Spread of Muscle Spasms in Hemifacial Spasm

Conte, Antonella; Falla, Marika; Diana, M.; Bologna, Matteo; Suppa, Antonio; Fabbrini, A; Colosimo, Carlo; Berardelli, Alfredo; Fabbrini, Giovanni

doi:10.1002/mdc3.12106

Cited by 10 publications

(3 citation statements)

References 12 publications

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“…Patients with an age of symptom onset >45 years had a faster progression rate. Conte et al ( 15 ) showed that the spread latency correlated with disease duration and inversely correlated with age of onset. They explained that this result implied that age negatively impacts the course of the disease and that aged facial nerve fibers were more prone to develop spread.…”

Section: Discussionmentioning

confidence: 99%

Analysis of risk factors related to the progression rate of hemifacial spasm

Xu,

Gu,

Yuan

et al. 2024

Front. Neurol.

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IntroductionAlthough there have been many researches on the etiology and risk factors with the onset of hemifacial spasm, researches on the risk factors related to progression rate are limited. This study aims to analyze the risk factors related to the progression rate of hemifacial spasm.MethodsThe study enrolled 142 patients who underwent microvascular decompression for hemifacial spasm. Based on the duration and severity of symptoms, patients were classified into rapid progression group and slow progression group. To analyze risk factors, univariate and multivariate logistic regression analyses were conducted. Of 142 patients with hemifacial spasm, 90(63.3%) were classified as rapid progression group, 52(36.7%) were classified as slow progression group.ResultsIn the univariate analysis, there were significant statistical differences between the two groups in terms of age of onset (P = 0.021), facial nerve angle (P < 0.01), hypertension (P = 0.01), presence of APOE ε4 expression (P < 0.01) and different degrees of brainstem compression in the Root Entry Zone (P < 0.01). In the multivariable analyses, there were significant statistical differences between the two groups in terms of age of symptom onset (P < 0.01 OR = 6.591), APOE ε4 (P < 0.01 OR = 5.691), brainstem compression (P = 0.006 OR = 5.620), and facial nerve angle (P < 0.01 OR = 5.758). Furthermore, we found no significant correlation between the severity of facial spasms and the progression rate of the disease (t = 2.47, P = 0.12>0.05).ConclusionAccording to our study, patients with facial nerve angle ≤ 96.5°, severer compression of the brainstem by offending vessels, an onset age > 45 years and positive expression of APOE ε4, may experience faster progression of hemifacial spasm.

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Section: Discussionmentioning

confidence: 99%

Analysis of risk factors related to the progression rate of hemifacial spasm

Xu,

Gu,

Yuan

et al. 2024

Front. Neurol.

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“…It usually starts by twitching over the orbicularis oculi and later worsens to involve the orbicularis oris, muscles of the cheek, and platysma. 1,2) Primary HFS is caused by vascular compression of the facial nerve within the root entry zone (REZ), whereas secondary HFS is associated with an underlying pathology, such as cerebellopontine angle tumor or vascular malformation. [3][4][5] Lee, et al 6) reviewed 2050 cases of HFS and found that only 9 were related to VS, including 6 that were associated with compression by the offending vessels.…”

Section: Introductionmentioning

confidence: 99%

Simultaneous Surgical Treatment of Vestibular Schwannoma and Hemifacial Spasm via Minimally Invasive Retrosigmoid Approach

Misron

Mfuko

Lee

et al. 2022

Korean J Otorhinolaryngol-Head Neck Surg

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The combination of vestibular schwannoma (VS) and hemifacial spasm (HFS) caused by a vascular loop is not frequently encountered. Surgical intervention using the retrosigmoid approach may enable the two diseases to be treated simultaneously. A 68-year-old male presented with progressive right HFS. MRI revealed a concurrent vascular loop and 3.2-mm intracanalicular VS. The retrosigmoid approach, together with microvascular decompression, was used to remove VS. Intraoperatively, compression by the vascular loop alone induced HFS although it was not related to VS. This finding is in contrast to the literature reports in which VS has been implicated in HFS. In our patient, when VS was completely removed, HFS immediately disappeared postoperatively.

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“…Although HFS is not fatal, it often leads to social embarrassment and interference with vision from involuntary eye closure leading to functional disability [ 1 – 3 ]. It is characterized by involuntary clonic or tonic contractions of the facial expression muscles, usually unilateral and rarely bilateral, beginning in the periorbital musculature usually starting in the low eyelid and progressing to the perioral, platysma and other facial expression muscles [ 4 ]. The symptoms of HFS are aggravated by stress, chewing, speech, light, cold stimuli and fatigue while relieved by quiet.…”

Section: Introductionmentioning

confidence: 99%

Hemifacial spasm is not affected by state of consciousness: a case report

Feng

Song

et al. 2021

Eur J Med Res

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Background Hemifacial spasm (HFS) is a movement disorder caused by mechanical compression of the facial nerve after it has left the brainstem and is characterized by brief or sustained twitching of the muscles innervated by that nerve. Often we observe spasm in an awakening situation. Actually contractions persist during sleep. To our knowledge, there were no reports on how HFS manifests under disturbance of consciousness. Here, we report a case of primary HFS in which the patient's symptoms persisted in a coma. Case presentation A 74-year-old female with right-sided primary HFS for 20 years and had received botulinum toxin injections in our hospital. Unfortunately she was carried to emergency department after traumatic right pneumothorax by accident. During the emergency treatment, she lost consciousness due to simultaneous cardiac arrest and respiratory arrest. She was then admitted to the emergency intensive care unit for further treatment. During her hospitalization, she was in a coma with stable vital signs and persisting symptoms of HFS. Thus, a multidisciplinary consultation was requested to identify whether it was focal cortical seizures involving the right-side facial muscles. Physical examination revealed brief involuntary clonic or tonic contractions accompanied with the ‘Babinski-2 sign’. A combination of relevant data, including her past history, clinical presentation and a negative computed tomography scan of the head, led to a diagnosis of right-sided HFS. As the symptoms of HFS are not life-threatening, the use of anticonvulsants is unnecessary. Conclusions For the layperson, it is crucial to seek a multidisciplinary consultation to obtain a correct diagnosis.

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Spread of Muscle Spasms in Hemifacial Spasm

Cited by 10 publications

References 12 publications

Analysis of risk factors related to the progression rate of hemifacial spasm

Analysis of risk factors related to the progression rate of hemifacial spasm

Simultaneous Surgical Treatment of Vestibular Schwannoma and Hemifacial Spasm via Minimally Invasive Retrosigmoid Approach

Hemifacial spasm is not affected by state of consciousness: a case report

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