This pilot study compared the effects of McKenzie and cervical stabilization exercises on proprioception, pain, disability, and deep neck flexor endurance in females aged 18-50 years with non-specific neck pain (NSNP). In this single-blind, randomized controlled pilot trial, 40 females (18-50 years) with chronic NSNP were allocated to McKenzie (Group A, n = 20) or stabilization (Group B, n = 20). Outcomes were assessed pre/post-intervention using JPE, VAS, NPADS, and deep neck flexor endurance tests. Both groups received three sessions/week for 4 weeks. Between-group analyses used two-way mixed ANOVA; ANCOVA was used to adjust for baseline differences in VAS and left-rotation JPE. Effect sizes were reported as ηp2 and Cohen's d. Although both interventions produced clinically significant within-group improvements across all measured outcomes, mixed ANOVA showed no significant Time × Group interactions for VAS, NPADS, endurance, or JPE flexion/extension/right rotation (all p > 0.05). A significant Time × Group interaction was initially observed for left-rotation JPE (F(1,38) = 7.486, p = 0.009, ηp 2 = 0.165). However, after adjustment for the baseline imbalance, ANCOVA showed no significant between-group difference in left-rotation JPE, indicating comparable efficacy between interventions. ANCOVA also confirmed no significant between-group difference in post-intervention VAS after baseline adjustment. All participants (100%) achieved the Minimal Clinically Important Difference (MCID) (≥2-point VAS reduction). In conclusion, both interventions are effective for NSNP, with comparable efficacy across most outcomes. After accounting for baseline differences, no significant between-group superiority was demonstrated, including for left-rotation proprioception.
The rise in mental health disorders has increased interest in novel natural therapeutic approaches beyond pharmacological interventions. Psychobiotics are live microorganisms that confer mental health benefits and have emerged as a promising intervention targeting the gut-brain axis. Evidence from preclinical studies demonstrated that psychobiotics can restore neurotransmitter balance by modulating pro-inflammatory cytokines and enhancing the expression of brain-derived neurotrophic factor. However, significant challenges remain, including the limited availability of clinical studies, determining optimal dosages, and understanding the long-term benefits of specific psychobiotic strains and their application in food matrices. This review highlights the findings from recent studies to identify psychobiotics' capability on tryptophan metabolism and their role in facilitating the synthesis of serotonin to propose a mechanistic framework for microbe-driven serotonin. While the eukaryotic pathways of serotonin biosynthesis are well defined, the specific mechanism by which bacteria contribute to this synthesis remains less understood; elucidating this metabolic link is essential. Beyond mechanism, this review evaluates the synergy between psychobiotics and food matrices to showcase the therapeutic approach to address the limitations of current interventions.
Exosome therapy is emerging as a promising neuroprotective strategy for Alzheimer's disease (AD). We evaluated and compared whether normal exosomes (NE) and modified exosomes (ME) derived from AD rat brain extract-treated rat bone marrow mesenchymal stem cells possess the potential to protect SH-SY5Y cells against streptozotocin (STZ) induced toxicity. The effect of exosomes on oxidative stress, inflammation and neuronal survival was evaluated. Further, antioxidant mechanism of exosomes by nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling was explored. Cells were exposed to 5 mM STZ and treated with NE and ME at an equivalent concentration of 50 µg/mL. Exosomes were characterized by specific exosomal markers, CD63 and CD9. Cell viability was assessed using the MTT assay. Neuronal growth and survival were evaluated by measuring brain-derived neurotrophic factor (BDNF) using ELISA and neuronal nuclei (NeuN) expression using immunocytochemistry. Intracellular reactive oxygen species (ROS) levels were determined using H2DCFDA, while inflammatory mediators, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified by ELISA. Expression levels of Nrf2 and HO-1 were also determined. Exosome treatment improved cell viability, reduced ROS, and lowered IL-6 and TNF-α levels. Immunocytochemistry quantification showed increased nuclear Nrf2 and HO-1 expression in exosome-treated cells. Moreover, our data indicate that ME derived from AD rat brain extract-treated rat bone marrow mesenchymal stem cells are more potent in protecting SH-SY5Y cells from STZ-induced oxidative stress and inflammation, possibly via Nrf2/HO-1 signaling, as compared to NE. These in vitro results support further preclinical evaluation of exosome-based strategies for AD.
