Stroke最新文献

Carotid atherosclerosis is a significant cause of incident and recurrent ischemic stroke, with risk not solely related to the degree of luminal stenosis. Multimodal imaging approaches, including positron emission tomography/computed tomography and positron emission tomography/magnetic resonance imaging, can provide anatomic and molecular evaluation of the atherosclerotic plaque in vivo. Plaque pathophysiology-including the key processes of inflammation and microcalcification-may help characterize stroke risk beyond conventional anatomic assessment alone. This review discusses the use of positron emission tomography in the investigation of carotid atherosclerosis, including methodological considerations, its contributions to our understanding of the underlying disease processes, and how imaging can be used in interventional trials. The clinical implications and potential future applications of positron emission tomography in the assessment and treatment of cerebrovascular disease are also examined.

The Stroke Treatment Academic Industry Roundtable convened a workshop regarding artificial intelligence (AI) and innovative clinical trial designs during the Stroke Treatment Academic Industry Roundtable XIII meeting on March 28, 2025. This forum brought together stroke physicians and researchers, and industry representatives to discuss the current use and future opportunities for AI and novel trial designs in acute stroke trials. AI already plays a substantial role in the treatment of acute stroke with regards to imaging but is poised to have a much larger impact in clinical care and research trials over the coming years. The quality and understanding of the data are used to train the AI, the human element needed to ensure training is successful, and the clinician and trialist at the bedside, the humans "in the loop," will be necessary to maximize AI's effectiveness in clinical practice and trials. Platform trials address multiple scientific questions in an area of medicine simultaneously within the same trial structure by sharing controls across multiple interventions. While platform trials increase efficiency and potentially decrease the time needed to answer important clinical scientific questions, they also can introduce complexity to standard workflows. Future acute ischemic stroke clinical trials should incorporate elements of pragmatic and patient-centered trial design when possible. Pragmatic trials aim to assess the effectiveness of treatments when they are implemented into routine clinical care rather than under idealized conditions. AI models and platform, pragmatic, and patient-centered trial designs are new tools to answer important clinical questions, but understanding how they work, their best uses, and their limitations is critical for accelerating successful new treatments for stroke.

Stroke is a leading cause of death and disability globally, with Asia disproportionately affected. A critical barrier to effective secondary prevention is the high prevalence of CYP2C19 loss-of-function alleles, present in almost 75% of South and East Asians, which reduce clopidogrel efficacy. Evidence from trials, including CHANCE-2 (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events), shows that genotype-guided alternatives, including ticagrelor and cilostazol, substantially lower recurrent stroke risk in loss-of-function carriers. Yet, clinical adoption remains limited by insufficient genetic testing infrastructure, cost, guideline gaps, and clinician training. Despite these challenges, genotype-guided therapy is both feasible and cost-effective, with the potential to reduce recurrent strokes, disability, and healthcare burden. Urgent action is required to implement precision antiplatelet strategies, update guidelines, and ensure equitable access, making pharmacogenomics a central component of stroke care in Asia.

Background: The Take Charge intervention-a conversation-based, community intervention to improve motivation, improved independence, and physical health 12 months after stroke in 2 randomized controlled trials with 572 participants. This article reports long-term outcomes for the 400 participants in the TaCAS study (Taking Charge After Stroke).

Methods: Follow-up study of a New Zealand multicenter, randomized, controlled, parallel-group trial. Outcomes were collected by postal questionnaire or telephone call. The TaCAS study recruited 400 participants discharged after stroke, randomized within 16 weeks to one of 3 groups: 1 session of the Take Charge intervention, 2 sessions 6 weeks apart, or no sessions (control). This study is of participants still alive and willing to answer a questionnaire 5 to 6 years after their index stroke, undertaken in 2022. The primary outcome was the Physical Component Summary of the Short Form 36, comparing the Take Charge intervention and control. Secondary outcomes were: Frenchay Activities Index; modified Rankin Scale (mRS); survival; and stroke recurrence. These outcomes were compared with those 12 months after stroke. Analysis was by ANOVA or logistic regression.

Results: Mortality data were available for all 400 participants, and functional data for 204/297 (69%) of survivors. The mean difference (95% CI) in Physical Component Summary between Take Charge and control groups was 2.8 (-0.8 to 6.5) units, P=0.12, and for independence (modified Rankin Scale score, 0-2) the odds ratio (95% CI) was 0.56 (0.28-1.16), P=0.11, both favoring Take Charge with similar point estimates to those after 12 months. Differences between Take Charge and control participants for Frenchay Activities Index scores, survival, and stroke recurrence were small and nonsignificant.

Conclusions: The clinically significant improvements in physical health and independence for Take Charge participants, observed at 12 months, were sustained 5 to 6 years after stroke, but no longer statistically significant.

Registration: URL: https://anzctr.org.au; Unique identifier: ACTRN12622000311752.

