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Purpose: Autonomic dysfunction is an underrecognized complication of acute ischemic stroke. The cortical regulation of sympathetic activation is predominantly lateralized to the right hemisphere and parasympathetic activation to the left hemisphere. However, prior evidence is lacking regarding ischemic lesions in unilateral hemisphere that concomitantly cause sympathetic and parasympathetic dysfunction., Case Report: We present the case of a 73-year-old woman with acute ischemic stroke in the left middle cerebral artery territory, whose neurological symptoms improved significantly after thrombolysis and endovascular thrombectomy. She presented residual scattered small infarctions involving the left insula and lateral parietal cortex. However, she experienced obvious autonomic symptoms that included orthostatic hypotension, which is indicative of sympathetic dysfunction, and micturition difficulty with exaggerated reflex tachycardia, indicative of parasympathetic dysfunction. The sympathetic and parasympathetic functions sequentially resolved on days 10 and 20 after stroke onset, respectively., Conclusion: The case revealed insight into the phenomenon and recovery course of concurrent sympathetic and parasympathetic dysfunction associated with ischemic lesions in the left hemisphere.

Early ischemic lesion on non-contrast computed tomogram (NCCT) in acute stroke can be subtle and need confirmation with magnetic resonance (MR) image for treatment decision-making. We retrospectively included the NCCT slices of 129 normal subjects and 546 ischemic stroke patients (onset < 12 h) with corresponding MR slices as reference standard from a prospective registry of Chang Gung Research Databank. In model selection, NCCT slices were preprocessed and fed into five different pre-trained convolutional neural network (CNN) models including Visual Geometry Group 16 (VGG16), Residual Networks 50, Inception-ResNet-v2, Inception-v3, and Inception-v4. In model derivation, the customized-VGG16 model could achieve an accuracy of 0.83, sensitivity 0.85, F-score 0.80, specificity 0.82, and AP 0.82 after using a tenfold cross-validation method, outperforming the pre-trained VGG16 model. In model evaluation, the customized-VGG16 model could correctly identify 53 in 58 subjects (91.37%) including 29 ischemic stroke patients and 24 normal subjects and reached the sensitivity of 86.95% in identifying ischemic NCCT slices (200/230), irrespective of supratentorial or infratentorial lesions. The customized-VGG16 CNN model can successfully identify the presence of early ischemic lesions on NCCT slices using the concept of automatic feature learning. Further study will be proceeded to detect the location of ischemic lesion., (© 2022. The Author(s).)

Background: Stroke is prevalent in patients with chronic kidney disease (CKD) and is associated with high mortality, but the causes of death after stroke among different CKD stages are not well known., Aims: We aimed to investigate whether the severity of CKD would impact on the causes of death after first-ever stroke., Methods: This retrospective multicenter cohort study included stoke patients with CKD between 2007 and 2012. The cause of death and date of death were ascertained by linking the National Death Registry Database of Taiwan. Clinical outcomes, 1-month, and 1-year mortality rates, and major causes of death were compared according to five CKD stages (G1 to G5) in the ischemic and hemorrhagic stroke separately., Results: Of these patients, 9,878 were first-ever ischemic stroke (IS) patients, and 1,387 were first-ever hemorrhagic stroke (HS) patients. Patients with CKD G5 had the highest one-year mortality rate with hazard ratio 5.28 [95%CI, 3.94-7.08] in IS and 3.03 [95%CI, 2.03-4.54] in HS when compared to G1 patients. Leading causes of one-year death after IS were stroke, cancer, and pneumonia in early (G1-3) CKD patients, while diabetes mellitus, CKD, and stroke itself contributed to the major mortality in CKD G5 patients. An inverse association between eGFR decrement and the proportion of deaths caused by stroke itself was observed in CKD G2-5 patients after IS. Stroke was the leading cause of one-year death among all CKD patients after HS., Conclusions: Asides from high mortality, late-stage CKD patients had different causes of death from early CKD patients after stroke. This study highlights the need to imply different treatment strategies in late-stage CKD post-stroke patients to improve their prognosis., Competing Interests: The authors have declared that no competing interests exist.

