These higher thalamic FA values noted during the interictal period which normalized during an attack are probably related to plastic peri-ictal modifications in regional branching and crossing of fibres. Whether these changes could be considered as the anatomical counterpart of the cyclical functional fluctuations previously observed in the neurophysiology of migraine remains to be determined.

BackgroundEpisodic migraine is characterized by decreased high-frequency somatosensory oscillations (HFOs), reflecting thalamo-cortical activity, and deficient habituation of low-frequency (LF-) somatosensory evoked potentials (SSEPs) to repetitive sensory stimulation between attacks. Here, we study conventional LF-SSEPs and HFOs in episodic migraineurs who developed chronic migraine (CM).MethodsThirty-four episodic (15 interictally [MOii], 19 ictally [MOi]) and 19 CM patients underwent right median nerve SSEPs. The patient groups were compared to a group of 20 healthy volunteers (HV) of comparable age and gender distribution. We measured the N20-P25 LF-SSEP 1st amplitude block and habituation, and, after applying a band-pass filter (450–750 Hz), maximal peak-to-peak latency and the amplitudes of the early and late HFOs.ResultsReduced early HFOs, lower 1st block LF-SSEPs and deficient habituation characterize MOii. Initially higher SSEP amplitudes and late normal habituation characterize both CM and MOi patients. After the digital filtration, both patient groups showed shortened latency peaks and normalization of early HFO amplitudes with increased late HFOs. When data of MO and CM patients were combined, the monthly number of days with headache negatively correlated with the LF-SSEP slope (r = −0.385, p = 0.006), which in turn negatively correlated with the 1st amplitude block (r = 0.568, p < 0.001).ConclusionsOur results show abnormalities in chronic migraine that are also reported during attacks in episodic migraineurs, namely early response sensitization and late habituation. The HFO analysis suggests that this sensory sensitization may be explained by an increase in the strength of the connections between the thalamus and cortex compared to episodic migraine between attacks. Whether this electro-functional behaviour is primary or secondary to daily headache, thus reflecting an electrophysiological fingerprint of the somatosensory system central sensitization process, remains to be determined.

Neurophysiological investigations have demonstrated that there are unique fluctuations in the migraine brain functional activity between the ictal and interictal periods. Here we investigated the possibility that there are fluctuations over time also in whole brain morphometry of patients affected by episodic migraine without aura (MO).Twenty-four patients with untreated MO underwent 3T MRI scans during (n = 10) or between attacks (n = 14) and were compared to a group of 15 healthy volunteers (HVs). We then performed voxel-based-morphometry (VBM) analysis of structural T1-weighted MRI scans to determine if changes in brain structure were observed over the course of the migraine cycle.Interictally, MO patients had a significantly lower gray matter (GM) density within the right inferior parietal lobule, right temporal inferior gyrus, right superior temporal gyrus, and left temporal pole than did HVs. Ictally, GM density increased within the left temporal pole, bilateral insula, and right lenticular nuclei, but no areas exhibited decreased GM density.These morphometric GM changes between ictal and interictal phases suggest that abnormal structural plasticity may be an important mechanism of migraine pathology. Given the functional neuroanatomy of these areas, our findings suggest that migraine is a condition associated with global dysfunction of multisensory integration and memory processing.

We designed this study to investigate possible correlations between variables measuring primary motor cortex excitability detected by single and paired-pulse transcranial magnetic stimulation (TMS) and the severity of clinical manifestations in patients with multiple sclerosis (MS). Thirty patients with MS in remission, 16 with relapsing-remitting (RR), 14 with secondary progressive disease (SP) and 17 healthy subjects participated in the study. In each subject, the central motor conduction time (CMCT) was calculated, and single-pulse and paired-pulse TMS at 3 and 10 ms interstimulus intervals was delivered over the primary motor cortex of the dominant hemisphere to measure the amplitude of motor-evoked potentials (MEPs), motor threshold (MTh), intracortical inhibition (ICI) and facilitation (ICF). Correlations were determined between the patients' TMS findings and magnetic resonance imaging (MRI) (lesion load) and clinical features (expanded disability status scale, EDSS score). EDSS scores were significantly higher in SPMS than in RRMS patients. The MTh was significantly higher, and the MEP was significantly smaller in SPMS patients than in RRMS patients and control subjects. All patients had longer CMCTs than healthy subjects. In all patients, paired-pulse TMS elicited an inhibited test MEP at the 3-ms ISI and a facilitated test MEP at the 10 ms ISI. Post hoc analysis showed that ICI was significantly lower in SPMS patients than in those with RRMS and healthy subjects. EDSS scores correlated significantly with TMS measures (MEP, ICI, CMCT and MTh), but not with MRI lesion load. It was found that intracortical excitability as measured with TMS differs according to the clinical course of MS; it remains normal in patients with low EDSS scores and is altered in patients with high EDSS scores.

We hypothesize that abnormal migraine cycle-dependent dynamics of connectivity between subcortical and cortical excitation/inhibition networks may contribute to clinical features of MO and recurrence of attacks.