Article

Natural history of headache after traumatic brain injury.

Department of Rehabilitation Medicine, University of Washington, Seattle, Washington 98195-6490, USA.
Journal of neurotrauma (Impact Factor: 3.97). 07/2011; 28(9):1719-25. DOI: 10.1089/neu.2011.1914
Source: PubMed

ABSTRACT Headache is one of the most common persisting symptoms after traumatic brain injury (TBI). Yet there is a paucity of prospective longitudinal studies of the incidence and prevalence of headache in a sample with a range of injury severity. We sought to describe the natural history of headache in the first year after TBI, and to determine the roles of prior history of headache, sex, and severity of TBI as risk factors for post-traumatic headache. A cohort of 452 acute, consecutive patients admitted to inpatient rehabilitation services with TBI were enrolled during their inpatient rehabilitation from February 2008 to June 2009. Subjects were enrolled across 7 acute rehabilitation centers designated as TBI Model Systems centers. They were prospectively assessed by structured interviews prior to inpatient rehabilitation discharge, and at 3, 6, and 12 months after injury. Results of this natural history study suggest that 71% of participants reported headache during the first year after injury. The prevalence of headache remained high over the first year, with more than 41% of participants reporting headache at 3, 6, and 12 months post-injury. Persons with a pre-injury history of headache (p<0.001) and females (p<0.01) were significantly more likely to report headache. The incidence of headache had no relation to TBI severity (p=0.67). Overall, headache is common in the first year after TBI, independent of the severity of injury range examined in this study. Use of the International Classification of Headache Disorders criteria requiring onset of headache within 1 week of injury underestimates rates of post-traumatic headache. Better understanding of the natural history of headache including timing, type, and risk factors should aid in the design of treatment studies to prevent or reduce the chronicity of headache and its disruptive effects on quality of life.

Full-text

Available from: Sureyya Dikmen, Apr 21, 2015
1 Follower
 · 
140 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Sports concussion headache (SCH) is common; yet poorly researched and understood. Somatic complaints including headache are frequently reported by both amateur and professional athletes. Although the literature is replete with reports of a high incidence of headache following sports concussive injuries, there is a dearth of evidence-based medicine to provide practitioners with an understanding of sports concussion headache risk factors, epidemiology, biomechanical risk factors and/or injury thresholds, aetiology, assessment, treatment or prognosis. Review: This article will provide readers with an overview of SCH based on the available literature (which as noted is limited); and, where evidence is lacking, information will be provided from the more general post-traumatic headache (PTHA) literature, the author’s extensive clinical experience and literature from parallel primary headache disorders. Incidence, pathoanatomy, neurobiology, classification, natural history and prognosis of sports concussion headache will be reviewed. Common, as well as less common, sports concussion headache sub-types will be discussed. General approaches to evaluation (including history taking and physical examination), as well as treatment approaches will also be addressed for specific headache subtypes. Lastly, directions for future research will be explored.
    Brain Injury 10/2014; 29(2). DOI:10.3109/02699052.2014.965213 · 1.86 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Headache is one of the most common symptoms following traumatic head injury. The mechanisms underlying the emergence of such post-traumatic headache (PTH) remain unknown but may be related to injury of deep cranial tissues or damage to central pain processing pathways, as a result of brain injury.MethodsA mild closed head injury in mice combined with the administration of cranial or hindpaw formalin tests was used to examine post-traumatic changes in the nociceptive processing from deep cranial tissues or the hindpaw. Histological analysis was used to examine post-traumatic pro-inflammatory changes in the calvarial periosteum, a deep cranial tissue.ResultsAt 48 h after head injury, mice demonstrated enhanced nociceptive responses following injection of formalin into the calvarial periosteum, a deep cranial tissue, but no facilitation of the nociceptive responses following injection of formalin into an extracranial tissue, the hindpaw. Mice also showed an increase in the number of activated periosteal mast cells 48 h following mild head trauma, suggesting an inflammatory response.Conclusion Our study demonstrates that mild closed head injury is associated with enhanced processing of nociceptive information emanating from trigeminal-innervated deep cranial tissues, but not from non-cranial tissues. Based on these finding as well as the demonstration of head injury-evoked degranulation of calvarial periosteal mast cells, we propose that inflammatory-evoked enhancement of peripheral cranial nociception, rather than changes in supraspinal pain mechanisms play a role in the initial emergence of PTH. Peripheral targeting of nociceptors that innervate the calvaria may be used to ameliorate PTH pain.
    European journal of pain (London, England) 09/2014; DOI:10.1002/ejp.583 · 3.22 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although the prevalence rate of chronic post traumatic headache (CPTHA) after mild traumatic brain injury (TBI) reaches up to 95%, its mechanism is unknown and little is known about the characteristics of the pain system in this condition. Our aim was to investigate the capabilities of two pain modulatory systems among individuals with CPTHA and study their association with CPTHA, here for the first time. Forty-six subjects participated; 16 with TBI and CPTHA, 12 with TBI without CPTHA, and 18 healthy controls. Testing included the measurement of heat-pain (HPT) and pressure-pain (PPT) thresholds in the forehead and forearm, pain adaptation to tonic noxious heat and conditioned pain modulation (CPM). The participants completed a post-traumatic stress disorder (PTSD) questionnaire. The two TBI groups did not differ in the TBI and background characteristics. However, TBI patients with CPTHA had significantly higher HPT and lower PPT in the cranium and higher PTSD symptomatology compared to TBI patients without CPTHA and healthy controls. Adaptation to pain and CPM were diminished in the CPTHA group compared to the two control groups. The intensity of CPTHA correlated negatively with cranial PPT, magnitude of pain adaptation and CPM. CPTHA intensity correlated positively with PTSD symptomatology. CPTHA appears to be are characterized by cranial hyperalgesia and dysfunctional pain modulation capabilities, that are associated with CPTHA magnitude. It is concluded that damage to pain modulatory systems along with chronic cranial sensitization underlies the development of CPTHA. PTSD may reinforce CPTHA and vice versa. Clinical implications are discussed.
    Journal of Neurotrauma 07/2014; 32(1). DOI:10.1089/neu.2014.3359 · 3.97 Impact Factor