YanHong Dong

The Montreal Cognitive Assessment (MoCA) is superior to the Mini-Mental State Examination (MMSE) for the detection of vascular cognitive impairment after acute stroke

BACKGROUND The majority of patient with post-stroke Vascular Cognitive Impairment (VCI) have Vascular Cognitive Impairment No Dementia (VCIND). The Mini-Mental State Examination (MMSE) has been criticized as a poor screening test for VCIND due to insensitivity to visuospatial and executive function impairments. The Montreal Cognitive Assessment (MoCA) was designed to be more sensitive to such deficits and may therefore be a superior screening instrument for VCIND. METHODS Stable patients within 14days of their index stroke without significant physical disability, aphasia, dysarthria, active psychiatric illness or pre-existing dementia were eligible. Cognitive and neurological measures were administered after informed consent. RESULTS 100 patients were recruited. Of the 57 patients with unimpaired MMSE scores, 18 (32%) patients had an impaired MoCA score. By comparison, only 2 out of the 41 (4.9%) patients with unimpaired MoCA scores had impaired MMSE scores. Moreover, MMSE domain subtest scores could not differentiate between groups of differing screening test results, whilst MoCA domain subtest scores (Visuospatial/Executive Function, Attention and Recall) could. CONCLUSION The MoCA is more sensitive than the MMSE in screening for cognitive impairment after acute stroke. Longitudinal studies are required to establish the prognostic value of MoCA and MMSE evaluation in the acute post-stroke period for cognitive impairment as defined by the standard method of formal neuropsychological evaluation 3-6 months after stroke.

The Montreal Cognitive Assessment is superior to the Mini-Mental State Examination in detecting patients at higher risk of dementia.

BACKGROUND To examine the discriminant validity of the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) in detecting patients with cognitive impairment at higher risk for dementia at a memory clinic setting. METHODS Memory clinic patients were administered the MoCA, MMSE, and a comprehensive formal neuropsychological battery. Mild cognitive impairment (MCI) subtypes were dichotomized into two groups: single domain-MCI (sd-MCI) and multiple domain-MCI (md-MCI). Area under the receiver operating characteristic curve (ROC) analysis was used to compare the discriminatory ability of the MoCA and the MMSE. RESULTS Two hundred thirty patients were recruited, of which 136 (59.1%) were diagnosed with dementia, 61 (26.5%) with MCI, and 33 (14.3%) with no cognitive impairment (NCI). The majority of MCI patients had md-MCI (n = 36, 59%). The MoCA had significantly larger AUCs than the MMSE in discriminating md-MCI from the lower risk group for incident dementia (NCI and sd-MCI) [MoCA 0.92 (95% CI, 0.86-0.98) vs. MMSE 0.84 (95% CI, 0.75-0.92), p = 0.02). At their optimal cut-off points, the MoCA (19/20) remained superior to the MMSE (23/24) in detecting md-MCI [sensitivity: 0.83 vs. 0.72; specificity: 0.86 vs. 0.83; PPV: 0.79 vs. 0.72; NPV: 0.89 vs. 0.83; correctly classified: 85.1% vs. 78.7%]. CONCLUSION The MoCA is superior to the MMSE in the detection of patients with cognitive impairment at higher risk for incident dementia at a memory clinic setting.

Brief screening tests during acute admission in patients with mild stroke are predictive of vascular cognitive impairment 3–6 months after stroke

