Risultati per: La nevralgia post-erpetica

Stroke, Volume 56, Issue Suppl_1, Page ATP1-ATP1, February 1, 2025. Background and Objective:The effect of time from onset to treatment on reperfusion in an extended time window remains unexplored. This study aimed to investigate the relationship between the time to treatment and the probability of reperfusion in acute ischemic stroke patients with large vessel occlusion treated with tenecteplase in an extended time window, using data from the Chinese Acute tissue-Based imaging selection for Lysis In Stroke Tenecteplase (CHABLIS-T) trials.Methods:This study included patients treated with intravenous tenecteplase from the CHABLIS-T1 and CHABLIS-T2 clinical trials, both of which screened patients in the extended window using CT perfusion (CTP) imaging. Major reperfusion was assessed through follow-up CTP or digital subtraction angiography (DSA) imaging. Time variables, including the time from last known normal (LKN) /symptom onset to hospital arrival/ administration of tenecteplase were entered as continuous, categorical, and cubic spline variables in multivariable logistic regression models to explore their association with the probability of post-thrombolytic reperfusion.Results:A total of 199 patients arrived within 4.5-24 hours from LKN were included in this study, of whom 67 achieved post-thrombolytic major reperfusion. Cubic spline analysis indicated a linear correlation between time variables and the probability of reperfusion. Therefore, time variables were entered as continuous or categorical variables in the regression models. Multivariable logistic regression analysis revealed that a longer time from LKN to hospital arrival was associated with a lower probability of major reperfusion (continuous variable: OR=0.998, P=0.018,Figure 1). Similarly, a longer time from LKN to thrombolysis was associated with a lower probability of reperfusion (continuous variable: OR=0.996, P=0.020,Figure 2; categorical variable: OR=0.043, P=0.005,Figure 3). The analysis of time from symptom onset to hospital arrival/thrombolysis and reperfusion drew similar resultsConclusion:In acute ischemic stroke patients with large vessel occlusion treated with tenecteplase in an extended time window, a longer time to treatment was associated with a lower probability of post-thrombolytic reperfusion. Therefore, rapid reperfusion treatment should still be required even in patients with large vessel occlusion in an extended time window with a good collateral flow, in order to optimize treatment effect.

Stroke, Volume 56, Issue Suppl_1, Page ADP56-ADP56, February 1, 2025. Introduction:We discovered a marked upregulation of MMP-12 levels in the brain following an ischemic stroke and demonstrated that reducing MMP-12 levels in otherwise healthy rodents decreases brain damage and facilitates functional recovery. This study aimed to assess the effectiveness of MMP-12 gene silencing in improving sensorimotor function recovery in aged mice and hypertensive rats.Methods:Both male and female C57BL/6 mice (≥16 months old) and male spontaneously hypertensive rats (SHRs) (2-3 months old) were subjected to 35-min and 1-h transient right middle cerebral artery occlusion (MCAO), respectively. Appropriate cohorts of animals (25 mice/group; 18 rats/group) received either control shRNA or MMP-12 shRNA plasmids (1 mg/kg) formulated as nanoparticles that were administered intravenously via tail vein 2 h after reperfusion. In mice, stroke symptoms were evaluated using the neurological deficit score at 2-4 hours and 1 day after reperfusion, while the modified neurological severity score was used in rats. Sensorimotor functions were assessed using the sticky tape test, pole test, and rotarod test at baseline (before MCAO) and at regular intervals post-MCAO (days 3, 5, and 7 in mice, and days 1, 3, 5, 7, and 14 in rats).Results:MMP-12 expression in the ischemic brain was significantly increased by 35-min MCAO in aged mice and 1-h MCAO in SHRs, as was previously observed in healthy young mice and rats that were subjected to 1-h and 2-h MCAO, respectively. In comparison to the control shRNA treatment, MMP-12 shRNA treatment facilitated a greater mean recovery of somatosensory function in aged mice (sticky tape latency was significant on day 3 and day 5; sticky tape interaction was significant on day 5) and in SHRs (sticky tape ratio was significant on day 14). Furthermore, MMP-12 shRNA treatment resulted in a greater mean recovery of motor function across all tested time points in aged mice (pole descent score was significant on day 7; rotarod latency was significant on day 7) and in SHRs (rotarod latency was significant on day 5 and day 14).Conclusions:Reducing MMP-12 expression in the ischemic brain facilitates the recovery of both somatosensory and motor function in aged mice and hypertensive rats after transient focal cerebral ischemia. Our findings further reinforce the potential benefits of MMP-12 gene silencing as a therapeutic approach for improving recovery outcomes in stroke patients.