Exercise has profound positive effects on cognitive function and brain health throughout different life stages. This systematic review aims to evaluate the multifaceted impacts of exercise on cognitive function, neuroplasticity, neurotransmitter expression, cerebrovascular function, and age-related cognitive decline across the lifespan. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines, we systematically searched PubMed, Web of Science, and Scopus databases for studies examining exercise interventions and cognitive function. Eligibility criteria included studies involving human participants across all age groups and animal models focusing on molecular mechanisms. The review employed qualitative synthesis to examine exercise modalities and age-specific effects. Risk of bias was assessed using the Joanna Briggs Institute Critical Appraisal Checklists. A total of 37 studies were included in the final synthesis (young adults: 2, middle-aged adults: 7, older adults/neurodegenerative diseases: 13, molecular mechanisms: 15). Regular physical activity, including aerobic, resistance, and combined training, significantly enhances cognitive abilities, promotes neuroplasticity, and mitigates age-related cognitive decline. Key molecular mechanisms include upregulation of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), and modulation of dopaminergic and serotonergic systems. Exercise serves as a potent non-pharmacological intervention for maintaining cognitive vitality and mental health. Limitations include heterogeneity in exercise protocols and outcome measures across studies. Future research should focus on multi-omics approaches to further elucidate cell-type-specific effects.
Hemorrhagic stroke (HS) remains a serious and potentially disabling complication following heart valve replacement (HVR). We aimed to evaluate the incidence and predictors of HS among mechanical HVR patients in Bangladesh. The Multidimensional Approach of Genotype and Phenotype In Stroke Etiology (MAGPIE) is an ambispective study recruited 568 consecutive HVR patients who had long-term (≥6 months) warfarin therapy between January 2010 and December 2024. Among the 568 HVR patients, 4.4% experienced HS, with a mortality rate of 52%, and the median age was 40 years (interquartile range [IQR]: 32-45). The median duration of warfarin uses among mechanical heart valve patients with HS varied by procedure: 63 months (IQR: 48-86) for mitral valve replacement, 60 months (12-85) for aortic valve replacement, 96 months (52-101.50) for double valve replacement, and 42 months (24-60) for patients undergoing coronary artery bypass grafting (CABG) with valve replacement. Additionally, a receiver operating characteristic curve analysis identified 104 months as the discriminatory threshold for warfarin therapy duration in predicting post-HVR HS onset. An age- and sex-adjusted logistic regression model identified severe pulmonary hypertension (odds ratio [OR] 4.44; 95% confidence interval [CI] 1.15-17.04; p = 0.02) and warfarin therapy duration ≥104 months (OR 1.99; 95% CI 1.00-3.76; p = 0.04) as independent predictors of HS in patients with mechanical HVR. Severe pulmonary hypertension was associated with a 4.4-fold higher risk and warfarin therapy beyond 104 months with a twofold higher risk of HS among patients with mechanical HVR.
Accumulating epidemiological and mechanistic evidence indicates that anti-inflammatory dietary patterns may attenuate systematic inflammation underlying chronic disease, including epilepsy (EP), a common and potentially debilitating neurological disorder frequently complicated by sleep disturbances. Herein, we aim to assess the inflammatory potential of habitual diets among individuals with EP, and co-occurring sleep disorders (SLDs). From 2013 to March 2020, 35,706 participants were enrolled in this study. EP status was defined based on reported use of antiepileptic drugs within the preceding 30 days. SLDs were assessed using questions on habitual sleep duration and validated self-reported sleep disturbances. Dietary inflammatory index (DII) and energy-adjusted DII (E-DII) scores were calculated using 24-h dietary recall data. Individuals with EP exhibited significantly higher DII and E-DII scores and a greater prevalence of SLDs compared with individuals without EP. In the fully adjusted model, participants in Quartile 4 of the DII score had significantly increased odds of EP and SLDs, relative to those in Quartile 1. Mediation analyses revealed that DII accounted for 2.650% to 6.234% of the association between EP and SLDs. In stratified analysis, an elevated prevalence of SLDs was observed across Quartile 2-4 for DII and in Quartile 2 and 4 for E-DII among individuals with EP. Individuals with EP consume diets with greater pro-inflammatory potential than those without EP. SLDs in this population are associated with higher dietary inflammatory burden-highlighting the need for evidence-informed, individualized nutritional guidance as part of comprehensive EP management.
