Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks: Correlations with thalamocortical activity and clinical features

Gianluca Coppola, Martina Bracaglia, Davide Di Lenola, Elisa Iacovelli, Cherubino Di Lorenzo, Mariano Serrao, Maurizio Evangelista, Vincenzo Parisi, Jean Schoenen, Francesco Pierelli

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Background We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features. Participants and methods Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)∗100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation. Results In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02). Conclusions 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.

Original languageEnglish
Pages (from-to)568-578
Number of pages11
JournalCephalalgia
Volume36
Issue number6
DOIs
Publication statusPublished - 2015

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Migraine without Aura
Somatosensory Cortex
Migraine Disorders
Healthy Volunteers
Ulnar Nerve
Somatosensory Evoked Potentials
Wrist
Electric Stimulation
Recurrence

Keywords

  • clinical features
  • evoked potentials
  • lateral inhibition
  • Migraine
  • thalamocortical activity

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks : Correlations with thalamocortical activity and clinical features. / Coppola, Gianluca; Bracaglia, Martina; Di Lenola, Davide; Iacovelli, Elisa; Di Lorenzo, Cherubino; Serrao, Mariano; Evangelista, Maurizio; Parisi, Vincenzo; Schoenen, Jean; Pierelli, Francesco.

In: Cephalalgia, Vol. 36, No. 6, 2015, p. 568-578.

Research output: Contribution to journalArticle

Coppola, Gianluca ; Bracaglia, Martina ; Di Lenola, Davide ; Iacovelli, Elisa ; Di Lorenzo, Cherubino ; Serrao, Mariano ; Evangelista, Maurizio ; Parisi, Vincenzo ; Schoenen, Jean ; Pierelli, Francesco. / Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks : Correlations with thalamocortical activity and clinical features. In: Cephalalgia. 2015 ; Vol. 36, No. 6. pp. 568-578.
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T1 - Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks

T2 - Correlations with thalamocortical activity and clinical features

AU - Coppola, Gianluca

AU - Bracaglia, Martina

AU - Di Lenola, Davide

AU - Iacovelli, Elisa

AU - Di Lorenzo, Cherubino

AU - Serrao, Mariano

AU - Evangelista, Maurizio

AU - Parisi, Vincenzo

AU - Schoenen, Jean

AU - Pierelli, Francesco

PY - 2015

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N2 - Background We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features. Participants and methods Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)∗100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation. Results In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02). Conclusions 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.

AB - Background We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features. Participants and methods Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)∗100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation. Results In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02). Conclusions 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.

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KW - evoked potentials

KW - lateral inhibition

KW - Migraine

KW - thalamocortical activity

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