Visual phenomena, decreased vision secondary to occipital lobe infarct

A 72-year-old white male presented with the report of experiencing two red lights shining into his eyes. This was episodic and first occurred two days earlier. He further reported that “half” of the vision was missing in each eye. This was more apparent when he looked at a clock. He added that his left eye had cleared, but his right eye remained somewhat blurry.

His contributory ocular history as a previous patient (2003–2010) included strabismic amblyopia (35 RT hypertropia OD), and a shotgun injury to forehead during a live-fire training as a teenager with some shrapnel remaining. He relocated in 2010.

One year ago, he suffered a stroke affecting the left side of his face. Bell’s palsy was ruled out. A CT scan was inconclusive for infarct; he did not receive an MRI due to the buckshot in forehead). Tests were performed elsewhere.

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His current medication history is extensive and remarkable for hypothyroidism, hypertension, hypercholesterolemia and heart disease.

• Diltiazem-ER 240 mg/d

• Nexium (esomeprazole, AstraZeneca) 40 mgqd

• Synthroid (levothyroxine sodium, Abbott Laboratories) 200 mcg/d

• Potassium chloride 10MEQ/d

• Lasix (furosemide, Sanofi Aventis) 40 mg bid

• Zocor (simvastatin, Merck) 20 mg HS

• Flonase (fluticasone, GlaxoSmithKline) 0.05% spray 1per nostril qd

• Pradaxa (dabigatran, Boehringer Ingelheim) 150 mg bid

• Digoxin 0.25 mg/d

• Testosterone 200 mg qd

• Finasteride 5 mg three times a week

• Fish oil 1,000 mg bid

• Vitamin B₁₂ 1,000 mcg twice a day

• Metamucil once a day

• Self-initiation of 87 mg aspirin two days ago (in addition to the Pradaxa)

Exam findings

Baseline examination findings showed visual acuities of OD 20/200 (pinhole 20/200); OS 20/40 (pinhole) 20/40. Goldmann tonometry showed intraocular pressures of 16 mm Hg in both eyes.

Pupils were miotic but reactive to light and accommodation without afferent pupillary defect. Cover testing revealed a constant three prism diopter right esotropia with 2 prism diopter right hypertropia. Ocular motilities were full in each eye.

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The patient’s blood pressure was 130/70 with pulse of 60 and regular. 

CenterVue Macular Integrity Assessment (MAIA) Microperimeter revealed a bilateral left inferior homonymous congruous macular quadrantanopsia (see Figure 1). Dilated fundus exam revealed a small “disk at risk” optic nerve head with subtle “pseudo” papilledema. Trace epiretinal membrane bilaterally was present. The left retina also displayed two areas of subretinal deposits that seem quiescent on OCT and a choroidal nevus (see Figures 2, 3).

Diagnosis

The macular objective visual findings suggest a specific area of post-chiasmal involvement. Because imaging studies involving MRI are contraindicated due to metallic foreign bodies, this was postulated based on the MAIA evidence.

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Plan and follow-up

Visual rehabilitation following occipital lobe infarct, as indicated by the macular findings, is challenging and often frustrating for both patient and provider. This patient was prescribed nitric oxide (Neo 40 Professional, HumanN) bid by mouth in an attempt to improve circulation through vasodilation from the indirect potentiation of a proprietary 425 mg nitric oxide blend secondary to the action of Vitamin B12, as (6S) – 5-methyltetrahydrofolic acid, and Vitamin C.

The patient was also placed on medical food Ocufolin (Ocufolin) bid that contains Vitamins B, C, D, and E, as well as zinc, lutein, zeaxanthin, N-acetylcysteine 180 mg, and (6S)-5-methyltetrahydrofolic acid 900 mcg. The two supplements were initiated to increase circulation and possibly circumvent additional events that could further affect his vision.

He was asked to return the following day.

At the one-day follow-up visit, visual acuity was unchanged in either eye. Humphrey’s 24-2 Visual field at threshold displayed a supra and infra-nasal field loss (no central visual-field depressions in the right eye (see Figure 4). A Humphrey’s 10-2 showed a left inferior macular quadrantopsia consistent with the objective macular sensitivity results (Figure 5).

A neurology consult to discover the etiology of the occipital lobe infarction was entertained. An MRI could not be performed, and CT scan is unlikely to image the likely lesion.

With information from the MAIA (scanning laser ophthalmoscope that places a white stimulus on a dark background on the retina while registering the retinal vasculature to counteract eye movements) and Humphrey’s 10-2, a diagnosis of occipital lobe infarct, by exclusion, was made.

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Communication with his neurologist was made and no additional treatment was recommended until reevaluation could be performed.

At the two-week follow-up visit, his best visual acuity was 20/10 OD, 20/30 OS. The MAIA (see time analysis) was stable to improving (Figure 6.)

The current treatment protocol was continued.

Discussion

The MAIA shows a defect on the retina and static perimetry shows congruent visual field loss.

It is designed to track very subtle changes in macular sensitivity by actively tracking retinal position while projecting a stimulus.¹

Unlike traditional visual field units that assume proper fixation while presenting a stimulus, the MAIA will adjust the stimulus being projected onto the retina to accurately test a specific area of the retina. The stimuli are registered to the retinal image to allow for a correlation between function and structure.

Follow-up examinations will place the stimuli in the exact position to the baseline exam and changes in function can be examined. In personal (PEW) discussions with numerous patients, both the objective (MAIA) and subjective data (static perimetry) provide motivators for adhering to medication recommendations.

MAIA has the advantage of objective data with good reliability and vessel registration on follow-up.¹ With this device, the same retinal areas are assessed each time.

Methylation, folate pathways, biopterin and transsulfuration pathways as well have been suggested as components of circulatory compromise. Recent references highlight the metabolic pathways and their consequences.^2-4

Optometrists in the near future will need to play a more proactive and holistic role in our patients’ care. This case illustrates the potential for visual rehabilitation enhancement with the use of supplements thought to have a positive impact.

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References:

1. Ellex. MAIA â€Â Macular Integrity Assessment. Available at: http://static1.1.sqspcdn.com/static/f/581090/18176760/1336935415477/MAIA_Overview.pdf?token=pg3FeV%2FlrxF6jv3kiwjA5SWmkJU%3D. Accessed 11/22/16.

2. Bhatia P, Singh N. Homocysteine excess: delineating the possible mechanism of neurotoxicity and depression. Fundam Clin Pharmacol. 2015 Dec;29(6):522-8.

3. McCully KS. Homocysteine Metabolism, Atherosclerosis, and Diseases of Aging. Compr Physiol. 2015 Dec 15;6(1):471-505

4. Lupoli R, Di Minno A, Spadarella G, Franchini M, Sorrentino R, Cirino G, Di Minno G. Methylation reactions, the redox balance and atherothrombosis: the search for a link with hydrogen sulfide. Semin Thromb Hemost. 2015 Jun;41(4):423-32.