Journal of Neurorestoratology最新文献

Background

Stroke is considered to be a leading cause of impairment. After experiencing strokes, patients are frequently left with impaired motor function, making it difficult to carry out daily tasks. The most extensively researched method for treating stroke patients in recent decades is CIMT (constraint-induced movement therapy), which was developed to treat upper limb deficits following stroke. CIMT entails limiting the use of the unaffected limb, altering behavior to increase the use of the affected limb, and finally, mass-training of the affected limb.

Objective

The current study aimed to determine the effectiveness of CIMT through TR for upper extremity function in stroke patients.

Materials and methods

Thirty post-stroke participants were selected on the basis of inclusion and exclusion criteria, and allocated into group A and group B. Group A was treated with CIMT in the physiotherapy department and group B was treated with CIMT through TR. Outcome measures were the Fugl-Meyer Assessment scale for upper extremities (FMA-UE), the Wolf Motor Function Test (WMFT), and the Motor Activity Log (MAL).

Results

Both groups showed significant improvements in FMA-UE, WMFT and MAL-A0U, MAL-Q0M scores. However, there were no significant differences between groups A and B in FMA-UE, WMFT, MAL-AOU, and MAL-QOM scores in the inter-group analysis.

Conclusion

CIMT via TR was equally effective than CIMT in physiotherapy department for upper extremity function in stroke. Further studies should be conducted to identify the long-term effectiveness of this approach.

Cerebrovascular disease is among the most common causes of permanent disability and mortality in adults and places immense pressure on health care resources. Metabolic diseases caused by susceptibility genes and unhealthy lifestyle play a key role in the development of cerebrovascular disease. Cardiometabolic disease is now well established and rapidly evolving. Cardiometabolic medicine, which considers metabolic issues and cardiovascular disease as an integrated whole, has been implemented in many countries worldwide. However, integrated management of metabolic risk factors and cerebrovascular disease is still in the initial stages. In this minireview, we propose a concept and definition of cerebrometabolic disease, describe its possible pathogenesis, summarize the recently proposed integrative therapeutic approach, and discuss future developments as well as challenges, with the aim of promoting a deeper understanding and integrated management of metabolic issues and cerebrovascular disease.

Background

Purinergic ligand-gated ion channel 7 receptor (P2X7R) is an ATP-gated cationic channel. It plays an important role in central nervous system diseases such as cerebral hemorrhage and Parkinson's disease, and is closely related to neuroinflammatory reactions associated with disease progression. In the present study, we evaluated the role of P2X7R in neuroinflammation and brain edema after traumatic brain injury (TBI). We also investigated the related mechanisms and potential therapeutic drugs.

Methods

In the in vivo experiments, C57BL/6 mice were randomly divided into four groups: Sham, TBI, TBI + A438079, or TBI + MCC950. The TBI model was constructed via controlled cortical impact, and mice then received saline, A438079, or MCC950 injections. Morphological damage to the brains of mice was observed by Nissl staining. Morphological and quantitative changes in microglia as well as P2X7R expression were observed via immunofluorescence. The water content of brain tissue was evaluated using the brain dry/wet weight ratio. In the in vitro experiments, lipopolysaccharides were used to stimulate murine microglial BV2 cells into an inflammatory activation state. The expression of P2X7R, interleukin (IL)-1β, IL-6, IL-12, tumor necrosis factor (TNF)-α, nuclear factor kappa-B (NF-κB), and NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasomes in BV2 cells was analyzed using enzyme-linked immunosorbent assay and Western blot. Moreover, an indirect co-culture technique was used to evaluate the effects of the neuroinflammatory model of BV2 cells on tight junction protein expression in mouse brain microvascular endothelial bEnd.3 cells.

