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At least 1,351 records · Page 75Linked to original sources
PubMed1991

Intraoperative facial nerve monitoring: prognostic aspects during acoustic tumor removal.

Intraoperative facial nerve monitoring with electrical stimulation (IFNMES) has become an integral part of acoustic tumor surgery. We reviewed the records of fifty-six patients who underwent translabyrinthine acoustic tumor removal with IFNMES. There was excellent correlation between intraoperative facial nerve activity and immediate postoperative facial nerve function (24 hours after surgery and at hospital discharge). Our data would suggest that patients who exhibit less than 500 microvolts of ongoing EMG activity during surgery, and who yield at least a 500-microvolt contraction when stimulated with 0.05 milliamps at the brainstem after tumor removal, can expect an excellent immediate facial nerve result (grade I or II).

Ear Neoplasms↗
PubMed1991

Facial nerve monitoring in acoustic tumor surgery.

Anatomic and functional preservation of the facial nerve during acoustic tumor surgery remains a primary goal. Intraoperative electromyographic facial nerve monitoring with auditory feedback has enabled the surgeon to more readily achieve this goal. We compared a group of monitored translabyrinthine acoustic tumor removals (N = 89) to a similar unmonitored group (N = 155) in regard to facial nerve function. Function was assessed immediately postoperatively, at time of discharge, and at 1 year postoperatively using the House six-point scale. Results were grouped as satisfactory, intermediate, or poor and were analyzed by tumor size. Facial nerve results were better at all time intervals in the monitored groups, although the difference was not statistically significant at the 1-year interval. There was no difference between monitored and unmonitored patients in the subgroups with tumors smaller than 2.5 cm in diameter. This study supports the usefulness of intraoperative facial nerve monitoring in improving facial nerve results, particularly in larger tumors.

Adult↗
PubMed1991

Facial nerve stimulation with cochlear implantation. VA Cooperative Study Group on Cochlear Implantation.

The course of the facial nerve may place it within the current field generated by an activated cochlear implant to produce incidental facial movement. We investigated the presence of facial nerve stimulation associated with cochlear implants in the VA Cooperative Study of Advanced Cochlear implants. Twelve of 82 patients enrolled in this study demonstrated facial nerve stimulation within 2 years of implant activation. Facial nerve stimulation in six patients with multiple channel implants (Nucleus or ineraid devices) either resolved spontaneously (n = 2), or was eliminated by deactivating basal (n = 2) or apical (n = 2) electrodes. Two of six patients with single-channel electrodes (3-M/Vienna devices) demonstrated facial nerve stimulation that resolved spontaneously (n = 2), resolved with lowering current output (n = 2), or was refractory to processor adjustment (n = 2). Intraoperative assessment in one of the refractory cases indicated that facial nerve stimulation resulted from current spread through the modiolus to activate the facial nerve. A variety of factors, including implant design, stimulus parameters, and local tissue impedances, may interact to produce incidental facial stimulation. Low-impedance pathways between the scala tympani and the modiolus may deserve increased recognition as an interactive factor in cochlear implant performance.

Adult↗
PubMed1979

Facial myokymia with polyradiculoneuropathy.

Two patients had bilateral facial myokymia in association with polyradiculoneuropathy. Characteristic electromyographic findings allow polyradiculoneuropathy to be differentiated from other causes of facial movements, and support the possibility that extraaxial facial nerve involvement is another cause of facial myokymia.

Adult↗
PubMed1983

Focal facial spasm.

An unusual case of focal facial spasm modified by factors affecting the peripheral facial nerve was investigated in a 32-year-old woman with involuntary contractions at the left mouth and nasal area. Voluntary facial movements were normal. The involuntary spasms ceased with digital pressure over the facial nerve in the left stylomastoid area. A difference between voluntary and these involuntary facial movements occurred both with local anesthetic blockade and with crushing of the facial nerve. Blink reflexes demonstrated unilateral left synkinesis, and facial EMG showed clonic discharges and individual motor units that discharged rapidly (200 Hz). Treatment with diphenylhydantoin, carbamazepine, and prednisone was ineffective. Neurolysis of the peripheral facial nerve resulted in temporary relief, whereas biofeedback controlled the spasms. Focal facial spasms may represent a disorder of the facial nucleus influenced by both peripheral and central mechanisms.

Adult↗
PubMed1984

Tic convulsif, the combination of geniculate neuralgia and hemifacial spasm relieved by vascular decompression.

A patient had combined otalgia and intractable unilateral facial spasm, relieved by microsurgical vascular decompression of the seventh and eighth cranial nerve complex in the cerebellopontine angle without section of the intermediate nerve. A dolicho-ectatic anterior inferior cerebellar artery compressed the seventh and eighth cranial nerves complex, suggesting that vascular compression of the intermediate nerve or of the sensory portion of the facial nerve may cause geniculate neuralgia. "Tic convulsif" seems to be a combination of geniculate neuralgia and hemifacial spasm. This combination could be due to vascular compression of the sensory and motor components of the facial nerve at their junction with the brainstem.

