Risultati per: Fisioterapia per il recupero post COVID-19

Stroke, Volume 56, Issue Suppl_1, Page ATP380-ATP380, February 1, 2025. Recent research on neurodegenerative diseases has highlighted a pathophysiological cascade characterized by abnormal lipid accumulation within the brain. Although progress has been made, the role of lipid metabolism following stroke remains unclear. This study aims to further explore changes in lipid metabolism after stroke, with a specific focus on the endoplasmic reticulum transmembrane protein 97 (TMEM97), which has emerged as a promising therapeutic target due to its critical role in cholesterol metabolism.Spatial transcriptomic analyses following experimental stroke induction in mice revealed neuronal upregulation of crucial genes involved in lipid metabolism pathways, including LDLR, acetyl-CoA acetyltransferase 1, and elongation of very long-chain fatty acids protein 6, indicating dynamic adaptations post-stroke or under cellular stressors.Initial findings demonstrate TMEM97 expression predominantly within neurons in vivo (mouse model). In an in vitro model of lipid starvation using mouse neural progenitor cells (MNPCs), pharmacological inhibition of lysosomal lipid release leads to increased expression of TMEM97. Interestingly, when TMEM97 was knocked down in MNPCs using lentiviral shRNA transfection, these cells exhibited no significant difference in neutral lipid accumulation compared to control cells. However, upon treatment with the lysosomal lipid release inhibitor, a significant increase in neutral lipid accumulation was observed exclusively in the TMEM97 knockdown cells.Furthermore, Thapsigargin-induced endoplasmic reticulum (ER) stress in the MNPCs reduced TMEM97 expression, while also increasing low-density lipoprotein (LDL) uptake and the mRNA levels of the LDL receptor (LDLR). The observed elevation of neuronal LDLR expression in vitro closely aligns with the heightened expression of LDLR in vivo, suggesting a coordinated modulation of lipid metabolism pathways triggered by ER stress in response to stroke or metabolic stress induction. This synchronous upregulation of LDLR underscores the crucial role of ER stress as a potential trigger for this regulatory response. Additionally, considering the known involvement of TMEM97 in lipid homeostasis within the ER, it further highlights the intricate interplay between these proteins in post-stroke lipid metabolism regulation.Our findings provide a compelling starting point for further exploring TMEM97’s significance in post-ischemic lipid homeostasis.

Stroke, Volume 56, Issue Suppl_1, Page ATP136-ATP136, February 1, 2025. Background:The STRACK project aims to improve post-stroke patient management and the transition from acute to primary care thanks to improvements in patient pathways and monitoring cardiovascular risk factors: heart failure, diabetes, atrial fibrillation, dyslipidemia and hypertension. Collaboration between primary care centers and hospital staff was essential for the project’s success by delivering personalized care and home monitoring devices to patients through access to a digital platform. STRACK was launched with a european value-based contracting process and Roche Diag. as partner.Methods:The three-year project was launched in May 2021, during first year all specialties and professionals participated in the development and planning of the project and were trained in the use of the devices and own digital platform.First STRACK patient was enrolled in May 2022. Once these post-stroke patients have been identified, they are given a personalized monitoring plan depending on the individuals’ risk factors, the personalized care and rehabilitation plans are tracked and followed. For a year post-discharge, a nursing and administrative team follows the data that the patient enters remotely or is automatically available on their mobile application.Results:STRACK has evolved the continuum of care by 421patient in July 2024 and ongoing, by integrating comprehensive monitoring of cardiometabolic risk factors (heart failure, diabetes, atrial fibrillation, dyslipidemia, hypertension) into a patient discharge plan, identified as key to avoiding stroke recurrence and improving control of vascular risk factors are monitored.Preliminary results of 231 patients (May 2022-2023) with full one year follow-up comparing with historical cohort (May 2018-2019) showed: Reduction in unnecessary visits (weighted): -26,3%. Reduction in admissions for stroke recurrence or related to stroke, (heart attack, angina, peripheral embolism, etc.): Stroke, 30days: -100%; Related to stroke, (365d: -47,7%; 30d: -57,0%). Reduction in cardiovascular admissions ( 30d: -100%; 365d: -31,4%). Best treatment adherence: 81,2% (72% previously)Conclusion:The great value of STRACK is knowing the evolution of stroke patients post-discharge through strict self-monitoring of clinical parameters, following prior health education. STRACK has managed to achieve reduction in stroke recurrence and adverse events and readmissions for cardiovascular risk factors, reducing emergency visits for vascular events.

