[Brain Protection of Muscone in Rats with Brain Injury].

OBJECTIVE: To observe cerebral protective effect of muscone (nasal administration) on traumatic brain injury model rats. METHODS: SD rats were divided into the sham-operation group, the model group, and the treatment groups according to random digit table, 50 in each group. Traumatic brain injury model was established by controlled cortical strike. Rats in the sham-operation group received surgery and anesthesia procedures only, with no strike. Muscone (1.8 mg/kg) was delivered to rats in the treatment group using in situ nasal perfusion, 30 min each time, twice daily for 7 successive days. Water content of brain tissue was detected in each group before intervention (T1), at day 3 of intervention (T2), day 5 of intervention (T3), and after intervention (T4), respectively. Expression levels of brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were detected using immunohistochemical analysis. RESULTS: Compared with the sham-operated group, water content of brain tissue increased (P < 0.05), and expression levels of NGF and BDNF decreased in the model group at T1, T2, T3, and T4 (P <0. 01). Compared with the model group, water content of brain tissue decreased (P < 0.05), and expression levels of NGF and BDNF increased (P < 0.01) in the treatment group at T1, T2, and T3. CONCLUSION: Nasal administration of muscone could reduce water content of brain tissue, alleviate cerebral edema, promote secretion of BDNF and NGF by olfactory ensheathing cells in traumatic brain injury rats.

[Treatment of Idiopathic Normal-Pressure Hydrocephalus by Wuling Powder Combined Ventriculo- peritoneal Shunt Surgery: an Efficacy Observation].

Objective To observe the clinical efficacy of Wuling Powder (WP) combined ventricu- loperitoneal shunt surgery in patients with idiopathic normal-pressure hydrocephalus (INPH). Methods Totally 56 INPH patients were randomly assigned to the control group and the treatment group, 28 in each group. All patients received ventriculoperitoneal shunt surgery. Three days after surgery patients in the treatment group took WP, while those in the control group took placebo decoction (one dose per day, once in the morning and once in the evening, 7 days as one course, a total of 6 courses after surgery). Mini- Mental State Examination (MMSE) score, the steps to turn around 180°, and Evan's index were tested be- fore surgery and 3 months after surgery. Adverse reactions were recorded in the two groups. Clinical effica- cy was assessed after 3 months of surgery. Results At month 3 after surgery 21 patients (80. 8%) were cured and 3 patients (11. 5%) were improved in the treatment group, with statistical difference when com- pared with the control group [14 cured (51. 9%) and 11 improved (40. 7%) ; P <0. 05]. Compared with be- fore surgery in the same group, levels of MMSE score increased and the steps to turn around 1800 were obviously reduced in the two groups at month 3 after surgery (both P <0. 05). Compared with the control group at month 3 after surgery, levels of MMSE score increased and the steps to turn around 1800 were ob- viously reduced in the treatment group (both P <0. 05). Conclusion In treating INPH patierts, WP com- bined ventriculoperitoneal shunt surgery was superior to the effect of using ventriculoperitoneal- shunt sur- gery alone.

Prognostic value of leptin: 6-month outcome in patients with intracerebral hemorrhage.

Leptin has recently been discussed as a novel biomarker for the clinical outcome of critical illness. This study aims to investigate the prognostic value of leptin with regard to long-term clinical outcomes in patients with intracerebral hemorrhage. In 50 healthy controls and 92 patients with acute spontaneous basal ganglia hemorrhage presenting to the emergency department of a large primary care hospital, we measured plasma leptin levels using an enzyme-linked immunosorbent assay in a blinded fashion. Plasma leptin levels on admission were considerably higher in patients than healthy controls. A significant correlation emerged between plasma leptin level and National Institutes of Health Stroke Scale score. A multivariate analysis identified plasma leptin level as an independent predictor for 6-month clinical outcomes including 6-month mortality and unfavorable outcome (Modified Rankin Scale score>2). Using receiver operating characteristic curves, we calculated areas under the curve for 6-month clinical outcomes. The predictive performance of leptin was similar to, but did not obviously improve that of National Institutes of Health Stroke Scale scores. Thus, leptin may help in the prediction of 6-month mortality and unfavorable outcome after intracerebral hemorrhage.

Copeptin is associated with one-year mortality and functional outcome in patients with acute spontaneous basal ganglia hemorrhage.

High plasma copeptin levels have been found to be associated with short-term poor outcome after intracerebral hemorrhage (ICH). We furthermore evaluate the relation of plasma copeptin levels to long-term outcome and early neurological deterioration after ICH. Fifty healthy controls and 89 patients with acute spontaneous basal ganglia hemorrhage were recruited in this study. Plasma copeptin concentrations on admission measured by enzyme-linked immunosorbent assay were considerably high in patients than healthy controls. A multivariate analysis identified plasma copeptin level as an independent predictor for 1-year mortality, 1-year unfavorable outcome (modified Rankin Scale score>2) and early neurological deterioration. A receiver operating characteristic curve showed that the predictive value of plasma copeptin concentration was similar to that of National Institutes of Health Stroke Scale scores for long-term poor outcome and early neurological deterioration. However, copeptin did not obviously improve the predictive values of National Institutes of Health Stroke Scale scores. Thus, increased plasma copeptin level is an independent prognostic marker of 1-year mortality, 1-year unfavorable outcome and early neurological deterioration after ICH.