Cases reported "Hemifacial Spasm"

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1/50. Endovascular treatment of hemifacial spasm associated with a cerebral arteriovenous malformation using transvenous embolization: case report.

    OBJECTIVE AND IMPORTANCE: To illustrate that decompression of the facial nerve by transvenous endovascular treatment may relieve hemifacial spasm (HFS) caused by dilated veins. CLINICAL PRESENTATION: A 35-year-old man suffered severe chronic right HFS associated with a dilated right lateral mesencephalic vein lying in the vicinity of the facial nerve. This nonessential vein was recruited as a secondary collateral drainage from an inoperable left temporo-occipital arteriovenous malformation. INTERVENTION: The lateral mesencephalic vein was reached through the superior petrosal sinus using a transfemoral venous approach and was occluded with interlocking detachable coils (Target therapeutics, Freemont, CA). There was complete remission of HFS without recurrence after 2.5 years of follow-up. CONCLUSION: This case report supports vascular compression in the pathogenesis of HFS and suggests that facial nerve injury is not essential for the therapeutic effect of surgical decompression.
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2/50. Relationship between cochleovestibular disorders in hemifacial spasm and neurovascular compression.

    OBJECTIVE: To investigate the evolution of cochleovestibular symptoms before, during, and after microvascular decompression (MVD) of the facial nerve in hemifacial spasm. STUDY DESIGN: Prospective study in patients with hemifacial spasm. Among our 13 patients who underwent MVD of the facial nerve from 1995 to 1997, 6 had associated cochleovestibular disorders confirmed by neurotologic tests. RESULTS: In four of these patients, a concomitant compression of the eighth and facial nerves was found at surgery. Preoperative magnetic resonance angiography studies had shown three cases of this double neurovascular compression. Intraoperative auditory brainstem response monitoring showed that interposition of Teflon between vessel and facial nerve was highly critical to the auditory function. Auditory brainstem response monitoring was used to guide the surgeon during this critical phase. Surgery improved at least one cochleovestibular symptom in each patient. CONCLUSIONS: The authors propose two pathophysiologic hypotheses. First, the concomitant facial and cochleo-vestibular symptoms may be due to a hyperactivity of both the facial and vestibular nuclei. According to theories about cryptogenic hemifacial spasm, the origin of this hyperactivity could be an ectopic excitation focus. However, the two nerves may have different sites of ectopic excitation. According to the second hypothesis, a pulsatile compression of the facial nerve may be transmitted to the eighth nerve. This could take place even if only the facial nerve is in contact with a vascular loop.
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3/50. ependymoma of the fourth ventricle presenting with hemifacial spasm. Report of a case.

    According to Gardner's hypothesis (1962) later confirmed by Jannetta (1982, 1985), hemifacial spasm can usually be related to a "vascular conflict" which takes place inside the cerebellopontine angle (CPA). Occasionally, the causative lesion can be identified as a mass encasing the facial nerve at its root exit zone (REZ) from the brain stem. The hemifacial spasm has been rarely reported in presence of a contralateral CPA mass ("false localising sign"). hemifacial spasm in patients with masses in anatomical regions other than the CPA has to be considered exceptional. The case of an adult man harboring an ependymoma of the fourth ventricle whose only neurological sign was a left hemifacial spasm is reported. The rarity of such a condition prompted us to review the literature. Particular attention has been paid to the possible pathogenetic mechanisms and their therapeutic implications.
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4/50. 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.
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5/50. Postoperative oblique sagittal MR imaging of microvascular decompression for hemifacial spasm.

    Pre-operative and postoperative oblique sagittal gradient-echo magnetic resonance (MR) imaging was used to evaluate micro-vascular decompression of the facial nerves in 26 patients with hemifacial spasm. The pre-operative MR images were divided into two groups as follows: 22 images in Group I, clear imaging of a high-intensity line and/or spot at the root exit zone (REZ) of the facial nerve; and 4 in Group II, and unreliable image around the REZ. Surgery found that the causative vessel was the vertebral artery (VA) in 9 cases and the anterior inferior cerebellar artery (AICA) or the posterior inferior cerebellar artery (pica) in 13 cases in Group I, and the AICA or the pica in the 4 cases in Group II. Postoperative MR imaging showed clear decompression as the high-intensity line and/or spot completely separated from the REZ by a low- and/or iso- intensity area in 9 cases of VA compression repositioned to the petrous dura matter, in 11 cases of pica or AICA compression treated by shredded Teflon pledgets in Group I and in 3 cases in Group II. Postoperative MR imaging showed an incomplete separation of any high-intensity line and/or spot in the REZ in 2 cases of pica or AICA compression in Group I and in one in Group II. The outcome was excellent in 22 of 23 cases with clear decompression, and in 1 of 3 cases of unclear decompression. hemifacial spasm persisted in 3 cases. Oblique sagittal gradient-echo MR imaging is a useful method for postoperative follow-up which can demonstrate changes around the REZ of the facial nerve if hemifacial spasm recurs.
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6/50. The treatment with alendronate in hemifacial spasm associated with Paget's disease of bone.

