Sports concussion headache.

http://informahealthcare.com/bij ISSN: 0269-9052 (print), 1362-301X (electronic) Brain Inj, Early Online: 1–14 ! 2014 Informa UK Ltd. DOI: 10.3109/02699052.2014.965213

REVIEW ARTICLE

Sports concussion headache Nathan D. Zasler1,2,3,4,5 Concussion Care Centre of Virginia, Ltd., Richmond, VA, USA, 2Tree of Life Services, Inc., Richmond, VA, USA, 3VCU Department of Physical Medicine and Rehabilitation, Richmond, VA, USA, 4Department of Physical Medicine and Rehabilitation, University of Virginia, Charlottesville, VA, USA, and 5 University of Virginia Brain Injury and Sports Concussion Institute, Charlottesville, VA, USA

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Abstract

Keywords

Background: Sports concussion headache (SCH) is common; yet poorly researched and understood. Somatic complaints including headache are frequently reported by both amateur and professional athletes. Although the literature is replete with reports of a high incidence of headache following sports concussive injuries, there is a dearth of evidence-based medicine to provide practitioners with an understanding of sports concussion headache risk factors, epidemiology, biomechanical risk factors and/or injury thresholds, aetiology, assessment, treatment or prognosis. Review: This article will provide readers with an overview of SCH based on the available literature (which as noted is limited); and, where evidence is lacking, information will be provided from the more general post-traumatic headache (PTHA) literature, the author’s extensive clinical experience and literature from parallel primary headache disorders. Incidence, pathoanatomy, neurobiology, classification, natural history and prognosis of sports concussion headache will be reviewed. Common, as well as less common, sports concussion headache subtypes will be discussed. General approaches to evaluation (including history taking and physical examination), as well as treatment approaches will also be addressed for specific headache subtypes. Lastly, directions for future research will be explored.

Cephalalgia, concussion, headache, mild traumatic brain injury, sports concussion

Introduction The topic of sports concussion has recently received much attention in the media, as well as the scientific literature. One significant common somatic sequela of sports concussion is that of post-traumatic headache (PTHA) or, more specifically, sports concussion headache (SCH). There is a dearth of evidence-based, prospective literature examining risk factors, incidence, prevalence, pathomechanics, pathoaetiology, classification, evaluation, treatment and/or prognosis of sports injury-related headache, whether post-concussive or otherwise. SCH, when associated with traumatic brain injury (TBI), typically occurs in the context of mild TBI or concussion; therefore, the term ‘sports concussion headache’. Headache is one of the most common somatic complaints seen in general medical practice and certainly the most common physical complaint following concussion and TBI in general [1, 2]. It is a common co-morbidity associated with sports trauma [3, 4]. There remains debate regarding the correlation of TBI severity with headache incidence [5, 6], but this has not been specifically addressed relative to SCH. Post-concussive headaches do not necessarily occur due to the Correspondence: Nathan D. Zasler, MD, FAAPM&R, FAADEP, DAAPM, CBIST, Concussion Care Centre of Virginia, Ltd., 3721 Westerre Parkway, Suite B, Richmond, VA 23233, USA. Tel: 804-3461803. Fax: 804-346-1956. E-mail: [email protected]

History Received 8 January 2014 Revised 28 July 2014 Accepted 14 August 2014 Published online 7 October 2014

concussion itself but often times are the result of head impact injury and/or cervical whiplash-type injuries [2]. The terms PTHA and SCH (which may be fine as ‘umbrella’ terms) do not convey any real information of value regarding the specific headache aetiology or underlying headache diagnosis, nor do they guide treatment of the headache disorder. Use of such general terms (e.g. PTHA or SCH) may; therefore, cause practitioners and others to misattribute the headache disorder to traumatic brain injury when in fact it’s cause may be extra-cerebral [2, 7, 8], whether associated with sports injury or otherwise. Historically, SCH was seen as a singular headache disorder with some quoting an incidence of headache occurring in nearly 90% of all sports concussions [9]. Current consensus opinion is shifting away from an Ockham’s razor approach to PTHA and by implication SCH diagnosis and a greater appreciation of the diverse biopsychosocial factors that may influence symptom presentation and promulgation [10]. There is also a growing understanding of the potential role of a number of different pain generators in SCH/PTHA [2]. How exactly specific headache phenotypes differ in sports injuries vs. other traumatic injuries, if at all, has yet to be determined. Additionally, the acute, sub-acute and chronic variants of sports concussion headache, as with PTHA in general, have not been rigorously studied relative to incidence, prevalence, aetiology, evaluation, treatment and/or prognosis.


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Similarly, risk factors for SCH and vulnerabilities for developing chronic SCH have received little attention. Some literature suggests that SCH, including post-traumatic migraine (PTM), is associated with protracted recovery from sports-related concussion, greater level of post-concussive symptom complaints, as well as more impairment on subacute neuropsychological testing [11–15]. Research examining the impact, if any, of SCH on balance testing via such instruments as the Balance Error Scoring System (BESS) has shown disparate results [16, 17]. What role genetic loading risk factors [12], pre-existing neck pain and/or headache, concurrent whiplash injury, athlete ‘preparedness’ for impact (i.e. player sees the blow coming and tenses up), dizziness, athlete sex, anatomic variables across players including sex differences, cultural influences, affective disorders and/or characterological traits have on SCH incidence, severity and duration are unknown at this point in time. Interestingly, pre-season neck pain, dizziness and/or headaches may, in and of themselves, be risk factors for subsequent concussion in certain athletes [18]. SCH can be associated with poorer performance on neuropsychological testing [19], altered sleep efficiency, changes in personality (i.e. irritability and decreased frustration tolerance), depression and anxiety [2, 20].

Classification There remains controversy on the best way to classify posttraumatic headache, in general, and sports concussion headaches, more specifically. Use of the current IHS International Classification of Headache Disorders (ICHD) system [22] which relies on descriptive elements for each headache category without any attribution to physical assessment findings may, in this author’s experience, result in misclassification of headache sub-types and, in particular, overdiagnosis of post-traumatic migraine headaches. This concern has recently been echoed by Evans [23]. What role classification systems, such as ICHD or ICD-10 [24], have in refining the assessment or treatment of any type of PTHA including SCH remains to be seen. These classification systems have been criticized on numerous levels and some have advocated for changes to occur in the manner in which such headache are classified [25, 26]. Additionally, no one has, as of yet, examined the correlation, if any, between diagnoses made based on either the ICHD or ICD-10 classification systems and clinical diagnosis based on history and exam findings of patients with PTHA including SCH. The ICHD III PTHA categories are divided up as noted in Table I, but as is noted there is no specific classification for SCH. The ICD-10 divides post-traumatic headache into several broad categories: post-traumatic headache, unspecified; acute post-traumatic headache and chronic post-traumatic headache, with each category having a separate category of intractable vs. not intractable. Although, there are classifications for other types of headache that may be applicable to causes of headache after trauma, they would not, by definition, fall under ‘post-traumatic headache’ by ICD-10 criteria. Again, like the ICHD, ICD-10 has no specific classification for SCH. Patients with ‘minor head trauma and no confirmatory signs’ are grouped in a separate classification.

