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At least 19 recordsLinked to original sources
PubMed2001

Fully endoscopic vascular decompression of the facial nerve for hemifacial spasm.

Hemifacial spasm is an uncommon disorder manifesting as a unilateral, involuntary, sporadic contraction of the musculature innervated by the seventh cranial nerve. Although debated, the etiology of hemifacial spasm is generally accepted as compression of the facial nerve by vessels of the posterior circulation. Early surgical techniques were ineffective and fraught with morbidity. Over the past 25 years microvascular decompression surgery has allowed the safe and effective treatment of hemifacial spasm. Recent reports combining microsurgical and endoscopic techniques have documented the advantages of the endoscope in exposing the anatomy of this region. Enhanced visualization allows a less traumatic dissection and increases the surgeon's ability to locate nerve-vessel conflicts often difficult to identify through the limited view of the microscope. This article reviews the history of hemifacial spasm and describes the first three cases of fully endoscopic vascular decompression for hemifacial spasm, emphasizing the advantages of this novel surgical approach.

Case Reports↗
PubMed1991

Occult pontine glioma in a patient with hemifacial spasm.

Hemifacial spasm due to an intracranial mass lesion is rare. We describe a 29-year-old man with hemifacial spasm successfully treated with botulinum A toxin injections for 2 years. The development of acquired diplopia secondary to acquired sixth cranial nerve palsy prompted investigation. Computed tomography done at the time of original diagnosis and on three other occasions (concentrating on the brain stem and cerebellopontine angle) failed to demonstrate an intracranial mass lesion. Magnetic resonance imaging (MRI) showed a large mass lesion in the pons presumed to be a glioma. Patients with hemifacial spasm who have atypical features, especially those with associated neurologic findings, should be screened for tumours. Our case illustrates the superiority of MRI in demonstrating pontine gliomas causing hemifacial spasm.

Adult↗
PubMed1994

Botulinum toxin treatment in patients with hemifacial spasm.

Hemifacial spasm is nearly always a unilateral disease of the facial musculature and is characterized by involuntary tonic or clonic cramps that considerably reduce the affected patient's quality of life. In the past, a number of different conservative and operative therapeutic procedures have been applied for the treatment of hemifacial spasm. In many cases these attempts failed to control the disease permanently or resulted in unwanted, sometimes strong, side effects. We report our own experiences with botulinum therapy in 29 patients with hemifacial spasm (78 therapeutic sessions). In our patients the mean duration of an effect after treatment with botulinum toxin was 18.2 weeks. Side effects were rare. Our results since 1990 at the University of Göttingen demonstrate that subcutaneous application of toxin from Clostridium botulinum to involved facial muscles represents a reliable method for successful treatment of hemifacial spasm.

Adult↗
PubMed1999

Gabapentin as treatment for hemifacial spasm.

Hemifacial spasm, a life-long condition characterized by involuntary unilateral contractions of the facial muscles, is a disabling disorder often resulting in patient irritation and social embarassment. Its probable etiology is neurovascular compression of the facial nerve at its root exit zone. The current medical treatment consists of either baclofen or anticonvulsant drugs, with limitation due to side effects or low efficacy. In recent years botulinum toxin injection and microvascular decompression of the facial nerve have been shown to be highly successful. However, both procedures share some complications and require special techniques. We present 5 patients affected by hemifacial spasm who responded well to the novel anticonvulsant drug gabapentin. Gabapentin was administered at a dose ranging from 900 to 1,600 mg daily, with rapid and clear improvement of spasms and absence of any remarkable adverse effects. Our findings suggest that gabapentin may be an effective treatment for patients with hemifacial spasm with a very good ratio of therapeutic effects to side effects when compared with other drugs currently used.

Acetates↗
PubMed1993

MR imaging of vascular compression in hemifacial spasm.

