerebral Venous Thrombosis

Transcranial Stimulation and Pathophysiological Considerations

J. Straub, MD; M. R. Magistris, MD; J. Delavelle, MD T. Landis, MD

From the Departments of Neurology (J.S., M.R.M., T.L.), and Radiology (J.D.), University Hospital of Geneva, Geneva, Switzerland.

Correspondence to Dr J. Straub, c/o Dr M.R. Magistris, Clinique de Neurologie, Hôpital Cantonal Universitaire de Genève, CH-1211 Genève 14, rue Micheli-du-Crest 24, Switzerland. E-mail judith.straub{at}hcuge.ch

Abstract

Background—Cranial nerve palsy in cerebral sinovenous thrombosis (CVT) is rare, its pathophysiology remains unclear, and data from electrophysiological examinations in such patients are missing.

Case Description—We report the case of a 17-year-old woman with familial protein S deficiency who was admitted with extensive multiple CVT. Two weeks after onset of symptoms, she developed isolated right peripheral facial palsy, and MR venography showed segmental occlusion of the ipsilateral transverse sinus. Complete recovery of facial palsy occurred concomitant with recanalization of the transverse sinus. Facial neurography, including transcranial magnetic stimulation of the facial nerve and related motor cortex, ruled out a coincidental idiopathic palsy and revealed conduction block proximal to the facial canal.

Conclusions—Facial palsy in our patient was caused by transient neurapraxia in the intracranial segment of the nerve. We suggest that elevated venous transmural pressure in the nerve’s satellite vein, which belongs to the affected drainage territory of the transverse sinus, might have caused venous blood-brain barrier dysfunction in the intrinsic vascular system of the nerve, with leakage of fluids and ions into the endoneurial space and thus an increase in interstitial resistance.

Key Words: cerebral thrombosis • cranial nerves • neural conduction • protein S deficiency • transcranial magnetic stimulation

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