Abstract
The ICHD-II criteria for post-traumatic headache (PTH) are strictly outlined. PTH can be subdivided into an acute and a chronic forms, the former likely nociceptive in nature, the latter likely neuropathic. The time of transition between the acute and the chronic forms is artificial and in the future should be better based on clear clinical or rather biological data. Chronic PTH often presents as one of the primary headache syndromes, e.g. migraine or tensiontype headache. Its biology is poorly understood and whether it merely represents the expression of the primary headache or it has a distinct pathogenesis remains unclear. The frontal lobe is often affected in traumatic head injury. Its dysfunction can cause an array of clinical consequences that have an impact on the patient's symptomatology and therapeutic outcome. Its recognition is likely to improve patient management quality.
Keywords
The International Classification of Headache Disorders, 2nd Edition (ICHD-II) addresses head and/or neck injury-related headache in category five (1). Headache related to head injury is subdivided into acute and chronic and then further subdivided into due to moderate/severe injury or due to mild injury.
A severe head injury is considered by these criteria as having at least one of the following features:
Loss of consciousness longer than 30 min;
Glasgow Coma Scale score less than 13;
Amnesia longer than 48 h; or
Abnormal imaging.
A mild head injury is defined by the following:
loss of consciousness less than 30 min, if any;
symptoms and signs of concussion, if any; or
Glasgow Coma Scale score at least of 13.
Post-traumatic headache (PTH) starts within 7 days of the trauma. When acute it lasts less than 3 months.
As far as headache due to neck injury is concerned, it also is divided into acute and chronic and the cause is presumed to be whiplash (sudden and significant deceleration/acceleration of neck). Whiplash has to be accompanied by pain at the time of the trauma.
Finally, ICHD-II created a category of headache due to intracranial haematoma, itself due to a trauma, specifically referring to an epidural or a subdural haematoma. Imaging must demonstrate the bleed. In the former, the epidural haematoma precedes the headache by no more than 24 h and must resolve within a maximum of 3 months of surgical treatment. In the latter, the headache follows the haematoma by 24–72 h and resolution is not a criterion.
The last two categories are headache due to other head and/or neck trauma, subdivided into acute and chronic, and postcraniotomy headache, also divided into acute or chronic. The craniotomy is of course presumed to be traumatic. There is no probable PTH, yet patients may have functional impairment after trauma in which the relationship between headache and injury may be difficult to establish.
It is worthwhile reflecting on the relationship between post-traumatic syndrome and head/neck injury. While it seems intuitive that the head injury could cause a number of aspects of the post-traumatic syndrome because of macroscopic lesions such as contusions, the potentially major deceleration imparted on the brain during a whiplash injury can also cause microscopic axonal injury, which, along with the significant pain and decreased mobility, contributes to the disability of post-traumatic syndrome. There may also be a direct cognitive impact of a neck injury but this remains unclear; this may require specific investigation. As it is common for head injury to be associated with neck injury, teasing out the contribution of each into the post-traumatic syndrome may be difficult if not impossible.
Another clinical challenge is the distinction between acute and chronic PTH. First, one could consider an acute PTH as an incipient chronic PTH. If clinical symptoms are similar, a common mechanism could be inferred, and thus the distinction between the two categories would be artificial. Conversely, if there is a clear symptomatic distinction the time in which those features statistically change has to differentiate the acute from the chronic form, as opposed to the artificial landmark currently set at 3 months. In the first classification of the International Headache Society this landmark was 2 months. It was based on a now-old observation that a steep decline in headache and, conversely, a steep incline in neuroticism and disability, took place between 2 and 6 months after the trauma (2). It was therefore considered that the chronic form was less biological and more psychological in nature. However, the second classification set 3 months as the landmark, even in the absence of biological evidence. Rather than a time landmark, the classification could consider either a biological or reliable clinical measure to provide the actual distinction between acute and chronic.
Chronic PTH typically presents as one of the following: chronic tension-type headache, chronic or transformed migraine, cervicogenic headache, cluster headache, or other. The classification could consider including these categories. The current recommendation is to code them separately. It is advised that if the PTH is de novo after the injury it should be considered strictly secondary but if it represents an aggravation of a pre-existing headache it be considered primary or primary plus secondary but never strictly secondary. A relevant yet unanswered question is whether the biology of a primary-like headache as mentioned above is the same with or without a chronic PTH component. The trauma is likely to exert its effect on the physiopathology of the headache, yet this remains putative. Although the similarity in symptomatology is obvious (3), further studies are warranted.