Hemifacial spasm is related to vascular compression of the root entry zone of the facial nerve at the brainstem by elongated tortuous vessels of the vertebrobasilar arterial system. In this study, we performed MR imaging in 16 patients with hemifacial spasm and investigated the vascular structures in bilateral-cerebellopontine angles and the relationship of each vessel to the root entry zone of the facial nerve. MR examination was performed with a 0.5 tesla MRI system, and MR angiography (3D time-of-flight) was obtained. Of 15 patients in whom both the nerve and vessels were clearly visible and could be observed to contact each other at the root entry zone, in 11 the tortuous artery could be identified by name. In only 1 patient was the contact between the nerve and vessel indeterminate, due to nonvisualization of the vessel around the facial nerve at its root entry zone. These findings suggest that MRI is a useful screening method in the preoperative assessment of hemifacial spasm.

Adult↗
PubMed1982

Position-dependent hemifacial spasm.

Hemifacial spasm developed in a 32-year-old man following a brain stem stroke. This stroke followed a self-induced head movement, which is a rare cause of such events. The clonic movements were often related entirely to the position of the head. Carbamazepine was successful in treating the spasm and may be indicated in the medical treatment of this disorder. The differential diagnosis and treatment of hemifacial spasm are discussed.

Adult↗
PubMed1999

An unusual cause of hemifacial spasm.

Hemifacial spasm (HFS) is a movement disorder characterized by involuntary paroxysmal chronic contractions of the facial musculature. The usual cause is vascular compression of the seventh cranial nerve, at its exit zone from the brain stem. We report a case of left hemifacial spasm, in a 66-year-old woman, in which the neuroradiological investigation with magnetic resonance imaging showed a hypervascular soft tissue mass arising from the left skull base, in the jugular foramen. This lesion was thought highly likely to be a glomus jugulare tumour. While the usual occurrence of tumour compression causing HFS has been previously recognized, the association of glomus jugulare tumours presenting with HFS has not. The importance of this association is discussed. Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗
PubMed1990

Secretion of tears in patients with hemifacial spasm.

Hemifacial spasm can cause abnormal tear secretion on the affected side. Thirty patients with this disease were examined using the Schirmer's test without topical anesthetic. Twelve of them showed more tear secretion on the affected side than on the unaffected side. The average Schirmer test value was 30.4 +/- 12.3 mm (+/- SD) on the affected side in the patients and 17.4 +/- 10.9 mm (n = 148) in the control subjects (P less than 0.001). Microvascular decompression surgery reduced the hypersecretion of tears. The results suggest that compression of the facial nerve by a blood vessel causes an excitatory stimulus for tear secretion in patients with hemifacial spasm.

Adult↗
PubMed2002

[Clinical aspects and treatment of 95 patients with hemifacial spasm].

Hemifacial Spasm (HFS) is considered a peripheral disease of the facial nerve caused by vascular compression at the nerve root in the pontocerebellar angle. We aimed to study the natural course of HFS and especially, to examine the relationships with psychological status or physical activities, in order to assess the possible role of the facial nucleus in the pathogenesis. Ninety-five consecutive patients with HFS, 52 men and 43 women, with a mean age of 62 + 12.7 years and a mean disease duration of 7.5 + 6.5 years, were personally interviewed by 2 of the authors (SB and HK). A detailed questionnaire was completed with direct and indirect questions regarding the relationship between the severity of the spasms and emotional status or physical activity. We found strong association between emotional stress and tiredness and aggravation of the spasms in 85% and 54% of the patients, respectively. Talking increased the spasm severity in 58% of the patients and eating or drinking aggravated the spasm in 28% of the patients. Physical activity, head position, the season of the year or the time during the day had no effect on the clinical status. Botulinum toxin was injected to 78 patients with an overall subjective rate of improvement of > 70% in 74% of the patients (23% graded their rates of improvement as > 90%). In conclusion, HFS is a movement disorder of the facial nerve which is highly influenced by emotional status to support an involvement of the facial nucleus in the pathogenesis. Botulinum toxin is a very effective long term treatment for this disorder.