Stroke, Volume 56, Issue Suppl_1, Page AWP16-AWP16, February 1, 2025. Introduction:Currently, no level A evidence exists for the optimal rescue strategy for cases at high risk for re-occlusion following endovascular thrombectomy (EVT) in acute ischemic stroke. Glycoprotein IIb/IIIa inhibitors, which inhibit platelet aggregation and adhesion, show promise as adjunctive therapy, potentially yielding favorable outcomes, especially in residual stenosis cases.Methods:In this retrospective review study, we included patients aged ≥18 who underwent EVT at a comprehensive stroke center with TICI 2b or 2c outcome (admitted between 2019 – 2024), who were noted to have high-risk residual stenosis on angiography after EVT. We defined high-risk post-EVT stenosis as any stenosis with ≥50% lumen stenosis, associated dissection, re-occlusion during thrombectomy, and severe residual luminal irregularity. We excluded patients who had a clear contraindication to Eptifibatide, received a stent, or if the luminal stenosis was related to reactive vasospasm and any cases with TICI 0, 1, or TICI 3 scores.Results:Our sample size was 60 (51.7% male, 48.3% female, mean age 63.9). Mean National Institute of Health Stroke Scale (NIHSS) on admission was 16.6; 36.7% (n=22) received eptifibatide. The rate of re-occlusion was significantly lower in patients who received eptifibatide compared to those who did not (9.1% vs. 36.8%, p=0.032). There was no difference in pre-stroke modified Rankin scale (mRS), NIHSS on admission, mortality, discharge mRS, or 90-day mRS between these two groups, nor between patients who received intravenous thrombolysis (IVT) vs. those who did not. However, among the 16 patients who received IVT, those who also received eptifibatide had significantly lower mean discharge NIHSS (5.0 vs. 13.6, p=0.028), discharge mRS (1.3 vs. 4.5, p=0.009), and 90-day mRS (1.0 vs. 4.1, p=0.038) than those who did not. Ordinal logistic regression of discharge mRS and 90-day mRS in IVT recipients with vs. without eptifibatide usage also revealed significant odds of lower mRS at both timepoints with eptifibatide (OR 7.23, p=0.011 and OR 5.2, p=0.030 respectively).Conclusions:Eptifibatide use is associated with lower re-occlusion rates in patients with residual high-risk stenosis after EVT. Among IVT recipients with post-EVT residual stenosis, eptifibatide use is associated with improved discharge mRS, discharge NIHSS, and 90-day mRS. Given our limited sample size, these findings need to be evaluated further with larger Randomized Control Trials.

