Stroke最新文献

Background: Patients with cervical artery dissection (CeAD) may experience a recurrent dissection, but its frequency, risk factors, and clinical implications are not well defined. We aimed to determine the risk, associated factors, and clinical impact of recurrent CeAD.

Methods: The STOP-CAD study (Antithrombotic Treatment for Stroke Prevention in Cervical Artery Dissection) was a multicenter international retrospective observational study of patients with CeAD treated between January 2015 and June 2022. Recurrent dissection was defined as a CeAD occurring at least 7 days after the diagnosis of the index event that affects a different artery or a different segment of the same artery. Patients were followed from day 7 up to 2 years. The absolute risk of recurrent CeAD over time was calculated using Kaplan-Meier survival estimates. Multivariable logistic and Cox regression models were used to assess predictors of CeAD recurrence.

Results: Of the 4023 patients included in STOP-CAD, 3836 (median age 46 years, 45% women) were eligible for this analysis. During a median (interquartile range) follow-up of 295 (97-720) days, 88 (2.29%) patients had a CeAD recurrence. Median time-to-recurrent CeAD was 53 (interquartile range, 18-157) days. The estimated risk of recurrent CeAD at 2 years was 3.22% (95% CI, 2.59%-4.00%). In multivariable analyses, younger age (adjusted odds ratios, 0.98 [95% CI, 0.96-0.99]), migraine (adjusted odds ratio, 1.88 [95% CI, 1.14-3.07]), and fibromuscular dysplasia (adjusted odds ratio, 2.90 [95% CI, 1.66-5.06]) were associated with CeAD recurrence, while presenting with an ischemic stroke was associated with a lower likelihood of recurrence (adjusted odds ratio, 0.47 [95% CI, 0.29-0.75]). These associations with CeAD recurrence over time were confirmed by Cox regression analyses. Among the 88 patients with recurrent CeAD, only 5 had accompanying ischemic events (3 strokes, 2 transient ischemic attacks).

Conclusions: In this retrospective study, recurrent CeAD was uncommon, approximately half of the events were diagnosed within the first 2 months of the index event, and recurrent events rarely caused new ischemic events. Younger age, migraine, absence of ischemic stroke at presentation, and signs of fibromuscular dysplasia may help identify high-risk patients.

Background: Lp-PLA2 (lipoprotein-associated phospholipase A2) is a sensitive biomarker of vascular inflammation and atherosclerosis. This study evaluated the influence of Lp-PLA2 activity on the efficacy and safety of ticagrelor-aspirin versus clopidogrel-aspirin among patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles.

Methods: The CHANCE-2 trial (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events-II) randomized 6412 patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles to receive ticagrelor-aspirin or clopidogrel-aspirin. This subgroup study included patients with available baseline Lp-PLA2 activity measurements, stratified by the median value of 188.4 nmol/min per milliliter. The primary efficacy and safety outcomes were stroke recurrence and severe or moderate bleeding events within 90 days. Associations between treatment and outcomes were assessed using multivariable Cox proportional hazards models, adjusting for a history of hyperlipidemia.

Results: A total of 5919 patients were included (mean age, 64.4 years; 33.9% female). Among patients with low Lp-PLA2 activity, ticagrelor-aspirin reduced the 90-day risk of recurrent stroke compared with clopidogrel-aspirin (5.4% versus 7.4%; adjusted hazard ratio, 0.72 [95% CI, 0.54-0.97]). In patients with high Lp-PLA2 activity, no significant difference was observed (6.9% versus 8.2%; adjusted hazard ratio, 0.84 [95% CI, 0.65-1.09]). The P value was 0.45 for the treatment × Lp-PLA2 activity interaction effect on stroke recurrence. The risk of bleeding associated with ticagrelor-aspirin did not differ across Lp-PLA2 activity levels.

Conclusions: In patients with minor stroke or transient ischemic attack carrying CYP2C19 loss-of-function alleles, elevated Lp-PLA2 activity did not significantly modify the efficacy or safety of dual antiplatelet therapy. Further research is needed to clarify the potential role of Lp-PLA2 in guiding individualized treatment decisions.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04078737.

Most people with spontaneous intracerebral hemorrhage (ICH) have hypertension, which is the strongest modifiable predisposing (risk) factor. However, multiple long-term medical conditions and other known predisposing factors for ICH usually coexist with hypertension, indicating that the causal pathway is multifactorial, and the term hypertensive ICH is oversimplistic. In this review, we integrate the highest quality evidence and our clinical experience in a framework to attribute multiple predisposing factors, underlying pathologies, and precipitating factors as the cause of ICH. In clinical practice, this framework supports physicians to take a holistic approach to treatment and prevention of ICH. In research, this framework shows how existing classification systems for the cause of ICH include underlying macrovascular, microvascular, and other structural pathologies but few predisposing or precipitating factors. Furthermore, this framework can inform the development of a more holistic classification system and expose knowledge gaps, including how predisposing factors lead to underlying pathologies and why only some people with these pathologies experience ICH.

Background: Cerebrovascular disease is prevalent in older adults and is associated with cognitive impairment. Although the association between brain infarcts and cognition has been widely investigated, the contribution of vascular disease to cognitive impairment has been less studied, particularly in non-White populations. We investigated the epidemiological and clinical characteristics of vascular disease phenotypes and their association with cognitive abilities in a diverse population.