Brain Inj, Early Online: 1–14

Table I. 5.1 Acute headache attributed to traumatic injury to the head 5.1.1 Acute headache attributed to moderate or severe traumatic injury to the head 5.1.2 Acute headache attributed to mild traumatic injury to the head 5.2 Persistent headache attributed to traumatic injury to the head 5.2.1 Persistent headache attributed to moderate or severe traumatic injury to the head 5.2.2 Persistent headache attributed to mild traumatic injury to the head 5.3 Acute headache attributed to whiplash 5.4 Persistent headache attributed to whiplash 5.5 Acute headache attributed to craniotomy 5.6 Persistent headache attributed to craniotomy

There are a number of problems with the current systems used for PTHA classification that have been pointed out by several practitioners/scientists [2, 23, 27]. The ICHD III classification system uses criteria that are primarily concerned with the temporal onset and pathoaetiological relationship of the headache to the trauma and not with the clinical features of the headache condition. ICHD III criteria for PTHA require that headache onset occurs within 7 days of the traumatic event or regaining consciousness. This temporal onset criterion appears to have been determined only on the basis of empiricism due to the lack of good evidence-based medicine to determine the same with an acknowledgement by most of many reported cases having longer lag times prior to headache onset. ICDH distinguishes between acute posttraumatic headaches (those which persist less than 3 months after injury) and persistent post-traumatic headache (persisting longer than 3 months). It should be noted, however, that this timeframe is disparate with typical definitions for chronic pain, which is traditionally defined as pain lasting longer than 6 months. Each of these conditions is further divided into headache following mild vs. severe head trauma (note that ‘head trauma’ and not ‘brain injury’ is used as the phraseology; again confounding not only the definitional criteria, but also research based on the same). Whiplash-induced headache is also included in the latest version of the ICHD, but the mechanisms and site of pain generation are not stipulated. It should also be noted that ICHD defines post-traumatic headaches as a singular disorder and does not distinguish the headache mechanistically in terms of migraine, tension, neuralgic, cervicogenic or other causes under the posttraumatic rubric; although all these conditions and others exist as separate diagnostic entities in the classification system. When a headache occurs for the first time in close temporal relation to trauma or injury to the head and/or neck, it is coded as a secondary headache attributed to the trauma or injury. This remains true when the new headache has the characteristics of any of the primary headache disorders. When a pre-existing headache with the characteristics of a primary headache disorder becomes chronic or is made significantly worse, in close temporal relation to such trauma, both the initial headache diagnosis and the secondary posttraumatic headache should be given. Delayed-onset persistent headache attributed to mild traumatic injury to the head may

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be used when the interval between injury and headache onset is greater than 7 days [22]. In more severe brain injury, the patient’s neurocognitive and/or neurobehavioural status may limit their ability to identify and/or appreciate head pain to be able to report it ‘early’, even after regaining consciousness. Further confounding the determination of time of onset of headache after sports concussion across injury severity are various factors including: the injured player may have other significant trauma with more painful post-traumatic conditions (e.g. neck injury, long bone fractures and/or extremity ligamentous injury, among other conditions) than their headache, causing them to focus their attention on the more painful body part; post-traumatic confusion and/or post-traumatic amnesia (neurogenic or drug induced); administration of pain medications or pathology that may not manifest pain right away.

Problematic issues in the SCH literature One significant concern when examining the extant literature on SCH is the rampant nomenclature misuse across studies as related to brain, head and neck injuries, as well as a lack of consistent use of parallel research methodologies across studies including historical data provided, injury details, headache classification methods, nature of physical/neurological hands-on exams (if done at all), among other issues. Another concern is the overt focus on concussion/TBI as the main or sometimes even sole underlying pathoaetiologic explanation for SCH. Athletes may suffer from headache of non-traumatic aetiologies including exertional, effort induced, dehydrational, pharmacological (as related to both prescribed and non-prescribed drugs) and sport device triggered headache that must be differentiated from SCH, as well as sports-related traumatic headache that is not due to concussion, particularly when occurring concurrently [28, 29]. Surprisingly, all three recent consensus/position papers dealing with sports concussion [30–32], as well as a review article comparing the conclusions of the aforementioned guideline recommendations [33], neglected to stipulate any guidelines or recommendations for SCH prevention, classification, pathoaetiology determination or methodologies for either evaluation or treatment; even though headache remains the most commonly reported somatic complaint following sports concussion. The American Medical Society Sports Medicine Position Statement on Concussion and Sports [33] did include a brief mention of migraines as a risk factor for concussion, as well as concussion being a risk factor for triggering migraine. Headache treatment was also briefly mentioned, including notation of the fact that there were posttraumatic headache sub-types including migraine, tension and occipital neuralgia . . . without any elaboration of any other potential causes of SCH being made. The guidelines also noted general pharmacological and physical modality interventions but did not stipulate what types of headaches might respond to which specific intervention(s). Currently, there are no evidence-based guidelines regarding classification, assessment and/or treatment of sports concussion headache and, for that matter, post-traumatic headache in general [2, 34].

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Pathoanatomy and neurobiology of sports concussion headache Potential sources of head pain that may be relevant in the assessment of a patient presenting with SCH include the dura, venous sinuses, cranial cavities including sinuses, eye socket, ear, nasal and oral pharynx. The skin, nerves, muscles and periosteum of the cranium are all pain sensitive. Cervical/cranial joint capsules (including the temporomandibular joint), cervical facets/zygapophyseal joints, peripheral nerves (supra-orbital, trochlear, greater occipital, lesser occipital as well as third occipital nerves) and the cervical sympathetic plexus may all be primary nociceptive pain generators that produce local or referred head pain [2]. Given the nature of sports injuries, it is certainly possible to incur various types of trauma to the aforementioned structures including but not limited to impact injuries (both long and short impulse), stretch injuries of various tissues (both rotational and linear), penetrating injuries, shearing/ tearing injuries and compression, as well as herniation-related forces. One of the most common, yet often overlooked, sources of head pain following a sports concussion is referred cervical pain. This type of pain is typically associated with acceleration–deceleration insults, also referred to as whiplash associated disorders or WAD, which may result in cervicogenic headache [2, 35]. Such injuries can produce an array of pain generators, including but not limited to myofascial pain emanating from any of the four layers of posterior cervical musculature, as well as anterolateral cervical musculature; traumatic neuralgias (as noted above), osseous somatic dysfunction, disc herniation and/or rupture, ligamentous injury and/or facet joint trauma (with potential for osteoarthropathy and/or traumatic injury to the medial branches of the dorsal ramus) [2]. The aforementioned injuries can be seen in the absence of TBI, mild or otherwise, and should always be considered in the context of identifying the specific pain generators contributing to the SCH. There is no consensus on the exact pathophysiology of PTHA or for that matter SCH. There are likely different mechanisms involved across patients and the potential for multiple pain sources (including psychogenic ones) in the same patient should always be considered. Central mechanisms involving increased brainstem nociceptive neuropeptides such as calcitonin gene-related peptide and substance P, as well as glial fibrillary acidic protein-positive astrocytes, may be associated with persistent allodynia related to somatosensory cortex injury [36, 37]. How relevant some of these proposed mechanisms are to human post-traumatic headache including SCH remains to be seen. Others have speculated that the pathophysiology of post-traumatic headache is shared with the pathophysiology of brain injury itself relative to inflammatory responses which could persist beyond timeframes for actual beneficial physiological effect leading to secondary injuries due to alterations in neuronal excitability, axonal integrity, central processing, as well as other changes [38]. Various other mechanisms have been proposed including ones involving the trigeminovascular system (given that the trigeminal nerve is the major peripheral nerve for transmitting pain stimuli in the head),

