Occipital Lobe

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Unilateral occipital lobe lesions, which are commonly due to vascular insults or primary and metastatic neoplastic lesions, cause a contralateral congruous homonymous hemianopia respecting the vertical meridian. Posterior cerebral artery infarction may produce a hemianopia with macular sparing (rather than macular splitting), and this feature is specific to occipital lobe-related hemianopias. Proposed mechanisms include the dual vascular supply of the occipital poles, bilateral representation of the maculae, and test artifact due to poor central fixation by the patient. Restricted lesions of the upper or lower banks of the calcarine cortex cause quadrantic field defects.

Bilateral upper or lower bank disturbances produce altitudinal hemianopias respecting the horizontal meridian. Homonymous hemianopic central scotomas are a telltale sign of a unilateral occipital lobe tip disturbance. Acuity is preserved with unilateral occipital lobe damage, but it can be impaired with bilateral geniculocalcarine lesions. Any level of visual acuity is possible with bilateral retrochiasmal lesions, but the acuities should be symmetrical unless there is superimposed anterior visual pathway disease.

Hemianopias that are stroke-related are often isolated, unless a proximal posterior cerebral artery occlusion leads to a third-nerve palsy, ataxia, or ipsilateral hemiparesis from mesencephalic involvement, and memory or personality changes from mesial-temporal or thalamic involvement. A patient with a unilateral hemianopia due to occipital lobe

infarction has a normal optokinetic response. In contrast, one with a hemianopia owing to an occipital lobe mass with edema extending into the parietal lobe may have an abnormal optokinetic response when the targets are drawn ipsilaterally to the lesion (Cogan's rule).

Cortical blindness, characterized by absent blink to threat and optokinetic responses, results from bilateral occipital lobe involvement. Clinically, patients with cortical blindness can be distinguished from those with pregeniculate lesions by the presence of intact pupillary light responses. Cortically blind patients may confabulate visual perceptions or deny their blindness (Anton's syndrome). Some of these patients have additional contributory cerebral lesions that alter recognition, memory, and behavior.

Unusual features observed following occipital lobe injury include unconscious vision in the blind hemifield (blindsight) and the recovery of motion perception (Riddoch's phenomenon). A "second," more primitive, retinal-tectal-pulvinal subcortical, extrastriate visual pathway has been proposed as a possible explanation. Polyopia (single objects appearing as several), palinopsia (persistence of visual images), and optic allesthesia (abnormal object orientation in space) are other unusual phenomena resulting from occipital, occipitoparietal, or occipitotemporal lesions.

Migrainous phenomena can involve the occipital lobes and manifest with transient hemianopic phenomena, with or without scintillations or phosphenes, followed by headache. Some patients experience only the visual prodrome without the headache (acephalgic migraine). In rare instances, a complicated migraine may lead to occipital lobe infarction and a fixed hemianopic defect.

In elderly patients, the differential diagnosis of occipital lobe dysfunction also includes Alzheimer's disease and hemorrhagic infarction due to amyloid angiopathy. Hypertensive encephalopathy or eclampsia can produce cortical blindness or transient hemianopias in patients of any age. Infectious causes include encephalitis, abscesses, progressive multifocal leukoencephalopathy, and Creutzfeldt-Jakob disease. In children, meningoencephalitis, adrenoleukodystrophy, and MELAS may be responsible for hemianopias. Ictal or postictal hemianopias are rare.

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