Sensory processing patterns affect headache severity among adolescents with migraine

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Abstract

Objective

To evaluate the relationship between pain catastrophizing level, sensory processing patterns, and headache severity among adolescents with episodic migraine.

Background

Catastrophizing about pain is a critical variable in how we understand adjustment to pain and has a unique contribution in predicting pain intensity. Recent reports found that migraine is also related to enhanced sensory sensitivity. However, the relationship between pain severity, pain catastrophizing level and sensory sensitivity requires greater study especially among adolescents.

Methods

Participants were 92 adolescents aged 13–18 years, 40 with episodic migraine and 52 healthy controls. The migraine patients were prospectively recruited from outpatient pediatric neurology clinics. All participants completed the Adolescent/Adult Sensory Profile (AASP), and the Pain Catastrophizing Scale for children (PCS-ch). The migraine groups also completed the PedMIDAS, which measures Headache related disability.

Results

Adolescents with migraine had significantly lower tendency to seek sensory input than healthy controls. Elevated rumination and helplessness correlated with higher migraine pain severity. Tendency to avoid sensory input predicted the migraine related disability level. They also significantly higher pain catastrophizing level than healthy controls, as seen in enhanced rumination ( p ≤ 0.001) and helplessness ( p ≤ 0.05).

Conclusions

Sensory processing difficulties are common among adolescents with episodic migraine. Sensory avoidance may be related to pain experience, and pain catastrophizing and disability level.

Trial registration

ISRCTN ISRCTN73824458. Registered 28 September 2014. retrospectively registered.

Related collections

Most cited references 41

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Pathophysiology of Migraine: A Disorder of Sensory Processing.

Peter J Goadsby, Philip Holland, Margarida Martins-Oliveira … (2017)

Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.

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Theoretical perspectives on the relation between catastrophizing and pain.

Michael Sullivan, Beverly Thorn, Jennifer Haythornthwaite … (2001)

The tendency to "catastrophize" during painful stimulation contributes to more intense pain experience and increased emotional distress. Catastrophizing has been broadly conceived as an exaggerated negative "mental set" brought to bear during painful experiences. Although findings have been consistent in showing a relation between catastrophizing and pain, research in this area has proceeded in the relative absence of a guiding theoretical framework. This article reviews the literature on the relation between catastrophizing and pain and examines the relative strengths and limitations of different theoretical models that could be advanced to account for the pattern of available findings. The article evaluates the explanatory power of a schema activation model, an appraisal model, an attention model, and a communal coping model of pain perception. It is suggested that catastrophizing might best be viewed from the perspective of hierarchical levels of analysis, where social factors and social goals may play a role in the development and maintenance of catastrophizing, whereas appraisal-related processes may point to the mechanisms that link catastrophizing to pain experience. Directions for future research are suggested.

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Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain.

Rodrigo Noseda, Rami Burstein (2013)

Scientific evidence supports the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation, and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory, and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. Data supporting the activation and sensitization of the trigeminovascular system include the progressive development of cephalic and whole-body cutaneous allodynia during a migraine attack. In addition, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex. Copyright © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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Author and article information

Contributors

Jacob Genizi: genizij@gmail.com

Journal

Journal ID (nlm-ta): J Headache Pain

Journal ID (iso-abbrev): J Headache Pain

Title: The Journal of Headache and Pain

Publisher: Springer Milan (Milan )

ISSN (Print): 1129-2369

ISSN (Electronic): 1129-2377

Publication date (Electronic): 6 May 2020

Publication date PMC-release: 6 May 2020

Publication date Collection: 2020

Volume: 21

Issue: 1

Electronic Location Identifier: 48

Affiliations

[1 ] GRID grid.414529.f, Pediatric Neurology Unit, , Bnai Zion Medical Center, ; Haifa, Israel

[2 ] GRID grid.414529.f, Department of Pediatrics, , Bnai Zion Medical Center, ; Haifa, Israel

[3 ] GRID grid.6451.6, ISNI 0000000121102151, Bruce and Ruth Rappaport Faculty of Medicine, , Technion, ; Haifa, Israel

[4 ] GRID grid.12136.37, ISNI 0000 0004 1937 0546, Department of Pediatric Neurology, Schneider Children’s Medical Center, Petach Tikva, Sackler Faculty of Medicine, , Tel Aviv University, ; Tel Aviv, Israel

[5 ]Child Development and Pediatric Neurology Service, Meuhedet-Northern Region, Haifa, Israel

[6 ] GRID grid.414529.f, Division of Allergy and Clinical Immunology, , Bnai Zion Medical Center, ; Haifa, Israel

[7 ] GRID grid.18098.38, ISNI 0000 0004 1937 0562, Occupational Therapy Department, , University of Haifa, ; Haifa, Israel

Article

Accession ID: PMC7203579 Pmcid ID: PMC7203579 Pmc-uid ID: 7203579 Publisher ID: 1119

DOI: 10.1186/s10194-020-01119-0

PMC ID: 7203579

PubMed ID: 32375649

SO-VID: 3ac1a32a-211d-4119-8320-bf5e46622794

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 8 March 2020

Date accepted : 28 April 2020

Custom metadata

Keywords: Sensory processing,Adolescents,Migraine,Pain catastrophizing level,Headache

Data availability:

Keywords: Sensory processing, Adolescents, Migraine, Pain catastrophizing level, Headache

Sensory processing patterns affect headache severity among adolescents with migraine

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Abstract

Objective

Background

Methods

Results

Conclusions

Trial registration

Related collections

New directions in predictive processing

Most cited references 41

Pathophysiology of Migraine: A Disorder of Sensory Processing.

Theoretical perspectives on the relation between catastrophizing and pain.

Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain.

Author and article information

Contributors

Journal

Affiliations

Article

History

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