title: Triptan-induced disruption of trigemino-cortical connectivity.
abstract: OBJECTIVE
  The 5-HT1B/D agonists (triptans) are specific headache medications that have no effect on pain as such. Although they are routinely used in the treatment of acute migraine attacks, the underlying mechanisms of action are still a matter of debate.
  
  
  METHODS
  Forty-three healthy participants underwent fMRI while receiving trigemino-nociceptive stimulation and control stimuli in a standardized fMRI paradigm. Using a crossover, double-blind, placebo-controlled design, 21 participants (10 women, mean age 26.9, range 20-37 years) received sumatriptan and 22 participants (11 women, mean age 25.5, range 22-32 years) received acetylsalicylic acid (ASA). Administration of medication and saline was randomized between participants of each group resulting in half of the participants receiving saline and the other half receiving the respective medication during the first fMRI data acquisition.
  
  
  RESULTS
  While mean pain intensity ratings did not differ significantly between control and medication nor between medications, we found a significant blood oxygen level-dependent signal increase in the trigeminal nuclei and the thalamus after sumatriptan treatment compared with placebo or ASA. In addition, we specifically looked for the pharmacologic modulation of functional coupling between trigeminal nuclei and higher brain areas, i.e., trigemino-cortical pathways, and found a strong coupling during the saline condition, which was altered by sumatriptan but not after ASA administration.
  
  
  CONCLUSIONS
  These data suggest that a specific functional inhibition of trigemino-cortical projections is one of the reasons that triptans, unlike pain killers, act highly specifically on headache and migraine but not pain as such.
authors.affiliation: From the Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
authors.forename: Inga L
authors.initials: IL
authors.lastname: Kröger
authors.affiliation: From the Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. a.may@uke.de.
authors.forename: Arne
authors.initials: A
authors.lastname: May
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects*; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009434:Neural Pathways / Q000187:drug effects; D059225:Nociception / Q000187:drug effects*; D058825:Serotonin 5-HT1 Receptor Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D012965:Sodium Chloride; D018170:Sumatriptan / Q000008:administration & dosage / Q000494:pharmacology*; D013788:Thalamus / Q000187:drug effects*; D014278:Trigeminal Nuclei / Q000187:drug effects*; D055815:Young Adult
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D058825:Serotonin 5-HT1 Receptor Agonists; D012965:Sodium Chloride; D018170:Sumatriptan; D001241:Aspirin