Cortical silent period duration in medication overuse headache changes according to the drug overused

Background Episodic migraineurs recorded interictally have shortened cortical silent period (SP), as a result of reduced activation of GABAB-ergic circuits in the motor cortex. In episodic migraine cortical activation fluctuates depending on the migraine cycle, whereas in chronic daily headache due to medication overuse (MOH) it seems locked in a pre-ictal state, it is of interest thus to study the cortical SP in patients with MOH. Material and methods We recorded the transcranial magnetic stimulation (TMS) induced SP in perioral muscle in 36 MOH patients, 12 migraine without aura patients studied interictally (MO), and 13 controls. MOH patients were sub-grouped in patients who overused triptans (n = 9), nonsteroidal anti-inflammatory drugs (NSAIDs) (n = 12), and combination of both (n = 15) drugs. We delivered high intensity magnetic stimuli through a figure-of-eight coil over the hotspot for the perioral muscles, while subjects maximally activated target muscles, and recorded the electromyographic responses with surface electrodes placed bilaterally. Results MO patients had shorter SP than controls (p = 0.021). Despite as a whole group patients with MOH had normal SP duration (p = 0.314), the subgroup of triptan overusers had significantly shorter SP than controls (p = 0.005) and NSAIDs overusers (p = 0.119) or both medications combined (p = 0.847). Monthly tablets intake, but not disease history, correlated positively with SP duration (r = 0.476, p = 0.003) in the whole group of MOH. Discussion In patients with MOH the activation of motor cortical inhibitory interneurons is greater than in episodic migraneurs studied interictally, and it is similar to that observed in controls. SP normalisation takes place in the MOH subgroup who overuse NSAIDs, whereas SP duration remains short in patients who overuse triptans alone. This finding confirms that in chronic migraineurs the overuse of NSAIDs or triptans changes the cortical physiology distinctly, and it shows that such distinctive effect is also exerted on cortical inhibitory circuits.