The Lesion Causing Continuous Facial Myokymia in Multiple Sclerosis

Jacobs, Lawrence; Kaba, Samer E.; Pullicino, Patrick

doi:10.1001/archneur.1994.00540230053012

Cited by 58 publications

(41 citation statements)

References 19 publications

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“…Pathological examination of the brainstem of patients with myokymia have demonstrated lesions of the pontine tegmentum and basis pontis (3,18,20) or demyelinating lesions of both the intra-axial (1 9) and extra-axial facial nerve (5). Demyelination can be associated with an increase in the affected fibers' excitability leading to both spontaneous and induced discharges as demonstrated both experimentally (17) and in common clinical experience (e.g.> tic doloreux).…”

Section: Discussionmentioning

confidence: 99%

“…The EMG shows continuous irregular discharges of individual facial motor units. Facial myokymia can occur in patients with brainstem disorders such as multiple sclerosis, pontine glioma, and syringobulbia or with proximal facial nerve lesions both within and adjacent to brainstem (1)(2)(3)(4)(5)(6). The condition can also be benign appearing in otherwise normal individuals during fatigue or after excessive alcohol ingestion (4).…”

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confidence: 99%

“…Occasionally motor units discharge in short bursts followed by a brief period of quiescence. The EMG of facial myokymia is easily distinguished from other 'spontaneous' facial motor activities accompanying hemifacial spasm, motor tics, palatal myoclonus, and focal cortical seizures (2)(3)(4).…”

mentioning

confidence: 99%

“…The pathophysiology underlying facial myokymia is unknown but has been athibuted to a disorder of the motor neurons in facial nucleus induced by lesions either within or adjacent to that structure, by lesions remote from facial nucleus but affecting inputs to the facial nucleus, or by lesions of the facial nerve within (3) or close to the brainstem (5).…”

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Experimental facial myokymia in cat

Zaaroor

Starr

1997

Acta Neurologica Scandinavica

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Introduction – The objective of this study was to describe facial myokymia in experimental animals accompanying kainic acid affects on facial motor neurons. Material & methods – Anesthetized cats were injected with kainic acid into the pons adjacent to the facial nucleus. Facial movements appeared shortly after the injections and facial electromyographic potentials were recorded. Cats were killed up to 4 weeks later, the brainstems were processed histologically, and the number of neurons in the facial nucleus counted. Results – Cats receiving injection of kainic acid adjacent to facial nucleus all developed spontaneous writhing movements of the face ipsilateral to the injection site, clinically resembling facial myokymia in humans. Transient facial paresis, lasting several weeks, appeared in some of the cats. Facial myokymia occurred independent of histological evidence of neuronal loss in facial nucleus, whereas facial paresis occurred in all but one of the animals with significant neuronal loss in the facial nucleus. Placing a needle into the superior olive without injecting kainic acid or injections of kainic acid into cochlear nucleus was not accompanied by facial myokymia or subsequent facial paresis. Conclusion – Facial movements in cats similar to myokymia in humans accompanies kainic acid injections adjacent to the nucleus of the facial nerve.

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Section: Discussionmentioning

confidence: 99%

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Experimental facial myokymia in cat

Zaaroor

Starr

1997

Acta Neurologica Scandinavica

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“…In some cases it can be secondary to pontine tumors acoustic neuroma, metastatic disease or multiple sclerosis; vascular disorders, tuberculomas, syringobulbia, Guillain-Barré syndrome, multiple system atrophy (MSA), spinocerebellar ataxia type 3 (SCA3), cysticercosis, autosomal dominant striatonigral degeneration, or Bell's palsy [5] and even autoimmune. In our patient myokymia was idiopathic.…”

Section: Letter To Editormentioning

confidence: 99%