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Craniofacial Pain
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
Hemifacial spasm is sometimes painful. Patients with longstanding facial palsy sometimes complain of pain on the affected side of the face, particularly when contracture of the facial muscles develops following a lower motor neurone palsy, or when hemifacial spasm develops.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
It is not to be confused with HEMIFACIAL SPASM which, although it can initially present as a blepharospasm-like condition, is in fact a more generalized disorder of the facial musculature (but only on one side of the face). It does however form a part of MEIGE SYNDROME (also known as segmental cranial dystonia). In this there is blepharospasm as well as jaw clenching, involuntary mouth opening and tongue extension, which of course also interfere with SPEECH PRODUCTION. Meige syndrome has been found to be associated with the presence of LEWY BODIES in the SUBSTANTIA NIGRA and LOCUS COERULEUS (as they are in Parkinson's disease) and there is evidence of decreased DOPAMINE activity in the STRIATUM.
Usefulness of intraoperative monitoring in microvascular decompression for hemifacial spasm: a systematic review and meta-analysis
Published in British Journal of Neurosurgery, 2022
Lyndon Sprenghers, Robin Lemmens, Johannes van Loon
Hemifacial spasm (HFS) is a rare, functional, neurological disease. The most frequent cause is compression of the facial nerve at the root exit zone of the brainstem by a conflicting vessel.1,2 Hemifacial spasm is not a life-threatening disorder, but it has a major impact on quality of life. Because of the functional nature of the disease, balancing the possible complications and adverse effects with the possible benefits of the therapy is of the utmost importance. Botulinum toxin injection is often the first step in treatment for hemifacial spasms. If patients do not respond to botulinum toxin injections, microvascular decompression (MVD) surgery can be effective. When hemifacial spasms are caused by compression, surgery is the best treatment. Surgical decompression of the conflicting blood vessels can give very good results and is the only treatment that can give a lasting cure. In one systematic review complete resolution of symptoms was achieved in 91.1% of the patients, with low rates of symptom recurrence. Complications of this surgery are uncommon and generally transient.3
Comparison of preseptal and pretarsal onabotulinum toxin an injection in patients with hemifacial spasm
Published in International Journal of Neuroscience, 2021
Ayşen Tuğba Canbasoğlu Yılmaz, Murat Yılmaz, Mehmet Fevzi Öztekin
An indication for treatment exists when a patient feels impaired in his/her quality of life by the disease or if functional impairments are present. The therapeutic options for hemifacial spasm range from simple application of heat to medication treatment and botulinum injections to microvascular decompression surgery. In hemifacial spasm, complications of a major surgical procedure reduce the rate of choice of a major surgical intervention [4]. Botulinum toxin (BTX) injections have yielded very favorable results in this disease, where systemic drug treatment is often not effective [5]. The primary effect of BTX was blockade and chemodenervation at the neuromuscular junction. BTX injection, which is performed selectively to relieve unintentional contractions, causes a decrease in overactivity without leading to a significant weakness, depending on the dose and site of administration [6]. The crucial disadvantage of this treatment modality is its limited effectiveness; the injections have to be repeated at intervals of 3–4 months [5,6].
Two-dimensional structure analysis of hemifacial spasms and surgical outcomes of microvascular decompression
Published in Neurological Research, 2021
Shiyuan Han, Yongning Li, Zhimin Li, Xin Wang, Jun Gao
Hemifacial spasm (HFS) is characterized by paroxysmal unilateral contractions of facial muscles that are typically caused by ephaptic hyperactivation of the VII cranial nerve (CN). Primary HFS typically begins in the fifth and sixth decades of life with a female predilection, usually occurring in the left side [1].HFS often leads to social embarrassment, which leads to a diminished self-image and a reduced quality of life [2]. More importantly, HFS episodes may pose vital consequences in the work environment that cannot afford any mistakes such as driving a car or performing an operation. Thus, the problem of HFS must receive necessary attention and be treated properly. Neurovascular conflict (NVC) in the root exit zone (REZ) of VII CN is considered to be the leading cause of HFS [1,3]. The REZ of the VII CN is a transition area between central oligodendrocytes and peripheral Schwann cells, at which the facial nerve is susceptible to local demyelination [4,5]. Myelination serves as a natural inhibitor of ephaptic transmission. Eventually, local demyelinated areas impulsively compressed by vessels lead to excessive or abnormal firing of the VII CN either by neighboring neurons or by facial motor nuclei [6–9]. Although it is basically considered a vascular compression syndrome, primary HFS is reported to be absent in 10% to 20% individuals with NVC in the REZ according to imaging tests [10,11]. Obviously, the underlying pathogenesis of HFS still remains to be further illuminated.