Cases reported "Facial Nerve Diseases"

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1/7. hemifacial spasm caused by pontine glioma: case report and review of the literature.

    hemifacial spasm (HFS) is an involuntary paroxysmal contractions of the facial musculature, caused generally by vascular compression of the seventh cranial nerve at its root exit zone from the brain stem. The case of an adult man harbouring brain stem glioma (BSG) whose only neurological signs were left HFS and mild facial weakness is reported. Radiological and neurophysiological findings are described. No responsible vessel could be identified during surgery, but the causative lesion was found to be an astrocytic tumour encasing the facial nerve at its root exit zone from the brain stem. The rarity of such a condition prompted us to review the literature. Nine cases, including our patient presenting with HFS caused by BSG, are reviewed.
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2/7. Hemorrhagic acoustic schwannoma: radiological and histopathological findings.

    A 49-year-old man on anticoagulation treatment with phenprocoumon presented with acute right sided 7th and 8th cranial nerve palsy, acute hearing loss, headache, vertigo, and vomiting. CT and MRI revealed a cerebellopontine angle tumor 15mm in diameter and acute intratumoral hematoma. A cellular schwannoma composed predominantly of Antoni A tissue with dilated thin-walled vessels, surrounded by old hemorrhage with hemosiderin-laden macrophages was found histologically.
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3/7. hemifacial spasm caused by a venule: case report.

    The syndrome of hemifacial spasm occurs as a consequence of compression, almost universally by blood vessels, of the root entry zone of the facial nerve. The vascular compression is usually obvious at operation, but may be subtle. The author describes a case in which a venule running in an anterior-posterior direction across the caudal aspect of the root entry zone of the facial nerve, which was thought to be causing the spasm, was coagulated and divided. A small, more distal arteriole, probably not contributory, was decompressed away from the nerve. After operation, the patient improved gradually, and she remains free of facial spasm or weakness. This is the most subtle vascular compression seen by the author and his colleagues in over 400 microvascular decompressions for hemifacial spasm.
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4/7. hemifacial spasm in childhood and adolescence.

    hemifacial spasm (HFS), a hyperactive dysfunction of the facial nerve, is rarely seen in young people. Between 1984 and 1994, we treated 924 patients with HFS by microvascular decompression at our institution. Of these, 8 (0.9%) were younger than 30 years. In most of the older patients with HFS, the offending artery which compresses the root exit zone was elongated, redundant, and focally arteriosclerotic as a result of hemodynamic effects due to aging or hypertension. On the other hand, the offending artery did not exhibit such characteristic changes of the vasculature in children and adolescents with HFS. In all of the young patients who underwent initial microvascular decompression at our clinic, the arachnoid membrane around the facial nerve was thickened and encased the artery, resulting in compression of the root exit zone of the facial nerve. Such thickening of the arachnoid surrounding the offending vessel may play an important role in the pathogenesis of HFS by trapping and encasing the artery to compress the root exit zone, particularly in the young patients.
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5/7. 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.
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6/7. hemifacial spasm caused by vascular compression of the distal portion of the facial nerve. Report of seven cases.

    It is generally accepted that hemifacial spasm (HFS) and trigeminal neuralgia are caused by compression of the facial nerve (seventh cranial nerve) or the trigeminal nerve (fifth cranial nerve) at the nerve's root exit (or entry) zone (REZ); thus, neurosurgeons generally perform neurovascular decompression at the REZ. Neurosurgeons tend to ignore vascular compression at distal portions of the seventh cranial nerve, even when found incidentally while performing neurovascular decompression at the REZ of that nerve, because compression of distal portions of the seventh cranial nerve has not been regarded as a cause of HFS. Recently the authors treated seven cases of HFS in which compression of the distal portion of the seventh cranial nerve produced symptoms. The anterior inferior cerebellar artery (AICA) was the offending vessel in five of these cases. Great care must be taken not to stretch the internal auditory arteries during manipulation of the AICA because these small arteries are quite vulnerable to surgical manipulation and the patient may experience hearing loss postoperatively. It must be kept in mind that compression of distal portions of the seventh cranial nerve may be responsible for HFS in cases in which neurovascular compression at the REZ is not confirmed intraoperatively and in cases in which neurovascular decompression at the nerve's REZ does not cure HFS. Surgical procedures for decompression of the distal portion of the seventh cranial nerve as well as decompression at the REZ should be performed when a deep vascular groove is noticed at the distal site of compression of the nerve.
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7/7. Atypical hemifacial spasm.

    Among 155 cases of hemifacial spasm (HFS), the authors found two cases of atypical HFS (1.3%) in which spasm started with the orbicularis oris and buccinator muscles, and gradually spread upward to involve the orbicularis occuli muscle, whereas the reverse process is usually seen in cases of typical HFS. The compression site in cases of atypical HFS is the posterior/rostral aspect of the facial nerve (FN), whereas it was the anterior/caudal aspect of the FN in all cases of typical HFS except for one. The meatal loop of the anterior inferior cerebellar artery (AICA) compressed the FN when the vessel passed between the FN and the eighth cranial nerve (8th N). These findings suggest that the topographical organization in the FN in the cerebellopontine cistern may be reversed to a peripheral distribution: the fibres on the posterior/rostral side of the FN innervate the lower part of the facial muscles, and those in the anterior/caudal side of the nerve innervate the upper part of the facial muscles. When examining patients with HFS, we must very carefully determine whether patients have typical or atypical HFS, to determine whether blood vessels (usually the meatal loop of the AICA) between the FN and the 8th N as well as at the root exit zone of the FN are to be decompressed.
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