Subcortical Vascular Dementia Patients Research Articles

Evaluation of cerebrovascular hemodynamics in vascular dementia patients with a new individual computational fluid dynamics algorithm

BackgroundCerebral hemodynamic disorders are involved in the occurrence and progression of vascular dementia (VaD), but the methods to detect hemodynamics remainmultifarious and uncertain nowadays. We aim to exploit a computational fluid dynamics (CFD) approach by static and dynamic parameters, which can be used to detect individual cerebrovascular hemodynamics quantitatively. MethodsA patient-specific CFD model was constructed with geometrical arteries on the magnetic resonance angiography (MRA) and hemodynamic parameters on ultrasound Doppler, by which, the structural and simulated hemodynamic indexes could be obtained, mainly including the cerebral arterial volume (CAV), the number of visible arterial outlets, the total cerebral blood flow (tCBF) index and the total cerebrovascular resistance (tCVR) index. The hemodynamics were detected in subcortical vascular dementia (SVaD) patients (n = 38) and cognitive normal controls (CNCs; n = 40). ResultsCompared with CNCs, the SVaD patients had reduced outlets, CAV and tCBF index (all P ≤ 0.001), increased volume of white matter hyperintensity (WMH) and tCVR index (both P ≤ 0.01). The fewer outlets (OR = 0.77), higher Hachinski ischemic score (HIS) (OR = 3.65), increased tCVR index (OR = 1.98) and volume of WMH (OR = 1.12) were independently associated with SVaD. All hemodynamic parameters could differentiate the SVaD patinets and CNCs, especially the composite index calculated by outlets, tCVR index and HIS (AUC = 0.943). Fewer outlets and more WMH increased the odds of SVaD, which were partly mediated by the tCBF index (14.4% and 13.0%, respectively). ConclusionThe reduced outlets, higher HIS and tCVR index may be independent risk factors for the SVaD, and a combination of these indexes can differentiate SVaD patients and CNCs reliably. The tCBF index potentially mediates the relationships between hemodynamic indexes and SVaD. Although all simulated indexes only represented the true hemodynamics indirectly, this CFD model can provide patient-specific hemodynamic alterations non-invasively and conveniently.

Association of the Irregular 3-Dimensional Shape of White Matter Hyperintensities with Cognitive Function

Introduction: The irregular shapes of white matter hyperintensities (WMHs) are associated with poor cognitive function, diabetes, or lacunes. However, the association between the WMH shape and dementia remains understudied. We investigated the association between the calculated shape index of WMH and the diagnosis of dementia and cognitive function. Methods: The inverse sphericity index (ISI_WMH) and volume of WMHs (VOL_WMH) were compared among 82 participants with normal cognition, 82 with Alzheimer’s dementia (AD), and 82 with subcortical vascular dementia (SVD). We examined the associations of ISI_WMH and VOL_WMH with the modified Hachinski Ischemic Score (mHIS), diagnosis of AD and SVD, and cognitive test scores, using linear, multinomial, or hierarchical linear regression models. Results: The mHIS was associated with both ISI_WMH (β = 0.326, p < 0.001) and VOL_WMH (β = 0.299, p < 0.001). Both ISI_WMH and VOL_WMH were associated with the SVD diagnosis (odds ratio [OR] = 2.685, p = 0.002, ISI_WMH; OR = 2.597, p = 0.005, VOL_WMH), but not with AD. The SVD diagnosis was better explained when the multinomial regression model included both ISI_WMH and VOL_WMH instead of VOL_WMH alone (χ² = 20.768, df = 2, p < 0.001). The Trail Making Test-D (TMT-D) scores of the SVD patients were associated with both ISI_WMH (β = 0.308) and VOL_WMH (β = 0.293). Conclusion: An irregular WMH shape may be associated with the high cerebrovascular component of cognitive impairment and the diagnosis and low cognitive flexibility of SVD, which may improve the prediction of SVD diagnosis when used in combination with WMH volume.

