Neurology International最新文献

Background: Ischemic stroke (IS) remains a leading global cause of mortality, recurrence, and long-term disability, with survivors also at risk of post-stroke dementia (PSD) and cognitive impairment (PSCI). The precise impact of statin therapy across different IS populations, including those with cardioembolic/atrial fibrillation (CE/AF) strokes and patients with low-baseline low-density lipoprotein (LDL) cholesterol, remains unclear, as does the influence of statin timing, intensity, type, and solubility.

Methods: We conducted the Impact of Statin Therapy on the Risk of Stroke Recurrence, Mortality, and Dementia After Ischemic Stroke (ISMARDD) meta-analysis, synthesizing evidence from 51 studies (n = 521,126), to evaluate the association between post-stroke statin therapy and key outcomes: all-cause mortality, stroke recurrence, cognition, and C-reactive protein (CRP). PSD was defined as new, persistent cognitive decline meeting standard diagnostic criteria, and PSCI as measurable but sub-threshold cognitive deficits. Random-effects models were used, and certainty was assessed with the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework.

Results: Statin therapy significantly reduced all-cause mortality within 3 months (OR 0.32), at 1 year (OR 0.35), and beyond 1 year (OR 0.56). Stroke recurrence was modestly reduced both within 1 year (OR 0.77) and after 1 year (OR 0.76). Statin use was associated with a lower risk of PSD (OR 0.74) but not PSCI overall. Benefits extended to CE/AF-related strokes and patients with low-baseline LDL cholesterol, both showing significantly lower mortality with statin use. Early initiation (<24 h) was linked with reduced recurrence, though effects of statin intensity, type, and solubility were inconsistent. Statins also significantly reduced CRP levels, underscoring anti-inflammatory and pleiotropic mechanisms.

Conclusions: The ISMARDD study demonstrates that statins confer survival benefit and selective cognitive protection (notably reduced PSD risk) after ischemic stroke, with modest recurrence benefit, supporting their broad use in secondary prevention. These findings highlight the need for precision-guided approaches tailored to stroke subtype, pharmacogenomics, and treatment timing to optimize therapeutic outcomes.

Objectives: We aimed to determine temporal patterns of blood-brain barrier (BBB) dysfunction, edema formation and functional recovery in acute stroke.

Materials and methods: Patients of two observational studies on ischemic and hemorrhagic stroke between 2006 and 2019 were analyzed. Blood-brain barrier dysfunction was assessed using the cerebrospinal fluid-to-plasma albumin ratio. Edema formation was measured on all available imaging scans during hospital stay. Relative edema was defined as the ratio of edema volume to stroke volume. Multivariable regression models were applied to analyze associations and calculate predicted probabilities.

Results: Overall, 138 stroke patients, 103 (74.6%) with ischemic stroke and 35 (25.4%) with hemorrhagic stroke, were analyzed. The predicted probability of substantial BBB dysfunction was approximately 46 (37-55) % among patients analyzed on 1 day after symptom onset and declined with increasing time, thereafter reaching 10 (3-29) % on day 30. The maximal extent of edema was lower in ischemic versus hemorrhagic stroke (relative edema: 1.5 [1.2-1.8] vs. 2.6 [1.9-4.5], p = 0.003) and occurred earlier after stroke onset (5.9 [4.6-8.5] days vs. 12.3 [9.7-16.4] days, p = 0.009). BBB dysfunction was associated with increased edema formation (adjusted relative edema: 4.0 [2.8-4.5] vs. 2.3 [1.8-3.0], p = 0.037) and lower chances of functional recovery (20/48 [41.7%] vs. 51/90 [56.7%], adjusted Odds Ratio: 0.37 [0.16-0.88], p = 0.025) in both ischemic and hemorrhagic stroke patients.

Conclusions: BBB dysfunction frequently occurred in acute ischemic and hemorrhagic stroke and was associated with secondary injury and worse clinical outcomes. Future studies should evaluate BBB dysfunction as a potential therapeutic target using advanced imaging techniques early after stroke onset. Edema formation was aggravated and prolonged in hemorrhagic versus ischemic stroke.

