Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

Gianluca Coppola1, Antonio Currà, Cherubino Di Lorenzo

  • 1G.B. Bietti Eye Foundation-IRCCS, Dept of Neurophysiology of Vision and Neurophthalmology, Rome, Italy. gianluca.coppola@uniroma1.it

BMC Neurology
|January 4, 2011
PubMed
Abstract

Insights

Medication-overuse headache (MOH) patients show increased cortical sensitization and lack of habituation in somatosensory evoked potentials (SEPs). This sensory sensitization may contribute to compulsive drug use in MOH.

Area of Science:

  • Neuroscience
  • Clinical Neurology

Background:

  • Medication-overuse headache (MOH) is a common and disabling neurological disorder.
  • Central sensitization is a key factor in MOH pathophysiology.
  • The electrophysiological profile of central sensitization in MOH is not well understood.

Purpose of the Study:

  • To investigate differences in somatosensory evoked potential (SEP) sensitization and habituation between patients with MOH and episodic migraine without aura (MOA).
  • To explore the role of central sensitization in the pathophysiology of MOH.

Main Methods:

  • Median-nerve SEPs were recorded in patients with MOH, episodic MOA (interictally and ictally), and healthy controls.
  • SEP sensitization was assessed by initial amplitude (block 1), and habituation by amplitude changes across three sequential blocks.

Main Results:

  • Episodic migraineurs showed a lack of SEP habituation between attacks.
  • Patients with MOH exhibited larger initial SEP amplitudes and failed to habituate, indicating increased cortical sensitization.
  • SEP amplitudes were lowest in triptan overusers and those with longer migraine history, and highest in those with longer headache chronification.

Conclusions:

  • The somatosensory cortex in MOH patients, particularly those overusing NSAIDs, demonstrates heightened sensitization.
  • This sensory sensitization may contribute to the behavioral sensitization driving compulsive medication intake.
  • Findings suggest drug-induced alterations in central serotoninergic pathways may underlie MOH pathophysiology.