Acute headache attributed to trauma or injury to the head and/or neck is defined by the International Headache Society (ICHD 3) as a headache occurring within 7 days of a 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) is the most common symptom of concussion, often a result of a sport injury, fall, blunt trauma or motor vehicle collision. 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. Nerve entrapment may also result from trauma and cause pain.
Epidemiology including risk factors and primary prevention
PTH is more frequent after mild TBI (mTBI) than moderate or severe TBI, and resembles multiple types of headache, such as migraine-type or tension-type headaches.2 Migraine-type headaches are more prevalent and can occur in patients regardless of either a pre-injury history or family history of migraine.3
PTH’s account for approximately 4% of all symptomatic headache disorders and is known to be one of the most common consequences of mTBI.4 Annually, it is estimated that 69 million people experience a traumatic brain injury worldwide, with > 3.8 million individuals in the United States being diagnosed with a mTBI yearly.5 Additionally, population-based studies estimate the one-year prevalence of persistent PTH to be .21%, with a lifetime prevalence of 4.7% in men and 2.4% in women. A considerably negative socioeconomic effect has also been reported among people with PTH, as 35% do not return to work within 3 months post-injury.6 PTH appears to be most common after mTBI compared to moderate or severe injury, most commonly resulting from motor vehicle related events (24-58%), followed by falls (24-45%), sport related events (3-18%), and violence 5-7%).7
Risk factors (for PTH)
Risk factors for acute PTH in adults with moderate or severe TBI include prior moderate to severe headaches and female gender.8 Evidence suggests the migrainous type of HA in sports-related concussion was associated with cognitive impairment and protracted recovery in a cohort study.
Risk factors are variably reported in the pediatric population. Several studies have reported a trend toward female gender and adolescence being risk factors.9 Repetitive head injuries did not predict occurrence or recovery from PTH.9 Developmental disorders, psychiatric disorders, history of headaches or migraines can influence concussion recovery time.10
In professional athletes, risk factors included a history of prior concussion, longer sport exposure, and the presence of the ApoE4 gene.11,12
Once a concussion occurs, common triggers for PTH include physical or cognitive exertion, sleep deprivation, changes in environment, dehydration, and emotional stress.13
Several sporting agencies have changed rules of play and advocated use of protective equipment to reduce the risk or TBI. Although 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 acutely following concussion may limit the severity and longevity of post-concussion headaches, noting prolonged rest is no longer a mainstay of concussion management.14
A blow to the head or body can transmit rotational and angular acceleration forces to the brain leading to straining of neural elements and disruption of the neuronal membrane. This leads to cortical spreading depression, changes in intracellular sodium and calcium, extracellular potassium and excess release of opioids and excitatory amino acids, such as beta-endorphins and glutamate.15 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 resulting in centrally derived pain.16 While trigeminal nerve injury is rare, it can induce facial pain often described as a headache. More common are traumatically induced supraorbital or supratrochlear neuralgias, which occur more frequently than maxillary nerve neuralgias.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation overtime)
The presentation of post-traumatic headache is heterogeneous and can be classified into specific phenotypes that can help 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 stereotypical stimuli including bright lights, stress, dehydration, poor sleep, and certain foods, which can last from 4 to 72 hours, typically followed by headache-free periods.17
People may have headaches induced by cervical spine injury, trigeminal autonomic cephalgia-like pain or entrapment-type headaches. People with cervicogenic postconcussional disorder (PCD) typically present with neck pain and stiffness, fatigue, and fogginess, dizziness with movement or prolonged neck stabilization. Pain often originates in the occipital region, which radiates 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. Those with PCD do not experience early concussion-related symptoms on graded aerobic treadmill testing.18
New onset headaches may also present as tension type headaches and secondary supraorbital neuralgia. Whereas tension type headaches are typically described as a pressing or tightening quality in a band-like distribution, supraorbital neuralgia may be described as a generalized dull pain with intermittent short sharp or burning exacerbations in the frontal or periorbital area, and in rare instances may have signs or symptoms of sensory dysfunction on the affected forehead.
Babcock et al demonstrated that 29.3% of children aged 5 to 18 years had headaches 3 months after TBI.19 Barlow et al reported that among patients presenting to an emergency department three months after mTBI, 11% of mTBI patients were symptomatic compared to 0.5% of those with extracranial injuries (ECI). 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 subjects with symptoms at 1 year continued to report headache.20
Specific secondary or associated conditions and complications
PTH is part of a complex set of symptoms that constitute post-concussive syndrome, now more commonly referred to as “persistent post-concussion symptoms”. 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).
Essentials of Assessment
Determining the specific headache pattern guides treatment. The history should focus on mechanism and timing of injury, headache characteristics, presence of risk factors, exacerbating conditions, and presence of any atypical symptoms or neurological deficits prompting 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.
Headache characteristics will help determine the type of headache, Factors such as location (unilateral vs generalized) characteristic (gripping vs throbbing), and associated symptoms (photophobia, nausea and vomiting) can help differentiate PTH phenotype. Changes in vision, hearing and balance can be associated or be triggers for headaches. Details regarding the course of headache improvement or deterioration and response to different treatment should be sought.
