Evaluating Transient Monocular Vision Loss

A transient monocular loss of vision (TMVL) should always scream VASCULAR EVENT! It’s basically a stroke or a TIA of the eye. But how does this happen, what vessels are affected, and how do the patient’s symptoms clue you into a more accurate diagnosis of amaurosis fugax? In this week’s BrainWaves episode, we review all of these in great detail:

We open the episode, as we do most of the time, with a quick anatomy review. It’s nice to

Image under public domain.

actually know what parts of the eye we’re talking about.

The retina receives vascular supply from the central retinal artery, a branch of the ophthalmic artery which originates from the internal carotid. The central retinal artery courses deep through the optic nerve to supply the superficial 2/3 of the retinal neural layers whereas the posterior ciliary arteries—also branches off the ophthalmic—travel outside of the optic nerve and supply the outer 1/3 of the retina and the optic nerve head just below the surface of the globe. Finally, the optic nerve head receives an anastomotic blood supply from the central retinal artery and posterior ciliary arteries. After oxygen and nutrients are extracted here, blood eventually circulates out of the globe, exiting via the central retinal vein.

A semi-comprehensive differential diagnosis of TMVL, by Biousse and Trobe, is found here:

A temporary occlusion of the ophthalmic artery is responsible for amaurosis fugax in many cases. This causes profound vision loss, often to the degree of No Light Perception because it blocks both the retinal and choroidal circulation. In these cases, the retina becomes white and edematous and no cherry red spot is seen because the choroid is not perfused. Vision returns after fewer than 5 minutes in most causes of amaurosis, and the patient should be evaluated urgent using carotid vessel imaging and echocardiography. Certainly, Giant Cell Arteritis is an alternative  cause of amaurosis fugax as well and must be considered carefully. See below.

Retinal ischemia, on its own, is a painless experience–minus the anxiety and panic of having lost your vision of course. In a central retinal artery occlusion, the entire retina is devoid of oxygen and the patient’s vision is reduced to finger counting or light perception vision only and a cherry red spot may be seen on the fundus examination. Central retinal artery occlusions may be embolic, for instance, from a plaque that has dislodged from a stenosed carotid bifurcation, or vasculitic, for instance from Giant Cell Arteritis. In an embolic CRAO, an embolus may be seen in the central retinal artery on ophthalmic examination. Giant cell arteritis would present usually with other typical symptoms such as headache, jaw claudication, scalp tenderness, and symptoms of polymyalgia rheumatica due to the overlap between these conditions. Laboratory studies such as ESR and CRP would be helpful in making the diagnosis and steroids should be instituted rapidly to avoid contralateral vision loss or stroke.

The optic nerve itself is susceptible to vascular compromise. Occlusion of the posterior ciliary arteries which provide blood flow to the anterior optic nerve (the optic disc) is not currently thought to be an embolic process in the same manner as a CRAO or BRAO. Anterior ischemic optic neuropathy, or AION is far more common than the posterior version (PION). AION occurs when perfusion to the optic nerve head is compromised and optic disc swelling is observed. The possibility of Giant Cell Arteritis must be considered in an older adult and typically causes significant vision loss and may be associated with many of the symptoms described earlier. Alternatively, non-arteritic ischemic optic neuropathy may occur in younger adults who have other vascular risk factors and a crowded optic disc appearance. PION is a much rarer condition and is caused by reduced perfusion to the posterior optic nerve. It causes acute vision loss without optic disc swelling in two major circumstances. The first is GCA. The second is in the post-operative setting when bloodflow to an optic nerve is compromised, often in prone-positioned surgery or in significant systemic hypotension.

Other symptoms that may be helpful in order to narrow your differential:

A lot of the time you may not find anything on the workup, and some tests may leave you with more questions than answers. But I think that this episode will open your eyes into the world of TMVL.

 

[Jim Siegler]


The content in this episode was vetted and approved by Imran Jivraj.

REFERENCES

Biousse V and Trobe JD. Transient monocular visual loss. Am J Ophthalmol. 2005;140:717-21.

Kattah JC, Wang DZ and Reddy C. Intravenous recombinant tissue-type plasminogen activator thrombolysis in treatment of central retinal artery occlusion. Arch Ophthalmol. 2002;120:1234-6.

Schumacher M, Schmidt D, Jurklies B, Gall C, Wanke I, Schmoor C, Maier-Lenz H, Solymosi L, Brueckmann H, Neubauer AS, Wolf A, Feltgen N and Group EA-S. Central retinal artery occlusion: local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology. 2010;117:1367-75 e1.

Ravits J and Seybold ME. Transient monocular visual loss from narrow-angle glaucoma. Archives of neurology. 1984;41:991-3.

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