Cerebral blindness is characterized by absence of blink to threat and optokinetic responses with normal fundi and preserved pupillary light reflexes. It results from bilateral retrogeniculate dysfunction. Anton’s syndrome refers to visual loss that is characterized by denial of blindness. While it classically presents in the form of cortical blindness, which is defined by bilateral occipital cortex involvement, to our knowledge, bilateral optic radiation involvement has not been previously described.

A 28 year old right handed man with a history of type one diabetes mellitus, hypertension, hyperlipidemia, and alcohol use, initially presented with diabetic ketoacidosis. He developed cardiac arrest for eight minutes, with hypoxemic and hypercarbic respiratory failure. He later had pulseless electrical activity arrest for three minutes. His hospital course was complicated by septic shock requiring pressors and acute renal failure requiring dialysis. A CT scan of head was obtained showing acute supratentorial and infratentorial infarcts. Neurologic exam was notable for preserved pupillary light reflexes, no blink to threat bilaterally, preserved voluntary eye movements, denial of blindness, and quadriparesis with greater weakness on the left. When asked to identify objects, the patient made incorrect guesses. MRI brain showed bilateral supratentorial and infratentorial border zone infarcts affecting the optic radiations bilaterally. The patient did not recover vision during the hospitalization.

This patient’s presentation is unusual as, to our knowledge, there have been no previously described cases of Anton’s syndrome resulting from bilateral optic radiation infarcts. While Anton’s syndrome may result from different pathological lesions in multiple locations along the visual pathways, this expands the spectrum of Anton’s syndrome resulting from cerebral infarction.