Introduction: Stroke is one of the leading causes of death and disability worldwide. In this context, early activation of the Stroke Code and a structured neurorehabilitation approach are key determinants of patients' functional outcomes. Objectives: We aimed to evaluate the impact of Stroke Code activation on the functional prognosis of patients who have suffered an ischemic stroke, analyzing the time-dependent relationship and the effectiveness of reperfusion therapies. Additionally, we sought to examine the role of nursing in inpatient neurorehabilitation. Methods: A systematic review was conducted following the PRISMA 2020 guidelines. Scientific studies published between 2020 and 2025 were reviewed across five databases: PubMed; Cochrane Library; Dialnet; Web of Science; and Scopus. Eligibility criteria were applied, and validated tools were used to assess methodological quality and risk of bias. Results: Thirteen studies were included, involving a total sample of 80,555 patients. Age; lesion volume; and time to treatment were found to be key prognostic factors. Early implementation of reperfusion therapies (thrombolysis and/or thrombectomy), combined with nursing-led neurorehabilitation interventions, significantly improved neurological status, functional independence, and quality of life. Conclusions: Stroke Code activation has a significant positive influence on functional prognosis. Reducing treatment delays and optimizing reperfusion therapies are critical. Furthermore, the role of nursing in hospital-based neurorehabilitation is essential to support patient recovery and functionality.

Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system, which can lead to physical and cognitive disability, fatigue, depression, and sleep disturbance, all of which may impair quality of life (QoL). While the physical disability is widely known to influence the QoL, the relative contributions of cognitive impairment, fatigue, and sleep quality remain incompletely defined.

Objectives: To evaluate the relationship between QoL, physical and cognitive disability, sleep quality, fatigue, and depression in people with MS (PwMS), and to explore phenotype-specific differences between relapsing and progressive forms.

Methods: In this monocentric cross-sectional study, 112 PwMS underwent physical assessment (EDSS, MSFC), cognitive testing (SDMT, PASAT, MoCA, MMSE), and QoL evaluation (MSIS-29, EQ-5D, EQ-VAS, MSNQ). A subgroup of 29 patients also completed the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), Modified Fatigue Impact Scale (MFIS), and Beck Depression Inventory (BDI). Correlation and group analyses were performed.

Results: Progressive MS patients showed greater physical disability (mean EDSS 5.8 vs. 2.6, p < 0.001), poorer cognitive performance, and lower QoL. Across the cohort, QoL strongly correlated with physical disability (EDSS) and cognitive performance (SDMT), with physical measures showing stronger associations. In relapsing MS, physical and cognitive impairment were linked to reduced QoL, whereas in progressive MS, physical disability predominated. In the sleep subgroup, poorer PSQI scores, longer sleep latency, and daytime sleepiness correlated with higher fatigue (MFIS), depressive symptoms (BDI), and reduced QoL (MSIS-29, EQ-5D).

Conclusions: QoL in MS reflects the combined burden of physical disability, cognitive impairment, fatigue, depression, and poor sleep quality, with phenotype-specific patterns. While physical disability is the main QoL determinant in progressive MS, cognitive deficits with slowed processing speed play an important role in relapsing MS. Comprehensive, multidimensional assessment, including sleep and mood screening, may support individualized management strategies in MS.

Background/Objectives: Psychogenic non-epileptic seizures (PNES) are seizure-like episodes not caused by abnormal brain activity, often linked to emotional dysregulation, dissociation, and altered interoceptive awareness. Standardized treatments are limited. This study aimed to explore the feasibility and preliminary psychological effects of a group-based mindfulness-based intervention (MBI) in individuals with PNES. Methods: This single-arm, pre-post pilot study (no control group) enrolled fifteen participants in two cycles of an 8-week MBI delivered either in-person or online. Twelve participants completed pre/post self-report assessments of depression (BDI-II), anxiety (STAI-Y1), perceived stress (PSS-10), sleep quality (PSQI), dissociation (DES-II), meteoropathy (METEO-Q), mindfulness (FFMQ), and interoceptive awareness (MAIA). Results: The intervention was well tolerated (dropout rate: 20%). Trend-level, non-significant improvements emerged for depressive symptoms (p = 0.092, r = 0.564) and sleep quality (p = 0.078, r = 0.591). A significant reduction was observed in the FFMQ Describing subscale (p = 0.045, r = 0.697). No significant changes were found in anxiety, perceived stress, or interoceptive awareness, although certain MAIA subscales indicated small, non-significant increases. Conclusions: Despite the limited sample size and absence of a control group, these preliminary findings support the feasibility and acceptability of MBIs for PNES, warranting further controlled investigations.

