Acute Phase Of Stroke Research Articles

The effectiveness of thrombolytic therapy in the acute phase of ischemic stroke based on the experience of the rural community of the Lublin Province in eastern Poland

Background: Intravenous thrombolysis - recombinant tissue plasminogen activator is currently popular among the recommended treatments for fresh ischemic stroke, mainly within 4 – 5 hours of the first symptoms. Still too many patients are delayed or not eligible for causal treatment because of a time out. Despite the growing public awareness associated with brain vascular diseases, there are still environments where it seems inadequate. This mainly applies to rural areas. Evaluation of the effectiveness of thrombolytic therapy in the acute phase of ischemic stroke on the background of differences related to the time of measurement. The aim of the study was to assess the effectiveness of thrombolytic therapy in the acute phase of ischemic stroke based on the experience of the rural community of the Lublin Province in eastern Poland. Methods: The diagnostic survey method with the survey technique was used. A standardized research tool was used - the National Institute of Health Stroke Scale (NIHSS). The study involved 81 patients of the Department of Neurology - Stroke Unit of the Provincial Specialist Hospital in Lublin, reporting their place of residence in rural areas. Results: The biggest difference in patients treated with alteplase was observed in measurements between day 1 and 10 (Z = 3.951, p <0.001), where the average NIHSS score on the first day it brought M = 10.36, and on the 10th day M = 4.04. A slight difference in NIHSS scores was observed in patients who did not receive thrombolytic therapy. The largest difference was observed between day 1 and 10 (Z = 5.408 p <0.001), where the average NIHSS score on day 1 was M = 9.08 and on 10. M = 5.21. Conclusions: Among patients who received thrombolytic therapy there was a faster improvement in neurological status compared to patients who did not receive such treatment.

The incidence of aspiration pneumonia in acute ischemic stroke patients in relation to early insertion of nasogastric tube feeding

Background Stroke is the acute onset of cerebral ischemia. Dysphagia with difficult swallowing is one of the common complications during the course of acute stroke, its incidence varies between 29–67%. Pneumonia is the second most common cause of death during the acute phase of stroke, with up to 20% mortality rate. In patient with risk of dysphagia or deficient oral intake, enteral feeding will be recommended. Objective Study the effect of early insertion of nasogastric tube for feeding on incidence of aspiration pneumonia in acute ischemic stroke patients with abnormal water swallow test. Methods The study was carried out in Alexandria Main University Hospital on 40 patients with acute ischemic stroke. Patients with abnormal water swallow test were classified into two groups: Group A: Insertion of nasogastric tube on admission after diagnosis. Group B: Giving intravenous fluids, minerals and traces for the first 48 h then inserting nasogastric tube on the third day. Results By comparing the patients in both groups, there was no statistical significant difference between them as regards; age, gender, comorbidities, and APACHE II score on admission. There was a statistical significant difference between both groups regarding fever, CRP level, WBCs, hypoxic index and the length of hospital stay. Conclusion Inserting Nasogastric tube insertion on admission in acute stroke patients may increase the incidence of aspiration pneumonia than being non-oral for 48 h before insertion on the third day as it affects the duration of ICU and hospital stay.

Machine learning-based prediction of post-stroke cognitive status using electroencephalography-derived brain network attributes.