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occipital nerve dysfunction, cervicogenic referred pain and central pain pathway disruption, among others [39].


Sports-related injury and headache Although most injuries involving TBI in sports that result in headache complaints will be classified as concussions, implying mild TBI (MTBI), it is certainly possible to see more substantive injuries that result in complicated MTBI, moderate TBI or even severe TBI. The evaluating clinician, whether on the field or in the hospital or clinic, must therefore use appropriate screening assessments to rule-out a more substantive brain injury when there is a complaint of headache following a sports-related traumatic event. There are now devices used to screen for extra-axial bleeds on the field that may significantly improve screening of injured players [40, 41]. Additionally, clinical signs including paralysis, papilloedema, anisocoria and/or progressive neurological impairment have been shown to be red flags for a more serious brain insult. The presence of post-traumatic confusion, amnesia, drowsiness and emesis may also be markers of a more substantive injury, whether or not associated with loss of consciousness, and should be managed with caution [42]. As previously mentioned, concussionrelated headache in sports must also be differentiated from other forms of sports-related headache [43]. Headaches may be seen transiently following so-called concussive convulsions [44]. These traumatic, but typically benign events, previously believed to be epileptic phenomena, are now thought to be a brief traumatic functional decerebration resulting from loss of cortical inhibition. Concussive convulsions typically occur within seconds of head impact and typically last no more than several minutes. They do not necessitate specific therapy and do not carry any increased risk of long-term epilepsy [44]. A topic of ongoing, substantive debate and controversy is that of chronic traumatic encephalopathy in athletes and its relation to repetitive concussive and/or sub-concussive injuries. Within that debate, there exists an additional point of contention relating to the causal relationship and incidence of headache in such cases. There are methodological concerns about CTE research relative to the absence of asymptomatic groups of athletes with a history of multiple concussions who have had brain histological studies done post-mortem to compare with the symptomatic group of concussed players. How much can be said about headache in this particular group of patients is debatable; however, McKee et al. [45] have noted that headaches were commonly reported by the athlete’s families in stages l and II, less commonly in stage III and not at all in stage IV [46]. No one has examined whether these headaches are predominantly psychogenic, tension, cervicogenic, migraine or some combination of the aforementioned . . . or of some other origin. Neither has anyone addressed why these headaches would be more common in milder forms of CTE neuropathology than more advanced forms. If headache was in fact a by-product of the disorder, then one would logically expect more, not less, headache with advancing disease. Another area of some controversy is that of whiplash triggered exacerbation of type I Arnold-Chiari malformation


(ACM) symptoms [47]. An ACM is a congenital variant involving downward herniation of the cerebellar tonsils through the foramen magnum and is graded on a I–III scale. Type I malformations are usually asymptomatic but can present, after apparently insignificant trauma, with a wide range of possible symptoms including, most importantly, headache. Studies have shown that upright scanning is apparently much more sensitive at picking up this anatomical variant when compared with recumbent imaging [48]. Treatment is traditionally surgical with decompressive surgery or, alternatively, but less commonly de-tethering of the spinal cord.

Natural history and prognosis Although there is now some limited methodologically sound literature examining the natural history of PTHA, there is even less such data on the natural history of SCH [49, 50]. No one has, as of yet, tried to demarcate the differences in natural history of the various sub-types of SCH or, for that matter, PTHA relative to examining the course of headache disorder for those with tension type headache, migraine, cervicogenic headache or occipital neuralgic headache, among other sub-types. There is not much known about headache prognostication after sports-related concussion/brain injury; mainly due to the fact that little has been done to investigate this headache disorder in a blinded, prospective manner over any substantive length of time as related to risk factors for more persistence of SCH or, as noted above, it’s natural history. Based on the extant PTHA literature, it is known that traumatically triggered headaches may often be persistent and, in general, are not promulgated by ongoing litigation [51], although no one has, as of yet, addressed validity and effort issues in the context of any type of SCH/PTHA study. Seifert [52] noted that the majority of those patients with SCH reported resolution of headache complaints within a few months from the time of initial injury, with general PTHA literature evidencing rates at 1 year post-injury to be between 8.4–35%, with almost 25% reporting non-remitting headaches attributable to their original injury at 4 years post-trauma. He also acknowledged the challenge of return to play decisions in athletes with persisting headache. Issues that are relevant in this context include differentiating whether their condition was an exacerbation of a pre-existing headache disorder, a new onset headache unrelated to the trauma or a de novo post-traumatic headache. In the context of any discussion of prognosis, one must consider how accurately patients with PTHA/SCH were actually diagnosed relative to their specific pain generators. Given the aforementioned, it is difficult to know if patients were correctly treated for their headache disorders. A recent comprehensive, systematic review of prognosis and return to play after sports concussion surprisingly made no comments on SCH/PTHA [11]. Confounding variables including pre-injury headache history, genetic loading, athlete sex and body morphology, injury biomechanics and forces, cultural issues, pain chronicity, pain coping resources (both internal and external), pre-injury characterological traits, social support, litigation (if any) and

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other factors may all play a role in the ultimate prognosis following sports-related injury and headache. Delayed recovery may, in part or whole, be related to multiple factors including inappropriate diagnosis and/or treatment, iatrogenic promulgation of SCH (i.e. via use of medications that produce medication overuse headache), as well as psychiatric disorders including substance abuse.