Background/Objectives: Cognitive decline is common in ageing, ranging from mild to severe manifestations. Although several modifiable risk factors have been identified, they are typically examined individually. This study aimed to identify latent profiles based on combinations of dementia risk factors and to quantify the associations with cognitive impairment in a European population of older adults. Methods: Based on the SHARE HCAP project, we conducted a retrospective longitudinal study by linking individual data from wave 6 (2015) and wave 9 (2021-2022). The sample included 2685 individuals aged 50+. The study outcome was cognitive status, assessed using standardised neurological tests and questionnaire and categorised as normal cognition, mild cognitive impairment (MCI), or severe cognitive impairment (SCI). The exposures included clinical, psychosocial, and lifestyle variables. Latent Class Analysis (LCA) was applied to identify distinct profiles, and multinomial logistic regression models were carried out to estimate associations between latent profiles and cognitive status, expressed as odds ratios (ORs) with 95% confidence intervals (CI). Results: The study sample included 2326 participants, of whom 25.1% with MCI and 9.4% with SCI. Through LCA, we identified four profiles: Low-risk, Combined Cluster, Inactive Behaviour, and Cardiometabolic Risk. Compared with the Low-risk profile, the odds of MCI were significantly higher for Combined Cluster profile (OR = 3.11; 95% CI: 2.38-4.06) and CR (OR = 1.44; 95% CI: 1.07-1.93). For SCI, elevated odds were observed for Combined Cluster (OR = 7.30; 95% CI: 4.47-11.92), Cardiometabolic Risk (OR = 2.31; 95% CI: 1.31-4.05), and Inactive Behaviour (OR = 1.87; 95% CI: 1.01-3.48). Conclusions: Four latent profiles were identified, each showing distinct associations with MCI and SCI. The Combined Cluster-characterised by poor mental health, limited physical activity, and hypertension-showed the highest odds of cognitive impairment. Public health strategies should prioritise integrated actions against these risk factors.

Autism spectrum disorder (ASD) is a complex, heterogenous, and prevalent neurodevelopmental disorder characterized by core symptoms, including social communication deficits, restrictive interests, and repetitive behaviors. Although environmental factors contribute to the etiology of ASD, the disorder has a strong genetic basis, although the specific genes involved in causing or contributing to the disorder remain to be conclusively identified. Whereas previous studies have focused on the cerebral cortex, hippocampus, and associated brain regions to uncover the underpinnings of ASD, emerging evidence indicates that dysfunction of the cerebellum is one of the most consistent associates of ASD. Traditionally thought to function solely in motor control, more recent studies have established that projections from the cerebellum make mono- and polysynaptic connections to a variety of non-motor areas including the cerebral cortex, hypothalamus, and hippocampus, and is involved in a range of cognitive, sensory, and behavioral functions. While several reviews of the molecular underpinnings of ASD have focused on the other brain regions, primarily the cortex, in this review we describe the key role that the cerebellum plays in the development of ASD and then focus on genetic variations that cause ASD, focusing on genes expressed and studied in the cerebellum. We have divided the ASD-associated genes in two subgroups-those that have been identified through a candidate gene approach with knowledge of their function in the cerebellum and their relationship to ASD subsequently confirmed in experimental models, and those identified through unbiased genetic analyses of individuals with ASD, many of which have not yet been characterized extensively and/or not studied in animal models. We also provide recently reported information on non-genetic factors that combine with genetic factors to promote ASD. Together, we hope our review will provide information on recent and significant findings related to the cerebellar underpinnings in ASD.

Background: Pronator teres syndrome is a rare proximal median neuropathy caused by compression of the median nerve at various points. It is a rare condition, and many times it is mistaken for carpal tunnel syndrome. Methods: There are many authors who refer to the pronator syndrome as a compression of the median nerve at several potential sites of en-trapment in the region of the antecubital fossa, more proximal compression at the Liga-ment of Strutters, and more distally, including lacerus fibrosus within the pronator teres muscle and the anterior interosseous nerve. Results: The diagnostic difficulties in a patient with severe right forearm pain during elbow flexion and pronation are presented. Routine test results, including MRI of the right elbow joint, nerve conduction study of the brachial plexus and ulnar nerve, and electromyographic study of the muscles of the right upper ex-tremity, were normal. Ultrasonography showed an enlarged pronator teres muscle. Conclusions: The patient underwent surgical removal of the lacertus fibrosus. All symptoms resolved.