    The association of Paget's disease of bone and hemifacial spasm has rarely been reported. hemifacial spasm is often associated with compression of the facial nerve by a vascular loop at the point where the nerve leaves the brainstem before traversing the cerebellopontine angle. It is believed that narrowing of the cerebellopontine angle cistern caused by Paget's disease increases the chance of vascular compression of the facial nerve. Whilst specific antipagetic therapy such as calcitonin has been used with good response in hemifacial spasm associated with Paget's disease, the usefulness of the newer bisphosphonates is not clear. A 65-year-old woman with hemifacial spasm associated with Paget's disease was treated with alendronate, and the hemifacial spasm became very infrequent 4 months after commencement of the therapy.
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7/50. hemifacial spasm caused by a contralateral vertebral artery: case report.

    BACKGROUND: hemifacial spasm is usually caused by compression of the facial nerve by ipsilateral blood vessels. Compression of the facial nerve root exit zone by a contralateral tortuous vertebral artery is very rare. methods: This 68-year-old woman presented with left-sided hemifacial spasm and was found to have compression of the left facial nerve by the tortuous vertebrobasilar artery, as revealed by magnetic resonance imaging and magnetic resonance angiography. Retromastoid craniectomy demonstrated compression of the left facial nerve root exit zone by the distal portion of the right vertebral artery. The vertebrobasilar junction and both vertebral arteries were moved laterally from the facial nerve and a muscle implant was interposed between the brainstem and the right vertebral artery. RESULTS: The patient has remained free of hemifacial spasm for a follow-up period of 27 months. CONCLUSIONS: Compression of the facial nerve by the contralateral tortuous vertebral artery may produce hemifacial spasm. A transposed large vessel can be secured by a sling technique or by interposing a soft implant between the brainstem and the vertebral artery.
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8/50. Remission of hemifacial spasm after proximal occlusion of vertebrobasilar dissecting aneurysm with coils: case report.

    intracranial aneurysm is a rare cause of hemifacial spasm and most of the previously reported cases are treated with surgical microvascular decompression. Authors report a case of hemifacial spasm caused by a dissecting aneurysm located at the vertebrobasilar junction which improved after endovascular obliteration of the affected vertebral artery with coils.The patient was a 69-year-old man with 20 months' history of left hemifacial spasm. A vertebral angiogram showed an irregular dilatation of the right vertebral artery associated with aneurysmal dilatation at the vertebrobasilar junction. Endovascular obliteration of the abnormally dilated right vertebral artery proximal to the vertebrobasilar junction was performed. The hemifacial spasm gradually improved after the embolisation and disappeared 6 months later. Endovascular proximal obliteration of the vertebral artery may have changed the hemodynamic force inside the aneurysm and eliminated the vascular compression at the root exit zone of the facial nerve.
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9/50. hemifacial spasm due to cerebellopontine angle meningiomas--two case reports.

    A 54-year-old female and a 49-year-old female presented with complaints of hemifacial spasm. Both patients underwent surgery to remove cerebellopontine angle meningiomas. In one case, no vascular compression was observed at the root exit zone. The tumor was removed subtotally leaving residual tumor adhered to the lower cranial nerves. The hemifacial spasm disappeared immediately after the operation. The residual tumor was treated using gamma knife radiosurgery. In the other case, the root exit zone of the facial nerve was compressed by both the tumor and anterior inferior cerebellar artery and the tumor was removed totally. Postoperatively, the hemifacial spasm disappeared, but the patient suffered facial nerve paresis and deafness that was probably due to intraoperative manipulation. However, the facial nerve paresis gradually improved. cerebellopontine angle meningioma with hemifacial spasm must be treated by surgical resection limited to preserve cranial nerve function. Subtotal removal with subsequent radiosurgery to treat the remaining tumor tissue is one option for the treatment of cerebellopontine angle meningioma.
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10/50. Therapeutic considerations in cerebellopontine angle lipomas inducing hemifacial spasm.

    lipoma is a very rare tumour at the cerebellopontine angle. We report a case of incomplete hemifacial spasm, associated with a lipoma involving and compressing both facial and acoustic nerves at their origin in the brainstem. The patient was treated with medical therapy (botulinum toxin A) and surgery. We present a review of the last ten years of the literature, with particular regard to management.
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