Neurodevelopment is a highly ordered, precisely regulated process that establishes the neurobiological foundations of cognition, thought, emotion, and behavior. Neurodevelopmental disorders (NDDs) display marked phenotypic and genetic heterogeneity and variably impair learning, daily functioning, and social adaptation. As a key epigenetic mechanism, histone lysine methylation shapes chromatin accessibility and transcriptional programs, exerting central roles in neural stem cell fate decisions, neuronal migration and circuit assembly, as well as synaptic plasticity and learning and memory. Focusing on the activating histone H3 lysine 4 (H3K4) methylation marks (H3K4me1/2/3), this review synthesizes evidence for the bidirectional regulation mediated by "writers" (the KMT2/SET/DOT1) and "erasers" (the KDM/LSD and KDM5) in NDDs, including Kabuki syndrome, Wiedemann-Steiner syndrome, autism spectrum disorder, and schizophrenia. We further outline how animal models, patient-derived brain organoids, and multi-omics atlases enhance mechanistic insight, and we discuss the translational potential of small-molecule interventions, and metabolic modulation. Together, we summarize how the precise balance of methylation writing and erasure-and its crosstalk with DNA methylation and histone acetylation-forms an epigenetic network that drives neurodevelopmental programs. Targeting this network offers testable therapeutic avenues for NDDs.
Flavone derivatives of natural products are often synthesized to enhance their structural specificity, target selectivity, and bioavailability. The current study aimed to examine the neuroprotective efficacy of flavone derivative in diabetic associated neurodegenerations through systematic assessments of in-silico and in-vivo. The synthesized flavone (2-phenyl-4H-chromen-4-one) was characterized by NMR spectroscopy and FTIR. The in-vivo assessments were performed by following the serum biochemistry of homeostatic model assessment (HOMA), antioxidant and histopathology of cortex and hippocampus. The in-silico assessment of molecular docking showed -6.6 Kcal/mol with dipeptidyl peptidase-4 enzyme (DPP4), -7.8 with acetylcholinesterase (AChE), and -9.5 with butyrylcholinesterase (BuChE). The diabetic neurodegeneration model was induced by the chemical induction method and treated with the test compound at a dose of 40 mg/kg in comparison to sitagliptin. The treatment of the test compound showed significant alterations in the cortex and hippocampus region with mitigated neuronal injuries which endorsed by expressions targeted genes including glucose transporter 3 (GLUT-3), glycogen synthase kinase 3 beta (GSK-3β), microtubule associated protein (MAP)-Tau, and peroxisome proliferator-activated receptor gamma (PPARγ). Furthermore, the lipid profile and oxidative stress were ameliorated significantly by the course of treatment. In conclusion, the synthesized flavone has significant capability to promote neuroprotective effects in diabetes associated neurodegeneration through mitigating oxidative stress and modulating the expression of the targeted genes, thereby alleviating neuronal injuries.
Aging closely correlates with impaired cognitive abilities, including learning, attention, and memory. These impairments are typically linked to disturbances in dopaminergic signaling and hippocampus theta oscillations, two essential processes involved in memory encoding and novelty detection. This review examines the relationship between theta oscillation activity and dopaminergic novelty detection processes, offering a fresh framework for improving adult cognitive function through virtual reality (VR)-based methods. The specific purpose of this review is to investigate how dopaminergic novelty detection and theta oscillations can be leveraged through VR-based adaptive interventions to enhance cognitive function in aging populations. It investigates how exposure to new stimuli in a VR setting may activate dopaminergic neurons and induce synchronized theta rhythms to improve memory and learning. The potential for adaptive VR systems that adjust task difficulty and novelty based on real-time neural feedback is also clarified by this review. By combining results from behavioral, electrophysiological, and neuroimaging research, it supports the development of tailored, non-invasive therapies that focus on the neurological underpinnings of cognitive decline. This approach is promising for reducing age-related cognitive decline and enhancing cognitive resilience throughout life.
