Background This study aims to preliminarily evaluate the role of Guide Chi and Regulate Spirit(GCRS) Tuina in enhancing walking function in post-stroke patients with walking dysfunction; secondly, by using functional near-infrared spectroscopy (fNIRS), it investigates the effect of GCRS Tuina on the restoration of brain function in this patient population. Methods Participants in the control group received 4-week rehabilitation treatment, while those in the Combined Tuina Group (CTG) additionally received GCRS Tuina therapy for another 4 weeks on this basis. Functional Ambulation Category (FAC), Fugl - Meyer Assessment Scale for Lower Extremity Motor Function (FMA - LE), and Modified Barthel Index (MBI) were evaluated at the baseline and after 4 treatment weeks. A gait and motion analysis system was used to measure step length, stride, walking speed, and step frequency. FNIRS was used to measure the resting-state functional connectivity(FC) strength, as well as the β - value and HbO2 concentration mean during the walking task. Results A total of 60 participants completed the randomized, and 53 completed the trial and entered the statistical analysis. Compared with the Single Rehabilitation Group(SRG), the CTG group had higher FAC, FMA-LE, and MBI scores after 4 weeks. After the treatment course, the standardized step length, stride, walking speed, and step frequency of the CTG were higher than SRG. At the Region of Interest(ROI) level, the CTG exhibited 13 inter-ROI FC strengths that were higher than SRG, and the differences could survive the FDR correction (PFDR<0.05). Under the walking task, the CTG group had higher β values in 18 channels and higher Oxyhemoglobin(HbO2) concentrations in 19 channels than the SRG (PFDR <0.05). Conclusion GCRS Tuina therapy can significantly improve patients' walking function, enhance lower limb motor ability and daily living ability. It can improve walking efficiency. Tuina can significantly increase the FC and enhance the activation levels and HbO2 concentrations. The stimulation of Tuina may help reconstruct the brain's motor control network, restore impaired motor function, promote the occurrence of neural plasticity, strengthen the neural circuits in the cognitive-motor-sensory cortex to improve walking function. Trial registration This study has been registered with the International Traditional Medicine Clinical Trial Registry (ITMCTR2024000654).

Purpose:Inflammation plays a role in cerebral small vessel disease (CSVD) pathophysiology. This study aimed to explore the association of the fibrinogen-to-albumin ratio (FAR), a novel inflammatory marker, with CSVD burden in patients with transient ischemic attack (TIA). Patients and Methods:From October 1, 2022, to November 30, 2023, continuous patients with TIA were recruited in the study. The total CSVD burden score and modified total CSVD burden score were used to assess the severity of CSVD. Multivariable regression analysis was used to explore the correlation between the FAR and CSVD in TIA patients. Results:A total of 455 participants were recruited, of whom 225 (48.35%), according to the total CSVD burden score, and 181 (40.67%), according to the modified CSVD burden score were finally identified as moderate-severe CSVD. Spearman correlation analysis showed that levels of FAR correlated with the total CSVD (r=0.392, P<0.001) and the modified total CSVD burden scores (r=0.379, P<0.001). Multivariable logistic regression analysis showed that FAR was independently associated with moderate-severe CSVD, both as a continuous variable and as a tertile variable (P<0.001). Conclusion:The level of FAR on admission was independently associated with the severity of CSVD in patients with TIA.

Studies have found that the phosphatase actin regulatory factor 1 expression can be related to stroke, but it remains unclear whether changes in phosphatase actin regulatory factor 1 expression also play a role in traumatic brain injury. In this study we found that, in a mouse model of traumatic brain injury induced by controlled cortical impact, phosphatase actin regulatory factor 1 expression is increased in endothelial cells, neurons, astrocytes, and microglia. When we overexpressed phosphatase actin regulatory factor 1 by injection an adeno-associated virus vector into the contused area in the traumatic brain injury mice, the water content of the brain tissue increased. However, when phosphatase actin regulatory factor 1 was knocked down, the water content decreased. We also found that inhibiting phosphatase actin regulatory factor 1 expression regulated the nuclear factor kappa B signaling pathway, decreased blood-brain barrier permeability, reduced aquaporin 4 and intercellular adhesion molecule 1 expression, inhibited neuroinflammation, and neuronal apoptosis, thereby improving neurological function. The findings from this study indicate that phosphatase actin regulatory factor 1 may be a potential therapeutic target for traumatic brain injury.

