Abstract
BackgroundThe interictal deficit of habituation to repetitive visual stimuli in migraine patients could be due to deficient intracortical inhibition and/or to low cortical pre-activation levels. Which of these abnormalities contributes more to the habituation deficit cannot be determined with the common methods used to record transient visual responses.We investigated lateral inhibition in the visual cortex during the migraine cycle and in healthy subjects by using differential temporal modulations of radial windmill-dartboard (WD) or partial-windmill (PW) visual patterns.MethodsTransient (TR-VEP) and steady-state visual-evoked potentials (SS-VEP) were recorded in 65 migraine patients (21 without and 22 with aura between attacks; 22 patients during an attack) and in 21 healthy volunteers (HV). Three stimulations were used in each subject: classic checkerboard pattern (contrast-reversion 3.1Hz), WD and PW (contrast-reversion ~4Hz). For each randomly presented stimulation protocol, 600 sweeps were acquired and off-line partitioned in 6 blocks of 100. Fourier analysis allowed data to extract in SS-VEP the fundamental (1H) and the second harmonic (2H) components that reflect respectively short-(WD) and long- range lateral inhibition (attenuation of 2H in WD compared to PW).ResultsCompared to HV, migraineurs recorded interictally had significantly less habituation of the N1-P1 TR-VEP component over subsequent blocks and they tended to have a smaller 1st block amplitude. 1H amplitude in the 1st block of WD SS-VEP was significantly greater than in HV and habituated in successive blocks, contrasting with an amplitude increase in HV. Both the interictal TR-VEP and SS-VEP abnormalities normalized during an attack. There was no significant between group difference in the PW 2H amplitude and its attenuation. When data of HV and migraine patients were combined, the habituation slope of WD-VEP 1H was negatively correlated with that of TR-VEP N1-P1 and with number of days since the last migraine attack.ConclusionThese results are in favour of a migraine cycle-dependent imbalance between excitation and inhibition in the visual cortex. We hypothesize that an interictal hypoactivity of monaminergic pathways may cause a functional disconnection of the thalamus in migraine leading to an abnormal intracortical short-range lateral inhibition that could contribute to the habituation deficit observed during stimulus repetition.
Highlights
The interictal deficit of habituation to repetitive visual stimuli in migraine patients could be due to deficient intracortical inhibition and/or to low cortical pre-activation levels
We found an increase in 1st harmonic (1H) SS-Visual Evoked Potential (VEP) amplitude during windmilldartboard (W-D) visual stimulation, reflecting the degree of short-range lateral inhibition, in migraine patients between attacks compared to healthy volunteers
The second distinctive finding in our study is that interictally, after the initial increase, the 1H W-D decreased in amplitude, i.e. habituated over sequential blocks, contrasting with the amplitude increase, i.e. potentiation, found in healthy volunteers (HV). We propose that this habituation of shortrange inhibition may contribute to induce the interictal lack of habituation of TR-VEP N1-P1 seen in migraine patients. This interpretation is supported by the inverse correlation we found between habituation of TR-VEP N1-P1 and that of the 1H SS-WD-VEPs: In other words, the more marked the VEP habituation deficit the more pronounced the habituation of short-range lateral inhibition
Summary
The interictal deficit of habituation to repetitive visual stimuli in migraine patients could be due to deficient intracortical inhibition and/or to low cortical pre-activation levels Which of these abnormalities contributes more to the habituation deficit cannot be determined with the common methods used to record transient visual responses. That the cortical dysexcitability in migraine could be due to abnormal thalamic control, namely to so-called “thalamocortical dysrhythmia” is suggested by studies of high frequency oscillations in spontaneous EEG and visual or somatosensory evoked potentials [6,7,8] This concept may reconcile the advocates of excessive excitation and deficient inhibition, since a deficient thalamo-cortical drive, i.e. a low level of cortical preactivation, results in a dysfunction of both inhibitory and excitatory cortical neurons [9]. Which of excitatory or inhibitory mechanisms contribute more to the habituation deficit cannot be determined with the methods commonly used to evoke visual responses that reflect the summation of both excitatory and inhibitory postsynaptic potentials [10]
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