Berberine (BBR) exerts an effective protection for diabetic retinopathy (DR), but the underlying key molecular mechanism remains unknown; this study investigated the protective mechanism of BBR on DR by alleviating cell pyroptosis. A rat DR model was established and treated with BBR, and histological analyses, including hematoxylin and eosin staining, Nissl staining, and immunofluorescence, were executed to evaluate tissue changes. Core target genes were identified using the GeneCards database, Venn diagram analysis, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein-protein interaction networks, and molecular docking. Validation of key genes was performed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot, and RNA interference. BBR improved retinal morphology, reduced edema, and restored the arrangement of retinal ganglion cells in DR rats. BBR significantly reduced the levels of pyroptosis markers such as IL-1β and IL-18, which were elevated in DR. Network pharmacology identified 10 hub genes, with six genes (JUN, STAT3, AKT1, TP53, IL-1B, EGFR) further analyzed. BBR reversed DR-induced upregulation of JUN, STAT3, and AKT1 at both the mRNA and protein levels, as confirmed by RT-qPCR and Western blot. Silencing these genes enhanced cell viability and amplified BBR's protective effects. Altogether, BBR alleviates retinal inflammation and pyroptosis in diabetic retinal ganglion cells by targeting JUN, STAT3, and AKT1, providing insights into its therapeutic potential for DR.
Abstract Alzheimer's disease (AD) pathogenesis is characterized by the accumulation of amyloid beta (Aβ) deposits in the cerebral parenchyma and vasculature, a condition referred to as cerebral amyloid angiopathy (CAA). Besides the full‐length form, Aβ deposits showed a highly heterogenous composition due to the action of different proteolytic enzymes. N‐terminal Aβ peptides have shown higher aggregation propensity and toxicity compared to the other truncated forms, with species starting at residue phenylalanine 4 (Aβ4‐x) being more neurotoxic than the others. Thus, Aβ4‐x species have drawn attention in AD pathogenesis, potentially offering novel therapeutic targets to halt or reverse disease progression. Antibodies targeting specifically Aβ4‐x species were designed with the aim of preventing their aggregation and promoting their clearance counterbalancing their neurotoxic effect. This work provides an update on monoclonal and polyclonal antibodies developed to specifically target Aβ4‐x species in AD and CAA preclinical studies (in vitro and in vivo models).
Obsessive-compulsive disorder (OCD) is a common and disabling, as well as underdiagnosed, neuropsychiatric condition characterized by involuntary and unwanted obsessions and/or compulsions, often accompanied by states of severe anxiety, distress and shame, as well as other comorbid disorders. Despite the extensive literature available to date, only some of the neurobiological mechanisms underlying the symptomatic manifestations of the disorder have been clarified, underlining the need for further research. The brain structures involved are hippocampus, amygdala, striatum, thalamus, dorsolateral prefrontal cortex, anterior cingulate cortex, and orbitofrontal cortex; furthermore, most studies have mainly focused on the expressive modalities and on the individual structural and functional alterations of the brain, generating sometimes conflicting data. The aim of this article is therefore to summarize and bring together the main evidence collected so far on what would appear to be the neuroanatomical correlates and mechanisms underlying the disorder and its manifestations, to provide a sufficiently clear and complete overview.
Visual impairment has been recognized as a potential risk factor for depressive symptoms (DS) in diabetes patients, yet the role of visual function in predicting DS remains unexplored. This study aims to develop and validate a predictive model for DS risk in type 2 diabetes mellitus (T2DM) patients in community health settings, incorporating a visual function index (VF14). We conducted a cross-sectional study involving 542 T2DM patients from four community health centers in Guiyang. Univariate and multivariate logistic regressions identified significant predictors, while 10 machine learning algorithms were employed to construct the predictive model. Model performance was assessed using such metrics as receiver operating characteristic curves, accuracy, sensitivity, specificity, F1 score, Brier score, C-index, calibration curves, and decision curve analysis. A restricted cubic spline (RCS) analysis evaluated the score-dependent risk profiles between the VF14 and DS. Key predictors included body mass index (BMI), self-reported glycemic status, age-related macular degeneration, glycated hemoglobin (HbA1c), and VF14. Among the models, the gradient boosting machine exhibited the robust predictive performance, with an area under the curve of 0.73 and sensitivity of 0.72. The Shapley additive explanations analysis identified VF14, BMI, and HbA1c as the top risk factors. RCS analysis revealed a score-dependent risk profile between VF14 and DS risk. This study introduces a clinically interpretable tool for early DS risk stratification in T2DM patients, offering potential for improved risk assessment and timely intervention in community health settings.
