Cases Of Hemifacial Spasm Research Articles

Hemifacial Spasm Due to a Large Distant Ipsilateral Posterior Fossa Meningioma

A rare case of hemifacial spasm due to an ipsilateral foramen magnum/clival meningioma is described. Magnetic resonance imaging demonstrated that the tumor was located distant to the cranial nerve VII/VIII complex. Resolution of the ipsilateral hemifacial spasm was noted after complete resection of the tumor. The mechanism of hemifacial spasm was likely due to displacement and distortion of the brain stem from the lesion distant to the cranial nerve VII/VIII complex. In our review of the literature this is the first reported case of an ipsilateral posterior fossa meningioma causing hemifacial spasm from indirect mass effect.

半側顔面けいれんに対して低周波しん通電療法を行った６例

半側顔面けいれんに対して低周波しん通電療法を行った６例

Hemifacial spasm caused by a pilocytic astrocytoma of the fourth ventricle

An 11-year-old male in whom hemifacial spasm was the presenting sign of a pilocytic astrocytoma within the fourth ventricle is reported. The child’s hemifacial spasm decreased substantially after resection of the tumor. Hemifacial spasm is largely a disease of adults and only rarely is attributed to brain tumors. In contrast, this marks the fifth case of hemifacial spasm reported in a child, three of which have been attributed to tumors of the fourth ventricle.

Combined hyperactive dysfunction syndrome of the cranial nerves: trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia: 11-year experience and review.

A pathological condition caused by vascular compression at the root entry/exit zone of the cranial nerves is designated hyperactive dysfunction syndrome (HDS) of the cranial nerves. Patients with HDS who exhibited a combination of trigeminal neuralgia (TN), hemifacial spasm (HFS), and/or glossopharyngeal neuralgia were retrospectively reviewed, to study the incidence, etiological factors, and demographic characteristics for this combined HDS group. Medical and surgical records were analyzed for 41 patients with combined HDS, of 1472 consecutive patients with HDS who were treated between 1984 and 1994. The combined HDS group accounted for 2.8% of all patients with HDS; 19 patients (1.3%) exhibited bilateral symptoms, i.e., 14 cases of TN, 3 of combined TN and HFS, and 2 of HFS. Twenty-two patients (1.5%) exhibited ipsilateral symptoms, i.e., 19 cases of TN and HFS and 3 of TN and glossopharyngeal neuralgia. Excluding three patients whose symptoms were associated with brain tumors or arteriovenous malformations, this patient group was older (63.2 versus 55.3 yr, P = 0.0009) and exhibited an increased percentage of associated hypertension (47.4 versus 17.5%, P = 0.000008), with a female predominance (86.8 versus 71.3%, P = 0.07), compared with the single HDS group. Thirty-six of these patients underwent a total of 61 microvascular decompression procedures, with favorable outcomes. The offending vessels were similar to those in single HDS, which were usually conventional and multiple. The associated etiological factors for vascular compression syndromes were more evident in the combined HDS group than in the single HDS group. Progressive arteriosclerotic vasculoarchitectural changes of the vertebrobasilar system, accelerated by aging and hypertension, bring about the development of combined HDS, with a remarkable female predominance.

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.

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.

EMG guided treatment of painful legs, moving toes wdith botulinum toxin A

To compare the electrophysiological excitability characteristics of the facial nucleus and related structures in hemifacial spasm (HFS), post-facial palsy synkinesis (PFPS) and facial myokymia (FM).Facial F-waves, blink reflex recoveries and magnetically elicited silent periods (SP) were prospectively studied in 17 HFS, 17 PFPS, 8 FM cases and in 13 controls. Earlier unpublished observations on abnormal impulse transmission in 36 HFS and 29 PFPS cases were also included.Enhanced F-waves were recorded on the symptomatic side in PFPS and HFS cases with a tendency to be more pronounced in PFPS. HFS and PFPS groups both showed an earlier blink reflex recovery, more prominent in PFPS patients, when stimulated and/or recorded on the symptomatic side. Unelicitable SPs were encountered after 24/39 stimulations in 5 patients with PFPS and rarely in HFS cases. Duration of elicitable SPs did not change remarkably. FM group had similar characteristics as normal controls in the 3 electrophysiological tests. Latencies of the lateral and synkinetic spread responses were significantly prolonged in the earlier PFPS group as compared to HFS. In two-point stimulation, both groups showed a greater latency shift in late responses, again more pronounced in PFPS.PFPS and HFS cases had similar enhanced excitability patterns at the facial nucleus and related brain-stem structures, more marked on the symptomatic side and more obvious in the PFPS group. Findings elicited in the FM group were thought to be caused by asynchronous hyperactivity of facial motoneurons.In this comparative electrophysiological study, similar excitability patterns were found in HFS and PFPS groups, albeit with different intensities.

Hemifacial spasm: evaluation and management options.