Results

Levels of P2X7R, IL-1β, IL-6, IL-12, TNF-α, NF-κB, and NLRP3 inflammasomes were significantly higher in the TBI group than in the Sham group. TBI also increased the brain edema degree and tight junction protein expression levels. By targeting P2X7R (with A438079) or NLRP3 (with MCC950), we were able to inhibit neuroinflammation and alleviate brain edema.

Conclusions

Targeting P2X7R may help to reduce neuroinflammation and brain edema secondary to acute TBI by inhibiting the NF-κB/NLRP3 inflammasome pathway. P2X7R may be an innovative therapeutic target in TBI.

Background

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder. Despite its biological underpinnings, ASD is yet diagnosed based on behavioral assessments. The importance of early ASD detection is supported by a large body of evidence. Early diagnosis can facilitate more effective interventions, reducing the socioeconomic costs and improving the quality of life of both children with ASD and their families. This study aims to investigate the expression patterns of ASD-related microRNAs (miRNAs) in Iranian children with ASD compared with matched neurotypical controls, to identify candidate miRNA biomarkers.

Method

Validation of ASD-related miRNAs was performed using the qRT-PCR method in plasma samples from 20 ASD and 20 unaffected individuals. Differentially expressed miRNAs were identified based on relative quantification analysis. Then, the diagnostic potential of each candidate miRNA was assessed using receiver operating characteristics (ROC) curve analysis.

Results

Based on statistical and bioinformatics analyses, eight miRNAs were recommended as candidate biomarkers. Furthermore, differential expression of five of these miRNAs—miR-146a-5p, miR-338-3p, miR-181b-5p, let-7a-5p, and miR-140-3p—was confirmed experimentally by qRT-PCR (p-value < 0.05) based on a t-test. miR-140-3p was not further detected as significant by the Mann–Whitney test. The sensitivity, specificity, and area under the ROC curve were calculated for each validated miRNA and fell in the ranges of 75%–91%, 66.67%–83.33%, and 74%–90%, respectively.

Conclusions

This study revealed a panel of high-confidence differentially expressed miRNAs, which requires further investigation in larger sample sizes and by other validation tests. These findings could be a step forward in the field of ASD biomarker discovery.

Introduction

Functional connectivity across large-scale networks is crucial for the regulation of conscious states. Nonetheless, our understanding of potential alterations in the temporal dynamics of dynamic functional connectivity (dFC) among patients with disorders of consciousness (DOC) remains limited. The present study aimed to examine different time-scale spatiotemporal dynamics of electroencephalogram oscillation amplitudes recorded in different consciousness states.

Methods

Resting-state electroencephalograms were collected from a cohort of 90 patients with DOC. The sliding window approach was used to create dFC matrices, which were subsequently subjected to k-means clustering to identify distinct states. Finally, we performed state analysis and developed a decoding model to predict consciousness.

Results

There was significantly lower dFC within the forebrain network in patients with unresponsive wakefulness syndrome than in those with a minimally conscious state. Moreover, there were significant differences in temporal properties, mean dwell time, and the number of transitions in the high-frequency band at different time scales between the unresponsive wakefulness syndrome and minimally conscious state groups. Using the multi-band and multi-range temporal dynamics of dFC approach, satisfactory classification accuracy (approximately 83.3 %) was achieved.

Conclusion

Loss of consciousness is accompanied by an imbalance of complex dynamics within the brain. Both transitions between states at short and medium time scales in high-frequency bands and the forebrain are important in consciousness recovery. Together, our findings contribute to a better understanding of brain network alterations in patients with DOC.

