Background: It is not yet clear whether nutritional status is associated with post-stroke cognitive impairment (PSCI). We examined the geriatric nutritional risk index (GNRI) on the domain-specific cognitive outcomes 3 months after a stroke. Methods: A total of 344 patients with acute ischemic stroke were included for the analysis. The GNRI was calculated as 1.489 × serum albumin (g/L) + 41.7 × admission weight (kg)/ideal body weight (kg) and was dichotomized according to the prespecified cut-off points for no risk and any risks. The primary outcome was PSCI, defined as having adjusted z-scores of less than −2 standard deviations in at least one cognitive domain: executive/activation, memory, visuospatial and language. Multiple logistic regression and linear regression analyses were performed to investigate the association between the GNRI and cognitive outcomes. Results: Seventy (20.3%) patients developed PSCI 3 months after a stroke. The mean GNRI was 106.1 ± 8.6, and 59 (17.2%) patients had low (<98) GNRI scores. A low GNRI was independently associated with the PSCI after adjusting for age, sex, education, initial stroke severity, stroke mechanism and left hemispheric lesion (odds ratio, 2.04; 95% confidence interval, 1.00–4.14). The GNRI scores were also significantly associated with the z-scores from the mini-mental status examination and the frontal domain (β = 0.04, p-value = 0.03; β = 0.03, p-value = 0.03, respectively). Conclusions: A low GNRI was independently associated with the development of PSCI at 3 months after an ischemic stroke. The GNRI scores were specifically associated with the z-scores of the global cognition and frontal domain cognitive outcomes.

Blood pressure variability (BPV) is associated with higher cardiovascular morbidity risks; however, its association with cognitive decline remains unclear. We investigated whether higher BPV is associated with faster declines in cognitive function in ischemic stroke (IS) patients. Cognitive function was evaluated between April 2010 and August 2015 using the Mini-mental State Examination (MMSE) and Montreal Cognitive Assessment in 1,240 Korean PICASSO participants. Patients for whom baseline and follow-up cognitive test results and at least five valid BP readings were available were included. A restricted maximum likelihood–based Mixed Model for Repeated Measures was used to compare changes in cognitive function over time. Among a total of 746 participants (64.6 ± 10.8 years; 35.9% female). Baseline mean-MMSE score was 24.9 ± 4.7. The median number of BP readings was 11. During a mean follow-up of 2.6 years, mean baseline and last follow-up MMSE scores were 25.4 ± 4.8 vs. 27.8 ± 4.4 (the lowest BPV group) and 23.9 ± 5.2 vs. 23.2 ± 5.9 (the highest BPV group). After adjusting for multiple variables, higher BPV was independently associated with faster cognitive decline over time. However, no significant intergroup difference in cognitive changes associated with mean systolic BP was observed. Further research is needed to elucidate how BPV might affect cognitive function.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral small-vessel disease caused by mutations in the NOTCH3 gene. Classical pathogenic mechanisms are associated with cysteine gain or loss, but recent studies suggest that cysteine-sparing mutations might have a potential role as a pathogen. In comparison with CADASIL patients in Western countries, there are several differences in Asian patients: (1) prevalent locus of NOTCH3 mutations (exons 2–6 [particularly exon 4] vs. exon 11), (2) age at symptom onset, (3) prevalence of cerebral microbleeds and hemorrhagic stroke, (4) clinical symptoms, and (5) severity of white matter hyperintensities and typical involvement of the anterior temporal pole in magnetic resonance imaging. Both ethnicity and founder effects contribute to these differences in the clinical NOTCH3 spectrum in different cohorts. More functional investigations from diverse races are needed to clarify unknown but novel variants of NOTCH3 mutations. This review may broaden the spectrum of NOTCH3 variants from an Asian perspective and draw attention to the hidden pathogenic roles of NOTCH3 variants.