Background and Objectives : Neurodegeneration and vascular burden are the two most common causes of post-stroke cognitive impairment. However, the interrelationship between the plasma beta-amyloid (Aβ) and tau protein, cortical atrophy and brain amyloid accumulation on PET imaging in stroke patients is undetermined. We aimed to explore: (1) the relationships of cortical thickness and amyloid burden on PET with plasma Aβ40, Aβ42, tau protein and their composite scores in stroke patients; and (2) the associations of post-stroke cognitive presentations with these plasma and neuroimaging biomarkers. Methods : The prospective project recruited first-ever ischemic stroke patients around 3 months after stroke onset. The plasma Aβ40, Aβ42, and total tau protein were measured with the immunomagnetic reduction method. Cortical thickness was evaluated on MRI, and cortical amyloid plaque deposition was evaluated by 18F-florbetapir PET. Cognition was evaluated with Mini-Mental State Examination (MMSE), Geriatric Depression Scale (GDS), Dementia Rating Scale-2 (DRS-2). Results : The study recruited 24 stroke patients and 13 normal controls. The plasma tau and tau*Aβ42 levels were correlated with mean cortical thickness after age adjustment. The Aβ42/Aβ40 ratio was correlated with global cortical 18F-florbetapir uptake value. The DRS-2 and GDS scores were associated with mean cortical thickness and plasma biomarkers, including Aβ42/Aβ40, tau, tau*Aβ42, tau/Aβ42, and tau/Aβ40 levels, in stroke patients. Conclusion : Plasma Aβ, tau, and their composite scores were associated with cognitive performance 3 months after stroke, and these plasma biomarkers were correlated with corresponding imaging biomarkers of neurodegeneration. Further longitudinal studies with a larger sample size are warranted to replicate the study results. [ABSTRACT FROM AUTHOR]

Background: Low lipid level is associated with better cardiovascular outcome. However, lipid paradox indicating low lipid level having worse outcomes could be seen under acute injury in some diseases. The present study was designed to clarify the prognostic significance of acute-phase lipid levels within 1 day after admission for stroke on mortality in first-ever statin-naïve acute ischemic stroke (IS) and hemorrhagic stroke (HS). Methods: This observational study was conducted using the data collected from Stroke Registry In Chang-Gung Healthcare System (SRICHS) between 2009 and 2012. Patients with recurrent stroke, onset of symptoms >1 day, and history of the use of lipid-lowering agents prior to index stroke were excluded. Stroke was classified into IS and hypertension-related HS. The primary outcomes were 30-day and 1-year mortality identified by linkage to national death registry for date and cause of death. Receiver operating characteristic (ROC) curve analysis and multivariate Cox proportional hazard models were used to examine the association of lipid profiles on admission with mortality. Results: Among the 18,268 admitted stroke patients, 3,746 IS and 465 HS patients were eligible for analysis. In IS, total cholesterol (TC) <163.5 mg/dL, triglyceride (TG) <94.5 mg/dL, low-density lipoprotein (LDL) <100 mg/dL, non-high-density lipoprotein cholesterol (non-HDL-C) <130.5 mg/dL, and TC/HDL ratio <4.06 had significantly higher risk for 30-day/1-year mortality with hazard ratio (HR) of 2.05/1.37, 1.65/1.31, 1.68/1.38, 1.80/1.41, and 1.58/1.38, respectively, compared with high TC, TG, LDL, non-HDL-C, and TC/HDL ratio (p < 0.01 in all cases). In HS, lipid profiles were not associated with mortality, except HDL for 30-day mortality (p = 0.025) and high uric acid (UA) concentrations for 30-day and 1-year mortality (p = 0.002 and 0.012, respectively). High fasting glucose and high National Institute of Health Stroke Scale (NIHSS) score at admission were associated with higher 30-day and 1-year mortality in both IS and HS and low blood pressure only in IS (p < 0.05). Synergic effects on mortality were found when low lipids were incorporated with high fasting glucose, low blood pressure, and high NIHSS score in IS (p < 0.05). Conclusions: Lipid paradox showing low acute-phase lipid levels with high mortality could be seen in statin-naïve acute IS but not in HS. The mortality in IS was increased when low lipids were incorporated with high fasting glucose, low blood pressure, and high NIHSS score. [ABSTRACT FROM AUTHOR]

