Microvascular decompression for hemifacial spasm: focus on late reoperation
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The objective of this study is to investigate late repeat microvascular decompression (MVD) with persistent or recurrent hemifacial spasm (HFS) and to compare the clinical characteristics, intraoperative findings, complications, and outcomes with first MVD. We analyzed MVDs performed at the University of Pittsburgh Medical Center between January 1, 2000 and December 31, 2007. Thirty-three patients who underwent late redo MVDs were classified as group I and 243 patients who underwent their first MVD as group II. Clinical data were collected to analyze the difference between the two groups. The mean follow-up period was 54.48 months (range, 9–102 months). There is no significant difference in preoperative clinical characteristics (gender, age, side of MVD, botox usage, facial weakness) between the two groups. In present study, we found a vein as the offending vessel in significantly more number of patients who underwent repeat MVD as compared to first MVD (P = 0.02). The lateral spread response disappeared in 66 % of patients during repeat MVDs, which is not different from those undergoing their first MVD. No difference in the relief rate was found during the immediate postoperative, discharge, or follow-up stages between repeat and first MVD. Moreover, no difference was found in the incidence of complications between repeat MVD and first MVD. Late repeat MVD for HFS is an effective and safe procedure. No specific preoperative clinical characteristics were identified in patients with repeat MVD. Intraoperative monitoring with lateral spread response (LSR) is an effective tool to evaluate adequate decompression. In patients with persistent LSR at the end of the procedure, facial nerve compression from a vein should be examined. We believe that it is important to undergo a repeat MVD for failed HFS relief irrespective of the timing of the operation.
KeywordsHemifacial spasm Microvascular decompression Reoperation Lateral spread response Botox
The authors acknowledge the collaboration of all of the staff and technical members at the Center for Clinical Neurophysiology, Department of Neurological Surgery, University of Pittsburgh Medical Center.
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