Author(s): Steven Flanagan, MD, Jessica Rivetz, MD
Originally published: November 11, 2011 Last updated: May 22, 2025
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Disease/Disorder

Definition

Acute post traumatic headache attributed to trauma or injury to the head and/or neck is defined by the International Headache Society (ICHD 3) as a secondary headache occurring within 7 days of head or neck trauma, within 7 days after regaining consciousness, and/or within 7 days of being able to report pain after the injury but lasting less than 3 months. After 3 months, it is referred to as a persistent post-traumatic headache.1 Post-traumatic headache (PTH) encompasses a broad range of headache phenotypes, including migraine-like, tension-like, trigeminal autonomic cephalalgias, cervicogenic, and cluster-like headaches.2

Etiology

Post traumatic headache (PTH) is the most common symptom after a concussion (also known as mild TBI), often resulting from a sports injury, fall, blunt trauma or motor vehicle collision. Biomechanical forces imparted to the head 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. Nerve entrapment may also result from trauma and cause pain.2,3,4

Epidemiology including risk factors and primary prevention

PTH resembles other headache phenotypes, such as but not limited to, migraine-type or tension-type headaches.1 Migraine-type headaches are more prevalent and can occur post-trauma regardless of pre-injury history or family history of migraine.

PTH’s account for approximately 4% of all symptomatic headache disorders and are known to be one of the most common and debilitating consequences of concussion.5 According to a recent systematic review, an estimated 69 million people annually experience a TBI worldwide with the vast majority of injuries being classified as mild.6 The reported range of PTH following concussion is 30-70%. The incidence of PTH persisting > 6 months post-injury is inversely related to TBI severity, with 50-60% incidence reported after concussion, and 30-35% incidence reported following moderate-to-severe TBI.4,7 The prevalence of PTH in children and adolescents following concussion is 43-60%.4,8 Prevalence of PTH among athletes and military personnel is likely underreported, making it challenging to accurately ascertain incidence, frequency and duration of symptoms.9 Approximately 15-20% of individuals post-concussion reportedly suffer from chronic PTH at 1-year post-injury.4,10 Up to 35% of people with PTH are unable to return to work post-trauma, suggesting it is a considerable contributor to post-injury disability.11

Risk factors

PTH is more common following concussion as opposed to moderate or severe TBI. Risk factors for acute PTH in adults with moderate or severe TBI include a history of migraine and/or other moderate to severe headache phenotype, younger age, female gender,12 greater injury severity, and premorbid mental health issues such as anxiety and depression.4 Migrainous type headache in sports-related concussion has been reported to be associated with cognitive impairment and protracted recovery.12  

Risk factors are variably reported in the pediatric population. Several studies report a trend toward female gender and adolescence. Repetitive head injuries did not predict occurrence or recovery from PTH.13 Developmental disorders, psychiatric disorders, history of headaches and migraines have been shown to increase recovery time from PTH and from TBI in general.14

In professional athletes, reported risk factors include a history of prior concussion, longer sport exposure, and the presence of the ApoE4 gene.15,16

Common triggers for PTH include physical or cognitive exertion, sleep deprivation, changes in environment, dehydration, and emotional stress.17

Primary prevention

Several sporting agencies have changed rules of play and advocated for both the use of protective equipment and improved coach and player education to reduce the risk of TBI. Although these changes have reduced the incidence of moderate to severe TBI, the evidence supporting the use of special equipment in reducing concussion or PTH remains unproven.18

An appropriate period of p physical and cognitive rest acutely following concussion may limit the severity and longevity of PTH. However, prolonged rest is no longer a mainstay of concussion management.19 Guidelines for returning to play after a concussion or other injury include a gradual, stepwise process with increasing levels of activity guided by athlete symptoms as intensity of exercise increases.20    

