Untersuchung der zirkadianen Rhythmik der Exzitabilität des menschlichen Motorkortex bei Patienten mit juveniler myoklonischer Epilepsie mittels Transkranieller Magnetstimulation

Juvenile myoclonic epilepsy (JME) is a common form of primary generalised epilepsy, which is characterised by myoclonic and generalised tonic-clonic seizures. Typically, seizures occur within the first two hours after awakening. Despite various studies concerning clinical, electrophysiological and genetic characteristics of JME the underlying pathomechanisms remain unclear. Especially the circadian rhythm of motorcortical excitability of patients with JME is still unknown. Transcranial magnetic stimulation (TMS) offers the opportunity to repeatedly measure the excitability of human motor cortex in-vivo and non-invasive. The aim of this study was to characterise possible circadian changes of motorcortical excitability in patients with JME and their comparison to healthy controls. In the present study single- and paired-pulse TMS was used to measure the following parameters of motorcortical excitability: motor thresholds (MT), intracortical inhibition (ICI), intracortical facilitation (ICF) and cortical stimulation induced silent period (CSP). All parameters were assessed in the evening and within the first two hours after awakening in the morning. Statistical analysis was performed by parametric and nonparametric tests (ANOVA, Wilcoxon-signed-rank-Test, Mann-Whitney-U-Test). In this explanatory study, the level of significance of each test was set at p<0.05. There were no significant intraindividual differences (p>0.05) in JME patients for all parameters between the evening and the morning testing. The intraindividual comparison of healthy controls also revealed no significant circadian changes. Furthermore, the interindividual comparison between these groups showed no significant differences in the morning or in the evening, respectively. The parameters of motorcortical excitability tested in this study showed no significant intra- or interindividual daytime dependent changes. Similar to absence epilepsy, this may be due to the involvement of rather subcortical structures in JME (e.g. the thalamus) which can not be selectively characterised by TMS. However, it can not be excluded that anticonvulsive drugs taken by JME patients in the present analysis disguised possible intracortical changes. Despite the anticonvulsant medication with increasing effect on MT no significant change of motor thresholds could be detected in patients. Thus, a reduced MT in JME may be concluded. This hypothesis should be verified in future investigations in non-treated patients.