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      MRI Findings in Patients with a History of Failed Prior Microvascular Decompression for Hemifacial Spasm: How to Image and Where to Look

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          Abstract

          A minority of patients who undergo microvascular decompression for hemifacial spasm do not improve after the first operation. We sought to determine the most common locations of unaddressed neurovascular contact in patients with persistent or recurrent hemifacial spasm despite prior microvascular decompression.

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          Most cited references18

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          Microvascular decompression for hemifacial spasm.

          The authors report the results of 782 microvascular decompression procedures for hemifacial spasm in 703 patients (705 sides), with follow-up study from 1 to 20 years (mean 8 years). Of 648 patients who had not undergone prior intracranial procedures for hemifacial spasm, 65% were women; their mean age was 52 years, and the mean preoperative duration of symptoms was 7 years. The onset of symptoms was typical in 92% and atypical in 8%. An additional 57 patients who had undergone prior microvascular decompression elsewhere were analyzed as a separate group. Patients were followed prospectively with annual questionnaires. Kaplan-Meier methods showed that among patients without prior microvascular decompression elsewhere, 84% had excellent results and 7% had partial success 10 years postoperatively. Subgroup analyses (Cox proportional hazards model) showed that men had better results than women, and patients with typical onset of symptoms had better results than those with atypical onset. Nearly all failures occurred within 24 months of operation; 9% of patients underwent reoperation for recurrent symptoms. Second microvascular decompression procedures were less successful, whether the first procedure was performed at Presbyterian-University Hospital or elsewhere, unless the procedure was performed within 30 days after the first microvascular decompression. Patient age, side and preoperative duration of symptoms, history of Bell's palsy, preoperative presence of facial weakness or synkinesis, and implant material used had no influence on postoperative results. Complications after the first microvascular decompression for hemifacial spasm included ipsilateral deaf ear in 2.6% and ipsilateral permanent, severe facial weakness in 0.9% of patients. Complications were more frequent in reoperated patients. In all, one operative death (0.1%) and two brainstem infarctions (0.3%) occurred. Microvascular decompression is a safe and definitive treatment for hemifacial spasm with proven long-term efficacy.
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            Microvascular decompression of cranial nerves: lessons learned after 4400 operations.

            Microvascular decompression has become an accepted surgical technique for the treatment of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and other cranial nerve rhizopathies. The senior author (P.J.J.) began performing this procedure in 1969 and has performed more than 4400 operations. The purpose of this article is to review some of the nuances of the technical aspects of this procedure. A review of 4415 operations shows that numerous modifications to the technique of microvascular decompression have occurred during the last 29 years. Of the 2420 operations performed for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia before 1990, cerebellar injury occurred in 21 cases (0.87%), hearing loss in 48 (1.98%), and cerebrospinal fluid (CSF) leakage in 59 cases (2.44%). Of the 1995 operations performed since 1990, cerebellar injuries declined to nine cases (0.45%), hearing loss to 16 (0.8%), and CSF leakage to 37 (1.85% p < 0.01, test for equality of distributions). The authors describe slight variations made to maximize surgical exposure and minimize potential complications in each of the six principal steps of this operation. These modifications have led to decreasing complication rates in recent years. Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.
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              Neurovascular compression findings in hemifacial spasm.

              It is generally accepted that hemifacial spasm (HFS) is caused by pulsatile vascular compression upon the facial nerve root exit zone. This 2-3 mm area, considered synonymous with the Obersteiner-Redlich zone, is a transition zone (TZ) between central and peripheral axonal myelination that is situated at the nerve's detachment from the pons. Further proximally, however, the facial nerve is exposed on the pontine surface and emerges from the pontomedullary sulcus. The incidence and significance of neurovascular compression upon these different segments of the facial nerve in patients with HFS has not been previously reported. The nature of neurovascular compression was determined in 115 consecutive patients undergoing their first microvascular decompression (MVD) for HFS. The location of neurovascular compression was categorized to 1 of 4 anatomical portions of the facial nerve: RExP = root exit point; AS = attached segment; RDP = root detachment point that corresponds to the TZ; and CP = distal cisternal portion. The severity of compression was defined as follows: mild = contact without indentation of nerve; moderate = indentation; and severe = deviation of the nerve course. Success in alleviating HFS was documented by telephone interview conducted at least 24 months following MVD surgery. Neurovascular compression was found in all patients, and the main culprit was the anterior inferior cerebellar artery (in 43%), posterior inferior cerebellar artery (in 31%), vertebral artery (in 23%), or a large vein (in 3%). Multiple compressing vessels were found in 38% of cases. The primary culprit location was at RExP in 10%, AS in 64%, RDP in 22%, and CP in 3%. The severity of compression was mild in 27%, moderate in 61%, and severe in 12%. Failure to alleviate HFS occurred in 9 cases, and was not related to compression location, severity, or vessel type. The authors observed that culprit neurovascular compression was present in all cases of HFS, but situated at the RDP or Obersteiner-Redlich zone in only one-quarter of cases and rarely on the more distal facial nerve root. Since the majority of culprit compression was found more proximally on the pontine surface or even pontomedullary sulcus origin of the facial nerve, these areas must be effectively visualized to achieve consistent success in performing MVD for HFS.
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                Author and article information

                Journal
                American Journal of Neuroradiology
                AJNR Am J Neuroradiol
                American Society of Neuroradiology (ASNR)
                0195-6108
                1936-959X
                April 10 2015
                April 2015
                April 2015
                November 27 2014
                : 36
                : 4
                : 768-773
                Article
                10.3174/ajnr.A4174
                7964296
                25430858
                25a325a0-066d-412f-8b71-b213c7d87132
                © 2014
                History

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