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We describe a patient presented with sequential events of hemifacial spasm, cerebral infarction and fatal subarachnoid hemorrhage. All of them are seemingly separate entities. Radiological examination revealed that the cause was vertebrobasilar dolichoectasia (VBD) coexisting with a giant saccular
Two cases of hemifacial spasm received microvascular decompression. Both of them had histories of hypertension and coronary insufficiency. The two cases died on the 12th postoperative day because of cerebrovascular accident. We think that the death was associated with the poor facilities,
Botulinum toxin type A (BTX-A) has been used to treat several neurological conditions such as sialorrhea, hyperhydrosis, dystonia, hemifacial spasm, spasticity and pain. Although spasticity has been successfully treated with BTX-A, few are the authors studying the use of BTX-A to treat shoulder pain
BACKGROUND
Hemifacial spasm (HFS) is caused by vascular compression of the VII cranial nerve at its root exit zone from the brainstem. Microvascular decompression (MVD) is the only treatment option that offers the prospect of a definitive cure for HFS. We conducted the first systematic review on the
Hemifacial spasm (HFS) is frequently caused by vascular compression of the facial nerve. Vertebrobasilar dolichoectasia (VBDE) may cause vascular crowding in the limited space of the posterior fossa, increasing the chance of vascular compression of the facial nerve. We investigated the prevalence of
: Microvascular decompression (MVD) is curative treatment for primary Hemifacial Spasm, in cases where a vascular loop impinges on the facial nerve. Surgical techniques for MVD may be extended to MVD of the glossopharyngeal nerve and trigeminal nerve in cases of primary glossopharyngeal neuralgia
Hemifacial spasm developed in a 32-year-old man following a brain stem stroke. This stroke followed a self-induced head movement, which is a rare cause of such events. The clonic movements were often related entirely to the position of the head. Carbamazepine was successful in treating the spasm and
BACKGROUND
The aim of this study was to determine the clinical characteristics and patients ' perception of hemifacial spasm (HFS) in Singapore.
METHODS
A clinical survey of 137 consecutive patients with HFS seen in our Botulinum Toxin Clinic over a 15-month period was undertaken.
RESULTS
Forty-six
Hemifacial spasm (HFS) due to direct compression of the facial nerve by a dolichoectatic vertebrobasilar artery is rare. Vessels are often non-compliant and tethered by critical brainstem perforators. We set out to determine surgical strategies and outcomes for this challenging disease. All patients
OBJECTIVE
Hemifacial spasm (HFS) is caused by arterial or venous compression of cranial nerve VII at its root exit zone. Traditionally, microvascular decompression of the facial nerve has been an effective treatment for posterior inferior and anterior inferior cerebellar artery as well as venous
Over the last decades microvascular decompression (MVD) has been established as the curative treatment of the primary Hemifacial Spasm (HFS), proven to be linked in almost all cases to a neurovascular compression of the facial nerve. Because the disease is not life-threatening and MVD not totally
When used therapeutically, botulinum toxin (BT) has to be injected into its target tissues. All manufacturers warn not to do so in patients with oral anticoagulation to avoid haematoma. We wanted to study the haematoma frequency (HF) in patients with anticoagulation receiving BT therapy. 32 patients
To analyze disease presentation, treatment, and clinical course of a consecutive series of patients with primary cerebellopontine angle (CPA) epidermoids.
Forty-seven consecutive patients with previously untreated CPA epidermoids.
Observation and microsurgery.
Disease- and treatment-associated
Venous angiomas were found to be the most common cerebral vascular malformations, composing 63% of such lesions in two autopsy series. Annual bleeding risk associated with venous angiomas is about 0.22 % per year. Venous angiomas are generally silent lesions because of their dynamic features, and