Cause of transient monocular visual loss may be difficult to ascertain, expert says

January 1, 2006

With the widespread availability of OCT, clinical can easily examine the vitreous interface.

Chicago-Transient monocular visual loss, also known as amaurosis fugax, can be a real puzzle for the neuro-ophthalmologist because by the time the patient has been referred, the more commonly known causes have already been ruled out, explained Cameron F. Parsa, MD, who spoke at the Neuro-ophthalmology Subspecialty Day Meeting during the American Academy of Ophthalmology annual meeting.

"The only advances [in identifying embolic causes] have been technical in nature," explained Dr. Parsa, assistant professor of ophthalmology, Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore. "We use Doppler ultrasonography rather than ophthalmodynamometry to determine the presence of cholesterol plaques or degree of carotid stenosis. Transesophageal echocardiography is used instead of transthoracic echocardiography to detect calcific plaques in the heart and aorta. We also have improved ability to identify prothrombotic factors in the blood."

Neural-mediated causes

With the clear-cut causes ruled out, the neuro-ophthalmologist may have to look a little deeper and consider mechanisms that are neither embolic or compressive for transient visual loss.

Hans E. Killer, MD, and colleagues photographically documented in the literature in 2003 a case of focal constriction of retinal vessels with corresponding visual field defects, which lasted several hours and then resolved. The patient also presented with a migraine headache at the same time, Dr. Parsa noted.

"So how does this focal vasoconstriction occur?" Dr. Parsa said. Unlike vessels elsewhere in the body, there is no sympathetic innervation of the retinal vasculature. "We think it may be regulated by signals from neural and glial cells, known as neurovascular coupling. We know that potassium plays an important role in this."

In cases of witnessed retinal vasoconstriction, most patients also had migraine headaches. Ultimately, the "underlying local dysfunction" points to retinal neural or glial cells, Dr. Parsa said.

Non-ischemic causes

In 1994 William F. Hoyt, MD, proposed that ephaptic neural transmission in the retina might be another mechanism producing amaurosis fugax, during a symposium organized by the American Academy of Ophthalmology and the North American Neuro-Ophthalmology Society.

"Such side-by-side, rather than synapse-to-synapse, axonal signaling can occur under various conditions, temporarily incapacitating neuronal function," Dr. Parsa said.

In the neurologic literature in 2001, Peter J. Goadsby, MD, PhD, reviewed the concept of "cortical spreading depression," which consists of a transient suppression of all neuronal activity that slowly advances across the brain cortex. This ephaptic "depolarization wave" is now the accepted cause of cerebral migraine. "It is, in fact, glial-cell mediated and linked to electrolyte concentration, particularly potassium surrounding the glial cells," Dr. Parsa said.

In the laboratory, researchers have shown this spreading depression to be possible in the amphibian and chick retina, he said.

Although spreading depression can be elicited in the retina in vitro, Dr. Parsa posed the following question: "What non-vascular event could affect M�glial cells in the retina in vivo, alter the electrolyte balance, and trigger spreading depression?"

Posterior vitreous detachment

The answer could be posterior vitreous detachment, he said. Vitreous separation was first discussed as a possible etiology for amaurosis fugax in 1994 by Barrett Katz, MD, and Dr. Hoyt. Recently this year, they published cases of gaze-evoked amaurosis secondary to vitreopapillary traction.