Eyelid Myokymia 

Updated: Jan 03, 2022
Author: Byron L Lam, MD; Chief Editor: Edsel B Ing, MD, PhD, MBA, MEd, MPH, MA, FRCSC 

Overview

Practice Essentials

Eyelid myokymia is typically benign, self-limited, and not associated with any disease. Intervention is usually unnecessary. Botulinum toxin injections are the treatment of choice when needed. Rarely, eyelid myokymia may occur as a precursor of hemifacial spasm, blepharospasm, Meige syndrome, spastic-paretic facial contracture, multiple sclerosis, autoimmune disease, and brainstem lesions (eg, pontine glioma). MRI with contrast to image the central and peripheral pathways of the facial nerve is warranted in rare cases. Medication related eyelid myokymia rarely occurs with agents such as topiromate, clozepine, flunarizine, and gold salts.[1]

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. The contractions are periodic and last seconds to hours.

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, multiple sclerosis. autoimmune disease, and brainstem lesions (eg, pontine glioma). Medication related eyelid myokymia rarely occurs with agents such as topiromate, clozepine, flunarizine, and gold salts.

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, multiple sclerosis. autoimmune disease, and brainstem lesions (eg, pontine glioma). Medication related eyelid myokymia rarely occurs with agents such as topiromate, clozepine, flunarizine, and gold salts.

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.

 

Presentation

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, clozepine, flunarizine, or gold salts has been uncommonly associated with eyelid myokymia.[2]

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, spastic-paretic facial contracture, multiple sclerosis, autoimmune disease, and brainstem lesions (eg, pontine glioma) 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.

 

DDx

Diagnostic Considerations

Hemifacial spasm - Unilateral facial contraction due to seventh nerve dysfunction

Essential blepharospasm

Meige syndrome - Blepharospasm and oral facial dystonia

Spastic-paretic facial contracture - Unilateral tonic facial contracture due to pontine dysfunction, associated usually with multiple sclerosis, and brainstem tumors or vascular lesions

Differential Diagnoses

 

Workup

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) with GAD is not needed for typical eyelid myokymia but should be considered to image the central and peripheral pathways of the facial nerve when other coditions such as facial myokymia, hemifacial spasm, or spastic paretic facial contracture is suspected, as well as when eyelid myokymia is continuous.

 

Treatment

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.[3, 4, 5, 6, 7]

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, multiple sclerosis, autoimmune disease, and brainstem lesions (eg, pontine glioma).

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

 

Medication

Medication Summary

Pharmacotherapy is used rarely to reduce symptoms when needed. 

Toxins

Class Summary

May inhibit transmission of impulses in neuromuscular tissue.

OnabotulinumtoxinA (BOTOX®)

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.

 

Questions & Answers