Migraine triggers and habituation of visual evoked potentials

Lisicki, Marco; Ruiz-Romagnoli, Emiliano; Piedrabuena, Raúl; Giobellina, Roberto; Schoenen, Jean; Magis, Delphine

doi:10.1177/0333102417720217

Cited by 19 publications

(11 citation statements)

References 13 publications

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“…19 In a recent study, migraineurs with mental stress as a trigger had deficient habituation in VEP whereas those without had preserved habituation. 20 Following repetitive transcranial magnetic stimulation (rTMS), Bohotin et al 25 reported improvement in VEP amplitude and habituation in migraine patients, whereas reverse was observed in the healthy controls. Authors suggested that deficient interictal habituation in migraineurs might be due to a reduced pre-activation excitability level of the visual cortex.…”

Section: Discussionmentioning

confidence: 99%

“…19 There are only few studies correlating sensitization and impaired habituation of VEP with migraine triggers and migraine characteristics. 20,21 Understanding the neuronal behavior may be helpful in choosing the appropriate drug for migraine prophylaxis. In this study, we report sensitization and impaired habituation of pattern reversal visual evoked potential (PRVEP), and their correlation with chronicity of disease, migraine triggers and migraine characteristics.…”

Section: Introductionmentioning

confidence: 99%

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Neuronal Dysexcitability May Be a Biomarker of Migraine: A Visual Evoked Potential Study

2017

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We report neuronal sensitization and impaired habituation in migraine using pattern reversal visual evoked potential (PRVEP) and correlate these with clinical characteristics of migraine. Sixty-five migraineurs and 30 healthy controls were included. A detailed clinical examination was done and migraine characteristics, including migraine trigger, photophobia, phonophobia, and allodynia were noted. Consecutive 5 blocks of PRVEP were recorded averaging 100 epochs at 3 Hz stimuli. The amplitude of N75 and P100 were measured. Amplitude of first block was considered for sensitization, and impaired habituation was considered if any subsequent block was not suppressed. Migraineurs had sensitization of P100 (14.01 ± 6.02 vs 11.60 ± 5.17 µV; P = .049), but not of N75 (42.22 ± 4.79 vs 11.08 ± 4.56 µV; P = .27) compared with the controls. Impaired habituation of N75 was more marked and persisted up to fourth block of VEP recoding. Impaired habituation of P100 was significant only in the third block. Baseline N75 and P100 amplitudes were higher in females, and N75 was also higher in those with longer duration of illness. These phenomena did not correlate with visual triggers. Sensitization and impaired habituation were marked during headache. Based on the PRVEP findings, it may be concluded that migraineurs have sensitization of P100 and impaired habituation of N75 especially during headache. These phenomena may be useful for therapeutic monitoring.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuronal Dysexcitability May Be a Biomarker of Migraine: A Visual Evoked Potential Study

2017

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“…25 A recent study looked at the relationship between triggers and the neurophysiological marker of habituation of visual evoked potentials. 26 They came up with the interesting finding that individuals with migraine who reported stress as a trigger factor differed in terms of habituation to individuals with migraine who did not report stress as a trigger factor, leading to the suggestion that the former group might constitute a distinct subset within the migraine spectrum. How a trigger precipitates headaches is an important question, but mechanisms of action do not seem a viable basis for classifying triggers with the current state of knowledge.…”

Section: Classification Of Headache Triggersmentioning

confidence: 99%

“…One hypothesis is that different migraine triggers activate a wide variety of brain areas, but that there is a common descending pathway accounting for the activation of meningeal nociceptors leading to the perception of pain, 24 whilst another hypothesis is that the pain of migraine has its origin in the cortex, but the immediate generator resides in the brainstem 25 . A recent study looked at the relationship between triggers and the neurophysiological marker of habituation of visual evoked potentials 26 . They came up with the interesting finding that individuals with migraine who reported stress as a trigger factor differed in terms of habituation to individuals with migraine who did not report stress as a trigger factor, leading to the suggestion that the former group might constitute a distinct subset within the migraine spectrum.…”