Objectives To determine the prognostic value of brief cognitive screening tests administered in the subacute stroke phase (initial 2 weeks) for the detection of significant cognitive impairment 3–6 months after stroke, the authors compared the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE). Methods Patients with ischaemic stroke and transient ischaemic attack were assessed with both MoCA and MMSE within 14 days after index stroke, followed by a formal neuropsychological evaluation of seven cognitive domains 3–6 months later. Cognitive outcomes were dichotomised as either no–mild (impairment in ≤2 cognitive domains) or moderate–severe (impairment in ≥3 cognitive domains) vascular cognitive impairment. Area under the receiver operating characteristic (ROC) curve analysis was used to compare discriminatory ability. Results 300 patients were recruited, of whom 239 received formal neuropsychological assessment 3–6 months after the stroke. 60 (25%) patients had moderate–severe VCI. The overall discriminant validity for detection of moderate–severe cognitive impairment was similar for MoCA (ROC 0.85 (95% CI 0.79 to 0.90) and MMSE (ROC 0.83 (95% CI 0.77 to 0.89)), p=0.96). Both MoCA (21/22) and MMSE (25/26) had similar discriminant indices at their optimal cutoff points; sensitivity 0.88 versus 0.88; specificity 0.64 versus 0.67; 70% versus 72% correctly classified. Moreover, both tests had similar discriminant indices in detecting impaired cognitive domains. Conclusions Brief screening tests during acute admission in patients with mild stroke are predictive of significant vascular cognitive impairment 3–6 months after stroke.

Prevalence of cognitive impairment in Chinese: Epidemiology of Dementia in Singapore study

Objective To study the prevalence of and associated factors for cognitive impairment and dementia in community dwelling Chinese from Singapore. Methods This study includes Chinese subjects from the Epidemiology of Dementia in Singapore (EDIS) study, aged ≥60 years, who underwent comprehensive examinations, including cognitive screening with the locally validated Abbreviated Mental Test and Progressive Forgetfulness Questionnaire. Screen positive participants subsequently underwent extensive neuropsychological testing and cerebral MRI. Cognitive impairment no dementia (CIND) and dementia were diagnosed according to internationally accepted criteria. The prevalence of cognitive impairment and dementia were computed per 5 year age categories and gender. To examine the relationship between baseline associated factors and cognitive impairment, we used logistic regression models to compute odd ratios with 95% CI. Results 1538 Chinese subjects, aged ≥60 years, underwent cognitive screening: 171 (15.2%) were diagnosed with any cognitive impairment, of whom 84 were CIND mild, 80 CIND moderate and seven had dementia. The overall age adjusted prevalence of CIND mild was 7.2%; CIND moderate/dementia was 7.9%. The prevalence increased with age, from 5.9% in those aged 60–64 years to 31.3% in those aged 75–79 years and 44.1% in those aged ≥80 years. Multivariate analysis revealed age, diabetes and hyperlipidaemia to be independently associated with cognitive impairment. Conclusions In present study, the overall prevalence of cognitive impairment and dementia in Chinese was 15.2%, which is in the same range as the prevalence reported in Caucasian and other Asian populations.

Association of silent lacunar infarct with brain atrophy and cognitive impairment

Objective Silent lacunar infarct (SLI) is associated with cognitive decline and linked to an increased risk of stroke and dementia. We examined the association of SLI with MRI measures of cortical thickness, subcortical and lateral ventricular shapes and cognition in 285 ethnic Chinese elderly. Methods SLI, cortical thickness, shapes of subcortical and ventricular structures were quantified using MRI. The cognitive performance was assessed using comprehensive neuropsychological tests. Linear regression was used to examine associations among SLI, brain measures and cognition. Results SLI was associated with atrophy in multiple subcortical structures, ventricular enlargement and widespread cortical thinning. Both SLI and atrophy were independently related to poorer performance in attention, memory and language domains. Only SLI was associated with visuomotor speed and executive function, while atrophy mediated the association between SLI and visuoconstruction. Conclusions Our findings support a vascular contribution to neurodegeneration and cognitive impairment.

Lipoxin A4 methyl ester ameliorates cognitive deficits induced by chronic cerebral hypoperfusion through activating ERK/Nrf2 signaling pathway in rats.