Common SCH sub-types Based on the extant literature, which is predominantly focused on headache classification using ICHD criteria, SCH most commonly is due to tension headache followed by migraine. Some question this ‘neurological dogma’ based on the overlap in presenting symptoms that can lead to confusion regarding the specific headache aetiology and associated pain generator(s) [2, 23]. Further research is needed to better edify specific variants of PTHA/SCH based not only on ICHD but also on bedside clinical exam and consideration of other factors like injury mechanics, body morphometrics, psychological factors, among other potential variables that may be important in delineating specific headache generators. SCH headache sub-types Musculoskeletal headache Musculoskeletal headache is classically characterized as a cap-like discomfort, but varies with the offending musculature. Any clinician evaluating an athlete after a sport injury should be familiar with myofascial pain and trigger point referral patterns [53, 54]. Sternocleidomastoid trigger points, for example, are notorious for referring pain retro- or periorbitally; whereas, trigger points in the clavicular portion of the sternocleidomastoid muscle can refer to the external ear, causing earache/head pain. Musculoskeletal pain may be constant or intermittent, relieved by application of heat, cold, massage and many overthe-counter medications including NSAIDs. There may be autonomic components such as dizziness or tinnitus due to specific muscle myofascial dysfunction [54]. Within the broad category of musculoskeletal headache, other aetiologies beyond the almost omnipresent myofascial pain include craniomandibular syndrome, cervical zygapophyseal joint disorders (see section below on cervicogenic headache) and craniospinal somatic dysfunction. In craniomandibular disorders, there may be internal derangement of the tmporomandibular joint and almost always a myofascial component related to muscles of mastication (temporalis, pterygoids or masseters) [55]. Temporomandibular joint (TMJ) dysfunction (TMJD) or craniomandibular syndrome is almost always seen following direct trauma to the craniomandibular complex when traumatic in origin. This type of trauma can produce focal headache and is also frequently overlooked as a primary or contributory cause of SCH. In TMJ, clicking, popping or malocclusion of the jaw may be noticed [2]. Cervicogenic headache These types of headaches may be related to dysfunction of the facet joints, occipital neuralgia, post-traumatic myofascial


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pain and/or cervical vertebral somatic dysfunction. Others have hypothesized that chronic pain following cervical acceleration–deceleration type injuries may be due to central sensitization. Obligatory for the diagnosis is unilateral head pain without side-shift and symptoms or signs of cervical involvement, the latter which could include provocation of pain by neck movement or by external pressure to the upper posterior neck, concurrent cervicalgia or reduced cervical range of motion. Bilateral occurrence may be seen on occasion. Most patients present with unilateral sub-occipital pain, as well as secondary oculofrontotemporal discomfort/ pain, particularly when the pain generators in question are more flared. This type of headache is commonly mislabelled as migrainous [56, 57]. Dysfunction of the cervical zygapophyseal joints, particularly at C2 and C3, may refer pain to the head. Familiarity with the cervical root sensory dermatomes and sclerotomes is, therefore, critical in the context of differential diagnostic assessment of such patients. Treatment considerations include intra-articular injection of local anaesthetic or block of the medial branches of the dorsal rami supplying the joint. It is important for clinicians to be able to differentiate referred pain that is dermatomal from referred pain of other origins including sclerotomal, ligamentous/tendinous and myofascial. Craniocervical somatic dysfunction may occur secondary to trauma and cause headache (both primary and referred). These osseous disorders are typically treated with manual, chiropractic and/or osteopathic manipulative and/or muscle energy techniques designed to realign dysfunctional units. Careful cervical physical examination is paramount in the context of evaluating an athlete with SCH [58]. Cervical mobilization and manipulation may be effective in the treatment of SCH, although there is no literature specific to this population. Various manipulative techniques may be used, but caution should be exercised with high velocity procedures due to risk of cervical fracture and/or vertebral artery injury, which are generally avoided by not mobilizing the neck in extension. Cervicogenic headache is a common cause of SCH, although there is a dearth of literature examining headache sub-types in this group of patients as previously noted. Some have argued that cervicogenic pathology and referred headache pain is likely the most common cause of post-traumatic headache [59]. Studies suggest that, in appropriate cases, manual therapy, exercise and blocks (diagnostic, as well as therapeutic) may play important roles in modulating cervicogenic headache pain [2]. Neuritic and neuralgic head pain Neuritic scalp pain may occur from local blunt trauma, surgical scalp incision or penetrating scalp injuries. Occasionally, neuromatous lesions may form after scalp nerve injury and serve as a pain nidus. Pain complaints may vary from dysesthetic ‘numbness’ type discomfort on touching of the affected area of scalp to lancinating-type pain that spontaneously occurs without provocative actions. Neuralgic pain may occur secondary to occipital (greater and/ or lesser), third nerve occipital, supra-orbital and/or infraorbital neuralgia as the most common clinical post-traumatic


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cephalic and/or facial neuralgias seen in clinical practice associated with PTHA; although, other post-traumatic neuralgias/neuropathies may occur [2]. Occipital neuralgia (ON) may occur following cervical acceleration–deceleration type injuries, as well as direct trauma to the craniocervical junction. ON may be perpetuated by contraction or myodystonia of the splenius muscle, which it penetrates. Pain is typically felt at the craniocervical junction and the sensory distribution of the nerve (e.g. C2 or C3). The affected nerve is tender to palpation which generally replicates the pain associated with the headache (e.g. stabbing quality), with numbness in the sensory distribution of the nerve. There is frequently referral of pain into the ipsilateral frontotemporal scalp and less frequently retro-orbitally secondary to ephaptic transmission between the proximal part of the C2 origin of the nerve and the ophthalmic branch of the fifth cranial nerve [60]. Third occipital headache has also been described and has been shown to be a fairly common cause of chronic postwhiplash headache. The posterior division of the third cervical nerve has a medial branch which runs between the semispinalis capitis and cervicis and pierces the splenius and trapezius, ending in the skin. While under the trapezius, it gives off a branch called the third occipital nerve, which pierces the trapezius and ends in the skin of the lower part of the back of the head, lying just medial to the greater occipital nerve and communicating with it [61]. Whether the aetiology is local neuroma formation in scar tissue in the scalp or a neuralgia, the pharmacological interventions are essentially the same and include nonsteroidal anti-inflammatories (NSAIDs), tricyclic antidepressants (TCAs) and anticonvulsants, particularly gabapentin and pregabalin. Injection of local anaesthetic with or without steroid may also be indicated for both diagnostic and therapeutic purposes for neuritic and neuralgic pain disorders [62, 63]. For greater and lesser occipital neuralgia and, in particular, for third occipital nerve headache, clinicians should be familiar with the anatomy of the region given risks of aberrantly placed injections into major vascular structures (see Figure 1). In either of the aforementioned situations, myofascial pain may be a secondary or perpetuating pain generator and must be treated, as well on a concurrent basis. Another treatment option that has garnered success is the use of topical compounded pain medications, particularly for more diffuse scalp or post-craniotomy or impact injury dysesthetic type pain [2]. An exciting treatment option for certain posttraumatic neuralgias is neuromodulation with either implantable units or, more attractively, external units such as Cefaly [64–66]; although these techniques are relatively new and await further testing for this class of headache as they have been FDA approved, at this point, for only migraine. Rarely, surgical decompression or nerve lysis (surgical or via cryotherapy) is necessary for these types of neuralgic cephalalgias; although long-term pain palliation is rarely achieved with surgical intervention. Post-traumatic migraine Post-traumatic migraine (PTM), also referred to as trauma trigger migraine (TTM), is well described in the sports


