Juhee Chin

Seoul Neuropsychological Screening Battery-Dementia Version (SNSB-D): A Useful Tool for Assessing and Monitoring Cognitive Impairments in Dementia Patients

The Seoul Neuropsychological Screening Battery (SNSB) is one of the standardized neuropsychological test batteries widely used in Korea. However, it may be a bit too lengthy for patients with decreased attention span; and it does not provide the score of global cognitive function (GCF), which is useful for monitoring patients longitudinally. We sought to validate a dementia version of SNSB (SNSB-D) that was shorter than the original SNSB and contained only scorable tests with a GCF score of 300. We administered SNSB-D to patients with mild cognitive impairment (MCI) (n=43) and Alzheimers disease (AD) (n=93), and normal controls (NC) (n=77). MCI and AD groups had GCF scores significantly different from NC group, and GCF scores were able to distinguish patients with Clinical Dementia Rating of 0.5 and 1. Test-retest reliability was high, with a correlation coefficient of 0.918 for AD, 0.999 for MCI, and 0.960 for NC. The GCF score significantly correlated with the Mini-Mental State Examination (MMSE). Through ROC-curve analysis, GCF scores were found to yield more accurate diagnoses than the MMSE. The SNSB-D is a valid, reliable tool for assessing the overall cognitive function, and can be used to monitor cognitive changes in patients with dementia.

Clinical Significance of Microbleeds in Subcortical Vascular Dementia

Background and Purpose— Despite many studies investigating the association between the ischemic changes and cognitive impairment in subcortical vascular dementia (SVaD), few studies correlated cognitive impairment with microbleeds (MBs) frequently seen in SVaD. Methods— Participants consisted of 86 patients with SVaD who fulfilled the criteria proposed by Erkinjuntti et al. Results— MBs occurred in 73 of 86 (84.9%) patients with SVaD. MBs were most commonly distributed in the cortex, and the cortical MBs were most pronounced in the temporoparietal area. A multiple regression showed that the number of cerebral MB was an independent predictor of cognitive impairment in multiple domains and the severity of dementia even after controlling confounding factors such as age, education, ischemic severity, and number of lacunes. Conclusion— These results indicate that cerebral MB is one of the important factors that cause cognitive impairments in SVaD.

Cortical Thinning in Vascular Mild Cognitive Impairment and Vascular Dementia of Subcortical Type

Amnestic mild cognitive impairment (MCI) is known to be a preclinical stage of Alzheimers disease (AD). Similarly, MCI associated with small‐vessel disease (svMCI), might be a forme froste of subcortical vascular dementia (SVaD). Patterns of cortical thinning in addition to the ischemia rating on MRI may further elucidate the clinical characteristics and pathogenesis of SVaD and svMCI. We tried to determine if svMCI differs from SVaD in the distribution of cortical atrophy, which may help understand the hierarchy between svMCI and SVaD and possibly also how svMCI evolves into SVaD.

Subcortical Vascular versus Amnestic Mild Cognitive Impairment: Comparison of Cerebral Glucose Metabolism

Most studies on mild cognitive impairment (MCI) have been focused on amnestic MCI (aMCI) that is the preclinical stage of Alzheimers disease (AD). In contrast, only a few studies have involved patients in the preclinical stages of subcortical vascular dementia (subcortical vascular MCI, svMCI). We tried to compare the overall glucose metabolism in patients with svMCI with that of patients with aMCI.

Cortical thinning related to periventricular and deep white matter hyperintensities

Previous studies showed that white matter hyperintensities (WMH) are related to cognitive decline in patients with mild cognitive impairment (MCI) or dementia. Moreover, periventricular WMH (periventricular white matter hyperintensities (PWMH)) and deep WMH (deep white matter hyperintensities (DWMH)) may have different effects on cognition. The purpose of this study is to investigate the contributions of PWMH and DWMH to the topography of cortical thinning and to investigate the relationship among WMH, cortical thinning, and cognitive impairments. Participants included 226 patients with Alzheimers disease or subcortical vascular dementia, and 135 patients with amnestic MCI or subcortical vascular MCI. Cortical thickness was measured using the surface based method. The topography of cortical thinning related to WMH was distributed in the frontal and perisylvian regions, which was similar to that of PWMH. In contrast, there were only small areas of cortical thinning inversely associated with DWMH, which were distributed in medial frontal and lingual gyrus. PWMH, but not DWMH, were associated with the frontal thinning and executive dysfunction; where both PWMH and frontal thinning were independently associated with executive dysfunction. Our results suggest that PWMH are associated with frontal thinning, which is further associated with frontal executive dysfunction.

Anatomical heterogeneity of Alzheimer disease Based on cortical thickness on MRIs

Objective: Because the signs associated with dementia due to Alzheimer disease (AD) can be heterogeneous, the goal of this study was to use 3-dimensional MRI to examine the various patterns of cortical atrophy that can be associated with dementia of AD type, and to investigate whether AD dementia can be categorized into anatomical subtypes. Methods: High-resolution T1-weighted volumetric MRIs were taken of 152 patients in their earlier stages of AD dementia. The images were processed to measure cortical thickness, and hierarchical agglomerative cluster analysis was performed using Wards clustering linkage. The identified clusters of patients were compared with an age- and sex-matched control group using a general linear model. Results: There were several distinct patterns of cortical atrophy and the number of patterns varied according to the level of cluster analyses. At the 3-cluster level, patients were divided into (1) bilateral medial temporal–dominant atrophy subtype (n = 52, ∼34.2%), (2) parietal-dominant subtype (n = 28, ∼18.4%) in which the bilateral parietal lobes, the precuneus, along with bilateral dorsolateral frontal lobes, were atrophic, and (3) diffuse atrophy subtype (n = 72, ∼47.4%) in which nearly all association cortices revealed atrophy. These 3 subtypes also differed in their demographic and clinical features. Conclusions: This cluster analysis of cortical thickness of the entire brain showed that AD dementia in the earlier stages can be categorized into various anatomical subtypes, with distinct clinical features.