Methods: In a Brazilian population-based clinicopathological study (recruitment between 2004 and 2024), inclusion criteria were age at death ≥18 years and the availability of an informant. Clinical information and cognitive abilities were assessed through informant interviews. Hyaline arteriolosclerosis (HA) was evaluated in 13 brain areas and categorized as absent, mild, moderate, or severe. Moderate/severe HA defined microvascular disease (Micro[+]). Intracranial atherosclerosis in the circle of Willis was similarly classified, with moderate/severe cases defining macrovascular disease (Macro[+]). Four vascular profiles were compared: Micro[+]/Macro[+], Micro[-]/Macro[+], Micro[+]/Macro[-], and Micro[-]/Macro[-]. Linear regression models adjusted for sociodemographic, clinical, and cerebrovascular/neurodegenerative lesions evaluated the association of cognition with vascular profiles, and microvascular and macrovascular diseases separately.

Results: Of 2418 participants, 834 with missing data were excluded, yielding a final sample of 1584 individuals (mean age, 74.3±13.4 years; 776 [49%] women; 982 [62%] White). Microvascular disease was slightly more frequent (31%) than macrovascular (29%). Regarding vascular profiles, 788 (50%) participants were Micro[-]/Macro[-], 334 (21%) Micro[+]/Macro[-], 301 (19%) Micro[-]/Macro[+], and 161 (10%) Micro[+]/Macro[+]. Micro[+] participants were older and more frequently women, and had worse cognitive abilities. Vascular groups were similar regarding most clinical comorbidities. HA (β, 0.81 [95% CI, 0.25-1.36]; P=0.004) and Micro[+]/Macro[+] phenotype (β, 1.25 [95% CI, 0.38-2.12]; P=0.005) were associated with worse cognitive abilities compared with HA-negative and Micro[-]/Macro[-] participants, respectively.

Conclusions: HA was as frequent as intracranial atherosclerosis. HA and the vascular phenotype with both microvascular and macrovascular diseases were associated with worse cognition.

Spasticity and related motor disorders are common and often disabling complications after stroke, affecting an estimated 30% to 80% of survivors. Spasticity can impair functional mobility, reduce independence, and increase caregiver burden. Secondary complications, including pain, restricted range of motion, skin breakdown, and joint contractures, further degrade quality of life, limit rehabilitation outcomes, and increase health care costs. Despite the availability of options to manage spasticity and mitigate its effects, timely diagnosis and intervention remain key challenges. Many patients receive treatment only after spasticity has become well established, and others receive no treatment at all due to persistent disparities in recognition, access, and delivery of treatment for spasticity, contributing to long-term disability and increased costs of care. This scientific statement reviews the rationale, established and emerging evidence, and strategic approaches for improving early recognition and intervention for poststroke spasticity. Early intervention is defined as treatment initiated within the first 3 months after stroke onset, potentially before development of secondary impairment from poorly controlled spasticity. Recognizing spasticity as a multidomain clinical syndrome-including involuntary muscle overactivity, impaired voluntary motor control, and passive tissue remodeling-offers important opportunities to improve timely diagnosis and treatment. Progress will also depend on a deeper understanding of the time course and pathophysiology of spasticity through both animal and human models. This scientific statement also outlines strategies to close gaps in recognition and care, including expanding and training the specialist workforce; developing innovative, scalable approaches for early detection and management; and strengthening care pathways and access to meet the substantial unmet needs of patients with poststroke spasticity.

Background: Persistent compromised hand function is one of the most common long-term deficits after stroke. It is related to dysfunction of the primary motor cortex (M1) and corticospinal tract (CST) as assessed by magnetic resonance imaging-derived estimates of CST lesion load or by transcranial magnetic stimulation-derived measures, such as motor evoked potential (MEP) status. However, substantial interindividual variability remains with these measures. We tested whether a novel measure, mean motor disconnectivity (MMD), explains additional variation in the hand function of subacute stroke patients.

Methods: Thirty-two participants (15 M/17 F; age, 58.6±9.65 years) after unilateral ischemic stroke involving the CST and related upper extremity weakness were studied within 4 weeks of stroke in a cross-sectional study design at Emory University between 2015 and 2021. The primary outcome measure was skilled hand function assessed using the Jebsen-Taylor test. Gross hand function and proximal UE function were secondary outcome measures. Transcranial magnetic stimulation was used to measure MEP status. Lesion masks were hand-drawn on each participant's structural magnetic resonance imaging image and were used to calculate lesion volume, CST lesion load, and MMD across a 20-region bilateral motor network consisting of the precentral gyrus, postcentral gyrus, thalamus, caudate, putamen, and brainstem regions. MMD is the mean of the disconnection values across the 20×20 nodes of this network of the adult human connectome; disconnection values quantify how severely a participant's lesion disrupts structural connectivity between region pairs.

Results: Univariable analysis indicated MEP status (MEP+/-), CST lesion load, and MMD were significantly correlated with preserved hand function; lesion volume was not. Adding MMD to a model containing MEP status significantly improved the fit of a multivariable model.

Conclusions: MMD explains additional variability in skilled hand function after accounting for MEP status, suggesting that disconnectivity measures capture stroke impact on motor areas beyond M1.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02544503.