Figure 1. Anatomy of the upper posterior cervical region with specific reference to C2 terminal branches of the greater and lesser occipital nerves. Reprinted fom Zasler et al. [112], with permission.

concussion [4, 23, 67–71] and general TBI literature, although its true incidence and long-term impact remains debated, in part because use of traditional classification systems in the absence of clinical exam may over-estimate its occurrence [2, 23] and in part because of the limitations of the measurement properties of headache-specific outcomes scales [72]. Patients with PTM may have a genetic predisposition to development of migraine following trauma to either the head/brain and/or neck [2, 23]. There is inadequate information to stipulate how acute PTM may differ mechanistically and otherwise from chronic PTM, if at all. PTM pain is typically described as a throbbing, unilateral pain that can be exacerbated by coughing and bending over. Cold may help, but heat usually makes the pain worse. There may be associated nausea, vomiting or anorexia. Hemicranial allodynia may occur after central sensitization takes place, which is a bad prognostic sign for triptan efficacy moving forward [2]. PTM is typically seen in children, adolescents and young adult, although there is a substantive literature on its occurrence in professional athletes [73–78]. The migraine attack may present variably including with visual disturbance (i.e. temporary blindness), change in level of consciousness or with hemiparesis or brain-stem symptoms (i.e. basilar migraine); however, an aura may be absent. A severe headache, nausea and vomiting typically follow. Symptoms of acute post-trauma migraine typically begin within 1–10 minutes after a blow to the head, but are not triggered by blows to the rest of the body. The attack usually resolves within a few to 24 hours. On rare occasion, neurologic deficits may not totally clear [79]. Trauma triggered migraines have been reported with soccer, football, rugby, volleyball and wrestling [73–78]. Because of the differences in participation level between girls and boys in contact sports, these headaches have historically been believed to occur more commonly in boys


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and young men; although there have been some dissenting opinions on this [12]. The clinical presentation of PTM is similar to other migraine attacks. The incidence of spontaneous migraine is much higher in children with trauma triggered migraine. A positive family history of migraine is seen in over 70% of children with this variety of headache [79]. Bennett et al. [80] of the University of Nebraska reviewed three members of a university football team, aged 18–21 years old, who were evaluated because of migraine symptoms precipitated by head trauma. This study analyzed the clinical data from these cases, as well as eight previously reported in athletes. The head trauma was usually minor and not associated with amnesia. Visual, motor, sensory or confusional signs and symptoms began after a short symptom-free interval. Symptoms lasted for 15–30 minutes and were followed by a headache frequently accompanied by nausea and vomiting. In nine of 11 cases, the attacks re-occurred with subsequent head trauma [80]. As per Seifert [52], if the neurologic evaluation is nonfocal and the headache appears to be consistent with migraine, imaging studies may not be necessary. Matthews [81] noted that, because of the widespread and erroneous belief that complicated migraine is associated with vascular anomalies, patients (or their parents) often fear that they have a more serious condition. If there are no physical abnormalities, neurodiagnostic investigations are generally not required. Rather, in children participating in otherwise routine physical activities, observation may be sufficient. In the athlete who plays full contact sport, an additional concern associated with acute headache onset following trauma is the possibility of traumatic intracranial haemorrhage. According to Bennett et al. [80], participation should be continued only after a thorough neurological evaluation. The athlete should be apprised of their condition and any abnormalities found on examination. The evaluating specialist should warn the patient to report to the team physician or trainer if neurological symptoms recur, including headache. Athletes should not return to play with persistent headache symptoms, either at rest or with physical or cognitive exertion [30–33]. It is recommended that readers stay abreast of current sports concussion guidelines regarding return to play recommendations, which go beyond the scope of this particular paper. Due to central overlap of primary nociceptive afferents involved in migraine headache and those related to cervical sensory nerves, the patient with SCH may present with a combination of vascular, neuralgic and/or musculoskeletal headache pain generators, all of which may require treatment. Sensory nerve fibres in the descending tract of the trigeminal nerve (TN) connect with sensory fibres from C1–C3 and, possibly, C4 cervical roots, which explains, at least in part, referred pain mechanisms between the neck and TN sensory receptive fields [2]. Based on the aforementioned, cervical nociceptive pain generators may also promulgate migraine through the trigeminocervical complex and, therefore, must be addressed as part and parcel of comprehensive migraine assessment and treatment [2] (see Figure 2). The aim of treatment of migraine headache is to prevent or reduce the frequency of the onset of headache (prophylactic treatment) and/or to abort a headache rapidly should it occur


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Figure 2. Schematic representation of interconnectivity between the spinal nucleus and tract of cranial nerve V, upper three cervical roots and the ophthalmic branch of the fifth cranial nerve through the Gasserian ganglion. Reprinted fom Zasler et al. [112], with permission.

(as well as sustain the headache relief once aborted). The precise trigger for migraine or vascular headache following sports concussion/trauma remains unknown. Based on primary headache disorder treatment of migraine, prophylactic migraine medications include NSAIDs, beta-blockers, calcium channel blockers, TCA’s and AEDs (i.e. topiramate, valproic acid, gabapentin) as more traditional treatments; however, these interventions, as with others, have not been formally and prospectively studied in SCH. Naturopathic agents such as butterbar and feverfew, as well as therapies such as B complex vitamins and magnesium supplementation, in addition to complementary treatments, may also augment treatment response [82, 83] based on primary headache migraine literature. Abortive medications may include ergot derivatives, dihydroergotamine derivatives, triptans, parenteral atypical antipsychotics and/or opiates or combination medications (i.e. NSAID with triptan), among other drugs, but only a smattering of information is available on their use (triptans specifically) for sports concussion migraine [84]. Triptans, as a class, may be ineffective if their use is delayed and allodynia develops. Botulinum toxin may be used for treatment of chronic migraine headache; although, there is no current approved indication for its use in SCH/PTHA related migraine headache. Botulinum toxin may exert a therapeutic effect for this type of headache not only through muscle relaxation but also through inhibiting release of sensitizing neurotransmitters such as glutamate and substance P [85]. If patients experience chronic daily headache and use abortive analgesics, they are at risk for developing rebound or medication over-use headache (MOH) (see below). Caffeine over-use may also contribute to patients becoming refractory to abortive migraine medications containing this substance.

