Microvascular Decompression to Treat Hemifacial Spasm: Long-term Results for a Consecutive Series of 143 Patients

Samii, M.; Günther, Thomas; İaconetta, Giorgio; Muehling, Michael; Vorkapic, Peter; Samii, Amir

doi:10.1097/00006123-200204000-00005

Cited by 184 publications

(127 citation statements)

References 38 publications

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“…HFS, with spasm relief achieved in 86% to 97% of patients. 3,4,[6][7][8]10,11,15,20,24 Culprit NVC in HFS is almost always found at the fREZ. We and others have emphasized that this area comprises exposed centrally myelinated facial nerve fibers as they emerge at the pontomedullary sulcus (i.e., RExP), then ascend approximately 8 mm attached along the pontine surface (AS) before detaching from the brainstem (RDP) and finally transitioning to peripheral myelin a few millimeters more distal along the nerve (TZ) to the cisternal portion.…”

Section: Repeat Mvd Techniquementioning

confidence: 99%

“…15,17 Surgical cure of HFS can be achieved with microvascular decompression (MVD) surgery, as pioneered by Jannetta in 1967, 12 and several series have demonstrated high rates of success and safety. 3,4,[6][7][8]10,11,13,20,21 The aim of this surgery is to alleviate culprit neurovascular compression (NVC) upon the facial nerve, most commonly at the facial root exit zone (fREZ). Only in rare cases is HFS caused by severe NVC of the cisternal portion of the facial nerve.…”

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confidence: 99%

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Failed microvascular decompression surgery for hemifacial spasm due to persistent neurovascular compression: an analysis of reoperations

Bigder¹,

Kaufmann²

2016

JNS

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H emifacial spasm (HFS) is relatively rare, with an estimated incidence of 0.8 per 100,000 persons/year and an estimated prevalence of 7.4 per 100,000 men and 14.5 per 100,000 women. 2 The disease typically begins as infrequent twitches of an eyelid that progress over time in intensity, frequency, and extent of involvement of the ipsilateral facial muscles. HFS may cause significant disability due to annoying and distracting twitches and forceful spasms, and also by the loss of binocular vision associated with involuntary eye closure. The greatest impact on the quality of life for many patients is the psychological and social impact of the facial disfigurement caused by the disorder. 15,17 Surgical cure of HFS can be achieved with microvascular decompression (MVD) surgery, as pioneered by Jannetta in 1967, 12 and several series have demonstrated high rates of success and safety. 3,4,[6][7][8]10,11,13,20,21 The aim of this surgery is to alleviate culprit neurovascular compression (NVC) upon the facial nerve, most commonly at the facial root exit zone (fREZ). Only in rare cases is HFS caused by severe NVC of the cisternal portion of the facial nerve.4,5 The extent of the fREZ, however, has been variably defined and is often considered as only the Obersteiner-Redlich zone of transition between central oligodendrocytes and peripheral Schwann cell-derived myelin, just distal to the facial nerve detachment from the lateral pons. 19 We have previously em- OBJectiVe Microvascular decompression (MVD) surgery for hemifacial spasm (HFS) is potentially curative. The findings at repeat MVD in patients with persistent or recurrent HFS were analyzed with the aim to identify factors that may improve surgical outcomes. methOdS Intraoperative findings were determined from review of dictated operative reports and operative diagrams for patients who underwent repeat MVD after prior surgery elsewhere. Clinical follow-up was obtained from the hospital and clinic records, as well as telephone questionnaires. reSultS Among 845 patients who underwent MVD performed by the senior author, 12 had been referred after prior MVD for HFS performed elsewhere. Following repeat MVD, all patients improved and complete spasm resolution was described by 11 of 12 patients after a mean follow-up of 91 ± 55 months (range 28-193). Complications were limited to 1 patient with aggravation of preexisting hearing loss and mild facial weakness and 1 patient with aseptic meningitis without sequelae. Significant factors that may have contributed to the failure of the first surgery included retromastoid craniectomies that did not extend laterally to the sigmoid sinus or inferiorly to the posterior fossa floor in 11 of 12 patients and a prior surgical approach that focused on the cisternal portion of the facial nerve in 9 of 12 patients. In all cases, significant persistent neurovascular compression (NVC) was evident and alleviated more proximally on the facial root exit zone (fREZ). cONcluSiONS Most HFS patients will achieve spasm relief with thorough allevia...