Age of Onset↗
PubMed2005

Cryptic cerebellopontine angle neuroglial cyst presenting with hemifacial spasm.

Hemifacial spasm (HFS) is commonly caused by a vascular loop compressing the Root Exit Zone (REZ) of the facial nerve. We report a case of HFS caused by a vascular loop that was abnormally displaced by a neuroglial cyst not seen in Magnetic Resonance Imaging (MRI). Microvascular decompression (MVD) was planned and the patient underwent a key-hole retromastoid posterior fossa exposure. A cystic lesion was found in the cerebellopontine angle (CPA), located around the seventh and eighth cranial nerves extending from the porous acousticus to the brainstem REZ of the facial nerve. The cyst wall was partially excised revealing the region of the neurovascular conflict. MVD of the facial nerve was performed with immediate postoperative complete resolution of the patient's symptoms.

Adult↗
PubMed1997

Benign congenital hemifacial spasm.

Hemifacial spasm (HFS) is characterized by involuntary, irregular contraction of the muscles innervated by one facial nerve. Usually, it is caused by facial nerve injury either due to microvascular compression or a posterior fossa tumor, but it also occurs without apparent cause. It is rare in children; no congenital cases have yet been reported. We report the first case of congenital HFS in a term newborn delivered by forceps after a normal labor. Multimodal evoked potentials, electroencephalogram, computed tomography of the petrous bone, as well as brain magnetic resonance imaging and angiography disclosed no abnormalities. Serial neurodevelopmental examinations and video recordings performed until 8 months of age documented a normal neurodevelopmental status and a tendency for spontaneous diminution of the HFS. An intrauterine facial nerve injury as the causative factor of HFS, being responsible for its benign course, is proposed.

Blepharospasm↗
PubMed2001

Unusual causes of hemifacial spasm.

Hemifacial spasm (HFS) has been defined as consisting of brief clonic jerking movements of the facial musculature, beginning in the orbicularis oculi with downward spreading to other facial muscles. HFS, perhaps the most common of the abnormal involuntary facial movements, has been classically ascribed to vascular loop compression at the root exit zone of the facial nerve. Causes other than such vascular loops are rare in the medical literature. Here we present three case studies in which the phenomenology of the HFS was atypical in onset and evolution. Using these three patients as introduction to the topic, we reviewed the literature of all cases of HFS with causes other than the vascular loop. In these three cases, HFS was caused by (1) a parotid gland tumor, (2) a cerebellopontine angle meningioma, and (3) an acoustic schwannoma. We also discuss the radiological findings as well as possible differences in the genesis of HFS and phenomenology in such cases and present recommendations on how to evaluate these patients.

Adenocarcinoma↗
PubMed2005

Safety, effectiveness, and duration of effect of BOTOX after switching from Dysport for blepharospasm, cervical dystonia, and hemifacial spasm dystonia, and hemifacial spasm.