Stroke, Volume 56, Issue Suppl_1, Page ADP28-ADP28, February 1, 2025. Background:Microglia-mediated inflammatory response directly affects ischemic stroke outcome. Autophagy is crucial in inflammatory response after cerebral ischemia. NLRC5 can be a positive or negative regulator of inflammatory signaling cascades, but its role after ischemic stroke is unstudied.Methods:Single-cell RNA sequencing and immunofluorescence staining were used to explore the expression and localization of NLRC5 in mice brain. Conditional (microglia-specific) NLRC5-knockout mice (TMEM119CreERTNLRC5f/f) and their littermate control mice (NLRC5f/f) were subjected to MCAO. Histopathological and behavioral methods were performed to assess ischemic injury in mice. In vitro, oxygen-glucose deprivation (OGD) and OGD neuronal supernatant were used to stimulate microglia to simulate post-stroke inflammatory microenvironment. Primary microglia were extracted from litters of wide type and NLRC5-global-KO mice for proteomic detection after OGD. Mass spectrometry was used to investigate the interaction of NLRC5 with other proteins. A series of cellular and molecular biological techniques were used to evaluate the proinflammatory response, autophagy activity and protein–protein interactions etc.Results:mRNA and protein expression of NLRC5 were increased after MCAO from 1 to 7 days. NLRC5 was mainly expressed in microglia rather than neurons and astrocytes. After MCAO, the cerebral infarction volume of TMEM119CreERTNLRC5f/fmice was smaller than that ofNLRC5f/fmice, and neurological impairment was slighter. In the ischemic penumbra tissue of TMEM119CreERTNLRC5f/fmice, autophagy level increased, microglia activation decreased, and inflammation decreased. In vitro experiments, NLRC5 knockdown promoted autophagy level of primary microglia and BV2 in the inflammatory environment, and the inflammatory response was reduced. Proteomic results showed that after OGD, the autophagy levels of NLRC5-global-KO primary microglia were increased compared to that of wide type mice. Additionally, the protein levels of EIF5A, EIF5A hypusination and ATG3 increased in NLRC5-KO primary microglia after OGD. Mass spectrometry revealed that NLRC5 could bind to EIF5A. Specific binding sites and mechanisms need further study.Conclusions:Down-regulation of microglia NLRC5 can increase hypusination level of EIF5A, increase ATG3 transcription, thus promote autophagy, inhibit neuroinflammation, and protect brain injury after ischemic stroke.

Stroke, Volume 56, Issue Suppl_1, Page ATP284-ATP284, February 1, 2025. Enrichment is the prospective use of any patient characteristic to select a study population at higher risk in which detection of a drug effect is more likely than it would be in an unselected population. Patients with post-stroke cognitive impairment (PSCI) found to have higher risk of stroke recurrence in a recently completed meta-analysis. The goal of this study is to test whether PSCI based patient selection may represent enrichment strategy for secondary stroke prevention clinical trial. This is a subgroup analysis of Insulin Resistance Intervention after Stroke (IRIS) trial. In IRIS trial, patients were randomized to receive pioglitazone vs. placebo and had a baseline Modified Mini-Mental State Examination (3MS, where 3MS ≤ 88 was indicative of global PSCI. The primary endpoint of the study was recurrent stroke or MI. We estimated the hazard ratio (HR) for the effect of pioglitazone among those with global PSCI. To determine the sample size for a subsequent trial enriched by including only subjects with global PSCI, we make the following assumptions: (1) time to event follows an exponential distribution in both the pioglizone and placebo groups where the hazard rate for the placebo group is assumed to be the same as in the IRIS trial among those with global PSCI; (2) hazards for the pioglitizon and placebo groups are proportional over the course of the study; and (3) subjects are randomized to pioglitazone or placebo in equal proportions.Data on n = 3,338 patients of original cohort of n = 3,876 were analyzed, and n = 473 among them had PSCI at baseline. During 5-years of follow-up, n=246 patients experienced recurrent stroke, and n = 118 had MI. In patients with PSCI HR was 0.56 (95% CI 0.34 – 0.92) suggesting a 44% reduction in the hazard rate for secondary stroke or MI after 5 years of follow-up in the pioglitizone group compared to the placebo. If we conservatively assume that the true HR = 0.56 (closer to the null of HR = 1 than what was observed in the IRIS trial), then a total sample size of n= 967 willl proivde 90% power using a two-sided log-rank test at the 5% significance level. This conservative sample size corresponds to a 75% reduction in the sample size that was required for the IRIS Trial. PSCI screening may represent enrichment strategy for secondary stroke prevention clinical trial potentially reducing sample size by 75%. PSCI screening-based enrichment can be tested in phase 2 secondary stroke prevention trial.

