Peripheral nerve hyperexcitability syndrome: A clinical, electrophysiological, and immunological study.

INTRODUCTION: Peripheral nerve hyperexcitability syndrome (PNHS) is characterized by muscle fasciculations and spasms. Nerve hyperexcitability and after-discharges can be observed in electrophysiological studies. Autoimmune mechanisms play a major role in the pathophysiology of primary PNHS. METHODS: We retrospectively conducted a case-control study recruiting patients with clinical and electrophysiological features of PNHS. Control patients were diagnosed with other neuronal or muscular diseases. Contactin-associated protein2 (CASPR2) and leucine-rich glioma-inactivated1 (LGI1) antibodies were examined. RESULTS: A total of 19 primary PNHS patients and 39 control patients were analyzed. The most common symptoms for the case group were fasciculations (11/19) and muscle spasms (13/19). Case group patients were likely to demonstrate electrodiagnostic findings of nerve hyperexcitability (17/19) and after-discharges in the tibial nerve (19/19). We found high prevalence of CASPR2 (9/19) and LGI1 (6/19) antibodies in the case group. DISCUSSION: Primary PNHS patients were likely to show after-discharges in the tibial nerve. The pathogenesis of PNHS is autoimmune CASPR2 and LGI1 antibodies are possible pathogenic antibodies for primary PNHS.

[Expression of cyclophilin A/CD147 in carotid atherosclerotic plaque and the intervention of atorvastatin].

OBJECTIVE: To explore the expression of CyPA and CD147 in rabbit models of vulnerable carotid atherosclerotic plaque and the therapeutic effect of atorvastatin.
 METHODS: Twenty-four male New Zealand rabbits were randomly divided into 3 groups. Eight rabbits were served as a normal diet group (Group A), and the remaining 16 rabbits underwent balloon-induced endothelial injury in the right carotid artery and thereafter were fed on high-cholesterol diet (1% cholesterol) for 12 weeks, then they were divided into 2 groups: a AS group (Group B), an atorvastatin group [Group C, 2.5 mg/(kg.d)]. 4 weeks later, plaque disrupture was triggered by China Russell's viper venom and histamine. Serum levels of TC, TG, LDL-C and HDL-C were measured at different timepoint. The damaged carotid arteries were collected to undergo pathological examination. The macrophage, expression of CyPA and CD147 were detected by immuno-histochemical analysis, and the mRNA levels of CyPA and CD147 were examined by reverse transcription polymerase chain reaction (RT-PCR).
 RESULTS: Compared with the Group A, the serum levels of TC and LDL-c in the Group B and Group C were significantly increased (all P<0.01). Compared with the Group B, the serum levels of TC and LDL-c in the Group C were reduced significantly after atorvastatin intervention for 4 weeks (all P<0.01). The plaques disruption and thrombosis occurred in 4 out of the 6 rabbits in the Group B, while only 1 rabbit demonstrated plaques disruption and thrombosis in the Group C. Compared with the Group B, the levels of CyPA, CD147 and macrophage in carotid atherosclerotic plaque in the Group C were decreased significantly (all P<0.01).
 CONCLUSION: The up-regulation of CyPA and CD147 may be involved in pathogenesis of vulnerable carotid atherosclerotic plaque. Atorvastatin could stabilize the plaque through inhibiting the CyPA and CD147 expression.

[Perioperative intensive statin therapy improves outcomes in patients with ischemic stroke undergoing middle cerebral artery stent implantation].

OBJECTIVE: To investigate whether intensive statin therapy during the perioperative period improves outcomes in patients undergoing middle cerebral artery (MCA) stent implantation for ischemic stroke. METHODS: Forty patients with ischemic stroke undergoing delayed stent implantation in our department from January, 2010 to November, 2014 were randomized to intensive statin group (atorvastatin, 80 mg/day, 3 days before till 3 days after intervention; n=20) and standard therapy group (atorvastatin, 20 mg/day, n=20). All the patients received long-term atorvastatin treatment thereafter (20 mg/day). Serum levels of C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1), and soluble extracellular matrix metalloproteinase inducer (EMMPRIN/CD147) were measured at 24 h before and 24 h after the intervention. The primary end point was procedure-related intra-stent thrombosis, 1-month incidence of major adverse cerebrovascular events (stroke, transient ischemic attack, in-stent restenosis, death or unplanned revascularization). RESULTS: The basic clinical data were similar between the two groups before the intervention (P>0.05). In the intensive therapy group, the levels of CRP, VCAM-1, and sCD147 were significantly lower at 24 h after the intervention than the levels before intervention (P<0.05) and the postoperative levels in the standard therapy group (P<0.05). The levels of CRP, VCAM-1, and sCD147 were all increased after the intervention in the standard therapy group (P>0.05). The incidence of primary end point was lower in intensive therapy group than in standard therapy group (P<0.05). CONCLUSION: In patients undergoing MCA intravascular stent implantation for ischemic stroke, perioperative intensive statin therapy improves the patients' outcomes, reduces the levels of CRP, VCAM-1 and sCD147 molecules, and lowers the incidences of cerebrovascular events.

Effect of minocycline on carotid atherosclerotic plaques.

OBJECTIVES: To investigate whether minocycline could attenuate the expression of extracellular matrix metalloproteinase inducer (CD147) and matrix metalloproteinase (MMP)-9 and enhance stability of atherosclerotic plaques. METHODS: Twenty-four New Zealand rabbits underwent balloon-induced endothelial injury of right carotid artery and were fed 1% cholesterol diet for 16 weeks. From week 12 to week 16, the animals were intervened with minocycline (2·5 mg kg(-1) d(-1), group A), atorvastatin (2·5 mg kg(-1) d(-1), group B) or were not treated with drugs (group C). After 16 weeks, all the rabbits were sacrificed by Chinese Russell's viper venom and histamine injection, then serum and right common carotid arteries were collected for biochemical, histological, and reverse transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: A rabbit model of atherosclerotic vulnerable plaques was established. Minocycline significantly increased the thickness of the plaque fibrous caps and decreased the positive staining area of macrophages in group A. When compared with group C, CD147, and MMP-9 expression in both mRNA and protein level were remarkably reduced in group A and B (P < 0·05). However, there was no significant difference between group A and B. Serum TC and low-density lipoprotein cholesterol (LDL-C) levels were decreased in the Atorvastatin group (P < 0·05), while minocycline had no obvious influence on the serum lipid levels. The incidence of plaque ruptures in group A (14·3%) and group B (14·3%) was lower than that in group C (66·7%, P < 0·05). CONCLUSIONS: Minocycline intervention significantly reduced the activity of CD147, MMP in plaque and histologically enhanced plaque stabilization. Minocycline was equally effective as Atorvastatin.