Higher Cortical Lesions

Patients with lesions of visual association areas may have visual field defects if striate cortex is involved, but their visual complaints frequently cannot be explained by field loss alone. Further investigation often allows more accurate characterization of their symptoms.

Inferior occipital lobe dysfunction, involving the lingual and fusiform gyri, results in a contralateral homonymous upper quadrantanopia and abnormal color vision in the contralateral hemifield (cerebral hemiachromatopsia). With left-sided lesions when the splenium of the corpus callosum or adjacent periventricular white matter is involved, alexia without agraphia (or pure alexia or "word blindness") may be observed. This represents a disconnection syndrome characterized by a right homonymous field defect and inability to retrieve lexical visual information processed in the intact right occipital lobe.

Visual agnosia (the inability to recognize visual objects), in the absence of significant afferent visual pathway disruption, suggests bilateral medial occipitotemporal lesions disrupting the inferior longitudinal fasciculus, which is a white matter tract connecting striate cortex with the visual association areas of the temporal lobe. Prosopagnosia, a visual agnosia specific for faces, results from similar lesions. Defective motion perception is observed with lesions of Brodmann area 39 or lateral occipitotemporal cortex.

Neglect or inattention to visual, tactile, or auditory stimuli in the left hemifield; dressing and constructional apraxia; and spatial disorientation suggest right hemispheric lesions. Neglect can occur without a hemianopia. Large parietal lesions frequently cause both, however, and in affected patients it may be difficult to separate dense visual neglect from field loss. The severity of neglect ranges from complete inattention to all stimuli in the left hemifield to subtle visual neglect of objects to the left only when stimuli are presented simultaneously on both sides of midline (double simultaneous stimulation).

Balint's syndrome is characterized by optic ataxia (a defect in reaching under visual guidance), simultanagnosia (an inability to recognize a whole picture despite the ability to perceive its parts), and ocular apraxia (a defect in voluntary eye movements). The symptom complex is caused by bilateral occipitoparietal lesions that are important for visual attention and foveal refixation. One or all elements may be present. Because the lesions commonly involve upper banks of occipital cortex, Balint's syndrome is commonly associated with inferior altitudinal field defects. Watershed infarctions are the usual cause.

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