EC Ophthalmology

We report a sixty-one years old male, who presented with complaints of blurring of vision in his right eye for two weeks along with floaters and headache. Best corrected visual acuity (BCVA) was recorded as 20/30 and 20/20 in his right and left eye respectively. A relative afferent pupillary defect (RAPD) was noted in the right eye. Fundus examination revealed disc edema in the right eye with unremarkable fundus in the left eye. The color vision, contrast sensitivity, Amsler’s grid evaluation and intraocular pressure (IOP) were within normal limits. Perimetry showed a superior altitudinal field defect in the right eye with unremarkable perimetry in the left eye. Keeping the diagnosis of non-arteritic anterior ischemic optic neuropathy (NA-AION), intravenous Methylprednisolone was started in pulse dose for three days. Appropriate investigations such as the Erythrocyte sedimentation rate (ESR) and complete blood count were ordered. After the completion of intravenous methyl-prednisolone for three days, the patient started complaining of weakness in the lower limbs and confusion. Neurological opinion was sought which revealed no significant abnormalities. The patient was sent to a cardiologist and an electrocardiogram (ECG) showed evidence of non-sustained ventricular tachycardia (NSVT). Magnetic resonance imaging (MRI) of the brain revealed an acute lacunar infarct involving the right thalamus (Right anterior thalamic-geniculate perforator territory infarct) with chronic ischemic microangiopathic changes. The patient was started on anti-hypertensive, anticoagulants, and oral steroids with the tapering dosage by the cardiologist.

Here is our aim to report a case of NA-AION which eventually led to a stroke that was induced by acute infarct of the anterior thalamic-geniculate perforator in an elderly patient.

 Keywords: Non-Arteritic Anterior Ischemic Optic Neuropathy; Disc Edema; Magnetic Resonance Imaging

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