Background: Coronary artery disease (CAD) may coexist with extracranial carotid artery stenosis (ECAS), but the influence of CAD on procedure-related complications after carotid artery stenting (CAS) has not been well investigated. The study aimed to determine the impact of CAD on the occurrence of peri-CAS cerebral ischemic lesions on diffusion-weighted imaging (DWI) scanning. Methods: Coronary angiography was performed within six months before CAS. DWI scanning was repetitively done within 1 week before and after CAS. Clinical outcome measures were stroke, angina, myocardial infarction and death within 30 days. Results: Among 126 patients (69.5±9.0 years) recruited for unilateral protected CAS, 33 (26%) patients had peri-CAS DWI-positive lesions. CAD was noted in 79% (26 in 33) and 48% (45 in 93) of patients with and without peri-CAS DWI-positive lesions (OR, 4.0; 95% CI, 1.6–10.0; P = .0018), and the number of concomitant CAD on coronary angiography was positively correlated with the risk for peri-CAS DWI-positive lesions (P = .0032). In patients with no CAD (n = 55), asymptomatic CAD (n = 41) and symptomatic CAD (n = 30), the occurrence rates of peri-CAS DWI-positive lesions were 13%, 41% and 30% (P = .0048), and the peri-CAS stroke rates were 2%, 7% and 0% (P = .2120). Conclusions: The severity of morphological CAD and the presence of either symptomatic or asymptomatic CAD are associated with the occurrence of peri-CAS cerebral ischemic lesions. [ABSTRACT FROM AUTHOR]

Background: The objective is to study whether the cardiovascular protective effects of colchicines could be applied to non-cardiogenic ischemic stroke (IS) patients. Patients and Methods: Non-cardiogenic IS patients were identified from the National Health Insurance Research Database. Eligible patients were divided into chronic and non-chronic use categories based on their long-term status of colchicine use. The non-chronic use category was subdivided into (1) non-user and (2) new user groups while the chronic use category was divided into (3) former user and (4) long-term user groups according to the patient's recent status of colchicine use. Inverse probability of treatment weights for propensity scores was used to balance the baseline characteristics. The primary outcome was recurrent IS, which was compared within the non-chronic use and chronic use categories. Results: In the non-chronic use category, the number of patients was 355,498 and 912 in the non-user and new user groups, respectively. In the chronic use category, the number of patients was 4737 and 4354 in the former user and long-term user groups, respectively. In the non-chronic use category, patients in the new user group had a marginally lower risk of recurrent IS at 6-months (subdistribution hazard ratio [SHR], 0.95; 95% confidence interval [CI], 0.94–0.97) and 2-years (SHR, 0.92; 95% CI, 0.91–0.93) follow up. In the chronic use category, patients in the long-term user group also had a marginally lower risk of recurrent IS at 6-months (SHR, 0.87; 95% CI, 0.86–0.88) and 2-years (SHR, 0.87; 95% CI, 0.86–0.88) follow up. The effect of colchicine on the reduced risk of recurrent IS was more favorable in patients who also used statins. Conclusions: Recent colchicine use in acute non-cardiogenic IS patients is associated with marginal fewer incidences of recurrent IS. Patients with concurrent statin use may have more profound protective effects. [ABSTRACT FROM AUTHOR]

Background: The 18F-THK-5351 radiotracer has been used to detect the in vivo tau protein distribution in patients with tauopathy, such as Alzheimer’s disease and corticobasal syndrome. In addition, 18F-THK-5351 can also monitor neuroinflammatory process due to high affinity to astrogliosis. We aimed to explore 18F-THK-5351 distribution patterns and characteristics in patients with recent ischemic stroke.Results: Fifteen patients received 18F-THK-5351 positron emission tomography (PET) and diffusion tensor imaging (DTI) approximately 3 months after ischemic stroke. A region of interest (ROI) was placed in the peri-ischemic area and was mirrored on the contralateral side as the control, and a proportional value was derived from the ratio of the peri-ischemic ROI value over the mirrored ROI value. Increased 18F-THK-5351 retention was observed in the areas around and remote from the stroke location. The proportional 18F-THK-5351 values were negatively correlated with the proportional fractional anisotropy values (r = − 0.39, P = 0.04).Conclusion: 18F-THK-5351 PET imaging provides a potential tool for in vivo visualization of the widespread ischemia-related changes associated with a microstructural disruption in recent ischemic stroke patients. [ABSTRACT FROM AUTHOR]