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Post-traumatic headache: epidemiology and pathophysiological insights

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@article{cc27334c00f54856b656a510eadd62d4,
title = "Post-traumatic headache: epidemiology and pathophysiological insights",
abstract = "Post-traumatic headache (PTH) is a highly disabling secondary headache disorder and one of the most common sequelae of mild traumatic brain injury, also known as concussion. Considerable overlap exists between PTH and common primary headache disorders. The most common PTH phenotypes are migraine-like headache and tension-type-like headache. A better understanding of the pathophysiological similarities and differences between primary headache disorders and PTH could uncover unique treatment targets for PTH. Although possible underlying mechanisms of PTH have been elucidated, a substantial void remains in our understanding, and further research is needed. In this Review, we describe the evidence from animal and human studies that indicates involvement of several potential mechanisms in the development and persistence of PTH. These mechanisms include impaired descending modulation, neurometabolic changes, neuroinflammation and activation of the trigeminal sensory system. Furthermore, we outline future research directions to establish biomarkers involved in progression from acute to persistent PTH, and we identify potential drug targets to prevent and treat persistent PTH.",
author = "H{\aa}kan Ashina and Frank Porreca and Trent Anderson and Amin, {Faisal Mohammad} and Messoud Ashina and Schytz, {Henrik Winther} and Dodick, {David W}",
year = "2019",
month = "10",
doi = "10.1038/s41582-019-0243-8",
language = "English",
volume = "15",
pages = "607--617",
journal = "Nature Reviews Neurology",
issn = "1759-4758",
publisher = "Nature Publishing Group",
number = "10",

}

RIS

TY - JOUR

T1 - Post-traumatic headache

T2 - epidemiology and pathophysiological insights

AU - Ashina, Håkan

AU - Porreca, Frank

AU - Anderson, Trent

AU - Amin, Faisal Mohammad

AU - Ashina, Messoud

AU - Schytz, Henrik Winther

AU - Dodick, David W

PY - 2019/10

Y1 - 2019/10

N2 - Post-traumatic headache (PTH) is a highly disabling secondary headache disorder and one of the most common sequelae of mild traumatic brain injury, also known as concussion. Considerable overlap exists between PTH and common primary headache disorders. The most common PTH phenotypes are migraine-like headache and tension-type-like headache. A better understanding of the pathophysiological similarities and differences between primary headache disorders and PTH could uncover unique treatment targets for PTH. Although possible underlying mechanisms of PTH have been elucidated, a substantial void remains in our understanding, and further research is needed. In this Review, we describe the evidence from animal and human studies that indicates involvement of several potential mechanisms in the development and persistence of PTH. These mechanisms include impaired descending modulation, neurometabolic changes, neuroinflammation and activation of the trigeminal sensory system. Furthermore, we outline future research directions to establish biomarkers involved in progression from acute to persistent PTH, and we identify potential drug targets to prevent and treat persistent PTH.

AB - Post-traumatic headache (PTH) is a highly disabling secondary headache disorder and one of the most common sequelae of mild traumatic brain injury, also known as concussion. Considerable overlap exists between PTH and common primary headache disorders. The most common PTH phenotypes are migraine-like headache and tension-type-like headache. A better understanding of the pathophysiological similarities and differences between primary headache disorders and PTH could uncover unique treatment targets for PTH. Although possible underlying mechanisms of PTH have been elucidated, a substantial void remains in our understanding, and further research is needed. In this Review, we describe the evidence from animal and human studies that indicates involvement of several potential mechanisms in the development and persistence of PTH. These mechanisms include impaired descending modulation, neurometabolic changes, neuroinflammation and activation of the trigeminal sensory system. Furthermore, we outline future research directions to establish biomarkers involved in progression from acute to persistent PTH, and we identify potential drug targets to prevent and treat persistent PTH.

U2 - 10.1038/s41582-019-0243-8

DO - 10.1038/s41582-019-0243-8

M3 - Review

VL - 15

SP - 607

EP - 617

JO - Nature Reviews Neurology

JF - Nature Reviews Neurology

SN - 1759-4758

IS - 10

ER -

ID: 58653435