The brain regions that are critically associated with visual neglect have become intensely disputed. In particular, one study of middle cerebral artery (MCA) stroke patients has claimed that the key brain region associated with neglect is the mid portion of the superior temporal gyrus (STG), on the lateral surface of the right hemisphere, rather than the posterior parietal lobe. Such a result has wide-ranging implications for both our understanding of the normal function these cortical areas and the potential mechanisms underlying neglect. Here, we use novel high resolution MRI protocols to map the lesions of 35 right-hemisphere patients who had suffered either MCA or posterior cerebral artery (PCA) territory stroke. For patients with MCA territory strokes, the critical area involved in all neglect patients was the angular gyrus of the inferior parietal lobe (IPL). Although the STG was damaged in half of our MCA neglect patients, it was spared in the rest. For PCA territory strokes, all patients with neglect had lesions involving the parahippocampal region, on the medial surface of the temporal lobe. PCA patients without neglect did not have damage to this area. We conclude that damage to two posterior regions, one in the IPL and the other in the medial temporal lobe, is associated with neglect. Although some neglect patients do have damage to the STG, our findings challenge the recent influential proposal that lesions of this area are critically associated with neglect. Instead, our results implicate the angular gyrus and parahippocampal region in this role.

BackgroundHuntington's disease (HD) is a fatal inherited neurodegenerative disease, caused by a

Disturbances in the white matter connections of the sensorimotor cortex can be demonstrated not only in manifest HD but also in premanifest gene carriers. Connectivity measures are well related to clinical functioning. DTI measures can be regarded as a potential biomarker for HD, due to their ability to objectify changes in brain structures and their role within brain networks.

We investigated single-word reading in normal subjects and patients with alexia following a left occipital infarct, using PET. The most posterior brain region to show a lateralized response was at the left occipitotemporal junction, in the inferior temporal gyrus. This region was activated when normal subjects, patients with hemianopic alexia and patients with an incomplete right homonymous hemianopia, but no reading deficit, viewed single words presented at increasing rates. This same area was damaged in a patient with pure alexia ("alexia without agraphia") and no hemianopia, who read words slowly using a letter-by-letter strategy. Although the exact level of the functional deficit is controversial, pure alexia is the result of an inability to map a percept of all the letters in a familiar letter string on to the mental representation of the whole word form. However, the commonest deficit associated with "pure" alexia is a right homonymous field defect; an impairment that may, by itself, interfere with single-word reading because of inability to see the letters towards the end of a word. The relative contributions of pure and hemianopic alexia in individual patients needs to be assessed, as the latter has been shown to respond well to specific rehabilitation programmes.

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