Magnesium is an essential nutrient involved in a wide range of physiological activities to maintain normal brain functions. So far, magnesium has been recognized as a cofactor for over 600 enzymatic reactions within the body. Importantly, magnesium deficiency has been implicated in the pathogenesis of various dementia-related diseases containing cardiovascular diseases and Alzheimer’s disease (AD). With increased aging, the incidence and prevalence of dementia are expected to rise dramatically double every 20 years worldwide. Accumulating evidence indicates that dementia-related diseases are associated with low magnesium levels, and dietary magnesium intake can improve cognitive function. Many studies have revealed that magnesium ions act as a natural Ca²⁺ blocker to inhibit calcium overload and halt the course of AD by blocking N-methyl-D-aspartate receptors and thus inhibiting neuronal overactivation. In addition, magnesium ions can inhibit glial cell-mediated neuroinflammation by down-regulating pro-inflammatory cytokines and oxidative stress, which have been implicated in the development of chronic age-related diseases. Thus, magnesium may be a target for the prevention and treatment of neurological diseases. Taken together, maintaining an optimal magnesium balance may help in the prevention of cognitive decline and dementia. In this review, we summarize our current understanding of the role of magnesium in dementia, highlighting recent progresses in the field.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a relatively common inherited arterial smooth muscle cell disease. The genetic defect is localized to the notch homolog protein 3 (NOTCH3) gene on chromosome 19q12 and is due to a missense variant in NOTCH3. The main clinical manifestations are transient ischemic attacks and repeated stroke, with cognitive impairments leading to dementia, migraine with aura, and mental/emotional disorders. To date, there is no specific therapeutic option, with only symptomatic supportive treatment for the symptoms of acute stroke, migraine, dementia, and mental abnormalities. Here, we provide a case report of a Chinese patient with CADASIL and a mutation in exon 4 of the NOTCH3 gene (p.Arg133Cys). The patient mainly exhibited recurrent cerebral infarction and affective disorder. Antidepressant treatment combined with repetitive transcranial magnetic stimulation significantly improved the depressive symptoms of the patient.

Objective

To retrospectively analyze the distribution characteristics of pathogenic bacteria in the cerebrospinal fluid (CSF) of patients with severe intracranial infection after craniotomy and treatment results. The aim was to provide a clinical basis and reference for improving treatment for severe intracranial infections.

Methods

This was a retrospective analysis of the distribution of pathogenic bacteria and the therapeutic effect for 43 patients who developed severe intracranial infections after craniotomy. All patients had positive CSF cultures and were treated in two hospitals in Beijing from May 2015 to May 2020. All patients received an intravenous injection of sensitive antibiotics combined with a CSF lateral ventricle catheter or lumbar cistern drainage. Antibiotic lavage treatment was administered through an external drain.

Results

The CSF bacterial culture results for the 43 patients showed 34 single-strain infections (26 Gram-positive bacteria and 8 Gram-negative bacteria) and 9 multistrain infections. Fifty-two pathogenic strains were isolated, namely 32 Gram-positive bacteria (61.54%), 18 Gram-negative bacteria (34.61%), and 2 fungi (3.85%). After combined treatment, 29 patients (67.44%) were cured; treatment was effective for 7 patients (16.28%) and ineffective for 7 patients (16.28%). After 6 months of follow-up, the 36 surviving patients were cured of infection. The Glasgow Outcome Scale score results showed that 5 of the 36 (13.9%) patients had a persistent vegetative state; 13 (36.1%) had severe disability; 12 (33.3%) had moderate disability; and 6 (16.7%) had mild disability.

Conclusion

CSF pathogenic bacteria in patients with intracranial infection after craniotomy were mainly Gram-positive bacteria, primarily Staphylococcus epidermidis. A small number of patients had mixed bacterial infections. Owing to the presence of implanted devices in patients who underwent ventriculoperitoneal shunt surgery, the antibacterial therapeutic effect was worse than that for other types of postoperative infections. Therefore, when initial intravenous antibiotics are ineffective, the shunt device should be removed or replaced as soon as possible. When initial intravenous antibiotics are ineffective and severe intracranial infection occurs, a combined treatment plan should be adopted. That is, CSF drainage and antibiotic lavage should be performed cautiously with the intravenous injection of sensitive antibiotics. Our clinical data confirmed that postoperative neurosurgical infection could lead to different degrees of nerve dysfunction, which should be considered.