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Neuro-ophthalmology

Eyelid Myokymia

Eyelid myokymia is an involuntary, fine, undulating contraction of the orbicularis oculi muscle. It is described as a “relatively slow movement like a worm wriggling.” It is the most common form of facial myokymia and the most frequently encountered spasm disorder.

Usually unilateral and more common in the lower eyelid. The contraction is sustained but not forceful, and in many cases it is self-limiting (resolves spontaneously). Unlike voluntary or reflex blinking, it is characterized by spontaneous and localized contraction.

Hyperfunction of the facial nerve is considered the essence of the pathology. Most cases are idiopathic, and anxiety, fatigue, and stress have been proposed as triggers.

Q How common is eyelid myokymia?
A

Eyelid myokymia is the most commonly encountered disorder among spasmodic conditions. It is said that many people experience it at least once in their lifetime, and it follows a benign and self-limiting course.

Patients complain of twitching on one side of the eyelid, more commonly in the lower eyelid. The symptom is uncomfortable but does not cause vision loss or pain.

It tends to worsen under the following conditions:

  • Fatigue and sleep deprivation: the most common trigger
  • Mental stress and anxiety: exacerbate symptoms
  • Caffeine and alcohol intake: excessive consumption worsens symptoms
  • Prolonged screen time: associated with eye strain

Symptoms last from seconds to hours and appear intermittently. They usually disappear within days to weeks.

Clinical Findings (Findings Confirmed by Physician Examination)

Section titled “Clinical Findings (Findings Confirmed by Physician Examination)”

Fine, repetitive contractions of the orbicularis oculi muscle, especially in the lower eyelid, are observed. The following are characteristic:

  • Range of contraction: Only a part of the orbicularis oculi muscle moves. It does not lead to difficulty opening the eyes.
  • Induction: Involuntary movements can be induced by repeated forceful eye closure.
  • Traction test: Gentle traction on the eyelid temporarily reduces the movements.
  • No eyebrow involvement: No synchronous eyebrow depression. This is an important distinguishing feature from hemifacial spasm.
  • Eye movement: Contraction may rarely cause slight eye movement.

Bilateral or upper eyelid involvement is rare but has been reported.

The exact cause of eyelid myokymia is not fully understood. Most cases are idiopathic.

Main triggers include:

  • Excessive caffeine intake
  • Anxiety and psychological stress
  • Sleep deprivation
  • Prolonged screen time
  • Post-viral infection
  • Alcohol and smoking

Associations with specific medications have also been reported.

  • Clozapine
  • Flunarizine
  • Topiramate
  • Gold salts
  • Metformin: isolated case reports

Rarely, central nervous system disorders can be the cause. In addition to multiple sclerosis, brain tumors, and brainstem lesions, eyelid myokymia due to trigeminal schwannoma has also been reported1).

Q Will reducing caffeine cure eyelid myokymia?
A

Caffeine is one of the main triggers of eyelid myokymia, and reducing intake may improve symptoms. However, since triggers are multifactorial, it is advisable to also ensure adequate sleep and reduce stress. For details, see the section on “Standard Treatments” (#5-standard-treatment).

Eyelid myokymia is a clinical diagnosis, and there are no specific tests. Diagnosis is based on characteristic orbicularis oculi contractions that are not initiated by voluntary movement.

Repeated forceful eyelid closure can induce involuntary movements, which is a diagnostic clue.

It is important to differentiate from the following conditions:

ConditionKey differentiating features
Hemifacial spasmSynchronous twitching spreading to the corner of the mouth. Accompanied by eyebrow drooping.
Essential blepharospasmBilateral. Accompanied by photophobia and dry eye sensation. Chronic progressive.
Meige syndromeComplicated by facial involuntary movements such as lip dyskinesia.

In eyelid myokymia, only a part of the orbicularis oculi muscle moves, and it does not lead to difficulty opening the eye. The fact that it is unilateral and not accompanied by synchronous eyebrow depression is useful for differentiating it from hemifacial spasm. Sometimes it cannot be distinguished from early hemifacial spasm, and follow-up observation may be necessary.

In the following cases, consider neuroimaging (MRI or CT).

