BackgroundProspective memory (PM) is one of the most important cognitive domains in everyday life. The neuronal basis of PM has been examined by a large number of neuroimaging and neuropsychological studies, and it has been suggested that several cerebral domains contribute to PM. For these activation studies, a constellation of experimental PM trials was developed and adopted to healthy subjects. In the present study, we used a widely used clinical PM assessment battery to determine the lesions attributable to PM failure, with the hypothesis that lesion-symptom analysis using diffusion tensor imaging (DTI) in subjects with diffuse axonal injury (DAI) can reveal the neuronal basis of PM in everyday life.ResultsFourteen DAI patients (age: range of 18-36, median 24) participated in this study. PM failure was scored in the range of 0-6 using three sub-tests of the Rivermead Behavioural Memory Test. The PM scores of DAI patients were in the range of 2-6 (median 4.5, inter-quartile range 2.25). The severity of axonal injury following DAI was examined using fractional anisotropy (FA), one of the DTI parameters, at voxel level in each subject. We then obtained clusters correlated with PM failure by conducting voxel-based regression analysis between FA values and PM scores. Three clusters exhibited significant positive correlation with PM score, the left parahippocampal gyrus, left inferior parietal lobe, and left anterior cingulate.ConclusionsThis is the first lesion-symptom study to reveal the neuronal basis of PM using DTI on subjects with DAI. Our findings suggest that the neuronal basis of PM is in the left parahippocampal gyrus, left inferior parietal lobe, and/or left anterior cingulate. These findings are similar to those of previous activation studies with loading experimental PM tasks.

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Patients with brain damage completed reversal and nonreversal shift-learning tasks and we compared their performance with that of normal adults. The overall group differences revealed that many patients could not reach the task criterion regardless of the location of damage and the shift condition of the task. When we compared patients with subcortical and cortical damage, we also found no group differences with regard to the total number of trials required to reach the learning criterion and in terms of their learning processes during shift learning. However, when we compared patients with subcortical and unilateral cortical damage, the results revealed that the learning processes of patients with subcortical damage were normal, whereas the patients with unilateral cortical damage showed lesion-specific effects on shift learning. These findings are discussed in light of previous developmental findings and the proposed role of subcortical structures in learning.

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