The status of cerebral perfusion and its restoration level play a vital role in the prognosis and clinical decision making of many neurosurgical diseases. As such, gold standard methods including CT, MR and ICP monitoring, which can indicate and measure cerebral perfusion and restoration, have been widely adopted to evaluate whether or not a patient has recovered from neurofunctional disabilities. This robust combination of methods, however, is confronted with a growing number of contradictions in recent years due to its inability to measure the status of cerebral reperfusion in microvasculature level, even though this has been shown to determine neurofunctional restoration as well or even better. To this date, nevertheless, we have very limited imaging methods that could evaluate human cerebral microperfusion both safely and accurately under most neurosur-gical conditions. We herein report a new method of acquiring a patient's cerebral microperfusion status non-invasively which could display the precise distribution of microvasculature in deep cerebral regions with a resolution of similar to 30 mu m, using everyday bed-side ultrasonography combined with a computerized super-resolution reconstruction algorithm. Using this imaging modality, we found that a patient's cerebral microperfusion might not be improved by some routine administrations even though the gold standard method had yielded the opposite conclusions. Our imaging modality retains the safe, portable feature of ordinary ultrasonography while possesses the extraordinary super-resolution nature, which enables an efficient, precise diagnosis of cerebral perfusion. Most importantly, the super resolution nature of this method may also facilitate early-stage evaluation of a patient's neurofunctional restoration level and avoid overoptimistic conclusions from conventional angi-ography or ICP monitoring.

Background According to the pathoanatomic classification system, progressive hemorrhagic injury (PHI) can be categorized into progressive intraparenchymal contusion or hematoma (pIPCH), epidural hematoma (pEDH), subdural hematoma (pSDH), and traumatic subarachnoid hemorrhage (ptSAH). The clinical features of each type differ greatly. The objective of this study was to determine the predictors, clinical management, and outcomes of PHI according to this classification. Methods Multivariate logistic regression analysis was used to identify independent risk factors for PHI and each subgroup. Patients with IPCH or EDH were selected for subgroup propensity score matching (PSM) to exclude confounding factors before evaluating the association of hematoma progression with the outcomes by classification. Results In the present cohort of 419 patients, 123 (29.4%) demonstrated PHI by serial CT scan. Of them, progressive ICPH (58.5%) was the most common type, followed by pEDH (28.5%), pSDH (9.8%), and ptSAH (3.2%). Old age (≥ 60 years), lower motor Glasgow Coma Scale score, larger primary lesion volume, and higher level of D-dimer were independent risk factors related to PHI. These factors were also independent predictors for pIPCH, but not for pEDH. The time to first CT scan and presence of skull linear fracture were robust risk factors for pEDH. After PSM, the 6-month mortality and unfavorable survival rates were significantly higher in the pIPCH group than the non-pIPCH group (24.2% vs. 1.8% and 12.1% vs. 7.3%, respectively, p < 0.001), but not significantly different between the pEDH group and the non-pEDH group. Conclusions Understanding the specific patterns of PHI according to its classification can help early recognition and suggest targeted prevention or treatment strategies to improve patients’ neurological outcomes.

Traumatic brain injury (TBI) could highly induce coagulopathy through breaking the dynamic balance between coagulation and fibrinolysis systems, which may be a major contributor to the progressive secondary injury cascade that occurs after TBI. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibition is reported to exert neuroprotection in TBI, making it a potential regulatory target involved in TBI-induced coagulation disorder. PTEN level is controlled in a major way by E3 ligase-mediated degradation through the ubiquitin-proteasome system. The C terminus of Hsc70-interacting protein (CHIP) has been shown to regulate proteasomal degradation and ubiquitination level of PTEN. In the present study, CHIP was overexpressed and knocked down in mouse brain microvascular endothelial cells (bEnd.3) and tissues during the early phase of TBI.In vitrocell proliferation, cell apoptosis, migration capacity, and invasion capacity were determined. The changes of procoagulant and apoptosis molecules after TBI were also detected as well as the micrangium density and blood-brain barrier permeability afterin vivoTBI.In vitroresults demonstrated that CHIP overexpression facilitated bEnd.3 cell proliferation, migration, and invasion and downregulated cell apoptosis and the expressions of procoagulant molecules through promoting PTEN ubiquitination in a simulated TBI model with stretch-induced injury treatment.In vivoexperiments also demonstrated that CHIP overexpression suppressed post-TBI apoptosis and procoagulant protein expressions, as well as increased microvessel density, reduced hemorrhagic injury, and blood-brain barrier permeability. These findings suggested that the upregulation of CHIP may attenuate apoptosis and procoagulant activity, facilitate brain repair, and thus exerts neuroprotective effects in TBI.

