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13 Articles in Volume 11, Issue #4
Diagnosing and Managing Hand Osteoarthritis
Difficult Migraine Patient
Electromagnetic Applications In Biology and Medicine
Excerpt from the Book Avoiding Opioid Abuse While Managing Pain
Hormone Therapies: Newest Advance in Pain Care
Make the Family Your Best Friend
Medications for Chronic Pain—Opioid Analgesics
Nonpharmacologic Remedies for Back Pain During Pregnancy
Reconsidering and Revising Evidence-Based Practice in Pain Medicine: Steps Toward Sustaining the Profession?
The Value of Blood Analysis for Compliance Monitoring
Treatment of Neuropathic Pain: The Role of Unique Opioid Agents
Understanding Potential Complications Of Epidural Steroid Injections
Unmasking Post-traumatic Headache

Unmasking Post-traumatic Headache

Highly prevalent and underrecognized, post-traumatic headache is a complex and often refractory complication of traumatic brain injury.

Post-traumatic headache (PTH) is arguably the most controversial topic in headache medicine, especially in light of recent press reports surrounding both high-profile athletes and combat soldiers who are at particular risk for traumatic brain injuries (TBIs) and resultant PTH. Although the Centers for Disease Control and Prevention (CDC) estimate that 1.7 million TBIs occur in the United States every year, this is felt to be a gross underestimate because individuals with mild or rapidly resolving symptoms may not report their injuries or seek medical care.1-3

Among US athletes alone, the true incidence of concussion is felt to approach 3.8 million cases per year.2 An estimated 30% to 90% of individuals with a history of TBI will have PTH,4,5 and (after adjusting for depression and post-traumatic stress disorder [PTSD]) PTH is the only symptom significantly associated with TBI in combat soldiers.6 Similarly detailed epidemiologic studies on acute and chronic PTH in concussed athletes have not been reported but are likely forthcoming.

Recently, the National Football League (NFL) and the National Hockey League (NHL) have taken measures to protect players against illegal contact to the head and have promoted the awareness and recognition of concussion.7,8 These efforts have helped to legitimize TBI and its long-term effects as a public health concern of great importance and have prompted a surge of new studies investigating the mechanism of acute head injury and the treatment and management of PTH.

Concussion Common Among Athletes

Concussions were a near-daily topic throughout the 2010-2011 football season and were the focus of the NFL’s recent crackdown on illegal hits to the head. Few examples were more iconic than the hit by James Harrison of the Pittsburgh Steelers on Mohamed Massaquoi of the Cleveland Browns, which was featured on the November 1, 2010, cover of Sports Illustrated. This illegal hit resulted in a $75,000 fine for Harrison (later reduced to $50,000) and a game-ending concussion for Massaquoi.

Growing interest in player safety likely resulted in the recent recommendation by the NFL that all teams incorporate standardized sideline testing in the 2011-2012 season, including cognitive, neurological, and balance assessments for all players suspected of having a concussion.7 Concurrently, the NHL has also focused attention on concussion this season with adoption of stricter rules to eliminate blindside hits and hits where the head appears to be the principal target.

Additionally, autopsy studies on former athletes have revealed evidence of chronic traumatic encephalopathy (CTE), emphasizing the long-term sequelae of repeated TBIs.8 The recent death of former NHL star Bob Probert again brought TBI to the forefront and has placed under scrutiny the acceptance of fighting in hockey—currently the only professional sport that continues to allow this behavior.8 Although the elimination of fighting continues to be a topic of much controversy, most concussion experts agree that fighting places players at needless risk for TBI.

Incidence on the Rise

The incidence of concussions has increased over the past 20 years and may be due, in part, to the increased size, speed, and strength of athletes, which translates to an increase in the frequency and magnitude of the contacts they experience.2 Ironically, many have felt that technological improvements made in protective gear have led to a paradoxical increase in the number of concussions and TBIs in both combat soldiers and athletes.6,9 Specifically, newer innovations in protective military combat gear have made head trauma more survivable, leaving the soldier susceptible to the consequences of concussive forces.6

With regard to protective gear in sports, it has also been suggested that improved technology has led to more aggressive and potentially dangerous play, as athletes have become less fearful of the physical consequences of inappropriate tackling or checking techniques, including leading with or targeting the head.9 Because concussion results from both direct and indirect forces, it has become clear that newer helmet designs are not the definitive answer to preventing TBI. As an accompaniment to improved technology, attention should be also focused on increased player awareness and preparation for high-velocity impacts and development of a culture in spectator sports that admonishes and punishes hits to the head.