Patho–anatomy/physiology

The pathophysiological mechanisms of PTH remain under investigation noting they likely vary depending on the headache subtype. However, mechanisms common to both migraine and TBI appear to be involved. These include: impaired descending pain modulation, neurometabolic changes (e.g., changes in intracellular sodium and calcium and extracellular potassium), neuroinflammation, cortical spreading depression, in addition to the release of excess calcitonin-gene-related peptide (CGRP), opioids and excitatory amino acids (e.g., beta-endorphins and glutamate).11 The persistence of PTH may be more closely linked to neuroinflammation and the activation of the trigeminal system, similar to what is seen in migraines, rather than solely to TBI mechanisms. TBI can cause immediate structural damage that contributes to PTH. This includes cerebral contusion, damage to cerebral blood vessels, and axonal shearing, along with the subsequent metabolic and inflammatory changes occurring with secondary injury.2 People with PTH who have no previous migraine history often show hypersensitivity to CGRP, a neuropeptide involved in trigeminal pain transmission and migraine initiation. Activation of trigeminal nociception arising from injury to the upper cervical roots by forced flexion and extension of the neck may trigger the trigeminal nucleus caudalis resulting in centrally derived pain. While direct trigeminal nerve injury is rare, it can induce facial pain often described as a headache. Referred cervical paraspinal musculoskeletal pain, due to muscle strain/sprain or contusion, can also contribute to PTH.21 Individuals presenting with a headache originating at the posterior skull base should be evaluated for greater occipital neuralgia. This arises from compression or irritation of the greater occipital nerve, typically presenting as a paroxysmal, lancinating, or stabbing pain lasting from seconds to minutes. PTH may also arise from direct trauma to the supraorbital or supratrochlear nerves.22       

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation overtime)

New onset/acute

The presentation of PTH is heterogeneous and best classified by phenotype that helps guide targeted therapy.

Migrainous PTH is characterized by paroxysmal attacks of unilateral, severe, throbbing, or pulsating headaches, often accompanied by photo- and/or phonophobia, nausea, and vomiting, at times preceded by an aura. These headaches can be provoked by bright lights, stress, dehydration, poor sleep, and certain foods, typically lasting to 72 hours, followed by headache-free periods.23  

New-onset PTH may also present as tension-type headaches or as secondary arising from a peripheral nerve injury. Tension-type headaches present with a pressing or tightening quality in a band-like distribution. Nerve injury, such as to the greater occipital or supraorbital nerve may result in headache described as a generalized dull pain with intermittent short sharp or burning exacerbations in the corresponding sensory distribution, with or without signs or symptoms of sensory dysfunction.4

Cervicogenic-type headaches (or cervicalgia) may be unilateral or bilateral, often associated with restricted neck ROM, neck and shoulder discomfort, and pain radiating to the oculo frontotemporal areas. Other symptoms include fatigue, fogginess, and dizziness with movement or after prolonged neck stabilization, with symptoms exacerbated by poor posture, weight training and running. Common findings on physical exam include paraspinal and sub-occipital muscle tenderness and spasm, decreased cervical spine range of motion, and dizziness. Autonomic symptoms such as photophobia, phonophobia, nausea, and vomiting occur less commonly compared to migraine-type headaches.24  

Local pain, referred pain and impairment of sensory integration and postural control, secondary to injury, may also contribute to headache symptomatology.21

Acute headache following moderate-to-severe TBI may also be due to meningeal or subarachnoid irritation in the setting of hemorrhages.2

Chronic/stable

Approximately one-third of children aged 5 to 18 report persistent headaches 3 months post trauma, meeting the definition for persistent PTH.25 One study indicated children and adolescents presenting to an ED 3 months post-concussion were significantly more likely to complain of headaches compared to those with extracranial injuries. The prevalence of PCS decreased over time with only 2.3% of concussion patients having persistent symptoms at 1 year, compared to 0.01% in the extracranial injury group. All of those subjects with symptoms at 1 year continued to report post-concussive symptoms that could not be explained by trauma, family dysfunction, or maternal psychological adjustment.26

Specific secondary or associated conditions and complications

PTH is part of a complex set of symptoms that constitute “persistent post-concussion symptoms” (PCS). These symptoms can be categorized into five clinical domains: somatic, cognitive or emotional symptoms, physical signs, behavioral changes, cognitive impairment and sleep disturbances.