Stroke, Volume 56, Issue Suppl_1, Page AWP78-AWP78, February 1, 2025. Introduction:Dysphagia affects approximately 30-80% of ischemic stroke patients. While most patients recover swallowing functions within a week, 10-50% may experience persistent issues for up to six months post-stroke. Early enteral access is critical for providing hydration, nutrition, and medication to these patients. Stroke patients often require specialized nutritional support through feeding tubes. At a large urban academic comprehensive stroke center, we identified an opportunity to develop a model that supports and streamlines feeding tube placement for this population to enhance care quality and improve patient outcomes.Methods:This retrospective study evaluated enteral feeding support in 43 post-acute stroke patients from October 2023 through July 31st. We compared tube placements and outcomes between nursing staff and a dietitian-led enteral access team. Nursing staff used standard NG tube procedures, while the dietitian-led team employed advanced techniques, including an electromagnetic device and bridle retention system to enhance tube stability and reduce need for replacements. We also assessed discharges to acute rehabilitation with bridled small-bore tubes who would have otherwise required PEG placement.Results:Out of 43 patients, 7 patients had NG tubes placed by nursing staff and 36 by the dietitian-led team. All 7 patients required replacement and were ultimately escalated to the dietitian-led team. The dietitian-led team achieved greater tube stability using advanced techniques and required only 1 replacement. A total of 13 patients were discharged to rehabilitation with bridled tubes.Conclusion:In conclusion, we found that a dietitian-led enteral access team can maintain high-quality care and satisfaction through advanced enteral tube placement techniques. Additionally, a subset of patients were able to defer PEG placement allowing for additional time for recovery from dysphagia. Future considerations include evaluating nurse workload reduction, decreased hospital stays, and accelerated rehabilitation placement with early, secure enteral access.

Stroke, Volume 56, Issue Suppl_1, Page A158-A158, February 1, 2025. Introduction:Clearing necrotic tissue from lesions by microglia/macrophage is crucial for recovery after acute ischemic stroke (AIS). Lysosomal activity is key for efferocytosis. In the chronic phase, reduced lysosomal activity impairs clearance, causing residual debris and worsening cognitive impairment. Migrasomes, formed during cellular migration, help maintain other organelles like mitochondria.Hypothesis:This study explored how migrasomes in microglia/macrophage help load damaged lysosomes for expulsion, preserving lysosomal quality and efferocytosis post-stroke.Methods:Male C57BL/6 mice including wild-type (WT) andTspan14conditional knockout (Tspan14fl/flLyz2Cre, TSPAN14 CKO) underwent transient middle cerebral artery occlusion (tMCAO). Migrasome production and TSPAN14 expression were evaluated through staining and nano flow cytometry. Neurobehavioral performance was measured by rotarod, foot fault, novel object recognition, and water maze tests up to 14 days post-stroke. In vitro, bone marrow-derived macrophages (BMDM) were cultured with blebbistatin to inhibit migrasome production. BMDM efferocytosis of dead neurons was assessed by staining and flow cytometry.Results:In cultures, 76.9% of migrasomes from BMDM engulfing dead neurons contained damaged lysosomes. Inhibiting migrasome production in BMDM impaired efferocytosis and increased damaged lysosome accumulation. TSPAN14 on the lysosomal membrane mediated lysosome sorting into migrasomes. Migrasomes from TSPAN14 CKO BMDM engulfing dead neurons had 62.3% less lysosomal content than those from WT BMDM, though their numbers were similar (P

Stroke, Volume 56, Issue Suppl_1, Page A156-A156, February 1, 2025. Background:Brain inflammation following ischemic stroke exacerbates neuronal injury. Early immune cell infiltration into the brain after ischemia is correlated with increased risk of subsequent stroke and higher three-month mortality. However, direct mechanisms that underly this immune cell recruitment remain unclear, preventing the development of successful therapeutics. Recent work has identified mast cells as early responders in stroke that incite inflammation, yet how these cells are activated remains unknown. We hypothesized that Mrgprb2, a mast cell receptor known to trigger neurogenic inflammation, initiates mast cell activity in stroke, and that inhibition of this receptor can attenuate stroke injury.Methods:We performed MCA occlusion (MCAO) on wild-type and Mrgprb2-null (Mrgprb2-/-) mice and assessed stroke volume, and behavior. We used flow cytometry and ELISA for immune cell and cytokine profiling to evaluate inflammation. Human stroke patient dura and blood was sampled to assess mast cell activity and to identify potential ligands for Mrgprb2 activation. Lastly, we used osthole, a Mrgprb2 inhibitor, as a post-MCAO treatment to determine if pharmacologic inhibition can attenuate post-stroke deficits in mice.Results:We found that Mrgprb2 is activated in meningeal mast cells after stroke, causing mast cell degranulation and release of chemokines that attract immune cells. Mrgprb2-/-mice exhibited reduced brain inflammation after stroke, leading to attenuated infarct size, and reduced mortality. Further, we show evidence that Mrgprb2-/-mice recruited fewer skull bone marrow neutrophils into the brain, suggesting a novel mechanism whereby mast cells regulate skull bone marrow recruitment. We demonstrated that the human ortholog of this receptor, MRGPRX2, is expressed in human meningeal mast cells, and that these cells are activated in stroke patients. Further, substance P, a known ligand of Mrgprb2/X2, is increased in stroke patient serum. Lastly, osthole-treated mice have reduced post-stroke brain inflammation and improved functional outcomes, confirming that pharmacologic inhibition of Mrgprb2 is a promising therapeutic strategy.Conclusions:Our study identifies Mrgprb2 as a key receptor which triggers mast cell activity in stroke and initiates brain inflammation. Mrgprb2/X2 provides a specific and druggable target to attenuate post-stroke inflammation and holds potential to meaningfully alter the clinical course for stroke patients.

