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Show Journal of Neuro- Ophthalmology 15( 1): 43- 44, 1995. © 1995 Raven Press, Ltd., New York Adie's Tonic Pupil Secondary to Migraine Valerie A. Purvin, M. D. A 46- year- old woman observed transient unilateral mydriasis during a classic migraine attack. One week later she experienced a similar episode after which anisocoria was persistent. Subsequent examination showed the clinical and pharmacologic features of a postganglionic parasympathetic paresis ( Adie's tonic pupil). This case confirms the hypothesis that transient mydriasis accompanying migraine is due to interruption of parasympathetic innervation rather than sympathetic overactivity. Key Words: Adie's pupil- Tonic pupil- Migraine- Episodic mydriasis. Transient unilateral pupillary dilation may occur as an isolated phenomenon or as an accompaniment to an episode of migraine ( 1- 3). While sometimes referred to as a manifestation of " autonomic instability," the exact mechanism of this form of mydriasis is uncertain. We report a patient who experienced transient pupillary dilation during a migraine attack followed by permanent mydriasis after a second episode thus enabling us to localize the site of the responsible lesion. From the Midwest Eye Institute, Methodist Hospital of Indiana, and Departments of Ophthalmology and Neurology, Indiana University Medical Center, Indianapolis, Indiana, U. S. A. Address correspondence and reprint requests to Dr. Valerie A. Purvin, Midwest Eye Institute, 1800 N. Capitol Avenue, Indianapolis, IN 46202, U. S. A. CASE REPORT A 46- year- old woman experienced sudden onset of flashing, brightly colored lights on January 6, 1988. These photopsias initially occupied the central field but moved out to the periphery over 10 minutes, leaving a scotoma in their wake. At 20 minutes after onset the lights abated, and vision returned to normal. She had had a mild headache that morning, which worsened with onset of her visual disturbance. During this episode she looked in a mirror and discovered right pupillary dilation. Following resolution of her visual disturbance, she continued to experience a throbbing bifrontal headache associated with photophobia for several hours. She was finally able to sleep, and upon awakening noted her headache had resolved and her pupils were of equal size. One week later she suffered a similar episode with the same sequence of events; however, this time the right pupil failed to return to its normal size. Her past medical history was significant for recurrent headaches for approximately 20 years. These were typically throbbing, associated with photophobia, precipitated by stress, and relieved by sleep. She had been treated with Lopressor for episodic tachyarrhythmia in the past with improvement of her headaches; however, this medication had been discontinued. Other medical problems included obesity and arthritis. Her only regular medication was daily aspirin. 43 44 V. A. PURVIN She was referred for neuro- ophthalmologic consultation 1 month after onset of anisocoria. Visual acuity was 20/ 20 in each eye at distance and Jl at near. Color vision, Goldmann perimetry and fundus examination were normal. Pupils measured 6 mm RE and 5 mm LE constricting to 5 mm RE and 3.5 mm LE in light. The right pupil was very sluggishly reactive to light with a slightly better response to near effort. This near response was slow, as was redilation upon distance fixation. The right pupil was slightly ovoid, and biomicroscopy revealed areas of segmental hypokinesis from 5 to 8 o'clock and from 11 to 1 o'clock. Following instillation of 0.125% pilocarpine, pupils measured 3 mm RE and 4 mm LE. Ocular motility was entirely normal. Deep tendon reflexes were normally active. A computed tomographic scan of the head with contrast was normal, as were serologic tests for syphilis. She was treated with beta- blockers, with a subsequent decrease in headache frequency. Reexamination 2 months later showed similar findings. DISCUSSION Localization of the lesion causing episodic unilateral pupillary dilation has been hampered by its fleeting nature. Such transient mydriasis could be due to excessive sympathetic activity causing spasm of the iris dilator or to interruption of the parasympathetic innervation to this iris sphincter. In the latter case, the site of the lesion could be either preganglionic ( as in ophthalmoplegic migraine) or postganglionic ( affecting the cilary ganglion or short ciliary nerves). Our patient suffered an attack of classic migraine associated with dilation of the right pupil that resolved within a few hours. Following a second similar episode, right pupillary dilation persisted. A tonic response to near effort, observation of segmental denervation with biomicroscopy, and pharmacologic evidence of cholinergic supersensitivity all pointed to a lesion of the postganglionic parasympathetic fibers, that is, an Adie's tonic pupil. Most cases of Adie's pupil are thought to be the consequence of a viral infection of the ciliary ganglion ( 4). This ganglion may also be damaged by other infectious agents, trauma, surgery, tumors, and ischemia. The ciliary ganglion receives its blood supply primarily from the posterior lateral ciliary artery and from the lateral muscular arterial trunk ( 5). Ischemia of this ganglion is rare. Specific causes have included quinine toxicity ( 6) and giant cell arteritis ( 7). Migrainous vasospasm affecting these arteries could lead to transient local ischemia causing reversible mydriasis. Unusually severe or prolonged spasm might cause permanent infarction with a residual Adie's pupil as seen in our patient. Based on the frequent occurrence of migraine in a group of patients with Adie's pupil, Massey ( 8) speculated that the two entities might be causally related. However, there are no previous reports linking the two disorders temporally in a specific patient. While migraine is unlikely to be a common cause of Adie's pupil, this case is of interest for the light it sheds on the mechanism of transient unilateral mydriasis accompanying migraine in some patients. Acknowledgments: I gratefully acknowledge the helpful comments of Dr. H. Stanley Thompson. REFERENCES 1. Hallett M, Cogan D. Episodic mydriasis in otherwise normal patients. Arch Ophthalmol 1970; 84: 130- 6. 2. Edelson R, Levy D. Transient benign unilateral pupillary dilation in young adults. Arch Neurol 1974; 31: 12- 14. 3. Woods D, O'Connor P, Fleming R. Episodic unilateral mydriasis and migraine. Am ] Ophthalmol 1984; 98: 229- 34. 4. Thompson HS. A classification of " tonic pupils." In: Thompson HS, Daroff R, Frisen L, Glaser JS, Sanders MD, eds, Topics in neuro- ophthalmol. Baltimore: Williams & Wilkins; 1979: 95- 6. 5. Eliskova M. Blood vessels of the ciliary ganglion in man. Br J Ophthalmol 1973; 57: 766- 72. 6. Gangitano JL, Keltner JL. Abnormalities of the pupil and visual- evoked potentials in quinine amblyopia. Am ] Ophthalmol 1980; 89: 425- 30. 7. Bronster DJ, Rudolph SH, Shanzer S. Pupillary light- near dissociation in cranial arteritis: a case report. Neuro-ophthalmol 1983; 3: 65- 70. 8. Massey EW. Pupillary dysautonomia and migraine: is Adie's pupil caused by migraine? Headache 1981; 21: 143- 6. J Ncuro- Ophthahnol, Vol. 15, No. 1, 1995 |