More than half of patients with acute ischemic stroke develop post-stroke cognitive impairment (PSCI), a significant barrier to future neurological recovery. Thus, predicting cognitive trajectories post-AIS is crucial. Our primary objective is to determine whether brain network properties from electroencephalography (EEG) can predict post-stroke cognitive function using machine learning approach. We enrolled consecutive stroke patients who underwent both EEG during the acute stroke phase and cognitive assessments 3 months post-stroke. We preprocessed acute stroke EEG data to eliminate low-quality epochs, then performed independent component analysis and quantified network characteristics using iSyncBrain®. Cognitive function was evaluated using the Montreal cognitive assessment (MoCA). We initially categorized participants based on the lateralization of their lesions and then developed machine learning models to predict cognitive status in the left and right hemisphere lesion groups. Eighty-seven patients were included, and the accuracy of lesion laterality prediction using EEG attributes was 97.0%. In the left hemispheric lesion group, the network attributes of the theta band were significantly correlated with MoCA scores, and higher global efficiency, clustering coefficient, and lower characteristic path length were associated with higher MoCA scores. Most features related to cognitive scores were selected from the frontal lobe. The predictive powers (R-squared) were 0.76 and 0.65 for the left and right stroke groups, respectively. Estimating EEG-based network properties in the acute phase of ischemic stroke through a machine learning model has a potential to predict cognitive outcomes after ischemic stroke.

Association of Pulse Pressure Fluctuation During Hospitalization With Adverse Outcomes Within 3 Months After Ischemic Stroke.

Pulse pressure (PP) depends on heart function and arterial wall elasticity, which is closely related to the incidence of ischemic stroke. However, the association of PP fluctuation during hospitalization with adverse outcomes after ischemic stroke remains unclear. The present study included 3,971 patients with ischemic stroke. The primary outcome was the composite outcome of death or vascular events within 3 months after ischemic stroke. PP fluctuation was reflected by successive variation of PP (PP-SV). The cumulative incidence rates of the primary outcome were the highest in the patients in the highest quartiles of PP-SV (P < 0.05). The multivariable-adjusted hazard ratios (95% confidence intervals) of the primary outcome in the highest quartiles were 1.86 (1.03-3.38) for death or vascular events, and 2.15 (1.06-4.37) for vascular events (all Ptrend < 0.05). Multivariable-adjusted restricted cubic spline analyses showed linear associations of PP-SV during hospitalization with the primary outcome (P for linearity <0.05). Large PP fluctuation during hospitalization was associated with increased risks of adverse outcomes within 3 months after ischemic stroke, which provided valuable new insight for blood pressure management in the acute phase of ischemic stroke. Controlling PP fluctuation may be contributing to improving prognosis after ischemic stroke.

12/15-lipoxygenase inhibition attenuates neuroinflammation by suppressing inflammasomes.

Lipoxygenases (LOXs) have essential roles in stroke, atherosclerosis, diabetes, and hypertension. 12/15-LOX inhibition was shown to reduce infarct size and brain edema in the acute phase of experimental stroke. However, the significance of 12/15-LOX on neuroinflammation, which has an essential role in the pathophysiology of stroke, has not been clarified yet. In this study, ischemia/recanalization (I/R) was performed by occluding the proximal middle cerebral artery (pMCAo) in mice. Either the 12/15-LOX inhibitor (ML351, 50 mg/kg) or its solvent (DMSO) was injected i.p. at recanalization after 1 h of occlusion. Mice were sacrificed at 6, 24, and 72-h after ischemia induction. Infarct volumes were calculated on Nissl-stained sections. Neurological deficit scoring was used for functional analysis. Lipid peroxidation was determined by the MDA assay, and the inflammatory cytokines IL-6, TNF-alpha, IL-1beta, IL-10, and TGF-beta were quantified by ELISA. The inflammasome proteins NLRP1 and NLRP3, 12/15-LOX, and caspase-1 were detected with immunofluorescence staining. Infarct volumes, neurological deficit scores, and lipid peroxidation were significantly attenuated in ML351-treated groups at 6, 24, and 72-h. ELISA results revealed that the pro-inflammatory cytokines IL-1beta, IL-6, and TNF-alpha were significantly decreased at 6-h and/or 24-h of I/R, while the anti-inflammatory cytokines IL-10 and TNF-alpha were increased at 24-h or 72-h of ML351 treatment. NLRP1 and NLRP3 immunosignaling were enhanced at three time points after I/R, which were significantly diminished by the ML351 application. Interestingly, NLRP3 immunoreactivity was more pronounced than NLRP1. Hence, we proceeded to study the co-localization of NLRP3 immunoreactivity with 12/15-LOX and caspase-1, which indicated that NLRP3 was co-localized with 12/15-LOX and caspase-1 signaling. Additionally, NLRP3 was found in neurons at all time points but in non-neuronal cells 72 h after I/R. These results suggest that 12/15-LOX inhibition suppresses ischemia-induced inflammation in the acute and subacute phases of stroke via suppressing inflammasome activation. Understanding the mechanisms underlying lipid peroxidation and its associated pathways, like inflammasome activation, may have broader implications for the treatment of stroke and other neurological diseases characterized by neuroinflammation.