Background: The phosphatase actin regulator-1 (PHACTR-1) gene on chromosome 6 encodes an actin and protein phosphatase 1 (PP1) binding protein, Phactr-1, which is highly expressed in brain tissues. Phactr-1 expression is involved in physiological and pathological cerebral microvascular events. This study aimed to investigate the role of expression of Phactr-1 in a mouse brain capillary endothelial cell line, bEnd.3, by knockdown the PHACTR-1 gene. Material/Methods: Three bEnd.3 cell groups were studied, CON (normal control cells), NC (control scramble transfected cells), and KD (cells with PHACTR-1 gene knockdown). The PHACTR-1 gene was knocked down using transfection with small hairpin RNA (shRNA). In the three cell groups cell proliferation, migration, and apoptosis were studied by MTT and colony formation assays, transwell and scratch assays, and flow cytometry. The related cell pathways of associated with Phactr-1 knockdown were studied by Western blot. Results: Phactr-1 knockdown suppressed bEnd.3 cell proliferation and migration, promoted cell apoptosis, and down- regulated the expressions of migration-associated proteins, including matrix metalloproteinase (MMP)-2 and MMP-9 and upregulated apoptosis-associated proteins, including Bax, Bcl-2, cleaved caspase-3, and caspase-3. Conclusions: Phactr-1 was shown to have a role in the inhibition of endothelial cell proliferation and migration, promoted cell apoptosis, and regulated matrix metalloproteinases and apoptosis-associated proteins. These findings indicate that the expression of the Phactr-1 should be studied further in the cerebral microvasculature, both in vitro and in vivo, regarding its potential as a diagnostic and therapeutic target for cerebral microvascular disease.

Posttraumatic hydrocephalus (PTH) is a disorder of disturbed cerebrospinal fluid (CSF) dynamics after traumatic brain injury (TBI). It can lead to brain metabolic impairment and dysfunction and has a high risk of clinical deterioration and worse outcomes. The incidence and risk factors for the development of PTH after decompressive craniectomy (DC) has been assessed in previous studies, but rare studies identify patients with higher risk for PTH among all TBI patients. This study aimed to develop and validate a risk scoring system to predict PTH after TBI. Demographics, injury severity, duration of coma, radiologic findings, and DC were evaluated to determine the independent predictors of PTH during hospitalization until 6 months following TBI through logistic regression analysis. A risk stratification system was created by assigning a number of points for each predictor and validated in an independent cohort. The model accuracy was assessed by the area under the receiver operating characteristic curve (AUC). Of 526 patients in the derivation cohort, 57 (10.84%) developed PTH during 6 months follow up. Age > 50 yrs (Odd ratio [OR] = 1.91, 95% confidence interval [CI] 1.09–3.75, 4 points), duration of coma ≥1 w (OR = 5.68, 95% CI 2.57–13.47, 9 points), Fisher grade III (OR = 2.19, 95% CI 1.24–4.36, 5 points) or IV (OR = 3.87, 95% CI 1.93–8.43, 7 points), bilateral DC (OR = 6.13, 95% CI 2.82–18.14, 9 points), and extra herniation after DC (OR = 2.36, 95% CI 1.46–4.92, 5 points) were independently associated with PTH. Rates of PTH for the low- (0–12 points), intermediate- (13–22 points) and high-risk (23–34 points) groups were 1.16%, 35.19% and 78.57% (p < 0.0001). The corresponding rates in the validation cohort, where 17/175 (9.71%) developed PTH, were 1.35%, 37.50% and 81.82% (p < 0.0001). The risk score model exhibited good-excellent discrimination in both cohorts, with AUC of 0.839 versus 0.894 (derivation versus validation) and good calibration (Hosmer-Lemshow p = 0.56 versus 0.68). This model will be useful to identify patients at high risk for PTH who may be candidates for preventive interventions, and to improve their outcomes.

