Investigation of the effects of continuous theta burst transcranial magnetic stimulation in patients with migraine

Corresponding Author: Melek Çolak-Atmaca E-mail: melekcolakdr@gmail.com Submitted: 14 January 2018 Accepted: 19 June 2018 Available Online Date: 24 July 2018 You may cite this article as: Çolak-Atmaca M, Çiftçi-Kavaklıoğlu B, Aldan MA, et al. Invesigation of the effects of continuous theta burst transcranial magnetic stimulation in patients with migraine. Neurol Sci Neurophyisol 2018; 35(4): 177-182. Presented in: This study was presented as an oral presentation at the 30th National Clinic Neurophysiology EEG-EMG Congress, 16-20 April 2014, Antalya (S20). Abstract Objective: Repetitive transcranial magnetic stimulation (rTMS) allows the non-invasive investigation of synaptic plasticity. Theta-burst stimulation (TBS) is a modified form of rTMS that induces synaptic plasticity. Our objective was to evaluate cortical excitability using paired-pulse transcranial magnetic stimulation (ppTMS) before and after continuous TBS (cTBS) in healthy controls and patients with migraine. Methods: The study included 17 patients with migraine without aura and 18 healthy volunteers. Motor evoked potential (MEP) amplitudes, motor threshold (MT), intracortical inhibition (ICI), intracortical facilitation (ICF), and cortical silent period (CSP) were assessed using a figure-of-eight–shaped coil with a magnetic stimulator. cTBS was applied following baseline assessments; the results of ICI, ICF, and CSP at baseline and post-cTBS were compared between patients with migraine and healthy controls. Results: There were no differences in baseline MT, CSP, and ICI parameters between patients with migraine and healthy controls; ICF was not achieved and a decrease in MEP amplitudes (80±52%) was found in most patients with migraine. After cTBS, ICF was not achieved in most subjects in both groups and a significant TIME effect (F=9.124 p=0.005) in addition to TIME x GROUP interaction (F=7.129 p=0.012) was noted, indicating a more significant decrease in the controls than in patients with migraine. Conclusion: Baseline ICF was not achieved in patients with migraine, and after cTBS, ICF was not achieved in either group; the inhibitory effect of cTBS was absent in patients with migraine. These findings indicate impairment of glutamatergic circuits to be a major culprit in the pathogenesis of migraine.