The Role of Endothelinergic and Nitroxidergic Reactions in Predicting the Functional Outcome in Patients with Ischemic Stroke of Different Severity

The aim of this study was to assess the value of nitric oxide (NO) and endothelin-1 (ET-1) serum concentrations as potential biomarkers for predicting the functional outcome in patients with acute ischemic stroke. Material and methods. A total of 37 patients diagnosed with ischemic stroke and admitted to a multidisciplinary vascular center were included in the study. The patients were divided into two groups based on the severity of neurological deficits as determined by the National Institutes of Health Stroke Scale (NIHSS): Group 1 consisted of 20 patients with NIHSS scores 15, and Group 2 consisted of 17 patients with NIHSS scores 15. The functional outcome was assessed using the NIHSS absolute values and the degree of disability measured by the Modified Rankin Scale (mRS) by comparing the values before and after baseline treatment. Lab evaluation included quantitative assessment of stable NO and ET-1 metabolites in patient’s serum at admission and on day 10 of hospital stay. The SPSS Statistics V23.0 for Windows software package, Python programming language, and Pandas and SciPy libraries were used for statistical data processing. Results. Group 1 patients demonstrated a statistically significant decrease in NIHSS (P=0.0013) and mRS (P0.0001) scores, which was indicative of a favorable functional outcome. Group 2 patients showed some recovery of only neurological deficit measured by NIHSS scale (P=0.0012), changes in degree of disability by mRS were statistically insignificant. On Day10 of hospital stay, both groups showed a clinically significant increase in ET-1 content, and slight change in NO concentration. NIHSS score demonstrated a significant negative correlation with baseline ET-1 concentrations: R=–0.82, P=0.00023 — in Group 1; R=–0.55, P=0.00075 — in Group 2. Modified RS scores showed negative correlation with NO (R=–0.50, P=0.00044) and ET-1 (R=–1.0, P=0.0074) concentrations in Group 1, and positive correlation with NO (R=0.55, P=0.0023) and ET-1 (R=0.33, P=0.04) concentrations in Group 2. Conclusion. Monitoring of NO and ET-1 serum concentrations provides valuable insights for personalized assessment of the anticipated functional outcome in patients with cerebral ischemia. Further research and the development of prognostic mathematical models are needed to validate the use of endothelial function markers as predictive indicators of patients' recovery potential during the acute phase of ischemic stroke.

The cell-specific roles of Nrf2 in acute and chronic phases of ischemic stroke.

Ischemic stroke refers to the sudden loss of blood flow in a specific area of the brain. It is the fifth leading cause of mortality and the leading cause of permanent disability. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) controls the production of several antioxidants and protective proteins and it has been investigated as a possible pharmaceutical target for reducing harmful oxidative events in brain ischemia. Each cell type exhibits different roles and behaviors in different phases post-stroke, which is comprehensive yet important to understand to optimize management strategies and goals for care for stroke patients. In this review, we comprehensively summarize the protective effects of Nrf2 in experimental ischemic stroke, emphasizing the role of Nrf2 in different cell types including neurons, astrocytes, oligodendrocytes, microglia, and endothelial cells during acute and chronic phases of stroke and providing insights on the neuroprotective role of Nrf2 on each cell type throughout the long term of stroke care. We also highlight the importance of targeting Nrf2 in clinical settings while considering a variety of important factors such as age, drug dosage, delivery route, and time of administration.

