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临床试验/NCT01382017
NCT01382017已完成不适用

Effects of Lacosamide on Human Motor Cortex Excitability: a Transcranial Magnetic Stimulation Study

University of Kiel1 个研究点 分布在 1 个国家目标入组 18 人开始时间: 2011年6月最近更新:
适应症
干预措施
相关药物

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

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 Comparator

Placebo arm

干预措施: Placebo (Drug)

Lasosamide 200

Experimental

Lacosamide 200 mg

干预措施: Lacosamide (Drug)

Lacosamide 400

Experimental

Lacosamide 400 mg

干预措施: Lacosamide (Drug)

Carbamazepine 600

Active Comparator

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

申办方类型
Other
责任方
Principal Investigator
主要研究者

Nicolas Lang

PD Dr. med.

University of Kiel

研究点 (1)

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