Neurology International最新文献

Background: The management of spontaneous intracerebral hemorrhage (ICH) has centered around controlling blood pressure in order to prevent hematoma expansion (HE). Rate-pressure product (RPP) has emerged as a hemodynamic marker that accounts for heart rate (HR) and systolic blood pressure (SBP), both of which are crucial in modifying shear stress to the vasculature. We hypothesized that RPP in the pre-hospital hyperacute phase is positively associated with initial hematoma volume and HE. Methods: We analyzed 263 patients with primary ICH from the Field Administration of Stroke Therapy-Magnesium (FAST-MAG) study with initial and interval neuroimaging. RPP was calculated as the product of HR and SBP in pre-hospital and pre-treatment phases, stratified into quintiles. HE was defined by volume expansion of >6 mL or >33% from baseline volume on repeat neuroimaging performed within 48 h of the first scan. The primary outcome was the initial hematoma volume by quintiles of hyperacute RPP. The secondary outcome was the occurrence of HE across RPP quintiles. Multivariable logistic regression was used to assess the degree to which RPP affects HE. Results: Of the 263 patients analyzed, 116 (44%) had HE. The proportion of patients with HE or the initial hematoma volume was not statistically significant across RPP quintiles overall. HE was significantly more common in female patients or patients on anticoagulation. Conclusions: Elevated RPP was not associated with increased initial hematoma volume or subsequent HE in the hyperacute period after spontaneous ICH. Future research is necessary to determine the clinical importance of RPP as a biomarker in the clinical outcome of ICH.

Background: Sleep-disordered breathing (SDB) and intracerebral hemorrhage (ICH) share a bidirectional relationship: SDB may increase ICH risk, while ICH can induce or exacerbate SDB. However, the prevalence and characteristics of post-ICH SDB remain poorly defined.

Objective: To estimate the prevalence of SDB among ICH survivors and examine associated clinical factors, including the relative burden of obstructive (OSA) versus central sleep apnea (CSA).

Methods: A systematic review and meta-analysis were performed across PubMed, Scopus, CINAHL, and ClinicalTrials.gov. Studies assessing SDB in adults with ICH using American Academy of Sleep Medicine (AASM) category 1-4 diagnostic devices were included. Random-effects models estimated pooled prevalence at varying apnea-hypopnea index (AHI) thresholds, with subgroup analyses by setting, timing, geography, and diagnostic factors.

Results: Seventeen studies met inclusion criteria. Pooled SDB prevalence was 85% (95% CI: 80-91%) at AHI > 5, with 49% (95% CI: 42-57%) experiencing moderate SDB (AHI > 15), and 21% (95% CI: 15-27%) experiencing severe SDB (AHI > 30). The prevalence of OSA predominated 73% (95% CI: 64% to 82%),while CSA occurred in 5% (95% CI: 2-9%), corresponding to a pooled RR of 7.44 and OR of 53.08 for OSA versus CSA.

Conclusions: SDB-primarily OSA-is highly prevalent following ICH, underscoring the need for early, routine screening and intervention to improve neurological and cardiovascular outcomes.

Background/Objectives: Dementia represents a growing public health challenge. The WHO Global Action Plan on the Public Health Response to Dementia emphasizes early detection, risk reduction, and innovation as key priorities. Mild Behavioral Impairment (MBI), defined as the emergence of persistent neuropsychiatric symptoms in older individuals, represents a potential marker of early neurodegeneration and possible window for early intervention. This review explores the role of MBI in dementia prevention, mapping current evidence within the WHO Global Action Plan framework. Methods: A comprehensive search was performed in PubMed, Scopus, and the official WHO website, during 1 September 2025-10 November 2025, without time restrictions. Eligible sources included original clinical studies, reviews, and policy documents addressing MBI, dementia prevention, and public health. Data were thematically synthesized according to the seven objectives of WHO: (1) dementia as a public health priority, (2) dementia awareness and friendliness, (3) dementia risk reduction, (4) dementia diagnosis, treatment, care and support, (5) support for dementia carers, (6) information systems for dementia, and (7) dementia research and innovation. Results: Accumulating evidence indicates that MBI assessment can capture early behavioral manifestations of neurodegenerative and other forms of dementia, correlating with fluid, neuroimaging and genetic biomarkers. Integrating MBI screening through the easy-to-administer MBI Checklist (MBI-C) into clinical and community-based care, including telemedicine pathways and research, may enhance early identification and personalized interventions, enrich the pool for clinical trials, and facilitate research in biomarker and therapy. MBI-related research further supports its integration in remote digital monitoring and population-based prevention. Conclusions: Embedding MBI-informed screening and interventions into national dementia strategies aligns with WHO objectives for early, equitable and scalable prevention and brain health.

