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Premorbid undernutrition has been proven to have an adverse effect on the prognosis of stroke patients. The evaluation of nutritional status is important, but there is no universally accepted screen methodology. We aimed to use the geriatric nutritional risk index (GNRI) for evaluating the effect of premorbid undernutrition on short-term outcomes in patients with acute ischemic stroke. A total of 1,906 patients were included for analysis. Baseline characteristics were collected. We evaluated the nutritional status of the patients using the GNRI and body mass index(BMI). The GNRI was calculated as {1.519×serum albumin(g/dL) + 41.7×present weight (kg)/ideal body weight (kg)}. All patients were categorized into four groups on the basis of the GNRI score. Among the included patients, 546 patients had an unfavorable outcomes. The proportion of patients with moderate and severe risk, assessed in GNRI, was significantly higher in the unfavorable outcome group compared to the favorable outcome group (33.3% vs 15.0%). The increased risk of premorbid undernutrition was associated with an increased risk of unfavorable outcome in a dose-response manner after adjusting for covariates. This study demonstrated that GNRI was associated with poor prognosis in patients with acute ischemic stroke. GNRI may be used to screen patients at high risk for unfavorable outcome.

Inflammation plays an important role in atherosclerosis and its complications. Since a dysregulated inflammatory response is associated with early neurological deterioration (END), serum neutrophil-to-lymphocyte ratio (NLR) could be a marker of END as well. In this study, we evaluated the relationship between the serum NLR and END in patients with ischemic stroke due to large-artery atherosclerosis (LAA). We evaluated consecutive patients with ischemic stroke due to LAA between January 2010 and December 2015. END was defined as an increase ≥ 2 on the total NIHSS score or ≥ 1 on the motor NIHSS score within the first 72 hours of admission. The NLR was calculated by dividing the absolute neutrophil count by the absolute lymphocyte count. Of the 349 included patients, 18.1% (n = 63) had END events. In multivariate analysis, serum NLR was independently associated with END (adjusted odds ratio, 1.08; 95% confidence interval [1.00-1.16], P = 0.043). Time to admission, and in-situ thrombosis and artery-to-artery embolization mechanisms were also significantly associated with END events. In an analysis of the relationship between serum NLR and vascular lesion burden, serum NLR was positively correlated with both the degree of stenotic lesions (P for trend = 0.006) and the number of vessel stenosis (P for trend = 0.038) in a dose-response manner. We also compared serum NLR by the stroke mechanisms: patients with hypoperfusion or in-situ thrombosis had the highest levels of NLR: however, only those with in-situ thrombosis had significantly higher NLR in the END group compared to the non-END group (P = 0.005). Serum NLR levels were associated with END events in patients with ischemic stroke due to LAA. Since NLR was also closely correlated with the underlying vascular lesions, our results indicated clues for mechanisms of END events.

Proton pump inhibitors (PPIs) are widely used for the treatment of gastrointestinal diseases. However, recent studies have shown that chronic PPI use is associated with the progression of endothelial senescence and cerebrovascular diseases. We hypothesized that PPI users might be vulnerable to fast progression of cerebral small vessel disease (SVD) with cumulative effects. Four hundred and eleven patients, who underwent brain magnetic resonance imaging, more than twice between January 2010 and December 2016 were screened. Patients aged < 50 years, and those who had concomitant diseases that might affect the progression of cerebral SVD were excluded. Baseline characteristics were collected. We evaluated the severity of SVD using the Fazekas score, the number of cerebral microbleeds (CMBs), and assessed the progression of SVD or CMBs based on the cumulative dose of PPIs. Among the included patients (N = 137), 39 were PPI ever-users. Univariate Cox regression analysis showed that PPI use was independently associated with the progression of Fazekas score only in the deep white matter hyperintensities (WMH) (hazard ratio [HR] 2.891, 95% confidence interval [CI] 1.210–6.906, P = 0.017). In multivariate Cox regression analysis, long-term PPI use was associated with a progression of Fazekas score in the deep WMH (HR 3.453, 95% CI 1.027–9.475, P = 0.045). However, PPI use was not associated with the progression of CMB. The present study results suggest that long-term use of PPIs is associated with the progression of deep cerebral WMH. Further research is needed using a large number of patients to validate this relationship.

