Early decompressive surgery improves long-term prognosis in patients with intracerebral hemorrhage.

BACKGROUND: Multiple studies have shown that early decompressive surgery in patients with intracerebral hemorrhage can effectively limit hematoma expansion, reduce perihematomal edema, and improve prognosis. However, these studies are limited by small sample sizes and short follow-up times. OBJECTIVE: To analyze the effect of early decompressive surgery on the long-term prognosis of patients with cerebral hemorrhage and identify the influencing factors for poor prognosis. METHODS: A retrospective analysis of 78 patients with cerebral hemorrhage admitted between January 2020 and December 2022 was conducted. Patients were divided into early and delayed surgery groups for comparison of outcomes such as mortality rate, modified Rankin Scale score, and Short Form-36 scores. Additionally, factors influencing long-term prognosis were analyzed through logistic regression based on significant differences observed between groups. RESULTS: The early decompressive surgery group showed superior outcomes with lower mortality rates, modified Rankin Scale (mRS) scores, hematoma expansion rates, and perihematomal edema volumes compared to the delayed surgery group (P< 0.05). Additionally, age, preoperative Glasgow Coma Scale (GCS) score, preoperative hematoma volume, and a history of hypertension or diabetes were identified as independent prognostic factors for patients with cerebral hemorrhage, with odds ratios (ORs) greater than 1. CONCLUSIONS: Early decompressive surgery can improve the long-term prognosis and quality of life of patients with cerebral hemorrhage, reduce mortality rates, and decrease hematoma expansion and perihematomal edema. Older patients, those with higher preoperative hematoma volume and GCS score, and those with coexisting hypertension and diabetes should be given special attention to decrease the occurrence of adverse prognosis.

Advantages of Small Bone-Window Craniotomy Under Microscope Combined Postoperative Intracranial Pressure Monitoring in the Treatment of Hypertensive Intracerebral Hemorrhage.

OBJECTIVE: The aim of this study is to analyze the clinical effect of small bone-window craniotomy with microscope combined postoperative ICP monitoring, and further explore an appropriate treatment for HICH patients. METHODS: One hundred fifty patients with HICH were selected according to inclusion and exclusion criteria and divided into 3 groups at random, 50 each group. Patients in 3 groups were treated with conventional craniotomy, small bone-window craniotomy and small bone-window craniotomy combined ICP monitoring respectively. The surgical efficiency, treatment effect and outcomes were recorded and analyzed. RESULTS: The intraoperative blood loss and operation time of small window groups were significantly less than that of conventional group, and the hematoma clearance rate in small window groups were significantly higher than in conventional group (P < 0.05). Compared with conventional group, the hospital stays and mannitol dose used were less in small window groups and least in small window combined ICP monitoring group (P < 0.05). The complication rate in small window combined ICP monitoring group was 10%, which was significantly lower than in conventional group (26%, P < 0.05), while no significant difference was found between small window group (18%) compared with the other 2 groups respectively (P > 0.05). The difference of morality rate between 3 groups wasn't significant (P > 0.05). Three treatment significantly increased the Barthel index score, and the improvement of small window combined ICP monitoring group was significantly higher than in other 2 groups respectively (P < 0.05), while the difference between this two groups wasn't significant (P > 0.05). CONCLUSION: Small bone-window craniotomy is more efficient and convenient than conventional craniotomy in the treatment of HICH. In the meantime, small bone-window craniotomy simultaneous with ICP monitoring significantly improved clinical effect and treatment outcomes of HICH patients.

Decompressive craniectomy protects against hippocampal edema and behavioral deficits at an early stage of a moderately controlled cortical impact brain injury model in adult male rats.

A decompressive craniectomy (DC) has been shown to be a life-saving therapeutic treatment for traumatic brain injury (TBI) patients, which also might result in post-operative behavioral dysfunction. However, there is still no definite conclusion about whether the behavioral dysfunction already existed at an early stage after the DC operation or is just a long-term post-operation complication. Therefore, the aim of the present study was to analyze whether DC treatment was beneficial to behavioral function at an early stage post TBI. In this study, we established a controlled cortical impact injury rat model to evaluate the therapeutic effect of DC treatment on behavioral deficits at 1 d, 2 d, 3 d and 7 d after TBI. Our results showed that rats suffered significant behavioral and mood deficits after TBI compared to the control group, while decompressive craniectomy treatment could normalize MMP-9 expression levels and reduce hippocampal edema formation, stabilize the expression of Synapsin I, which was a potential indicator of maintaining the hippocampal synaptic function, thus counteracting behavioral but not mood decay in rats subjected to TBI. In conclusion, decompressive craniectomy, excepting for its life-saving effect, could also play a potential beneficial neuroprotective role on behavioral but not mood deficits at an early stage of moderate traumatic brain injury in rats.

Hydrogen-rich water attenuates brain damage and inflammation after traumatic brain injury in rats.

