To investigate the mechanisms underlying the evolution of unilateral spatial neglect (USN) due to cerebral infarction, the cerebral oxygen metabolism was measured quantitatively by positron emission tomography (PET). Out of 189 consecutive patients with right hemisphere lesions who underwent PET, we recruited 13 patients (group A) who exhibited USN at the time of PET examination, 11 patients (group B) who had already recovered from USN, and 27 patients (group C) with right hemisphere infarction who failed to present with USN throughout. Eight normal volunteers (group NV) served as controls. Statistical comparisons were performed on the local values of the cerebral metabolic rate of oxygen (CMRO
2) from the region of interest (ROI) in the right dorsolateral frontal lobe, superior temporal gyrus, inferior parietal lobule, cingulate gyrus, basal ganglia and thalamus which are associated with USN. We also obtained CMRO
2 values for the contralateral areas. As compared with group C or NV, there were significant decreases in CMRO2 in the right frontal, right temporal and right parietal lobes, right basal ganglia, right thalamus and bilateral cingulate gyri in groups A and B. Except for the left inferior parietal lobule, no significant differences in regional CMRO
2 were noted between groups A and B. These findings indicate that extensive right hemisphere lesions may produce USN, but no specific brain region is associated with its recovery. Different from aphasics, no definite relationship is evident between recovery from USN and the role of the contralateral left hemisphere. This could be explained partly by the complexity of the pathogenetic mechanisms underlying USN.
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