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Section: Repeat Mvd Techniquementioning

confidence: 99%

mentioning

confidence: 99%

Failed microvascular decompression surgery for hemifacial spasm due to persistent neurovascular compression: an analysis of reoperations

Bigder¹,

Kaufmann²

2016

JNS

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“…The 2 patients with poor results underwent re-operation and showed com plete disappearance of spasms (Table 7). 14, [17][18][19] Estimation of the compressing vessel and the incidence of each vessel causing compression Preoperative vertebral angiography in patients with hemifacial spasm allows the exclusion diagnosis of aneurysms and arteriovenous anomalies, and the esti mation of the site of the compressing vessel site. Recntly, MRI has often been used for diagnosis of hemifacial spasm.20-23 However oblique sagittal gra dient echo MRI discriminated between the AICA and PICA, with a true positivc rate of 75.9%.…”

Section: Surgical Resultsmentioning

confidence: 99%

Angiographic manifestations and operative findings with 70 cases of hemifacial spasm: relation of common trunk anomalies

2003

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Abstract. The relations between angiographic manifestations and operative findings of hemifacial spasm were studied in 70 cases between 1988 and 2001. Vertebral angiography was performed, and Towne, straight AP, and lateral projections were routinely examined. The dominant anterior inferior cerebellar artery (AICA) directly compressed the facial nerve root exit zone in 26 cases, the dominant posterior inferior cerebellar artery (PICA) in 20, the AICA in 13, the PICA in 2, and the vertebral artery (VA) in 9. Compression by multiple vessels was observed in 11 cases. Anatomical variations of the affected AICA and PICA were classified into 3 groups according to their origins and distributions of blood supply: normal distribution of AICA and PICA in 18%, common trunk anomaly with domi nant AICA (basilar artery origin) in 48% and common trunk anomaly with dominant PICA (vertebral artery origin) in 34%. Analyses of the angiograms revealed significantly increased numbers of common trunk anomalies compared with cases with normal angiograms. In 18 of the 20 cases of unilateral common trunk anomalies, facial nerves were compressed by the dominant artery. Preoperative verte bral angiograms may clarify the offending vessels and their sites in most hemifacial spasm cases, thus increasing the safety of surgical interventions. (Keio J Med 52 (3): 189-197, September 2003)

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“…The cause of hemifacial spasm is the vascular compression by an artery or arteries at the nerve root exit zone (REZ) of the 7 th nerve in more than 95% of cases (1,2,(4)(5)(6)8,9,15,20). Microvascular decompression has been established for the treatment of hemifacial spasm (12,15).…”

Section: Introductionmentioning

confidence: 99%

Microvascular decompression for hemifacial spasm due to four offending vessels: a case report

Choi

Choi²,

Rhee³

2011

Turkish Neurosurgery

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A 65-year-old woman presented with left facial involuntary movement and facial palsy for eight years. Brain magnetic resonance image (MRI) and magnetic resonance angiography (MRA) revealed multiple vascular compression of facial nerve root exit zone (REZ). Standard retromastoid suboccipital craniectomy and arachnoid dissection were performed. Right vertebral artery (VA), left VA, left anterior inferior cerebellar artery (AICA), and left posterior inferior cerebellar artery (PICA) compressed the facial nerve in that order. The offending vessels were dissected away from the facial nerve and transposed sequentially. Teflon was interposed between the arteries and the nerve. Electrophysiological monitoring showed disappearance of the abnormal hemifacial spasm response during the operation. The offending vessels were right VA, left VA, left AICA, and left PICA. Postoperatively, the patient's involuntary movement was completely resolved. We report a rare case of hemifacial spasm caused by four offending vessels that was treated by microvascular decompression (MVD) with wide arachnoid dissection.

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Microvascular Decompression to Treat Hemifacial Spasm: Long-term Results for a Consecutive Series of 143 Patients

Cited by 184 publications

References 38 publications

Failed microvascular decompression surgery for hemifacial spasm due to persistent neurovascular compression: an analysis of reoperations

Failed microvascular decompression surgery for hemifacial spasm due to persistent neurovascular compression: an analysis of reoperations

Angiographic manifestations and operative findings with 70 cases of hemifacial spasm: relation of common trunk anomalies

Microvascular decompression for hemifacial spasm due to four offending vessels: a case report

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