Adult↗
PubMed1984

Miller Fisher syndrome: clinical and electrophysiologic evidence of peripheral origin in 10 cases.

Clinical and electrophysiologic data recorded in patients with Fisher syndrome characterized by ophthalmoplegia, ataxia, and areflexia are presented. Cases with limb weakness or pleocytosis in the CSF were excluded, according to Fisher. Ten patients were selected. All had hand and foot numbness. A large amount of protein without cell reaction was found during the third week of illness in serial CSF examinations. EMGs showed very slight limb involvement without spontaneous activity, and in most cases, facial muscles exhibited a denervation pattern. Distal motor nerve conduction velocity on limbs and F wave latencies were normal, whereas the sensory nerve action potentials were altered in all but one case when tested (seven out of eight cases). By means of blink reflex study performed in four patients, no significant pattern of brainstem dysfunction was discovered. The authors discuss the preeminent role of peripheral nerve lesions with regard to the ataxia and ophthalmoplegia.

Adolescent↗
PubMed1985

Vascular compression, hemifacial spasm, and multiple cranial neuropathy.

Hemifacial spasm is usually an isolated symptom resulting from facial nerve root compression. Three patients had, in addition, tinnitus, hearing loss, facial sensory loss, diminished gag reflex, dysphagia, and dysarthria. Acoustic reflexes were abnormal, and facial nerve conduction studies showed evidence of ephaptic transmission and ectopic excitation. Brain CT and metrizamide cisternography were normal. Surgical exploration showed compression of cranial nerve roots by posterior inferior cerebellar artery branches. After decompression, symptoms abated, and electrical signs of hemifacial spasm disappeared. Vascular compression of nerve roots in the cerebellopontine recess may cause multiple cranial neuropathy.

Aged↗
PubMed1983

Early correction of orbicularis oculi paralysis with an encircling silicone prosthesis.

Fifteen patients with paralysis of the 7th and 5th nerves or the 7th nerve alone were treated with an encircling silicone prosthesis. There has been no serious ocular complication observed over the last 3 years. The prosthesis has been removed in 9 of the 15 patients in whom good 7th nerve recovery has occurred. In the remaining 6 patients, the prosthesis is being well tolerated.

Cranial Nerve Diseases↗
PubMed1984

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.

Brain Stem↗
PubMed1984

Contralateral trigeminal nerve dysfunction as a false localizing sign in acoustic neuroma: a clinical and electrophysiological study.

A 49-year-old woman presented with right facial sensory impairment due to trigeminal nerve dysfunction caused by a contralateral acoustic neuroma. The mechanism of the falsely localizing trigeminal involvement is probably displacement and distortion of the brain stem by the large mass lesion and not increased intracranial pressure. A preoperative orbicularis oculi reflex study was abnormal and indicative of right trigeminal nerve dysfunction; after surgical removal of the tumor, the orbicularis oculi reflex study was normal. We conclude that a false localizing sign of trigeminal nerve dysfunction can occur rarely on the contralateral side in patients with large posterior fossa tumors, especially tumors arising from the cerebellopontine angle, and should be considered in the differential diagnosis of hemifacial sensory disturbance.

Brain Diseases↗
PubMed1987

Hemifacial spasm in young people treated with microvascular decompression of the facial nerve.

Hemifacial spasm (HFS) in childhood is extremely rare. Two patients with HFS in childhood and eight adults who had the onset of HFS before the age of 20 were treated with microvascular decompression of the facial nerve at the nerve root entry zone. The two children were both girls and had typical HFS on the right side. Of the eight adults, five were men and three were women. Six had typical and two had atypical HFS. Six had HFS on the left side, and two had HFS on the right. Vascular cross compression was found at the nerve root entry zone in all cases. The average follow-up period was 7.3 years (range, 1 1/2 to 11 years). All but one patient had complete relief of their HFS immediately or after delay. In one adult, the compressing artery could not be decompressed without damaging the nerves. One adult patient had two recurrences 1 year after the first operation and 6 months after the second; this patient had complete relief after a third operation. Complications included temporary mild facial weakness in four patients and moderate hearing impairment in the patient who had three operations. These results are comparable to those of HFS of adult onset. Microvascular decompression is recommended as the treatment of choice for HFS during childhood.

Adolescent↗
PubMed1995

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.

Adolescent↗
PubMed1995

Hemifacial spasm resulting from cerebellopontine angle lipoma: case report.

A case of hemifacial spasm associated with a cerebellopontine angle lipoma is described. Both the seventh and the eighth cranial nerves were incorporated and distorted within this tumor, which seemed to be the cause of hemifacial spasm and other cranial nerve dysfunctions, but obvious vascular elements were not included. To identify a cerebellopontine angle lesion as a lipoma is very important in surgical management. Magnetic resonance imaging is essential to the differential diagnosis of the cerebellopontine angle lesion.

Aged↗