Essentials of Assessment

History

PTH, like other primary headaches, is a clinical diagnosis. Determining the specific headache pattern guides treatment. The history should focus on mechanism and timing of injury, headache characteristics, presence of risk factors, exacerbating and alleviating factors, and presence of any atypical symptoms or neurological deficits that would warrant further diagnostic testing.

Important initial injury details to elicit include the mechanism of injury, the presence or absence of loss of consciousness, post-traumatic amnesia or seizure, symptoms experienced at the time of injury, and initial and subsequent medical management.

Determining headache phenotype and characteristics is crucial for diagnosis and treatment. These include headache location (unilateral vs generalized), quality (gripping vs throbbing); associated symptoms (e.g., photophobia, phonophobia, nausea and vomiting); duration; change in quality and/or severity over time; and   provoking and alleviating factors. Changes in vision, hearing and balance can be associated symptoms, noting various types of visual and auditory stimuli may trigger   headaches. Details regarding the course of headache improvement or deterioration and response to different treatment are important to obtain.

Although PTH presents similarly to common headache subtypes, it is associated with somatic and cognitive symptoms such as fatigue, confusion, disorientation, distractibility, amnesia, and impaired concentration. These symptoms should be elicited and addressed as needed as part of a comprehensive rehabilitation treatment plan.

Clinicians should inquire about comorbid conditions and risk factors, including but not limited to sleep disorders; underlying psychiatric disorders or acute symptoms (such as anxiety, depression, PTSD); learning disabilities; previous cervical spine injuries; vestibular dysfunction; prior TBI’s; and pre-morbid neuro-ophthalmological conditions such as strabismus or convergence insufficiency.

Physical examination

It is important to perform thorough neurological and musculoskeletal examinations, including a cognitive and vestibular assessment. The visual system consists of a wide neurological network that is prone to injury after a TBI. As a result, vision and ocular symptoms may worsen and contribute to headaches.27 Therefore, a focused vestibulo-ocular examination including testing of convergence, smooth pursuits, saccades and the vestibulo-ocular reflex is critical. Additionally, all patients should undergo an examination of the jaw, temporomandibular joint and cervical spine that includes range of motion, palpation, and provocative ligament and cervical dizziness testing.

Functional assessment

Obtaining information on how headache effects basic and instrumental ADLs as well as vocational and recreational activities is helpful in assessing their impact on daily function. The Migraine Disability Assessment questionnaire (MIDAS) is a 5-item survey that helps clinicians track the impact of PTH on daily life.25

Formal assessment tools such as the Sport Concussion Assessment Tool – 6th Edition, (SCAT6) may be helpful in risk stratifying patients presenting with concussion type symptoms. The SCAT6 is used as part of on-field assessment as well as in the office within 72 hours post-injury, but no more than 7 days post-injury. After 7 days, clinicians can use the Sports Concussion Office Assessment Tool (SCOAT6) for adults and children, which was introduced at the 6th International Conference on Concussion in Sport, Amsterdam, October 2022.28

Laboratory studies

There are no routine blood tests to assess for PTH. Some preliminary studies have suggested the use of biomarkers such as S100B or neuron specific enolase (NSE) serve as prognostic tools.29 Patients with an elevated S100 calcium-binding protein B drawn six hours after TBI may be more likely to have persistent PTH symptoms at six months. In addition, increased NSE levels were directly associated with severity of headache after six months. However, there is insufficient data to support the use of biochemical serum and cerebral spinal fluid biomarkers in diagnosing or prognosticating PTH.30,31 Similarly, the significance of genetic markers in the management of concussion risk or injury outcome is unclear at this time.32

