Effect of hyperbaric oxygen treatment on patients with heatstroke complicated by multiple organ dysfunction:A retrospective study.

Background: The benefits of hyperbaric oxygen (HBO) in treating animals with heat stroke (HS) have been established. This study aims to retrospectively analyze the effect of HBO on multiple organ dysfunction following HS in humans. Methods: Retrospective data were collected from patients with HS admitted to our hospital in the past 7 years. Patients were categorized into groups based on whether they received HBO therapy. The study compared various factors, including sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation-Ⅱ (APACHE-Ⅱ) scores, mortality rates, neurological function scores, serum myocardial enzyme levels, liver, kidney, and coagulation function indicators, blood routine results, electrolyte levels, and modified Barthel index (MBI) score for standard daily living ability before treatment and after 2 and 4 weeks of treatment. Results: The mortality rates in the HBO and control group were 0% and 8.49%, respectively. Upon admission, the HBO group had higher SOFA and APACHE-Ⅱ scores and lower neurological, coagulation, and liver functions than those of the control group. HBO treatment significantly improved SOFA, APACHE-Ⅱ, and neurological scores while relieving levels of alanine aminotransferase, aspartate aminotransferase, creatinine, and myocardial enzymes. Additionally, it mitigating lymphocyte and platelet count decline caused by HS. The MBI score was significantly enhanced after treatment in the HBO group. Conclusions: Clinical practice advocates administering HBO therapy to patients with severe illness, organ damage, and nerve impairment. Compared with conventional treatment, combined HBO therapy demonstrated superior efficacy in alleviating multiple organ dysfunction and improving daily living ability in patients with HS.

Analysis of Clinical Symptoms of Guillain-Barré Syndrome Induced by Heat Stroke: Three Case Reports and Literature Review.

Background: Heat stroke is a potentially fatal condition that is caused by elevated core temperature. Guillain-Barré syndrome (GBS) induced by heat stroke is extremely rare and has only been reported in few case reports. The purpose of this case study was to evaluate the clinical symptoms, neuroelectrophysiological and imageological features of GBS after heat stroke. Methods: We reviewed our hospital records and previously published reports to find the cases of GBS after heat stroke. The clinical, imageological, and electrophysiological profiles, treatment and prognosis were presented and analyzed. Results: We retrieved three cases of GBS induced by heat stroke from our hospital, which presented as lesions on multiple cranial and peripheral nerves and albuminocytologic dissociation in the cerebrospinal fluid. All of these patients had disorders of consciousness at the early stage of heat stroke and a "pseudo-recovery period" after they recovered from coma after heat stroke. After immunoglobulin administration and immunoregulation therapy, these patients' neurological deficiencies were relieved significantly. But there are still disabilities and almost totally reliant on others. Conclusions: The number of the cases of GBS induced by HS reported in this study has been the most in the recent 5 years. Clinicians should pay attention to patients with heat stroke with sustained coma and the sudden quadriplegia. Early, exact and timely diagnosis and treatment of GBS need to be performed, to accelerate recovery and improve prognosis.

Memantine ameliorates tau protein deposition and secondary damage in the ipsilateral thalamus and sensory decline following focal cortical infarction in rats.

Previous studies have reported that memantine presents evidence of therapeutic benefits in several animal models of ischemic stroke and neurodegenerative diseases. However, the effect of memantine on secondary damage in the ipsilateral thalamus after focal cortical infarction remains undefined. Present study investigated whether memantine has a protective effect on secondary damage in the ipsilateral thalamus after focal cerebral infarction in rats. At 24 h after distal middle cerebral artery occlusion (MCAO), rats in the memantine and vehicle groups were intraperitoneal injected with memantine and isopycnic vehicle, respectively, was once daily administered for consecutive 7 days. Infarct size was evaluated through Nissl staining and sensory decline determined using adhesive removal test. Secondary thalamic damage was assessed using Nissl staining and immunofluorescence 8 days after MCAO. Immunoboltting was used to identify tau and apoptosis-associated proteins in the ipsilateral thalamus after MCAO. Results revealed that memantine ameliorated sensory decline compared to the vehicle controls. Subsequently, tau phosphorylated at threonine 231 (p-tau-231), glycogen synthase kinase3ßpY216 (GSK3ßpY216) and protein phosphatase 2A (PP2ApY307) were reduced by memantine, causing greater reduction in neuronal loss and inhibition of reactive astrogliosis in the ipsilateral ventroposterior thalamic nucleus (VPN) compared with the vehicle groups. In addition, increase in secondary damage-induced TUNEL-positive cells was blunted by memantine, as demonstrated by the significant reduction in expression of apoptosis-associated proteins. Our results suggest that memantine has a neuro-protective effect on secondary damage in the ipsilateral thalamus following MCAO by inhibiting the activity of GSK3ßpY216/PP2ApY307 and down regulating the levels of p-tau-231 protein.

[Factors affecting recovery of consciousness in patients with disorders of consciousness following brain trauma: a logistic regression analysis].

OBJECTIVE: To explore the factors that affect the recovery of consciousness in patients with disorders of consciousness following brain trauma. METHODS: We analyzed the data of 114 patients with disorders of consciousness following brain trauma admitted for rehabilitation. Bilateral logistic regression analysis was used to explore the factors that affected the recovery of the patients' consciousness. A logistic regression model was established and the ROC curve was drawn to obtain the optimal threshold of the prognostic model. RESULTS: Univariate analysis showed that vegetative state duration (P<0.001), CRS-R scores (P<0.001), hydrocephalus (P=0.037), hypertonia (P=0.034), central fever (P=0.035), paroxysmal sympathetic hyperactivity (PSH) (P=0.004), and epilepsy seizures were correlated with the recovery of consciousness. Logistic multivariate analysis showed that central fever (OR=3.493, P=0.044), vegetative state duration (OR=1.016, P=0.008), PSH (OR=4.223, P=0.034) and CRS-R scores (OR=0.640, P=0.002) all significantly affected the recovery of consciousness. The χ2 value of the Hosmer-Lemeshow test was 10.214 (P=0.250), and the goodness of fit of this model indicated an outstanding fitting (c=0.91). CONCLUSIONS: The presence of PSH is the one of the most important factor followed by centric fever to affect the outcome of patients with disorders of consciousness. A lower CRS-R score and a longer duration of vegetative state also predict a poor recovery of consciousness in these patients.