Neural precursor cell delivery induces acute post-ischemic cerebroprotection, but fails to promote long-term stroke recovery in hyperlipidemic mice due to mechanisms that include pro-inflammatory responses associated with brain hemorrhages

BackgroundThe intravenous delivery of adult neural precursor cells (NPC) has shown promising results in enabling cerebroprotection, brain tissue remodeling, and neurological recovery in young, healthy stroke mice. However, the translation of cell-based therapies to clinical settings has encountered challenges. It remained unclear if adult NPCs could induce brain tissue remodeling and recovery in mice with hyperlipidemia, a prevalent vascular risk factor in stroke patients.MethodsMale mice on a normal (regular) diet or on cholesterol-rich Western diet were exposed to 30 min intraluminal middle cerebral artery occlusion (MCAO). Vehicle or 106 NPCs were intravenously administered immediately after reperfusion, at 3 day and 7 day post-MCAO. Neurological recovery was evaluated using the Clark score, Rotarod and tight rope tests over up to 56 days. Histochemistry and light sheet microscopy were used to examine ischemic injury and brain tissue remodeling. Immunological responses in peripheral blood and brain were analyzed through flow cytometry.ResultsNPC administration reduced infarct volume, blood–brain barrier permeability and the brain infiltration of neutrophils, monocytes, T cells and NK cells in the acute stroke phase in both normolipidemic and hyperlipidemic mice, but increased brain hemorrhage formation and neutrophil, monocyte and CD4+ and CD8+ T cell counts and activation in the blood of hyperlipidemic mice. While neurological deficits in hyperlipidemic mice were reduced by NPCs at 3 day post-MCAO, NPCs did not improve neurological deficits at later timepoints. Besides, NPCs did not influence microglia/macrophage abundance and activation (assessed by morphology analysis), astroglial scar formation, microvascular length or branching point density (evaluated using light sheet microscopy), long-term neuronal survival or brain atrophy in hyperlipidemic mice.ConclusionsIntravenously administered NPCs did not have persistent effects on post-ischemic neurological recovery and brain remodeling in hyperlipidemic mice. These findings highlight the necessity of rigorous investigations in vascular risk factor models to fully assess the long-term restorative effects of cell-based therapies. Without comprehensive studies in such models, the clinical potential of cell-based therapies cannot be definitely determined.

From Admission to Discharge: Predicting National Institutes of Health Stroke Scale Progression in Stroke Patients Using Biomarkers and Explainable Machine Learning.

As a result of social progress and improved living conditions, which have contributed to a prolonged life expectancy, the prevalence of strokes has increased and has become a significant phenomenon. Despite the available stroke treatment options, patients frequently suffer from significant disability after a stroke. Initial stroke severity is a significant predictor of functional dependence and mortality following an acute stroke. The current study aims to collect and analyze data from the hyperacute and acute phases of stroke, as well as from the medical history of the patients, in order to develop an explainable machine learning model for predicting stroke-related neurological deficits at discharge, as measured by the National Institutes of Health Stroke Scale (NIHSS). More specifically, we approached the data as a binary task problem: improvement of NIHSS progression vs. worsening of NIHSS progression at discharge, using baseline data within the first 72 h. For feature selection, a genetic algorithm was applied. Using various classifiers, we found that the best scores were achieved from the Random Forest (RF) classifier at the 15 most informative biomarkers and parameters for the binary task of the prediction of NIHSS score progression. RF achieved 91.13% accuracy, 91.13% recall, 90.89% precision, 91.00% f1-score, 8.87% FNrate and 4.59% FPrate. Those biomarkers are: age, gender, NIHSS upon admission, intubation, history of hypertension and smoking, the initial diagnosis of hypertension, diabetes, dyslipidemia and atrial fibrillation, high-density lipoprotein (HDL) levels, stroke localization, systolic blood pressure levels, as well as erythrocyte sedimentation rate (ESR) levels upon admission and the onset of respiratory infection. The SHapley Additive exPlanations (SHAP) model interpreted the impact of the selected features on the model output. Our findings suggest that the aforementioned variables may play a significant role in determining stroke patients' NIHSS progression from the time of admission until their discharge.

