Cortical blindness is loss of vision due to bilateral visual cortical damage (usually hypoxic-ischemic in origin), or bilateral subcortical lesions affecting the optic radiations. A small central field around the fixation point may be spared (macula sparing). Pupillary reflexes are preserved but optokinetic nystagmus cannot be elicited.
Cortical blindness may result from:
- Bilateral (sequential or simultaneous) posterior cerebral artery occlusion;
- "Top of the basilar syndrome";
- Cerebral anoxia;
- Bacterial endocarditis;
- Wegener’s granulomatosis;
- Coronary or cerebral angiography (may be transient)
- Epilepsy (transient);
- Cyclosporin therapy, e.g., following organ transplantation.
If acute in onset (i.e., vascular), cortical blindness may ultimately evolve to prosopagnosia via visual object agnosia.
Patients with cortical blindness may deny their visual defect (Anton’s syndrome, visual anosognosia) and may confabulate about what they "see."