Stroke, Volume 56, Issue Suppl_1, Page ADP26-ADP26, February 1, 2025. Introduction:Short interspersed nuclear elements (SINEs) are an abundant class of noncoding retrotransposons that can be transcribed by RNA polymerase III. Some SINEs have also been shown to act as genomic enhancers, thus giving rise to what are known as enhancer SINE-RNAs (eSINE-RNAs). The function of these novel RNAs within the post-stroke brain remains virtually unexplored. In this study, we map the genome-wide cortical expression of eSINE-RNAs in response to stroke, characterize their cell-type&subcellular localization, and determine their role in affecting post-stroke infarct volumes.Methods:Ischemic stroke was induced in male C57BL/6N mice using 1h middle cerebral artery occlusion (MCAO) followed by 6h of reperfusion (or sham surgery). Genome-wide RNA-seq and H3K27ac ChIP-seq (n=3/group/experiment) were performed on ipsilateral cortices to identify stroke-responsive enhancer RNA transcripts, which were then overlaid with genomic SINEs to identify eSINE-RNAs. Immunohistochemistry and RNA-FISH were used in tandem to determine the cell-type and subcellular localization of several highly expressed eSINE-RNAs. Select eSINE-RNAs were ablated via intracerebroventricular injection of antisense oligonucleotides followed by 1h MCAO and 24h reperfusion. Infarct volumes following knockdown were evaluated using cresyl violet staining (n=5-7/group).Results:We discovered 46 eSINE-RNAs upregulated in the cortex following MCAO, 33 of which were unique to stroke and not detected in the sham group. These RNAs were derived from several families of SINEs, including 24 from the B1 family, 20 from the B2 family, and one each from the less ubiquitous ID and MIR families. The expression of several abundant eSINE-RNAs was specific to the nuclei of neurons within the prospective infarct and peri-infarct territories, including the sensorimotor cortex and hippocampus. Ablation of select eSINE-RNAs resulted in significantly higher infarct volumes versus controls, suggesting that these eSINE-RNAs serve a neuroprotective role in the brain following ischemic stroke.Conclusion:Our study is the first report to characterize the expression of eSINE-RNAs in the post-stroke brain and begin to elucidate their function as regulators of post-stroke pathophysiology. Our results suggest that the transcription of eSINE-RNAs represents a robust neuroprotective response to transient focal ischemia, thus positioning them as potential molecular targets for modulating post-stroke outcomes.

Stroke, Volume 56, Issue Suppl_1, Page AWP294-AWP294, February 1, 2025. Background:Racial disparities have been well described in cardiovascular disease. However, the impact of race on the risk of stroke among infective endocarditis (IE) patients is not well understood.Objective:This study aims to investigate the racial disparities in the risk of stroke and clinical outcomes among IE patients.Method:The TriNeTX Global Collaborative Network database was used to identify patients aged ≥18 years of age from January 2000 to May 2023 which included IE patients. Patients were categorized into two groups, one with Black or African American and another with White race patients. Both groups were followed for 12 months. Propensity score-matched analysis (PSM) (1:1) was performed on age, gender, BMI, hypertension, diabetes mellitus, chronic kidney disease, hemoglobin level, LDL level, left ventricular ejection fraction and various drugs including beta blockers, ACEi and ARBi. Primary outcome was ischemic stroke, while secondary outcomes were all-cause mortality, heart failure, cardiogenic shock, MACE (composite of all-cause mortality, heart failure, and ischemic stroke), and acute kidney injury (AKI).Result:After 1:1 propensity score matching, the study cohort comprised 9, 814 Black patients and 9, 814 White patients. The mean age of patients was comparable between both groups (59.8 and 63.1 years). IE patients were having a comparable risk of ischemic stroke among both the races after 1 month (RR, 1.17 (95% CI: 0.96-1.42), P = 0.11), however, the risk of ischemic stroke was significantly higher among Black patients after 1 year (RR, 1.18 (95% CI:1.02-1.36), P = 0.024) when compared with White patients. Black patients were having a significantly higher risk of all-cause mortality after one month (RR, 0.818 (95% CI: 0.74-0.89), P