The role of NOTCH3 variants in Alzheimer's disease and subcortical vascular dementia in the Chinese population

Aims NOTCH3 gene mutations predominantly cause cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, a common etiology of subcortical vascular dementia (SVaD). Besides, there may be a pathogenic link between NOTCH3 variants and Alzheimer's disease (AD). We aimed to study the role of NOTCH3 variants in AD and SVaD patients.MethodsWe recruited 763 patients with dementia (667 AD and 96 SVaD) and 365 healthy controls from the Southern Han Chinese population. Targeted capture sequencing was performed on NOTCH3 coding and adjacent intron regions to detect the pathogenic variants in AD and SVaD. The relationship between common or rare NOTCH3 variants and AD was further analyzed using Plink1.9.ResultsFive known pathogenic variants (p.R182C, p.C201S, p.R544C, p.R607C, and p.R1006C) and two novel likely pathogenic variants (p.C201F and p.C1061F) were detected in 16 SVaD patients. Additionally, no pathogenic or likely pathogenic variants were found in AD patients. NOTCH3 was not associated with AD in either single‐variant association analysis or gene‐based association analysis.ConclusionOur findings broaden the mutational spectrum of NOTCH3 and validate the pathogenic role of NOTCH3 mutations in SVaD, but do not support the notion that NOTCH3 variation influences the risk of AD.

Changes in Microvascular Morphology in Subcortical Vascular Dementia: A Study of Vessel Size Magnetic Resonance Imaging.

Background: Cerebral small vessel disease is the most common cause of subcortical vascular dementia (SVaD). Unfortunately, conventional imaging techniques do not always demonstrate the microvascular pathology that is associated with small vessel disease. The purpose of this study was to evaluate the changes in the microvascular structure of SVaD and to identify how the microvascular changes in vessel size, detected with imaging, affect the gray matter.Methods: Ten SVaD patients and 12 healthy controls underwent vessel size imaging with gradient-echo and spin-echo sequences before and after contrast agent injection. Four microvessel index maps, including total blood volume fraction (BVf), mean vessel density (Q), mean vessel diameter (mVD), and vessel size index (VSI) were calculated. ROI value of each microvessel parameter was compared between SVaD patients and controls. Voxel-wise comparison of microvessel parameters was also performed to assess the regional difference. The relationship between the microvessel parameters in white matter and total gray matter volume (TGV) were assessed.Results: Both mVD and VSI were significantly different between the SVaD and controls in the ROI-based comparisons (unpaired t-test, p < 0.05). mVD and VSI were significantly increased in the SVaD group at the subcortical, periventricular white matter, basal ganglia, and thalami compared with the controls (FDR corrected, p < 0.05). VSI in the white matter areas were significantly negatively correlated with TGV (r = −0.446, p < 0.05).Conclusions: The increase of mVD and VSI in SVaD patients reflects the damage of the microvessels in the white matter, and these changes may lead to the damage of the gray matter.

Distinct Patterns of Rich Club Organization in Alzheimer’s Disease and Subcortical Vascular Dementia: A White Matter Network Study

Recent advances in neuroimaging technology have shown that rich club organization in human brain networks plays a crucial role in global communication and cognitive functionality. In this study, we investigated rich club organization within white matter structural brain networks in two common types of dementia, Alzheimer's disease (AD) and subcortical vascular dementia (SVaD). We recruited 30 AD patients ([11C] Pittsburgh compound-B (PiB) PET positive), 39 SVaD patients (PiB negative), and 72 age-, gender-, and education-matched cognitively normal (CN) subjects. Rich club organization was significantly disrupted in both dementia patient groups, which exhibited higher rich club coefficients than the CN group. Rich club organization in the patient groups was primarily disrupted over the left frontal and left middle temporal areas when compared to the CN group. The number of rich club nodes was significantly reduced in the dementia groups, which was more severe in SVaD (p = 0.0107, permutation-based t-test). Although rich club organization was disrupted both in the patient groups, its disruption pattern is different between them. The rich-club connections normalized by degree-and-strength preserved random networks were significantly increased in the dementia groups with SVaD more severely, and feeder connections were reduced more significantly than in AD. Furthermore, SVaD patients exhibited more sporadic disruption in white matter connectivity than AD patients, with local connections showing a more significant degree of deterioration. Combined with the distinct disruption in rich club nodes, these findings may imply a differing role for rich club organization in AD and SVaD, due to different pathological mechanisms.

