Long latancy reflexes and cortikal relay time in epilepsy

SUMMARY Aim: Epilepsy is a disease of central nervous system and mainly depended to excitability of cortical neuronal population. Some electrophysiological parameters like cortical motor thresholds (ME), cortical silent periods (KSP) reflecting the excitability of cortical neuronal activity have been studied in epilepsy in many studies. However, some reflexes originating from sensorimotor cortex like long latency reflexes obtained from intrinsic hand muscles has never been studied in epilepsy, previously. In this study our aims were evaluating of these reflexes in patients with epilepsy and comparing of the results with more conventional parameters like ME and KSP. Materials and Methods: Fifthy-two patients (39 female and 13 male) with epilepsy and 20 healthy controls (12 female and 8 male) were included to the study. All participants gave informed consent for the study. After the clinical evaluation, routine EEG investigation was performed. Thereafter, electrophysiological investigations were performed. Initially, upper extremity somatosensorial evoked potentials were recorded. Then long latency evoked potentials evoked by electrical stimulation of median nerve and motor evoked potentials evoked by transcranial magnetic stimulation were recorded. Cortical relay time were calculated by the using of these parameters. Discussion and Results: Cortical relay time (KGZ) was shortenned in patients with JME. However, difference did not reach to significance statistically. Additionally, this parameter was increased in patients with generalised epilepsy (extra JME). However, significant difference was not observed between generalised epilepsy and JME and generalise epilepsy and controls. Amplitude of ULR2 was increased in patients with JME in comparison with controls and patients with generalised epilepsy. Additionally, mean latency of ULR2 was shortened in patients with JME however, the difference did not reach statistical significance. Level of motor thresholds (ME) was significantly decreased in patients with JME in comparison with controls and other epileptics. These findings suggested that there was an increased excitability may be due to a dysfunction in the cortical inhibitör interneuronal activity in the motor cortex in patients with JME. However, silent periods did not show any significant change between patients and controls. Additionally, we evaluated the effects of valproic acid and levetiracetam on the electrophysiological parameters. However, no effect was demonstrated. We concluded that MEs was most sensitive parameter in the demonstration of cortical excitability in JME. However, it seems that the evaluation of ULRs and analysis of KGZ did not give significant information in epilepsy. Evaluation of both pre and post treatment periods to demonstration of effect of antiepileptics on electrophysiological parameters should be performed in further studies.