Stroke, Volume 56, Issue Suppl_1, Page ADP13-ADP13, February 1, 2025. Background:People with stroke are at high risk of dementia. There have been reductions in stroke case fatality and disability but temporal trends in the incidence and absolute burden of post-stroke dementia have not been described.Methods:We did a population-wide analysis of over 15 million people in Ontario, Canada between 2002-2022. Using linked administrative databases, we identified all 90-day dementia-free survivors of first acute ischemic stroke or intracerebral hemorrhage (ICH). We evaluated dementia incidence from 90-days after stroke onwards using a validated definition which included hospitalization, physician claims, and dementia medications. We calculated 1-year and 5-year incidence of dementia as percentages and per 100 person-years for each fiscal year, age-/sex-standardized by the 2002 population and with follow-up until March 2022. We stratified incidence trends by sex, stroke type, and severity (90-day home time of

Stroke, Volume 56, Issue Suppl_1, Page ATP264-ATP264, February 1, 2025. Introduction:Children with cardiac diseases are at an increased risk to develop ischemic stroke that can lead to lifelong neurological deficits. Blood pressure is an important modifiable factor associated with poor neurological outcomes. However, there lacks sufficient evidence to provide patient specific blood pressure guidelines post pediatric ischemic stroke.Objective:We evaluated blood pressure mean and changes in pediatric patients with cardiac diseases within the first 48hours cardiac critical care unit (CCCU) after an arterial ischemic stroke.Method:We conducted a retrospective study of children diagnosed with acute arterial ischemic stroke admitted to the CCCU. We reviewed data on demographics, clinical outcome, radiologic, hemodynamic parameters, and medication. Ischemic lesion volume size was obtained from Diffusion-Weighted Imaging by a full-trained neuroradiologist. Blood pressure percentile was obtained based on age, sex, and the 50thheight range. We contrasted the blood pressure with age and admission year matched CCCU controls without a history of stroke. We used linear regression to model blood pressure trends, t-test to compare continuous data, and chi square analyses to compare discrete data points.Results:Twenty-nine stroke patients (34% female, median age 2.1 years and range 17 years) were included. The majority of patients aged up to 3 years-old, presented with congenital heart defects (69%). Older patients presented more often with acquired heart disease (40%). Blood pressure means and trends differed by age, cardiac disease, and neurological outcomes. Younger patients and those with congenital heart defects had higher blood pressure compared to controls. Older patients or those with acquired heart diseases tended to have lower systolic blood pressure and higher diastolic blood pressure than their control. A third of patients with neurological deficits presented with an average blood pressure greater than the 95thpercentile, while patients with normal neurological status at discharge all had an average blood pressure inferior to the 50thpercentile. Higher blood pressure was associated with worst neurological outcomes, and larger ischemic brain volume size.Conclusion:Patients with cardiac disease have age and cardiac anomaly specific blood pressure after an acute ischemic stroke. Further research into these differences and blood pressure management in this group is crucial to lessening the burden of stroke on this at risk population.

Stroke, Volume 56, Issue Suppl_1, Page ADP31-ADP31, February 1, 2025. Introduction:CT perfusion maps (CTP) can estimate the ischemic core in acute ischemic stroke based on distinctive cerebral blood flow (CBF) thresholds. However, metabolic factors beyond perfusion influence the tissue tolerance to ischemia and the infarct growth rate.Hypothesis:We hypothesize that patients with lower hemoglobin and higher blood glucose levels exhibit reduced cerebral tissue resilience to hypoperfusion and will show larger ischemic core underestimation volume (ICuV) compared to other patients with normal hemoglobin and blood glucose levels.Methods:Large vessel occlusion stroke patients investigated with baseline CTP undergoing thrombectomy with near-complete reperfusion and without parenchymal hemorrhage from the ESCAPE-NA1 trial were included. Patients were subdivided into anemic (Hgb

