Effects of Lacosamide on Human Motor Cortex Excitability: a Transcranial Magnetic Stimulation Study
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 入组人数
- 18
- 试验地点
- 1
- 主要终点
- TMS measures of cortical excitability
研究概览
简要总结
This study has been designed to explore dose-depended effects of lacosamide (LCM) on motor cortex excitability with TMS in a randomized, double-blind, placebo-controlled crossover trial in young healthy human subjects, and to compare the pattern of excitability changes induced by LCM with those of carbamazepine (CBZ). LCM selectively enhances slow inactivation of voltage-gated sodium channel, and, in contrast to CBZ, does not affect steady-state fast inactivation (Errington et al., 2006). The enhancement of slow inactivation of sodium channels by LCM is a novel manner to modulate sodium channels and leads to normalization of activation thresholds and a reduced pathophysiological hyper-responsiveness, thereby effectively controlling neuronal hyperexcitability without affecting physiological activity (Beyreuther et al., 2007). Therefore, it is thought that LCM, compared to CBZ, will be better tolerated in clinical settings while being as or even more effective in controlling seizure activity. On the basis of the results from nonhuman studies, it is hypothesized that the TMS profile of LCM will be distinguishable from that of CBZ. CBZ, like other 'classical' sodium channel blockers such as phenytoin, predominantly demonstrated elevated TMS motor thresholds indicating reduced neuronal membrane excitability, without developing significant changes of synaptic intracortical inhibition and facilitation (Ziemann et al., 1996; Chen et al., 1997; Lee et al., 2005). Because of its novel mode of action it can only be speculated which TMS parameters LCM might affect. For example, more than exclusively affecting neuronal membrane excitability, LCM could possibly also affect inhibitory mechanisms such as short- and long-latency intracortical inhibition (Valls-Sole et al., 1992; Kujirai et al., 1993). This would in line with other well-tolerated modern antiepileptic drugs (Ziemann et al., 1996; Reis et al., 2002; Lang et al., 2006).
研究设计
- 研究类型
- Interventional
- 分配方式
- Randomized
- 干预模型
- Crossover
- 主要目的
- Basic Science
- 盲法
- Double (Participant, Investigator)
入排标准
- 年龄范围
- 18 Years 至 45 Years(Adult)
- 性别
- Male
- 接受健康志愿者
- 是
入选标准
- •right-handed
- •aged 18-45 years
排除标准
- •cardiac pacemaker
- •metal implants in the head
- •intake of any medication
- •previous neurologic, psychiatric, or chronic internal diseases
- •pregnancy or breastfeeding; drug, nicotine, or alcohol abuse
- •known or expected intolerance to soy beans, peanuts, LCM or CBZ; abnormal ECG with prolonged PQ-interval
- •participation in another clinical trial within the previous 8 weeks
研究组 & 干预措施
Placebo
Placebo arm
干预措施: Placebo (Drug)
Lasosamide 200
Lacosamide 200 mg
干预措施: Lacosamide (Drug)
Lacosamide 400
Lacosamide 400 mg
干预措施: Lacosamide (Drug)
Carbamazepine 600
Carbamazepine 600 mg
干预措施: Carbamazepine (Drug)
结局指标
主要结局
TMS measures of cortical excitability
时间窗: within 24h after intake of study medication
Transcranial magnetic stimulation (TMS) measurements included resting motor thresholds (RMT) and active motor thresholds (AMT), the intensity to evoke MEP of ∼1mV peak-to-peak amplitude (SI1mV), short-interval intracortical inhibition/intracortical facilitation (SICI/ICF), long-interval intracortical inhibition (LICI), short-interval intracortical facilitation (SICF), recruitment curves, MEP under tonic activation (aMEP), and cortical silent period (CSP), and MEP changes in response to short trains of repetitive TMS.
次要结局
未报告次要终点
研究者
Nicolas Lang
PD Dr. med.
University of Kiel