Ischemic stroke is one of the leading causes of death, and even timely treatment can result in severe disabilities. Reperfusion of the ischemic stroke region and restoration of the blood supply often lead to a series of cellular and biochemical consequences, including generation of reactive oxygen species (ROS), expression of inflammatory cytokines, inflammation, and cerebral cell damage, which is collectively called cerebral ischemia-reperfusion (IR) injury. Since ROS and inflammatory cytokines are involved in cerebral IR injury, injury could involve cellular senescence. Thus, we investigated whether senolytic therapy that eliminates senescent cells could be an effective treatment for cerebral IR injury. To determine whether IR induces neural cell senescence in vitro, astrocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). OGD/R induced astrocyte senescence and senescent cells in OGD/R-injured astrocytes were effectively eliminated in vitro by ABT263, a senolytic agent. IR in rats with intraluminal middle cerebral artery occlusion induced cellular senescence in the ischemic region. The senescent cells in IR-injured rats were effectively eliminated by intravenous injections of ABT263. Importantly, ABT263 treatment significantly reduced the infarct volume and improved neurological function in behavioral tests. This study demonstrated, for the first time, that senolytic therapy has therapeutic potential for cerebral IR injury.

Cerebral small vessel diseases (cSVDs) affect the prognosis of various types of ischemic stroke. Therefore, we evaluated the association between cSVD and the prognosis of cryptogenic stroke patients with active cancer. We enrolled patients diagnosed with cryptogenic stroke and active cancer from 2010 to 2016. Early neurological deterioration (END) was defined as a ≥ 2-point increase in the total NIHSS score or a ≥ 1-point increase in the motor NIHSS score within the first 72 h. We defined an unfavorable outcome as the modified Rankin Scale (mRS) score ≥ 3 points. We analyzed cSVD separately for each subtype including white matter hyperintensity (WMH), silent brain infarct (SBI), and cerebral microbleed (CMB). A total of 179 cryptogenic stroke patients with active cancer were evaluated. In the multivariable analysis, SBI was significantly associated with END (adjusted odds ratio = 3.97, 95% confidence interval: 1.53–10.33). This close relationship between SBI and END increased proportionally with an increase in SBI burden. However, WMH and CMB showed no significant association with END. None of the cSVD subtypes showed a statistically significant relationship with the 3-month unfavorable outcome. SBI was the only parameter closely associated with END in cryptogenic stroke patients with active cancer.

Background: The brain–gut axis has emerged as a potential target in neurodegenerative diseases, including dementia, as individuals with dementia exhibit distinct gut microbiota compositions. Fecal microbiota transplantation (FMT), the transfer of fecal solution from a healthy donor to a patient, has shown promise in restoring homeostasis and cognitive enhancement. Objective: This study aimed to explore the effects of FMT on specific cognitive performance measures in Alzheimer’s dementia (AD) patients and investigate the relationship between cognition and the gut microbiota by evaluating changes in gene expression following FMT. Methods: Five AD patients underwent FMT, and their cognitive function [Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Clinical Dementia Rating Scale Sum of Boxes (CDR-SOB)] was assessed before and after FMT. The patients’ fecal samples were analyzed with 16S rRNA to compare the composition of their gut microbiota. We also assessed modifications in the serum mRNA expression of patients’ genes related to lipid metabolism using serum RNA sequencing and quantitative real-time polymerase chain reaction. Results: Significant improvements in cognitive function, as measured by the MMSE (pre- and post-FMT was 13.00 and 18.00) and MoCA were seen. The MoCA scores at 3 months post-FMT (21.0) were the highest (12.0). The CDR-SOB scores at pre- and post-FMT were 10.00 and 5.50, respectively. Analysis of the gut microbiome composition revealed changes via 16S rRNA sequencing with an increase in Bacteroidaceae and a decrease in Enterococcaceae. Gene expression analysis identified alterations in lipid metabolism-related genes after FMT. Conclusion: These findings suggest a link between alterations in the gut microbiome, gene expression related to lipid metabolism, and cognitive function. The study highlights the importance of gut microbiota in cognitive function and provides insights into potential biomarkers for cognitive decline progression. FMT could complement existing therapies and show potential as a therapeutic intervention to mitigate cognitive decline in AD.

Stroke in cancer patients is not rare but is a devastating event with high mortality. However, the predictors of mortality in stroke patients with cancer have not been well addressed. D-dimer could be a useful predictor because it can reflect both thromboembolic events and advanced stages of cancer. In this study, we evaluate the possibility of D-dimer as a predictor of 30-day mortality in stroke patients with active cancer. We included 210 ischemic stroke patients with active cancer. The 30-day mortality data were collected by reviewing medical records. We also collected follow-up D-dimer levels in 106 (50%) participants to evaluate the effects of treatment response on D-dimer levels. Of the 210 participants, 30-day mortality occurred in 28 (13%) patients. Higher initial NIHSS scores, D-dimer levels, and CRP levels as well as frequent cryptogenic mechanism, systemic metastasis, multiple vascular territory lesion, hemorrhagic transformation, and larger infarct volume were related to 30-day mortality. In the multivariate analysis, D-dimer [adjusted OR (aOR) = 2.19; 95% CI, 1.46-3.28, P < 0.001] predicted 30-day mortality after adjusting for confounders. The initial NIHSS score (aOR = 1.07; 95% CI, 1.00-1.14, P = 0.043) and hemorrhagic transformation (aOR = 3.02; 95% CI, 1.10-8.29, P = 0.032) were also significant independent of D-dimer levels. In the analysis of D-dimer changes after treatment, the mortality group showed no significant decrease in D-dimer levels, despite treatment, while the survivor group showed the opposite response. D-dimer levels may predict 30-day mortality in acute ischemic stroke patients with active cancer.

