Reduced Short-Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks


Alaydin H. C. , VURALLI D. , Keceli Y., Can E., CENGİZ B. , Bolay H. B.

HEADACHE, cilt.59, sa.6, ss.906-914, 2019 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 59 Konu: 6
  • Basım Tarihi: 2019
  • Doi Numarası: 10.1111/head.13554
  • Dergi Adı: HEADACHE
  • Sayfa Sayıları: ss.906-914

Özet

Background and Objective Migraine attacks disrupt sensory information processing and may also disturb sensorimotor integration. This prospective pilot study aimed to assess the sensorimotor integration and inhibitory circuitry in the sensorimotor cortex using short-latency afferent inhibition (SAI) paradigm in migraine. Methods Twenty-five migraine without aura patients (10 interictal, 5 preictal, 10 ictal) and 16 healthy controls were enrolled. SAI was elicited by combining the right median nerve electrical stimulation and left motor cortical magnetic stimulation at the 21-millisecond interval. Mean motor evoked potential (MEP) amplitude ratio, recorded from right abductor pollicis muscle after single and conditioned stimulations, was calculated as SAI. Results Average MEP inhibition ratio after single and conditioned stimuli in healthy controls was not significantly different from interictal patients (45.1% +/- 20.3% vs 44.5% +/- 14.75% [P = .93]). However, SAI was significantly reduced during preictal/prodromal (-14.6% +/- 42.8% [P = .002]) and ictal/headache (-7.4% +/- 31.1% [P = .0001]) periods of migraine compared to healthy controls. Conclusion Pronounced decrease in SAI during preictal and ictal periods in migraine was shown for the first time. Instead of inhibition to a conditioned stimulus, facilitation in the sensorimotor cortex was detected both ictally and preictally. Preictal SAI results suggest the presence of increased excitability state several hours prior to the headache phase. This phenomenon could be related to the cortical hyperresponsivity to sensory stimuli and cognitive disturbances accompanying migraine attacks as SAI is modulated by cholinergic activity.