Acute headache attributed to trauma or injury to the head and/or neck is defined by the International Headache Society (ICHD 3 beta) as a headache occurring within 7 days of a head or neck trauma or within 7 days of being able to report pain after the injury but lasting less than 3 months1. After 3 months, it is called persistent Post-traumatic Headache1.
Post Traumatic Headache (PTH) is the most common symptom of concussion, often as a result of sports injury, falls or motor vehicle accidents. Biomechanical forces imparted to the brain can also be transmitted to the cervical spine resulting in a whiplash-type injury and cervicogenic headaches that are mediated by a combination of local inflammation, central sensitization, and sensory and autonomic pathway dysfunction.
PTH is more frequent after mild TBI (mTBI) than moderate or severe TBI, and can resemble migraine-type or tension-type headaches2. Migraine-type headaches are more prevalent, and can occur in patients with no pre-injury history but with a family history of migraines or in those with pre-injury migraine headaches3.
Epidemiology including risk factors and primary prevention
The National Electronic Injury Surveillance Centers reported approximately 3.4 million ED visits for sports and recreational related TBI between 2001 to 2012; the annual rate increased in both sexes in all age groups4. The 0-19 year age group were the most affected (70%). Most TBI in this age group were mild with 90% treated and released from the EDs4. Males had twice the rates of concussion. Bicycling, football and basketball were associated with the majority of injuries in males while bicycling, playground activities and horseback riding accounted for TBI in females.
Eisenberg et al reported 85% of children presented with headache following mTBI5. Meehan et al reported 93% PTH among high school students with concussion6. Kuczynski et al reported that 11% of pediatric patients who presented with mTBI had headaches 2 weeks after injury7.
Risk factors (for PTH)
Risk factors for acute PTH in adults with moderate or severe TBI include prior moderate to severe headaches and female gender8. Their findings showed that the migranous type of HA in sports-related concussion was associated cognitive impairment and protracted recovery in a cohort study.
In the pediatric population, risk factors are not consistent. Several studies have reported a trend toward female gender and adolescence being risk factors for PTH9,. Repetitive head injuries did not predict occurrence or recovery from PTH9. Developmental disorders, psychiatric disorders, history of headaches or migraines can influence concussion recovery time10.
In professional athletes, risk factors were associated with history of prior concussion, longer sport exposure, and ApoE4 gene11,12
Once a concussion occurs, common triggers for PTH include physical or cognitive exertion, sleep deprivation, changes in environment, dehydration, and emotional stress13
Several sporting agencies have changed rules of play and advocated use of protective equipment to reduce concussions. Though these changes have reduced the incidence of moderate to severe TBI, the benefit of special equipment in reducing concussion or PTH remains to be proven.
Physical and cognitive rest following concussion may limit the severity and longevity of post-concussion headaches.
During a concussive blow, rotational or angular acceleration forces are transmitted to the brain leading to straining of neural elements and disruption of the neuronal membrane. It has been postulated that this may lead to cortical spreading depression, changes in intracellular sodium, calcium and extracellular potassium, excess release of opioids and excitatory amino acids, such as beta-endorphins and glutamate14. This mechanism is well described in migraines, and may also be seen in PTH. Other possible contributors are trigeminal nociception or injury to upper cervical roots by forced flexion and extension of the neck which may trigger the trigeminal nucleus caudalis to cause centrally derived pain.15
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation overtime)
Migrainous PTH are characterized by paroxysmal attacks of unilateral, severe, throbbing, or pulsating headaches, which are frequently accompanied by photo- and phonophobia, nausea, and vomiting8. These headaches are typically provoked by stereotypical stimuli including bright lights, stress, dehydration, poor sleep, and certain foods and last from 4 to 72 h after which patients typically experience headache-free periods8. Typically PTH resolve within 7-10 days following the initial injury8. Cervicogenic PCD patients typically present with neck pain and stiffness, fatigue, and fogginess, dizziness with movement or prolonged neck stabilization. These headaches are often occipital, radiate to the temples and eyes, and are exacerbated by poor posture, weight training and running. Common findings include paraspinal and sub-occipital muscle tenderness and spasm, decreased cervical spine range of motion, and dizziness. Cervicogenic PCD patients do not experience an early symptom-limited threshold on graded aerobic treadmill testing15.