Transient plasticity response is regulated by histone deacetylase inhibitor in oxygen-glucose deprivation condition.

The pathological form of synaptic plasticity, ischemic long-term potentiation (iLTP), induced by oxygen and glucose deprivation (OGD), is implicated in the acute phase of stroke with the potentiation of N-methyl-D-aspartate receptor (NMDAR). While there has been widespread attention on the excitatory system, a recent study reported that γ-aminobutyric acid (GABA)ergic system is also involved in iLTP. Valproic acid (VPA), a histone deacetylase inhibitor, protects against ischemic damage. However, whether VPA regulates early phase plasticity in ischemic stroke remains unknown. The present study aims to investigate the potential role and mechanism of VPA in ischemic stroke. A brief exposure of OGD on the hippocampal slices and the induction of photothrombotic ischemia (PTI) were used as ex vivo and in vivo models of ischemic stroke, respectively. Using extracellular recordings, iLTP was induced in the hippocampal Schaffer collateral pathway following OGD exposure. VPA treatment abolished hippocampal iLTP via GABAA receptor enhancement and extracellular signal-regulated kinase (ERK) phosphorylation. Administration of VPA reduced brain infarct volume and motor dysfunction in mice with PTI. Moreover, VPA protected against ischemic injury by upregulating the GABAergic system and ERK phosphorylation, as well as by reducing of matrix metalloproteinase in a PTI-induced ischemic stroke model. Together, this study revealed the protection of VPA in ex vivo OGD-induced pathological form of neuroplasticity and in vivo PTI-induced brain damage and motor dysfunction through rescuing GABAergic deficiency and the pathological hallmarks of ischemia.

Periodic Limb Movements during Sleep in Acute Stroke: Prevalence, Severity and Impact on Post-Stroke Recovery.

Periodic Limb Movements during Sleep (PLMS) have been described to be frequently present in stroke patients. We aimed to evaluate the prevalence and severity of PLMS in acute stroke patients and clarify the association between PLMS and coexisting Sleep Disordered Breathing (SDB). Additionally, we focused on identifying variables that could independently predict the presence of PLMS in patients with acute stroke. The potential impact of PLMS on stroke outcome at three months was investigated as well. In this study, we performed overnight polysomnography on consecutive stroke patients within 72 h from symptom onset. Data regarding clinical and imaging characteristics were prospectively collected. National Institute of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS) and Epworth-Sleepiness Scale (ESS) were used to evaluate stroke severity on admission, stroke outcome at three months and history of daytime sleepiness, respectively. We documented PLMS and SDB using standard polysomnography criteria. We prospectively assessed 126 patients with acute stroke [109 with ischemic and 17 with hemorrhagic stroke, mean age 60 ± 11 years, 68% men, median NIHSS score on admission: 3 (IQR: 2-7)]. The overall rate of PLMS in our cohort was 76%, and the rate of SDB among patients with PLMS was 83%. PLMS detection rates differed significantly (p-value: <0.001) according to SDB, with PLMS prevalence increasing with greater SDB severity. SDB could independently (OR:4.869, 95% CI: 1.884-12.784, p-value: 0.001) predict the presence of PLMS in the acute stroke phase in multivariable analyses adjusting for potential confounders. Moreover, baseline stroke severity (NIHSS-score increase in per-1 point: OR: 0.819, 95% CI: 0.737-0.895, p-value < 0.001) and PLMS (OR:0.099, 95% CI: 0.009-0.482, p-value = 0.015) were significantly associated with the likelihood of excellent functional outcome (mRS-scores: 0-1) at 3 months. The common presence of mostly severe PLMS in patients with acute stroke and their negative effect on stroke outcomes point out the necessity for early PLMS detection and treatment.

