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At least 1,351 records · Page 75Linked to original sources
PubMed1997

Costs of treating dystonias and hemifacial spasm with botulinum toxin A.

Botulinum toxin (BTX) has become a safe and effective therapeutic tool in the treatment of a variety of neurological disorders, especially dystonias. One major disadvantage, however, is the high cost of a single injection of BTX. In this study of 835 patients, we calculated the cost of treatment with BTX serotype A (BTX-A) for different dystonias and hemifacial spasm. The annual expenditure per patient for BTX-A injections in this cohort totalled (mean +/- standard deviation) 1030 Deutschmarks (DM) [1996 values] +/- DM610 [$US570 +/- $US340; 230 +/- 130 pounds sterling (Pound)] for blepharospasm (n = 158), DM1450 +/- DM1520 ($US800 +/- $US830; 310 Pounds +/- 280 Pounds) for craniocervical dystonia (n = 148), and DM1480 +/- DM780 ($US810 +/- $US430; 330 Pounds +/- 180 Pounds) for oromandibular dystonia (n = 16), while the treatment of cervical dystonia consumed DM4590 +/- DM2060 ($US2520 +/- $US1130; 960 Pounds +/- 420 Pounds) [n = 362] per patient. In order to alleviate symptoms in patients with hemifacial spasm (n = 151), DM510 +/- DM270 ($US280 +/- $US150; 110 Pounds +/- 60 Pounds) had to be spent annually. The expenses for surgical therapy for cervical dystonia were DM10,120 +/- DM1900 (n = 54). No major differences concerning expenditure could be found in this study between the 2 available preparations of BTX. However, there appeared to be a lower rate of adverse effects with the Botox formulation, compared with the Dysport formulation, of BTX-A (this difference was statistically significant, i.e. p < 0.001). Although the cost of an individual injection is high, other cost factors also substantially contribute to the societal costs of adult-onset dystonias. Some of these costs may be attenuated with the use of BTX. The subjective and objective relief of these socially devastating and sometimes painful conditions rewards the expenditure associated with the use of BTX-A.

Adult↗
PubMed1991

Arteriovenous malformation in the cerebellopontine angle presenting as hemifacial spasm--case report.

A 64-year-old female was admitted with a 6-year history of right hemifacial spasm. Neurological examination and precontrast computed tomographic (CT) scanning showed no abnormality. Vertebral angiography disclosed, however, a small arteriovenous malformation (AVM) in the right cerebellopontine angle. A postcontrast CT scan demonstrated a high-density area in the right cerebellomedullary junction which appeared as a flow-void signal on magnetic resonance images. A right retromastoid craniectomy was performed to separate an enlarged and tortuous loop of the right anterior inferior cerebellar artery from the right facial nerve using a Teflon-felt sheet. The AVM was not excised. Postoperatively, she was completely free of hemifacial spasm.

Cerebellopontine Angle↗
PubMed1991

Hemifacial spasm caused by CP angle AVM associated with ruptured aneurysm in the feeding artery--case report.

A 66-year-old male presented with clinical features of hemifacial spasm. Cerebral angiograms disclosed an arteriovenous malformation (AVM) in the cerebellopontine angle. The hemifacial spasm was caused by a dilated feeding artery of the AVM compressing the facial nerve at the root exit zone. Surgery was not initially performed because of his age and absence of AVM rupture. However, the AVM was associated with a small aneurysm in the feeding artery, which rapidly grew during 20 days after discharge and ruptured causing subarachnoid hemorrhage. The aneurysm was clipped and the feeding artery of the AVM partially obliterated. Careful angiographic examination for associated aneurysms and consequent surgical obliteration to prevent hemorrhage are suggested in cases of AVM.

Aged↗
PubMed1995

Hemifacial spasm in Albright's hereditary osteodystrophy with pseudopseudohypoparathyroidism and nephrogenic diabetes insipidus--case report.

A 30-year-old male with Albright's hereditary osteodystrophy, pseudopseudohypoparathyroidism, and nephrogenic diabetes insipidus presented with hemifacial spasm persisting for 2 years. This association is extremely unusual. Angiography revealed markedly tortuous carotid and vertebral arteries inconsistent with his age. Neurovascular decompression of the left vertebral artery achieved only partial resolution of the spasm.

Adult↗
PubMed1996

Turbo spin-echo magnetic resonance imaging depiction of facial nerve compression by a vertebral artery in a patient with hemifacial spasm--technical note.

Turbo spin-echo magnetic resonance (MR) imaging of a patient with hemifacial spasm clearly demonstrated vascular compression of the facial nerve by the vertebral artery. The high resolution images of this method may be an appropriate alternative to preoperative cerebral angiography. Turbo spin-echo MR imaging is a diagnostic procedure of choice for patients with hemifacial spasm and possibly trigeminal neuralgia.

Adult↗
PubMed1980

Radiography of trigeminal neuralgia and hemifacial spasm.

