To account for inter-participant variability, outliers, coil positioning errors and, most importantly, participant comfort during data acquisition, we recommend creating a map with 80 stimuli and a 1.5 s ISI. This makes it possible to acquire TMS maps in 2 min, making mapping a more feasible tool to study short- and long-term changes in cortical organization.

Supplemental Digital Content is Available in the Text.Visual allodynia, the burden of hypersensitivity to light and patterns, is enhanced in migraine patients, particularly in those with migraine with aura and chronic migraine.

Background Migraine is associated with altered sensory processing and cortical responsivity that may contribute to susceptibility to attacks by changing brain network excitability dynamics. To gain better insight into cortical responsivity changes in migraine we subjected patients to a short series of light inputs over a broad frequency range (“chirp” stimulation), designed to uncover dynamic features of visual cortex responsivity. Methods EEG responses to visual chirp stimulation (10–40 Hz) were measured in controls (n = 24) and patients with migraine with aura (n = 19) or migraine without aura (n = 20). Average EEG responses were assessed at (i) all EEG frequencies between 5 and 125 Hz, (ii) stimulation frequencies, and (iii) harmonic frequencies. We compared average responses in a low (10–18 Hz), medium (19–26 Hz) and high (27–40 Hz) frequency band. Results Responses to chirp stimulation were similar in controls and migraine subtypes. Eight measurements (n = 3 migraine with aura; n = 5 without aura) were assigned as “pre-ictal”, based on reported headache within 48 hours after investigation. Pre-ictally, an increased harmonic response to 22–32 Hz stimulation (beta band) was observed ( p = 0.001), compared to interictal state measurements. Conclusions We found chirp responses to be enhanced in the 48 hours prior to migraine headache onset. Visual chirp stimulation proved a simple and reliable technique with potential to detect changes in cortical responsivity associated with the onset of migraine attacks.

Background: Epilepsy and migraine are paroxysmal neurological conditions associated with disturbances of cortical excitability. No useful biomarkers to monitor disease activity in these conditions are available. Phase clustering was previously described in electroencephalographic (EEG) responses to photic stimulation and may be a potential epilepsy biomarker. Objective: To investigate EEG phase clustering in response to transcranial magnetic stimulation (TMS), compare it to photic stimulation in controls and explore its potential as a biomarker of juvenile myoclonic epilepsy or migraine with aura. Methods: People with juvenile myoclonic epilepsy, migraine with aura and healthy controls underwent single-pulse TMS with concomitant EEG recording during the interictal period. We compared phase clustering after TMS with photic stimulation across the groups using permutation-based testing. Results: We included eight people with juvenile myoclonic epilepsy (five off medication, three on), 10 with migraine with aura and 37 controls. TMS and photic phase clustering spectra showed significant differences between epilepsy without medication and controls. Two phase clustering-based indices successfully captured these differences between groups. One participant was tested multiple times. In this case, the phase clustering-based indices were inversely correlated with the dose of anti-epileptic medication. Phase clustering did not differ between people with migraine and controls. Conclusion: We present methods to quantify phase clustering using TMS-EEG and show its potential value as of brain network activity in epilepsy. Our results suggest that the higher propensity to phase clustering is not shared between epilepsy and migraine.

Migraine patients often report (inter)ictal hypersensitivity to light, but the underlying mechanisms remain an enigma. Both hypo‐ and hyperresponsivity of the visual network have been reported, which may reflect either intra‐individual dynamics of the network or large inter‐individual variation in the measurement of human visual evoked potential data. Therefore, we studied visual system responsivity in freely behaving mice using combined epidural electroencephalography and intracortical multi‐unit activity to reduce variation in recordings and gain insight into visual cortex dynamics. For better clinical translation, we investigated transgenic mice that carry the human pathogenic R192Q missense mutation in the α1A subunit of voltage‐gated CaV2.1 Ca2+ channels leading to enhanced neurotransmission and familial hemiplegic migraine type 1 in patients. Visual evoked potentials were studied in response to visual stimulation paradigms with flashes of light. Following intensity‐dependent visual stimulation, FHM1 mutant mice displayed faster visual evoked potential responses, with lower initial amplitude, followed by less pronounced neuronal suppression compared to wild‐type mice. Similar to what was reported for migraine patients, frequency‐dependent stimulation in mutant mice revealed enhanced photic drive in the EEG beta‐gamma band. The frequency‐dependent increases in visual network responses in mutant mice may reflect the context‐dependent enhancement of visual cortex excitability, which could contribute to our understanding of sensory hypersensitivity in migraine.