Imaging

The American College of Radiology has criteria to determine the appropriateness of head and neck imaging in the setting of PTH. Head without IV contrast is the primary imaging modality for patients with acute head trauma to identify lesions requiring urgent neurosurgical intervention. Of note, no more than 10% of initial head CT imaging studies of those with concussion reveal trauma-related lesions, with fewer than 1% requiring neurosurgical intervention. Findings that warrant CT imaging acutely following head trauma with resultant headache includes moderate to severe head trauma (GCS < 13) and new or progressive neurological findings.33

The Canadian CT Head Rule helps determine when to perform a CT scan on patients with acute minor head injuries. The Canadian CT Head Rule recommends a CT scan for adults with minor head injuries who exhibit any of the following: Glasgow Coma Scale (GCS) score less than 15 two hours post-injury, signs of a skull fracture, or any history of loss of consciousness or amnesia longer than 30 minutes. Additionally, it suggests considering a CT scan for patients over 65 years of age, those treated with anticoagulants, or if there are persistent symptoms such as vomiting or severe headache.34

Brain MRI is the imaging modality of choice in patients with subacute or chronic PTH and is more often considered for follow-up imaging. This is especially pertinent in the setting of persistent and/or neurologic deficits that remain unexplained after initial head CT imaging, as it is more sensitive for subtle findings such as those seen in diffuse axonal injury. Other considerations for MRI imaging in the setting of headache include those associated with cough, exertion, or sexual activity (to exclude vascular pathology), presence of papilledema (to exclude elevated intracranial pressure), and headache related to changes in body position (to exclude intracranial hypotension typically in association with CSF leak).35

Supplemental assessment tools

Sideline testing (e.g. SCAT-6) or online concussion (e.g. Impact) testing can help identify athletes who are at risk of developing symptoms. The SCAT-6 is recommended for sideline testing in cases of suspected concussion. It is most appropriately used within the first 72 hours of injury, with diminishing utility by day 7.28

Early predictions of outcomes

As previously noted, PTH more commonly occurs following concussion than moderate to severe TBI.3 Headaches lasting more than 10 days have a poorer prognosis. Noise and light sensitivity and early onset migraine predict a more prolonged course. Symptom burden at the time of concussion may also be predictive of developing persistent post-concussion symptoms.36

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 environmental triggers are important educational considerations.

Rehabilitation Management and Treatments

Available or current treatment guidelines

No formal guidelines exist specifically for PTH, noting treatment is guided by headache type (e.g. migraine, cluster, tension, etc.).

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 in cases of suspected concussion in sporting events. The SCAT 6 guides clinical sideline assessment.

Treatment

First line treatments of headaches include proper hydration (non-caffeinated fluids) and nonsteroidal anti-inflammatory medications.17 Although there are no clinical trials in humans, ibuprofen (7.5–10 mg/kg) is recommended as a first-line treatment of acute migraine in children due to its analgesic and anti-inflammatory benefits.37 Acetaminophen (15 mg/kg) is also safe and well tolerated and probably effective in the treatment of children with acute migraine.38 Dosage should be limited to no more than 3 days per week (maximum 2 doses in the same day).37,38

If NSAIDs are ineffective in aborting migraine attacks, triptans may be considered.2 However, there is a theoretical risk of vasospasm, which may exacerbate hypoperfusion resulting in neurologic vascular injury. 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 triptan differ, but all should be limited to no more than 9 days per month to avoid rebound headaches. Caution is warranted in those with known ischemic heart disease, uncontrolled hypertension, suspected basilar or hemiplegic migraine, and women who experience migraine auras on hormonal birth control. 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 specifically studied in PTH populations.39

