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Unilateral Involuntary Eyelid Closure Induced by Diplopia That Did Not Remit With Contact Lens Occlusion

Tay, Eugene MSc, MRCSEd, MRCOphth; Plant, Gordon T. MA, MD, FRCP

Journal of Neuro-Ophthalmology: March 2005 - Volume 25 - Issue 1 - p 53-55
Letters to the Editor
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Moorfields Eye Hospital and Royal National Hospital for Neurology and Neurosurgery; London, England; E-mail: dr_eugenetay@yahoo.com

We report an unusual case of unilateral blepharospasm secondary to diplopia that did not remit even with contact lens occlusion.

A 50-year-old woman had diplopia on right gaze for 3 years. Examination revealed a right face turn, a complete right abduction deficit, and a partial deficit of right adduction and supraduction. The eyelids and pupils were normal. Magnetic resonance imaging revealed a right intracavernous meningioma. During follow-up, diminished supraduction of the OD and synkinetic elevation of the lid on adduction and infraduction developed, as well as absence of right incyclotorsion on attempted downward gaze, attributed to aberrant regeneration of a palsied third cranial nerve (Fig. 1). The face-turn increased and involuntary unilateral closure of the OD lids developed that was attributed to a desire to eliminate diplopia (Fig. 2).

FIG. 1

FIG. 1

FIG. 2

FIG. 2

Botulinum toxin injected into the right medial rectus failed to relieve primary position diplopia, so a right occlusive contact lens was fitted. Despite relief of the diplopia, the involuntary OD lid closure persisted. When the occlusive contact lens was removed and she occluded her OS, the OD lids opened briefly, but she experienced vertigo. A right upper lid crutch in conjunction with the right occlusive lens was unsuccessful. She was finally treated with botulinum toxin injection into the right orbicularis muscle. With the occluding contact lens in place in the OD, the OD lids remained open.

Several triggers of blepharospasm have been reported. These include bright lights, air, and cold (1). Elston (2) found that 57% of 272 blepharospasm patients had ophthalmological symptoms at the onset, mostly irritation and photophobia, but there was no evidence of ocular disease on examination. Jankovic and Orman (3) reported the lack of associated ocular signs in patients with blepharospasm who described ocular symptoms. Ocular irritation as a result of lagophthalmos from Bell's palsy is thought also to be a precipitating factor in those predisposed to blepharospasm (4). Precipitating triggers have been noted in other dystonias, such as local hand injury in those with writer's cramp (2).

It is possible that diplopia-activated brain stem mechanisms subserving unilateral eye closure in our patient resulted in involuntary eye closure that persisted despite contact lens occlusion and eventually required botulinum toxin treatment.

Eugene Tay MSc, MRCSEd, MRCOphth

Gordon T. Plant MA, MD, FRCP

Moorfields Eye Hospital and Royal National Hospital for Neurology and Neurosurgery; London, England; E-mail: dr_eugenetay@yahoo.com

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REFERENCES

1. Jankovic J, Havins WE, Wilkins RB. Blinking and blepharospasm. Mechanism, diagnosis, and management. JAMA. 1982;248:3160-4.
2. Elston JS, Marsden CD, Grandas F, Quin NP. The significance ophthalmological symptoms in idiopathic blepharospasm. Eye. 1988;2:435-9.
3. Jankovic J, Orman J. Blepharospasm: demograohic and clinical survey of 520 patients. Ann Ophthalmol. 1984;16:371-6.
4. Miwa H, Kondo T, Mizuno Y. Bell's palsy induced blepharospasm. J Neurol. 2002;249:452-4.
© 2005 Lippincott Williams & Wilkins, Inc.