Babcock et al demonstrated that 29.3% of children aged 5 to 18 years had headaches at 3 months after TBI16. Barlow et al reported that among patients presenting to an emergency department, three months after mTBI, 11% out of 670 mTBI patients were symptomatic compared to 0.5% of 197 extracranial injury (ECI) group. The prevalence of symptoms decreased over time with only 2.3% of mTBI patients having persistent symptoms at 1 year, compared to 0.01% in the ECI group. All of those patients with symptoms at 1 year continued to report headache17.
Specific secondary or associated conditions and complications
PTH is part of a complex set of symptoms that constitute post-concussive syndrome. These symptoms can be categorized into five clinical domains: somatic (headache), cognitive or emotional symptoms (lability), physical signs (LOC, amnesia), behavioral changes (irritability), cognitive impairment (decreased attention, memory impairments, slowed reaction times), and sleep disturbance (insomnia).
2. ESSENTIALS OF ASSESSMENT
History should be focused on the details of the injury, headache characteristics and risk factors for persistent symptoms.
Initial injury details that are important to elicit from the athlete include the mechanism of injury, the presence of loss of consciousness, post-traumatic amnesia or seizure; concussion symptoms experienced at the time of injury, and initial and subsequent medical management of the injury.
Characteristics of the headache to determine type of headache, whether migrainous, tension or otherwise should be obtained. Symptoms such as location (unilateral vs generalized) characteristic (gripping vs throbbing), associated symptoms (photophobia, nausea and vomiting), can help differentiate the types. Changes in vision, hearing, balance can be associated or be triggers for headaches. Details regarding the course of the headaches-improvements or deterioration, response to different treatment strategies should be sought.
Pre-existing medical conditions that may impact concussion recovery and symptom duration include previous concussions, non-specific or migraine headaches, ADHD or learning disorders, psychiatric conditions such as depressive or anxiety disorders, previous cervical spine injuries, and pre-existing neuro-ophthalomological conditions such as strabismus or convergence insufficiency are important. A family history of psychiatric disorders and migraine headaches may also predispose patients to post-concussion symptoms or conditions.
The physical examination in PTH comprises of a complete neurological evaluation including cognition and balance testing such as Balance Error Scoring System.
In symptomatic patients a focused vestibulo-ocular examination including testing of convergence, smooth pursuits, saccades, vestibulo-ocular reflex, visual acuity, visual fields, color vision, as well as fundoscopy is required. All patients should undergo an examination of the jaw, temporomandibular joint, cervical spine that includes range of motion, palpation, and provocative ligament and cervical dizziness testing. Those that report a history of intermittent vertigo should undergo the Dix-Hallpike maneuver to test for benign paroxysmal positional vertigo (BPPV).
History of headache and its effect on basic and instrumental ADL vocation and recreation should be elicited. The MIDAS (Migraine Disability Assessment questionnaire) is a 5-item questionnaire that can help clinicians track the impact of PTH on daily life18.
No recommendations have been made for routine blood tests.
There is also insufficient data that biochemical serum and cerebral spinal fluid biomarkers of brain injury to justify the routine use of these biomarkers clinically19,20.
Similarly, the significance of genetic markers in the management of sports concussion risk or injury outcome is unclear at this time 21
CT scans are usually not indicated in concussions except when there are suspicion of intracranial hemorrhage in athletes who have LOC, posttraumatic amnesia, persistently altered mental status (Glasgow Coma Scale ,15), focal neurologic deficit, evidence of skull fracture on examination, or signs of clinical deterioration. Some authors suggest that any athlete with loss LOC (grade 3 concussion) should have a CT scan22. However, this recommendation remains controversial. In a study of 712 patients with LOC or amnesia and a perfect GCS, the prevalence of abnormal CT scans was 9%, with less than 1% requiring surgical intervention23. In an emergency department-based study by Papa et al, the percentage of abnormal CT scans in adult patients increased from 13% for patients with a perfect GCS score to 37% for those with a GCS score of 1320.Athletes with a brief LOC are at no higher risk for long-term neurologic sequelae, and indications for imaging should not differ from those listed above23. CT scanning continues to be the imaging study of choice in evaluating an acute head injury as it is better at imaging acute hemorrhage, requires less time and is a better tool for monitoring patients than magnetic resonance imaging (MRI).