Objective The surgical treatment and curative effect of transcranial subfrontal unroofing retrobular tumor resection are introduced and the prognosis is discussed.Methods The clinical data of 13 patients with retrobular tumors treated in our department were collected retrospectively.All the patients underwent surgery through subfrontal unroofing approach to discuss the surgical challenges,which involved tumor removal,visual function preservation and cosmetic reconstruction.Results Total resection of the tumors was achieved in 9 cases( 8 angioma and 1 optic nerve neurinoma),subtotal resection in 2 optic nerve neurinoma cases,and the partial resection in 1pserdotumor and 1 hamartoma.Seven patients were followed-up for 6 months( 6 patients was lost during follow-up).Of 7 patients,the visual acuity was improved in 6 patients and remained unchanged in 1 patient.Conclusion Retrobular tumor can be treated safely by transcranial approaches which provides a better exposure of the orbital cavity and tumors.

目的 通过对进展性脑挫伤患者的凝血指标进行动态检测,探讨在进展过程中关键凝血指标的变化.方法 对95例进展性脑挫伤患者进行临床资料分析,检测伤后24h～7d内格拉斯哥昏迷评分(GCS)、凝血酶原时间(PT)、激活部分凝血酶原时间(APTT)、纤维蛋白原含量(FIB)、D-二聚体浓度(D-dimer)、纤维蛋白降解产物(FDP)以及其变化趋势.分析其中与死亡率、格拉斯哥预后评分(GOS)相关的危险因素.结果 进展性脑挫伤各组患者中入院评分、D-二聚体及纤维蛋白原含量与死亡率、GOS评分相关.结论 凝血指标对进展性脑挫伤患者预后判断具有临床指导意义,入院评分越低,D-二聚体浓度越高,纤维蛋白原含量越高预后越差.其中以双额叶及颞叶部位进展性脑挫伤预后较差.

AbstractThis meta-analysis examined whether early decompressive craniectomy (DC) can improve control of intracranial pressure (ICP) and mortality in patients with traumatic brain injury (TBI).Medline, Cochrane, EMBASE, and Google Scholar databases were searched until May 14, 2015, using the following terms: traumatic brain injury, refractory intracranial hypertension, high intracranial pressure, craniectomy, standard care, and medical management. Randomized controlled trials in which patients with TBI received DC and non-DC medical treatments were included.Of the 84 articles identified, 8 studies were selected for review, with 3 randomized controlled trials s having a total of 256 patients (123 DCs, 133 non-DCs) included in the meta-analysis. Patients receiving DC had a significantly greater reduction of ICP and shorter hospital stay. They also seemed to have lower odds of death than patients receiving only medical management, but the P value did not reach significance (pooled odds ratio 0.531, 95% confidence interval 0.209–1.350, Z = 1.95, P = 0.183) with respect to the effect on overall mortality; a separate analysis of 3 retrospective studies yielded a similar result.Whereas DC might effectively reduce ICP and shorten hospital stay in patients with TBI, its effect in decreasing mortality has not reached statistical significance.

Objective: To identify the early changes of serum neuroglobin and Nogo-A concentrations and the relations to traumatic brain injury (TBI) severity and prognosis.Methods: Serum samples were obtained and analyzed from 34 patients with TBI within the first 96h after injury. Comparative analysis combined with Glasgow Coma Scale (GCS) scores and the 6-month prognosis of these patients was performed.Results: Significant correlations were found between peak serum neuroglobin and Nogo-A concentrations and a patient's GCS score on admission (p<0.001). The mean peak serum neuroglobin and Nogo-A concentrations were both significantly higher in patients with an unfavorable outcome at 6 months after injury (p<0.05).Conclusions: Serum neuroglobin and Nogo-A levels could be suggested as biomarkers for predicting TBI severity and prognosis.