Centiloid method evaluation for amyloid PET of subcortical vascular dementia

Reference region selection is important for proper amyloid PET analysis, especially in subcortical vascular dementia (SVaD) patients. We investigated reference region differences between SVaD and Alzheimer’s disease (AD) using Centiloid scores. In 57 [C-11] Pittsburgh compound B (PiB) positive (+) AD and 23 PiB (+) SVaD patients, we assessed standardized PiB uptake and Centiloid scores in disease-specific cortical regions, with several reference regions: cerebellar gray (CG), whole cerebellum (WC), WC with brainstem (WC + B), pons, and white matter (WM). We calculated disease group differences from young controls (YC) and YC variance according to reference region. SVaD patients showed large effect sizes (Cohen’s d > 0.8) using all reference regions. WM and pons showed larger YC variances than other regions. Findings were similar for AD patients. CG, WC, and WC + B, but not WM or pons, are reliable reference regions for amyloid imaging analysis in SVaD.

Correlations between Gray Matter and White Matter Degeneration in Pure Alzheimer\u2019s Disease, Pure Subcortical Vascular Dementia, and Mixed Dementia

Alzheimer’s disease dementia (ADD) and subcortical vascular dementia (SVaD) both show cortical thinning and white matter (WM) microstructural changes. We evaluated different patterns of correlation between gray matter (GM) and WM microstructural changes in pure ADD, pure SVaD, and mixed dementia. We enrolled 40 Pittsburgh compound B (PiB) positive ADD patients without WM hyperintensities (pure ADD), 32 PiB negative SVaD patients (pure SVaD), 23 PiB positive SVaD patients (mixed dementia), and 56 normal controls. WM microstructural integrity was quantified using fractional anisotropy (FA), axial diffusivity (DA), and radial diffusivity (DR) values. We used sparse canonical correlation analysis to show correlated regions of cortical thinning and WM microstructural changes. In pure ADD patients, lower FA in the frontoparietal area correlated with cortical thinning in the left inferior parietal lobule and bilateral paracentral lobules. In pure SVaD patients, lower FA and higher DR across extensive WM regions correlated with cortical thinning in bilateral fronto-temporo-parietal regions. In mixed dementia patients, DR and DA changes across extensive WM regions correlated with cortical thinning in the bilateral fronto-temporo-parietal regions. Our findings showed that the relationships between GM and WM degeneration are distinct in pure ADD, pure SVaD, and mixed dementia, suggesting that different pathomechanisms underlie their correlations.

Cerebral gray matter volume reduction in subcortical vascular mild cognitive impairment patients and subcortical vascular dementia patients, and its relation with cognitive deficits.

IntroductionSubcortical vascular mild cognitive impairment (svMCI) is the predementia stage of subcortical vascular dementia (SVaD). The aim of this research is to explore and compare cerebral gray matter (GM) volume reduction in svMCI patients and SVaD patients, and to investigate the relationship between cerebral GM volume reduction and cognitive deficits.MethodsThirty one svMCI patients, 29 SVaD patients, and 31 healthy controls were recruited in our research. They conducted neuropsychological tests and brain structural magnetic resonance imaging (MRI) examination. To detect cerebral GM volume reduction in svMCI patients and SVaD patients, we used statistical parametric mapping 8‐voxel‐based morphometry 8 (SPM8‐VBM8) method to analyze MRI data. To detect the relationship between cerebral GM volume reduction and cognitive deficits, multiple linear regression analysis was used.ResultsCompared with healthy controls, svMCI patients showed cerebral GM volume reduction in hippocampus and parahippocampal gyrus, insula and superior temporal gyrus. Compared with healthy controls, SVaD patients exhibited more atrophy which encompasses all of these areas plus anterior and middle cingulate, inferior temporal gyrus, orbitofrontal cortex, and superior frontal gyrus. In svMCI patients, cerebral GM volume reduction correlated with memory loss, attention dysfunction, and language dysfunction; in SVaD patients, besides those cognitive deficits, cerebral GM volume reduction correlated with more cognitive impairments, including executive dysfunction, neuropsychiatric symptom, and depression.ConclusionsOur findings prove that both svMCI patients and SVaD patients exhibit cerebral GM volume reduction and there may exist a hierarchy between svMCI and SVaD, and cerebral GM volume reduction in both svMCI patients and SVaD patients correlates with cognitive deficits, which can help us understand the mechanism of cognitive impairments in svMCI patients and SVaD patients, and diagnose SVaD at its early stage.

