Figure 6

Schematic representation of visual information processing pathway describing the neural network model that can encompass the present findings in both healthy volunteers and migraineurs. In the normal condition (left panel), in presence of a regular brainstem and thalamic activation, visual information travels normally across subcortical areas, then at the cortical level increases the firing rate of excitatory pyramidal cells at the beginning and of fast-spiking (FS) inhibitory interneurons during stimulus repetition. The latter leads to a normal inhibition in adjacent cortical columns manifesting as a decrement in short-range lateral inhibition (LI) followed by its recovery with increasing inhibition of pyramidal cell (modified from [59]). In the thalamo-cortical dysrhythmia model (right panel), used to explain our findings in migraine, the presence of an anatomical or functional disconnection of the thalamus from subcortical areas, causes a change of rhythmic thalamocortical activity that favour low frequency activity which at the cortical level will reduce firing rates of excitatory pyramidal cells at the beginning and of FS inhibitory interneurons during stimulus repetition. The latter leads to a disinhibition in adjacent cortical columns manifesting as a progressive increase in short range LI, the so-called “edge effect”, which, in our migraineurs, is followed by its recovery with increasing excitation of pyramidal cells (modified from [60]).