UNLABELLED Lipoxin A4 (LXA4) is known for its powerful anti-inflammatory function. Current studies in vitro suggest that LXA4 possesses novel antioxidant effect. The aim of this study is to examine whether Lipoxin A4 methyl ester (LXA4 ME) has neuroprotective effects against chronic cerebral hypoperfusion, and if so, whether the effects of LXA4 ME are associated with its potential antioxidant property. Adult male Sprague-Dawley rats were subjected to permanent bilateral common carotid artery occlusion (BCCAO) and randomly assigned into four groups: sham (sham-operated) group, vehicle (BCCAO+normal saline) group, LXA4 ME10 (BCCAO+LXA4 ME 10 ng per day) group and LXA4 ME100 (BCCAO+LXA4 ME 100 ng per day) group. LXA4 ME was administered through intracerebroventricular injection for 2 consecutive weeks. LXA4 ME significantly alleviated spatial learning and memory impairments, as assessed by Morris water maze and inhibited the loss of neurons in the CA1 region of the hippocampus. Biochemically, LXA4 ME phosphorylated extracellular signal regulated kinase (ERK) 1/2 and enhanced nuclear factor erythroid 2-related factor 2 (Nrf2) expression and its nuclear translocation, as well as NAD(P)H quinone oxidoreductase 1 (NQO1) expression. LXA4 ME reduced lipid peroxidative production in the hippocampus, as measured by immunohistochemical staining for 4-Hydroxynonenal (4-HNE). In addition, LXA4 ME significantly elevated the ratio of Bcl-2/Bax and decreased cleaved caspase-3 expression in the hippocampus. Therefore, these data suggest that LXA4 ME exerts beneficial effects on the cognitive impairment induced by chronic cerebral hypoperfusion through attenuating oxidative injury and reducing neuronal apoptosis in the hippocampus, which is most likely associated with the activation of ERK/Nrf2 signaling pathway.

Patterns of neuropsychological impairment in Alzheimer's disease and mixed dementia

BACKGROUND Mixed dementia (MD), i.e., the coexistence of Alzheimers disease (AD) and cerebrovascular disease (CVD), is a common dementia subtype. Few studies have attempted to establish the cognitive profiles of mild-moderate MD and compare it to the profiles of AD using a comprehensive neuropsychological test battery. We aimed to establish the neuropsychological profile of mild-moderate MD in relation to mild-moderate AD. METHODS Patients with consensus diagnoses of MD and AD of mild-moderate severity (Clinical Dementia Rating score of 1-2) were recruited from a memory clinic. Cognitive performance was measured by a formal neuropsychological battery covering domains of attention, language, verbal and visual memory, visuoconstruction, visuomotor speed and executive function. Cognitive domain scores are z-scores calculated using the mean and SDs of the AD group. ANCOVAs with age and education as covariates were employed to examine differences in mean score difference of cognitive domains and subtests between patients with MD and AD. RESULTS 151 patients were recruited with the majority of AD (n=96, 63.6%) and a minority of MD (n=55, 36.4%). There were no significant differences in the demographic characteristics of patients with MD and AD. However, patients with MD were significantly more impaired than AD patients in global cognitive composite, attention and visuoconstruction (global cognitive composite: -0.32±0.98 vs 0±1, p=0.011; attention: -0.32±0.90 vs 0±1, p=0.013; visuoconstruction: -0.27±0.99 vs 0±1, p=0.024, respectively). CONCLUSION The neuropsychological profile of patients with MD of mild-moderate severity is characterized by a poorer global performance, as well as attention and visuoconstruction than those with AD of mild-moderate severity.

Abnormalities of Cortical Thickness, Subcortical Shapes, and White Matter Integrity in Subcortical Vascular Cognitive Impairment

Subcortical vascular cognitive impairment (sVCI) is caused by lacunar infarcts or extensive and/or diffuse lesions in the white matter that may disrupt the white matter circuitry connecting cortical and subcortical regions and result in the degeneration of neurons in these regions. This study used structural magnetic resonance imaging (MRI) and high angular resolution diffusion imaging (HARDI) techniques to examine cortical thickness, subcortical shapes, and white matter integrity in mild vascular cognitive impairment no dementia (VCIND Mild) and moderate‐to‐severe VCI (MSVCI). Our study found that compared to controls (n = 25), VCIND Mild (n = 25), and MSVCI (n = 30) showed thinner cortex predominantly in the frontal cortex. The cortex in MSVCI was thinner in the parietal and lateral temporal cortices than that in VCIND Mild. Moreover, compared to controls, VCIND Mild and MSVCI showed smaller shapes (i.e., volume reduction) in the thalamus, putamen, and globus pallidus and ventricular enlargement. Finally, compared to controls, VCIND Mild, and MSVCI showed an increased mean diffusivity in the white matter, while decreased generalized fractional anisotropy was only found in the MSVCI subjects. The major axonal bundles involved in the white matter abnormalities were mainly toward the frontal regions, including the internal capsule/corona radiata, uncinate fasciculus, and anterior section of the inferior fronto‐occipital fasciculus, and were anatomically connected to the affected cortical and subcortical structures. Our findings suggest that abnormalities in cortical, subcortical, and white matter morphology in sVCI occur in anatomically connected structures, and that abnormalities progress along a similar trajectory from the mild to moderate and severe conditions. Hum Brain Mapp 35:2320–2332, 2014.

