Journal of Central Nervous System Disease最新文献

Background: Action Observation Therapy (AOT) and Neuromuscular Electrical Stimulation (NMES) are widely adopted techniques for upper-limb rehabilitation in post-stroke patients. Although AOT and NMES are individually effective, studies investigating a potential synergistic effect on enhancing rehabilitative outcomes are lacking. Objectives: This study aims at comparing the effect of AOT and NMES applied together (AOT-NMES) on muscle synergies with respect to either AOT alone or a Motor Neutral Observation treatment alone (MNO, involving neither AOT nor NMES) on motor function recovery of upper limb. Design: Randomized Controlled Trial (RCT) with n = 60 post-stroke patients with resulting upper limb disability, randomly allocated (1:1:1 ratio) in three interventional arms: AOT-NMES (n = 20), AOT (n = 20) and MNO (n = 20). Methods and Analyses: All rehabilitation treatments will consist of n°15 60 min-long rehabilitative sessions. Primary outcome measure will be upper limb motor function, assessed using the Fugl-Meyer Assessment scale for upper limb (FM-UL), collected at the baseline (T0), post-intervention (T1) and at follow-up (T2, 6-months after T1). Other outcome measures will be collected through a multidimensional evaluation including assessing stroke-associated quality of life, neurophysiological data, biomechanical and MRI measures. The innovative protocol will also be evaluated for usability and safety. Discussion: We expect to determine the efficacy, usability and safety of the AOT-NMES rehabilitation approach for the recovery of upper limb motor function in post-stroke patients. The obtained results will also help reveal the neural underpinnings of motor recovery, as assessed by neurophysiological data, biomechanical and MRI measures.

We present a case of paraneoplastic tumefactive demyelination in a 55-year-old female with an underlying anaplastic thyroid carcinoma (ATC), alongside a review of the literature on all cases of tumefactive demyelination associated with non-CNS neoplasia. In the presented case the patient developed a right-sided subacute sensorimotor hemiparesis. The initial cerebral MRI revealed a bilateral frontoparietal tumefactive mass lesion with marked gadolinium uptake and mass effect. Cerebrospinal fluid revealed CSF-specific oligoclonal bands type III, with negative cell count, protein and pathogen testing. Brain biopsy indicated demyelination and T-cell infiltrates and foamy macrophages. A body CT revealed an anaplastic thyroid carcinoma. Despite steroids, plasma exchange, rituximab, and cancer treatment, the patient died due to clinical fluctuation and cancer progression. In addition to our case 9 cases of tumefactive demyelinating have been reported in patients with newly diagnosed extracranial neoplasia, most commonly seminoma germ cell tumour (7/10). 8/10 (80%) of patients were male, with mean age at diagnosis was 52.9 years 95% C.I. [43.8, 62.0]. 5/10 patients presented with sensorimotor hemiparesis and/or confusion/neurocognitive deficits. 4/10 with visual deficits and 2/10 with aphasia. In all cases neoplasia was diagnosed simultaneously or after neurological manifestations. All cases presented initially as solitary lesions. A malignancy specific-treatment as well as steroid treatment in different regiments were applied. In addition in 2/10 plasmapheresis was implemented and 1/10 patients received intravenous immunoglobulins. In the majority of cases including the presented case partial neurological improvement was documented whereas malignancy usually progressed. To our knowledge, this is the first report of paraneoplastic tumefactive demyelination associated with an ATC highlighting the importance of a thorough workup in these patients. This is the first reported case of paraneoplastic tumefactive demyelination associated with ATC, underscoring the necessity of a comprehensive diagnostic approach in similar patients.

Background and purpose: Stroke has become a major public health problem. This paper aims to briefly review the current epidemiological characteristics, preliminary achievements, and national action strategies related to stroke prevention and control in China.

Methods: English and Chinese literature were searched on stroke epidemiological characteristics and more proactive strategies for its prevention and control in China. Potential papers related to this topic were identified from PubMed, Medline, Embase, Cochrane Library, Wanfang Database, SINOMED, and China National Knowledge Infrastructure databases, as well as the annual reports and websites of the People's Daily, the State Council, and the National Health Commission of the People's Republic of China.

Results: Stroke has been ranked among the top three causes of death in China, and has become a public health problem endangering people's health. High rates of incidence, mortality, and disability bring a heavy burden to stroke patients, families, and society. With China's economic development, urbanization, and population aging, the prevalence and incidence of stroke are still rising. Although some progress has been made in specialized stroke prevention and treatment in China, there is still much room for improvement. Curbing increasing stroke due to increased prevalence and suboptimal control of risk factors and unhealthy lifestyles is no longer just the efforts of medical service institutions. It still requires a more proactive national strategy and general mobilization of the whole people. Increased prevalence of stroke, survivors' unfavorable outcomes, and suboptimal rehabilitation also need specialized stroke care and the perfect Hierarchical Medical System within the regional medical consortium in China.

Conclusions: The current situation of stroke prevention and treatment is still very serious in China. In the future, the stroke prevention and treatment model will change from passive stroke treatment and risk factor control to a more proactive prevention model of health factor management.

Background: Alzheimer's disease (AD) is characterized by complex molecular alterations that complicate its pathogenesis and contribute to the lack of effective treatments. Mesenchymal stem cell-derived extracellular vesicles (EVs) have shown promise in AD models, but results across different EV subpopulations remain inconsistent.

