Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome Polo Pontino, Corso della Repubblica 79, 04100, Latina, Italy.
Università Cattolica del Sacro Cuore/CIC, Istituto di Anestesiologia, Rianimazione e Terapia del Dolore, Largo Agostino Gemelli 8, 00168, Rome, Italy.
J Headache Pain. 2020 Apr 16;21(1):34. doi: 10.1186/s10194-020-01104-7.
Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features.
SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation.
Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI.
The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine between attacks, but increased ictally.
短潜伏期传入抑制(SAI)由感觉传入引起的运动皮层抑制组成,取决于胆碱能丘脑皮质投射对抑制性 GABA 能皮质网络的兴奋作用。鉴于偏头痛中存在丘脑皮质节律紊乱的电生理证据,我们研究了偏头痛发作期间和发作间期的 SAI,并寻找其与体感适应、丘脑皮质激活和临床特征的相关性。
通过在腕部正中神经上用电刺激在个体体感诱发电位(SEP)N20 加上 2、4、6 或 8 ms 的随机刺激间隔条件下,获得经颅磁刺激诱导的运动诱发电位(MEP)的 SAI。我们招募了 30 名无先兆偏头痛患者,16 名发作间期(MO)患者,14 名发作期(MI)患者和 16 名健康志愿者(HV)。我们计算了未条件 MEP 振幅与 4 种条件 MEP 之间线性回归的斜率,作为 SAI 的衡量标准。我们还测量了 SEP 振幅适应和高频振荡(HFO),作为丘脑皮质激活的指标。
与 HV 相比,MO 患者在发作间期的 SAI、SEP 适应和早期 SEP HFO 显著降低,但在发作期增强。HV 中 SAI 程度与早期 HFO 幅度呈正相关,但 MO 或 MI 中无相关性。
SAI 和 SEP HFO 的偏头痛周期依赖性变化进一步证明,在发作间期,促进性丘脑皮质激活(对 SAI 的运动皮层 GABA 能网络)可能减少,但发作时增加。