Stroke, Volume 56, Issue Suppl_1, Page ADP11-ADP11, February 1, 2025. Introduction:We examined whether prestroke cardiovascular risk is associated with faster cognitive decline and higher dementia risk after stroke independent of prestroke cognition.Methods:We included 1,808 dementia-free individuals with incident stroke (91% ischemic, 7% hemorrhagic, 2% other; 52% women, 38% Black, median age 75) from 4 cohorts (1971-2019): Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, Framingham Offspring Study, and REasons for Geographic And Racial Differences in Stroke. We assessed prestroke atherosclerotic cardiovascular disease (ASCVD) risk with the American Heart Association’s Predicting Risk of cardiovascular disease EVENTs (PREVENT) 10-year ASCVD risk score, which has age and sex as risk factors. Outcomes were global cognition (primary), executive function, memory, and dementia. Linear mixed-effects and Cox regression models examined continuous and categorical (quintiles) 10-year ASCVD risk scores and adjusted for mean prestroke cognition, race, education, and cohort. Median (IQR) follow-up was 4.4 (2.0, 7.9) years for global cognition and 5.1 (2.4, 8.8) for dementia. Dementia cases totaled 142 at 5 years and 182 at 10 years.Results:Median (IQR) 10-year prestroke ASCVD risk was 14.0% (9.9%, 18.5%). Higher prestroke 10-year ASCVD risk was associated with lower adjusted initial poststroke global cognition, memory, and executive function (changes to intercept, Table 1). The quintile analysis showed a dose-response relationship between higher prestroke ASCVD risk and lower initial poststroke cognition scores (changes to intercept, Table 1). The overall stroke survivor group had unadjusted mean declines of -0.59 points/year (95%CI, -0.66 to -0.52 points/year; P

Stroke, Volume 56, Issue Suppl_1, Page ATP263-ATP263, February 1, 2025. Introduction:Children with arteriopathy are at an increased risk to develop ischemic stroke that can lead to lifelong neurological deficits. Blood pressure is an important modifiable factor associated with poor neurological outcomes. However, there is a lack of sufficient evidence to provide patient specific blood pressure guidelines post pediatric ischemic stroke.Objective:We aimed to evaluate blood pressure averages and changes in pediatric patients with arteriopathy within the first 48 hours in intensive care after an arterial ischemic stroke.Method:We conducted a retrospective study of children diagnosed with acute arterial ischemic stroke admitted to the pediatric intensive care unit (PICU). We reviewed data on demographics, clinical outcome, radiologic, hemodynamic signs, and medication within PICU. Ischemic lesion volume size was obtained from Diffusion-Weighted Imaging by a full-trained neuroradiologist. Blood pressure percentile was obtained based on age, sex, and the 50thheight rang. We also contrasted blood pressures of stroke patients with age and admission year matched controls without a history of stroke. We used linear regression to model blood pressure trends, t-test to compare continuous data, and chi square analyses to compare discrete data points.Results:Forty-five patients (49% female, median age 7.8 years, range age 17 years) were included. Arteriopathy disease included Dissection, Moyamoya, Focal Cerebral Arteriopathy and Vasculitis. Despite only a minority of patients being on vasoactive medications, patients with arteriopathy had higher blood pressures compared to age-matched control PICU patients in the first 48 hours. In addition, 31% of arteriopathy patients had an average systolic blood pressure greater than the 95thpercentile for the first two days after an acute arterial ischemic stroke, versus only 14% of their control (p-value < 0.05). Neurological deficits and increased brain ischemic lesion volume were associated with higher blood pressures.Conclusion:Understanding blood pressure trends and outcomes after an ischemic stroke in children at risk is crucial to guide the management of this modifiable factor. Blood pressure in children with arteriopathy is increased after an ischemic stroke compared to controls admitted to PICU. Further research into the etiology of differences observed here and blood pressure management is crucial to reducing the burden of pediatric ischemic stroke on this at risk population.