Abstract Traumatic brain injury (TBI) causes significant mortality. Dexmedetomidine (DEX) shows neuroprotective potential in animals, but clinical evidence remains inconsistent. We evaluated the impact of early DEX, initiated within 48 h of admission with a treatment duration of at least 4 h, on survival in intensive care unit (ICU) patients with TBI using the Medical Information Mart for Intensive Care‐IV (MIMIC‐IV) database. Outcomes included 28‐day, hospital, and 1‐year mortality, analyzed via propensity score matching (PSM), multivariable Cox models, and subgroup analyses. Of 2378 patients, 241 received DEX. After PSM (235 pairs), early DEX use significantly reduced 28‐day (HR 0.45, 95% CI 0.30–0.69, p < 0.001) and hospital mortality (HR 0.25, 95% CI 0.15–0.42, p < 0.001). These results remained robust across sensitivity analyses. Similarly, 1‐year mortality decreased (HR 0.64, 95% CI 0.47–0.87, p < 0.01) and further supported by the Boruta algorithm, although inverse probability of treatment weighting analysis showed only a non‐significant trend (p = 0.08). Survival benefits were more pronounced in patients aged <65 and those requiring mechanical ventilation. In conclusion, early DEX use is associated with improved short‐ and long‐term survival in ICU patients with TBI, particularly in younger individuals and those requiring mechanical ventilation. Randomized controlled trials are warranted to establish causality.
Cranial-irradiation is associated with tissue damage resulting in neurocognitive impediments that adversely influence patient quality of life. Administration of radiation directly to the tumor may extend to the neighboring healthy tissues, which may induce acute to persistent oxidative stress, lessening neurogenesis, neuroinflammation, as well as vascular alterations, leading to neurocognitive sequelae as a result of decline in neuronal structural complexity as well as synaptic connections. Almost all the medications indicated in the treatment of irradiation-triggered brain injury work via signaling pathways that are associated with lessening chronic oxidative stress, which is considered a consequence of the inflammatory response, reduction of edema, as well as microglia activation. Some agents have both preventative as well as therapeutic potential via the amalgamation of both neuroprotective and therapeutic mechanisms above. Thus, in this review, agents such as baicalein, troxerutin, epigallocatechin gallate, quercetin, melatonin, valproic acid, lithium, neurosteroid progesterone as well as minocycline have been implicated as neuroprotective agents for irradiation-induced neurological deficits. Also, agents such as glucocorticoids, methylphenidate, vitamin E, bisdemethoxycurcumin, phosphodiesterases, edaravone, pioglitazone and fenofibrate, glutamate antagonists, human urinary kallidinogenase, bevacizumab, as well as hyperbaric oxygen have been implicated as therapeutic agents for irradiation-induced neurological deficits. Furthermore, agents such as angiotensin-converting enzyme, 3-N-butyl-phthalide, stem cell therapy, sphingosine-1-phosphate, gangliosides, and neurotrophins have been implicated as combined potential neuroprotective and therapeutic agents for irradiation-induced neurological deficits. The aim of this review is to elucidate the potential neuroprotective and therapeutic agents above and their mechanisms for irradiation-induced neurological deficits after brain irradiation.
Facial expression recognition (FER) has emerged as a pivotal interdisciplinary research domain that bridges computer science, psychology, neuroscience, and medicine. By mapping the FER scientific knowledge graph, this study aimed to explore the technological evolution and forecast future trends in this field. The study collected and cleaned the research on emotion perception in the Web of Science (WoS) database, and utilized the software CiteSpace (version 6.4R1) and R (BiblioShiny packages) software to create a scientific knowledge map. K-means was used for cluster analysis, and then the latent Dirichlet allocation (LDA) was employed to extract popular topics from the text of each cluster. Uniform manifold approximation and projection (UMAP) was utilized to reduce high-dimensional embeddings to a two-dimensional space. From a regional perspective, research is mainly distributed in countries or regions such as North America, Western Europe, East Asia, India, and Australia. Research on facial emotion recognition has focused primarily on neuroscience, psychiatry, and psychology. With the rapid development of computer technology, the interdisciplinary intersection is becoming increasingly important as FER has shown strong potential in identifying rare and neurological diseases. Furthermore, the evolution of artificial intelligence (AI) has transformed facial expression feature extraction from manual methodologies to machine learning-based approaches. The rapid development of computer algorithms and AI has greatly improved the accuracy and speed of facial emotion recognition. As a technology capable of detecting instantaneous emotional changes, FER holds promising prospects in fields such as neuroscience, emotion analysis, and pain assessment.