Radiographic findings in 68 patients with trigeminal neuralgia and 24 patients with hemifacial spasm are reviewed. The relative value of various radiographic diagnostic procedures is discussed. Trigeminal neuralgia and hemifacial spasm are usually caused by vascular compression of the trigeminal root entry zone and facial nerve exit zone respectively. Computed tomography (CT) of the posterior fossa is the only radiographic screening procedure required. Angiography should be reserved for patients in whom CT findings suggest an aneurysm or tumor.

Adult↗
PubMed2003

Angiographic manifestations and operative findings with 70 cases of hemifacial spasm: relation of common trunk anomalies.

The relations between angiographic manifestations and operative findings of hemifacial spasm were studied in 70 cases between 1988 and 2001. Vertebral angiography was performed, and Towne, straight AP, and lateral projections were routinely examined. The dominant anterior inferior cerebellar artery (AICA) directly compressed the facial nerve root exit zone in 26 cases, the dominant posterior inferior cerebellar artery (PICA) in 20, the AICA in 13, the PICA in 2, and the vertebral artery (VA) in 9. Compression by multiple vessels was observed in 11 cases. Anatomical variations of the affected AICA and PICA were classified into 3 groups according to their origins and distributions of blood supply: normal distribution of AICA and PICA in 18%, common trunk anomaly with dominant AICA (basilar artery origin) in 48% and common trunk anomaly with dominant PICA (vertebral artery origin) in 34%. Analyses of the angiograms revealed significantly increased numbers of common trunk anomalies compared with cases with normal angiograms. In 18 of the 20 cases of unilateral common trunk anomalies, facial nerves were compressed by the dominant artery. Preoperative vertebral angiograms may clarify the offending vessels and their sites in most hemifacial spasm cases, thus increasing the safety of surgical interventions.

Adult↗
PubMed1985

Audiometric abnormalities in hemifacial spasm.

One-hundred forty-three patients with hemifacial spasm (HFS) as a primary disorder were evaluated pre- and postoperatively by pure-tone and speech audiometry, determination of thresholds for the acoustic middle ear reflex, and recording of auditory brainstem responses. We found an unusual 'notch' in the pure-tone audiograms of 16 patients (11%) and a low-frequency up-sloping pure-tone threshold in another 17 patients (12%). Because such abnormalities occur rarely, it may be assumed that they are related to these patients' primary disorder. All of the patients underwent microvascular decompression to relieve their spasms, and it was confirmed during surgery that in all patients the seventh cranial nerve was compressed at its root entry zone by vascular structures. It is therefore assumed that the abnormality of pure-tone threshold function noted in 23% of the patients with HFS was caused by compression of the auditory nerve by the same vessel as that which compressed the facial nerve. Since the changes in the pure-tone threshold occurred in the mid- and low-frequency range, it is assumed that low-frequency fibers constitute the outer part of the auditory nerve at its entrance into the human brainstem.

Audiometry, Pure-Tone↗
PubMed1987

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.

Adult↗
PubMed1976

Segmental arterial spasm in patients with total brain infarction.

An arteriographic investigation has shown that segmental spasm occurs in a relatively high frequency of patients with total brain infarction (12 of 30), and if spasm at the origin of arterial branches is included, the frequency is still higher (19 of 30). The phenomenon is possibly a sign of changed sympathetic tone, the pathophysiological significance of which is discussed.

Adolescent↗
PubMed1976

Cerebral arterial spasm. Part 5: in vitro contractile activity of vasoactive agents including human CSF on human basilar and anterior cerebral arteries.

In vitro experiments were performed with a small volume chamber to determine the contractile activity of various vasoactive agents on human basilar and anterior cerebral arteries. Cumulative log-dose response curves were obtained for most of the agents tested including serotonin and three different prostaglandins; many of these curves were found to be similar to curves previously obtained with canine cerebral arteries. It was concluded from these similarities that canine cerebral arteries are a good in vitro model for studying human cerebral arterial spasm. It was also demonstrated that human cerebrospinal fluid, collected up to 17 days after a subarachnoid hemorrhage from patients with clinical and angiographic evidence of cerebral arterial spasm, would cause large, dose-dependent contractions in human anterior cerebral arteries.

Adolescent↗
PubMed1994

Coexistent trigeminal neuralgia, hemifacial spasm, and hypertension: preoperative imaging of neurovascular compression. Case report.

The case is reported of a 60-year-old woman with left-sided trigeminal neuralgia, hemifacial spasm, and hypertension. Compression of the left trigeminal, facial, and vagus nerves by the anterior and posterior inferior cerebellar arteries and a persistent trigeminal artery variant were demonstrated by magnetic resonance angiography using a novel sequence. At operation the angiographic appearances were confirmed, and decompression was performed with the placement of polyvinyl sponge at all three levels. Postoperatively, the patient had complete relief from the trigeminal neuralgia and hemifacial spasm and has sustained normotension without medication.

Arteries↗
PubMed1996

Trigeminal neuralgia and hemifacial spasm as false localizing signs in patients with a contralateral mass of the posterior cranial fossa. Report of three cases.