MRI is the imaging study of choice for patients with prolonged symptoms (> 7 d) or for a late change in an individual’s neurologic signs or symptoms. A study by Strauss et al identified early diffusion tensor imaging (DTI) biomarkers of mild traumatic brain injury that significantly predicted outcomes at 1 year following injury24. The study found that abnormally high fractional anisotropy is significantly associated with better outcomes and might represent an imaging correlate of post-injury compensatory processes24,25
Although positron emission tomography (PET) scanning, functional MRIs (fMRIs) diffusion tensor imaging, magnetic resonance spectroscopy, functional connectivity) have demonstrated some compelling findings, these tests are used mainly in a research setting26,27,28.
Different electrophysiological recording techniques (eg, evoked response potential (ERP), cortical magnetic stimulation and electroencephalography) although promising have not shown consistent difference from controls.
Detailed neuro-psychologic testing is employed more often in athletes who are at the professional level or in mTBI research but should be offered to all patients who have persistent symptoms. When evaluating an athlete’s performance on the neuropsychological tests, it is best to compare results with previous testing, if available.
The National Hockey League (NHL), National Football League (NFL), Major League Baseball (MLB) as well as many college teams are utilizing limited neuro-psychologic testing to document the possible prolonged effects of presumed minor head injuries and to assist the clinician in determining possible retirement issues29.
Supplemental assessment tools
Sideline testing (e.g. SCAT-3, King-Devick) or online concussion (e.g. Impact) testing can help identify athletes who are at risk of developing symptoms. The SCAT-3 has been recommended by the Zurich, incorporates the Maddocks’ questions and the Standardized Assessment of Concussion (SAC)30.
EARLY PREDICTIONS OF OUTCOMES
No correlation exists between injury severity and post-concussion HA. Headaches lasting more than 10 days have poorer prognosis. Noise and light sensitivity and early onset migraine predict a more prolonged course. Symptom burden at the time of the concussion may also be predictive of post-concussion syndrome.
Social role and social support system
Patient and family education regarding PTH and its distinction from other types of headaches and brain injury, prognosis and expected recovery is important. Avoiding cognitive overexertion and/or the environment to the triggering of symptoms and headaches is an important measure.
Physical and cognitive rest is recommended until the acute symptoms resolve, especially in the first 24 to 48 hours. The athlete may return to play when symptom free and not taking any medications that could mask or modify symptoms. Implementation of a graded return-to-play program is recommended, starting with minimal activity and gradually increasing intensity every 24 hours so long as the athlete remains asymptomatic There is evidence that exercise potentially offers a neuroprotective effect through the activation of specific neuronal circuits, resulting in enhanced vascularization and neuronal proliferation30.
A letter that helps the school/employer and patient understand this connection between cognitive overexertion, physical problems and symptoms and suggesting appropriate accommodations often is helpful. The CDC’s HeadsUp program and the AAP both describe plans for returning children and adolescents to school.31, 32
3. REHABILITATION MANAGEMENT AND TREATMENTS
Available or current treatment guidelines
No formal guidelines exist for PTH. There are guidelines for concussion management in general and in the athlete.
Initial evaluations and recommendations
The consensus recommendations for sideline assessment include initially considering cervical spine injury, immediate full assessment by a health care provider and removal from play. The Sport Concussion Assessment Tool, Version 3 (SCAT3), has been developed to guide the clinical assessment at the sidelines.