Portuguese version of Wechsler Memory Scale–3rd edition’s utility with demented elderly adults

ABSTRACTThe purpose of this study is to analyze the utility of the Portuguese version of the Wechsler Memory Scale-3rd edition (WMS-III) with demented elderly people, namely its capacity to detect and discriminate between subcortical vascular dementia (SVD) and Alzheimer's disease (AD). We assessed early demented patients (SVD = 16; AD = 36) aged 65 or older who were compared to a control group (n = 40). Both clinical groups were adequately matched in terms of disease severity, overall cognitive functioning, depressive symptomatology, and pre-morbid intelligence. Between-group's differences were evaluated using the Quade's rank analysis of covariance. We also computed indexes and subtests optimal cut-off scores, and the corresponding sensitivity, specificity, and positive and negative predictive values, which were able to successfully discriminate between patients and healthy subjects. The SVD patients had a better overall memory performance than AD patients on the majority of the indexes and the delayed condition subtests of the WMS-III. The AD patients only showed a better performance on digit span subtest. Several measures discriminated patients from healthy subjects. This study suggests some recommendations for the diagnostic accuracy of the Portuguese version of WMS-III in dementia and about differential diagnosis between SVD and AD.

Distinctive Resting State Network Disruptions Among Alzheimer's Disease, Subcortical Vascular Dementia, and Mixed Dementia Patients.

Recent advances in resting-state functional MRI have revealed altered functional networks in Alzheimer's disease (AD), especially those of the default mode network (DMN) and central executive network (CEN). However, few studies have evaluated whether small vessel disease (SVD) or combined amyloid and SVD burdens affect the DMN or CEN. The aim of this study was to evaluate whether SVD or combined amyloid and SVD burdens affect the DMN or CEN. In this cross-sectional study, we investigated the resting-state functional connectivity within DMN and CEN in 37 Pittsburgh compound-B (PiB)(+) AD, 37 PiB(-) subcortical vascular dementia (SVaD), 13 mixed dementia patients, and 65 normal controls. When the resting-state DMN of PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(+) AD patients displayed lower functional connectivity in the inferior parietal lobule while the PiB(-) SVaD patients displayed lower functional connectivity in the medial frontal and superior frontal gyri. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the DMN in the posterior cingulate gyrus. When the resting-state CEN connectivity of PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(-) SVaD patients displayed lower functional connectivity in the anterior insular region. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the CEN in the inferior frontal gyrus. Our findings suggest that in PiB(+) AD and PiB(-) SVaD, there is divergent disruptions in resting-state DMN and CEN. Furthermore, patients with combined amyloid and SVD burdens exhibited more disrupted resting-state DMN and CEN than patients with only amyloid or SVD burden.

The Difference of Verbal Fluency Task Performance between Alzheimer’s Disease and Subcortical Vascular Dementia: CREDOS (Clinical Research Center for Dementia of South Korea) Study

Background: The verbal fluency test consists of two separate tests of semantic fluency and phonemic fluency. The performance patterns of these tests differ with the type of dementia. We studied the patterns of verbal fluency between Alzheimer's disease (AD) and subcortical vascular dementia (SVaD), and assessed the clinical utility of these tests. Methods: The 1,475 selected participants comprised 73 normal control sub jects, 673 patients with amnestic mild cognitive impairment (aMCI), 535 AD patients, 42 patients with subcortical vascular mild cognitive impairment (svMCI), and 152 SVaD patients. We analyzed the z-score for the total number of animal items as a semantic fluency index and the z-score of the phonemic total score as a phonemic fluency index. Results: The performance of semantic fluency was lower than that of phonemic fluency in all groups. The SVaD group showed the worst scores and abnormal performances on both tests, while the AD group presented abnormal performance only for semantic fluency. Dividing the patients with dementia according to severity revealed a different pattern between AD and SVaD for the clinical dementia rating (CDR) stage of 0.5. The performance of the AD group declined gradually with CDR. However, the SVaD group performed very poorly in both tests even for very mild dementia (CDR stage of 0.5). The aMCI and svMCI groups exhibited similar performance patterns. Conclusions: The pattern of semantic and phonemic fluency was not clinically useful at the MCI stage, but it could be helpful in differentiating AD and SVaD in the early stage of dementia. J Korean Neurol Assoc 34(1):14-22, 2016

Effects of amyloid and vascular markers on cognitive decline in subcortical vascular dementia.

