Lack of habituation causes high intensity dependence of auditory evoked cortical potentials in migraine.

Migraineurs are characterized interictally by lack of habituation, or even potentiation, of cortical evoked potentials during repetitive stimulation and by a strong intensity dependence of auditory evoked potentials (IDAP). To determine whether these two features of sensory processing are interrelated, we have studied them simultaneously on the same recordings of auditory evoked potentials (AEPs). AEPs were obtained at four different stimulation intensities in 14 patients suffering from migraine without aura (MO) and 14 healthy volunteers (HV). For each intensity, 120 trials were averaged off-line globally and over four sequential blocks of 30 trials. IDAP was expressed by the amplitude/stimulus intensity function (ASF slope) for global and block averages. Habituation was calculated as the percentage amplitude variation between the first and fourth blocks for each stimulus intensity. The IDAP slope for global averages was higher in MO (1.05 +/- 0.27 microV/10 dB) than in HV (0.64 +/- 0.45 microV/10 dB) (P = 0.008), but IDAP slopes for block averages were greater in MO only at the fourth block (P = 0.048). First block amplitudes tended to be lower in MO, except at 80 dB. There was a potentiation of AEP amplitudes at every stimulus intensity in MO, contrasting with habituation in HV. IDAP slopes were negatively correlated with mean habituation percentages in pooled data from patients and controls (r = -0.610; P = 0.0006). This study confirms that IDAP is higher in migraineurs than in healthy controls. It also shows that the AEP habituation is replaced by potentiation at all stimulus intensities. The negative correlation found between IDAP and habituation suggests that the latter is able to have a strong influence on the former and perhaps even lead to it. In migraine, the habituation deficit amplifies the IDAP and may thus be the causal functional abnormality. We propose that it is due to a decreased pre-activation level of sensory cortices, a hypothesis also supported in this study by the lower amplitude of first AEP blocks in patients.