Background: Early hematoma expansion is a major determinant of poor outcomes after spontaneous intracerebral hemorrhage (ICH). Identifying reliable predictors of hematoma expansion may facilitate risk stratification and timely interventions. This study aimed to evaluate clinical, laboratory, and radiological factors associated with early hematoma expansion within 24 h.

Methods: We retrospectively analyzed consecutive patients with spontaneous ICH admitted to a tertiary hospital in Korea between 2009 and 2021. Inclusion criteria were aged ≥ 18 years, primary spontaneous ICH, baseline non-contrast CT (NCCT), and follow-up CT within 24 h. Clinical, laboratory, and medication histories were collected, and NCCT/CT angiography (CTA) imaging markers (spot sign, blend sign, hypodensity, swirl sign, black hole sign, island sign, mean hematoma density) were evaluated. Early hematoma expansion was defined as an absolute volume increase ≥6 cm³ or a relative increase ≥33% on follow-up CT. Multivariate logistic regression identified independent predictors.

Results: Among 899 screened patients, 581 met inclusion criteria (mean age 61.6 years; 59.7% male). Seventy-eight patients (13.4%) experienced early hematoma expansion. Independent predictors included CTA spot sign (adjusted OR 9.001, 95% CI 4.414-18.354), blend sign (OR 3.054, 95% CI 1.349-6.910), mean hematoma density <60 HU (OR 2.432, 95% CI 1.271-4.655), male sex (OR 2.902, 95% CI 1.419-5.935), and statin use (OR 2.990, 95% CI 1.149-7.782). Prior antiplatelet therapy was associated with a reduced risk of hematoma expansion (OR 0.118, 95% CI 0.014-0.981).

Conclusions: Early hematoma expansion occurred in 13.4% of patients and was predicted by a combination of CTA and NCCT markers, as well as clinical and pharmacological factors. Spot sign remained the strongest predictor, while NCCT features such as blend sign and low hematoma density also provided practical prognostic value. These findings underscore the multifactorial pathophysiology of ICH expansion and highlight the importance of integrating imaging, clinical, and therapeutic variables into prediction models to improve early risk stratification and guide targeted interventions.

Objectives: Pulmonary embolism (PE) is an uncommon but potentially fatal complication of acute ischaemic stroke (AIS). Its global burden and prevention remain incompletely defined. We performed a systematic review and meta-analysis (PEARL-AIS) to estimate prevalence, risk factors, outcomes, and prophylactic efficacy, with GRADE evidence appraisal. Methods: Following PRISMA 2020 and MOOSE guidelines, five databases (PubMed, Embase, Cochrane, Scopus, Web of Science) were searched (1995-2024). The protocol was prospectively registered (OSF s25ny). Random-effects models (DerSimonian-Laird; REML sensitivity) were used to pool prevalence and odds ratios; heterogeneity was evaluated with I², Cochran's Q, and τ². Influence (leave-one-out) and subgroup analyses for prevalence and mortality of PE in AIS were explored. Bias was assessed using the Modified Jadad Scale; overall certainty was graded with the GRADE framework. Results: Twenty-four studies met the inclusion criteria (n = 25,666,067), of which seventeen studies (n = 23,637,708) contributed to pooled prevalence analyses. The pooled prevalence of PE after AIS was 0.40% (95% CI 0.33-0.49), approximately six-fold higher than in the general population, with considerable heterogeneity (I² > 90%, Cochrane classification). The pooled mortality among AIS patients with PE was 12.9% (95% CI 1.6-31.7). Mortality risk was significantly higher in AIS patients with PE (OR 4.96, 95% CI 2.98-8.24). Atrial fibrillation (29%), cancer (19%), and smoking (23%) were common; hypertension (54%) and diabetes (23%) were prevalent but not predictive, with diabetes showing a paradoxical protective association (OR 0.88, 95% CI 0.84-0.92). Pharmacological prophylaxis was associated with a reduced risk of PE (OR 0.64, 95% CI 0.46-0.90; I² = 0%), supported by moderate-certainty evidence. Conclusions: PE is an uncommon but often fatal complication of AIS. Traditional venous thromboembolism predictors underperform in this context, suggesting a stroke-specific thromboinflammatory mechanism linking the brain and lung axis. Despite considerable heterogeneity and low-to-moderate certainty of evidence, pharmacological prophylaxis demonstrates a consistent protective effect. Systematic PE surveillance and tailored prophylactic strategies should be integral to contemporary stroke care, while future studies should refine risk stratification and elucidate the mechanistic underpinnings of this brain-lung thromboinflammatory continuum.