Late-onset sporadic Alzheimer's disease (LOAD) is the most common form of dementia. The disease is characterized by progressive loss of memory and behavioral changes followed by neurodegeneration of all cortical areas. While the contribution of genetic and environmental factors is important, advanced aging remains the most important disease risk factor. Because LOAD does not naturally occur in most animal species, except humans, studies have traditionally relied on the use of transgenic mouse models recapitulating early-onset familial Alzheimer's disease (EOAD). Hence, the development of more representative LOAD models through reprograming of patient-derived cells into neuronal, glial, and immune cells became a necessity to better understand the disease's origin and pathophysiology. Herein, and focusing on neurons, we review current work in the field and compare results obtained with two different reprograming methods to generate LOAD patient's neuronal cells: the induced pluripotent stem cell and induced neuron technologies. We also evaluate if these models can faithfully mimic cellular and molecular pathologies observed in LOAD patients' brains.

Background: Simulation-based training may offer a useful approach to support skill acquisition in neurointerventional stroke treatment without exposing patients to procedural risks. As the global demand for thrombectomy rises, training strategies that ensure procedural competence while addressing workforce constraints are increasingly important. With this pilot study, we aim to generate a hypothesis as to whether additional exposure of trainees to mechanical thrombectomy could benefit from simulator training on top of the standard training carried out on flow models. This study was designed as an exploratory pilot investigation and was not able to provide inferential or confirmatory statistical conclusions.

Methods: Six novice participants (advanced clinical-year medical students with completed anatomical and preclinical training, but without previous exposure to catheter-based interventions) performed two neurointerventional tasks, vascular access and mechanical thrombectomy (MTE), on flow models. After a baseline assessment, three participants received standard model-based training (control group), and three received additional simulator training using a high-fidelity angiography simulator (Mentice VIST G5). Performance was reassessed after four weeks using technical and clinical surrogate metrics, which were ranked and descriptively analyzed.

Results: No relevant differences were observed between groups for the vascular access task. In contrast, the simulator group demonstrated a trend toward improved performance in the MTE task, with greater gains in efficiency, autonomy, and procedural safety.

Conclusions: Our findings indicate a possible benefit of even brief simulator exposure for skill acquisition for complex endovascular procedures such as MTE. While conventional training may suffice for basic skills, simulation may be particularly helpful in supporting learning in more advanced tasks.

Background/Objectives: Post-traumatic epileptogenesis is a frequent and clinically relevant consequence of traumatic brain injury (TBI), often contributing to worsened neurological and functional outcomes. In patients experiencing early post-injury seizures, rehabilitative strategies that support recovery while considering increased epileptogenic risk are needed. This case study explores the potential benefits of combining neurofeedback (NFB) with motor therapy on cognitive and motor recovery. Methods: A patient hospitalized for severe TBI who experienced an acute symptomatic seizure in the early post-injury phase underwent baseline quantitative EEG (qEEG), neuromotor, functional, and neuropsychological assessments. The patient then completed a three-week rehabilitation program (five days/week) including 30 sensorimotor rhythm (SMR) NFB sessions (35 min each) combined with daily one-hour motor therapy. qEEG and clinical assessments were repeated post-intervention and at 6-month follow-up. Results: Post-intervention qEEG showed significant reductions in Delta and Theta power, reflecting decreased cortical slowing and enhanced neural activation. Relative power analysis indicated reduced Theta activity and Alpha normalization, suggesting improved cortical stability. Increases were observed in Beta and High-beta activity, alongside significant reductions in the Theta/Beta ratio, consistent with improved attentional regulation. Neuropsychological outcomes revealed reliable improvements in global cognition, memory, and visuospatial abilities, mostly maintained or enhanced at follow-up. Depressive and anxiety symptoms decreased markedly. Motor and functional assessments demonstrated meaningful improvements in motor performance, coordination, and functional independence. Conclusions: Findings suggest that integrating NFB with motor therapy may support recovery processes and be associated with sustained neuroplastic changes in the early post-injury phase after TBI, a condition associated with elevated risk for post-traumatic epilepsy.