Objectives: This study investigates proteomic and transcriptomic data from publicly available postmortem AD brain datasets to identify molecular changes at both the gene and protein levels. These findings are then compared with the proteomes of various EV subpopulations, differing in size and distribution, to determine the most promising subtype for compensating molecular degeneration in AD.

Design: We conducted a comprehensive analysis of 788 brain samples, including 481 AD cases and 307 healthy controls, examining protein and mRNA levels to uncover AD-associated molecular changes. These findings were then compared with the proteomes of different EV subpopulations to identify potential therapeutic candidates.

Methods: A multi-omics approach was employed, integrating proteomic and transcriptomic data analysis, miRNA and transcription factor profiling, protein-protein network construction, hub gene identification, and enrichment analyses. This approach aimed to explore molecular changes in AD brains and pinpoint the most relevant EV subpopulations for therapeutic intervention.

Results: We identified common alterations in the cAMP signaling pathway and coagulation cascade at both the protein and mRNA levels. Distinct changes in energy metabolism were observed at the protein level but not at the mRNA level. A specific EV subtype, characterized by a broader size distribution obtained through high-speed centrifugation, was identified as capable of compensating for dysregulated mitochondrial proteostasis in AD brains. Network biology analyses further highlighted potential regulators of key therapeutic proteins within this EV subtype.

Conclusion: This study underscores the critical role of proteomic alterations in AD and identifies a promising EV subpopulation, enriched with proteins targeting mitochondrial proteostasis, as a potential therapeutic strategy for AD.

Cognitive impairment encompasses a spectrum of disorders marked by acquired deficits in cognitive function, potentially leading to diminished daily functioning and work capacity, often accompanied by psychiatric and behavioral disturbances. Alzheimer's disease (AD) and Post-stroke cognitive impairment (PSCI) are significant causes of cognitive decline. With the global population getting older, AD and PSCI are becoming major health concerns, underscoring the critical necessity for successful treatment options. In recent years, various non-invasive biophysical stimulation techniques, including ultrasound, light, electric, and magnetic stimulation, have been developed for the treatment of central nervous system diseases. Preliminary clinical studies have demonstrated the feasibility and safety of these techniques. This review discuss the impact of 40 Hz multisensory stimulation on cerebral function, behavioral outcomes, and disease progression in both animal models and individuals exhibiting cognitive deficits, such as AD and PSCI. Furthermore, it summarizes the potential neural pathways involved in this therapeutic modality by synthesizing evidence from a variety of studies within the field. Subsequently, it evaluates the existing constraints of this technique and underscores the potential advantages of 40 Hz multisensory stimulation therapy for individuals with cognitive deficits, with the goal of enhancing the management and care of AD and PSCI.

Background: In conjunction with more sensitive culture and molecular diagnostic testing modalities, simultaneous or sequential infection with more than 1 vector borne zoonotic pathogen is being increasingly documented in human patients. On a frequent basis, many people are exposed to apparently healthy, but infected, domestic and wild animals, the arthropod vectors with which these animals have co-evolved, and the bacterial, protozoal and other pathogens for which various animals are reservoirs. Unsuspected zoonotic transmission by scratch, bite, or vector exposures can result in chronic, indolent, or potentially life-threatening infections.

Methods: In December 2016, at 2 years of age, a male child residing in Ontario, Canada received facial scratches from a feral cat. In August 2018, seizures began 8 days after the child developed a focal, suspected insect bite rash. In June 2019, potential mold toxicity in the child's bedroom was assessed by fungal culture and urinary mycotoxin assays. Beginning in January 2022, Bartonella spp. serology (indirect fluorescent antibody assays), polymerase chain reaction (PCR) amplification, DNA sequencing, and enrichment blood and brain cultures were used on a research basis to assess Bartonella spp. bloodstream and central nervous system (brain biopsy) infection. In 2024, using recently developed PCR and DNA sequencing targets, Babesia species infection was retrospectively assessed due to the rash observed in 2018.

Results: Although there was historical cat and suspected tick exposures, serological testing for Bartonella henselae and Borrelia burgdorferi were repeatedly negative. Sequential neurodiagnostic testing partially supported a diagnosis of Rasmussen's encephalitis. Astrogliosis was the only brain biopsy histopathological abnormality. Bartonella henselae DNA was amplified and sequenced from enrichment cultures of brain tissue. Retrospectively, Babesia odocoilei and Babesia divergens-like MO-1 infections were confirmed by amplification and sequencing of DNA extracted from enrichment blood cultures processed in January 2022, from blood and brain tissue cultures in June 2022, and blood in January and June 2023.

Conclusions: Infection with B. henselae, B. odocoilei, and B. divergens-like MO-1, complicated by mycotoxin exposure, created a complex clinical scenario for this child, his parents, and his doctors.

Under normal physiological conditions, gut microbiota and host mutually coexist. They play key roles in maintaining intestinal barrier integrity, absorption, and metabolism, as well as promoting the development of the central nervous system (CNS) and emotional regulation. The dysregulation of gut microbiota homeostasis has attracted significant research interest, specifically in its impact on neurological and psychiatric disorders. Recent studies have highlighted the important role of the gut- brain axis in conditions including Alzheimer's Disease (AD), Parkinson's Disease (PD), and depression. This review aims to elucidate the regulatory mechanisms by which gut microbiota affect the progression of CNS disorders via the gut-brain axis. Additionally, we discuss the current research landscape, identify gaps, and propose future directions for microbial interventions against these diseases. Finally, we provide a theoretical reference for clinical treatment strategies and drug development for AD, PD, and depression.