First line treatments of headaches include proper hydration (non-caffeinated fluids) and nonsteroidal anti-inflammatory medications13. Although there are no clinical trials in humans, Ibuprofen (7.5–10 mg/kg) is recommended as first-line treatment of acute migraine in children due to its analgesic and anti-inflamatory benefits33. Acetaminophen (15 mg/kg) is also safe and well tolerated and probably effective in the treatment of children with acute migraine34. Dosage should be limited to no more than 3 days per week (maximum 2 doses in the same day)33,34.
If NSAIDs are not effective, triptans may be considered35,36,37. However, there is a theoretical risk of vasospasm which may exacerbate hypoperfusion resulting in vascular injury to the brain. The efficacy of triptans has been studied in adults soldiers but not pediatric population37. Imaging should be done prior to triptan administration in any child with headache and persistent altered mental status or focal neurological findings. Triptans should be taken at the onset of headache and can be repeated 2 hours later if needed. The dosage recommendations for each of the 7 triptan differ, but all should be limited to no more than 9 days per month to avoid rebound headaches. Caution should be used in patients with known ischemic heart disease, uncontrolled hypertension, or suspected basilar or hemiplegic migraine. Administration within 24 hours of an ergot derivative or other serotonin agonists and during or within 2 weeks of monoamine oxidase inhibitor use should be avoided. At present, three triptans are FDA approved for use in pediatric migraine, almotriptan in children above 12, rizatriptan in children above 6 , and most recently, zolmitriptan nasal spray in children above 12. However, the safety and efficacy of triptans have not been studied in PTH.38,
Another option to triptans are anti-epileptic drugs, anti-depressants or beta-blockers39,40,41. Anti-epileptic drugs such as topiramate should also be used judiciously in the setting of cognitive complaints, as these medications could potentially exacerbate these symptoms. For tension type HA, tricyclics (nortriptyline 25-75 mg per day) may be preferred41.
Non-pharmacological treatment alternatives include physical therapy and cervical manipulation, cognitive behavioral therapy, transcutaneous nerve stimulators, biofeedback, and relaxation therapy. The treatment of PTH often necessitates a multidisciplinary approach due to the heterogeneous nature of symptomatology and the variability of clinical presentation42,43.
Subacute or chronic phase
Rebound headache from analgesic overuse, which was present in 20% to 45% of patients in one study, often responds to analgesic withdrawal. In a retrospective study of adolescent patients with concussion, overuse of analgesics following injury exacerbated concussion-related headaches or made them chronic41.
Opioids, steroids, barbiturate hypnotics, and lidocaine injections have not been well studied in the pediatric population for any headache phenotype, and therefore no recommendation has been made regarding its use. They should be avoided in patients with persistent PTH. There is increasing evidence that these compounds may cause long-term detrimental effects and there is a risk of long-term dependence and the development of MOH, specifically in patients who may be prescribed opioid or barbiturate containing medications.
There is no clear evidence to help guide the clinician on the timing of initiation of preventive therapy in children to decrease the likelihood of developing persistent PTH. In general, prophylaxis should be limited to those children and adolescents whose headaches occur with sufficient frequency and/or severity to warrant a daily medication, a minimum of 1 headache per week or 3–4 headaches per month to justify initiating and to limit the duration to a period of 4–6 months. Tricyclic antidepressants, such as amitriptyline and nortriptyline, anti-epileptics such as topiramate, valproic acid, gabapentin, and zonisamide, and beta-blockers, like propranolol, as well as supplements such as melatonin and magnesium have been studied and found useful.
Consultation with a headache specialist or brain injury medicine physician is indicated for patients who have prolonged symptoms. Neuropsychologic consultation may also be considered to document and remediate any deficits that may interfere with the return to sport, school, or work.
Coordination of care
Parallel practice: Consider cognitive behavioral management strategies, especially if prominent psychosocial issues exist.
Communication with the school or workplace early in the treatment process to make provisions for cognitive rest can lessen symptom frequency/severity. These accommodations include frequent rest breaks, more time for tests, provision of class notes, etc.
Multidisciplinary: Participation in a formal pain rehabilitation program may be needed if HA pain becomes refractory to treatment and is functionally limiting.
