Transient Visual Loss in a Marathon Runner, Ocular Migraine
by Jeffrey Dach MD

A 55 year old female marathon runner noticed recurrent visual disturbance in one eye when exercising. Later, the patient reported the visual loss persisted and was associated with intermittent headaches. The patient presented to the ER, emergency room, and extensive CAT scan and MRI imaging studies in the hospital were all normal. The patient was referred to a neurologist. After reviewing the negative imaging studies with CAT angiography and MRI, the diagnosis of cerebral infarction was excluded, and the neurologist  suggested the diagnosis of transient ishemic attack (TIA) and the platelet inhibitor, aspirin, was prescribed. Following this, the patient was seen by a neuro-opthalmologist who entertained the diagnosis of Transient Loss of Vision (Amaurosis Fugax) associated with retinal artery spasm, also called Ocular Migraine. The neuro-opthalmologist prescribed nifedipine, a calcium channel blocker drug. Symptoms were relieved when the patient took the nifedipine, and symptoms returned when the drug was stopped.

Header Image:

A) Normal Ophthalmoscopic image of the retina of right eye of the patient during an asymptomatic period (A) (Green Arrows show normal retinal vessels) and Image (B) was taken during an attack provoked by climbing stairs, and Image C taken after resting recovery period returning to normal. 

B) After Climbing Stairs. A pale optic disc, a more distinct fovea, and a narrowing of all branches of the retinal arteries and veins, obtained 1 minute 54 seconds after the acute visual loss.(Red Arrows Showed Narrowed Retinal Vessels)

C) Recovery Image after Resting: Normal diameter of all retinal vessels, obtained 2 minutes 15 seconds after the acute visual loss and 10 seconds after the return of vision in the right eye. (No Arrows on this one. All Normal). Images Courtesy of:  Jehn, Andrea, et al. “Exercise-induced vasospastic amaurosis fugax.” Archives of Ophthalmology 120.2 (2002): 220-222.

Transient Loss of Vision (Amaurosis Fugax) associated with retinal artery spasm, also called Ocular Migraine can be a diagnostic dilemma to the neurologist and may be difficult to distinguish from retinal artery embolism. Useful tests include vascular imaging studies, and retinal photography by a neuro-ophthalmologist. An extensive neuro-imaging work-up is usually all normal. This includes a neuro-ophthalmologic examination (with a gonioscopy), computerized visual field testing, visual-evoked potentials, a general and cardiovascular clinical examination, echocardiography, Holter monitoring, magnetic resonance angiography, and transcranial and transorbital Doppler and duplex ultrasonography. Blood evaluation is also normal. This includes complete blood cell count, blood chemical analyses, blood coagulation studies, and tests for thyroid function, erythrocyte sedimentation rate, antinuclear antibodies, cryoglobulins, Lyme disease, and anticardiolipin antibodies. If the episodes of visual disturbance are exercise induced, retinal photography of the fundus may document typical findings of retinal artery spasm. A Doppler ultrasonographic study during an attack may show transient reduction of blood flow in the central retinal artery. Fluorescein angiography of the retina may be useful. Calcium channel blocker nifedipine may be effective in certain patients with exercise-induced vasospastic amaurosis fugax.

In 2021, Carlos Tello, PhD reviewed ocular migraines and wrote:

Calcium channel blockers such as nifedipine and verapamil work by reducing sudden contractions of the eye’s arteries, which reduces the release of serotonin and the occurrence of “spreading depressions” . In a clinical trial on 9 people suffering from ocular migraines, the use of calcium channel blockers halted all episodes. When the treatment was discontinued, the ocular migraines returned [29]. Calcium channel blockers have a rapid onset of action. Nifedipine tablets placed under the tongue were able to block ocular migraines within 30 seconds in one patient and within 10 minutes in another [31].

Side effects of calcium channel blockers include [32]: Accumulation of fluids in the body, causing swelling (peripheral edema). Overproduction of diluted urine (polyuria). Acid reflux. Enlargement of the gums (gingival hyperplasia). It is not advised to take calcium channel blockers with beta-blockers [30]. Calcium channel blockers are not recommended in people with heart, kidney, and liver failure, low blood pressure, and sick sinus syndrome [32]. Reference: Retinal or Ocular Migraines: Symptoms, Causes & Treatments. Written by Carlos Tello, PhD (Molecular Biology) | Last updated: November 3, 2021 https://selfhacked.com/blog/retinal-or-ocular-migraines/

Conclusion: Exact diagnosis of amarosis fugax (ocular migraine) may be difficult with multiple possibilities to be considered. Once embolic disease and other causes such as vasculitis and gluten sensitivity are excluded, a trial with calcium channel blockers such as nifedipine  may prove beneficial.