Stroke, Volume 56, Issue Suppl_1, Page A114-A114, February 1, 2025. Introduction:Post-stroke neuroinflammation is a hallmark of ischemic stroke. This study investigates the role of IGSF6 in microglia during ischemic stroke and its contribution to neuroinflammatory responses and brain injury following stroke.Methods:IGSF6 expression was examined in murine microglia under various inflammatory stimuli. Using a middle cerebral artery occlusion (MCAO) model, we evaluated the impact of microglialIgsf6knockdown (Igsf6-KD) on neuroinflammation and ischemic outcomes. Pro-inflammatory cytokine levels were measured using qPCR and ELISA in bothIgsf6-KD and wild-type (WT) mice, and functional outcomes were assessed through neurological tests. Subcellular localization and cytokine trafficking studies were conducted using immunofluorescence, electron microscopy, and protein interaction assays.Results:IGSF6 expression was significantly upregulated in microglia following MCAO. Knockdown of Igsf6 in microglia resulted in reduced secretion of pro-inflammatory cytokines (TNF, IL-6, CCL2, CCL5) at day 1 post-stroke, despite unchanged mRNA levels. Morphological analysis of microglia fromIgsf6-KD mice revealed a less reactive phenotype. Additionally,Igsf6-KD mice exhibited a reduction in infarct volume and improved functional outcomes, including enhanced performance on rotarod, grip strength, and foot-fault tests.Mechanistically, IGSF6 was shown to localize to the trans-Golgi network (TGN) and mediate cytokine trafficking. Knockdown ofIgsf6disrupted this process, reducing the secretion of key cytokines without affecting their transcription or translation.Conclusions:Microglial IGSF6 exacerbates post-stroke neuroinflammation by promoting the secretion of pro-inflammatory cytokines. Its knockdown attenuates neuroinflammatory responses, reduces ischemic brain injury, and improves functional recovery. These findings highlight the detrimental role of IGSF6 in stroke pathology and suggest that targeting IGSF6 may offer therapeutic benefits for mitigating neuroinflammation and improving outcomes after ischemic stroke.

Stroke, Volume 56, Issue Suppl_1, Page ADP41-ADP41, February 1, 2025. Introduction&Objective:Stroke care is fragmented with reported 30-day readmission rates as high as 10-15%. Novel, cost effective strategies to improve care coordination and address social determinants of care are needed. We sought to evaluate the clinical and financial impact of a home-based stroke care delivery model colloquially called Stroke Mobile (SM).Methods:Patients discharged to home, home health, rehab or skilled nursing facility followed by home from an Ochsner Health hospital in the New Orleans region between July 2021 through December 2022 with stroke (ischemic stroke, TIA, ICH) and on a value-based contract were eligible for the study. Patients were seen at home by an RN and health educator within 30 days of discharge followed by monthly for 3 consecutive months. Thereafter, patients were seen periodically as determined by the care team up to a year. Patients seen by the SM team were compared to a propensity matched control group comprising of patients eligible for care service by the SM team but not enrolled in the program during the study period. Propensity score matching was performed using age, gender, race and chronic conditions as covariates and “nearest neighbor” algorithm with 1:3 match ratio. Parametric (independent sample t-test) and non-parametric (Wilcoxon rank sum, Chi-square) tests were used to test the difference in overall cost (per member per month (pmpm)), 30-day readmissions, and cost of readmission between groups with an error rate set to

Stroke, Volume 56, Issue Suppl_1, Page A123-A123, February 1, 2025. Introduction:Neurology follow-up appointments are an essential part of post-stroke care, treatment and secondary stroke prevention. We aimed to determine factors contributing to patient attendance at neurology appointments and its impact on 90-day outcomes and readmissions.Methods:Retrospective analysis on acute ischemic stroke (AIS) patients with care coordinated by a nurse navigator from 7 hospitals (January 2021-March 2024). Patients excluded if: died during index hospitalization, discharged to hospice or long term acute care hospitals, or had incomplete data. Primary outcome: factors contributing to patients attending post-discharge neurology appointments and secondary outcome: 90 day all cause readmission rates utilizing binomial stepwise logistic regression models. Ninety-day utility weighted modified rankin scale (UWmRS) evaluated using hierarchical linear regression. Sensitivity analyses examined secondary outcomes in patients discharged home. Subgroup analysis compared latency of patient follow up and association of 90 day all cause readmission rates using a binomial stepwise logistic regression. All outcome analyses were adjusted for potential confounding variables as identified in the univariate analyses.Results:A total of 6121 AIS patients were evaluated, after exclusions 3450 were included in this study. Patients were more likely to attend a neurology appointment if discharged home,OR=1.47 [95%CI,1.23, 1.74],p

