Prophylactic treatment of migraine with β-blockers and riboflavin: Differential effects on the intensity dependence of auditory evoked cortical potentials

Peter S. Sándor, Judit Áfra, Anna Ambrosini, Jean Schoenen

Research output: Contribution to journalArticle

84 Citations (Scopus)

Abstract

Objective.-To investigate the influence of different pharmacological treatments on the intensity dependence of auditory evoked cortical potentials in migraineurs. Background.-Between attacks, patients with migraine show abnormalities in cortical information processing and decreased brain mitochondrial energy reserve. Both are most probably relevant for migraine pathogenesis, and they could be differentially modified by prophylactic drug therapy. Design.-The intensity dependence of the auditory evoked cortical potentials is, on average, increased in migraine. We have studied this intensity dependence in 26 patients before and after a 4-month period of prophylaxis with beta-blockers (n = 11, all migraine without aura; metoprolol or bisoprolol) or riboflavin (n = 15, migraine without aura: 13, migraine with aura: 2). Recordings were performed at least 3 days before or after an attack. Results.-After the treatment with beta-blockers, the intensity dependence of the auditory evoked cortical potentials was significantly decreased (before: 1.66 ± 1.02 μV/10 dB; after: 0.79 ± 1.06 μV/10 dB, P = .02). The decrease in intensity dependence was correlated significantly with clinical improvement (r = .69, P = .02). There was no change in intensity dependence after riboflavin treatment (before: 1.80 ± 0.81 μV/10 dB; after: 1.56 ± 0.83 μV/10 dB, P = .39), although the majority of patients showed improvement. Conclusions.-These results confirm that beta-blockers and riboflavin act on two distinct pathophysiological mechanisms. Combining both treatments might enhance their efficacy without increasing central nervous system side effects.

Original languageEnglish
Pages (from-to)30-35
Number of pages6
JournalHeadache
Volume40
Issue number1
DOIs
Publication statusPublished - 2000

Fingerprint

Auditory Evoked Potentials
Riboflavin
Migraine Disorders
Migraine without Aura
Bisoprolol
Migraine with Aura
Metoprolol
Therapeutics
Automatic Data Processing
Central Nervous System
Pharmacology
Drug Therapy
Brain

Keywords

  • Auditory evoked cortical potentials
  • Beta-blockers
  • Intensity dependence
  • Migraine
  • Prophylactic treatment
  • Riboflavin

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Prophylactic treatment of migraine with β-blockers and riboflavin : Differential effects on the intensity dependence of auditory evoked cortical potentials. / Sándor, Peter S.; Áfra, Judit; Ambrosini, Anna; Schoenen, Jean.

In: Headache, Vol. 40, No. 1, 2000, p. 30-35.

Research output: Contribution to journalArticle

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N2 - Objective.-To investigate the influence of different pharmacological treatments on the intensity dependence of auditory evoked cortical potentials in migraineurs. Background.-Between attacks, patients with migraine show abnormalities in cortical information processing and decreased brain mitochondrial energy reserve. Both are most probably relevant for migraine pathogenesis, and they could be differentially modified by prophylactic drug therapy. Design.-The intensity dependence of the auditory evoked cortical potentials is, on average, increased in migraine. We have studied this intensity dependence in 26 patients before and after a 4-month period of prophylaxis with beta-blockers (n = 11, all migraine without aura; metoprolol or bisoprolol) or riboflavin (n = 15, migraine without aura: 13, migraine with aura: 2). Recordings were performed at least 3 days before or after an attack. Results.-After the treatment with beta-blockers, the intensity dependence of the auditory evoked cortical potentials was significantly decreased (before: 1.66 ± 1.02 μV/10 dB; after: 0.79 ± 1.06 μV/10 dB, P = .02). The decrease in intensity dependence was correlated significantly with clinical improvement (r = .69, P = .02). There was no change in intensity dependence after riboflavin treatment (before: 1.80 ± 0.81 μV/10 dB; after: 1.56 ± 0.83 μV/10 dB, P = .39), although the majority of patients showed improvement. Conclusions.-These results confirm that beta-blockers and riboflavin act on two distinct pathophysiological mechanisms. Combining both treatments might enhance their efficacy without increasing central nervous system side effects.

AB - Objective.-To investigate the influence of different pharmacological treatments on the intensity dependence of auditory evoked cortical potentials in migraineurs. Background.-Between attacks, patients with migraine show abnormalities in cortical information processing and decreased brain mitochondrial energy reserve. Both are most probably relevant for migraine pathogenesis, and they could be differentially modified by prophylactic drug therapy. Design.-The intensity dependence of the auditory evoked cortical potentials is, on average, increased in migraine. We have studied this intensity dependence in 26 patients before and after a 4-month period of prophylaxis with beta-blockers (n = 11, all migraine without aura; metoprolol or bisoprolol) or riboflavin (n = 15, migraine without aura: 13, migraine with aura: 2). Recordings were performed at least 3 days before or after an attack. Results.-After the treatment with beta-blockers, the intensity dependence of the auditory evoked cortical potentials was significantly decreased (before: 1.66 ± 1.02 μV/10 dB; after: 0.79 ± 1.06 μV/10 dB, P = .02). The decrease in intensity dependence was correlated significantly with clinical improvement (r = .69, P = .02). There was no change in intensity dependence after riboflavin treatment (before: 1.80 ± 0.81 μV/10 dB; after: 1.56 ± 0.83 μV/10 dB, P = .39), although the majority of patients showed improvement. Conclusions.-These results confirm that beta-blockers and riboflavin act on two distinct pathophysiological mechanisms. Combining both treatments might enhance their efficacy without increasing central nervous system side effects.

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