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Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions

Emerging evidence suggests mild traumatic brain injury related headache (MTBI-HA) is a form of neuropathic pain state. Previous supraspinal mechanistic studies indicate patients with MTBI-HA demonstrate a dissociative state with diminished levels of supraspinal prefrontal pain modulatory functions a...

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Autores principales: Flowers, Matthew, Leung, Albert, Schiehser, Dawn M, Metzger-Smith, Valerie, Delano-Wood, Lisa, Sorg, Scott, Kunnel, Alphonsa, Wong, Angeline, Vaninetti, Michael, Golshan, Shahrokh, Lee, Roland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358489/
https://www.ncbi.nlm.nih.gov/pubmed/34365850
http://dx.doi.org/10.1177/17448069211037881
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author Flowers, Matthew
Leung, Albert
Schiehser, Dawn M
Metzger-Smith, Valerie
Delano-Wood, Lisa
Sorg, Scott
Kunnel, Alphonsa
Wong, Angeline
Vaninetti, Michael
Golshan, Shahrokh
Lee, Roland
author_facet Flowers, Matthew
Leung, Albert
Schiehser, Dawn M
Metzger-Smith, Valerie
Delano-Wood, Lisa
Sorg, Scott
Kunnel, Alphonsa
Wong, Angeline
Vaninetti, Michael
Golshan, Shahrokh
Lee, Roland
author_sort Flowers, Matthew
collection PubMed
description Emerging evidence suggests mild traumatic brain injury related headache (MTBI-HA) is a form of neuropathic pain state. Previous supraspinal mechanistic studies indicate patients with MTBI-HA demonstrate a dissociative state with diminished levels of supraspinal prefrontal pain modulatory functions and enhanced supraspinal sensory response to pain in comparison to healthy controls. However, the relationship between supraspinal pain modulatory functional deficit and severity of MTBI-HA is largely unknown. Understanding this relationship may provide enhanced levels of insight about MTBI-HA and facilitate the development of treatments. This study assessed pain related supraspinal resting states among MTBI-HA patients with various headache intensity phenotypes with comparisons to controls via functional magnetic resonance imaging (fMRI). Resting state fMRI data was analyzed with self-organizing-group-independent-component-analysis in three MTBI-HA intensity groups (mild, moderate, and severe) and one control group (n = 16 per group) within a pre-defined supraspinal pain network based on prior studies. In the mild-headache group, significant increases in supraspinal function were observed in the right premotor cortex (T = 3.53, p < 0.001) and the left premotor cortex (T = 3.99, p < 0.0001) when compared to the control group. In the moderate-headache group, a significant (T = −3.05, p < 0.01) decrease in resting state activity was observed in the left superior parietal cortex when compared to the mild-headache group. In the severe-headache group, significant decreases in resting state supraspinal activities in the right insula (T = −3.46, p < 0.001), right premotor cortex (T = −3.30, p < 0.01), left premotor cortex (T = −3.84, p < 0.001), and left parietal cortex (T = −3.94, p < 0.0001), and an increase in activity in the right secondary somatosensory cortex (T = 4.05, p < 0.0001) were observed when compared to the moderate-headache group. The results of the study suggest that the increase in MTBI-HA severity may be associated with an imbalance in the supraspinal pain network with decline in supraspinal pain modulatory function and enhancement of sensory/pain decoding.
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spelling pubmed-83584892021-08-13 Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions Flowers, Matthew Leung, Albert Schiehser, Dawn M Metzger-Smith, Valerie Delano-Wood, Lisa Sorg, Scott Kunnel, Alphonsa Wong, Angeline Vaninetti, Michael Golshan, Shahrokh Lee, Roland Mol Pain Research Article Emerging evidence suggests mild traumatic brain injury related headache (MTBI-HA) is a form of neuropathic pain state. Previous supraspinal mechanistic studies indicate patients with MTBI-HA demonstrate a dissociative state with diminished levels of supraspinal prefrontal pain modulatory functions and enhanced supraspinal sensory response to pain in comparison to healthy controls. However, the relationship between supraspinal pain modulatory functional deficit and severity of MTBI-HA is largely unknown. Understanding this relationship may provide enhanced levels of insight about MTBI-HA and facilitate the development of treatments. This study assessed pain related supraspinal resting states among MTBI-HA patients with various headache intensity phenotypes with comparisons to controls via functional magnetic resonance imaging (fMRI). Resting state fMRI data was analyzed with self-organizing-group-independent-component-analysis in three MTBI-HA intensity groups (mild, moderate, and severe) and one control group (n = 16 per group) within a pre-defined supraspinal pain network based on prior studies. In the mild-headache group, significant increases in supraspinal function were observed in the right premotor cortex (T = 3.53, p < 0.001) and the left premotor cortex (T = 3.99, p < 0.0001) when compared to the control group. In the moderate-headache group, a significant (T = −3.05, p < 0.01) decrease in resting state activity was observed in the left superior parietal cortex when compared to the mild-headache group. In the severe-headache group, significant decreases in resting state supraspinal activities in the right insula (T = −3.46, p < 0.001), right premotor cortex (T = −3.30, p < 0.01), left premotor cortex (T = −3.84, p < 0.001), and left parietal cortex (T = −3.94, p < 0.0001), and an increase in activity in the right secondary somatosensory cortex (T = 4.05, p < 0.0001) were observed when compared to the moderate-headache group. The results of the study suggest that the increase in MTBI-HA severity may be associated with an imbalance in the supraspinal pain network with decline in supraspinal pain modulatory function and enhancement of sensory/pain decoding. SAGE Publications 2021-08-08 /pmc/articles/PMC8358489/ /pubmed/34365850 http://dx.doi.org/10.1177/17448069211037881 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Research Article
Flowers, Matthew
Leung, Albert
Schiehser, Dawn M
Metzger-Smith, Valerie
Delano-Wood, Lisa
Sorg, Scott
Kunnel, Alphonsa
Wong, Angeline
Vaninetti, Michael
Golshan, Shahrokh
Lee, Roland
Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title_full Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title_fullStr Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title_full_unstemmed Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title_short Severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
title_sort severities in persistent mild traumatic brain injury related headache is associated with changes in supraspinal pain modulatory functions
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358489/
https://www.ncbi.nlm.nih.gov/pubmed/34365850
http://dx.doi.org/10.1177/17448069211037881
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