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Keywords:

  • migraine without aura;
  • pattern reversal-visual evoked potentials;
  • nociceptive blink reflex;
  • habituation

Background.—Lack of habituation, as reported in migraine patients between attacks for evoked cortical responses, was also recently found for the nociceptive blink reflex (nBR) mediated by brainstem neurons. It is not known if both brain stem and cortical habituation deficits are correlated in the same patient, which would favor a common underlying mechanism.

Objective.—To search for intraindividual correlations between habituation of pattern reversal-visual evoked potentials and that of the nociception-specific blink reflex in migraineurs and in healthy volunteers (HV).

Methods.—We recorded 15 HV and 15 migraine without aura patients between attacks. Habituation for visual evoked potentials was measured by comparing the N1–P1 amplitude change (%) between the first and sixth block of 100 sequential averaged responses. Habituation for the nBR was defined as the percentage change of the R2 response area between the 1st and 10th block of five averaged EMG responses, elicited by stimulating the right side every 2 minutes for 32 minutes. We also calculated the slope of N1–P1 amplitude and R2 response area changes from the first to the last response and the correlation with attack frequency.

Results.—A significant habituation deficit in both cortical and brain stem evoked activity characterized on average the group of migraineurs compared to controls. In migraine patients, but not in HV, we found a significant positive correlation between habituation of pattern reversal-visual evoked potentials and that of the nociception-specific blink reflex both for the degree of habituation between first and last blocks of averagings (r = 0.703; P= .003) and for the habituation slope (r = 0.751; P= .001). Moreover, nBR habituation was positively correlated with attack frequency (r = 0.548; P= .034).

Conclusion.—The positive correlation between visual evoked potential and nBR habituations is consistent with the idea that in migraine the same neurobiological dysfunction might be responsible for the habituation deficit both in cortex and brain stem. As nBR habituation increases with attack frequency, its interictal deficit is unlikely to be due to trigeminal sensitization.