Bilateral Cortical Blindness due to Bilateral Occipital Infarcts without Anosognosia

Abstract

Bilateral cortical blindness refers to the total loss of vision in the presence of normal pupillary reflexes and in the absence of Ophthalmological disease resulting from bilateral lesions of the striate cortex in the occipital lobes. In most cases, these patients deny their blindness and their behavior is as if they have an intact vision. We report the case of an 84-year-old man with bilateral cortical blindness resulting from bilateral occipital lobe infarcts. The patient presented this infrequent clinical condition after acute bilateral infarction of the occipital lobes possibly due to cardiac embolism resulting from atrial fibrillation of unknown duration. Subcutaneous administration of low molecular weight heparin in therapeutic doses resulted in neurological improvement in the first four days. Interestingly, the visual symptoms were complicated neither by anosognosia nor by memory impairment. Cortical blindness and Anton’s syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease could be the background in a bilateral cortical blindness, as in our patient. To our knowledge, this is the first reported case with bilateral cortical blindness due to simultaneous bilateral occipital infarcts but without anosognosia. Bilateral cortical blindness refers to the total loss of vision in the presence of normal pupillary reflexes and in the absence of Ophthalmological disease resulting from bilateral lesions of the striate cortex in the occipital lobes. In most cases, these patients deny their blindness and their behavior is as if they have an intact vision. We report the case of an 84-year-old man with bilateral cortical blindness resulting from bilateral occipital lobe infarcts. The patient presented this infrequent clinical condition after acute bilateral infarction of the occipital lobes possibly due to cardiac embolism resulting from atrial fibrillation of unknown duration. Subcutaneous administration of low molecular weight heparin in therapeutic doses resulted in neurological improvement in the first four days. Interestingly, the visual symptoms were complicated neither by anosognosia nor by memory impairment. Cortical blindness and Anton’s syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease could be the background in a bilateral cortical blindness, as in our patient. To our knowledge, this is the first reported case with bilateral cortical blindness due to simultaneous bilateral occipital infarcts but without anosognosia.