| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3045389 | Clinical Neurophysiology | 2012 | 7 Pages |
ObjectiveIt has been demonstrated that the early part of 600 Hz High Frequency Oscillations (HFOs), probably generated in the terminal part of thalamo-cortical somatosensory radiations, are abnormally reduced between attacks in migraineurs. We aimed at verifying whether spontaneous clinical fluctuations in migraine are correlated to HFO changes.MethodsWe recorded somatosensory evoked potentials in 28 migraine patients. Clinical fluctuations (number of attacks in the 6 months preceding and following the test) were correlated to the HFOs’ amplitudes. Moreover, eight out of 28 patients underwent a longer follow-up, including HFO control and clinical observation during the 12 months following the baseline recording.ResultsThe amplitude of early presynaptic HFOs was significantly correlated to the clinical evolution, since spontaneous worsening was associated with reduced presynaptic HFOs, whereas spontaneous improvement was associated with enhanced presynaptic HFOs (correlation test, p < 0.05). No correlation was found between the amplitude of postsynaptic HFOs and clinical fluctuations. Patients undergoing longer follow-up showed substantially unchanged HFOs, accordingly with their stable clinical condition.ConclusionsHFOs’ enhancement in spontaneously improved patients can reflect the increased activity of brainstem arousal related structures, which in turn increases the thalamo-cortical drive and the cortical lateral inhibition mediated by GABAergic interneurons.SignificanceHFOs’ recording could represent a useful tool in the functional assessment of migraine.
► High Frequency Oscillations (HFOs) changes were recorded in 28 migraine patients and correlated to spontaneous clinical fluctuations. ► Presynaptic HFOs were enhanced in spontaneously improved patients, whereas they were abnormally reduced in worsening ones. ► HFO recording could represent a useful marker to evaluate migraine progression and neurophysiological underpinnings of prophylactic drugs.