This meta-analysis examined whether early decompressive craniectomy (DC) can improve control of intracranial pressure (ICP) and mortality in patients with traumatic brain injury (TBI).Medline, Cochrane, EMBASE, and Google Scholar databases were searched until May 14, 2015, using the following terms: traumatic brain injury, refractory intracranial hypertension, high intracranial pressure, craniectomy, standard care, and medical management. Randomized controlled trials in which patients with TBI received DC and non-DC medical treatments were included.Of the 84 articles identified, 8 studies were selected for review, with 3 randomized controlled trials s having a total of 256 patients (123 DCs, 133 non-DCs) included in the meta-analysis. Patients receiving DC had a significantly greater reduction of ICP and shorter hospital stay. They also seemed to have lower odds of death than patients receiving only medical management, but the P value did not reach significance (pooled odds ratio 0.531, 95% confidence interval 0.209-1.350, Z=1.95, P=0.183) with respect to the effect on overall mortality; a separate analysis of 3 retrospective studies yielded a similar result.Whereas DC might effectively reduce ICP and shorten hospital stay in patients with TBI, its effect in decreasing mortality has not reached statistical significance.

Objective T o explore the anatomical features of recurrent artery of Heubner( RAH) of C hinese people. Methods T he number, routes, outer diameter, branches, and perfused areas of RAHs of 90 cerebral hemispheres from 45 brain samples fixed by formalin of 10% were observed and measured by the operation microscope. Results A total of 128 RAHs were found in 45 brain samples. T here were 1- 3 RAHs in each cerebral hemisphere. T he average number was( 1. 42 ± 0. 62) mm. T he RAH started from 8 mm of the horizontal proximal segment to 3 mm of the distal segment of anterior communicating artery( AC oA). T he average distance was( 0. 46 ± 1. 29) mm from the distal end of AC oA. T he outer diameter was 0. 05- 1. 20 mm and the average outer diameter was( 0. 64 ± 0. 24) mm. T he length was 12- 56 mm and the average length was( 30. 41 ± 10. 24) mm. T he RAH supplied the cortex as well as the cerebral parenchyma. Conclusion RAH has anatomical variations. It is clinically helpful to identify anatomical features of RAH and its relationships with A1 segment of AC oA, orbitofrontal artery, and frontalpolar artery.

Decompressive craniectomy (DC) is widely used to treat intracranial hypertension following traumatic brain injury (TBI) or cerebral vascular disease. Many studies have discussed complications of this procedure, and hydrocephalus is a common complication of DC. To further evaluate the relationship between DC and hydrocephalus, a review of the literature was performed. Numerous complications may arise after DC, including contusion or hematoma expansion, epilepsy, herniation of the cortex through a bone defect, CSF leakage through the scalp incision, infection, subdural effusion, hydrocephalus and "syndrome of the trephined". Several hydrocephalus predictors were identified; these included DC, distance from the midline, hygroma, age, injury severity, subarachnoid or intraventricular hemorrhage, delayed time to craniotomy, repeated operation, and duraplasity. However, results differed among studies. The impact of DC on hydrocephalus remains controversial.

Both delayed posttraumatic intracerebral hemorrhage and epidural hematoma have been well described in the neurosurgical literatures. However, delayed posttraumatic acute subdural hematoma which happens more than a week with a rapid progress after mild traumatic brain injury and causes death of patient is rarely reported. We show two such cases and briefly review the literature and discuss the probable pathogenesis of their rapid progress.

Aim: To study the variation in microsurgical anatomy of posterior circulation of the Circle of Willis in Chinese adult population to provide anatomical guide for high-risk vascular and cranial base surgery. Methods: Forty-six Chinese adult cadaveric brain specimens fixed in formalin were dissected, examined, measured, and photographed under light microscopy. Results: Over 60% of the posterior communicating arteries (PCoAs) in 46 cases (92 samples, both sides) were found to have differences in diameter between the 2 sides. About 50% of cases showed variation in length of >2 mm. Approximately 50% of the samples appeared to have a normal anatomic relationship between posterior communicating artery and the posterior cerebral artery (PCA). The occurrence rate of perforating branches from the precommunicating segment of the PCA (P1) was 98%. The angle of the basilar artery with bilateral PCA was measured as 45 to 150 degrees (mean 105 degrees). Conclusions: Variation in diameter, length, and/or other anatomic factors occurred in more than 50% of cases in the posterior circulation of the Circle of Willis.