Vascular loop compression syndrome of the facial nerve is well documented as a cause of hemifacial spasm (HFS). These unilateral synchronous contractions of facial musculature are a cause of cosmetic defomity, social embarrassment and often mild facial weakness in longstanding cases. However, other documented causes of HFS include tumor infiltration, aneurysms, primary congenital cholesteatoma, herpes zoster oticus and primary facial nerve neuromas. Therefore, a knowledgeable diagnostic evaluation is necessary to avoid pitfalls of improper management. Advances in imaging techniques that aid in uncovering the etiology of HFS are reviewed. We now combine three modalities — computed tomography (CT), magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) — to avoid pitfalls in the management of this uncommon disabling condition. We also present 11 cases of hemifacial spasm; five patients did not have vascular loop compression as the underlying cause for their spasm.

Botulinum toxin: preferred treatment for hemifacial spasm.

This paper retrospectively analyses the clinical data of 65 consecutive cases of hemifacial spasm. A benign etiology was clinically evident in the majority of cases. Neuroradiologic investigation ruled out serious intracranial pathology in atypical cases. Trials of oral medication in 26 patients were consistently unsuccessful. Fifty-one patients had repeated lid and facial muscle injections of botulinum toxin during a period of 8 years. The mean duration of effective relief from spasm following an initial treatment was 18.9 weeks. This effect did not diminish with repeated injections.

Hemifacial spasm associated with a cerebellopontine angle arachnoid cyst in a young adult

There are no reported cases of hemifacial spasm associated with an arachnoid cyst in the literature. We report the first case of hemifacial spasm with an ipsilateral cerebellopontine angle arachnoid cyst in a 25-year-old man. The patient underwent evacuation of the arachnoid cyst by a partial membranectomy without any beneficial effect, and finally got rid of the hemifacial spasm by reexploration and microvascular decompression of the facial nerve. The operative findings and results revealed that the cyst produced deviation of the ipsilateral posterior inferior cerebellar artery, which was secondarily in contact with the root exit zone of the facial nerve.

Vestibular Nerve Injury as a Complication of Microvascular Decompression

Abstract We report a case of hemifacial spasm in which hearing was well preserved after microvascular decompression, but the vestibular nerve was injured selectively. We review the pathophysiological mechanisms relevant to this complication in the light of results of animal experimental studies we have conducted. In addition, we discuss the clinical significance of this particular type of cranial nerve injury.

Vestibular nerve injury as a complication of microvascular decompression

We report a case of hemifacial spasm in which hearing was well preserved after microvascular decompression, but the vestibular nerve was injured selectively. We review the pathophysiological mechanisms relevant to this complication in the light of results of animal experimental studies we have conducted. In addition, we discuss the clinical significance of this particular type of cranial nerve injury.

Arteries in contact with the cisternal portion of the facial nerve in autopsy cases: Mmicrosurgical anatomy for neurovascular decompression surgery of hemifacial spasm

The cisternal portion of the facial nerve and its contact arteries were examined anatomically in relation to neurovascular decompression surgery to treat hemifacial spasm. Thirty-five sides of brains from 20 autopsied adult patients were examined under a surgical microscope (× 5- × 25). One attaching point was found on 10 facial nerves, two points on 20 nerves, and three points on four nerves. More than two thirds of the facial nerves were attached at two points: the root exit zone and the distal cisternal portion. In a case of distal attachment, the contact artery formed an arterial-nerve complex with the distal portions of the facial and acoustic nerves. The arterial attachment at the root exit zone was evident on 24 of the 35 facial nerves (69%), and most of the contact arteries were the anterior inferior cerebellar artery and its branches. In five nerves, the root exit zone was attached at two points to arteries. The anatomy of autopsied brains without hemifacial spasm is not identical to that of actual clinical cases of hemifacial spasm; nevertheless, the results do aid in intraoperative anatomical orientations.

Botulinum A toxin treatment for eyelid spasm, spasmodic torticollis and apraxia of eyelid opening

Botulinum-A toxin (botAtox) was used in the treatment of blepharospasm (BS), idiopathic hemifacial spasm (HFS), idiopathic spasmodic torticollis (ST) and apraxia of eyelid opening (AEO). The injection of 7.5-30 U botAtox per eye spread over 3 or 4 sites in the palpebral part of orbicularis palpebrae (OP) reduced palpebral spasm in 12/13 cases of BS and in 7/8 cases of HFS. The effect lasted for 14.5 weeks on average (range 4-30 weeks). Palpebral ptosis (lasting 1-3 weeks) was the most frequent side effect (16/107 eyes treated) but was not related to dose of botAtox or number of inoculation sites. Injection of 60-160 U botAtox into the sternocleidomastoid, trapezius and splenius capitis muscles reduced ST objectively in 1/4 patients for about 4 weeks. In the other patients the reduction or abolition of the hypertrophy of the previous hyperactive muscles was accompanied by persistence or rearrangement of the dystonia pattern, suggesting a change in the pattern of activity of the neck muscles after botAtox. 5 U botAtox per eye spread over 4 sites in the OP significantly reduced the frequency of the episodes of involuntary eyelid closure in 2 patients with AEO but not BS. The therapeutic effect lasted for 7 months after the first treatment and for 8 months after the second in a 46 year old woman with a 6 month history while the second patient (72 year old parkinsonian) has now completed her 3rd month of treatment.

Baclofen in hemifacial spasm.

