Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

IMPORTANCE Type 2 diabetes is expected to accelerate age-related peripapillary retinal nerve fiber layer (pRNFL) loss, but limited information on the rate of reduction in pRNFL thicknesses in patients with type 2 diabetes is available. OBJECTIVE To investigate longitudinal changes in pRNFL thickness in patients with type 2 diabetes, with or without diabetic retinopathy (DR). DESIGN, SETTING, AND PARTICIPANTS A total of 164 eyes of 63 healthy individuals and 101 patients with type 2 diabetes (49 patients without DR [non-DR group] and 52 patients with mild to moderate nonproliferative DR [NPDR group]) were enrolled in this prospective,

Assessment of functional independence and residual disability is very important for measuring treatment outcome after stroke. The modified Rankin Scale (mRS) and the modified Barthel Index (MBI) are commonly used scales to measure disability or dependence in activities of daily living (ADL) of stroke survivors. Lack of consensus regarding MBI score categories has caused confusion in interpreting stroke outcomes. The purpose of this study was to identify the optimal corresponding MBI and modified Rankin scale (mRS) grades for categorization of MBI. The Korean versions of the MBI (K-MBI) and mRS were collected from 5,759 stroke patients at 3 months after onset of stroke. The sensitivity and specificity were calculated at K-MBI score cutoffs for each mRS grade to obtain optimally corresponding K-MBI scores and mRS grades. We also plotted receiver operating characteristic (ROC) curves of sensitivity and specificity and determined the area under the curve (AUC). The K-MBI cutoff points with the highest sum of sensitivity and specificity were 100 (sensitivity 0.940; specificity 0.612), 98 (sensitivity 0.904; specificity 0.838), 94 (sensitivity 0.885; PLOS ONE | https://doi.

Background and Purpose— The theory of cognitive reserve (CR) was introduced to account for individual differences in the clinical manifestation of neuropathology. This study investigated whether CR has a modulating effect on cognitive impairment and recovery after stroke. Methods— This study is an interim analysis of the Korean Stroke Cohort for Functioning and Rehabilitation. A total of 7459 patients with first-ever stroke were included for analysis. Education, occupation, and composite CR scores derived from those 2 variables were used as CR proxies. Scores from the Korean version of the Mini-Mental State Examination analyzed for 30 months after stroke onset were analyzed. Results— Lower CR increased the risk of cognitive impairment after stroke. The odds ratio was 1.89 (95% CI, 1.64–2.19) in patients with secondary education and 2.42 (95% CI, 2.03–2.90) in patients with primary education compared with patients with higher education. The odds ratio was 1.48 (95% CI, 1.23–1.98) in patients with a skilled manual occupation and 2.01 (95% CI, 1.42–2.83) in patients with a nonskilled manual occupation compared with patients with a managerial or professional occupation. In the multilevel model analysis, the Korean version of the Mini-Mental State Examination total score increased during the first 3 months (1.93 points per month) and then plateaued (0.02 point per month). The slopes were moderated by the level of education, occupation, and composite CR score: the higher the level of education, occupation, or CR score, the faster the recovery. In the older adult group, the Korean version of the Mini-Mental State Examination scores showed a long-term decline that was moderated by education level. Conclusions— Education and occupation can buffer an individual against cognitive impairment caused by stroke and promote rapid cognitive recovery early after stroke. In addition, higher education minimizes long-term cognitive decline after stroke, especially in older patients. Clinical Trial Registration— URL: https://www.clinicaltrials.gov . Unique identifier: NCT03402451.

Diabetes is expected to accelerate age-related ganglion cell-inner plexiform layer (GC-IPL) loss, but there is limited information on the rate of reduction in GC-IPL thicknesses. We aimed to evaluate the reduction rate of GC-IPL thickness in diabetic patients, and to compare the rates between patients without and with diabetic retinopathy (DR). We included 112 eyes of 112 patients with diabetes [49 eyes without DR (no-DR group) and 63 eyes with mild to moderate non-proliferative DR (NPDR group)] and 63 eyes of 63 normal controls (control group) in this study. Macular GC-IPL thickness in all participants was measured for 3 years at 1-year intervals. The reduction rates of GC-IPL thickness were determined by linear mixed models and compared among the three groups. The estimated reduction rates of the average GC-IPL thickness in the no-DR (−0.627 μm/year) and NPDR (−0.987 μm/year) groups were 2.26-fold (p = 0.010) and 3.56-fold (p = 0.001) faster, respectively, than the control group (−0.277 μm/year). Age, duration of diabetes, and baseline average GC-IPL thickness were associated with longitudinal changes in average GC-IPL thickness. The GC-IPL reduction rate was significantly faster in diabetic patients, with and without DR. Physicians should therefore be aware that GC-IPL damage continues even if there is no DR. Diabetic retinopathy (DR), the most common complication of diabetes, is the leading cause of preventable visual impairment 1,2. In general, DR is clinically defined based on the observation of abnormal fundus vascular lesions, such as microaneurysms, hemorrhages, hard exudates, and cotton wool spots. However, experimental and clinical studies have shown that neurodegenerative changes, including loss of ganglion cells and glial reactivity, are also early events in the pathogenesis of DR 3-5. The loss of ganglion cells affects retinal ganglion cell layer and retinal nerve fiber layer (RNFL) thickness, and reduced thickness of these layers has been detected in clinical and animal studies 3,6-8. Optical coherence tomography (OCT) is a reliable method for quantitative structural evaluation of inner retinal layers, including of the thickness of the peripapillary RNFL (pRNFL) and macular ganglion cell-inner plexiform layer (GC-IPL), where such parameters could be useful for evaluating various conditions, such as retinal neuro-ophthalmic disease and glaucoma 9-11. Progressive changes in GC-IPL thickness can be identified by serial analysis of OCT measurements, and this trend-based analysis could be useful to understand the pathogenesis of certain conditions. Although microvascular abnormalities represent the classic hallmarks of DR, recent studies have reported that diabetic retinal neurodegeneration (DRN) occurs in patients without DR and DRN, which antecedes DR 12-15. The presence of age-related loss of retinal ganglion cells has been demonstrated histologically, and a progressive reduction in GC-IPL thickness, as measured by OCT, has also been reported 16. Abnormal systemic and eye conditions may accelerate th...