To determine the independent and synergistic effects of amyloid and small vessel disease (SVD) burden on longitudinal cognitive decline in patients with subcortical vascular dementia (SVaD). A longitudinal cohort study was conducted involving patients from outpatient clinics of 2 tertiary referral centers. Sixty-one patients with SVaD were prospectively recruited and underwent MRI, 11C-Pittsburgh compound B (PiB) PET at baseline, and a 3-year annual neuropsychological follow-up. Effects of PiB positivity and SVD markers (white matter hyperintensities [WMH], lacunes, and microbleeds) on longitudinal cognitive decline were evaluated using generalized estimation equation after controlling for age, sex, education, APOE4 allele, and follow-up interval. When individual neuropsychological tests were used as outcome measures, PiB positivity was associated with faster cognitive decline in attention, visuospatial, visual memory, and global cognition function. Higher WMH burden was associated with faster cognitive decline in attention, visuospatial, visual recognition memory, and semantic/phonemic fluency function, whereas lacunes and microbleeds had no significant effects. When global dementia rating (Clinical Dementia Rating sum of boxes) was considered as an outcome measure, however, only PiB positivity was associated with faster cognitive decline. Significant interactions between PiB positivity and higher SVD burden were found to affect cognitive decline in semantic word fluency (from WMH burden) and global dementia rating (from microbleed burden). In SVaD patients, amyloid burden, independently or interactively with SVD, contributed to longitudinal cognitive decline. Amyloid deposition was the strongest poor prognostic factor.

Survival in Subcortical Vascular Dementia: Predictors and Comparison to Probable Alzheimer's Disease in a Tertiary Memory Clinic Population

Background: Subcortical vascular dementia (SVaD) is one of the most common dementias, after Alzheimer's disease (AD) dementia. Few survival analyses in SVaD patients have been reported. Methods: The dates and causes of death of 146 SVaD and 725 AD patients were included. We used the Cox proportional hazards model to compare survival between SVaD and AD patients and to explore possible factors related to survival of SVaD patients. Results: The median survival time after the onset of SVaD (109 months) was shorter than that recorded for AD (152 months). The most common cause of death in SVaD was stroke (47.1%). Factors associated with shorter survival in SVaD were late onset, male sex, worse baseline cognition, absence of hypertension and a family history of stroke. Conclusions: Stroke prevention may be important in SVaD treatment because 47.1% of SVaD patients died of stroke. A family history of stroke and absence of hypertension were associated with a shorter survival in SVaD, suggesting the existence of genetic or unknown risk factors.

White matter microstructural changes in pure Alzheimer's disease and subcortical vascular dementia.

Recent studies have demonstrated that Alzheimer's disease (AD) and subcortical vascular dementia (SVaD) have white matter (WM) microstructural changes. However, previous studies on AD and SVaD rarely eliminated the confounding effects of patients with mixed Alzheimer's and cerebrovascular disease pathologies. Therefore, our aim was to evaluate the divergent topography of WM microstructural changes in patients with pure AD and SVaD. Patients who were clinically diagnosed with AD and SVaD were prospectively recruited. Forty AD patients who were Pittsburgh compound B (PiB) positive [PiB(+) AD] without WM hyperintensities and 32 SVaD patients who were PiB negative [PiB(-) SVaD] were chosen. Fifty-six cognitively normal individuals were also recruited (NC). Tract-based spatial statistics of diffuse tensor imaging were used to compare patterns of fractional anisotropy (FA) and mean diffusivity (MD). Compared with the NC group, the PiB(+) AD group showed decreased FA in the bilateral frontal, temporal and parietal WM regions and the genu and splenium of the corpus callosum as well as increased MD in the left frontal and temporal WM region. PiB(-) SVaD patients showed decreased FA and increased MD in all WM regions. Direct comparison between PiB(+) AD and PiB(-) SVaD groups showed that the PiB(-) SVaD group had decreased FA across all WM regions and increased MD in all WM regions except occipital regions. Our findings suggest that pure AD and pure SVaD have divergent topography of WM microstructural changes including normal appearing WM.

