Eyelid Myokymia

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Background

Myokymia is characterized by spontaneous, fine fascicular contractions of muscle without muscular atrophy or weakness. Eyelid myokymia results from fascicular contractions of the orbicularis oculi muscle. Eyelid myokymia is typically unilateral, with the most common involvement being one of the lower eyelids. When multiple eyelids are involved, the fascicular contractions of each eyelid are independent of each other.

In most cases, eyelid myokymia is benign, self-limited, and not associated with any disease. Intervention is usually unnecessary. Rarely, eyelid myokymia may occur as a precursor of hemifacial spasm, blepharospasm, Meige syndrome, spastic-paretic facial contracture, and multiple sclerosis.

Pathophysiology

Consisting of involuntary fine undulating contractions across the striated muscle, the pathophysiology of eyelid myokymia is not well understood. The contractions are nonsynchronous semirhythmic discharges of motor units discharging at a rate of 3-8 Hz. The discharges have intervals of 100-200 ms between individual motor bursts. The contractions are transient and intermittent. The focus of irritation is most likely the nerve fibers within the muscle. Pontine dysfunction in the region of the facial nerve nucleus also has been suggested. Possible precipitating factors include stress, fatigue, and excessive caffeine or alcohol intake.

Epidemiology

Frequency

United States

The incidence and prevalence of eyelid myokymia are unknown, but symptoms of eyelid myokymia are frequently encountered in the ophthalmic clinic.

Mortality/Morbidity

Eyelid myokymia is a benign and self-limited condition in most patients, but, in some cases, it may be a precursor of hemifacial spasm, blepharospasm, Meige syndrome, spastic-paretic facial contracture, facial myokymia, and multiple sclerosis.

Age

Eyelid myokymia usually occurs in adults but may occur at any age.

Prognosis

Prognosis is excellent in most cases.

Patient Education

For excellent patient education resources, see eMedicineHealth's patient education article BOTOX® Injections.

History

Patients with eyelid myokymia usually note sporadic "jumping" or "twitching" of one of the lower eyelids. Eyelid myokymia may also involve one of the upper eyelids or multiple eyelids. The irregular contractions are usually unilateral and may occur intermittently for days to months.

In rare cases, the contractions may be severe enough to move the eye to produce oscillopsia.

A history of stress, fatigue, and excessive caffeine or alcohol intake may be present. The use of topiramate in migraineurs has been questioned as a cause of eyelid myokymia.[1]

Physical

Fine fascicular nonsynchronous contractions of the orbicularis oculi may be visible if the patient has the contractions during examination. If present, the contractions are usually intermittent and are more apparently felt by the patient than visible to the observer. The symptoms often improve when the eyelid is pulled manually. Rarely, the contractions may be vigorous enough to cause movement of the globe, producing fine nystagmuslike eye movements.

If the eyelid myokymia is associated with contraction of other parts of the face, hemifacial spasm, blepharospasm, Meige syndrome, and spastic-paretic facial contracture should be excluded. Activation of the facial muscles (eg, big smile, eyelids squeezed shut) helps to determine if the eyelid myokymia is associated with contractions of other parts of the face.

Causes

The cause is unknown but may be associated with stress, fatigue, and excessive caffeine or alcohol intake.

Demyelination and brainstem lesions are rarely found in patients thought to have eyelid myokymia.

Imaging Studies

A complete cranial nerve examination should be performed.

If the myokymia is not seen in the office, patients should be encouraged to video-document their episodes.

Brain magnetic resonance imaging (MRI) is not needed for typical eyelid myokymia but should be considered if facial myokymia, hemifacial spasm, or spastic paretic facial contracture is suspected, as well as when eyelid myokymia is continuous.

Medical Care

Reassurance and reduction in precipitating factors, if identifiable, are appropriate for many patients.

When symptoms are severe, local subcutaneous botulinum toxin A (BOTOX®) injections of 2.5-5 units each to the affected eyelid region provide relief for 12-18 weeks. If the upper eyelid is involved, the injections should not be placed near the levator palpebrae; otherwise, ptosis lasting weeks will result.[2, 3, 4, 5, 6]

Adverse effects include temporary lid laxity, which may produce lagophthalmus, exposure keratopathy, ptosis, and diplopia.

The efficacy of other agents has not been proven.

Diet

Excessive caffeine and possibly alcohol intake may be associated with eyelid myokymia.

Activity

Excessive physical exertion may be associated with eyelid myokymia.

Prevention

If precipitating factors can be identified, avoidance can reduce the frequency of episodes.

Long-Term Monitoring

Rarely, eyelid myokymia may occur as a precursor of blepharospasm, Meige syndrome, hemifacial spasm, facial myokymia, spastic-paretic facial contracture, and multiple sclerosis.

Advise patients to return for reexamination, if there is a change in symptoms.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

OnabotulinumtoxinA (BOTOX®)

Clinical Context:  Blocks neuromuscular conduction by binding to receptor sites on motor nerve terminals, entering the nerve terminals and inhibiting the release of acetylcholine. One treatment is usually sufficient, but in persistent cases, the injection may be repeated in 4-6 mo. Injection should be used only when symptoms are severe or when oscillopsia is present. Treatment of pediatric patients is not recommended.

Class Summary

May inhibit transmission of impulses in neuromuscular tissue.

What is eyelid myokymia?What is the pathophysiology of eyelid myokymia?What is the prevalence of eyelid myokymia in the US?What is the morbidity of eyelid myokymia?Which age groups have the highest prevalence of eyelid myokymia?What is the prognosis of eyelid myokymia?Which clinical history findings are characteristic of eyelid myokymia?Which physical findings are characteristic of eyelid myokymia?What causes eyelid myokymia?Which conditions are included in the differential diagnoses of eyelid myokymia?What are the differential diagnoses for Eyelid Myokymia?What is the role of imaging studies in the workup of eyelid myokymia?How is eyelid myokymia treated?Which dietary modifications are used in the treatment of eyelid myokymia?Which activity modifications are used in the treatment of eyelid myokymia?How is recurrent eyelid myokymia prevented?What is included in the long-term monitoring of eyelid myokymia?What is the goal of drug treatment for eyelid myokymia?Which medications in the drug class Toxins are used in the treatment of Eyelid Myokymia?

Author

Byron L Lam, MD, Professor, Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Edsel Ing, MD, MPH, FRCSC, Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Active Staff, Michael Garron Hospital (Toronto East Health Network); Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital, Canada

Disclosure: Nothing to disclose.

Additional Contributors

Ron W Pelton, MD, PhD, Private Practice, Colorado Springs, Colorado

Disclosure: Nothing to disclose.

References

  1. Medrano-Martínez V, Pérez-Sempere A, Moltó-Jordá JM, Fernández-Izquierdo S, Francés-Pont I, Mallada-Frechin J, et al. Eyelid myokymia in patients with migraine taking topiramate. Acta Neurol Scand. 2015 Aug. 132 (2):143-6. [View Abstract]
  2. Baldwin MR, Barbieri JT. Association of Botulinum neurotoxins with synaptic vesicle protein complexes. Toxicon. 2009 Apr 8. [View Abstract]
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  12. Reinecke RD. Translated myokymia of the lower eyelid causing uniocular vertical pseudonystagmus. Am J Ophthalmol. 1973 Jan. 75(1):150-1. [View Abstract]
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  14. Scott AB. Botulinum toxin for blepharospasm. Spaeth G, Katz LJ, Parker KW, eds. Current Therapy in Ophthalmic Surgery. Toronto: Decker; 1989. 322-324.
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