Cognitive screening improves the predictive value of stroke severity scores for functional outcome 3–6 months after mild stroke and transient ischaemic attack: an observational study

Objectives To investigate the prognostic value of the neurocognitive status measured by screening instruments, the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE), individually and in combination with the stroke severity scale, the National Institute of Health Stroke Scale (NIHSS), obtained at the subacute stroke phase or the baseline (≤2 weeks), for functional outcome 3–6 months later. Design Prospective observational study. Setting Tertiary stroke neurology service. Participants 400 patients with a recent ischaemic stroke or transient ischaemic attack (TIA) received NIHSS, MoCA and MMSE at baseline and were followed up 3–6 months later. Primary outcome measures At 3–6 months following the index event, functional outcome was measured by the modified Rankin Scale (mRS) scores. Results Most patients (79.8%) had a mild ischaemic stroke and less disability (median NIHSS=2, median mRS=2 and median premorbid mRS=0), while a minority of patients had TIA (20.3%). Baseline NIHSS, MMSE and MoCA scores individually predicted mRS scores at 3–6 months, with NIHSS being the strongest predictor (NIHSS: R2 change=0.043, p<0.001). Moreover, baseline MMSE scores had a small but statistically significant incremental predictive value to the baseline NIHSS for mRS scores at 3–6 months, while baseline MoCA scores did not (MMSE: R2 changes=0.006, p=0.03; MoCA: R2 changes=0.004, p=0.083). However, in patients with more severe stroke at baseline (defined as NIHSS>2), baseline MoCA and MMSE had a significant and moderately large incremental predictive value to the baseline NIHSS for mRS scores at 3–6 months (MMSE: R2 changes=0.021, p=0.010; MoCA: R2 changes=0.017, p=0.021). Conclusions Cognitive screening at the subacute stroke phase can predict functional outcome independently and improve the predictive value of stroke severity scores for functional outcome 3–6 months later, particularly in patients with more severe stroke.

Ankle-Brachial Index, Cognitive Impairment and Cerebrovascular Disease in a Chinese Population

Background: Previous studies have assessed the association between ankle-brachial index (ABI) and cognition, mainly using brief cognitive tests. We investigated whether ABI was associated with cognition independent of neuroimaging markers of cerebrovascular disease. Methods: Chinese subjects (n = 278, aged ≥60 years) were recruited from the ongoing Epidemiology of Dementia in Singapore (EDIS) Study. Ankle and brachial blood pressures were measured, and low ABI was defined as ≤0.9. A neuropsychological battery was utilized to determine cognition. Cognitive impairment no dementia (CIND) and dementia were diagnosed according to standard diagnostic criteria. Magnetic resonance imaging (MRI) was used to obtain semiquantitative and quantitative markers of cerebrovascular disease and atrophy. Results: A low ABI was related to the presence of intracranial stenosis (odds ratio, OR = 1.71; 95% confidence interval, CI: 1.13-2.59), but not with the presence of infarcts, microbleeds or grey matter, white matter and white matter lesion volumes. Furthermore, a low ABI was associated with poorer overall cognitive function and CIND-moderate/dementia (OR = 2.26; 95% CI: 1.11-4.59), independent of cardiovascular risk factors, and the MRI markers related to cerebrovascular disease and atrophy. Conclusion: We found an association between a low ABI and cognitive impairment, independent of any MRI marker of cerebral small vessel disease or large artery atherosclerotic disease.