Stroke, Volume 56, Issue Suppl_1, Page A162-A162, February 1, 2025. Background:Preceding respiratory tract infections (RTIs) caused by bacteria or viruses are associated with worse stroke outcomes, likely due to an exaggerated inflammatory immune response, endothelial dysfunction, platelet activation, and coagulopathy. Recent studies have revealed increased plasma von Willebrand factor (VWF) levels and reduced ADAMTS13 activity (the risk factors for stroke) in patients with RTIs, including COVID-19. However, it remains unclear whether an imbalance in the VWF–ADAMTS13 axis plays a causative role in the pathophysiology ofS. aureus- or COVID-19-associated stroke severity or is merely an associative marker of disease status.Objective:To examine whether an imbalance in the VWF–ADAMTS13 axis is a causal link between RTIs and stroke severity.Methods:Wild-type (WT) mice (3–4 months old) were infected intranasally with sublethal doses ofS. aureus(on days 0, 2, and 5) or mouse-adapted SARS-CoV-2 (on day 0). On day 6 (S. aureus) or day 3 (SARS-CoV-2), the infection was confirmed to be localized in the lungs (but not in the brain) and the plasma VWF levels and ADTMTS13 activity were quantified. In another set of experiments, WT,Vwf−/−, andAdamts13−/−mice (3–4 months old) with respective littermate controls were subjected to transient (30 or 45 min) cerebral ischemia (filament stroke model) followed by reperfusion. For theS. aureusexperiments, brain infarcts were assessed on day 2 post-reperfusion and functional outcomes (corner test, wire hanging test, modified neurological severity score, and rotarod test) on week 1 and 4 post-reperfusion. For the SARS-CoV-2 experiments, brain infarcts and functional outcomes (the Bederson score) were assessed on day 1 post-reperfusion.Result:We demonstrated thatS. aureusor SARS-CoV-2 infection localized to the lungs in the WT mice resulted in increased (2–3 fold) plasma VWF levels and reduced ADAMTS13 activity, concomitant with larger infarcts and worse functional outcomes (P

Stroke, Volume 56, Issue Suppl_1, Page AWMP41-AWMP41, February 1, 2025. Introduction:Post-stroke cognitive decline (PSCD) is a common complication of strokes, and early assessment is crucial. However, outpatient cognitive assessment protocols are inconsistent, leading to missed diagnoses of PSCD. A potential solution is the XpressO application, introduced in 2023 by the creators of the Montreal Cognitive Assessment (MoCA). Because XpressO is self-paced, it can be completed by patients while waiting for an appointment and hence can assess cognition without impacting clinic workflow.Hypothesis:This study aims to investigate the feasibility of using the XpressO online self-administered cognitive assessment and compare its ability to detect PSCD with the MoCA short form (MoCA-sf) at our out-patient stroke clinic.Methods:Patients at the clinic with a history of ischemic or hemorrhagic strokes were included. We used