The global transition to digital health offers a critical opportunity to transform health care delivery, particularly in low- and middle-income countries. Stroke care exemplifies the need for timely, coordinated, and longitudinal management across health systems. Although substantial progress has been achieved, low- and middle-income countries continue to encounter persistent challenges, including infrastructural deficiencies, digital inequity, fragmented governance structures, and limitations within the health care workforce. Nonetheless, scalable digital health interventions, such as telestroke networks, mobile health platforms, artificial intelligence-supported diagnostics, and telerehabilitation programs, have demonstrated efficacy and impact across diverse contexts. The central challenge has, thus, shifted from technological development to the systemic integration of these solutions within existing health infrastructures. Crucially, low- and middle-income countries must not be perceived solely as passive recipients of technology but as active agents of innovation, developing efficient, adaptive, and culturally attuned models prioritizing community engagement and a holistic conception of health. To realize the transformative potential of digital health, it is imperative to invest not only in technological infrastructure but also in promoting digital literacy, establishing robust ethical and regulatory frameworks, fostering cross-sectoral partnerships, and creating inclusive innovation ecosystems. Only through such a comprehensive, human-centered approach can digital health effectively serve as a catalyst for more equitable, resilient, and sustainable health systems, particularly for populations residing in resource-constrained settings.

Background: Acute ischemic stroke models often rely on anesthesia, which alters neurovascular coupling and limits real-time functional assessment. We tested the hypothesis that an awake mouse model of thromboembolic stroke, combined with multimodal imaging, would reveal very early cerebrovascular dynamics and connectivity changes predictive of final lesion outcomes.

Methods: Male Swiss mice (6-8 weeks old; 30-40 g; n=60) were implanted with a cranial headplate and habituated to restraint and imaging. One microliter pneumatic injection of murine thrombin (1 IU) into the distal middle cerebral artery induced in situ clot formation. Twenty minutes postocclusion, mice received intravenous rtPA (recombinant tissue-type plasminogen activator; Alteplase, 10 mg/kg; 10% bolus/90% infusion over 40 minutes, n=31) or saline (n=29). Primary outcomes included lesion volume (T2-weighted magnetic resonance imaging at 24 hours), brain perfusion (ASL magnetic resonance imaging), cerebral blood volume variations (ultrafast Doppler US imaging), resting-state connectivity, and neurovascular coupling to whisker stimulation (functional ultrasound imaging). Sample size (n=12 per group for imaging) was based on prior variability. Statistical analyses included unpaired t tests, repeated-measures ANOVA with Dunnett or Tukey post hoc, and simple linear regression; significance set at P<0.05.

Results: At 24 hours, rtPA reduced lesion volumes by 36.7% (10.97±4.7 versus 17.33±5.92 mm³ in controls; t₅₈=4.624; P<0.0001). ASL magnetic resonance imaging revealed a 66.5±9.9% CBF drop at 1 hour (F=48.63; P<0.0001) and a 51.2±45.1% hyperperfusion at 24 hours compared with baseline (F=11.67; P=0.0024). CBV declined by 59.2±12.9% at 10 minutes and partially recovered with rtPA at 1 hour (+87.3±30.6%; P=0.0165). Early hypoperfused area (10 minutes) predicted final lesion observed at 24 hours (R²=0.6465; P=0.0016). Resting-state connectivity shift of 12.0° at 10 minutes was mitigated by rtPA by 1 hour (14.8° versus 3.6°; P<0.01). Whisker-evoked CBV responses were abolished ipsilaterally at 10 minutes (-100.5±3.3%; P=0.0038) and showed partial recovery by 24 hours with rtPA (+37.2% relative to 10 minutes). At this time point, responses no longer differed significantly from baseline (P=0.093), indicating a modest but functionally meaningful recovery despite marked interindividual variability.

Conclusions: Awake thromboembolic stroke model with early functional ultrasound imaging completed with magnetic resonance imaging uncovers rapid blood flow perturbations and connectivity disruptions that are sensitive to rtPA and predictive of final lesion outcome. This platform enhances translational relevance by enabling hypothesis-testing of novel thrombolytics under physiologically intact conditions.

Background: White matter hyperintensities (WMHs), the neuroimaging markers of cerebral small vessel disease, have been associated with adverse neurological recovery after stroke. However, their role in poststroke aphasia, an acquired language disorder affecting approximately one-third of stroke survivors, remains unclear. This review synthesizes evidence on the relationship between WMHs and poststroke aphasia, focusing on severity and recovery across stroke phases, associations with cognitive outcomes, and the influence of hemispheric lateralization.

Methods: This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Literature search was performed across PubMed, Scopus, and Web of Science. Thirteen studies met eligibility criteria, examining the impact of WMH severity on language and cognitive deficits in patients with poststroke aphasia. Correlation and regression analyses were the predominant statistical approaches to evaluate associations and control for confounders.

Results: Greater WMH burden was significantly associated with more severe language impairments in the chronic (6 studies, n=443), subacute (3 studies, n=117), and mixed subacute-chronic phases (1 study, n=42), particularly in object naming, word fluency, and spoken comprehension. Preliminary evidence suggests periventricular WMHs may be more linked to aphasia severity than deep WMHs, whereas treatment-related findings remain inconclusive. In the acute phase, 2 studies (n=288) found no association between WMH burden and either aphasia severity or treatment response. In chronic aphasia (4 studies, n=392), WMHs were also linked to poorer cognitive performance, especially in nonverbal reasoning and executive functions. Hemispheric assessment varied, with some studies focusing on the contralesional side to reduce lesion-related confounding, while others used bilateral measures, limiting comparability.

Conclusions: WMHs may represent neuroimaging biomarkers of language and cognitive dysfunction in chronic and subacute poststroke aphasia. Future studies with standardized imaging protocols and larger samples are needed to clarify their prognostic value and personalize rehabilitation strategies.

Registration: URL: https://www.crd.york.ac.uk/PROSPERO/; Unique identifier: CRD42024582826.