Stroke, Volume 56, Issue Suppl_1, Page ATP36-ATP36, February 1, 2025. Stroke, the leading cause of adult disability, necessitates new therapeutic strategies informed by a deeper understanding of brain repair mechanisms. This pilot study investigates the role of parvalbumin inhibitory interneurons (PV-INs) in post-stroke recovery using wide-field optical imaging (WFOI) and optogenetics. PV-INs, the largest subclass of GABAergic interneurons, are crucial in regulating cortical excitability and mediating activity-dependent plasticity. However, their specific function in stroke recovery remains unclear.Here we use 5 aged mice expressing Channelrhodopsin (ChR2) in PV-INs and the red-shifted genetically encoded calcium indicator, jRGECO1a, driven by the Thy1 promoter to allow for simultaneous optogenetic targeting of PV-INs and mesoscopic imaging of excitatory activity. Photothrombosis was induced in the left primary somatosensory forepaw cortex and subsequent optogenetic photostimulation of PV-INs, calcium, and hemodynamic imaging was conducted pre- and post-stroke to map PV-IN circuitry and assess changes in cortical activity.Preliminary results revealed significant disruptions in homotopic resting-state functional connectivity and cortical activity one-week post-stroke. Power maps indicated reduced activity in the somatosensory, hindpaw, and parietal cortices, with electrical forepaw stimulation showing decreased activity in both left and right primary somatosensory forepaw regions. Contralesional excitation increased in the retrosplenial and parietal cortices during forepaw stimulation. Further, optogenetic stimulation of PV-INs pre-stroke showed increased inhibition, while post-stroke stimulation resulted in less ipsilesional inhibition and more global excitation. Behavioral assessments using the cylinder rearing test indicated a 26% decrease in right forepaw use post-stroke, aligning with imaging findings.Ongoing studies aim to extend these observations by including a larger cohort of aged mice and a cohort of young mice at 1-, 4-, and 8- weeks post-stroke to examine age-related differences in PV-IN-mediated plasticity during stroke recovery. These studies will elucidate the critical contributions of PV-INs to post-stroke plasticity and recovery, potentially guiding new therapeutic approaches for stroke rehabilitation.

Stroke, Volume 56, Issue Suppl_1, Page ATP62-ATP62, February 1, 2025. Introduction:Education for post-acute stroke patients is crucial for several reasons: recovery and rehabilitation, prevention of recurrence, empowerment, caregiver support, and health literacy. Education equips patents and their families with the knowledge/tools needed to manage the long-term effects of a stroke and overall well-being.Background:Mary Greeley Medical Center (MGMC) leadership identified a lack of compliance in patient education in the post-acute setting for stoke survivors. In 2019, only 60% of stoke patients in the MGMC Acute Rehabilitation Unit (ARU) received the necessary education to be successful at discharge.Objective:To use the best practices outlined by the American Heart Association’s (AHA) guidelines and increase our compliance to greater than 75% of all stroke patients in the ARU setting receiving education on; stroke warning signs, individualized risk factors, prevention, medication management, caregiver education, and after visit follow up.Methods:Our intervention involved implementing a standardized checklist in stroke patients’ rooms, clearly outlining essential educational components. This streamlined approach facilitated real-time assessment of education needs by both staff and patients. Upon admission, stroke patients received an informative packet containing AHA materials. We upgraded patient entertainment systems to include stroke-related educational videos. All educational documentation was integrated into the electronic medical record, enhancing accessibility for both staff and patients via MyChart. Caregivers can access this education via mobile devices. Nursing leaders engaged with patients during rounds to ensure effective utilization of these educational tools.Results:Over a five-year period, the implementation of improved patient education strategies led to a consistent increase in the proportion of patients receiving stroke education in the MGMC ARU. Starting from a baseline of 60% in 2019, the rate rose to 84% during 2020/2021, and further to 91% in 2022. The data for 2023 reflects a continuation of this positive trend. Leadership played a pivotal role by regularly assessing adherence to the education protocol and making continuous enhancements to the educational delivery process.Conclusions:The standardization of educational requirements and increasing the accessibility of a variety of learning platforms has increased staff compliance with providing the necessary education to stroke patients in the MGMC ARU.