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Post-traumatic tension headache Tension-type headache (TTHA) is one of the most common primary headache disorders and, like many other headache conditions, can be considered a spectrum disorder. Per ICDHIII diagnostic categories for TTHA include: infrequent episodic TTHA, frequent episodic TTHA, chronic TTHA and probable TTHA. Advances in basic pain and clinical research have improved the understanding of the pathophysiologic mechanisms of tension-type headache. Increased excitability of the central nervous system generated by repetitive and sustained pericranial myofascial input may be responsible for the transformation of episodic tension-type headache into the chronic form. Both muscular and psychogenic factors are believed to be associated with tension-type headache [2]. How such stress might be involved in the pathogenesis of TTHA after TBI is unclear; however, it would certainly seem to be warranted to investigate the interactions of stress post-TBI, in its myriad dimensions, with disease pathogenesis and perpetuation including TTHA. The mechanisms by which trauma, either to the neck, cranium or cranial adnexal structures or the brain itself may trigger tension type headaches are poorly understood. TTHA may result from an interaction between changes in the descending control of second order trigeminal brain stem nociceptors and inter-related peripheral changes, such as myofascial mediated pain and/or pericranial muscles nociceptive afferent input. Stress and negative emotional states (mediated through limbic circuitry) have been theorized to trigger such headaches through central mechanisms. What role TBI itself has in triggering such headaches is unclear. With more frequent episodes of headache, central changes become increasingly more important. With greater duration, long-term sensitization of nociceptive neurons and decreased activity in the anti-nociceptive system gradually leads to chronic TTHA. Current consensus is that peripheral mechanisms are most likely involved in episodic TTHA and central mechanisms play a more important role in chronic TTHA. There is still debate as to whether the pain in TTHA originates from peripheral (e.g. myofascial) vs. central origins, with the latter also theorized to occur due to hyperexcitability of the trigeminal caudal nucleus and other structures involved with pain processing [86]. Recent studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of CTTH by sensitizing pain pathways. Patients with CTTH typically have increased muscle and skin pain sensitivity, demonstrated by decreased mechanical, thermal and electrical pain thresholds [86]. Abnormal CNS pain processing may be linked to hyperexcitability of central nociceptive neurons (both cortically and sub-cortically) and may underlie the pathophysiology of CTTH. Additionally, some have speculated that there may also be a dysfunction in pain inhibitory systems [87]. Treatment of TTHA should include pharmacotherapy, both acute and prophylactic, as well as non-pharmacologic approaches [87]. The mainstay of acute pharmacotherapy is NSAIDs, sometimes in conjunction with caffeine, sedatives and/or tranquilizers. Adequate doses of NSAIDs must be utilized prior to labelling a trial as a failure. There is no scientific evidence to support the use of traditional muscle


relaxants in TTHA. Prophylactic pharmacotherapy for TTHA is much more diversified, with various drug classes being utilized including tricyclic antidepressants, tizanidine, botulinum toxins and certain SNRIs such as venlafaxine [82]. Nitric oxide synthase inhibitors may also hold therapeutic promise but are not in clinical use at this time. Nonpharmacological treatments may include relaxation therapy, as well as EMG biofeedback, cognitive behavioural therapies including stress management, limited contact treatment, spinal manipulation [2, 88], physical therapy when apropos including postural retraining and muscle trigger point therapies [89], use of modalities such as heat and cold therapies and, lastly, oromandibular treatment in selected patients [2]. Uncommon sub-types of sports concussion headache Various dysautonomic headaches have been reported and, although rare, should be considered in the differential diagnostic work-up of a patient with SCH [90–92]. Clues to a dysautonomic source of headache pain include a unilateral episodic throbbing pain in association with hyperactive sympathetics involving the ipsilateral face during the attack (miosis, sweating) but between attacks, a mild Horner’s syndrome. Post-traumatic trigeminal autonomic headaches have also been reported. Post-traumatic cluster headache and paroxysmal hemicrania are relatively rare types of post-traumatic headache, although case reports have been published on both following trauma [93, 94]. It should be noted, however, that with less common headache variants there is always a question about the causal relationship of the injury to the headache and/or its persistence. The literature is scant in proving a causal link between trauma and these headache sub-types. Arterial dissections of the carotid, as well as the vertebral artery, may also be seen following sports-related trauma, although they are rare [95, 96]. Both can be associated with headache and neck pain. The challenge for the clinician conducting the earliest assessment is to recognize signs of arterial dissection in patients presenting with head and neck pain as early identification and treatment reduces the risk of stroke and death. When suspected, the evaluating clinician should immediately have the patient transferred for emergency evaluation by a neurosurgeon and/or interventional neuroradiologist. The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae, producing an intimal tear. After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischaemic event or suffer a stroke. Early presentation of cervical artery dissection can be very subtle and the inciting incident may be so benign that the patient may not even remember it. While affecting only 8% of patients, the triad of headache, ipsilateral oculosympathetic paresis (i.e. partial Horner’s syndrome) and contralateral stroke symptoms is very concerning for carotid artery dissection. Headache is present in up to 75% of patients. The headache of carotid artery dissection may be gradual in onset or thunderclap. The quality of the headache is neither sensitive nor specific for carotid


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artery dissection. Neither bruits nor pulsatile tinnitus is sensitive or specific for dissection. Patients with vertebral artery dissection present with unilateral headache with signs and symptoms consistent with lateral medulla ischaemia [97]. Although rare in this context, lateral medulla ischaemia, also known as Wallenberg’s syndrome, is characterized by dysmetria, ataxia, ipsilateral hemiplegia and contralateral loss of pain and temperature sensation [98]. Patients may complain of double vision, dizziness and vomiting. Most, but not all, patients with vertebral artery dissection have a headache. Headache is severe, unilateral and often posterior-occipital. Whereas patients with carotid artery dissection may present with a wide variety of types of headaches, the quality of the headache in vertebral artery dissection is much more consistently unilateral and severe. Almost half of patients have neck pain of gradual onset. Less commonly, patients will present with isolated neck pain and no headache. On exam, patients may have neck tenderness with palpation. When compared to carotid artery dissection, vertebral artery dissection is more likely to affect younger patients and is more common in women [96, 99].

Table II. SCH/PTHA headache historical points.

Medication over-use headache

including measures of behavioural and cognitive coping, measures of general health functioning, specific pain domain inventories and/or general psychological measures, in particular, the Minnesota Multiphasic Personality Inventory-2nd Edition (MMPI-2). There are also additional pain assessment measures with built-in response bias indicators. Clinicians should also be familiar with non-organic indicators on interview that may suggest the need for further assessment of functional contributors to the pain presentation, although these are likely less common overall in sports injuries, particularly at a professional level, than in cases involving post-traumatic headaches associated with secondary gain incentives (i.e. personal injury, worker’s compensation and/or disability claims) [20, 21]. Practitioners should also consider the use of headache diaries [102], as well as other tracking methodologies such as Migraine Disability Assessment (MIDAS) Questionnaire, headache Impact Test (HIT) and HIT-6, Chronic Pain Index (CPI), Headache Impact Questionnaire (HImQ) [103], among others to not only acquire history but to track it on an ongoing basis and positively impact treatment decisions. The Migraine Disability Assessment (MIDAS) questionnaire was developed to measure the functional effects headache have on daily function. Migraine sufferers answered five questions in three activity domains covering the previous 3-month period. They scored the number of lost days owing to headache in employment, household work and family and social activities. Sufferers also report the number of additional days with significant limitations to activity (defined as at least 50% reduced productivity) in the employment and household work domains. The total MIDAS score is obtained by summing the answers to the five questions as lost days due to headache. The score is categorized into four severity grades: Grade I ¼ 0–5 (defined as minimal or infrequent disability); Grade II ¼ 6–10 (mild or infrequent disability); Grade III ¼ 11–20 (moderate disability); Grade IV ¼ 21 and over (severe disability). Two other questions (A and B) are not