Consequences of Acute Brain Injury

Acute concussive head injuries are characterized by shifts in cellular ionic balance, leading to a profound disturbance of normal cellular physiology and a mismatch between cellular energy supply and demand. Immediately following a concussive head injury, neuronal and glial membrane activation leads to a release of neurotransmitters including glutamate, which results in activation of voltage-gated potassium channels and N-methyl-d-aspartic acid (NMDA) receptors. The resulting loss of intracellular potassium potentiates the potassium efflux that results via leakage from structural disruptions within cell membranes.10

In an effort to maintain normal ionic balance and resting membrane potentials, sodium/potassium (Na/K) pumps are taxed to pump potassium back into the cell and sodium and calcium back out. This excess energy demand results in glycolysis and, eventually, lactic acidosis. Simultaneously, the increased intracellular calcium becomes sequestered within the mitochondria, impairing adenosine triphosphate (ATP) production and further depriving the overburdened Na/K pumps of energy. As axons begin to sequester calcium, their integrity is also threatened. In experimental models of concussion, increased intracellular calcium and decreased cerebral blood flow may persist for several days after injury and ultimately result in cell necrosis and apoptosis.10

Magnetic resonance spectroscopy (MRS) demonstrates that these critical alterations in normal metabolic activity within the brain correlate with decreases in both N-acetylaspartate (NAA)-choline and the NAA-creatine ratio, indicating significant cellular derangements that may persist well after the resolution of clinical symptoms.11,12 Abnormalities in white matter tracts indicative of axonal disruption can also be found on diffusion weighted tensor imaging of the brain after TBI with a recovery period that mirrors the observations made in MRS.13,14 Crucially, the summation of these findings suggests that the brain remains in a metabolically vulnerable state for days to weeks after the time when a soldier is considered healthy enough to return to battle or when an athlete is considered safe to return to play. Successive concussive head injuries during this vulnerable period portend an even longer period that is required for the brain’s metabolic activity to return to normal.11

These data suggest that significant changes are overdue in the evaluation of TBI and concussive head injuries and will likely have a profound impact on return-to-play guidelines for athletes and perhaps also the formulation of algorithms regarding the management of TBI in combat soldiers.

Pathologically, repetitive head trauma is associated with cavum septum pallucidum and atrophy of the mammillary bodies and mesial temporal lobes with resultant ventricular dilation.15 On a microscopic level, the brains of athletes who were subjected to repetitive concussive head injures exhibit tau-immunoreactive neurofibrillary tangles, astrocytic tangles, neuropil neuritis, and b-amyloid plaques throughout the brain and spinal cord, mimicking the pathologic findings in Alzheimer’s disease.15

Evaluation and Diagnosis of PTH

Although there is little debate that new headache occurring in the context of a traumatic head injury is designated as secondary, some degree of diagnostic judgment is required in the evaluation of preexisting headache that is made worse after a head injury. In the latter instance, the primary headache disorder and the secondary headache from the traumatic injury may coexist—especially if the exacerbation of the primary headache has a clear temporal relationship to and improves along with the resolution of the injury.16

Criteria for the diagnosis of headache attributed to head injury only require that the headache occur within 7 days of the injury. No specific headache phenotype or characteristics need to be present to establish the diagnosis. The designation of 7 days as the window during which PTH should occur warrants further review, as this criterion may be too rigid and fail to capture all cases of PTH. For example, Theeler et al report that only 37% of soldiers felt to have PTH reported headache within 7 days of their TBI.17,18

Further distinctions within PTH can be made based on additional clinical criteria. Moderate/severe head injuries are distinguished from those that are mild based on the presence of a Glasgow Coma Scale (GCS) score less than 13, post-traumatic amnesia for more than 48 hours, loss of consciousness for more than 30 minutes, or the presence of a traumatic lesion such as intracranial hemorrhage or skull fracture. Additional distinctions between acute and chronic headaches depend on the duration of symptoms being either less than or more than 3 months. Other PTH categories within the International Classification of Headache Disorders, second edition (ICHD-II), include headaches that result from neck injuries (ie, whiplash injuries) and those that are determined to be secondary to traumatic intracranial hematomas.16

Post-traumatic headache is frequently multifactorial and may result from injury to any number of pain-sensitive structures in the head and neck. These include facet joints, muscular structures, and peripheral nervous structures such as the greater occipital or supraorbital nerves.5,19,20 Activation of afferent trigeminal pain fibers from the dura and intracranial vessels and/or dysfunction of the central structures involved with the modulation and processing of pain also may contribute to headache.20 PTH also may result from traumatic tears in the dura leading to orthostatic exacerbations resulting from cerebrospinal fluid (CSF) leak. Thus, a detailed history with specific attention to headache characteristics and triggers; thorough general, musculoskeletal, and neurologic examinations; and appropriate imaging studies are essential in establishing an accurate diagnosis and directed treatment plan. Information about the mechanism of injury, location of pain, timing of exacerbations, and aggravating/alleviating factors also provides useful diagnostic and therapeutic clues.4