In addition to abortive treatments, migraine prophylaxis can be achieved with various anticonvulsants, antidepressants, or beta-blockers.2 Anti-epileptic drugs such as topiramate should also be used judiciously following TBI as they may exacerbate TBI-induced cognitive impairments and fatigue. For tension type headaches, tricyclics (e.g., nortriptyline 25-75 mg per day) may be preferred.40 Propranolol is the beta-blocker of choice for migraine prophylaxis (10mg daily). Onabotulinumtoxin A is also FDA approved for prophylaxis in adults with chronic migraines, but not for children and adolescents under the age of 18. However, there is emerging evidence suggesting it is both safe and effective in adolescence. Studies examining it specifically for migrainous PTH are limited, noting 64% of service men with chronic PTH responded favorably in a retrospective consecutive case series.41

Migraine management may also be achieved through antagonism of the calcitonin gene-related peptide (CGRP) pathway. CGRP is released during migraines noting there is evidence that triptans lower CGRP levels. CGRP can cause cerebral artery dilation and degranulation of mast cells of the trigeminal vascular network, leading to nociception. Several CGRP inhibitors have been approved for migraine management (eptinezumab, galcanezumab, and fremanezumab, erenumab), which show promise in treating people refractory to other treatment modalities.42

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 presentation.43,44

Peripheral nerve blocks have been studied in people with PTH with promising results. Seventy-one percent of subjects with acute or persistent PTH reported almost complete pain relief with 2% lidocaine and epinephrine scalp injections, with 83% of those patients reporting migraine-like features.45   Occipital nerve blocks in people with occipital neuralgia has been shown to provide long-term relief of pain with an associated improvement in quality of life and decreased post-concussion symptoms.45,46 Depending on presentation and exam, other treatments can be considered. These include diagnostic and therapeutic supraorbital nerve blocks (i.e., pain, tenderness, hypoesthesia, and allodynia in the territory supplied by the supraorbital nerve) or sphenopalatine ganglion blocks (for severe acute migraine-type headache or acute trigeminal neuralgia).50

Subacute or chronic phase

Rebound headache from analgesic overuse, which was present in up to 45% of subjects 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 chronic.47

Opioids, steroids and barbiturate hypnotics have not been well-studied in the pediatric population. However, they should be avoided in people with persistent PTH as there is increasing evidence they may cause long-term detrimental effects. There is also a risk of long-term dependence and the development of medication headaches, specifically in those prescribed opioid or barbiturate-containing medications.49

Preventive therapy

There is no clear evidence to help guide the clinician on the timing of initiation of preventive migraine therapy in children. In general, prophylaxis should be limited to those children and adolescents whose migraine headaches occur with sufficient frequency and/or severity to warrant a daily medication, including a minimum of 1 headache per week or 3–4 headaches per month. Treatment in this population should be limited to a period of 4–6 months. Herbal and vitamin supplements, such as magnesium, feverfew (butterbur), vitamin B2 (riboflavin), and CoQ10, have shown to provide benefit for prevention and treatment of migraine-type post-traumatic headaches. For those refractory to more conservative medications and supplements, consideration should be given to using tricyclic antidepressants, anti-epileptics (such as topiramate, valproic acid, gabapentin, and zonisamide), and beta-blockers.48       

Consultations

Consultation with a headache specialist or brain injury medicine physician is indicated for patients who have prolonged symptoms.

Coordination of care

As with many conditions treated by physiatrists, an interdisciplinary approach to management may be considered. This includes referrals for cognitive behavioral management, especially if prominent psychosocial issues exist. Physical, occupational and speech therapy should be prescribed as needed based on the individual needs of the person being treated. Collaboration and communication with the school or workplace early in the treatment process to initiate accommodations can lessen symptom frequency and severity. These accommodations may include but are not limited to frequent rest breaks, more time for tests and assignments, and provision of class notes. Referral to a formal pain rehabilitation program may be needed if PTH becomes refractory to treatment and is functionally limiting.

Patient & family education

Education has been shown to have the biggest impact in managing post concussive symptoms. The patient and family should be informed of expected improvements over time.

