A correlative analysis between inflammatory cytokines and trigeminal neuralgia or hemifacial spasm.

BACKGROUND: It is necessary to understand the mechanism of trigeminal neuralgia (TN) and hemifacial spasm (HFS) in order to seek for an effective noninvasive remedy. As previous studies implied that inflammatory cytokines induced by demyelination following the nerve injury may be the initiated factor causing neuropathic pain, we attempt to analyze the correlation between cytokines and these hyperactive cranial nerve disorders. METHOD: The consecutive patients whose diagnosis were confirmed by microvascular decompression surgery as primary TN or HFS caused by vascular compression and healthy volunteers between March and May 2018 in XinHua Hospital Shanghai JiaoTong University School of Medicine were recruited. Preoperatively, venous blood was collected and the protein concentrations of IL-1ß, IL-2, IL-6, IL-8, IL-10, TNF-α and IFN-γ were determined with ELISA. Each cytokine was compared between the patients and healthy volunteers. RESULTS: Ultimately, 28 healthy volunteers as well as 44 TN and 47 HFS patients were enrolled in this investigation. The serum levels of IL-1ß, IL-6, IL-8 and TNF-α in either HFS or TN patients were significantly higher than that in healthy volunteers (p < 0.05), yet which were similar between TN and HFS patients (p > 0.05). Besides, there was a significantly correlation between IL-6 concentration and severity of HFS (r = 0.933, p < 0.05) or TN (r = 0.943, p < 0.05). DISCUSSION: Vascular compression of trigeminal or facial nerve roots may induce a rise in variety of cytokines, and IL-6 may play an important role in the signaling pathways to generate ectopic impulses from these cranial nerves.

Comparison of serum concentration of Ca, P, Mg, and Fe between hemifacial spasm patients and healthy controls; prospective randomized controlled study.

PURPOSE: In this study, we aimed to measure the serum vitamin D level in hemifacial spasmic (HFS) patients and show the role of HFS in the pathogenesis and place in etiology. MATERIALS AND METHODS: This study included 43 prospective newly diagnosed HFS patients and 43 healthy volunteers in the neurology clinic. The serum (Ca, P, Mg, Fe) concentration of 4 essential elements was measured with a biochemical device. The groups were correlated in terms of four essential element concentrations. The severity of the disease was measured using Lee's Quality of Life Scale and correlated with the concentration of four trace elements. The results were compared using the independent t-test and Mann-Whitney U-test. RESULTS: Concentration of serum Ca, P, and Mg in the HFS patients was found to be lower in the control group which was statistically significant (P < 0.05). There was no statistically difference between the groups in terms of Fe concentration (P > 0.05). There was no significant correlation between trace element concentration and severity of illness and daily life quality in the patient group. CONCLUSION: These results show us the role of HFS in the pathogenesis of these four trace elements and the importance of its location in etiology. We think that changes in the concentration of trace elements in HFS can lead to demyelinization, which may lead to spasm.

Blepharospasm with elevated anti-acetylcholine receptor antibody titer.

OBJECTIVES: To determine whether serum levels of anti-acetylcholine receptor antibody (anti-AChR-Abs) are related to clinical parameters of blepharospasm (BSP). METHODS: Eighty-three adults with BSP, 60 outpatients with hemifacial spasm (HFS) and 58 controls were recruited. Personal history, demographic factors, response to botulinum toxin type A (BoNT-A) and other neurological conditions were recorded. Anti-AChR-Abs levels were quantified using an enzyme-linked immunosorbent assay. RESULTS: The anti-AChR Abs levels were 0.237 ± 0.022 optical density units in the BSP group, which was significantly different from the HFS group (0.160 ± 0.064) and control group (0.126 ± 0.038). The anti-AChR Abs level was correlated with age and the duration of response to the BoNT-A injection. CONCLUSION: Patients with BSP had an elevated anti-AChR Abs titer, which suggests that dysimmunity plays a role in the onset of BSP. An increased anti-AChR Abs titer may be a predictor for poor response to BoNT-A in BSP.

Blepharospasm with elevated anti-acetylcholine receptor antibody titer / Blefaroespasmo com título elevado de anticorpos antirreceptores de acetilcolina

ABSTRACT Objective: To determine whether serum levels of anti-acetylcholine receptor antibody (anti-AChR-Abs) are related to clinical parameters of blepharospasm (BSP). Methods: Eighty-three adults with BSP, 60 outpatients with hemifacial spasm (HFS) and 58 controls were recruited. Personal history, demographic factors, response to botulinum toxin type A (BoNT-A) and other neurological conditions were recorded. Anti-AChR-Abs levels were quantified using an enzyme-linked immunosorbent assay. Results: The anti-AChR Abs levels were 0.237 ± 0.022 optical density units in the BSP group, which was significantly different from the HFS group (0.160 ± 0.064) and control group (0.126 ± 0.038). The anti-AChR Abs level was correlated with age and the duration of response to the BoNT-A injection. Conclusion: Patients with BSP had an elevated anti-AChR Abs titer, which suggests that dysimmunity plays a role in the onset of BSP. An increased anti-AChR Abs titer may be a predictor for poor response to BoNT-A in BSP.

RESUMO Objetivo: Determinar se os níveis séricos do anticorpo antirreceptor de acetilcolina (anti-AChR-Abs) estão relacionados aos parâmetros clínicos do blefaroespasmo (BSP). Métodos: Fora recrutados 83 adultos com BSP, 60 pacientes ambulatoriais com espasmo hemifacial (HFS) e 58 controles. Foi aplicado um questionário para registrar história pessoal, fatores demográficos, resposta à toxina botulínica tipo A (BoNT-A) e outras condições neurológicas. Os níveis de anti-AChR-Abs foram quantificados usando um ensaio imunoenzimático. Resultados: O nível de anti-AChR-Abs foi de 0,237 ± 0,022 unidades de densidade óptica (OD) no grupo BSP, significativamente diferente em comparação com o grupo HFS (0,160 ± 0,064) e o grupo controle (0,126 ± 0,038). O nível de anti-AChR-Abs se correlacionou com a idade e a duração da resposta à injeção de BoNT-A. Conclusão: Pacientes com BSP apresentaram títulos elevados de anti-AChR-Abs, o que sugere que a desimunidade desempenha um papel no surgimento de BSP. O aumento do título de anti-AChR-Abs pode ser um preditor de resposta insuficiente à BoNT-A em BSP.

The role of genetic factors in the development of hemifacial spasm: preliminary results.

Hemifacial spasm (HFS) has been reported to result from vascular compression of the facial nerve at the root entry zone. The pathogenesis of HFS is not completely understood. Some study groups described that the vascular compression was due to the morphological changes of the vessel such as vertebral artery shifting. In this study, radiological evidence of VA shifting was identified in 26 (59.1%) of 44 patients with 3D-TOF MRA. We hypothesized that a genetic factor might be present for vascular change and tried to find out the role of a genetic factor more susceptible to vascular change causing vascular compression. We examined a single nucleotide polymorphism (SNP) in the genes related to vascular change such as methylenetetrahydrofolate reductase (MTHFR), thymidylate synthase enhancer region (TSER), endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor (VEGF) polymorphisms. 43 HFS patients and 207 healthy controls were genotyped and fasting plasma homocysteine (pHcy) concentrations were measured. The SNPs were genotyped using polymerase chain reaction (PCR) amplification followed by digestion with the restriction enzyme. The pHcy levels were not significantly different between HFS patients and controls. No association was detected between the SNPs in the selected genes and susceptibility to HFS. However, further study will be needed to confirm these findings.