The Potential Role of RANTES in Post-Stroke Therapy.

One of the key response mechanisms to brain damage, that results in neurological symptoms, is the inflammatory response. It triggers processes that exacerbate neurological damage and create the right environment for the subsequent repair of damaged tissues. RANTES (Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted) chemokine(C-C motif) ligand 5 (CCL5) is one of the chemokines that may have a dual role in stroke progression involving aggravating neuronal damage and playing an important role in angiogenesis and endothelial repair. This study concerned patients with ischemic stroke (AIS), whose CCL5 concentration was measured at various time intervals and was compared with the control group. In addition, the effect of this biomarker on neurological severity and functional prognosis was investigated. Compared to healthy patients, a higher concentration of this chemokine was demonstrated in less than 4.5 h, 24 h and on the seventh day. Differences in CCL5 levels were found to be dependent on the degree of disability and functional status assessed according to neurological scales (modified Rankin Scale, National Institutes of Health Stroke Scale). In addition, differences between various subtypes of stroke were demonstrated, and an increase in CCL5 concentration was proven to be a negative predictor of mortality in patients with AIS. The deleterious effect of CCL5 in the acute phase of stroke and the positive correlation between the tested biomarkers of inflammation were also confirmed.

Macrophage and monocyte subsets in response to ischemic stroke.

Ischemic stroke is a leading cause of disability and mortality. Despite extensive efforts in stroke research, the only pharmacological treatment currently available is arterial recanalization, which has limited efficacy only in the acute phase of stroke. The neuroinflammatory response to stroke is believed to provide a wider time window than recanalization and has therefore been proposed as an attractive therapeutic target. In this review, we provide an overview of recent advances in the understanding of cellular and molecular responses of distinct macrophage populations following stroke, which may offer potential targets for therapeutic interventions. Specifically, we discuss the role of local responders in neuroinflammation, including the well-studied microglia as well as the emerging players, border-associated macrophages, and macrophages originating from the skull bone marrow. Additionally, we focus on the behavior of monocytes stemming from distant tissues, such as the bone marrow and spleen. Finally, we highlight aging as a crucial factor modulating the immune response, which is often neglected in animal studies. This article is protected by copyright. All rights reserved.

Brain Derived Neurotrophic Factor Methylation and Long-term Outcomes after Stroke Interacting with Suicidal Ideation.

This study aimed to evaluate the unexplored relationship between BDNF methylation, long-term outcomes, and its interaction with suicidal ideation (SI), which is closely associated with both BDNF expression and stroke outcomes. A total of 278 stroke patients were assessed for BDNF methylation status and SI using suicide-related item in the Montgomery-Åsberg Depression Rating Scale at 2 weeks post-stroke. We investigated the incidence of composite cerebro-cardiovascular events (CCVEs) during an 8-14-year period after the initial stroke as long-term stroke outcome. We conducted Cox regression models adjusted for covariates to evaluate the association between BDNF methylation status and CCVEs, as well as its interaction with post-stroke SI at 2 weeks. Higher methylation status of CpG 1, 3, and 5, but not the average value, predicted a greater number of composite CCVEs during 8-14 years following the stroke. The associations between a higher methylation status of CpGs 1, 3, 5, and 8, as well as the average BDNF methylation value, and a greater number of composite CCVEs, were prominent in patients who had post-stroke SI at 2 weeks. Notably, a significant interaction between methylation status and SI on composite CCVEs was observed only for CpG 8. The significant association between BDNF methylation and poor long-term stroke outcomes, particularly amplified in individuals who had post-stroke SI at 2 weeks, suggested that evaluating the biological marker status of BDNF methylation along with assessing SI during the acute phase of stroke can help predict long-term outcomes.

Ozanimod Differentially Preserves Human Cerebrovascular Endothelial Barrier Proteins and Attenuates MMP-9 Activity Following In Vitro Acute Ischemic Injury.