Treating clinicians should use medications to modulate SCH only when clinically indicated. There is a need for all prescribing clinicians to be aware of the risk of medication over-use headache (MOH) in athletes with SCH; although this issue has not been specifically addressed in prospective, controlled studies. MOH may be seen from over-use of a variety of analgesic and/or abortive headache agents including ergotamines, opiates, caffeine, triptans and/or barbiturates [100, 101]. Over-use of these medications may lead to development of chronic daily headache (CDH). Patients may become dependent on these symptomatic headache medications. Drug withdrawal normally results in worsening of the headache, particularly when medications are stopped suddenly as opposed to being slowly weaned with concurrent alternative headache management options prescribed. Headache medication over-use may also make headaches refractory to prophylactic headache medication [2].

Evaluation of PCH History Historical information regarding the mechanism of injury can help distinguish what types of headache pain generators might be expected. The physical forces involved in post-traumatic headache, in general, and SCH, more specifically, include impact and/or acceleration/deceleration (inertial) loading; the latter including ‘whiplash’ type injury to the neck. The more information gathered by the clinician regarding the headache history, the better able the clinician will be in determining the root cause(s) of the headache disorder [2]. The primary points to address in the context of taking a pain history are reviewed in Table II. There are also a number of well-validated and reliable pain assessment batteries that can be considered for use to supplement information derived during the interview,

Timing of headache onset. Pattern of progression of pain over time. Treatment history relative to pharmacologic and non-pharmacologic approaches that have either helped headache pain or made it worse. Frequency of pain. Severity of pain, typically rated using some type of pain scale (i.e. pain faces). ‘COLDER’ mnemonic—character of pain, onset, location, duration, exacerbation and relief. Trigger factors such as cognitive stress, physical activity, certain postures, among others. Associated symptoms such as nausea, emesis, aura, dizziness, blurred vision, photosensitivity and phonosensitivity. Functional consequences of pain (i.e. how this pain affects ability to perform work and non-work related activities). Determine if the patient had headache of any kind pre-dating the injury and, if so, whether it has been altered in any way post-injury. Review relevant medical records to increase understanding of potential pain generators based on the injury history including mechanics (if known). Check on family history of headache including genetic loading risk factors for migraine. Interview corroboratory sources, as persons with TBI may not have adequate insight into or memory regarding the accident, symptoms evolution and/or functional consequences of the headache disorder.


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scored, but were designed to provide the physician with clinically relevant information on headache frequency and pain intensity [103]. The HIT was first developed as a web-based test (at www.headachetest.com and www.amIhealthy.com). It is a dynamic questionnaire, with items derived from four validated headache questionnaires sampling all areas of headache impact (the Headache Disability Inventory [HDI], the HImQ, the MIDAS Questionnaire and the Migraine-Specific Quality of Life Questionnaire [MSQ]). Patients are questioned until clinical standards of score precision are met. Internet-HIT matches the questions asked to each patient’s severity level. In practice, five questions are sufficient to grade the majority of headache sufferers. Clinical standards of accuracy were met by 98% of migraine sufferers and 97%, 87% and 61% of people with severe, moderate and mild headaches, respectively, completing five or fewer questions [103]. HIT-6 is a paper-based, short-form questionnaire based on the Internet-HIT question pool, designed for people without access to the Internet. Six questions cover pain severity, loss of work and recreational activities, tiredness, mood alterations and cognition. Each question is scored on a 5-point scale, with the scores being added to produce the final score. HIT-6 scores are categorized into four grades, representing minimal, mild, moderate and severe headache impact. Studies have shown that HIT-6 is reliable and valid [103]. It should be noted, however, that studies assessing the test– re-test reliability of migraine outcome instruments in SCH are very limited [72]. Physical examination The physical examination of the athlete with headache following concussion or any magnitude TBI for that matter should take into consideration central and peripheral neurological, as well as musculoskeletal clinical exam findings [2, 12, 42]. It should be understood, however, that there are no studies determining the key or critical elements in the physical assessment of the patient with SCH or for that matter PTHA. The neurological evaluation should include an elemental neurological exam including full cranial nerve assessment (including cranial nerve 1 for olfactory function and, as relevant, oculovestibular testing), funduscopic exam (to rule out papilloedema), deep tendon reflexes including pathological reflexes, sensory exam including visual fields, motor exam and cerebellar assessment including measures of postural stability, assessment for meningismus and mental status evaluation [42]. Appropriate on-field cognitive screening should be performed in conjunction with follow-up cognitive testing off the field, as deemed clinically appropriate. Peripheral neurological examination should include the face, head and craniocervical junction, mainly focused on assessment for neuralgic and/or neuritic headache pain generators. The musculoskeletal evaluation should include inspection for body asymmetries (such as head tilt, shoulder droop, tilted pelvis, leg length discrepancy or asymmetric gait), postural assessment including head forward posture, rounded shoulders, stance, pelvic alignment, as well as assessment for


cervical and lumbar lordosis or lack thereof. Jaw range of motion and tracking, as well as spinal range of motion, particularly cervicothoracic, should be addressed in any patient with SCH. Auscultation for bruits should be done as appropriate over the carotids, closed eyes, temporal arteries and mastoids. The temporomandibular joint should also be auscultated, as indicated, for abnormal articular sounds. Palpatory exam should include the face, head (including TMJ and masticatory muscles), shoulder girdles and neck and must be done in a controlled, layer by layer fashion to truly localize pathology [2, 8, 104]. Other testing The clinical tests pertinent to assessment of the patient with SCH may also include cerebral and/or cervical imaging, electrophysiological testing, psychoemotional and pain adjustment/coping evaluation, as well as general functional assessment testing. Tests should only be ordered when it is anticipated that the results will have an impact on clarifying a diagnosis and/or treatment plan or facilitating prognostication. There are no specific guidelines for neurodiagnostic testing for SCH that have been established to date either by consensus expert opinion or evidence-based medicine. In patients with sports-related concussion and SCH of a more chronic nature (i.e. greater than 6 months), psychoemotional evaluation for depression, anxiety, PTSD and/or Axis II related traits/disorders become more critical to consider as with PTHA/chronic pain in general [20]. That being said, these affective conditions may occur much earlier after injury and should always be considered in the context of a thorough assessment of non-remitting SCH beyond the first few weeks post-trauma. Additionally, injured athletes with more chronic SCH should also be assessed for their pain coping and adjustment via appropriate psychological and pain evaluations. Athletes may tend to minimize complaints due to their desire to return to play, which may make both assessment and treatment more challenging. Often times, it is difficult to get insurance companies to approve evaluations; however, in chronic pain the incidence of affective disturbances is high and appropriate acknowledgement of these disorders and treatment can only facilitate pain modulation and functional improvement. When there are concerns regarding the veracity of pain reporting or general complaint validity, it is recommended to consider performing response bias testing and effort tests (ideally, both embedded and stand-alone), in addition to examining the evolution of signs and symptoms following the sports injury, the injury history and results of diagnostics and clinical exams, corroboratory reports from other players or family, among other factors that should be considered relevant to individual case analysis in the context of validity assessment [21].