Six patients with idiopathic hemifacial spasm refractory to the usually employed medications were successfully treated with baclofen. Adverse side effects were found in only 1 patient (memory loss) which was controlled with administration of piracetam. We suggest that there is an association between stress and certain cases of hemifacial spasm and that such stress related cases may respond positively to baclofen.

Mechanism of Hearing Disturbance after Microvascular Decompression

In 35 posterior fossa operations with intraoperative brain-stem auditory evoked potential (BAEP) monitoring, there were seven microvascular decompression (MVD) operations performed for five cases of hemifacial spasm and two of trigeminal neuralgia. Among these seven patients, three cases, two of hemifacial spasm and one of trigeminal neuralgia, showed postoperative hearing disturbance. In these cases, intraoperative BAEPs showed aggravations of all waveform components including wave I. Otoneurological examinations revealed the hearing disturbances were caused not only by retrocochlear lesions but also by cochlear lesions. These findings suggest that postoperative hearing disturbance after MVD surgery is deeply related to circulatory disturbance of the internal auditory artery.

Intracranial microvascular decompression for "cryptogenic" hemifacial spasm, trigeminal and glossopharyngeal neuralgia, paroxysmal vertigo and tinnitus: I. Surgical technique and results.

Intracranial microvascular decompression was performed in 21 out of 24 patients with hyperactive dysfunction of cranial nerves: 8 cases of hemifacial spasm, 12 of trigeminal neuralgia, 3 of glossopharyngeal neuralgia and 1 case of paroxysmal vertigo and tinnitus. In 21 cases an abnormal vascular loop was found to impinge on the root entry zone of the nerve in the brainstem. Dissection of this loop with decompression of the nerve resulted in long-lasting relief of symptoms in all but two patients who presented early recurrence; in one of these a second procedure was eventually successful. In two patients with trigeminal neuralgia a benign tumor of the cerebellopontine angle that had escaped preoperative diagnosis was present. Finally, in one case no compressive lesions were found. From the data of the literature and from our present experience microvascular decompression can be considered a safe as well as an effective procedure, affording a high success rate in conditions often or usually resistant to medical treatment and erroneously considered "idiopathic".

Treatment of tic douloureux and hemifacial spasm by posterior fossa exploration: therapeutic implications of various neurovascular relationships.

A series of 152 posterior fossa explorations for tic douloureux and hemifacial spasm has been reviewed with assessment of outcome at the last follow-up examination. Among 103 cases of tic followed for an average of 48.3 months, 79 patients (77%) obtained good or excellent symptomatic relief, and there were 24 failures or recurrences (23%). Of 48 cases of hemifacial spasm followed for an average of 42.1 months, there were good or excellent results in 42 cases (87.5%); only 6 patients (12.5%) experienced failure or recurrence. Patients noted to have arterial contact at the 5th nerve entry zone responded significantly better to microvascular decompression than did patients with no arterial contact. Further, patients noted to have anatomical distortion of the 5th nerve by an artery or wedging of an artery into the crevice between the nerve and the pons had significantly better outcomes after microvascular decompression than did patients with other kinds of arterial contact. Partial sensory rhizotomy proved to be a highly effective alternative to microvascular decompression in cases of doubtful neurovascular compression. It was not possible to define similar neuroanatomical criteria predictive of response to microvascular decompression in patients with hemifacial spasm.

Treatment of Tic Douloureux and Hemifacial Spasm by Posterior Fossa Exploration: Therapeutic Implications of Various Neurovascular Relationships

Abstract A series of 152 posterior fossa explorations for tic douloureux and hemifacial spasm has been reviewed with assessment of outcome at the last follow-up examination. Among 103 cases of tic followed for an average of 48.3 months. 79 patients (77%) obtained good or excellent symptomatic relief, and there were 24 failures or recurrences (23%). Of 48 cases of hemifacial spasm followed for an average of 42.1 months, there were good or excellent results in 42 cases (87.5%); only 6 patients (12.5%) experienced failure or recurrence. Patients noted to have arterial contact at the 5th nerve entry zone responded significantly better to microvascular decompression than did patients with no arterial contact. Further, patients noted to have anatomical distortion of the 5th nerve by an artery or wedging of an artery into the crevice between the nerve and the pons had significantly better outcomes after microvascular decompression than did patients with other kinds of arterial contact. Partial sensory rhizotomy proved to be a highly effective alternative to microvascular decompression in cases of doubtful neurovascular compression. It was not possible to define similar neuroanatomical criteria predictive of response to microvascular decompression in patients with hemifacial spasm.

Hemifacial spasm: treatment by posterior fossa surgery.

Nine cases of hemifacial spasm have been treated by posterior fossa exploration without mortality or significant morbidity. In only three was definite pathology found, but the hemifacial spasm was abolished in eight patients and markedly diminished in the remaining patient. The condition has reccurred in one patient. Microsurgical techniques make the operation safe and accurate. We suggest that this procedure is the best approach for hemifacial spasm requiring treatment. Where no definite pathology is found, the effectiveness of the procedure is probably due to fibrosis and hence mild trauma to the facial nerve induced by the sponge wrapped around the nerve.