Abstract
BackgroundPatients suffering from migraine with aura can have either pure visual auras or complex auras with sensory disturbances and dysphasia, or both. Few studies have searched for possible pathophysiological differences between these two subgroups of patients.MethodsMethods - Forty-seven migraine with aura patients were subdivided in a subgroup with exclusively visual auras (MA, N = 27) and another with complex neurological auras (MA+, N = 20). We recorded pattern-reversal visual evoked potentials (VEP: 15 min of arc cheques, 3.1 reversal per second, 600 sweeps) and measured amplitude and habituation (slope of the linear regression line of amplitude changes from the 1st to 6th block of 100 sweeps) for the N1-P1 and P1-N2 components in patients and, for comparison, in 30 healthy volunteers (HV) of similar age and gender distribution.ResultsVEP N1-P1 habituation, i.e. amplitude decrement between 1st and 6th block, which was obvious in most HV (mean slope −0.50), was deficient in both MA (slope +0.01, p = 0.0001) and MA+ (−0.0049, p = 0.001) patients. However, VEP N1-P1 amplitudes across blocks were normal in MA patients, while they were significantly greater in MA+ patients than in HVs.ConclusionsOur findings suggest that in migraine with aura patients different aura phenotypes may be underpinned by different pathophysiological mechanisms. Pre-activation cortical excitability could be higher in patients with complex neurological auras than in those having pure visual auras or in healthy volunteers.
Highlights
Patients suffering from migraine with aura can have either pure visual auras or complex auras with sensory disturbances and dysphasia, or both
Preliminary descriptive analysis showed that the visual evoked potentials (VEP) N1–P1 and P1–N2 peak-topeak amplitudes of the six blocks and the habituation slopes had a non-normal distribution
To define which comparison(s) contributed to the major effects, post hoc tests were performed with Tukey Honest Significant Difference (HSD) test
Summary
Patients suffering from migraine with aura can have either pure visual auras or complex auras with sensory disturbances and dysphasia, or both. Migraine with aura (MA) is defined as attacks of neurological symptoms that last no more than 60 min and may be followed or accompanied by headache (International Classification of Headache Disorders 3beta 2013). According to Rasmussen and Olesen [3], 51 % of migraine auras are purely visual, while 4 % comprise sensory symptoms in addition to the visual ones and 6 % language disturbances in addition to visual and sensory disturbances. The most likely cause of the migraine aura, Leão’s cortical spreading depression (CSD), consists of a brief neuronal depolarisation followed by a long-lasting wave of neuronal depression that often spreads posteroanteriorly in the occipital cortex and can reach the parietal and/or temporal lobes [4, 5]. In animal models CSD is able to activate peripheral and central trigeminovascular neurons that underlie the migraine headache [10, 11], knowledge is lacking on the possible relation of CSD to interictal neural alterations that may predispose to migraine attacks
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