Other causes of Amaurosis Fugax:

Embolic Stroke/vascular disease/Cerebrovascular Accident
Thrombophilia, genetic tendencey for clotting.
ANTIPHOSPHOLIPID SYNDROME (APS)
Gluten sensitivity
Giant cell arteritis
Retinal Artery Vasculitis
Associated conditions include migraine, cluster headache, temporal arteritis, polyarteritis nodosa, and eosinophilic vasculitis.

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References and Case Reports

1) Jehn, Andrea, et al. “Exercise-induced vasospastic amaurosis fugax.” Archives of Ophthalmology 120.2 (2002): 220-222.
episodes by climbing stairs, we had the opportunity to examine the patient several times during an attack. We could use fundus photography to observe and document the occlusion of the right central retinal artery (Figure 1). A Doppler ultrasonographic study during an attack showed a transient stopping of blood flow in the central retinal artery. We never observed a relative afferent pupillary defect during an attack. To our knowledge, this is the first report showing that the calcium channel blocker nifedipine may be effective in certain patients with exercise-induced vasospastic amaurosis fugax.

2) Suthahar, Y., et al. “A case of recurring Amaurosis Fugax.” NATIONAL JOURNAL OF NEUROLOGY 3 (2013): 85-87.
After much discussion, it was thought that WWs symptoms may possibly be attributed to carotid artery vaso-spasm [similar to the spasming of the coronary arteries in Prinz-metal angina]. She was initiated on Verapmil 120mg daily (calcium channel blocker) with surprising results. Her symptoms completely resolved and she experienced no reoccurrence as long as she complied with the verapmil.

(Winterkorn, et al. 1993) went a step further and gathered 9 patients with recurrent attacks of amaurosis fugax despite anti-platelet therapy and demonstrated complete symptom resolution in all patients through the use of calcium-channel blockers [nimodipine or verapamil]. He also established the return of symptomatic attacks once the treatment was withdrawn.

3) Winterkorn, Jacqueline, et al. “Treatment of vasospastic amaurosis fugax with calcium-channel blockers.” New England Journal of Medicine 329.6 (1993): 396-398.
After informed consent was obtained from each patient, treatment with calcium-channel blockers was initiated. When the initial dose was inadequate, the attacks continued but were less frequent and less severe. The dose was increased until an effective therapeutic dose was achieved (20 mg of nifedipine three times daily, 60 mg of a long-acting preparation of nifedipine a day, or 120 mg of a long-acting preparation of verapamil a day); thereafter, no patient had further attacks. Two patients stopped taking the calcium-channel blocker soon after they became free of symptoms, and two other patients skipped several doses of medication while traveling. In each of these four patients, the attacks of amaurosis fugax resumed within a few days and persisted until treatment with nifedipine was reinstated. More than one year after treatment was begun, all patients were still taking calcium-channel blockers, with no further recurrence of amaurosis fugax.

4) Retinal or Ocular Migraines: Symptoms, Causes & Treatments
Written by Carlos Tello, PhD (Molecular Biology) | Last updated: November 3, 2021

5) Park, Ji-Hyung, et al. “A case report of isolated orbital vasculitis mimicking retinal migraine: A potential cause of recurrent transient monocular blindness and ipsilateral headache.” Cephalalgia 39.6 (2019): 792-798.  Isolated orbital vasculitis should be considered in differential diagnosis of recurrent transient monocular blindness and ipsilateral headache. High-resolution vessel wall magnetic resonance imaging can be helpful for the diagnosis.

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Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
my web site: https://drjeffreydachmd.com/
my personal blog: www.jeffreydachmd.com 
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Menopausal Hormone Replacement, Health Benefits
Natural Thyroid Toolkit by Jeffrey Dach MD
Cracking Cancer Toolkit ebook
Cracking Cancer Toolkit print version
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www.naturalmedicine101.com
www.bioidenticalhormones101.com
www.truemedmd.com
www.drdach.com

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Published on June 11th, 2026 by Jeffrey Dach MD