Patient & familyeducation
Education has been shown to have the biggest impact in managing post concussive symtoms. The patient and family be informed of expected improvements over time, and importance of physical and cognitive rest in the early stages.
4. Gaps in the evidence–based knowledge
There is no laboratory or imaging correlates to PTH to verify diagnosis, severity or response to treatment. The mechanism of headache generation is not understood. Little is also known about the long term effects of multiple concussions, relation to mild cognitive impairments (MCI’s), chronic traumatic encephalopathy (CTE), and other adverse outcomes.
It has become evident, that athletes should not return to play on the day of injury, but there is limited understanding of the optimal amount of rest needed for recovery, ideal time frame to undertake graded aerobic treadmill testing and initiate sub-maximal aerobic exercise treatment to manage the PTH or other postconcussive symptoms.
5. Cutting edge/emerging and unique concepts and practice
Emerging therapy for PTH include use of IV ketorolac, prochlorperazine, metoclopramide, or ondansetron within 14 days of initial injury for intractable PTH. 86% of study subjects reported pain reduction (86 %), with 52 % reporting complete headache resolution44.
Onabotulinumtoxin A was approved by the FDA for use in chronic adult migraineurs in 2010; but there is limited experience in PTH or pediatric patients. In a retrospective consecutive case series of US servicemen treated with onabotulinum toxin A for chronic headaches after head injury (n = 64), 40.6% had at least 15 headache days per month with migraine features. Forty-one (64%) reported getting better45.
Peripheral Nerve Blocks have been used with dramatic results. 71% of patients(n=28) reported almost complete pain relief with 2% lidocaine with epinephrine scalp injections. Seeger et al performed a retrospective chart review including adolescent patients (mean age 15 years; n = 14) with PTH who received occipital nerve blocks. Sixty-four percent reported long-term response to the occipital nerve blocks, with associated improved quality of life and decreased post-concussion symptom scores46,47
Two small studies have also shown therapeutic benefits in the treatment of persistent PTH using transcranial magnetic stimulation (TMS) which has received FDA approval for treatment of migraine48.
- Olesen J . Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33(9):629–808.
- Lew HL, Lin PH, Fuh JL, et al.: Characteristics and treatment of headache after traumatic brain injury: a focused review. Am J Phys Med Rehabil. 2006; 85(7):619–27.
- Lucas S, Hoffman JM, Bell KR, et al.: A prospective study of prevalence and characterization of headache following mild traumatic brain injury. Cephalalgia2014; 34(2): 93–102.
- Victor G. Coronado, MD, MPH; Tadesse Haileyesus, MS; Tabitha A. Cheng, MD; Jeneita M. Bell, MD, MPH; Juliet Haarbauer-Krupa, PhD; Michael R. Lionbarger, MPH; Javier Flores-Herrera, MD, MPH; Lisa C. McGuire, PhD; Julie Gilchrist, MD.: J Head Trauma Rehabil Vol. 30, No. 3, pp. 185–197. Trends in Sports- and Recreation Related Traumatic Brain Injuries Treated in US Emergency Departments: The National Electronic Injury Surveillance System-All Injury Program (NEISS-AIP) 2001-2012
- Eisenberg MA, Meehan WP, Mannix R. Duration and course of post-concussive symptoms. 2014;133:999–1006.
- Meehan WP, d’Hemecourt P, Comstock RD. High school concussion in the 2008–2009 academic year: mechanism, symptoms, and management. Am J Sports Med. 2010;38(12):2405–9
- Kuczynski A, Crawford S, Bodell L, Dewey D, Barlow K. Characteristics of post-traumatic headaches in children following mild traumatic brain injury and their response to treatment: A prospective cohort. Dev Med Child Neurol.2013;55:636–641
- Kontos AP, Elbin RJ, Lau B, et al. Posttraumatic migraine as a predictor of recovery and cognitive impairment after sport-related concussion. Am J Sports Med. 2013;41(7):1497–504.
- McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med 2005;39:196–204.
- Bramley H, Heverley S, Lewis MM, et al. Demographics and treatment of adolescent posttraumatic headache in a regional concussion clinic. Pediatr Neurol.2015;52:493–498.
