Delayed Facial Palsy After Microvascular Decompression for Hemifacial Spasm.

OBJECTIVE: We explored the risk factors for the occurrence of delayed facial paralysis (DFP) after microvascular decompression (MVD) for hemifacial spasm (HFS). METHODS: A retrospective study was conducted of 636 patients who had undergone MVD for HFS by the same neurosurgery department of China-Japan Friendship Hospital from January 2006 to May 2016. Of the 636 patients, 50 (7.9%) had presented with DFP, which had developed from 2 to 60 days postoperatively (average, 12.9 ± 10.0005 days). All 50 patients with DFP had recovered completely within 10-300 days (average, 88.7 ± 61.389 days) after the onset of DFP. We randomly selected 100 patients from the 586 patients without DFP as the control group. Univariate and multivariate logistic analyses were used to analyze the risk factors involved in the occurrence of DFP. RESULTS: Univariate analysis showed that the disease course was the only factor associated with the development of DFP (P = 0.003). Furthermore, on multivariate logistic analysis, the course of HFS was the only risk factor associated with the development of DFP (P = 0.01). Additionally, the Spearman test revealed a positive correlation between the onset of DFP and the duration of the DFP symptoms (rs = 0.682; P < 0.001). CONCLUSION: Although DFP frequently occurred after MVD, it can recover spontaneously. The longer the course of HFS, the more frequently DFP will occur after MVD. The earlier that DFP develops, the shorter will be the time to recovery.

Danhong Injection Alleviates Mechanical Allodynia via Inhibiting ERK1/2 Activation and Elevates BDNF Level in Sciatic Nerve in Diabetic Rat.

Danhong injection (DHI) has been widely used in China for cardiocerebrovascular diseases treatments. And in this study, we demonstrated the therapeutic effect of DHI on experimental diabetic neuropathy for the first time. Methods. Streptozotocin- (STZ-) induced SD rats were used. In experiment 1, 4-week treatment with DHI or saline started 4 weeks after STZ injection; mechanical allodynia was measured before and every 2 weeks after STZ injection. In experiment 2, chronic intrathecal infusion of U0126 was conducted during the 8th week of diabetes. Phosphorylated and total ERK1/2 in spinal cord were analyzed by western blot. BDNF level in sciatic nerve was evaluated by ELISA. Results. DHI treatment significantly alleviated mechanical allodynia at the end of the study and downregulated the expression of phosphorylated ERK1/2 in spinal cord. In addition, DHI treatment also elevated brain-derived neurotrophic factor (BDNF) level in sciatic nerve of DPN rat. In experiment 2, inhibition of ERK1/2 activation was confirmed to result in the alleviation of mechanical allodynia. Conclusions. We demonstrated that DHI was able to alleviate mechanical allodynia in diabetic neuropathy rat through inhibiting the activation of ERK1/2. The reduction of BDNF content in sciatic nerve was also partially reversed by DHI treatment.

Two-Point Discrimination Predicts Pain Relief after Lower Limb Nerve Decompression for Painful Diabetic Peripheral Neuropathy.

BACKGROUND: Peripheral nerve decompression surgery has been reported to be effective for pain reduction in patients with painful diabetic peripheral neuropathy. The aim of this study was to characterize which patients may have more pain relief benefits in the lower limbs after nerve decompression surgery. METHODS: A retrospective study was conducted. Pain levels were measured with the Numerical Rating Scale. Treatment effects were classified by either substantial relief (at least 50 percent reduction in Numerical Rating Scale score compared with preoperative Numerical Rating Scale score) or nonsubstantial relief (<50 percent reduction or worse in Numerical Rating Scale score) at 12 months based on established criteria. Sex, age, body mass index, duration of diabetes mellitus, duration of diabetic peripheral neuropathy pain, preoperative Numerical Rating Scale score, and two-point discrimination were evaluated using univariate and logistic regression analysis. RESULTS: The mean preoperative Numerical Rating Scale score (8.65 ± 1.29) decreased significantly 6 days (3.56 ± 2.22; p < 0.01), 6 months (3.03 ± 2.11; p < 0.01), and 12 months (3.44 ± 2.36; p < 0.01) after surgery; 64.7 percent of patients had substantial pain relief at 12 months. According to univariate and logistic regression analysis, better two-point discrimination was associated with substantial pain relief (OR, 3.700; p = 0.046, logistic regression analysis). CONCLUSIONS: Nerve decompression surgery was able to alleviate pain in patients with painful diabetic peripheral neuropathy. Two-point discrimination may be a predictive factor for the prognosis of painful diabetic peripheral neuropathy after nerve decompression surgery. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, III.