Section: Classification Of Headache Triggersmentioning

confidence: 99%

Triggers of Primary Headaches: Issues and Pathways Forward

Martin

2020

Headache

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The triggers of primary headaches have considerable significance for our understanding and management of headache and migraine. Triggers explain the variance in headaches – why they occur when they do. Trigger management is generally viewed as an important component of a comprehensive treatment approach for headaches. Historically, however, triggers have not had a prominent place in the headache literature. This situation began to change 20 to 30 years ago, and the pace of change has increased exponentially in recent times. Nevertheless, the field is beset with issues that have held it back from achieving more. This review will focus on elaborating those issues with the goal of suggesting ways forward. The first issue considered will be the definition of a trigger, and how specific triggers are labeled. Consideration will then be given to a classification system for triggers. The review will discuss next the evidence relating to whether self‐reported triggers can, indeed, precipitate headaches, and how the capacity to elicit headaches may be acquired or extinguished. Attention will be given to the very important clinical issue of trigger management. Finally, the pathways forward will be proposed. Perhaps the most useful thing to accomplish at this point in time would be agreement on a definition of headache triggers, a list of triggers, and a classification system for triggers. This would greatly assist in comparing research on triggers from different research groups as well as eliminating some of the issues identified in this review. An authoritative body such as the American Headache Society or the International Headache Society, could establish a multidisciplinary committee that would complete these tasks. Consideration should also be given to incorporating triggers into the International Classification of Headache Disorders as an axis or via the use of codes, as this would raise the profile of triggers in assessment and management.

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“…If we transfer this concept to a disease such as migraine, it will illustrate the difference between the RFs for the “disease” and triggers for episodes. While “stress” and “not eating” [3, 4] do not necessarily explain why some people develop the “disease” of migraine, these stimuli may trigger an episode of migraine headache. Similarly, triggers such as “sitting” or “lifting awkwardly” may explain the reappearance of episodes of LBP but not necessarily the primary RFs for the underlying “disease” of LBP.…”

Section: Introductionmentioning

confidence: 99%

Can We Trust the Literature on Risk Factors and Triggers for Low Back Pain? A Systematic Review of a Sample of Contemporary Literature

Ardakani

Leboeuf‐Yde

Walker

2019

Pain Research and Management

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Background. Risk factors (RFs) for the “disease” of low back pain (LBP) are probably different from the triggers of new episodes of LBP. Investigating RFs for the onset of the “disease” and the triggers of LBP is problematic if researchers fail to discern the different types of pain-free status of participants at and before baseline. There is a difference between never having had LBP and having been pain-free for a certain period only. In this review, we assessed the dependability of contemporary literature on RFs and triggers of LBP, in relation to the “disease” and the episodes, respectively.Methods. A literature search from 2010 until 2017 was performed. Information on the definitions of LBP, potential RFs/triggers, and study design was extracted. Studies were reclassified based on the type of LBP concerning the “disease,” episode, or mixed/unclear/chronic. RFs and triggers were grouped into major domains, and positive associations listed, respectively, for the “disease” and episodes.Results. In 42 of the included 47 articles, it was not clear if the authors investigated RFs for the “disease” of LBP or triggers of new episodes. Only one study properly reported RFs for the onset of the “disease” of LBP, and four studies were deemed suitable to investigate triggers for a new episode of LBP. No study reproduced the results of other included studies.Conclusion. Trustworthy information regarding RFs and triggers of LBP is rare in the current literature. Future research needs to use precise definitions of LBP (onset of the “disease” vs. episodes) and nominate the timing of the associated factors in relation to the types of LBP as these are two critical factors when studying causes of LBP.

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Migraine triggers and habituation of visual evoked potentials

Cited by 19 publications

References 13 publications

Neuronal Dysexcitability May Be a Biomarker of Migraine: A Visual Evoked Potential Study

Neuronal Dysexcitability May Be a Biomarker of Migraine: A Visual Evoked Potential Study

Triggers of Primary Headaches: Issues and Pathways Forward

Can We Trust the Literature on Risk Factors and Triggers for Low Back Pain? A Systematic Review of a Sample of Contemporary Literature

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