Complicated migraine resulting in blindness due to bilateral retinal infarction.

Abstract

Retinal migraine is not uncommon, but permanent sequelae in the anterior visual pathway are rare. We describe the case ofa young woman in whom blindness developed over a six-year period due to recurrent episodes of migrainerelated occlusions of a branch retinal artery.Migraine occurs in 10-25% of the population' and is more common in women than in men. ' Eight months later, following an increase in the frequency of her migraine, she developed an occlusion of a macular branch of the right superotemporal arteriole which resulted in a permanent scotoma and a reduction of visual acuity on the right to 6/9.At the age of 20, again following an increase in the frequency of her migraine, she suddenly developed further loss of vision in the right eye due to an inferotemporal BRAO affecting the macula (Fig 1). On this occasion she was treated with the calcium channel blocker nimodipine and intravenous methyl prednisolone 1 g daily for three days. No visual recovery occurred.The patient had not been taking an oral contraceptive agent and had never been prescribed ergot derivatives. Her father, brother, and niece also suffer from migraine. EXAMINATIONA general medical examination revealed no significant abnormalities. In particular she was normotensive, the heart was clinically normal, and there were no carotid or orbital bruits. Slitlamp examination revealed normal anterior segments, and the intraocular pressures were 14 mm Hg in both eyes. After the most recent BRAO her visual acuity was counting fingers in the right eye and hand movements in the left. There was loss of the central and superotemporal visual field of the right eye and loss of all but the superotemporal quadrant of the left. Funduscopy showed an acute occlusion of the inferotemporal arteriole on the right and optic atrophy plus attenuation of the superior and inferior temporal arterioles on the left. A fluorescein angiogram, performed on the right eye two days after the inferior temporal BRAO (Fig 2) showed occlusion of the inferotemporal arteriole and evidence of the previous superior macular branch arteriolar occlusion. INVESTIGATIONSThe following investigations gave normal or negative results: full blood count, erythrocyte sedimentation rate, routine biochemical screen-

Oscillucusis and sudden deafness in a migraine patient

“…The most common migraine aura is visual, and metabolic studies of the brain suggest a primary neuronal basis with secondary vascular changes, such as vasospasm or vasodilatation depending on the phase of migraine [32][33] . In retinal migraine this vasospasm may result in blindness [34][35] , illustrating vasospasm to have occurred at some time during the migraine attack 12, 21,36. The pathophysiology of auditory symptoms is probably related with vasospasm of small arterioles within the cochlea and labyrinth, much as retinal migraine may involve only a subset of arterioles in the retina 11,12,22,37 . However controversy exists regarding its role in the production of the symptoms 29,37 .…”

Retinal Nerve Fibre Layer Thickness of Migraine Patients with or without White Matter Lesions

“…[15][16][17][18][19][20][21] According to Kara et al, 30 the retrobulbar circulation and flow haemodynamics in the left vertebral artery may be altered in both headache and headache-free periods in migraineurs without aura. Glenn et al 31 reported a case of complicated migraine due to bilateral retinal infarction. Beversdof et al 32 reported recurrent branch retinal infarcts in association with migraine.…”

Retinal Nerve Fibre Layer Thickness in Migraine Patients with or without Aura

“…[10][11][12] Using colour Doppler imaging, Kara et al 13 reported that central retinal artery and posterior ciliary artery vessel resistance was higher in patients with migraine in both headache and headache-free periods compared with the control group. All of these studies support the hypothesis of low perfusion and vascular retinal variations in migraine.…”

“…10,11 Retinal alterations described in the literature manifest as acute and chronic retinal damage. Migraine can lead to focal decrease in cerebral blood flow and perhaps in retinal circulation.…”