People with epilepsy often have other comorbidities (such as depression, stroke, obesity, migraine, autism spectrum disorder, anxiety, bipolar disorder, attention deficit hyperactivity disorder, etc.). Approximately 50% of adults with active epilepsy have at least one Comorbidities of epilepsy. Epilepsy comorbidities are often associated with worse quality of life and prognosis. Vagus nerve stimulation (VNS) is a neuromodulation technique that relies on electrical stimulation and was approved by the Food and Drug Administration (FDA) in 1997 for the treatment of epilepsy. In the process of exploring the efficacy and mechanism of VNS in the treatment of epilepsy, an additional benefit was unexpectedly found, that is, VNS can meliorate symptoms of a variety of comorbidities. Since the FDA approved VNS for the treatment of depression in 2005, VNS has shown increasingly bright prospects in the treatment of comorbidities. In addition to the approved indications, including depression, stroke, obesity and migraine, VNS in other neuropsychiatric comorbidities have shown great potential. From invasive implantable VNS (iVNS) to non-invasive transcutaneous VNS (tVNS), studies on the benefits of VNS in the treatment of epilepsy and its Comorbidities are also evolving. This article reviews the progress of clinical treatment and mechanism of VNS in the treatment of epilepsy comorbidities in recent years, with the aim to provide the best treatment strategy for epilepsy patients and research basis for scientific researchers. At the same time, the parameter Settings of previous and latest clinical trials of VNS for the treatment of epilepsy comorbidity were summarized and analyzed to provide more references for the clinical application of VNS.
ObjectiveTo determine the outcome of antiepileptic drugs (AEDs) withdrawal in patients who had been seizure-free for more than two years. MethodsPatients with epilepsy who had been seizure-free for at least two years and decided to stop AEDs therapy gradually were checked on every two months for seizure relapse. The inclusion criteria were:①diagnosis of epilepsy, defined as at least two unprovoked seizures at least 24 hours apart; ②patients remained seizure-free for at least 24 consecutive months during AEDs therapy; ③patients expressed a desire to discontinue AEDs therapy gradually and agreed to return for regular follow-ups; and④electroencephalogram (EEG) showed no epileptic discharge. The time to a seizure relapse and predictive factors were analyzed by survival methods, including sex; age at seizure onset; number of episodes; seizure-free period before AEDs withdrawal; duration of follow-up after AEDs withdrawal; AEDs tapering off period (taper period); results from brain MRI; EEG before seizure-free; EEG before drug withdrawal; seizure type (classified as generalized, partial, or multiple types based on history); the number of AEDs administered for long-term seizure control. A log-rank test was used for univariate analysis, and a Cox proportional hazard model was used for multivariate analysis. ResultsSixty-eight patients (39 male, 29 female) were admithed. The relapsed rate was 23.5%. Univariate analysis and multivariate Cox regression analysis indicated that multiple AEDs, hippocampal sclerosis and withdrawal time were significantly correlated with seizure recurrence and those were significant independent predictive factors, with hazard ratio were 0.861, 2.223 and 2.137 respectively. ConclusionsThe relapsed rate in our study was similar to other studies. Distinguishing variables, such as multiple AEDs, hippocampal sclerosis and withdrawal time, need to be considered when decide to withdraw. Therefore, our recommendation is that after two years of being seizure-free, patients could consider withdrawal unless they are hippocampal sclerosis patients.
ObjectiveThrough Sequenom iPEX system analyzed the genetic susceptibility in patients with Medial temporal lobe epilepsy (MTLE) which screening hyperpolarization-activated cyclic nucleotide gated channel (HCN) subunit HCN1 and HCN2 single nucleotide polymorphism blood samples. MethodsPatients with epilepsy who were diagnosed MTLE in our epileptic clinic from December 2013 to April 2016 were included in this study, total 143 cases. Healthy volunteers who received annual physical checkups were recruited to serve as controls total 120 cases. The group enter criterion according to a 2004 ILAE report mainly:①12~55 years old; ②attack forms:partial onset seizures or secondary tonic-closure-clonus attack, a common onset symptoms such as stomach gas rise feeling, sense of deja vu, automatism etc.; ③with or without febrile convulsions history; ④EEG displayed unilateral or bilateral temporal spike, sharp slow wave, or their spines slow-wave sample such as epilepsy wave; ⑤head MRI displayed hippocampal sclerosis. Exclusion criteria:①tumors; ②head MRI display focal cortical dysplasia (FCD). Using sequenom iPLEX technology platform to detect all the object of study of gene polymorphism sites total ten sites. All statistical tests were conducted using SPSS version 16.0. Resultsall sites fulfilled Hardy-Weinberg genetic balance. The results showed that HCN1 rs17344896 C/T, rs6451973 A/G and HCN2 rs12977194 A/G three polypeptide sites associated with MTLE, with statistical differences(P < 0.05). ConclusionHCN1 and HCN2 genetic suscepibility is one of possible mechanism of MTLE.