Treatment caveats The treating clinician should establish realistic treatment endpoints for the patient with SCH and get appropriate ‘buy-in’ from both the patient (and guardian as relevant), as well as the family. Appropriate management of concussion requires immediate removal of the athlete from the game and



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appropriate and timely health professional evaluation. Consensus recommendations exist for a subsequent period of rest, both cognitive and physical, until the patient is asymptomatic with graduated return-to-normal activities including sports participation [30–33, 46]. More specifically to the issue of SCH, there should also be education regarding headache treatment options including risks vs. benefits. The simplest, least invasive, lowest risk and most cost-effective management approaches that allow for optimization of patient compliance and maximal functional restoration should be used whenever possible. When pharmacologic agents are used, analgesia should be delivered with minimal adverse effects and inconvenience to the patient, with clearly defined treatment expectations, including education regarding medication side-effects. ‘Shot gun’ pharmacological treatments such as use of opiate analgesics as first line medication for SCH are to be strongly discouraged. If an opiate is considered at any point in the treatment process it should be clear to the patient and/or guardian that not all pain is opiate sensitive; and that such treatment may lead to both physical and psychological dependency, as well as potential adverse physiological effects if used more chronically. Opiates may also compound other TBI-related impairments including cognitive difficulties. If opiates are used, they should be used judiciously and with appropriate screening (i.e. Opiate Risk Tool) and monitoring procedures (including use of opiate/controlled substance agreements and random urine screens) [82, 105]. Proper communication should be maintained between the patient, the caregiver and treating clinician regarding response to individual pain treatment interventions. The treating clinician should maintain ongoing communication with any other clinicians involved with the patient’s health management to adequately co-ordinate clinical care. Evidence-based guidelines and meta-analyses should be referred to as guides to the specific use of pharmacological and non-pharmacological interventions as available in either PTHA or the parallel primary headache disorders, since none currently exist for treatment of SCH. Attempts should also be made to minimize polypharmacy and use drugs that can be dosed 1–2-times per day (as opposed to more), as both measures will improve compliance, decrease drug–drug interactions, improve quality-of-life and likely result in lower expense. Additionally, whenever possible, use of medications whose mechanism of action may impede neural plasticity (e.g. opiates, barbiturates, certain anticonvulsants) should be minimized or avoided [82]. Exercise is an under-prescribed treatment intervention in pain management including headache. Beneficial effects can include pain modulation on both a central and peripheral basis, weight control, positive affective modulation, benefits to brain function, improvement of general sense of well-being and improved general state of health [2, 20, 106–108]. The use of complementary medicine interventions in headache has become more accepted over the last two decades; however, for most of these interventions efficacy data is sorely lacking. Appropriate prescription of adaptive equipment, as well as an ergonomically modified school, home and/or work environments, may also add to overall management of SCH to facilitate greater pain modulation and tolerance.

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A variety of psychological methods may be appropriate to consider in the context of SCH pain management, either in conjunction with other interventions or as the sole intervention; however, these treatments have not been specifically evaluated in persons with SCH. Psychological interventions are underutilized treatment options for patients with chronic SCH. Behavioural treatment interventions for pain in persons with TBI should focus on coping with pain, modulation of affective responses to chronic pain and associated disability, as well as primary pain modulation [20, 109]. Behavioural interventional techniques including biofeedback, relaxation training, operant treatments, cognitive behavioural interventions, social and assertiveness skills training, imagery and hypnosis and habit reversal should also be considered [20, 110]. Ultimately, SCH (and PTHA for that matter) should not be either evaluated or treated in isolation or with a ‘blinders on’ approach [2, 25, 111]. It is a multidimensional phenomenon with biological, psychological and social contributors, among others that have yet to be fully identified.

Directions for future research Research on the topic of post-traumatic headache including sports concussion headache must use a common nomenclature and definitional criteria. One needs to elucidate mechanisms for PTHA and SCH and differentiate them from primary headache disorders, if in fact the mechanisms are unique. There needs to be an increased understanding regarding factors that increase risk for SCH and persistent SCH (i.e. greater than 6 months pain duration), as well as efforts made to find ways to modulate said risk factors to minimize medical and functional morbidity. There also needs to be development of an evidence-based medicine approach to classification that incorporates proper nomenclature use, injury and headache history, as well as headache features (based on both subjective patient report and physical exam findings), with appropriate integration of response bias and pain validity reporting checks, into a rational paradigm. One needs to develop standardized assessment protocols for each of the identified SCH sub-types. Randomized, controlled trials examining the natural history, evaluation, treatment and prognosis of SCH sub-types are crucial to moving the science forward in this area of brain injury medicine.

Acknowledgements A very special thanks to Emily Joyner, LPN, CMOM for her assistance in manuscript preparation and patience with my editing and revisions.

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

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Update on sports concussion.

Concussion Ethics and Sports Medicine.

Return to Sports After Concussion.

Appendix B: Sports concussion toolkit.

Sports concussion diagnosis and management.

Sports concussion management: part I.

Neuroimaging findings in pediatric sports-related concussion.

Brain injury special edition on sports concussion.

Causes and consequences of sports concussion.

Neurometabolic aspects of sports-related concussion.

Tackling the sports-related concussion crisis.

Neuroimaging evaluation of sports-related concussion.

Pediatricians' knowledge of current sports concussion legislation and guidelines and comfort with sports concussion management: a cross-sectional study.

Pediatric sports specific return to play guidelines following concussion.

The sports concussion picture: fewer 'pixels', more HD.

The history of neurosurgical treatment of sports concussion.

The Legal Landscape of Concussion: Implications for Sports Medicine Providers.

Investigating a Novel Measure of Brain Networking Following Sports Concussion.

A model of prevention of sports concussion in adults.

Epidemiology of sports-related concussion in seven US high school and collegiate sports.

Subject-specific increases in serum S-100B distinguish sports-related concussion from sports-related exertion.

Administration and environment considerations in computer-based sports-concussion assessment.

Vestibulo-ocular dysfunction in pediatric sports-related concussion.

Acute sports-related traumatic brain injury and repetitive concussion.