Hippocampal volume and shape in pure subcortical vascular dementia

The purposes of the present study were to explore whether hippocampal atrophy exists in pure subcortical vascular dementia (SVaD) as defined by negative 11C-Pittsburg compound-B (PiB−) positron emission tomography and to compare hippocampal volume and shape between PiB− SVaD and PiB positive (PiB+) Alzheimer's disease (AD) dementia. Hippocampal volume and shape were compared among 40 patients with PiB− SVaD, 34 with PiB+ AD, and 21 elderly with normal cognitive function (NC). The normalized hippocampal volume of PiB− SVaD was significantly smaller than NC but larger than that of PiB+ AD (NC > PiB− SVaD > PiB+ AD). Both PiB− SVaD and PiB+ AD patients had deflated shape changes in the cornus ammonis (CA) 1 and subiculum compared with NC. However, direct comparison between PiB− SVaD and PiB+ AD demonstrated more inward deformity in the subiculum of the left hippocampus in PiB+ AD. PiB− SVaD patients did have smaller hippocampal volumes and inward shape change on CA 1 and subiculum compared with NC, suggesting that cumulative ischemia without amyloid pathology could lead to hippocampal atrophy and shape changes.

Blood Viscosity in Subcortical Vascular Mild Cognitive Impairment with versus without Cerebral Amyloid Burden

Subcortical vascular dementia (SVaD) is a common form of dementia, attributed to ischemic small-vessel disease. Blood viscosity (BV) may contribute to the pathophysiology of SVaD. However, SVaD patients with coexisting amyloid deposition may not show differences in BV because their small-vessel disease may result from amyloid angiopathy independently of BV. We, therefore, hypothesized that BV might show different changes compared with control subjects in subcortical vascular mild cognitive impairment (svMCI) that refers to the prodromal stage of SVaD according to cerebral amyloid burden detected by the [(11)C] Pittsburgh compound B (PiB) PET (positron emission tomography), and apolipoprotein 4 (ApoE4) genotype (a known risk factor for vascular and parenchymal amyloid). Our subjects consisted of 33 healthy normal controls (NC), 28 patients with PiB(-) svMCI, and 12 with PiB(+) svMCI. They underwent scanning capillary tube viscometer measuring BV during systolic and diastolic phases. Compared with the NC group, the PiB(-) svMCI group showed increased diastolic blood viscosity (DBV) but no difference in systolic blood viscosity (SBV). By contrast, there was no significant difference in SBV and DBV between the NC and PiB(+) svMCI groups. Within the PiB(+) svMCI group, ApoE4(-) subgroup showed increased DBV compared with the ApoE4(+) subgroup. Increased DBV is an important contributor to the development of "pure" svMCI (ie, without cerebral amyloid deposition). The relationship between BV and PiB(+) svMCI differed according to ApoE genotype, suggesting that the pathogenesis of PiB(+) svMCI might also be heterogeneous.

Apraxia for differentiating Alzheimer&amp;rsquo;s disease from subcortical vascular dementia and mild cognitive impairment

Although ideomotor limb apraxia is considered to be a typical sign of cortical pathologies such as Alzheimer’s disease (AD), it has been also reported in subcortical neurodegenerative diseases and vascular lesions. We aimed to investigate the difference between AD, subcortical vascular dementia (SVaD) and mild cognitive impairment (MCI) patients by means of ideomotor limb apraxia frequency and severity. Ninety-six AD, 72 SVaD, and 84 MCI patients were assessed with the mini-mental status examination (MMSe), clinical dementia rating (CDR) and the apraxia screening test of TULIA (AST). Apraxia was significantly more frequent in the AD patients (32.3%) than in both of the SVaD (16.7%) and MCI (4.8%) patients. The frequency of apraxia was also significantly higher in SVaD patients than in MCI patients. AD patients had significantly lower apraxia scores than both SVaD and MCI patients. In addition, a significant difference was found between SVaD and MCI patients in terms of apraxia scores. These results suggest that the widespread belief of the association between apraxia and cortical dementias is not exactly correct. The significant difference between both of the dementia groups and the MCI patients suggests that the absence of apraxia can be an indicator for MCI diagnosis.