Computed tomography (CT) imaging of the head should be considered as part of the routine emergent evaluation of TBI—especially in the context of headache with focal neurologic signs or symptoms. The presence of neck pain with Horner’s syndrome warrants additional imaging of intra- and extracranial vessels to rule out arterial dissection. Persistent PTH may necessitate magnetic resonance imaging (MRI) of the brain and consideration of cervical spine imaging when signs or symptoms of radiculopathy, myelopathy, or skeletal injury to the neck are present. Contrast-enhanced MRI of the brain may reveal pachymeningeal enhancement or descent of the cerebellar tonsils in the presence of CSF leak; however, the absence of these findings does not fully eliminate this diagnosis, and additional studies such as radionuclide cisternography or computed tomography/magnetic resonance (CT/MR) myelography may be necessary.

Positron emission tomography (PET), MRS, and MR diffusion tensor imaging (DTI) have questionable utility in the routine evaluation of PTH but may be helpful in identifying abnormalities consistent with neuronal damage and axonal injury. The resolution of these abnormalities has been found to lag behind the resolution of concussion symptoms, which suggests that they may eventually have a role in the formulation of new return-to-play guidelines for athletes.

Given the higher prevalence of psychiatric disorders and cognitive impairment in PTH populations compared with controls, neuropsychometric testing should be considered and patients should be screened for depression, anxiety, and PTSD.21

Treatment of PTH

There have been no randomized, placebo-controlled studies of medications for the treatment of headache secondary to traumatic head injuries, and the majority of existing data have been obtained from small, retrospective studies.5,19 Because there are no formal recommendations for the treatment of PTH, providers generally apply the evidence-based treatment guidelines for the particular headache phenotype that the patient exhibits.19,20,22 Retrospective studies suggest that the most common PTH phenotype in the general population is tension-type headache, whereas military populations tend to most frequently exhibit PTH meeting criteria for migraine.5,17,18,23,24 Frequently, the clinical course of PTH is further complicated by the presence of medication overuse.

For PTH exhibiting the characteristics of tension-type headache, tricyclic antidepressants (TCAs) such as amitriptyline and nortriptyline are commonly used. Because TCAs are also efficacious in migraine, they have been reported in small retrospective studies to be efficacious in PTH exhibiting migrainous features.25,26 These agents have the potential for added benefit in patients with comorbid depression or sleep disturbances. One study also suggested the possible utility of dual therapy with amitriptyline and the beta-blocker propanolol.26

Because head and neck injuries may result in direct trauma to the greater occipital nerves and produce the clinical picture of occipital neuralgia, occipital nerve blockade may be effective for PTH.27 Although there is a paucity of evidence supporting the use of trigger point injections, supraorbital nerve blockade, and botulinum toxin injections in the management of PTH, their utility in some primary headache disorders suggests the need for further study in the context of PTH.5,22

Other uncontrolled studies have established the possible effectiveness of osteopathic cervical manipulation, biofeedback, relaxation, and physical therapy.19,28,29 Given the frequent comorbidity of depression, PTSD, mood changes, balance disorders, and sleep disturbances in the context of TBI, consultation for vestibular rehabilitation, sleep studies, and psychiatric evaluation may be beneficial.5,19,30 Cognitive-behavioral therapy may also be effective in PTH in combination with other treatments.31

Although several studies support the utility of various therapeutic options in the monotherapy of PTH, no one treatment is likely to be more beneficial than an individualized program including consultation with appropriate subspecialists in concert with both pharmacologic and nonpharmacologic treatments.32


PTH is a complex and often refractory complication of TBI; it is highly prevalent and underrecognized. The gravity of these disorders has recently drawn increased attention, especially in light of the clinical, radiographic, and pathologic abnormalities recently reported in high-profile athletes and soldiers with a history of TBI. Although TBI and concussion continue to be a topic of much debate and research, many questions regarding diagnosis, pathophysiology, treatment, and prognosis remain unanswered. The most common sequela of TBI is PTH, which can inflict a striking medical and social burden. Between the designation of TBI as the “signature injury” of the military conflicts in Iraq and Afghanistan and the increasing incidence of concussions in athletes of all levels and ages, healthcare providers are likely to see an increase in the incidence and prevalence of PTH.

Although the recognition of concussion and PTH has evolved, many cases go undetected or inadequately treated. This occurs in part because many patients with TBI may initially lack obvious symptoms despite having incurred a neurometabolic crisis severe enough to cause significant disability or death.

Despite technological advances in the prevention of TBI, there is a paucity of data with which to formulate adequate diagnostic and therapeutic guidelines for the acute treatment of concussion and PTH. This patient population undoubtedly poses a therapeutic challenge, and a multidisciplinary and multifaceted approach is paramount.

Post-Traumatic Headache (PTH)

Last updated on: November 2, 2012
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