Gaps in the Evidence–Based Knowledge

There are no laboratory or imaging correlates to PTH to verify diagnosis, severity or response to treatment. The natural history and prognosis of PTH is not well characterized. The clinical presentation of PTH is varied, and treatment is largely based on similar headache subtypes such as migraine and tension-type headaches. In addition, the definition of PTH is controversial as the presentation of symptoms can occur long after 7 days.

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. In one study, 86% of study subjects reported pain reduction, with 52 % reporting complete headache resolution.44 Small studies have also shown therapeutic benefits in the treatment of persistent PTH using transcranial magnetic stimulation (TMS), which is FDA-approved for treatment of migraine with beneficial effects on headache intensity and mood.47

References

  1. Olesen J. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition. Cephalalgia. 2013;33(9):629–808.
  2. Blumenfeld A, McVige J, Knievel K. Post-traumatic headache: Pathophysiology and management – A review. Journal of Concussion. 2022;6. doi:10.1177/20597002221093478
  3. 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.
  4. Mavroudis I, Ciobica A, Luca AC, Balmus IM. Post-Traumatic Headache: A Review of Prevalence, Clinical Features, Risk Factors, and Treatment Strategies. J Clin Med. 2023 Jun 23;12(13):4233. doi: 10.3390/jcm12134233. PMID: 37445267; PMCID: PMC10342432.
  5. Lucas S, Hoffman JM, Bell KR, et al.: A prospective study of prevalence and characterization of headache following mild traumatic brain injury. Cephalalgia 2014; 34(2): 93–102.
  6. Dewan, M. C., Rattani, A., Gupta, S., Baticulon, R. E., Hung, Y., Punchak, M., Agrawal, A., Adeleye, A. O., Shrime, M. G., Rubiano, A. M., Rosenfeld, J. V., & Park, K. B. (2019). Estimating the global incidence of traumatic brain injury. Journal of Neurosurgery, 130(4), 1080-1097. https://doi.org/10.3171/2017.10.JNS17352
  7. Kjeldgaard D., Forchhammer H.B., Teasdale T.W., Jensen R.H. Cognitive behavioural treatment for the chronic post-traumatic headache patient: A randomized controlled trial. J. Headache Pain. 2014;15:81.
  8. Zemek R., Barrowman N., Freedman S.B., Gravel J., Gagnon I., McGahern C., Aglipay M., Sangha G., Boutis K., Beer D., et al. Pediatric Emergency Research Canada (PERC) Concussion Team. Clinical Risk Score for Persistent Postconcussion Symptoms Among Children With Acute Concussion in the ED. JAMA. 2016;315:1014–1025. doi: 10.1001/jama.2016.1203. Erratum in JAMA 2016, 315, 2624.
  9. Lucas S, Blume HK. Sport-Related Headache. Neurol Clin. 2017 Aug;35(3):501-521. doi: 10.1016/j.ncl.2017.03.012. PMID: 28673412.
  10. Theeler B.J., Flynn F.G., Erickson J.C. Chronic daily headache in U.S. soldiers after concussion. Headache. 2012;52:732–738. doi: 10.1111/j.1526-4610.2012.02112.x.
  11. Ashina H, Porreca F, Anderson T, Amin FM, Ashina M, Schytz HW, Dodick DW. Post-traumatic headache: epidemiology and pathophysiological insights. Nat Rev Neurol. 2019 Oct;15(10):607-617. doi: 10.1038/s41582-019-0243-8. Epub 2019 Sep 16. PMID: 31527806.
  12. 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.
  13. 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.
  14. 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.
  15. Merritt VC, Ukueberuwa DM, Arnett PA. 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