- Merritt VC1, Ukueberuwa DM1, Arnett PA1. Relationship between the apolipoprotein E gene and headache following sports-related concussion.J Clin Exp Neuropsychol.2016 Nov;38(9):941-9. doi: 10.1080/13803395.2016.1177491. Epub 2016 May 18
- Moran LM1, Taylor HG, Ganesalingam K, Gastier-Foster JM, Frick J, Bangert B, Dietrich A, Nuss KE, Rusin J, Wright M, Yeates KO. Apolipoprotein E4 as a predictor of outcomes in pediatric mild traumatic brain injury. J Neurotrauma.2009 Sep;26(9):1489-95. doi: 10.1089/neu.2008.0767.
- Seifert, T. Post-Traumatic Headache Therapy in the Athlete Curr Pain Headache Rep (2016) 20: 41. doi:10.1007/s11916-016-0568-6
- Taylor AR, Bell TK. Slowing of cerebral circulation after concussional head injury: a controlled trial. Lancet. 1966;2:178–80
- Iovesan EJ, Kowacs PA, Oshinsky ML. Convergence of cervical and trigeminal sensory afferents. Curr Pain Headache Rep. 2003;7(5):377–83.
- Babcock L, Byczkowski T, Wade SL, et al. Predicting postconcussion syndrome after mild traumatic brain injury in children and adolescents who present to the emergency department.Arch Pediatr Adolesc Med. 2012;167:156–161.
- Barlow KM, Crawford S, Stevenson A, et al. Epidemiology of postconcussion syndrome in pediatric mild traumatic brain injury. 2010;126:e374-e381.
- Stewart WF et al.Validity of the Migraine Disability Assessment(MIDAS) score in comparison to a diary-based measure in a population sample of migraine sufferers.Pain 2000:88(1):41-52
- Begaz T, Kyriacou DN, Segal J, et al. Serum biochemical markers for post-concussion syndrome in patients with mild traumatic brain injury. J Neurotrauma 2006;23:1201–10.
- Papa L, Brophy GM, Welch RD, Lewis LM, Braga CF, Tan CN, et al. Time Course and Diagnostic Accuracy of Glial and Neuronal Blood Biomarkers GFAP and UCH-L1 in a Large Cohort of Trauma Patients With and Without Mild Traumatic Brain Injury.JAMA Neurol. 2016 May 1. 73 (5):551-60. [Medline].
- Terrell TR, Bostick RM, Abramson R, et al. APOE, APOE promoter, and Tau genotypes and risk for concussion in college athletes. Clin J Sport Med 2008;18:10–17.
- Stein SC, Ross SE. Mild head injury: a plea for routine early CT scanning.J Trauma. 1992 Jul. 33(1):11-3. [Medline].
- Jeret JS, Mandell M, Anziska B, et al. Clinical predictors of abnormality disclosed by computed tomography after mild head trauma.Neurosurgery. 1993 Jan. 32(1):9-15; discussion 15-6. [Medline].
- Strauss SB, Kim N, Branch CA, Kahn ME, Kim M, Lipton RB, et al. Bidirectional Changes in Anisotropy Are Associated with Outcomes in Mild Traumatic Brain Injury.AJNR Am J Neuroradiol. 2016 Jun 9. [Medline].
- Anderson P. Neuroimaging May Predict Recovery After Mild TBI. Medscape Medical News. Available at http://www.medscape.com/viewarticle/866419#vp_2. July 21, 2016; Accessed: July 25, 2016.
- Ptito A, Chen JK, Johnston KM. Contributions of functional magnetic resonance imaging (fMRI) to sport concussion evaluation. NeuroRehabilitation. 2007. 22(3):217-27. [Medline].
- Henninger N, Sicard KM, Li Z, et al. Differential recovery of behavioral status and brain function assessed with functional magnetic resonance imaging after mild traumatic brain injury in the rat. Crit Care Med. 2007 Nov. 35(11):2607-14. [Medline].
