That? Thats nothing. Dont even worry about it. Weve all said this to a patient at some time during our careers. When an individual presents with a common, benign condition, were often tempted to simply brush it off as nothing. We may think that were being reassuring, but the patient may see this as dismissive, callous and unprofessional.

Regardless of the condition, our patients deserve an explanation and an answer to their questions. If a therapy is available that can relieve their symptoms or speed the resolution of their signs, we must try to employ that therapy.

In the first part of this two-part series, well discuss eyelid myokymia, one of the more common nothings we see in clinical practice, and what we can do for patients who have this condition.

Myokymia Defined

Myokymia is defined as undulating contractions that spread across the affected striated muscle characterized electrophysiologically by rhythmic or semirhythmic bursts of a single motor unit discharging several times per second at a rate of 3 to 8Hz.1

In simpler terms, lid myokymia represents an involuntary misfiring of the neurons that innervate the orbicularis oculi muscle. This results in subtle twitching of the upper and/or lower eyelid.

The precise etiology of lid myokymia is unclear, although earlier studies suggest that it may represent a localized form of facial myokymia, a more ominous condition that is often associated with brainstem disease.2 However, more recent perspectives conclude that the ocular version is due to an isolated, self-limiting peripheral lesion and is completely benign.1

Signs and Symptoms

Eyelid myokymia typically affects young (most likely ages 20 to 40), otherwise healthy patients. They commonly report intermittent bouts of these ocular spasms at different times throughout the day; these bouts may persist for weeks to months.

Individuals who have myokymia may be more apt to suffer
exacerbations during times of high emotional stress or fatigue, extreme physical exertion or lack of sleep. Other associated factors include excessive consumption of caffeine, alcohol or tobacco.1 Occasionally, myokymia may be induced by ocular irritation or foreign body.

Individuals who have myokymia may be more apt to suffer exacerbations during times of high emotional stress or fatigue, extreme physical exertion or lack of sleep.

Vision is infrequently affected, except in rare cases of associated superior oblique myokymia; under such circumstances, the rhythmic contractions of the extraocular muscle will induce subjective oscillopsia and/or diplopia. Superior oblique myokymia may represent a more deep-seated condition, such as brainstem stroke, dural arteriovenous fistula, multiple sclerosis, vascular compression or intracranial tumor.

Be sure to differentiate eyelid myokymia from facial myokymia. Myokymia that involves the
orbicularis oculi muscle alone is virtually always benign. However, my-okymia that involves other facial muscles may be a sign of brainstem disease, especially pontine glioma.8,9


Patients with eyelid myokymia may display deep concern and anxiety regarding their condition, often incorrectly assuming that it represents a severe ocular or neurological problem. Equally frustrating is that the seemingly obvious lid movements are often completely imperceptible to others, thus the patient cannot even get validation of his or her symptoms from friends and family.

Fortunately, we can offer these patients reassurance and therapeutic intervention. For a small percentage of patients, simply explaining that the condition is benign and self-limiting may be satisfactory. Additionally, a review of caffeine, alcohol and tobacco habits is indicated for all patients who have myokymia.

Other factors associated with myokymia include excessive consumption of caffeine, alcohol or tobacco. Advise patients to cut back on these while symptoms remain.

Advise patients to discontinue or curtail the use of such products as long as their symptoms remain. Likewise, recommend that patients strive to get seven to eight hours of sleep every evening and that they utilize appropriate stress management strategies where applicable.

Patients who are exceedingly symptomatic may benefit from therapeutic measures. Anecdotally, topical antihistamines, such as anta- zoline or pheniramine maleate, may benefit these patients by prolonging the refractory period of the spasming orbicularis. Likewise, oral antihistamines (e.g., 12.5mg to 25mg promethazine q.d. to t.i.d.) or quinine (200mg to 300mg q.d. to t.i.d.) may be used for recalcitrant cases of lid myokymia, according to several well-known sources.10,11 However, realize that while these remedies have been suggested in the literature, there are no prospective clinical trials to date to confirm
that these treatments are actually beneficial.

For more severe or protracted courses of eyelid myokymia, some physicians now rely on a common cosmetic agent. Subcutaneous Botox injection (botulinum toxin A, Allergan) approved for the treatment of blepharospasm and
strabismus, has been successfully used in numerous cases of eyelid myokymia. Several reports suggest that just one injection can effectively induce permanent resolution of symptoms.1,12,13

Remember that while we may categorize a particular condition as benign, that does not necessarily mean the patient will be asymptomatic or indifferent to the problem. Whenever an individual takes the time and effort to seek our care, we must respond accordingly, and we must never trivialize any patients condition, no matter how common or mundane the diagnosis.

Next month, well discuss another common nothing we see in clinical practice: sub-conjunctival hemorrhage.

Drs Kabat and Sowka have no financial interest in any of the products mentioned.

1.Banik R, Miller NR. Chronic myokymia limited to the eyelid is a benign condition. J Neuroophthalmol 2004 Dec; 24(4):290-2.

2.Rubin M, Root JD. Electrophysiologic investigation of benign eyelid twitching. Electromyogr Clin Neurophysiol 1991 Sep; 31(6):377-81.

3.Webster R, Leslie S. Recurrent superior oblique myokymia in a patient with retinitis pigmentosa. Clin Exp Optom 2004 Mar; 87(2):107-9.

4. Geis TC, Newman NJ, Dawson RC. Superior oblique myo-kymia associated with a dural arteriovenous fistula. J Neuroophthalmol 1996 Mar;16(1): 41-3.

5. Miller NR, Newman NJ. Walsh and Hoyts Clinical Neuro-Ophthalmology: the Essentials, 5th ed. Philadelphia: Lippincott, Williams and Wilkins; 1999: 561.

6. Hashimoto M, Ohtsuka K, Suzuki Y, et al. Superior oblique myokymia caused by vascular compression. J Neuroophthalmol 2004 Sep; 24(3):237-9.

7. Morrow MJ, Sharpe JA, Ranalli PJ. Superior oblique myo-kymia associated with a posterior fossa tumor: oculographic correlation with an idiopathic case. Neurology 1990 Feb; 40(2):367-70.

8. Sharma RR, Mathad NV, Joshi DN, et al. Persistent facial myokymia: a rare pathognomic physical sign of intrinsic brain-stem lesions: report of 2 cases and review of literature. J Postgrad Med 1992 Jan-Mar; 38(1):37-40, 40A-40B.

9. Selvapandian S, Rajshekhar V. Facial myokymia as the presenting symptom of a pontine glioma. Neurol India 1999 Sep; 47(3):241-2.

10. Marren SE, Bartlett JD, Melore GG. Diseases of the Eyelids. In: Bartlett JD, Jaanus SD, eds. Clinical Ocular Pharmacology, 4th ed. Boston: Butterworth-Heinemann; 2001:485-522.

11. Lam BL. Myokymia. In: Fraunfelder FT, Roy FH, eds. Current Ocular Therapy, 4th ed. Philadelphia: WB Saunders; 1995:582.

12. Jordan DR, Anderson RL, Thiese SM. Intractable orbicularis myokymia: treatment alternatives. Ophthal Surg 1989 Apr; 20(4): 280-3.

13. Ruusuvaara P, Setala K. Long-term treatment of involuntary facial spasms using botulinum toxin. Acta Ophthalmologica 1990 Jun; 68(3):331-8.

Vol. No: 143:10Issue: 10/15/2006