BACKGROUND: Local injection of botulinum toxin type A is first-line treatment of blepharospasm, cervical dystonia, and hemifacial spasm; however, there is uncertainty about the optimal dose of toxin for each indication as well as dose-conversion ratios that should be used when switching products in clinical practice. OBJECTIVE: The goal of this study was to compare the safety, effectiveness, and duration of clinical effect of BOTOX and Dysport and Dysportdagger after drug switching (Dysport to BOTOX) among patients with movement disorders. METHODS: A total of 48 patients diagnosed with blepharospasm (n = 27), cervical dystonia (n = 12), or hemifacial spasm (n = 9) were evaluated during a single-arm, crossover-design study in which each patient was his/her own historical control using a 5:1 or 4:1 conversion ratio of Dysport to BOTOX units. Patients were assessed (using Jankovic, Visual Analog Scale, general pain scale, Toronto Western Spasmodic Torticollis Rating Scale [TWSTRS] scores) after the last injection of Dysport and the first injection of BOTOX. Moreover, each patient kept a diary during treatment to track onset and duration of therapeutic effect. RESULTS: Although BOTOX and Dysport were both clinically effective, this effect was more significant with BOTOX compared to Dysport based on TWSTRS for cervical dystonia (p = 0.012), and Jankovic scores for blepharospasm (p = 0.006). Longer duration of effect also was noted with BOTOX than with Dysport (blepharospasm, 62.2 days vs 47.4 days (p = 0.001); cervical dystonia, 64.3 days vs 44.6 days (p = 0.014); hemifacial spasm, 65.1 days vs 41.8 days (p < 0.014), respectively). Of the 48 patients, 19 experienced at least one adverse drug reaction (ADR) during Dysport treatment, with the most commonly reported ADRs being ptosis for blepharospasm and hemifacial spasm and neck weakness for cervical dystonia. No patient reported an ADR during BOTOX treatment. CONCLUSIONS: Results suggest therapeutic effectiveness is enhanced with BOTOX compared to Dysport at a dosing ratio between 5:1 and 4:1 (Dysport:BOTOX). Safety and duration of therapeutic effect also are enhanced with BOTOX. Further research is needed.

Adult↗
PubMed2004

Hemifacial Spasm.

Hemifacial spasm (HFS) is a peripheral movement disorder caused by direct or indirect compression or distortion of the root exit zone of the seventh cranial nerve, which is most commonly compressed by an arterial loop, but also may be compressed by a tumor, cyst, or aneurysm. All patients with HFS should undergo magnetic resonance imaging, with particular attention to the seventh cranial nerve. For patients with HFS who want treatment, there are three options. Oral medications, particularly anticonvulsants, may be useful, but the response rate is low and evidence is almost exclusively anecdotal. Local injection of botulinum toxin into the overactive muscles has a very high rate of success and virtually no serious side effects. Backed by controlled clinical trials, the authors consider it the treatment of choice. Microvascular surgical decompression has the advantage of being potentially curative, and obviates the need for chronic injections with botulinum toxin. However, surgery carries much greater risk than botulinum toxin and the spasm may recur. It is important that surgery is carried out by an experienced neurosurgeon to reduce the risk.

Journal Article↗
PubMed1997

Pitfalls in the diagnosis of hemifacial spasm.

Hemifacial spasm (HFS), a condition characterized by involuntary unilateral facial spasms, is a disabling disorder resulting in functional compromise, patient frustration, cosmetic deformity, and social embarrassment. Compression of the seventh nerve at the root entry zone via vascular loop is presently the most widely accepted causative theory. Although less common, there are other entities that can result in HFS. Basic evaluation, including a thorough history, physical examination, and magnetic resonance imaging (MRI) scan, is important to confirm the diagnosis and rule out other causes. The relation of vascular loop syndrome to HFS is well enough established that radiologic documentation of a vascular loop is probably not necessary in every case. Here we present 12 cases of HFS, 6 without VLS. The etiology and evaluation of HFS are reviewed.

Adult↗
PubMed1993

[Electrophysiological study of hemifacial spasm].

Hemifacial spasm is characterized by intermittent involuntary contractions of one or several groups of muscles innervated by the facial nerve. The possible causal mechanisms have been the subject of numerous publications. The pre-eminent work of Moller and Jannetta implicates the compression of the facial nerve at its point of entry into the central nervous system, the Root Entry Zone, while the physiopathology is poorly understood, two principle hypotheses emerge: 1) ephaptic transmission between injured fibers; 2) hyper excitability of the facial motor nucleus. Using standard electromyographic techniques and blink reflex studies, we were able to demonstrate hyperexcitability of the facial nucleus. The cause of this hyperexcitability remains unexplained. It could be the result of a permanent antidromic stimulation from a peripheral ectopic center of excitation.

Adult↗
PubMed2005

Botulinum toxin type A therapy for hemifacial spasm.

