In recent decades, the development of the neurosurgery has changed from the traditional anatomical model to the modern anatomical-functional model. The nerve functions are maximally protected while lesions are removed as far as possible. Neurophysiological monitoring especially somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) can directly reflect the integrity of the sensory and motor nerve conduction pathways of the nervous system. At present, it has been widely used in the neurosurgery, spinal surgery, vascular surgery and other surgical fields. In recent years, more and more clinical surgeries involved spinal surgery, intraoperative neurophysiological monitoring could timely find any reversible spinal cord damage such as mechanical stretch, ischemia, and anesthetic drugs, which not only improve the quality of surgery, reduce iatrogenic spinal cord injury, but also greatly improve the prognosis of patients and reduce postoperative neurological dysfunction and complications. In this paper, the research progress of neural electrophysiological monitoring techniques in spinal cord surgery is reviewed.

Objective To explore the clinical effect of transjugular intrahepatic portosystemic shunt (TIPS) and percutaneous transhepatic variceal embolization (PTVE) on the treatment of cirrhosis with esophageal gastric varices bleeding. Methods The data of 61 patients of liver cirrhosis combined with esophageal gastric varices bleeding who underwent the interventional treatment were included in the retrospective analysis. Patients were divided into two groups, PTVE treatment group (n=42), and TIPS treatment group (n=19). The success rate of clinical treatment, the rebleeding rate, the alleviation of varicose veins, the incidence of hepatic encephalopathy, survival rate and liver function parameters were compared between two groups. Results Two groups of surgery were successful. The portal vein pressure decreased obviously in TIPS group. The rebleeding rate was higher in PTVE group (78.6%) than that in TIPS group (63.2%). The total alleviation rate of esophageal gastric varices was significantly lower in PTVE group (50.0%) than that in TIPS group (89.5%, P<0.05). The incidence rates of hepatic encephalopathy were 14.3% and 26.3% for PTVE group and TIPS group respectively. The two-year cumulative survival rates of PTVE group and TIPS group were 95.2% and 89.5% respectively, and there was no statistically significant difference between two groups. After surgery, the liver function parameters were not significantly different from those determined before the treatment in PTVE group. At 1 month and 3 months after TIPS, the liver functions were declined obviously. At 6 and 12 months after the treatment, the liver functions were not significantly different from those determined before the treatment in PTVE group. Conclusion The surgery of TIPS is safe and ideal interventional treatment for cirrhosis with esophageal gastric varices bleeding, which has the lower rebleeding rate, better esophageal gastric varices alleviation rate and long term less influence in liver function.

Objective To investigate the inhibitory effects of N-acetylcysteine (NAC) on inflammatory factors after acute spinal cord injury, and the mechanisms thereof. Methods A total of 54 clean and healthy adult female SD rats were divided into three groups according to the principle of randomization:simple laminectomy group (Sham group), spinal cord injury group (SCI group) and N-acetylcysteine group (NAC group), with 18 rats in each group. The Sham group was treated with T9-10 laminectomy only without spinal cord injury. Aneurysm clamp was used to establish rat model of T9-10 spinal cord injury in SCI group and NAC group. At the time of 15 min and 12 h after injury, the rats of NAC group were injected N-acetylcysteine intraperitoneally (150 mg/kg). At the time of 24 h post modeling, 12 rats were sacrificed in each group for observing the severity of tissue injury by using hematoxylin-eosin (HE) staining (6 rats), and detecting the contents of inflammation factors including tumor necrosis factor (TNF)- α and interleukin (IL)- 6 by using enzyme- linked immunosorbent assay (ELISA) (6 rats). The remaining 6 rats in each group were raised for 8 weeks. During the first week, the ones in NAC group were injected NAC twice a day at 12 h intervals for 7 d. Additionally, the neurological function evaluation was performed at week 1, week 2, week 4, week 6 and week 8 after injury in rats by using the spinal cord injury motor function score (BBB) and the inclined plate test. Results The results of HE staining showed that the spinal cord was intact without hemorrhage and inflammatory cell infiltration in Sham group. The morphology and inflammatory status were significantly worse in SCI group than those in NAC group and Sham group. The results of ELISA showed that the expressions of TNF-αand IL-6 were significantly higher in SCI group and NAC group than those in Sham group (P<0.05), while the expression levels of TNF-αand IL-6 were significantly lower in NAC group than those of SCI group (P<0.05). The BBB scores and inclined plate test showed that both were significantly lower in SCI group and NAC group than those of Sham group (P<0.05), and the results were better in NAC group than those of SCI group. Conclusion NAC may promote the recovery of neurological function in rats by reducing the local inflammatory response through diminishing the contents of TNF-αand IL-6 in spinal cord.

Objective To explore the neuroprotective effects ofβ-aescinate on brain edema in rats of traumatic brain injury (TBI). Methods A total of 78 male SD (Sprague Dawley) rats were randomly divided into three groups: sham-operation group (Sham), traumatic brain injury group (TBI) andβ-aescinate group, with 26 rats in each group. Rats of Sham group were anesthetized and surgically prepared only, but were not induced by cortical contusion. Electronic brain cortical damage impactor (eCCI) was used for establishing TBI model in TBI group and β-aescinate group after opening the bone window. TBI group was only established TBI model, but no intervention. After establishment of TBI model in β-aescinate group, β-aescinate (5 mg/kg body weight) was intraperitoneally injected, once every 24 hours. The modified neurological severity scores (mNSS) was used for evaluating changes of neurological function. After 48 hours, SD rats were sacrificed for hematoxylin and eosin (H&E) staining (n=6). Additionally, water content of the brain tissue was evaluated using the wet-to-dry weight ratio (n=10). Evans blue assay was performed to investigate the blood-brain barrier (BBB) permeability (n=4). The expression of aquaporin 4 (AQP4) was measured by Western blot assay (n=6). Results Compared with the Sham group, neurologic deficit, increased brain water content and the expression of AQP4 were found in TBI group (all P<0.05). Moreover, BBB permeability was destroyed. However, β-aescinate can improve the neurological function, reduce the brain water content and significantly decrease the expression of AQP4 in TBI rats. The BBB permeability was significantly improved in treatment group (all P<0.05). Conclusion These findings suggest that β-aescinate can reduce cerebral edema and improve neurological outcome in SD rats after TBI. This neuroprotection may be related with the down-regulation of AQP4 protein.