Although PTH presents similarly to more common headache subtypes, it is often associated with somatic and cognitive symptoms such as fatigue, confusion, disorientation, distractibility, loss of memory surrounding the injury event, and impaired concentration. These symptoms should be elicited and treated as needed in conjunction with headache management as part of a comprehensive rehabilitation program.
Furthermore, clinicians should inquire about comorbid conditions and risk factors such as sleep disturbances, psychiatric disorders such as anxiety and depression, learning disorders, previous cervical spine injuries, vestibular dysfunction, post-traumatic stress disorder, prior TBI’s, and pre-existing neuro-ophthalmological conditions such as strabismus or convergence insufficiency.
It is important to perform a thorough neurological physical examination, 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.21 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.
History of headache and its effect on basic and instrumental ADL, vocation and recreation activities can be helpful is assessing the impact of PTH on daily function. The Migraine Disability Assessment questionnaire (MIDAS) is a 5-item questionnaire that can help clinicians track the impact of PTH on daily life.19
Formal assessment tools such as the Sport Concussion Assessment Tool – 5th Edition, (SCAT5) may be helpful in risk stratifying patients presenting with concussion type symptoms.22
There are no routine blood tests. Some preliminary studies have suggested the use of biomarkers such as S100B or neurone specific enolase (NSE) to help prognosticate.23 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 still insufficient data to support the use of biochemical serum and cerebral spinal fluid biomarkers in diagnosing or prognosticating PTH.24,25
Similarly, the significance of genetic markers in the management of concussion risk or injury outcome is unclear at this time.26
The American College of Radiology has criteria to determine the appropriateness of head and neck imaging in the setting of PTH. CT Head without IV contrast is the primary imaging modality for patients with acute head trauma, with the purpose of identifying lesions that may require neurosurgical intervention (e.g., hemorrhage, herniation, and hydrocephalus. Of note, only 10% or less of initial imaging studies of those with mTBI reveal positive CT findings, with less than 1% requiring neurosurgical intervention. Additional findings that would further warrant CT imaging acutely following head trauma with resultant headache includes moderate to severe head trauma (GCS < 13) and new or progressive neurological findings.
MRI Head 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 which may be seen in CSF leak).
Supplemental assessment tools
Sideline testing (e.g. SCAT-5) or online concussion (e.g. Impact) testing can help identify athletes who are at risk of developing symptoms. The SCAT-5 is recommended for sideline testing in cases of suspected concussion.27
Early Predictions of Outcomes
PTH more commonly occurs following mTBI than moderate to severe TBI.2 Headaches lasting more than 10 days have a poorer prognosis.28 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.
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 SCAT5 guides clinical sideline assessment.
First line treatments of headaches include proper hydration (non-caffeinated fluids) and nonsteroidal anti-inflammatory medications.13 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.29 Acetaminophen (15 mg/kg) is also safe and well tolerated and probably effective in the treatment of children with acute migraine.30 Dosage should be limited to no more than 3 days per week (maximum 2 doses in the same day).29,30
If NSAIDs are ineffective in ablating migraine attacks, triptans may be considered.31,32,33 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 should be used in patients with known ischemic heart disease, uncontrolled hypertension, suspected basilar or hemiplegic migraine and in 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.34
In addition to ablative treatments, migraine prophylaxis can be achieved with various anti-convulsants, anti-depressants or beta-blockers.35,36,37 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 HA, tricyclics (nortriptyline 25-75 mg per day) may be preferred.38
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.39
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.40,41
Onabotulinumtoxin A was approved by the FDA for use in adults with chronic migraines in 2010; but there is limited data regarding its effectiveness in PTH or in children. 64% of service men with chronic PTH responded favorably to treatment with onabotulinum toxin A in a retrospective consecutive case series.42
Peripheral Nerve Blocks have been studies in people with PTH with promising results. 71% 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.43 Seeger et al performed a retrospective chart review including adolescents with occipital neuralgia who received occipital nerve blocks. Sixty-four percent with occipital neuralgia reported long-term relief of pain following the blocks, with associated improvement in quality of life and decreased post-concussion symptom scores.43,44
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.45
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 over-use headaches, specifically in those prescribed opioid or barbiturate containing medications.
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. Tricyclic antidepressants, such as amitriptyline and nortriptyline, anti-epileptics such as topiramate, valproic acid, gabapentin, and zonisamide, and beta-blockers, as well as supplements such as melatonin and magnesium have been studied and found useful in adults.
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 with TBI being treated. Collaboration and communication with the school or workplace early in the treatment process to effectuate 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.41Two small studies have also shown therapeutic benefits in the treatment of persistent PTH using transcranial magnetic stimulation (TMS) which received FDA approval for treatment of migraine.45
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- 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
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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
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Christopher Yih, DO
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Jason Kessler, MD
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Danni Lu, MD
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