Open Access Open Badges Research article

Effects of light deprivation on visual evoked potentials in migraine without aura

Gianluca Coppola1*, Julien Crémers2, Pascale Gérard2, Francesco Pierelli34 and Jean Schoenen25

Author Affiliations

1 G.B. Bietti Eye Foundation-IRCCS, Dept of Neurophysiology of Vision and Neuroophtalmology, Rome, Italy

2 Headache Research Unit. University Dept. of Neurology, Liège University, Belgium

3 Dept of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome Polo Pontino, Latina, Italy

4 IRCCS-Neuromed, Pozzilli (IS), Italy

5 GIGA-Neurosciences, Liège University, Liège, Belgium

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BMC Neurology 2011, 11:91  doi:10.1186/1471-2377-11-91

Published: 27 July 2011



The mechanisms underlying the interictal habituation deficit of cortical visual evoked potentials (VEP) in migraine are not well understood. Abnormal long-term functional plasticity of the visual cortex may play a role and it can be assessed experimentally by light deprivation (LD).


We have compared the effects of LD on VEP in migraine patients without aura between attacks (MO, n = 17) and in healthy volunteers (HV, n = 17). Six sequential blocks of 100 averaged VEP at 3.1 Hz were recorded before and after 1 hour of LD. We measured VEP P100 amplitude of the 1st block of 100 sweeps and its change over 5 sequential blocks of 100 responses.


In HV, the consequence of LD was a reduction of 1st block VEP amplitude and of the normal habituation pattern. By contrast, in MO patients, the interictal habituation deficit was not significantly modified, although 1st block VEP amplitude, already lower than in HV before LD, further decreased after LD.


Light deprivation is thought to decrease both excitatory and subsequent inhibitory processes in visual cortex, which is in line with our findings in healthy volunteers. The VEP results in migraine patients suggest that early excitation was adequately suppressed, but not the inhibitory mechanisms occurring during long term stimulation and habituation. Accordingly, deficient intracortical inhibition is unlikely to be a primary factor in migraine pathophysiology and the habituation deficit.