Abstract: . . .  NC sample, CN+L, CI+L, D+L, and prAD). If this overall test was significant, each lacune group and the prAD group was compared to its control group, and the lacune groups were compared to each other. The association of imaging variables with each other, and with MMSE scores, was assessed using Spearman correlations (less affected by December (1 of 2) 2000 NEUROLOGY 55 1629 Statistical analysis. Page 5 a small number of cases than Pearson correlations). The degree to which imaging variables explained the same ver- sus independent aspects of the differences between groups was examined using partial correlation and step-wise mul- tiple logistic regression analyses. An analysis of regional gray matter atrophy in the D+L and prAD groups was performed. First, the mean and SD of percent cortical gray matter in each region was com- puted for the single control sample that was used for both D+L and prAD groups. Each D+L and prAD subjects percent cortical gray matter in each region was converted to a Z-score, using the control samples mean and SD for that variable. The mean 2-score for each variable for the D+L and prAD groups was then tested for difference . . .
. . .  secondary degeneration, or 3) subclinical ischemia. Note that neurofibrillary tangles were found in the hippocam- pus in all three autopsied cases of D+L (Braak and Bra& 11-IV). In one case, hippocampal sclerosis was found as well. Thus, the pathogenesis of hippocampal atrophy in SIVD is variable and may reflect a combina- tion of degenerative and ischemic pathologies. Cortical atrophy in SIVD might result from sec- ondary axonal and trans-synaptic degeneration fol- lowing primary subcortical injury. This would represent the structural corollary to the traditional notion that cortical hypoperfusion in SIVD results from functional deafferentation of cerebral cortex.4o Based on anatomic studies of frontal-subcortical cir- cuits in nonhuman primatestl predominant atrophy of the prefrontal cortex might be expected. Regional analyses in our lacune groups did not reveal prefer- ential atrophy of prefrontal cortex, as opposed to pa- rietal, temporal, or occipital cortex (see table 3). However, despite this pattern of diffuse atrophy, sec- ondary degeneration cannot be ruled out. Although prefrontal cortex is considered to be the primary area of connectivity, widespread areas of posterior multimodal association cortex and hippocampus are  . . .
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