Structural correlates of mild cognitive impairment: A clinicovolumetric study.

CONTEXT:: Annually 10-12% of patients with mild cognitive impairment (MCI) are likely to progress to Alzheimer's Disease (AD). The morphometric profile in stable non-converters has not been adequately characterized. AIMS: To determine the structural differences between amnestic MCI and early AD using volumetric magnetic resonance imaging (MRI) and its correlation with neuropsychological test performances. SETTINGS AND DESIGN:: This was a hospital-based case-control study. MATERIALS AND METHODS:: Twenty-four patients classified as having "non-progressor" MCI, 13 as having an early AD, and 25 controls, and assessed using neuropsychological evaluation, and three-dimensional T1-weighted 1.5T magnetic resonance maging (MRI) were included in the study. We used both voxel-based morphometry and automated regional volumetry to assess the topographical patterns of volume loss. STATISTICAL ANALYSIS USED: Post-hoc analysis of variance was done for comparison between means, and partial correlation analysis was done for correlating volumetric and cognitive measures. RESULTS:: Consistently, significant atrophy of the superior temporal gyrus, left hippocampus, and mesial frontoparietal regions were identified in patients with MCI in comparison to controls. Increased atrophy in the limbic regions, temporal neocortex, and precuneus was identified in patients with early AD in comparison to patients with MCI. While differences in retention and recall scores between the groups were independent of age and volumetric variables, significant correlations were observed between the learning and recall scores and the volume of hippocampus in patients with MCI as well as temporal neocortex in patients with AD. Atrophy of the superior temporal gyrus and mesial neocortical regions represents the structural correlate of amnestic MCI parallel to the development of hippocampal atrophy. CONCLUSIONS:: Identification of the pattern of volumetric abnormalities in patients with amnestic MCI in addition to atrophy of the medial temporal lobes necessitates a close follow up to continuously assess these patients for their progression to early AD.

Do quantified sleep architecture abnormalities underlie cognitive disturbances in amnestic mild cognitive impairment?

The study was designed to gauge association between occult sleep-related breathing disturbances and sleep architecture changes on cognitive trajectories in subjects with amnestic mild cognitive impairment (aMCI) relative to cognitively normal healthy controls, phenotyped by neuroimaging. Subjects with aMCI and normal cognition were prospectively recruited. Following standardized neuropsychological and sleep questionnaire assessment they underwent a single overnight polysomnography (PSG); multimodality MRI was used to ascertain age-corrected radiological differences between the 2 groups. The aMCI cohort was followed up longitudinally with serial cognitive assessments for the next 3 years. Thirty seven subjects with aMCI and 24 control subjects consented for evaluation. Although occult moderate to severe obstructive sleep apnea (OSA) was more prevalent in aMCI (43.6%) as opposed to controls (22.7%); higher median apnea-hypopnea index (AHI = 11.5) and total apnea-hypopnea time (26.6 min) were also noted in aMCI relative to controls (6.6 and 11.4 min respectively), the differences were not statistically significant. In the aMCI group, better sleep efficiency, longer duration of REM sleep correlated with higher associative learning, free-recall/recognition memory performance. Higher AHI had negative correlation with visual memory scores. However longitudinal cognitive trends in the aMCI group over 3 years reflected relative stability (only 5% progressed to AD) notwithstanding imaging differences from controls and appeared to be independent of sleep parameters. The study concluded that despite associations between sleep efficiency, REM sleep and sleep-related breathing variables with neuropsychological test-scores in aMCI, these appear to be comorbidities rather than causative factors for the degree of cognitive impairment or its longitudinal trajectory.

Post-stroke cognitive impairment - A cross-sectional comparison study between mild cognitive impairment of vascular and non-vascular etiology.

PURPOSE: To elucidate the cognitive profiles of post-stroke vascular mild cognitive impairment (VaMCI) in comparison to MCI of non-vascular etiology and cognitively normal healthy controls at a tertiary-care hospital in southern India. RESULTS: Logistic regression analysis adjusted for age and sex comparing VaMCI [N=50] with controls [N=27] revealed significant impairment in visual, verbal learning-recall and executive function scores. As compared to the MCI group [N=36], VaMCI had significantly higher scores on Weschler's Memory Scale (WMS) verbal subset delayed recall scores (p=0.045, odds ratio [OR]=2.62, 95% CI=1.02-6.76) with lower scores on WMS-visual immediate learning scores (p=0.042, OR=0.35, 95% CI=0.13-0.96), Rey Auditory Verbal Learning Test (RAVLT) total learning scores (p=0.001, OR=0.17, 95% CI=0.06-0.48) and 20 minute recall (p=0.026, OR=0.33, 95% CI=0.12-0.88), Delayed Matching to Sample test (DMS-48) abstract immediate (p=0.002, OR=0.20, 95% CI=0.07-0.56), abstract delayed recognition sub-sets (p=0.014, OR=0.28, 95% CI=0.10-0.78) and made more total errors on Wisconsin Card Sorting Test (WCST; p=0.040, OR=2.70, 95% CI=1.05-7.14) while the MCI group significantly had more commission errors on RAVLT (p≤0.001, OR=0.13, 95% CI=0.05-0.38) and WCST - perseverative errors (p=0.036, OR=0.30, 95% CI=0.10-0.93). Significant differences were noted in word-list learning-recall (p=0.012) and WMS verbal delayed recall (p=0.014) between VaMCI with mild versus moderate to severe deep white matter hyperintensities on neuroimaging. CONCLUSIONS: Cognitive impairment following minor stroke involves episodic verbal and visual memory over and above executive function in comparison to MCI of non-vascular etiology. Close cognitive followup is warranted with adequate risk stratification and management especially in the presence of sub-cortical leukoaraiosis which is contributory to cognitive decline in this group of patients.