Inflammation and oxidative stress are the two major causes of apoptosis after traumatic brain injury (TBI). Most previous studies of the neuroprotective effects of hydrogen-rich water on TBI primarily focused on antioxidant effects. The present study investigated whether hydrogen-rich water (HRW) could attenuate brain damage and inflammation after traumatic brain injury in rats. A TBI model was induced using a controlled cortical impact injury. HRW or distilled water was injected intraperitoneally daily following surgery. We measured survival rate, brain edema, blood-brain barrier (BBB) breakdown and neurological dysfunction in all animals. Changes in inflammatory cytokines, inflammatory cells and Cho/Cr metabolites in brain tissues were also detected. Our results demonstrated that TBI-challenged rats exhibited significant brain injuries that were characterized by decreased survival rate and increased BBB permeability, brain edema, and neurological dysfunction, while HRW treatment ameliorated the consequences of TBI. HRW treatment also decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1ß and HMGB1), inflammatory cell number (Iba1) and inflammatory metabolites (Cho) and increased the levels of an anti-inflammatory cytokine (IL-10) in the brain tissues of TBI-challenged rats. In conclusion, HRW could exert a neuroprotective effect against TBI and attenuate inflammation, which suggests HRW as an effective therapeutic strategy for TBI patients.

Procyanidins protects against oxidative damage and cognitive deficits after traumatic brain injury.

PRIMARY OBJECTIVE: Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates the events that result in protracted neuronal dysfunction and remodeling. Importantly, antioxidants can protect the brain against oxidative damage and modulate the capacity of the brain to cope with synaptic dysfunction and cognitive impairment. RESEARCH DESIGN: To date, however, no studies have investigated the effects of procyanidins (PC) on cognitive deficits after TBI. METHODS AND PROCEDURES: In the present study, rats with controlled cortical impact (CCI) were used to investigate the protective effects of procyanidins. MAIN OUTCOMES AND RESULTS: The results showed that procyanidins reduced the level of malondialdehyde (MDA) and elevated the level of glutathione (GSH) and the activity of superoxide dismutase (SOD). In addition, treatment with procyanidins, which elevated the levels of brain-derived neurotropic factor (BDNF), phosphorylation-cAMP-response element binding protein (pCREB), total CREB, and cyclic AMP (cAMP), improved cognitive performance in the Morris water maze after TBI. CONCLUSIONS: These results suggest that procyanidins appear to counteract oxidative damage and behavioral dysfunction after TBI through antioxidant activity and the up-regulation of cAMP/CREB signaling.

A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury.

Drinking is a risk factor for traumatic brain injury (TBI), and ethanol can aggravate the outcome by promoting brain edema. The mechanism involved is not fully understood. It has been confirmed that aquaporin-4 (AQP4) and vascular endothelial growth factor (VEGF) play pivotal roles in cytotoxic/vasogenic brain edema individually, and both of these proteins are downstream regulatory factors of hypoxia-inducible factor-1α (HIF-1α). In this study, we used a fluid percussion injury (FPI) model in rats to determine the effects of acute ethanol intake on the expression levels of HIF-1α, AQP4, and VEGF prior to FPI. The animals were sacrificed 1, 2, 3, and 4 days post-injury. We found that the expression levels of HIF-1α and AQP4 were significantly upregulated in the ethanol-pretreated groups, whereas the VEGF expression level was not. In addition, there was a positive correlation between HIF-1α and AQP4. The results of this study indicate that cytotoxic brain edema may play an important role in the early stage of FPI in ethanol-pre-treated animals and that HIF-1α and AQP4 might be involved.

Clinical characteristics and prognostic analysis of recurrent hemangiopericytoma in the central nervous system: a review of 46 cases.

Central nervous system hemangiopericytoma (HPC) is a malignant vascularized mesenchymal tumor with a high rate of recurrence. Because of its rarity, few clinical characteristics and prognostic analysis information regarding recurrent HPC exist for doctors to pursue optimal outcomes. Forty-six recurrent HPC cases treated at our hospital between 2004 and 2012 were compiled into a single database based on a retrospective review of patient records, which were used to summarize the clinical characteristics. The mean survival of the recurrent HPC patients in our cohort was 41.6 ± 4.4 months, with 1-, 2-, 3-, and 4-year survival rates of 80.4, 65.2, 59.2, and 53.8 %, respectively. Thirty patients (65.2 %) suffered their first tumor recurrence, with a mean survival of 36.9 ± 4.1 months. Sixteen patients (34.8 %) suffered a second or further tumor recurrence, with a mean survival of 39.7 ± 7.0 months. Eighteen patients (39.1 %) died of all causes during the follow-up period, with a mean survival of 14.2 ± 5.6 months. Univariate and multivariate regression analyses showed that factors associated with good prognosis included recurrence age over 35 years, an interval between the first and second recurrence of more than 1 year and a clear boundary of the recurrent tumor. Gross total resection with adjuvant external beam radiotherapy could independently delay tumor recurrence of the second or more times and prolong the postoperative survival; thus, this strategy should be pursued as the initial treatment.