Changes in subcortical structures in early- versus late-onset Alzheimer's disease

Patients with early-onset Alzheimers disease (EOAD) are reported to be different from those with late-onset Alzheimers disease (LOAD) in terms of neuropsychological and neuroimaging findings. In this study, we aimed to compare the longitudinal volume changes of 6 subcortical structures (the amygdala, hippocampus, thalamus, putamen, globus pallidus, and caudate nucleus) between patients with EOAD and LOAD for 3 years. We prospectively recruited 36 patients with probable Alzheimers disease (14 EOAD, 22 LOAD) and 14 normal control subjects. We analyzed the volume of subcortical structures using an automatic surface-based method. At baseline, there were no differences in the volumes of subcortical structures between patients with EOAD and LOAD. However, over 3 years of longitudinal follow-up, patients with EOAD showed more rapid volumetric decline in the caudate, putamen, and thalamus than patients with LOAD, which is consistent with neuropsychological results. Our findings suggested that the cognitive reserve theory might be applicable to explain different decline rates of the volumes of the basal ganglia and thalamus according to onset age.

Longitudinal changes of cortical thickness in early- versus late-onset Alzheimer's disease

Early-onset Alzheimers disease (EOAD) has been shown to progress more rapidly than late-onset Alzheimers disease (LOAD). However, no studies have compared the topography of brain volume reduction over time. The purpose of this 3-year longitudinal study was to compare EOAD and LOAD in terms of their rates of decline in cognitive testing and topography of cortical thinning. We prospectively recruited 36 patients with AD (14 EOAD and 22 LOAD) and 14 normal controls. All subjects were assessed with neuropsychological tests and with magnetic resonance imaging at baseline, Year 1, and Year 3. The EOAD group showed more rapid decline than the LOAD group in attention, language, and frontal-executive tests. The EOAD group also showed more rapid cortical thinning in widespread association cortices. In contrast, the LOAD group presented more rapid cortical thinning than the EOAD group only in the left parahippocampal gyrus. Our study suggests that patients with EOAD show more rapid cortical atrophy than patients with LOAD, which accounts for faster cognitive decline on neuropsychological tests.

The cortical neuroanatomy of neuropsychological deficits in mild cognitive impairment and Alzheimer's disease: A surface-based morphometric analysis

Patients with probable Alzheimers disease (AD) and the amnesic form of mild cognitive impairment (aMCI) often demonstrate several types of neuropsychological deficits. These deficits are often related to cortical atrophy, induced by neuronal degradation. The purpose of this study is to investigate whether different anatomic patterns of cortical atrophy are associated with specific neuropsychological deficits. The participants were 170 patients with AD and 99 patients with aMCI. All participants underwent the Seoul Neuropsychological Screening Battery (SNSB), which includes tests that assess attention, language, visuospatial functions, verbal and visual memory, and frontal/executive functions. Cortical atrophy (thinning) was quantified by measuring the thickness of the cortical mantle across the entire brain using automated, three-dimensional magnetic resonance imaging. The relationship between cortical thickness and neuropsychological performance was analysed using stepwise multiple linear regression analyses. These analyses (corrected P<.001) showed that several specific brain regions with cortical thinning were associated with cognitive dysfunction including: digit span backward, verbal and picture recall, naming and fluency, drawing-copying, response inhibition and selective attention. Some of the other functions, however, were not associated with specific foci of cortical atrophy (digit span forward, the word reading portion of the Stroop test, word and picture recognition). Our study, involving a large sample of participants with aMCI and AD, provides support for the postulate that cortical thinning-atrophy in specific anatomic loci are pathological markers for specific forms of cognitive dysfunction.

Mechanism of the Closing-in Phenomenon in a Figure Copying Task in Alzheimer’s Disease Patients

Abstract The “closing-in phenomenon” in figure copying tasks refers to a tendency to copy near the target, or to overlap the target to be copied. The mechanisms underlying the closing-in phenomenon have not been fully elucidated. We posit that closing-in may be related to the patients’ compensatory strategies to overcome visuospatial dysfunction or visuospatial working memory deficit. Thus, it is expected that as the complexity of the target figure or the distance from the target to the copying space is increased, the magnitude of closing-in will be increased. Thirteen patients with Alzheimer’s disease (AD) who demonstrated closing-in on a screening test and 15 healthy controls participated in this study. Each subject copied figures in conditions that varied in terms of figure complexity and distance from the target to the copying space. Neither figure complexity nor distance between the target and copying space affected the degree of closing-in in normal subjects. In contrast, in AD patients, the magnitude of closing-in increased as a function of figure complexity; however closing-in was unchanged by varying the distance from the target to the copying space. Our results suggest that copying near the target figure might be the patients’ strategy to compensate for their visuospatial dysfunction or visuospatial working memory deficits.