Should post-traumatic headaches be considered a post-concussive symptom?

The diagnostic terms cerebral concussion (or concussion) and mild Traumatic Brain Injury (mTBI) are generally considered to be roughly synonymous and both connote a traumatic insult to the brain resulting in disruption in cerebral functioning, if not frank injury to the brain. This letter will henceforth use the term, ‘mTBI’ synonymously with the term ‘concussion’, with both terms understood to imply cerebral dysfunction due to injury to the cerebrum.

mTBI can lead to the development of a number of symptoms that are often referred to as post-concussive symptoms (PCS); post-traumatic headaches (PTH) are generally considered to be a common (if not the most common) PCS [1] and are included in both the ICD-10 and DSM-4-TR diagnostic criteria for Post-Concussion Syndrome and Post-concussional Disorder, respectively. While PCS, including PTH [2], have long been recognized as being non-specific (i.e. may be caused or contributed to by factors other than mTBI), the ongoing inclusion of PTH as a PCS leads to the implication that PTH can be, or are, caused by cerebral injury/dysfunction caused by mTBI. Clinicians, for example, may teach persons who have suffered an mTBI that PTH is a symptom of the mTBI and further may make treatment decisions (e.g. return to play decisions, etc.) based on the ongoing presence of PTH (in addition to other PCS). Further, the presence of headache following an acceleration–deceleration event is often considered to raise suspicion for the diagnosis of mTBI. This letter seeks to raise, for future consideration and research, the possibility that PTH are not caused by mTBI and that clinical interventions based on inclusion of PTH as a PCS may ultimately be inappropriate and indeed may even have the potential for harm.

The pathophysiological mechanisms underlying PTH are poorly understood [1, 3, 4] and it is not at all clear that injury to the brain underlies all, or even some, PTHs. Experts in the management of PTH often recommend that the assessment and management of PTH proceed via identification of signs and symptoms of non-PTH headaches, such as tension headaches, vascular headaches such as migraines, cervicogenic headaches and medication rebound headaches; treatment recommendations are then based on the type of headache identified [3, 4] and appear to generally not be altered by the presence or absence of a history of mTBI. As summarized by Lenaerts [3], ‘Chronic PTH often presents as one of the primary headache syndromes, e.g. migraine or tension-type 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’ (p. 12). As will be evident from consideration of the ‘primary headache syndromes’ to which Lenaerts is referring, the pathophysiological mechanisms underlying these types of headaches do not require involvement of cerebral dysfunction; cerebral dysfunction caused by mTBI is not likely to directly cause these types of headaches. Indeed, it is of course known that the human brain lacks pain receptors and as such one cannot perceive pain from insult to the brain (e.g. this is a basis for the ability to conduct certain neurosurgical interventions with only ‘local’ freezing of pain sensitive structures such as the skin, meninges, etc.). Rather, PTHs appear, based on current knowledge, to be caused primarily by injury to the head (and neck), rather than injury to the brain. Based on these considerations, the consequent implication for clinicians and patients, then, is that PTHs appear not to reflect injury to the brain. This message may well serve to considerably reduce patient anxiety related to fear of ongoing brain dysfunction when experiencing ongoing PTH and may well lead to the need to reconsider treatment recommendations such as return-to-play and -work recommendations (e.g. the presence of ongoing PTH, as they are considered to be a PCS, is currently generally considered to be an indication to not return to play in contact sports or to work in situations of risk for mTBI).

Having said all of this, it is of course possible that insult to the brain may contribute to at least some PTH. For example, increased intracranial pressure caused by subdural haematomas and hydrocephalus may cause headaches; however, these conditions are, of course, relatively rare post-mTBI and are generally associated with additional symptoms. It is also at least possible, speculatively, that mTBI can produce changes in neuronal systems underlying perception or regulation of pain (e.g. impact on the opiate system; central pain syndromes, etc.). The available research data related to the pathophysiology of PTH do not, however, currently strongly support the likelihood of ‘cerebral’ causes of PTH in mTBI [3, 4]. Additional research would appear to be indicated.

Until such research is conducted, how should the issue of PTH as a PCS be addressed? One might argue that continuing to include PTH as a PCS, despite the apparent lack of evidence for a cerebral basis for PTH, is an appropriately ‘cautious’ approach and ought to be maintained until evidence mounts to indicate that PTH are not likely to be due to cerebral dysfunction caused by mTBI. Conversely and based on the author’s experience as a both a physician working with TBI patients and as an amateur hockey coach, the belief that PTH is due to ongoing cerebral dysfunction/injury can and does cause considerable stress and distress (and perhaps may, in turn, exacerbate headaches and other PCS?) and, as mentioned above, may lead to societal impact as with delaying return-to-play and -work. This letter is clearly, given the limitations of the research evidence, not intended to be a ‘demand’ for change; rather, the author hopes that the considerations briefly offered above will lead to future research, along with reconsideration by appropriate experts (related both to PTH and PCS), as to the risks, benefits and appropriateness of continuing to consider PTH a PCS. An alternative approach, until/if it is firmly established that concussive injury to the brain can/does cause PTH, may be to consider PTH a symptom that is ‘associated with’ mTBI, rather than a ‘true’ PCS.

Silver and Kay [5] recently proposed that the term PCS (and related terms) is itself invalid (given that multiple aetiologies may contribute to PCS) and proposed that the term’s use be discontinued with substitution instead of the term ‘persistent symptoms that occur after a concussion’ (p. 476). This proposal is consistent with and, hence, supportive of the concerns and proposals raised in this letter; however, the author suggests that Silver and Kay’s terminology be restricted to only those ‘PCS’ for which there is evidence of a probable cerebral pathophysiological contribution in at least some cases; based on the considerations briefly discussed above, this does not currently include PTH.

Declaration of interest

The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.