Infarcts of Both Inferior Parietal Lobules With Impairment of Visually Guided Eye Movements, Peripheral Visual Inattention and Optic Ataxia

Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic adenocarcinoma. The initial left-sided infarct induced right visual neglect, impairment of right-beating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OKN slow phase. The lesion on the left involved the upper part of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the SPL. As the oculomotor deficits and the peripheral visual inattention were bilateral after the second infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres. The zone damaged in common included a small part of the SPL, the superoanterior extremity of the angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all visually guided eye movements and in visual attention. It is further suggested that two corticofugal pathways are implicated in visually guided saccades, the first arising from the frontal eye fields and projecting directly onto the premotor structures in the brainstem, the second arising from the posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and including a relay in the superior colliculus before reaching the premotor structures. Lastly, the findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed occipitofrontal pathways coursing in the deep white matter of the parietal lobe.