Background: Chronic post-stroke spasticity often limits gait despite best-practice botulinum-toxin intramuscular injections (BTIs), whose benefit is constrained by short duration, dose ceilings, and tachyphylaxis. Cryoneurolysis (CNL) induces a reversible axonotmesis with preserved endoneurium, potentially providing longer tone reduction with fewer adverse effects, but its impact on whole-gait quality and its compatibility with implanted functional electrical stimulation (FES) remain poorly documented. Case presentation: A 43-year-old man, 12 years after right middle cerebral artery stroke, walked independently with an implanted common peroneal FES system but complained of effortful gait with left-knee "locking" and drop foot without FES. Multiple BTI series to triceps surae and quadriceps yielded only transient benefit. Two ultrasound-guided CNL sessions targeted tibial (soleus, medial gastrocnemius) and femoral (rectus femoris, vastus intermedius) motor branches. Quantitative gait analysis and fine-wire electromyography (EMG) were performed at baseline, 6 weeks after each CNL, and at 6 months, with and without FES. CNL produced immediate and sustained reductions in triceps surae and quadriceps overactivity, resolution of genu recurvatum, normalization of stiff-knee gait, improved ankle dorsiflexion, and increased swing phase knee flexion (>50°). Gait Deviation Index rose from 69 to 80 and Gillette Gait Index decreased by more than 50%, with preserved strength and without adverse events. Conclusions: Targeted, sequential CNL of tibial and femoral motor branches can safely deliver durable, clinically meaningful gait improvements when BTI has reached its ceiling and can act synergistically with implanted FES. Quantitative gait analysis and EMG sharpen clinical decision-making in spasticity management.

Background/objectives: Patients with acute severe neurological disorders often receive a transurethral indwelling catheter (TUIC) during their initial treatment. These TUICs often remain in place until the transfer to a rehabilitation or a long-term care facility. There are no systematic concepts for bladder management and no data regarding the impact on the catheter associated, health-related quality of life (HRQoL) in this patient group. The aim of this study was to investigate the impact of successful TUIC removal on the HRQoL of those affected and to contribute to the development of systematic bladder management.

Methods: A prospective longitudinal study was conducted on 33 patients treated at a neurological rehabilitation centre due to acute severe neurological disorders. The HRQoL was assessed using the SF-36 Health Survey prior to and following the TUIC removal. The influence of urinary incontinence was analysed. The mean differences were determined using a one-sample t-test adjusted for age and gender.

Results: TUIC removal was successful in 61.8% (21/33). The SF-36 Health Survey showed the following improvements (adj. mean diff., 95% CI, p-value): Mental Component Summary measure (4.36, 0.34; 8.38, p = 0.035), Role-Emotional (20.89, 0.54; 41.24, p = 0.045), Physical Functioning (10.03, 3.18; 16.88, p = 0.007). The comparison between incontinent and continent patients showed a poorer HRQoL for the incontinent group.

Conclusions: Successful TUIC removal has a positive influence on psychological/emotional aspects and physical functioning. Structured bladder management that considers the physical and psychological aspects of patients and nursing staff, as well as medical and economic aspects, should be pursued with vigour.

Background: Aging is traditionally characterized by progressive structural and cognitive decline; however, increasing evidence shows that the aging brain retains a remarkable capacity for reorganization. This adaptive neuroplasticity supports cognitive resilience-defined as the ability to maintain efficient cognitive performance despite age-related neural vulnerability.

Objective: To synthesize current molecular, cellular, neuroimaging, and electrophysiological neuromarkers that characterize adaptive neuroplasticity and to examine how these mechanisms contribute to cognitive resilience across aging.

Methods: This narrative review integrates findings from molecular neuroscience, multimodal neuroimaging (fMRI, DTI, PET), electrophysiology (EEG, MEG, TMS), and behavioral research to outline multiscale biomarkers associated with compensatory and efficient neural reorganization in older adults.

Results: Adaptive neuroplasticity emerges from the coordinated interaction of neurotrophic signaling (BDNF, CREB, IGF-1), glial modulation (astrocytic lactate metabolism, regulated microglial activity), synaptic remodeling, and neurovascular support (VEGF, nitric oxide). Multimodal neuromarkers-including preserved frontoparietal connectivity, DMN-FPCN coupling, synaptic density (SV2A-PET), theta-gamma coherence, and LTP-like excitability-consistently correlate with resilience in executive functions, memory, and processing speed. Behavioral enrichment, physical activity, and cognitive training further enhance these biomarkers, creating a bidirectional loop between experience and neural adaptability.

Conclusions: Adaptive neuroplasticity represents a fundamental mechanism through which older adults maintain cognitive function despite biological aging. Integrating molecular, imaging, electrophysiological, and behavioral neuromarkers provides a comprehensive framework to identify resilience trajectories and to guide personalized interventions aimed at preserving cognition. Understanding these multilevel adaptive mechanisms reframes aging not as passive decline but as a dynamic continuum of biological compensation and cognitive preservation.