Retinal Migraine Headache DISEASE entity

Migraine is a common and well-documented disorder first described in 1882 by Dr. Galezowski. Ocular or retinal migraines are generally defined as a transient monocular scotoma or loss of vision which is accompanied or followed by a headache within 60 minutes of visual symptoms onset.

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In some cases, persistent monocular visual loss and abnormal ophthalmological findings have been reported. The symptoms are usually transient. The pathophysiology of those persistent deficits is not clear.

Based on theories and pathophysiology of retinal migraine, precipitating factors for a retinal migraine are the same for migraine, with and without aura.

Factors include but are not limited to, emotional stress, high blood pressure, and hormonal contraceptive pills, as well as exercise, being at a higher altitude, dehydration, smoking, low blood sugar, and hyperthermia.

Comorbidity with lupus, atherosclerosis, and sickle cell disease increases the risk of having a retinal migraine.

A retinal migraine is a rare disorder, but the prevalence is not known. Data specific to retinal migraines do not exist, but migraines, in general, have a prevalence of 18.2% in females and 6.5% in male patients, with a higher prevalence in whites followed by blacks followed by Asians.

Retinal migraine can start as early as 7 years of age, but most cases start in the second decade and peak in the fourth decade of life.

Based on a study by Pradhan et al., it was found that 50% of retinal migraine patients said the vision loss was complete in one eye, up to 20% said it was just blurring, 12% reported an incomplete loss, 7% dimming, and 13% scotoma.

More than 75% of patients had a headache on the same side as the vision disturbance within an hour.

Twenty-nine percent of retinal migraine patients have a history of migraine headaches, and 50% have a family history of migraine headaches.

The pathophysiology of migraine remains controversial. One theory of ocular migraine is that it is due to vasospasm within the retinal or ciliary vasculature while others think it is a spreading depression of the neuron in the retina that is similar to the spreading depression of the cerebral cortex.

The spreading depression of the cerebral cortex is usually seen in the visual aura of a classic migraine; it has been observed in patients having an episode of retinal migraine, and vasoconstriction of both veins and arteries that could be diffuse or segmental.

It also can be noticed by ocular hypoperfusion on fundoscopy. Fluorescein angiography can confirm the diagnosis. The fluorescein angiogram shows delayed filling or occlusion of the central retinal artery and its branches with either normal ciliary circulation or patchy choroidal defects and capillary dropout.

Retinal migraine attacks are precipitated by similar factors as a migraine with aurae such as stress, smoking, hypertension, hormonal contraceptive pills, exercise, bending over, high altitude, dehydration, hypoglycemia, or excessive heat.

Strong family history in these patients suggests that a retinal migraine has a genetic predisposition but no clear pattern of inheritance has been described.

The vasospasm theory is controversial due to the complexity of the retinal vascular supply. The retina has dual circulation, central retinal artery supplies, inner retinal layers, lacks adrenergic innervation, maintains sensory nerves, and is auto-regulated.

The choroidal circulation supplies the posterior retina including the photoreceptors it carries adrenergic fibers without autoregulation.

Retinal Migraine Headache MANAGEMENT

If the attacks are infrequent, such as one per month, then treatment is not necessary. When attacks are more frequent, first-line therapy starts with lifestyle changes that include avoiding dietary triggers such as alcohol and caffeine, controlling stressors like high blood pressure, and ceasing to smoke.

If that does not help, then the patient must start a diary to help evaluate the success of the therapy and initiate prophylaxis therapy.

It is usually recommended to avoid ergot and beta-blockers in retinal migraines due to the increased incidence of irreversible vision loss.

Calcium channel blockers such as nifedipine and verapamil (most effective) are the mainstay of treatment here. Contraindications to calcium blockers include congestive heart failure, hypotension, sick sinus syndrome, cardiac conductive defects, concomitant, and renal or hepatic failure.

Other medications such as coumadin and heparin have been used in isolated cases of patients with antiphospholipid antibody syndrome and retinal migraine.

Aspirin and antiepileptic drugs have all been shown to reduce the severity of attacks. An abortive therapy is not used in this condition due to the brief duration of episodes; the main focus of treatment would be to reduce the recurrence of attacks.

Medications such as Triptans, ergots, and beta-blockers should be avoided in migraines with transient vision loss since there is a concern for exacerbation of vasoconstriction and increasing the risk of potential irreversible visual loss.

Retinal Migraine Headache COMPLICATIONS

Complications of a retinal migraine include central retinal artery occlusion (CRAO), retinal infarction, central retinal venous occlusion, branch retinal artery occlusion (BRAO), retinal hemorrhages that can lead to edema of the retina and disc, ischemia of choroid or optic nerve, and vitreous hemorrhage.

Many of those could lead to irreversible vision loss in the patient. It is important to avoid the use of triptans, ergots, and beta-blockers in migraines with transient vision loss secondary to the risk of potentiating vasoconstriction and increasing the risk of irreversible visual loss.

Would you have interest in taking retinal images with your smartphone?

Fundus photography is superior to fundus analysis as it enables intraocular pathologies to be photo-captured and encrypted information to be shared with colleagues and patients.

Recent technologies allow smartphone-based attachments and integrated lens adaptors to transform the smartphone into a portable fundus camera and Retinal imaging by smartphone.



  1. Pula JH, Kwan K, Yuen CA, Kattah JC. Update on the evaluation of transient vision loss. Clin Ophthalmol. 2016;10:297-303.
  2. Pradhan S, Chung SM. Retinal, ophthalmic, or ocular migraine. Curr Neurol Neurosci Rep. 2004 Sep;4(5):391-7.
  3. Ahmed M, Boyd C, Vavilikolanu R, Rafique B. Visual symptoms and childhood migraine: Qualitative analysis of duration, location, spread, mobility, colour and pattern. Cephalalgia. 2018 Dec;38(14):2017-2025.
  4. Reggio E, Chisari CG, Ferrigno G, Patti F, Donzuso G, Sciacca G, Avitabile T, Faro S, Zappia M. Migraine causes retinal and choroidal structural changes: evaluation with ocular coherence tomography. J Neurol. 2017 Mar;264(3):494-502.
  5. MacGregor EA. Migraine (Japanese Version). Ann Intern Med. 2017 Apr 04;166(7):JITC49-JITC64. 




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