Stroke, Volume 56, Issue Suppl_1, Page A150-A150, February 1, 2025. Background and Purpose:Stroke is a leading cause of long-term disability, often resulting in functional and cognitive impairments that significantly reduce quality of life. While racial and ethnic differences in clinical outcomes after stroke are well-documented, the impact of post-stroke disability on patient-centered outcome measures, which account for physical, emotional, and sociocultural factors, remains insufficiently understood. This study aimed to investigate racial and ethnic differences in post-stroke quality of life among participants in the SHINE trial.Methods:This is a post-hoc analysis of the Stroke Hyperglycemia Insulin Network Effort (SHINE) trial. Self-reported race, ethnicity, and the 12-item Stroke Specific Quality of Life (SSQOL) Scale at 90-day follow-up were used for correlation analyses, adjusted for age, sex, hypertension, diabetes, stroke size, recurrent stroke, and 90-day modified Rankin Scale. The SSQOL is a patient-centered outcome measure that assesses health-related quality of life specific to stroke survivors across 12 domains (Table 1).Results:A total of 907 ischemic stroke patients with hyperglycemia (mean age 65±12.8, 44.7% female, 80.9% with diabetes) were included in this study. At 90-day follow-up, no significant differences were found in overall SSQOL summary scores by race/ethnicity. However, Hispanic patients reported significantly lower scores in self-care (p < .0001) (Figure 1), vision (p = .015), and upper extremity function (p = .007), while Black patients reported lower energy (p = 0.012).Discussion:These findings indicate that Hispanic and Black stroke survivors experience lower quality of life in specific domains after adjusting for stroke severity and other potential confounders. In addition to clinical outcomes, it is crucial to understand stroke survivors’ perceptions of their quality of life which can inform more culturally competent care. Future research should validate these associations and examine the role of socio-economic factors in shaping post-stroke quality of life to promote effective and equitable care in line with the WHO 2030 Rehabilitation agenda.

Stroke, Volume 56, Issue Suppl_1, Page AWMP37-AWMP37, February 1, 2025. Introduction:Post-stroke fatigue (PSF) is a common and debilitating consequence of cerebrovascular accidents, potentially stemming from central and peripheral mechanisms. Recent studies have linked myasthenia gravis-related antibodies to PSF, though data on their role remains limited. Current treatments for PSF are often ineffective, underscoring the need for more research into its underlying causes and management.Objectives:This study investigates the presence of myasthenia gravis-related antibodies in patients with PSF after motor recovery, focusing on low-density lipoprotein receptor-related protein 4 (LRP4) and AGRIN antibodies. We aim to evaluate their clinical response to targeted therapies, excluding anti-AChR and anti-MuSK antibodies.Methods:We conducted a cross-sectional study involving patients with PSF who had undergone myasthenia antibody testing. The study cohort included individuals with fatigue following good motor recovery, who tested positive for LRP4 and AGRIN antibodies. Clinical, demographic, and imaging data were analyzed, with clinical response assessed using the Modified Rankin Scale (mRS) at follow-up.Results:Among 935 patients at the stroke unit over two years, 50 were tested for myasthenia antibodies due to PSF. Of these, 17 (34%) were positive for either anti-AGRIN (70.58%) or anti-LRP4 (64.71%) antibodies. Fatigue was reported by 82.35% of the antibody-positive patients. This group consisted of 35.29% females with a mean age of 66.7 years. Most had a history of ischemic stroke (88.23%), with 11.76% having experienced hemorrhagic stroke.All 17 patients received cholinergic medications, showing significant improvement in mRS scores. The Wilcoxon signed-rank test revealed a p-value of

