Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. It is caused by lesions of the retrochiasmal visual pathways, ie, lesions of the optic tract, the lateral geniculate nucleus, the optic radiations, and the cerebral visual (occipital) cortex (figure 1) [1-4]. Characteristics of the visual field abnormalities (type, form, size, and congruity), along with associated neurologic signs and symptoms, have been traditionally used for localizing pathologic lesions in the brain (table 1) [1-6].
Homonymous hemianopia is often disabling, causing difficulties with reading and visual scanning. Patients may fail to notice relevant objects or avoid obstacles on the affected side, causing collisions with approaching people or cars. They are not legally allowed to drive in most states. This has dramatic consequences on their vocational and private lives [1,7].
This topic will discuss homonymous hemianopia as a fixed deficit; it may be a transient phenomenon resulting from migraine, transient cerebral ischemia, or seizure. This is discussed separately. (See "Amaurosis fugax (transient monocular or binocular visual loss)", section on 'Causes of transient binocular visual loss'.)
Any type of intracranial lesion in the appropriate location can cause a homonymous hemianopia; however, vascular causes (cerebral infarction and intracranial hemorrhage) are the most frequent in adults, ranging from 42 to 89 percent, followed by brain tumors, trauma, surgical interventions, and other central nervous system diseases [1,8-13]. In children, neoplasms are the most common cause of homonymous hemianopia (39 percent), followed by cerebrovascular disease (25 percent) and trauma (19 percent) . Homonymous hemianopia after head trauma may be under recognized; multifocal brain injury is more common in this setting, contributing to other neurologic deficits that may overshadow the visual field defect .
Uncommon causes of homonymous hemianopia include multiple sclerosis, infections (encephalitis, abscess), degenerative dementia (posterior cortical atrophy), Creutzfeldt Jakob disease, adrenoleukodystrophy, seizures, and severe hyperglycemia [12,15-20] (See "Clinical manifestations and diagnosis of Alzheimer disease", section on 'Posterior cortical atrophy'.)