Endothelial integrity is critical in mitigating a vicious cascade of secondary injuries following acute ischemic stroke (AIS). Matrix metalloproteinase-9 (MMP-9), a contributor to endothelial integrity loss, is elevated during stroke and is associated with worsened stroke outcome. We investigated the FDA approved selective sphingosine-1-phosphate receptor 1 (S1PR1) ligand, ozanimod, on the regulation/activity of MMP-9 as well as endothelial barrier components (PECAM-1, claudin-5, and ZO-1) in human brain microvascular endothelial cells (HBMECs) following hypoxia plus glucose deprivation (HGD). We previously reported that S1PR1 activation improves HBMEC integrity; however, mechanisms underlying S1PR1 involvement in endothelial cell barrier integrity have not been clearly elucidated. We hypothesized that ozanimod would attenuate an HGD-induced increase in MMP-9 activity which would concomitantly attenuate the loss of integral barrier components. Male HBMECs were treated with ozanimod or vehicle and exposed to 3h of normoxia (21% O2) or HGD (1% O2). Immunoblotting, zymography, qRT-PCR, and immunocytochemical labeling techniques assessed processes related to MMP-9 and barrier markers. We observed that HGD acutely increased MMP-9 activity and reduced claudin-5 and PECAM-1 levels, and ozanimod attenuated these responses. In situ analysis via PROSPER, suggested that attenuation of MMP-9 activity may be a primary factor in maintaining these integral barrier proteins. We also observed that HGD increased intracellular mechanisms associated with augmented MMP-9 activation, however ozanimod had no effect on these select factors. Thus, we conclude that ozanimod has the potential to attenuate HGD mediated decreases in HBMEC integrity in part by decreasing MMP-9 activity as well as preserving barrier properties.

Poor control of modifiable cardiovascular risk factors among Congolese patients in the acute and sequelae phase of stroke : A cross-sectional study

PurposeTo assess the level of the control of the cardiovascular risk factors in patients with a history of stroke in the Democratic Republic of the Congo. MethodsThe level of the control of arterial hypertension, diabetes mellitus, and dyslipidemias was analyzed in two hundred and seventy-four (274) patients followed for stroke. ResultsAmong 188 patients with a prior diagnosis of arterial hypertension, only 100 (53.2%) were treated, 27 (27.0%) had their blood pressure well controlled [12.3% in acute stroke vs. 46.5% in sequelae phase; p = 0.0002]. Among 42 (71.2%) diabetics treated, 23 (63.9%) had glycaemia levels > 200 mg/dl, 60.0% in acute phase and 83.3% in sequelae phase (p = 0.28). Finally, 87.0% of the patients had a non-HDL-C > 85 mg/dl. ConclusionsThis study shows a poor control of modifiable cardiovascular risk factors in patients with very high cardiovascular risk due to stroke. There is a need for an effective program to combat non-communicable diseases in our environment.

The Clinical Variables Predicting the Acquisition of Independent Ambulation in the Acute Phase of Stroke: A Retrospective Study.

Predictive factors associated with independent ambulation post-stroke are less commonly reported for patients during the acute phase of stroke. This study aimed to identify the clinical variables predicting ambulation independence in the acute phase of stroke and test the superiority of their prediction accuracy. Sixty-nine patients, hospitalized in the acute phase for an initial unilateral, supratentorial stroke lesion, were divided into independent (n = 24) and dependent ambulation (n = 45) groups, with functional ambulation category scores of 4-5 and ≤ 3, respectively. They were evaluated upon admission using the modified Rankin scale (mRS), Stroke Impairment Assessment Set (SIAS) concerning the motor function of the lower extremities, Ability for Basic Movement Scale modified version 2 (ABMS2), and Functional Independence Measure (FIM). The scores of the four measures were significantly different between the groups. A univariate logistic regression analysis identified these variables as prognostic factors for independent ambulation. A receiver operating characteristic curve analysis identified the cutoff values (area under the curve) for the mRS, SIAS, FIM, and ABMS2 as 3 (0.74), 12 (0.73), 55 (0.85), and 23 (0.84), respectively. In summary, the FIM and ABMS2 may be more accurate in predicting ambulation independence in patients with stroke during the acute phase.

Transient Middle Cerebral Artery Occlusion Model of Stroke.

Stroke stands as a major cause of death or chronic disability globally. Nevertheless, existing optimal treatments are limited to reperfusion therapies during the acute phase of ischemic stroke. To gain insights into stroke physiopathology and develop innovative therapeutic approaches, in vivo rodent models of stroke play a fundamental role. The availability of genetically modified animals has particularly propelled the use of mice as experimental stroke models. In stroke patients, occlusion of the middle cerebral artery (MCA) is a common occurrence. Consequently, the most prevalent experimental model involves intraluminal occlusion of the MCA, a minimally invasive technique that doesn't require craniectomy. This procedure involves inserting a monofilament through the external carotid artery (ECA) and advancing it through the internal carotid artery (ICA) until it reaches the branching point of the MCA. After a 45 min arterial occlusion, the monofilament is removed to allow reperfusion. Throughout the process, cerebral blood flow is monitored to confirm the reduction during occlusion and subsequent recovery upon reperfusion. Neurological and tissue outcomes are evaluated using behavioral tests and magnetic resonance imaging (MRI) studies.

Correlation between Increased Leukocyte Counts in Patients with Acute Phase Hemorrhagic Stroke with Early Neurological Deterioration Events

Stroke is the second most common cause of death and the leading cause of disability worldwide. Hemorrhagic stroke occurs in 15% of stroke cases. Increased leukocyte counts in the acute phase of hemorrhagic stroke are believed to be related to the incidence of early neurological deterioration. This study aims to determine the relationship between increased leukocyte count and early neurological deterioration in hemorrhagic stroke patients while being treated at UKI General Hospital. This research is analytic research with a cross-sectional design. There were 38 research subjects. The sample was selected using total sampling with specified inclusion and exclusion criteria. The study subjects were grouped into leukocytosis with leukocyte values &gt; 11,000/µL blood and normoleukocytes with leukocyte ranges ranging from 4000-11000/µL blood. The data used is secondary data. The results of the study were processed using the SPSS computer program. It was found that early neurological deterioration in patients with leukocytosis was significantly higher than in patients with normoleucosis, with a Relative Risk of early neurological deterioration in patients with leukocytosis of 3.003 (CI 95%); p=0.031). A significant relationship exists between increased leukocyte count (leukocytosis) upon admission and early neurological deterioration while being treated for hemorrhagic stroke patients at the UKI General Hospital.

C-Reactive Protein Levels and Cognitive Decline following Acute Ischemic Stroke: A Systematic Review and Meta-Analysis.

Cognitive decline (CD) is devastating with a high incidence in patients after stroke. Although some studies have explored underlying associations between C-reactive protein (CRP) levels and cognitive decline after stroke, consistent results have not been obtained. Therefore, this meta-analysis aimed to explore whether or not higher levels of C-reactive proteins were associated with an increased risk of cognitive decline after stroke. To this end, PubMed, Embase, the Cochrane Library, and Web of Science were searched for eligible studies, and pooled effect sizes from eligible studies were calculated using random effect models. Furthermore, subgroups were established and meta-regression analyses were performed to explain the causes of heterogeneity. Eventually, nine studies with 3893 participants were included. Our statistical results suggested that the concentrations of peripheral CRP may be significantly increased for CD patients after stroke, compared to those of non-CD patients. Subgroup analyses showed that CRP was higher in CD than that in non-CD patients when the mini-mental state examination was used. A higher level of CRP in the acute phase of ischemic stroke may suggest an increased risk of CD after stroke. However, these results should be cautiously interpreted because of the limited sample sizes and the diversity of potential confounders in the studies included in this meta-analysis.