Amaurosis fugax is characterized by a sudden, monocular, painless, temporary
visual loss due to a hypoperfusion of retinal circulation. Some of the more
frequent causes include atheromatous disease of the internal carotid or ophthalmic
artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure
glaucoma, increased intracranial pressure, orbital compressive disease, a
steal phenomenon, and blood hyperviscosity or hypercoagulability.1 Vasospasm may account for many cases of unknown
Amaurosis fugax due to exercise-induced vasospasm has been described only
once, in 1989 by Imes and Hoyt.3 They described
6 healthy young adults who experienced visual loss precipitated by exercise.
Three of them had monocular visual loss.
Exercise-induced visual disturbances not due to a hypoperfusion of retinal
circulation include pigmentary glaucoma attacks, which may be painless,5 Uhthoff symptom after optic neuritis,6
and unformed hallucinations secondary to occipital lobe tumors.7
We describe 3 more patients with exercise-induced monocular transient visual
loss, probably caused by vasospasm.
For 5 years, a 65-year-old man experienced recurrent exercise-induced
transient monocular blindness. Visual symptoms consisted of a rapid progressive
visual field constriction in his right eye. If the patient did not stop exercising,
complete monocular blindness would occur. The events lasted from 30 seconds
to 3 hours. They regularly appeared during heavy sport activities such as
jogging or biking. During the 5 years, the frequency and strength of the attacks
continuously decreased. The patient was in excellent health, had participated
in sports regularly since his youth, and had no coronary risk factors. He
had no history of migraine. He underwent an extensive work-up that included
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. The
results were normal. Blood evaluation included a complete blood cell count,
blood chemical analyses, blood coagulation studies, and tests for thyroid
function, erythrocyte sedimentation rate, antinuclear antibodies, cryoglobulins,
syphilis, Lyme disease, and anticardiolipin antibodies. Because the patient
was regularly able to provoke such 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. Treatment with aspirin or nifedipine
had no effect.
Ophthalmoscopic image of the right eye of the patient from case 1
during an asymptomatic period (A) and during an attack provoked by climbing
stairs (B and C). B, 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. C, 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.
A 40-year-old physician saw us because of a single attack of a hemianopic
temporal scotoma in the left eye that had occurred during heavy physical activity.
The episode lasted about 30 minutes. By covering 1 eye, he noticed that the
defect was truly monocular. He had a history of migraine and had experienced
headaches or stomachaches several times after heavy bodybuilding. He had undergone
a work-up by internal medicine specialists for the stomachaches, which were
diagnosed to be of vasospastic origin. Treatment with aspirin before sports
participation reduced the degree of the symptoms. Results of a neuro-ophthalmologic
examination and kinetic perimetry were completely normal. Because of the patient's
history of chronic exercise-induced migraine and stomachache, the ocular symptoms
were considered by exclusion also to be caused by vasospasm, and no further
examinations were carried out.
For 14 years, a 45-year-old man experienced an exercise-induced transient
"graying out" in his right eye lasting from 30 seconds to 15 minutes. Covering
1 eye confirmed that the symptoms were monocular. Results of a neuro-ophthalmologic
examination, including a gonioscopy, were normal. Because this patient too
was able to provoke such episodes by climbing stairs, we were able to examine
him several times during an attack. We did not see any fundus abnormalities,
possibly because stopping exercise resulted in a rapid recovery of visual
acuity. However, immediate repeated automated perimetry after an attack showed
a reproducible mild constriction of the visual field in his right eye. The
left eye was always asymptomatic. A repeated intake of nifedipine resulted
in the successful prevention of visual symptoms and a normal right automated
perimetry finding after exercise. He had a history of thrombosis of the left
superficial femoral artery. At the time of the examinations, the patient was
not taking any medication. He had been smoking intermittently since he was
a young adult. He had no history of migraine. The same blood work-up as in
case 1 was performed, and results were found to be normal. Stress electrocardiographic
findings were normal. Results of transcranial and transorbital Doppler and
duplex ultrasonography were normal except for a slight hypoplastic right vertebral
artery. Further work-up was refused by the patient.
Vasospasm is a recognized cause of amaurosis fugax1,3
and also occurs in elderly patients.2 Associated
conditions include migraine, cluster headache, temporal arteritis, polyarteritis
nodosa, and eosinophilic vasculitis.
Our 3 patients had exercise-induced monocular attacks, probably caused
primarily by vasospasm. They illustrate the variety of transient monocular
visual symptoms and findings that occur with exercise. Our first patient experienced
rapid progressive visual field constriction. If exercising was not stopped,
complete monocular blindness would occur. Anophthalmoscopy revealed a transient
central artery occlusion (Figure 1).
Our second patient noticed a hemianopic temporal scotoma in his left eye.
The third patient described the visual loss as "graying out." Computerized
perimetry performed immediately after an attack revealed an ipsilateral mild
peripheral visual field constriction. In contrast to the 6 cases described
by Imes and Hoyt,3 one of our patients with
exercise-induced vasospasm had a late onset at age 60 years. Therefore, we
conclude that vasospasm may also occur in elderly patients with a recent onset
of exercise-induced amaurosis fugax.
Vasospastic amaurosis fugax is presumed to be caused by a vasospasm
or reduced arterial flow.2,4
Vasospasms could be caused by a vessel hypersensitivity to certain vasoconstrictors
released during physical exercise or by an inappropriate high release of such
mediators (eg, catecholamines, endothelin-1, or neuropeptide Y). Winterkorn
et al4 reported a successful treatment with
calcium channel blockers. In our first patient, neither aspirin nor the calcium
channel blocker nifedipine was able to reduce the severity of the attacks.
Our second patient was able to reduce the stomachaches by taking aspirin before
performing sports. Because he had had only 1 attack involving the visual system
and was comfortable with aspirin intake, calcium channel blockers were not
tried. In our third patient, nifedipine could successfully prevent attacks.
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.
Corresponding author and reprints: Daniel S. Mojon, MD, Department
of Neuro-Ophthalmology and Strabismus, Kantonsspital, 9007 St Gallen, Switzerland
Jehn A, Frank Dettwiler B, Fleischhauer J, Sturzenegger M, Mojon DS. Exercise-Induced Vasospastic Amaurosis Fugax. Arch Ophthalmol. 2002;120(2):220-222. doi: