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Unmasking Post-traumatic Headache

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

Last updated on: November 2, 2012
First published on: May 1, 2011