Stroke, Volume 56, Issue Suppl_1, Page ANS8-ANS8, February 1, 2025. Background and Purpose:Patients discharged home after a stroke are particularly vulnerable during the immediate post-discharge period. We identified significant gaps in post-discharge care for stroke patients at our Comprehensive Stroke Center, including inconsistent follow-up timing and a high rate of missed appointments. This initiative aimed to enhance the post-discharge process to improve care quality and reduce missed follow-ups.Methods:We implemented a streamlined follow-up process for stroke patients discharged home, aligning with the Centers for Medicaid and Medicare (CMS) definition of the Transitional Care Management (TCM). A Nurse Practitioner (NP) conducted inpatient rounds, coordinated follow-up appointments before discharge, and contacted patients within 24-48 hours. Patients were seen by the outpatient stroke NP within 7 to 14 days, either in clinic or via telemedicine. This process, compliant with CMS requirements and billable under TCM, was evaluated over seven months, focusing on clinic no-show rates and reimbursement compared to standard discharge practices.Results:Patients discharged home under our TCM model had a 3% no-show rate, significantly lower than the 14% observed in those discharged without TCM. All patients discharged home with TCM had a post-discharge follow-up appointment scheduled compared to 9% of patients discharged home without TCM who had no scheduled stroke follow-up. Additionally, using the appropriate CMS codes for TCM resulted in higher reimbursement and increased revenue compared to standard follow-up billing.Conclusions:Implementing this initiative aligned our discharge process with the CMS-recognized TCM model, improved scheduling of post-discharge follow-up appointments, reduced post-discharge clinic no-show rates, and increased departmental revenue.

Stroke, Volume 56, Issue Suppl_1, Page AWMP44-AWMP44, February 1, 2025. Background:The post-acute journey for stroke patients is highly variable. We evaluated patient and health-system factors that contribute to the variability in 1-year home time (HT) by employing unsupervised learning (cluster analyses) among Acute Ischemic Stroke (AIS) patients.Methods:Texas statewide medical claims data on post-stroke care transitions were extracted from a CMS Qualified Entity housing data for ≥80% of the population (including 100% of Medicare Fee-for-Service). Clinical information on a matched sub-population was linked from the EMR of a 7-hospital certified stroke health system. K-means clustering was performed on 1) the statewide dataset on post-discharge care utilization, and 2) the hospital dataset which further included clinical and acute care features. The optimal number (k) of cluster centers was compared algorithmically using direct (average silhouette) and gap statistic methods. Cluster performance, with respect to distinguishing high risk patients more likely to have low HT post-discharge (i.e., total 1-year home time of

Stroke, Volume 56, Issue Suppl_1, Page AWP367-AWP367, February 1, 2025. Introduction:Ischemia reperfusion injury (IRI) is a paradoxical and deleterious consequence of current interventions for acute ischemic stroke (AIS). Rapid restoration of oxygen to brain tissue upon reperfusion initiates mitochondrial reverse electron transport (RET) and production of reactive oxygen species (ROS), which exacerbate cell death. A pivotal role of the citric acid cycle intermediate succinate has been identified in driving RET post-reperfusion, whereby succinate accumulated during ischemia is rapidly reoxidized following reperfusion leading to a burst of ROS. Disodium malonate (DSM), a competitive inhibitor of succinate dehydrogenase, has been shown to attenuate RET ROS production following reperfusion and reduce infarct volume in rodent models. Here, we sought to evaluate the effect of DSM on infarct evolution post-reperfusion in a clinically-relevant sheep model of AIS for enhanced clinical translation.Methods:Male Merino sheep (N=13, 24-36 months, 62±6 kgs) underwent right pterional craniotomy and middle cerebral artery occlusion (MCAo) via aneurysm clip application for 4 hrs followed by reperfusion. Animals were pre-operatively randomized into vehicle (0.9% saline, N=5), medium dose DSM (0.5 mmole/min; N=4) and high dose DSM (1.0 mmole/min; N=4). Treatment was administered via right common carotid catheter at a rate of 15 mL/min for 10 min, starting 5 min prior to reperfusion. MCAo and reperfusion were confirmed on digital subtraction angiography (DSA). One hour following reperfusion, animals underwent magnetic resonance imaging (MRI) with a follow-up MRI performed 6 hours later. Infarct volume was calculated on diffusion weighted imaging (DWI) at each time-point to assess ischemic evolution.Results:All animals displayed evidence of MCAo and successful reperfusion following aneurysm clip removal (Figure 1). Infarct volume between groups was comparable at 1 hr post reperfusion (P >0.05), however, by 6 hrs infarct expansion was attenuated in animals receiving DSM compared with vehicles (P=0.0037). This was apparent in both the medium (P=0.006) and high (P=0.011) DSM groups.Conclusions:Intraarterial DSM administration reduces infarct expansion following reperfusion in a sheep model of MCAo. Evaluation of treatment efficacy in a larger cohort of animals is essential to address stroke therapeutic and industry roundtable (STAIR) guidelines and provide evidence to progress DSM to clinical trial for the treatment of IRI in AIS.