Reversible cerebral vasoconstriction syndromes (RCVS) is a rare disease that is characterized by reversible multifocal stenosis of the cerebral arteries with various clinical manifestations. Though the pathomechanism of RCVS was unclear, we reported RCVS related to the levonorgestrel-releasing intrauterine system (IUS). A previous healthy 36-year-old woman had thunderclap headache after implanting the levonorgestrel-releasing IUS a year ago. In the serial angiography, we initially found left vertebra artery (VA), and then additionally new stenosis of both anterior cerebral arteries and middle cerebral arteries (MCA). Bilateral MCA stenosis improved but developed stenosis of right VA after a week. The mean flow velocities of both MCA increased in the first transcranial doppler (TCD), but normalized in the follow up TCD. Levonorgestrel might act as the vasoconstrictitve factor that increased the level of endothelin-1, diminished the release of NO and raised oxidative low-density lipoprotein (LDL). Although the exact pathological mechanisms for RCVS were not yet elucidated, this case might help clinicians understand the mechanisms of RCVS.

Objectives: This study aimed to investigate whether transfusions and hemoglobin variability affects the outcome of stroke after an acute ischemic stroke (AIS). Methods: We studied consecutive patients with AIS admitted in three tertiary hospitals who received red blood cell (RBC) transfusion (RBCT) during admission. Hemoglobin variability was assessed by minimum, maximum, range, median absolute deviation, and mean absolute change in hemoglobin level. Timing of RBCT was grouped into two categories: admission to 48 h (early) or more than 48 h (late) after hospitalization. Late RBCT was entered into multivariable logistic regression model. Poor outcome at three months was defined as a modified Rankin Scale score ≥3. Results: Of 2698 patients, 132 patients (4.9%) received a median of 400 mL (interquartile range: 400–840 mL) of packed RBCs. One-hundred-and-two patients (77.3%) had poor outcomes. The most common cause of RBCT was gastrointestinal bleeding (27.3%). The type of anemia was not associated with the timing of RBCT. Late RBCT was associated with poor outcome (odd ratio (OR), 3.55; 95% confidence interval (CI), 1.43–8.79; p-value = 0.006) in the univariable model. After adjusting for age, sex, Charlson comorbidity index, and stroke severity, late RBCT was a significant predictor (OR, 3.37; 95% CI, 1.14–9.99; p-value = 0.028) of poor outcome at three months. In the area under the receiver operating characteristics curve comparison, addition of hemoglobin variability indices did not improve the performance of the multivariable logistic model. Conclusion: Late RBCT, rather than hemoglobin variability indices, is a predictor for poor outcome in patients with AIS.

Background: Poststroke hyperglycemia is associated with poor outcomes. Most prior studies used initial glucose as an indicator of poststroke hyperglycemia without considering glycemic control status at the time of stroke occurrence. We aimed to investigate the effect of an admission-glucose gap on short-term functional outcomes in acute ischemic stroke (AIS). Methods: We enrolled patients with AIS or transient ischemic attack who had been admitted within 7 days of symptom onset to three stroke centers from May 2016 to December 2019. The admission-glucose gap between estimated average glucose levels (eAG) and initial glucose level (eAG–initial glucose) was categorized into four groups. The short-term functional outcome was evaluated using the modified Rankin Scale (mRS) score at 3 months after stroke onset and was dichotomized. Results: Among 1332 included subjects, 548 (41.1%) had poor short-term functional outcomes. After adjusting for multiple variables, a severe negative glucose gap (eAG–initial glucose ≤ −50 mg/dL) was significantly associated with poor short-term functional outcome (OR, 1.573; 95% CI, 1.101–2.248). After dichotomizing glycemic control status, its significance was only maintained in the good glycemic control group (HbA1c < 6.5%) (OR, 1.914; 95% CI, 1.155–3.169). Conclusions: An elevated admission-glucose gap, in which the initial glucose level was much higher than the estimated glucose level was based on HbA1c, was associated with poor stroke prognosis. In addition to admission-glucose levels, glycemic control status at the time of stroke onset should be considered when predicting short-term stroke outcomes.