BACKGROUND: Hemifacial spasm is characterised by unilateral involuntary contractions of muscles innervated by the facial nerve. The usual cause is a vessel touching the facial nerve near its origin from the brain stem. Although it is a benign condition it can cause significant cosmetic and functional disability. It is a chronic disease and spontaneous recovery is very rare. The two treatments routinely available are microvascular decompression and Botulinum Toxin type A (BtA) muscular injections. OBJECTIVES: To determine whether botulinum toxin (BtA) is an effective and safe treatment for hemifacial spasm. SEARCH STRATEGY: We searched the Cochrane Movement Disorders Group trials register, the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2004), MEDLINE (1977 to December 2003), EMBASE (1977 to December 2003), and reference lists of articles. We also contacted drug manufacturers and researchers in the field. SELECTION CRITERIA: Randomised studies comparing BtA with placebo in people with hemifacial spasm. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Study authors were contacted for additional information. Adverse effects information was collected from the trials. MAIN RESULTS: We found only one small randomised, placebo-controlled trial involving 11 people. It was a crossover trial during which patients underwent four sets of injections, comparing placebo with three different doses of BtA - formulation Botox(r) (low dose: one-half of the intermediate dose; intermediate dose; and high dose: twice the intermediate dose), and one of placebo. In this trial BtA was superior to placebo. AUTHORS' CONCLUSIONS: The findings of this single eligible trial support the results of large, open, case-control studies showing a benefit rate between 76 and 100%. This effect size probably makes it very difficult to perform new large placebo controlled trials for hemifacial spasm. Despite the paucity of good quality controlled data, all the studies available suggest that BtA is effective and safe for treating hemifacial spasm. Future trials should explore technical factors such as the optimum treatment intervals, different injection techniques, doses, Bt types and formulations. Other issues include service delivery, quality of life, long-term efficacy, safety, and immunogenicity. BtA should be compared with surgical microvascular decompression.

Botulinum Toxins, Type A↗
PubMed2006

A comparative study of primary and secondary hemifacial spasm.

BACKGROUND: Hemifacial spasm (HFS) is a common movement disorder. OBJECTIVE: To evaluate possible differences in the demographic and clinical features between primary and secondary HFS. DESIGN: In-person interview using a standardized questionnaire to collect demographic and clinical data. SETTING: A multicenter study that included patients with HFS attending 3 Italian academic centers. Patients Two hundred fourteen patients with HFS. MAIN OUTCOME MEASURE: A complete neurological examination assessed the current muscle distribution of spasm and the presence of synkinetic movements between upper and lower facial muscles. RESULTS: The study sample comprised 214 patients with HFS, 81 men and 133 women, having a mean +/- SD age of 65.9 +/- 12.3 years; 164 patients were classified as having primary HFS and 50 patients (48 postparalytic and 2 symptomatic cases) were classified as having secondary HFS. Patients with primary and those with secondary HFS had similar mean +/- SD ages at onset (54.9 +/- 13.5 vs 57.0 +/- 12.8 years), male-female ratios (63:101 vs 18:32), right-sided-left-sided HFS (77:86 [1 bilateral] vs 21:28 [1 bilateral]), and frequencies of familial cases (2.9% vs 2.0%), respectively. Most patients (65.0%) with primary HFS had initial symptoms of periocular muscle contractions alone and had subsequent involvement of the lower facial muscles. Most patients (72.0%) with secondary HFS reported initial involvement of the upper and lower facial muscles simultaneously. Signs of synkinesis were present in primary (43.3%) and secondary (58.0%) HFS. CONCLUSIONS: Patients with primary and those with secondary HFS share common demographic and clinical features, including sex distribution, age at onset, affected side of HFS, synkinesis, and rarity of familial cases. Signs of synkinesis were present in significant proportions of patients with primary or secondary HFS. The 2 forms differed in clinical presentation.

Adolescent↗