- Kirov I, Fleysher L, Babb JS, et al. Characterizing ‘mild’ in traumatic brain injury with proton MR spectroscopy in the thalamus: Initial findings. Brain Inj. 2007 Oct. 21(11):1147-54. [Medline].
- Conder R1, Conder AA Neuropsychological and psychological rehabilitation interventions in refractory sport-related post-concussive syndrome. Brain Inj.2015;29(2):249-62. doi: 10.3109/02699052.2014.965209. Epub 2014 Oct 7.
- Griesbach GS. Exercise after traumatic brain injury: is it a double-edged sword. PM R. 2011;3(6 suppl 1):S64–72.
- “Returning to School After a Concussion: A Fact Sheet for School Professionals” Available from:http://www.cdc.gov/headsup/pdfs/schools/tbireturning_to_school-a.pdf
- Halstead ME, McAvoy K, Devore CD, Carl R, Lee M, Logan K. Returning to learning following a concussion.2013;132:948–957.
- Lewis D, Ashwal S, Hershey A, et al. Practice parameter: Pharmacological treatment of migraine headache in children and adolescents: Report of the American Academy of Neurology Quality Standards Subcommittee and the Practice Committee of the Child Neurology Society. 2004;63:2215–2224.
- Hamalainen ML, Hoppu K, Valkeila E, Santvuori P. Ibuprofen or acetaminophen for the acute treatment of migraine in children. 1997;48:103–107.
- Eiland L, Hunt M. The use of triptans for pediatric migraines.Pediatr Drugs. 2010;12:379–389.
- Kacperski J, O’Brien HL. Triptan use in pediatric migraine: Focus on rizatriptan.Neurol Futures. 2012;7:385–394.
- Erickson J. Treatment outcomes of chronic posttraumatic headaches after mild head trauma in US soldiers: An observational study. 2011;51:932–944.
- Kacperski J, O’Brien HL. Triptan use in pediatric migraine: Focus on rizatriptan.Neurol Futures. 2012;7:385–394.
- Packard R. Treatment of chronic daily posttraumatic headache with divalproex sodium. 2000;40:736–739.
- Ludvigsson J. Propranolol used in prophylaxis of migraine in children.Acta Neurologica. 1974;50:109–115.
- Blume HK. Pediatric headache: A review.Pediatr Rev. 2012;33:562–576.
- Blume HK, Brockman LN, Breuner CC. Biofeedback therapy for pediatric headache: Factors associated with response.2012;52:1377–1386.
- Campbell JK, Penzien DB, Wall EM. Evidence-based guidelines for migraine headache: Behavioral and physical treatments. US Headache Consortium 2000. Available from:http://www.aan.com/professionals/practice/pdfs/gl0089.pdf.
- Chan S, Burowski B, Byczkowski T, et al. Intravenous migraine therapy in children with posttraumatic headache in the ED. Am J Emerg Med. 2015;33:635–9.
- Yerry JA, Kuehn D, Finkel AG. Onobotulinum toxin a for the treatment of headache in service members with a history of mild traumatic brain injury: a cohort study. Headache. 2015;55(3):395–406
- Dubrosky AS, Friedman D, Kocilowicz H. Pediatric post-traumatic headaches and peripheral nerve blocks of the scalp: A case series and patient satisfaction survey. 2014;54:878–887.
- Seeger TA, Orr S, Bodell L, et al. Occipital nerve blocks for pediatric posttraumatic headache: A case series.J Child Neurol. 2015;30:1142–1146.
- Leung A, Shukla S, Fallah A, et al. Repetitive transcranial magnetic stimulation in managing mild traumatic brain injury-related headaches. Neuromodulation. 2015; E-pub ahead of print. doi:1111/ner.12364.
Original Version of the Topic
Jeffrey Thompson, MD. Post Concussion Headache.01/24/2013
Anne Felicia Ambrose, MD
Nothing to Disclose
MD, Raman Sharma, MD,
Nothing to Disclose
Soumabha Das, MD,
Nothing to Disclose
Raia Minassian, MD,
Nothing to Disclose
Hossam Eldin Mohamed, MD,
Nothing to Disclose