Background High quality cardiopulmonary resuscitation (CPR) is one of the key elements of the survival chain in cardiac arrest. Audiovisual feedback of chest compressions have been suggested to be beneficial by increasing the quality of CPR in the simulated cardiac arrests. Methods A prospective before and after study was performed to investigate the effect of a real-time audiovisual feedback system on CPR quality during in-hospital cardiac arrest in intensive care units from November 2018 to February 2022. In the feedback period, CPR was performed with the aid of the real-time audiovisual feedback system. The primary outcome was the percentage of compressions with both adequate depth (5.0–6.0 cm) and rate (100–120/minute). Results A total of 27,295 compressions in 30 cardiac arrests in the no-feedback period and 27,965 compressions in 30 arrests in the feedback period were analyzed. The percentage of compressions with both adequate depth and rate was 11.8% in the feedback period and 16.8% in the no-feedback period ( P  < 0.01). The percentage of compressions with adequate rate in the feedback period was lower than that in the no-feedback period (67.3% vs. 75.5%, P  < 0.01). The percentage of beyond-target depth with the feedback was significantly higher than that without feedback (64.2% vs. 51.4%, P  < 0.01). Conclusion Real-time audiovisual feedback system did not increase CPR quality and was associated with a higher percentage of compression depth deeper than the recommended 5.0–6.0 cm. It is essential to explore more effective ways of implementing feedback in real clinical settings to improve of the quality of CPR. Trial registration NCT03902873 (study start: Nov. 2018, initial release April 2019, retrospectively registered).

Inadequate cerebral perfusion is a risk factor for cerebral ischemia in patients with large artery steno-occlusion. We investigated whether prefrontal oxyhemoglobin oscillation (ΔHbO 2 , 0.6–2 Hz) was associated with decreased vascular reserve in patients with steno-occlusion in the large anterior circulation arteries. Thirty-six patients with steno-occlusion in the anterior circulation arteries (anterior cerebral artery, middle cerebral artery, and internal carotid artery) were included and compared to thirty-six control subjects. Patients were categorized into two groups (deteriorated vascular reserve vs. preserved vascular reserve) based on the results of Diamox single- photon emission computed tomography imaging. HbO 2 data were collected using functional near-infrared spectroscopy. The slope of ΔHbO 2 and the ipsilateral/contralateral slope ratio of ΔHbO 2 were analyzed. Among the included patients (n = 36), 25 (69.4%) had deteriorated vascular reserve. Patients with deteriorated vascular reserve had a significantly higher average slope of ΔHbO 2 on the ipsilateral side (5.01 ± 2.14) and a higher ipsilateral/contralateral ratio (1.44 ± 0.62) compared to those with preserved vascular reserve (3.17 ± 1.36, P  = 0.014; 0.93 ± 0.33, P  = 0.016, respectively) or the controls (3.82 ± 1.69, P  = 0.019; 0.94 ± 0.29, P  = 0.001). The ipsilateral/contralateral ΔHbO 2 ratio could be used as a surrogate for vascular reserve in patients with severe steno-occlusion in the anterior circulation arteries.

Background Herpes simplex encephalitis is the most common type of sporadic encephalitis worldwide. Frank intracerebral hemorrhage complicating the disease course in herpes simplex encephalitis patients is rare, especially cases where surgical decompression is necessary. Here, we report a previously healthy female with herpes simplex encephalitis who underwent surgical decompression due to temporal lobe hemorrhage. Case presentation A previously healthy 34-year-old Korean female presented with fever, myalgia and severe headache. Brain MRI showed a high T2 signal intensity change and diffuse swelling of the right temporal lobe. Polymerase chain reaction testing of the cerebrospinal fluid confirmed the presence of herpes simplex virus 1. The patient was admitted for close observation and intravenous acyclovir. On hospital day 3, she had a sudden onset of vomiting and severe headache. Brain CT showed frank temporal lobe hemorrhage. Despite aggressive medical treatment, she became increasingly drowsy. Ultimately, she underwent emergency right decompressive craniectomy, expansile duraplasty and intracranial pressure monitor insertion. The patient recovered fully without any neurological deficits or neuropsychological problems. She was discharged after completion of 2 weeks of acyclovir and returned 2 months later for cranioplasty. Conclusions Patients with severe herpes simplex encephalitis complicated by intracerebral hemorrhage or malignant cerebral edema should undergo aggressive medical treatment. Surgical decompression should also be actively considered in these severe cases to prevent further neurological deterioration.