Stroke, Volume 56, Issue Suppl_1, Page AWP123-AWP123, February 1, 2025. Background:Post-stroke fatigue is a common and debilitating issue, often linked to depression or neural damage. Emerging evidence suggests that myasthenia gravis (MG) may also play a role in post-stroke fatigue, offering a new perspective on patient management and long-term disability reduction.Objectives:This study aims to assess the incidence of de novo MG in stroke survivors following motor recovery over 18 to 24 months and compare findings with a healthy control group.Methods:Conducted at a tertiary care institution over two years, this prospective case-control study included ischemic and hemorrhagic stroke patients. Participants were recruited during the acute stroke phase and underwent evaluations for neuromuscular weakness and autoimmune disorders. They were monitored in a specialized stroke clinic for two years. Key variables included demographics, comorbidities, autoimmune disorders, stroke subtype, time since onset of stroke, and muscle fatigability. Age and sex-matched controls were assessed concurrently. Baseline and two-year follow-up measurements of acetylcholine receptor (AChR) antibodies were performed, and new antibodies were monitored. Participants with significant fatigability were tested for MG, and if confirmed, treated with cholinergic drugs.Results:The study involved 96 participants with a mean age of 60.45 years, predominantly male (63.86%). Ischemic stroke was most common (93.75%). Major risk factors included hypertension (12.5%), diabetes (5.20%), and dyslipidemia (3.12%), with 11.45% having autoimmune disorders. Of the 96 participants, 74 (77.08%) reported fatigability an average of 23.2 months post-stroke. Types of fatigability included neck (34.37%), proximal arm (11.46%), grip (19.80%), speech (5.21%), and eye (6.25%). Among 36 stroke patients with post-stroke fatigability and 36 controls re-evaluated at follow-up, 7 stroke patients tested positive for AChR antibodies compared to 1 control. Fisher’s Exact test showed a significant association between stroke and AChR-Ab positivity (p = 0.001), with an odds ratio of 7, suggesting a potential link between post-stroke fatigue and MG.Conclusion:The study highlights MG as a potential underrecognized factor in post-stroke fatigue. These findings may improve diagnostic and therapeutic strategies for stroke survivors and pave the way for further research into post-stroke immune alterations and MG development.