Trigeminal neuralgia and hemifacial spasm were false localizing signs in three patients with contralateral space-occupying mass lesions in the posterior cranial fossa. According to radiological observations, the brainstem was remarkably displaced and distorted toward the side contralateral to the mass in all three cases. In the two cases with trigeminal neuralgia, the fifth cranial nerve was embedded in a thick arachnoid membrane and strongly compressed and angulated between the brainstem and the petrous bone, but there was no apparent vascular involvement. In the case with hemifacial spasm, only the contralateral tumor was removed. Postoperatively, all three patients experienced complete cessation of the symptoms without recurrence. Based on the operative findings, the authors postulate that angulation and distortion of the axis of the cranial nerve due to the contralateral mass, accompanied by thickening of the arachnoid membrane around the nerve, play an important role in false localizing signs, particularly in patients with trigeminal neuralgia.

Adult↗
PubMed1996

Hemifacial spasm caused by a venous angioma. Case report.

The authors describe the case of a 53-year-old woman who suffered from a hemifacial spasm caused by a venous angioma in the posterior fossa. At operation the parenchymal segment of the angioma was preserved and vascular decompression was performed by placing pieces of shredded Teflon between the vessel and nerve. After decompression the patient was completely free from spasm.

Cerebral Angiography↗
PubMed1998

Neurovascular decompression of the eighth cranial nerve in patients with hemifacial spasm and incidental tinnitus: an alternative way to study tinnitus.

OBJECT: The authors sought to clarify the clinical characteristics of tinnitus resulting from neurovascular compression (NVC) of the eighth cranial nerve. METHODS: The authors explored the eighth cranial nerve in the cerebellopontine cistern during neurovascular decompression (NVD) of the facial nerve in 10 patients with hemifacial spasm who suffered from incidental tinnitus on the same side. The diagnosis of NVC of the eighth cranial nerve was confirmed in all patients. This condition was found in only seven of 114 patients with hemifacial spasm alone, indicating that NVC of the eighth cranial nerve is one of the causes of tinnitus (p < 0.001, chi-square test). The tinnitus resolved or was markedly improved after NVD of the eighth cranial nerve in eight patients (80%). Both pulsatile and continuous tinnitus responded well to NVD. All patients experienced various degrees of sensorineural hearing disturbance, but other neurotological examinations provided poor diagnostic value. CONCLUSIONS: It is the authors' opinion that sensorineural hearing loss and positive findings on magnetic resonance imaging are the most reliable evidence for the presence of tinnitus caused by NVC of the eighth cranial nerve.

Adult↗
PubMed2002

Hemifacial spasm associated with an ependymal cyst in the cerebellopontine angle. Case report.

No previous case of hemifacial spasm associated with an ependymal cyst has been reported in the literature. In this article the authors report the first case in which hemifacial spasm accompanied an ipsilateral cerebellopontine angle ependymal cyst in a 27-year-old woman. Cyst fenestration and arterial decompression of the facial nerve at the root exit zone resulted in complete resolution of the patient's symptoms. A histopathological study including immunohistochemical methods identified an ependymal cyst.

Adult↗
PubMed2005

Monitoring of facial muscle motor evoked potentials during microvascular decompression for hemifacial spasm: evidence of changes in motor neuron excitability.

OBJECT: Hemifacial spasm (HFS) is thought to be due to a hyperactive facial motor nucleus consequent to chronic neurovascular contact. The lateral spread (LS) response is presumed to reflect changes in facial motor neuron excitability. Facial muscle motor evoked potentials (MEPs) use the same efferent pathway as LS, therefore the authors speculated that these potentials should reflect differences consistent with changes at the facial motor nucleus level. METHODS: Monitoring of LS and bilateral facial MEP was performed in 10 consecutive patients undergoing MVD for HFS. Ipsilateral facial MEPs were monitored in 17 patients undergoing MVD for trigeminal neuralgia (TN). Latency, amplitude, and duration of the MEPs were compared before and after MVD. Following MVD the duration of ipsilateral MEPs decreased from 17.6 +/- 1.2 to 7.6 +/- 0.7 msec and their amplitude decreased from 269.9 +/- 66.3 to 76.5 +/- 26.2 microV (p < or = 0.01). These changes were consequent to the abolition of LS in eight of 10 patients and an approximately 50% reduction in two patients. The relationship between the reduction in MEPs and changes in LS was significant (p < 0.01). Control facial muscle MEPs (nonspastic side in patients with HFS and in those with TN) did not change significantly during the MVD procedure. Spasms were alleviated in nine of 10 patients, and there was no indication of facial nerve damage intraoperatively or postoperatively. CONCLUSIONS: Facial muscle MEPs represent a novel tool for studying the neurophysiological mechanisms of HFS in particular and monitoring the facial nerve in general. Data in this study support the hypothesis that the development of HFS and its alleviation with MVD are related to changes in facial motor nucleus activity.

Case-Control Studies↗