  • If symptoms persist for several weeks or more
  • If symptoms extend beyond the eyelid
  • If accompanied by neurological signs

These tests aim to rule out central nervous system diseases such as multiple sclerosis, brain tumors, and brainstem lesions. For persistent eyelid myokymia, it has been reported that the trigeminal blink reflex is useful for identifying the causative lesion 1).

Eyelid myokymia is usually benign and self-limiting, resolving within minutes to weeks. It often improves with physical and mental rest.

The basics of initial management are as follows:

  • Reassurance for the patient: Explain that it is a benign condition.
  • Removal of triggers: Stress reduction, adequate sleep, limiting caffeine and alcohol intake
  • Discontinuation or change of causative drugs: If drug-related causes are suspected

If symptoms persist for several weeks or more, consider the following.

  • Use of tranquilizers: May be effective for symptom relief
  • Botulinum toxin injection: Considered for refractory symptoms. Usually provides symptom relief for 3 to 4 months
  • Referral to a specialist: Consider referral to an oculoplastic surgeon or neuro-ophthalmologist.

In extremely rare cases, myectomy of the orbicularis oculi muscle has been reported for refractory cases.

Q What should I do if eyelid myokymia does not resolve on its own?
A

If it persists for more than a few weeks, it is advisable to see an oculoplastic surgeon or neuro-ophthalmologist. Imaging tests may be performed to rule out central nervous system disorders. Botulinum toxin injections may be considered for refractory cases.

Eyelid myokymia results from asynchronous discharges within the orbicularis oculi muscle. A single motor unit exhibits semi-rhythmic bursts (grouped discharges) firing at a frequency of 3–8 Hz. The discharges occur spontaneously but may be exacerbated by voluntary movements.

The essence of the condition is hyperexcitability of the facial nerve. Although it is thought to originate from the peripheral nerve, there have been reports of pontine lesions. When caused by central nervous system disease, involvement of the trigeminofacial reflex has been suggested. In the trigeminofacial reflex, the afferent pathway corresponds to the trigeminal nerve and the efferent pathway to the facial nerve.

Ito et al. (2023) reported a 57-year-old man with eyelid myokymia as the sole symptom of a trigeminal schwannoma in Meckel’s cave 1). Preoperative trigeminal blink reflex testing showed reduced R1 and R2 amplitudes on the affected side (R1 amplitude ratio: left/right = 0.05). Symptoms disappeared after surgery, and blink reflex amplitudes recovered (R1 amplitude ratio: 0.68). It was hypothesized that pulsatile stimulation of a blood vessel between the tumor and the nerve stimulated the trigeminal nerve, causing eyelid myokymia via the blink reflex.

This report indicates that afferent (trigeminal nerve) lesions can also cause persistent eyelid myokymia.


7. Latest Research and Future Prospects (Research Stage Reports)

Section titled “7. Latest Research and Future Prospects (Research Stage Reports)”

Regarding the mechanism of eyelid myokymia caused by trigeminal schwannoma, electrophysiological evaluation using trigeminal-evoked blink reflex is attracting attention 1). Previous reports have indicated that damage to the trigeminal trunk leads to decreased R1 and R2 amplitudes and prolonged latency, but in the case reported by Ito et al., only decreased amplitude was observed without prolonged latency.

The following mechanisms have been considered for this finding.

  • Sensitivity of R1 to acute changes: R1 is a monosynaptic circuit and reflects acute changes more sensitively than R2.
  • Phase cancellation of sensory nerve action potentials: In demyelinating lesions, only amplitude reduction may occur
  • Low sensitivity to small fibers: In afferent pathway disorders, R1 amplitude may decrease without latency prolongation

In the future, accumulation of similar cases is expected to further elucidate the pathogenesis of eyelid myokymia.


  1. Ito E, Sugita R, Saito R. Eyelid myokymia caused by a trigeminal schwannoma as determined by the trigeminal-evoked blink reflex. Clin Case Rep. 2023;11:e7086.
  2. Ahsan M, Nizami DJ. Metformin-induced eyelid myokymia. Indian J Pharmacol. 2024;56(5):358-360. PMID: 39687960.
  3. Khalkhali M. Topiramate-Induced Persistent Eyelid Myokymia. Case Rep Psychiatry. 2016;2016:7901085. PMID: 27293943.

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