Post-traumatic headache (PTH) is defined by the International Classification of Headache Disorders-2 (ICHD-2) as a headache arising within seven days after a head or neck injury.1
WHAT TYPE OF HEADACHE IS THE PTH?
Most forms of PTH resemble primary headache disorders such as migraine and tension type headaches.2 Other forms of PTH are related to temporal mandibular injury, occipital neuralgia, neck injuries, brain hemorrhages, low cerebrospinal fluid pressure due to CSF leak and carotid and vertebral artery dissections.3
WHAT TYPE OF INJURIES CAUSE PTH?
Post-traumatic headaches may occur due to a traumatic brain injury (TBI). TBI may be found in both military and civilian populations. In military personnel, TBI are most commonly caused by blast explosions (75 percent), falls (29 percent), vehicle accidents (22 percent), fragment or shrapnel (21 percent) and bullets (2 percent).2 In the civilian population, TBI are most commonly caused by motor vehicle accidents (45 percent), falls (30 percent), occupational accidents (10 percent), recreational accidents (10 percent), and assaults (5 percent).4 Falls account for most of TBIs in children between 0-4 years of age and adults over 75 years of age.5
WHAT IS THE LATENCY PERIOD BETWEEN TBI AND INITIATION OF HEADACHES?
The ICHD-2 used an arbitrary latency period of seven days from TBI to onset of headaches. This is intended to eliminate the possibility that PTH was caused by any etiology other than TBI. However, recent data showed that PTH develops in patients within a week (40 percent), within a month (20 percent), and beyond a month (40 percent) after a TBI.6 A latency period of three months is probably more acceptable.7
WHAT ARE MAIN RISK FACTORS TO DEVELOP PTH?
Female sex and prior history of headaches.2
WHAT ARE MOST COMMONLY ASSOCIATED SYMPTOMS TO PTH?
Post-traumatic stress disorder (PTSD) and sleep disorders can augment the severity of PTH. This can be seen especially in military personnel.2 Other symptoms include impaired attention and concentration, slowing of mental-processing speed, mood changes, personality changes, irritability, dizziness, vertigo, diplopia, decreased taste and smell.
WHAT IS THE EPIDEMIOLOGY?
There are 1.8 million cases of acute PTH and 400,000 chronic PTH cases every year in the United States civilian population.8 Military personnel and civilians, specifically amateur athletes, who sustained a TBI are at high risk of developing PTH. One study reports 37 percent of 978 US soldiers who sustained mild TBI developed PTH.9 Ten to twenty percent of amateur athletes with TBI develop PTH.10
HOW OFTEN DO POST-TRAUMATIC HEADACHES PERSIST?
In the civilian population, 78 percent of PTH may persist after three months,11 35 percent persist after one year,12 24 percent persist after two years,13 and 24 percent persist after four years.3,14 Ninety eight percent of the soldiers who met the criteria for deployment-related concussion have headaches after three months of deployment. The prevalence of chronic daily headaches (15 or more days of the month) in returning veterans with deployment-related concussion headaches was 20 percent.6,15
WHAT IS THE SEVERITY OF MOST OF THE TBI?
Majority of the TBI are mild TBI (mTBI). Chronic PTH occur mostly after a mild TBI (75.3 percent) and less frequently with moderate to severe TBI (32.1 percent).8 Mild TBI is defined as a TBI associated with no loss of consciousness or loss of consciousness of less than 30 minutes duration, post-traumatic amnesia up to a day, and associated with Glasgow Coma Scale (GCS) ≥13 with normal brain structural MRI.3,16
Moderate TBI is defined as a TBI associated with loss of consciousness more than 30 minutes, but less than 24 hours; posttraumatic amnesia more than a day, but less than seven days; associated with Glasgow Coma Scale (GCS) between 9-12 and, and normal or abnormal brain structural MRI. Severe TBI is defined as a TBI associated with loss of consciousness more than 24 hours; posttraumatic amnesia more than seven days ; associated with Glasgow Coma Scale (GCS) between 3-8 ; and with normal or abnormal brain structural MRI.2,3,16
WHAT IS THE PATHOPHYSIOLOGY?
PTH occur due to injury 1) of nociceptor afferent fibers from the trigeminal nerve innervating the anterior head and scalp, face, leptomeninges and blood vessels and 2) from distal branches from C2 and C3 cervical spinal roots such as the greater and lesser occipital nerves innervating the posterior head and scalp. These two pathways convey painful signals to the spinal trigeminal nucleus with activation of second-order neurons that results in the process of central sensitization.17 At the cellular level, TBI induces a neuroinflammatory changes via microglia activation with the release of proinflammatory molecules such as interleukenes 1β, 6, 8, and tumor necrosis factor (TNF). Inflammatory response also includes blood brain barrier abnormalities with extravasation of neurotrophils, plasma proteins, mast cell degranulation, and platelet aggregation.18 These neurochemical changes may trigger cortical spreading depression and release of calcium gene peptides from trigeminal nerve cell bodies. This will stimulate glia to release more inflammatory molecules causing more neuronal hyperexitability.19 Release of excitatory neurotransmitters such as acetylcholine, glutamate, and aspartate, and magnesium decrement and alter glucose metabolism are also implicated in PTH pathogenesis.17,20