  16. 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.
  17. Seifert, T. Post-Traumatic Headache Therapy in the Athlete Curr Pain Headache Rep (2016) 20: 41. doi:10.1007/s11916-016-0568-6
  18. Daneshvar DH, Baugh CM, Nowinski CJ, McKee AC, Stern RA, Cantu RC. Helmets and mouth guards: the role of personal equipment in preventing sport-related concussions. Clin Sports Med. 2011 Jan;30(1):145-63, x. doi: 10.1016/j.csm.2010.09.006. PMID: 21074089; PMCID: PMC2987604.
  19. Griesbach GS. Exercise after traumatic brain injury: is it a double-edged sword? PM R. 2011 Jun;3(6 Suppl 1):S64-72. doi: 10.1016/j.pmrj.2011.02.008. PMID: 21703583.
  20. Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2017 Jun;51(11):838-847. doi: 10.1136/bjsports-2017-097699.
  21. Dwyer, B., & Zasler, N. (2020, January 1). Post-traumatic cephalalgia. NeuroRehabilitation.
  22. Choi I, and Jeon SR. Neuralgias of the Head: Occipital Neuralgia. J Korean Med Sci. 2016 Apr;31(4):479-88. doi: 10.3346/jkms.2016.31.4.479. Epub 2016 Mar 9. PMID: 27051229; PMCID: PMC4810328.
  23. Ashina, H., et al. (2021). Post-traumatic headache attributed to traumatic brain injury: classification, clinical characteristics, and treatment.
  24. Piovesan, E.J., Kowacs, P.A. & Oshinsky, M.L. Convergence of cervical and trigeminal sensory afferents. Current Science Inc 7, 377–383 (2003). https://doi.org/10.1007/s11916-003-0037-x
  25. Babcock L, Byczkowski T, Wade SL, Ho M, Mookerjee S, Bazarian JJ. Predicting Postconcussion Syndrome After Mild Traumatic Brain Injury in Children and Adolescents Who Present to the Emergency Department. JAMA Pediatr. 2013;167(2):156–161. doi:10.1001/jamapediatrics.2013.434
  26. Barlow KM, Crawford S, Stevenson A, et al. Epidemiology of postconcussion syndrome in pediatric mild traumatic brain injury. 2010;126:e374-e381.
  27. Akhand, O., Balcer, L. J. & Galetta, S. L. (2019). Assessment of vision in concussion. Current Opinion in Neurology, 32 (1), 68-74.
  28. Patricios, J. S., Schneider, G. M., van Ierssel, J., Purcell, L. K., Davis, G. A., Echemendia, R. J., Fremont, P., Fuller, G. W., Herring, S. A., Harmon, K. G., Holte, K., Loosemore, M., Makdissi, M., McCrea, M., Meehan, W. P., 3rd, O’Halloran, P., Premji, Z., Putukian, M., Shill, I. J., Turner, M., … Schneider, K. J. (2023). Beyond acute concussion assessment to office management: a systematic review informing the development of a Sport Concussion Office Assessment Tool (SCOAT6) for adults and children. British journal of sports medicine, 57(11), 737–748. https://doi.org/10.1136/bjsports-2023-106897
  29. de Kruijk, J. R., et al. “Prediction of post-traumatic complaints after mild traumatic brain injury: early symptoms and biochemical markers. (Paper).” Journal of Neurology, Neurosurgery and Psychiatry, vol. 73, no. 6, Dec. 2002, pp. 727+. Gale OneFile: Health and Medicine.
  30. 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
  31. 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.
  32. 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].
  33. Shetty, V. S., Reis, M. N., Aulino, J. M., Berger, K. L., Broder, J., Choudhri, A. F., Kendi, A. T., Kessler, M. M., Kirsch, C. F., Luttrull, M. D., Mechtler, L. L., Prall, J. A., Raksin, P. B., Roth, C. J., Sharma, A., West, O. C., Wintermark, M., Cornelius, R. S., & Bykowski, J. (2016). ACR appropriateness criteria head trauma. Journal of the American College of Radiology, 13(6), 668–679. https://doi.org/10.1016/j.jacr.2016.02.023