目的 应用细菌纤维素膜修补兔硬脑膜缺损,观察植入后早期局部组织学改变以及炎症因子表达情况.方法 24只新西兰兔随机分为A、B两组,每组12只.所有动物经切除双侧硬脑膜制备2 cm×1 cm的缺损.A组动物的右侧硬脑膜缺损采用细菌纤维素膜修补,左侧硬脑膜缺损则不予修补,于术后第30、90、180天采集标本,行组织学检查.B组动物的右侧硬脑膜缺损采用细菌纤维素膜修补,左侧硬脑膜缺损以人工硬膜修补,于术后第7、14、21天采集修补部位组织,采用RT-PCR技术检测促炎症细胞因子白介素1β(IL-1β)、白介素6(IL-6)和肿瘤坏死因子α(TNF-α) mRNA的表达.结果 所有实验动物均存活,切口无感染.在A组的细菌纤维素膜修补侧,细菌纤维素膜均匀覆盖脑表面,与脑组织无粘连；外侧面纤维结缔组织增生,内侧面成纤维细胞排列均匀,新生血管形成,炎症反应轻微；在A组的未修补侧,大脑与皮下组织直接粘连.RT-PCR检测结果显示:术后各时间点,B组细菌纤维素膜修补侧IL-1 β和IL-6 mRNA表达水平均显著低于人工硬膜修补侧,两侧TNF-α mRNA表达水平相近.结论 采用细菌纤维素膜修复硬脑膜缺损,不易与脑组织形成粘连且早期炎症反应轻微.细菌纤维素膜可能成为理想的硬脑膜替代材料.

Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of head injury and often leads to a poor prognosis. Hemocoagulation disorder is recognized to have important effects on hemorrhagic or ischemic damages. We sought to assess if posttraumatic hemocoagulation disorders were associated with cerebral infarction, and evaluate their influence on outcome among patients with moderate or severe head trauma. In this study, PTCI was observed in 28 (10.57%) of the 265 patients within the first week after injury. In multivariate analysis, the thrombocytopenia (odds ratio (OR) 2.210, 95% confidence interval (CI) 1.065–4.674), abnormal prothrombin time (PT) (OR 3.241, 95% CI 1.090–7.648), D-dimer (>2 mg/L) (OR 7.260, 95% CI 1.822–28.076), or disseminated intravascular coagulation (DIC) scores (≥5) (OR 4.717, 95% CI 1.778–12.517) were each independently associated with an increased risk of PTCI. Admission Glasgow Coma Scale (GCS) score, abnormal activated partial thromboplastin time (APTT) and fibrinogen, and D-dimer (>2 mg/L) and DIC scores (≥5) showed an independent predictive effect on poor outcome. In conclusion, recognition of this important treatable cause of PTCI and the associated risk factors may help identify the group at risk and tailor management of patients with TBI.

Objective To investigate the value of 3.0T magnetic resonance imaging(MRI) in diagnosis of severe traumatic brain injury and outcome prediction.Methods Thirty-eight patients with severe traumatic brain injury were evaluated with MRI 4 to 6 weeks after injury,the lesion volumes in T1 and T2 weighted imaging and fluid attenuated inversion recovery(FLAIR) images were quantified and compared with simultaneous CT findings.The diffuse axonal injury(DAI) scores were recorded,and correlation analysis was performed with Glasgow coma scale(GCS) on admission and Glasgow outcome scale(GOS) 6 months after injury.Results MRI demonstrated more lesions than CT,especially for the corpus callosum and brain stem lesions.There were significant differences in DAI scores and lesion volumes in T1 and T2 weighted imaging and FLAIR images between different outcome groups(P0.05).DAI score had strongest correlation with GOS 6 months after injury(r=-0.854,P0.05),and the lesion volume detected by MRI was also negatively correlated with the outcome(P0.05).Conclusion 3.0T MRI is superior to CT in detection of intraparenchymal injury,especially for deep lesions.A quantitative study of the lesion volume and location demonstrated by MRI may play a role in outcome prediction.