Neural Substrates of Reserve Observed in a Non-Demented Aging Population

Cognitive decline in dementia does not correspond precisely to the amount of neurodegeneration in the brain. This discrepancy in brain damage and its clinical manifestation has been explicated by the concept of reserve. Brain reserve inferred from the brain size had moderate success in explaining the discrepancy, and numerous studies have reported the effects of education supporting cognitive reserve. Yet the neural substrates of reserve have been elusive. Utilizing optimized voxel-based morphometry, we have identified brain regions that were significantly smaller in individuals with low cognitive performance (LCP) compared to those with normal cognitive performance (NCP) in community-residing non-demented elderly people both with low educational attainment. It was assumed that the cognitive performance in this population reflected long-standing cognitive functioning of the individual, possibly the reserve, based on their stable follow-up performance and clinical interviews. Bilateral precuneus, right superior frontal gyrus and left middle frontal gyrus were smaller in individuals with LCP. Further, the LCP individuals had weaker correlation between the gray matter volume of those regions and the rest of the cortex. On the other hand, volume of these regions was more tightly correlated with the K-DRS Total score in these individuals. Finally, an outcome study of the community sample from which this study's participants were recruited from reported five times higher risk of dementia in the LCP group. Precuneus and prefrontal cortex are proposed as key sites comprising the neural substrates that underlie the reserve

Neural Substrates of Reserve Observed in a Non-Demented Aging Population

Cognitive decline in dementia does not correspond precisely to the amount of neurodegeneration in the brain. This discrepancy in brain damage and its clinical manifestation has been explicated by the concept of reserve. Brain reserve inferred from the brain size had moderate success in explaining the discrepancy, and numerous studies have reported the effects of education supporting cognitive reserve. Yet the neural substrates of reserve have been elusive. Utilizing optimized voxel-based morphometry, we have identified brain regions that were significantly smaller in individuals with low cognitive performance (LCP) compared to those with normal cognitive performance (NCP) in community-residing non-demented elderly people both with low educational attainment. It was assumed that the cognitive performance in this population reflected long-standing cognitive functioning of the individual, possibly the reserve, based on their stable follow-up performance and clinical interviews. Bilateral precuneus, right superior frontal gyrus and left middle frontal gyrus were smaller in individuals with LCP. Further, the LCP individuals had weaker correlation between the gray matter volume of those regions and the rest of the cortex. On the other hand, volume of these regions was more tightly correlated with the K-DRS Total score in these individuals. Finally, an outcome study of the community sample from which this study's participants were recruited from reported five times higher risk of dementia in the LCP group. Precuneus and prefrontal cortex are proposed as key sites comprising the neural substrates that underlie the reserve

Treatment of a Sequential Giant Fusiform Aneurysm of the Basilar Trunk

We report an exceptional case of a de novo giant fusiform aneurysm of the basilar trunk, which developed shortly after the therapeutic occlusion of the right internal carotid artery for a fusiform carotid aneurysm. It would appear to be appropriate to call this entity a sequential giant fusiform aneurysm. The patient was successfully treated with endovascular occlusion of the giant basilar trunk aneurysm following bypass surgery

Assessment of Tissue Viability Using Diffusion- and Perfusion-Weighted MRI in Hyperacute Stroke

OBJECTIVE: The aim of this study was to investigate the relationship between the diffusion and perfusion parameters in hyperacute infarction, and we wanted to determine the viability threshold for the ischemic penumbra using diffusion- and perfusion-weighted imaging (DWI and PWI, respectively). MATERIALS AND METHODS: Both DWI and PWI were performed within six hours from the onset of symptoms for 12 patients who had suffered from acute stroke. Three regions of interest (ROIs) were identified: ROI 1 was the initial lesion on DWI; ROI 2 was the DWI/PWI mismatch area (the penumbra) that progressed onward to the infarct; and ROI 3 was the mismatch area that recovered to normal on the follow-up scans. The ratios of apparent diffusion coefficient (ADC), the relative cerebral blood volume (rCBV), and the time to peak (TTP) were calculated as the lesions' ROIs divided by the contralateral mirror ROIs, and these values were then correlated with each other. The viability threshold was determined by using the receiver operating characteristic (ROC) curves. RESULTS: For all three ROIs, the ADC ratios had significant linear correlation with the TTP ratios (p < 0.001), but not with the rCBV ratios (p = 0.280). There was no significant difference for the ADC and rCBV ratios within the ROIs. The mean TTP ratio/TTP delay between the penumbras' two ROIs showed a significant statistical difference (p < 0.001). The cutoff value between ROI 2 and ROI 3, as the viability threshold, was a TTP ratio of 1.29 (with a sensitivity and specificity of 86% and 73%, respectively) and a TTP delay of 7.8 sec (with a sensitivity and specificity of 84% and 72%, respectively). CONCLUSION: Determining the viability thresholds for the TTP ratio/delay on the PWI may be helpful for selecting those patients who would benefit from the various therapeutic interventions that can be used during the acute phase of ischemic stroke