  34. Stiell IG, Wells GA, Vandemheen K, Clement C, Lesiuk H, Laupacis A, McKnight RD, Verbeek R, Brison R, Cass D, Eisenhauer ME, Greenberg G, Worthington J. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001 May 5;357(9266):1391-6. doi: 10.1016/s0140-6736(00)04561-x. PMID: 11356436.
  35. Utukuri, P. S., Shih, R. Y., Ajam, A. A., Callahan, K. E., Chen, D., Dunkle, J. W., Hunt, C. H., Ivanidze, J., Ledbetter, L. N., Lee, R. K., Malu, O., Pannell, J. S., Pollock, J. M., Potrebic, S. X., Setzen, M., Shih, R. D., Soares, B. P., Staudt, M. D., Wang, L. L., & Burns, J. (2023). ACR appropriateness criteria® headache: 2022 update. Journal of the American College of Radiology, 20(5). https://doi.org/10.1016/j.jacr.2023.02.018
  36. McConnell B, Duffield T, Hall T, et al. Post-traumatic Headache After Pediatric Traumatic Brain Injury: Prevalence, Risk Factors, and Association With Neurocognitive Outcomes. Journal of Child Neurology. 2020;35(1):63-70. doi:10.1177/0883073819876473
  37. 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.
  38. Hamalainen ML, Hoppu K, Valkeila E, Santvuori P. Ibuprofen or acetaminophen for the acute treatment of migraine in children. 1997;48:103–107.
  39. Kacperski J, O’Brien HL. Triptan use in pediatric migraine: Focus on rizatriptan.Neurol Futures. 2012;7:385–394.
  40. Blume HK, Brockman LN, Breuner CC. Biofeedback therapy for pediatric headache: Factors associated with response.2012;52:1377–1386.
  41. 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
  42. Mohanty D, Lippmann S. CGRP Inhibitors for Migraine. Innov Clin Neurosci. 2020;17(4-6):39-40.
  43. 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.
  44. 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.
  45. 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.
  46. 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.
  47. Leung A, Metzger-Smith V, He Y, Cordero J, Ehlert B, Song D, Lin L, Shahrokh G, Tsai A, Vaninetti M, Rutledge T, Polston G, Sheu R, Lee R. Left Dorsolateral Prefrontal Cortex rTMS in Alleviating mTBI Related Headaches and Depressive Symptoms. Neuromodulation. 2018 Jun;21(4):390-401. doi: 10.1111/ner.12615. Epub 2017 May 30. PMID: 28557049.
  48. Patel PS, Minen MT. Complementary and Integrative Health Treatments for Migraine. J Neuroophthalmol. 2019 Sep;39(3):360-369. doi: 10.1097/WNO.0000000000000841. PMID: 31403967; PMCID: PMC7769000.
  49. Garza, I., & Schwedt , T. J. (2024). Medication overuse headache: Etiology, clinical features, and diagnosis. UpToDate. https://www.uptodate.com/contents/medication-overuse-headache-etiology-clinical-features-and-diagnosis?source=related_link
  50. Fernandes L, Randall M, Idrovo LPeripheral nerve blocks for headache disordersPractical Neurology 2021;21:30-35.

Original Version of the Topic

Jeffrey Thompson, MD. Post Concussion Headache. 1/24/2013

Previous Revision(s) of the Topic

Anne Felicia Ambrose, MD, Raman Sharma, MD, Soumabha Das, MD, Raia Minassian, MD, Hossam Eldin Mohamed, MD. Post Concussion Headache. 3/24/2017.

Steven Flanagan, MD, Christopher Yih, DO, Jason Kessler, MD, Danni Lu, MD. Post Traumatic Headache. 12/1/2021

Author Disclosures

Steven Flanagan, MD
Nothing to Disclose

Jessica Rivetz, MD
Nothing to Disclose