Tanshinone IIA Improves Painful Diabetic Neuropathy by Suppressing the Expression and Activity of Voltage-Gated Sodium Channel in Rat Dorsal Root Ganglia.

Painful diabetic neuropathy (PDN) is one of the intractable complications of diabetes mellitus, which manifest as exaggerated pain perception. Previous studies showed that Tanshinone IIA (TIIA), one of the major bioactive extracts of Salvia miltiorrhiza Bunge, have obvious analgesic effect on different types of pain process, and the underlying analgesic mechanisms are not fully understood. The present study combined the behavioral, electrophysiological and biochemical methods to elucidate the analgesic mechanism of TIIA, using streptozotocin (STZ)-induced PDN rat models. Intraperitoneal injection (i.p.) of TIIA for 3 weeks in PDN rats significantly improved mechanical allodynia and thermal hyperalgesia. Patch clamp recordings showed that the excitability of dorsal root ganglion (DRG) nociceptive neuron was increased in diabetic state, and TIIA treatment effectively recovered the subnormality, which was achieved by preventing augments of both Tetrodotoxin-sensitive (TTX-resistant) and Tetrodotoxin-sensitive (TTX-S) sodium currents. Further, the protein expressions of voltage-gated sodium channels (VGSCs) α-subunits Nav1.3, Nav1.7 and Nav1.9 increased in DRG of diabetic rats and were normalized by TIIA application. In conclusion, this study provides evidence that the TIIA attenuated PDN by effecting VGSCs activities and expressions, indicating that the TIIA could be a promising agent for PDN treatment.

Enhanced Neuroprotective Effects of Coadministration of Tetrandrine with Glutathione in Preclinical Model of Parkinson's Disease.

Aim. In this study we examined the influence of tetrandrine (Tet) on the neuroprotective effects of glutathione (GSH) in the 6-hydroxydopamine- (6-OHDA-) lesioned rat model of Parkinson's disease (PD). Methods. Levels in the redox system, dopamine (DA) metabolism, dopaminergic neuronal survival, and apoptosis of the substantia nigra (SN) and striatum, as well as the rotational behavior of animals were examined after a 50-day administration of GSH + Tet (or GSH) and/or L-3,4-dihydroxyphenylalanine (L-dopa) to PD rats. Ethics Committee of Huashan Hospital, Fudan University approved the protocol (number SYXK2009-0082). Results. Administration of GSH or Tet alone did not show any significant effects on the factors evaluated in the PD rats. However, in the GSH + Tet group, we observed markedly decreased oxidative damage, inhibition of DA metabolism and enhanced DA synthesis, increased tyrosine hydroxylase- (TH-) immunopositive neuronal survival, and delayed apoptosis of dopaminergic neurons in the SN. Animal rotational behavior was improved in the GSH + Tet group. Additionally, coadministration of GSH + Tet appeared to offset the possible oxidative neurotoxicity induced by L-dopa. Conclusion. In this study, we demonstrated that tetrandrine allowed occurrence of the neuroprotective effect of glutathione probably due to inhibition of P-glycoprotein on 6-hydroxydopamine-lesioned rat models of Parkinson's disease, including rats undergoing long-term L-dopa treatment.

Glutathione prevents free fatty acids-induced oxidative stress and apoptosis in human brain vascular endothelial cells through Akt pathway.

AIMS: The damage of human brain vascular endothelial cells (HBVECs) is the key pathogenesis of diabetes-associated cerebral vascular complications. The aim of this study was to elucidate the effects of glutathione (GSH) on free fatty acids (FFAs)-induced HBVECs apoptosis, oxidative stress, and the involved possible signaling pathway. METHODS: After culturing HBVECs for 72 h with GSH and FFAs, we determined cell proliferation by CCK8, detected apoptosis by caspase-3 and Annexin V-FITC/PI staining, and judged oxygen stress by determining the reactive oxygen species (ROS) and the mitochondrial membrane potential (MMP). We investigated whether the Akt pathway was involved in FFAs-induced signaling pathway alteration and whether GSH influenced the above effects. RESULTS: After being cultured in 200 µM FFAs for 72 h, the HBVECs proliferation significantly decreased; HBVECs apoptosis increased; the ROS levels increased; and the HBVECs MMP subsequently decreased. FFAs induced a significant decrease in phosphorylated active Akt. These alterations were obviously prevented when 1 mM GSH was added to culture medium containing FFAs, and the above effects of GSH were blocked by Akt inhibitor. CONCLUSION: GSH may prevent FFAs-induced HBVECs damage, oxidative stress, and apoptosis through activating the Akt pathway.