The aetiologies of the head/neck injury can be multiple. Careful consideration of the cause of the injury in PTH enhances the understanding of its symptomatology and mechanisms, and improves its therapy and overall management. While motor vehicle collisions often include a whiplash and are by far the most common source of PTH, falls predominate in the elderly and either subdural haematoma-induced headache or cervicogenic headache occurs. Middle-aged patients frequently get head/neck injuries at the workplace, which increases the incidence of legal issues of liability. Leisure and sport activities are typically more seasonal. Self-inflicted injuries unfortunately represent the highest proportion of head injuries, especially gun shots in the United States. Assault and battery are not uncommon.
Factors involved in the genesis of PTH chronification could encompass central sensitization, itself potentially mediated by axonal injury affecting pain-inhibiting structures in the brain stem (4). Abnormal cortical processing could be another determinant (5). Other putative contributors include behavioural changes, medication (over)use, and certainly a genetic predisposition. Whether factors causing chronification of PTH overlap those in chronic migraine is unknown.
PTH outcome is worse with older age, female gender and depression and anxiety. Perceived headache disability appears attributed to depression (6).
Much has been said on the relationship between presence and/or severity of the PTH and post–traumatic syndrome overall, on one hand, and the severity of the head/neck injury, on the other. Studies seem to indicate a weak relationship at best, and others even an inverse relationship whereby milder injury could be more likely to provoke a headache later (7, 8). As to factors specifically pertinent to whiplash, unpreparedness of vehicle occupants, rear end-type collision and rotation of the head at the time of impact are significant (9). Similarly, correlation between disability and pain levels in cervicogenic PTH is poor (6). Disability due to combined head and neck injury is severe but the relative role of each in the headache is difficult to tease out. Two per cent of the population is disabled by overall traumatic brain injury in the USA according to the census of 2002, with a yearly incidence of 1.8 million traumatic brain injuries, of which 30–90% have PTH. Its occurrence appears to depend on the health care system. Over time, 44% of head and neck injuries are accompanied by chronic headache at 6 months, but beyond 1 year the head pain tends to become permanent (20% at 1 year, 3 years, 4 years). PTH causes more disability than primary headaches according to a study of 280 million subjects where 84% of chronic PTH patients had some degree of disability vs. 60% of primary headache patients. A recollection bias can occur, illustrated by the need to prompt patients about a history of trauma before the occurrence of the headache. It is interesting to observe that the outcome of chronic PTH remains unchanged by the settlement of a legal issue (12).
Post-traumatic syndrome encompasses variable degrees of the following. Besides the headache, patients can complain of: vertigo amnesia, decreased concentration and confusion, insomnia and fatigue, depression and anxiety, irritability and social disintegration. When one considers the features of frontal lobe syndrome, which is common with antero-posterior deceleration injuries, the italicized features mentioned could be attributed to that part of the brain. Frontal lobe syndrome may in time influence symptomatology, disease perception, therapeutic compliance and legal matters. It must be better recognized, especially in view of effective treatments such as cognitive-behavioural therapy.
It appears clear from the above issues that further, in-depth, clinical characterization is warranted.
Treatment of PTH remains difficult, especially in the chronic form, yet when thoughtfully applied can be very effective. Judiciously balancing therapy between acute, and nociceptive, pain, on one hand, and chronic, and probably neuropathic, pain, on the other, can be challenging. The choice between symptomatic analgesia and prophylaxis may be difficult. There is a risk of medication overuse headache that complicates the syndrome.
The therapy of chronic PTH is multifaceted and associates symptomatic pain relief, early pharmacoprophylaxis and a complementary therapy, including any combination of physical therapy, relaxation and biofeedback, among others (11, 12). Education remains paramount and often needs to involve the physician, nurse, physical therapist and social worker, as well as the family. Overall, this endeavour can be challenged by cognitive dysfunction. The patient needs to be reassured. The pathophysiology of the syndrome needs be explained and reasonable expectations should be given to the patients to avoid frustrating therapeutic limitations.
Finally, it is crucial to focus on function as a more relevant and reasonable outcome than complete pain relief.
The medical community at large should be aggressive in advocating for patients. A multidisciplinary approach is more cumbersome and costly but also more effective and it is important to emphasize it over time. It is formally recommended to separate medical and legal aspects (12).
In conclusion, the distinction between acute and chronic PTH syndrome needs further attention and a clinical and/or biological distinction needs be sought. PTH pathogenesis in mild injury remains unclear. The relative role of head and neck trauma in PTH is difficult. Finally, the impact of the frontal lobe syndrome in presentation and management needs be appreciated.
Patient and physician need to engage in education, and multidisciplinary therapy is recommended. Legal and medical issues should remain separate and the medico-legal system should decrease its reliance on investigations and emphasize clinical assessment.
Conflicts of interest
MEL has acted as a speaker for OrthoMcNeil Neurologics and Merck.