Stroke, Volume 56, Issue Suppl_1, Page AWMP76-AWMP76, February 1, 2025. Importance:The COVID-19 pandemic significantly disrupted healthcare systems worldwide, impacting the management of acute ischemic stroke (AIS). Understanding changes in AIS admissions, treatment patterns&outcomes during the pandemic is essential for optimizing stroke care in future public health crises.Objective:To evaluate the impact of the COVID-19 pandemic on AIS admissions, treatment utilization, complications&outcomes in the U.S. from 2016 to 2021, focusing on the pre-pandemic (2016-2019)&peri-pandemic (2020-2021) periods.Methods:A retrospective observational cohort study utilizing the National Inpatient Sample (NIS) nationwide database, analyzing weighted hospital discharge records over 6 years, encompassing urban, rural, teaching &non-teaching hospitals.Participants were AIS patients aged 18 years&older (n=3,154,154), identified using ICD-10 codes. Sociodemographic characteristics such as age, sex, race&comorbidities were evaluated. The mean patient age was 70.0 ± 0.03 years, with an average length of stay of 5.1 ± 0.01 days&an adjusted mean cost of $16,765 ± 71. Men accounted for 50.5% of the cohort. AIS hospitalizations from 2016 to 2021 were collected, comparing pre-&peri-pandemic periods. Primary outcomes included AIS admission trends, while secondary outcomes included reperfusion therapy utilization, intubation&ventilation rates, discharge disposition&complications.Results:AIS admissions increased from 507,920 in 2016 to 535,694 in 2021. A demographic shift was observed, with the proportion of male patients rising from 49.8% to 51.4%&the mean age decreasing from 70.3 to 69.7 years (p < 0.0001). Most patients were White (69.5% in 2016), but their proportion decreased over time, while Black, Hispanic&Asian/Pacific Islander cases increased (p 0.5734). Reperfusion therapy usage increased, with mechanical thrombectomy (MT) rising from 2.2% to 5.6% in 6 years. Intubation/ventilation rates grew from 4.8% pre-COVID to 5.5% peri-COVID (p < 0.0001). Subarachnoid&intracerebral hemorrhage rates had increased throughout the 6 years in the group with MT-only intervention (p .011&.002, respectively).Conclusions:The COVID-19 pandemic led to significant shifts in AIS hospitalization patterns, including changes in age distribution, increased reperfusion therapy use&rising complications. These findings highlight the need for adaptive public health strategies&resource allocation to maintain stroke care during future crises.

Stroke, Volume 56, Issue Suppl_1, Page AWMP51-AWMP51, February 1, 2025. Background:Obstructive sleep apnea (OSA) is common among patients with ischemic stroke and transient ischemic attack (TIA) and has been associated with poor outcomes. Guidelines recommend evaluating eligible patients with cerebrovascular events for OSA.Objective:to examine whether a quality improvement (QI) intervention could increase OSA testing post-stroke/TIA.Methods:ASAP (NCT04322162) was a stepped-wedge cluster-randomized trial evaluating the effectiveness of a QI intervention to increase OSA testing among ischemic stroke or TIA patients at intervention (N=6) vs. control sites (N=30). Recruitment was at the facility level. The study involved 3 phases: baseline, implementation, and sustainability. The primary outcome was: 30-day OSA diagnostic testing rate. Secondary outcomes were: 30-day continuous positive airway pressure treatment rate, and 90-day recurrent vascular event and readmission rates. ASAP was powered to detect a difference in the primary outcome: baseline vs. implementation. Generalized linear mixed-effects models with binomial distribution and log link fit to patient-level data with site-level random effects were used. The QI intervention included: a virtual kickoff (teams reviewed data, identified improvement opportunities, considered barriers and solutions to diagnosing OSA post-stroke/TIA, and action plan development); monthly collaborative conferences; web-based platform displaying quality data and resource library; and external facilitation.Results:Among 1747 patients at 6 intervention sites the diagnostic rate increased from 2.1% (baseline, 20/952) to 29.1% (implementation, 189/650); among 7454 patients at 30 control sites the 30-day diagnostic rate varied (0.6%-2.2%; adjusted odds ratio (aOR) 16.90 (95%CI, 9.49-30.10). The diagnostic rate during sustainability was 11.7% (17/145); aOR 3.58 (1.59-8.04). The 30-day treatment rate varied (0.0%-0.4%) at control sites and increased at intervention sites: 0.3% (baseline, 3/952) to 2.8% (implementation, 18/650; OR 14.22 (2.40-84.40). The treatment rate during sustainability was 0.7% (1/145); aOR 2.66 (0.13-56.21). 90-day readmission and recurrent event rates were lower during implementation and sustainability (vs. baseline); these changes were not statistically significant.Conclusions:QI approaches can markedly increase OSA testing among patients with acute cerebrovascular events. Additional work should identify strategies to increase treatment rates among stroke/TIA patients with OSA.