Neurological disorders represent one of the most pressing challenges in contemporary medicine, requiring tools that enable early diagnosis, targeted treatment, and deeper mechanistic understanding. Conventional biological agents such as antibodies, though widely used, often face limitations related to stability, brain penetration, cost, and integration into real-world platforms. Molecularly imprinted polymers (MIPs) have emerged as a promising synthetic alternative, capable of mimicking the molecular recognition functions of biological systems while offering enhanced robustness and customisability. MIPs provide key advantages, including high thermal and chemical stability, reusability, and design flexibility, making them especially attractive for neurological applications. In this review, we begin by presenting an overview of the main MIP formats applied in neurology, detailing their preparation, characterisation, and application-relevant advantages and limitations. We then explore the most actively investigated areas of MIP use in neurological diagnostics, research, and therapy, with a particular focus on: (i) nerve agents, (ii) neurotransmitters, and biomarkers, and (iii) drug development, drug delivery, and direct biological activity. Finally, we discuss the key challenges that currently hinder the clinical translation of MIPs in neurology, including poor biodegradability, in vivo biocompatibility concerns, and scalability, along with emerging strategies aimed at overcoming these barriers. We hope this analysis will serve as a useful reference for neuroscientists seeking novel material-based tools, as well as for materials scientists aiming to develop neurological applications of molecular imprinting.
Chemotherapy-induced peripheral neuropathy (CIPN) is a common complication in patients with malignant tumors during chemotherapy. The pathological mechanisms of CIPN remain unclear, and effective preventive and therapeutic strategies are still lacking, posing a major challenge in clinical practice. Aberrant activation of spinal glial cells, particularly microglia and astrocytes, is a key pathological hallmark of CIPN. Evidence from multiple animal models supports a causal link between glial activation and CIPN, suggesting that glial cells may serve as potential therapeutic targets. However, owing to the diversity of chemotherapy agents, the mechanisms of glial activation in CIPN differ and remain insufficiently characterized. This review takes spinal glial activation induced by peripheral nerve injury as its starting point, with a specific focus on microglia and astrocytes. It provides a systematic overview of their roles and mechanisms in CIPN caused by commonly used chemotherapeutic agents. The aim is to deepen understanding of CIPN pathogenesis and provide a foundation for developing targeted therapies.
The evolving research on the interactions between pain and mental disorders underscores the critical role of neuroimmune interplay in shaping pain perception and mental illness progression. This study employs bibliometric analysis to scrutinize the research landscape, identify emerging hotspots, and forecast future directions. A systematic review of literature from 2014 to 2023 was conducted using CiteSpace software for co-citation analysis, keyword co-occurrence, and burst detection to identify research hotspots and trends. The study examined developmental trends in pain and psychiatric disorder research, highlighting major research institutions and key themes. It unveils pivotal contributors and collaborative networks, showing significant growth in recent years. Emphasis is placed on neuroinflammation and neuroimmunomodulation interactions with mental illnesses. Keyword and thematic clustering analyses highlight the roles of microglial activation, inflammatory mediators, neurotransmitters, and emotional regulation processes. This study paves the way for future inquiries into neuroimmune mechanisms, the development of personalized treatment strategies, and an interdisciplinary approach to enrich our understanding of the biopsychosocial model in these conditions. Future studies should delve deeper into the molecular intricacies of these interactions to develop more effective therapeutic strategies, aiming to enhance patients' quality of life.
The appropriate acute treatment strategy for minor ischemic stroke, defined as National Institutes of Health Stroke Scale scores 5, is not as well‐defined. Prior studies have demonstrated mixed results regarding the effects of neurovascular interventions on minor stroke patients for optimizing the chances of symptomatic improvement. We performed a retrospective single‐center study across 6 years to determine the association between thrombolytics and the likelihood of clinical symptom improvement by 24 h in minor stroke patients across ages. Margin plots were derived from multivariable regression analyses. Of 1172 minor stroke patients, in patients <70 years of age, there was greater than 50% likelihood of improvement with any type of thrombolytic administration. When substratifying by type of thrombolytic, there is greater than 50% odds of improvement in patients <80 years of age treated with alteplase and <70 years of age treated with tenecteplase. Thus, the association between age and likelihood of benefit after thrombolytic treatment in minor stroke patients highlights particular minor stroke subpopulations, particularly younger patients, who may benefit from thrombolytic treatment.