Diffusion Tensor Imaging Changes Correlate with Clinical Progression in Vascular Mild Cognitive Impairment and Vascular Dementia of Subcortical Type

Departments of Neurology*, Radiology†, Inha University School of Medicine, Incheon; Department of Biomedical Engineering‡, Hanyang University, Seoul, Korea Background: Cerebral small vessel disease (SVD) induces vascular cognitive impairment (VCI) such as subcortical vascular dementia (SVaD) and subcortical vascular mild cognitive impairment (svMCI). We compared MRI parameters between SVaD and svMCI and determined which MRI parameters best correlated with cognitive function and disability on cross-sectional and longitudinal analyses within them. Methods: Twenty-four patients with SVaD and twelve with svMCI were recruited. They underwent multimodal MRIs including fluid-attenuated inversion recovery lesion load, lacunar infarct number, and fractional anisotropy (FA) and mean diffusivity (MD) from diffusion tensor imaging (DTI), neuropsychological testing, Sum of Boxes of Clinical Dementia Rating Scale (CDR-SB), Barthel Index, and the Korean version of a Geriatric Depression Scale (GDS-K). Seventeen patients were retested after 20 months for a brain MRI and clinical evaluation. Results: There were significant differences in average MD and peak height of MD histograms within normal-appearing brain tissue (NABT) between SVaD and svMCI patients. In the cross-sectional analysis, average MD within NABT significantly correlated with the composite neuropsychology score (r = -0.80, p< 0.001), the composite executive function score (r = -0.67, p< 0.001), and the CDR-SB (r = 0.54, p= 0.001), and the Barthel Index correlated with peak heights of the MD histograms (r = 0.37, p= 0.03) in NABT. Changes of CDR-SB was associated with changes of average MD within WMH (r = 0.57, p= 0.02), and changes of GDS-K was associated with changes of WMH volume (r = 0.51, p= 0.04) on a longitudinal scale. Conclusions: DTI parameters in NABT correlated with cognitive impairment and disability in VCI associated with SVD. Clinical progression of SVD was associated with some increment of WML volume and ultrastructural changes in WMH. Received: July 12, 2013 Revision received: September 9, 2013 Accepted: September 9, 2013

Motor intentional disorders in vascular mild cognitive impairment and vascular dementia of subcortical type

Subcortical vascular mild cognitive impairment (svMCI), a prodromal stage of subcortical vascular dementia (SVaD), is primarily associated with frontal injuries, whereas amnestic MCI (aMCI) is associated with temporoparietal injuries. Twenty-seven patients with svMCI, 20 with aMCI, 14 with SVaD, and 10 normal controls underwent motor intentional tasks (force initiation, development, maintenance, and termination) using a force dynamometer. Of the four motor intentional tasks, the maintenance task proved sensitive in differentiating svMCI from aMCI. In most motor intentional tasks, performances of svMCI patients were intermediate between those of controls and SVaD patients (initiation and termination: NC=aMCI=svMCI>SVaD; development: NC>aMCI=svMCI>SVaD; maintenance: NC=aMCI>svMCI=SVaD).

NEUROPSI battery subtest profile in subcortical vascular dementia and Alzheimer's disease.

ObjectiveTo investigate the diagnostic value of subtests of the NEUROPSI battery for differentiating subcortical vascular dementia (SVaD) from Alzheimer's disease (AD).MethodsThirteen patients with mild SVaD, 15 patients with mild probable AD, and 30 healthy controls, matched for age, education and dementia severity (in the case of patients), were submitted to the Mini-Mental State Examination (MMSE) and NEUROPSI battery. The performance of AD and SVaD groups on NEUROPSI subtests was compared. The statistical analyses were performed using Kruskal-Wallis, Chi-square and Mann-Whitney tests. The results were interpreted at the 5% significance level (p<0.05). Bonferroni's correction was applied to multiple comparisons (α=0.02).ResultsSVaD and AD patients showed no statistical difference in MMSE scores (SVaD=20.8 and AD=21.0; p=1.0) or in NEUROPSI total score (SVaD=65.0 and AD=64.3; p=0.56), suggesting a similar severity of dementia. The AD group performed worse on memory recall (<0.01) and SVaD group was worse in verbal fluency subtests (p=0.02).ConclusionNEUROPSI's memory and language subtests can be an auxiliary tool for differentiating SVaD from AD.