CHAPTER 6 Postconcussive Headache

NATHAN D. ZASLER, MD, FAAPM&R, FAADEP, DAAPM, CBIST • SARA ETHEREDGE, PT, DPT, CKTP, CCI, CMTPT

INTRODUCTION developing so-called “chronic” PCH remain debated Polytrauma, including traumatic brain injury, has been in part due to variable study methodology. Some liter- associated with significant pain sequelae.1 Postconcus- ature suggests that preinjury migraine is associated sive headache (PCH) has historically been viewed as a with protracted recovery from sports-related CBI, singular headache disorder with some quoting an inci- greater levels of postconcussive symptom complaints, dence of headache occurring in nearly 90% of concus- as well as more impairment on subacute neuropsycho- sive brain injuries (CBIs) with a fairly alarming rate of logical testing (particularly in females), although con- 6,7 chronicity. Whether PCH chronicity is a reflection of troversy remains. The bulk of the literature does our lack of understanding of the condition and/or a note a positive association between acute headache 6,7 consequence of suboptimal diagnoses remains to be symptom burden and protracted recovery from CBI. elucidated. The idea that PCH is a singular headache The effect genetic loading risk factors, preexisting disorder is now known to be an oversimplification of neck pain, and/or headache associated with whiplash a much more complex and variable pathoetiology that injury, impact preparedness, dizziness, sex, anatomic is often mixed with diverse biopsychosocial factors variables between males and females, cultural norms/ that may influence symptom presentation, pain adapta- perspectives, affective disorders, and characterological tion versus promulgation, and prognosis. Other factors traits have on influencing PCH incidence/reporting, such as base rate misattribution (e.g., migraine inci- severity, and duration are still debated. There is some dence in the military), sociocultural issues, nocebo ef- literature, however, that suggests that such factors may fects, and/or compensation/litigation must also be impact outcome. PCH can adversely impact neuropsy- e considered.2 4 Increased understanding regarding the chological testing performance, alter sleep quality and array of post-traumatic headache (PTHA) pain genera- behavior (e.g., irritability and decreased frustration tors following CBI has further emphasized the tolerance), as well as lead to secondary symptoms of complexity of PCH and the interrelationships of depression and anxiety and has also been associated 3,4 vascular, autonomic, peripheral nerve, muscular, with poorer outcomes from CBI. osseous/joint, and other contributors to such Terminology remains in limbo and there is no inter- e headaches.3 5 national consensus on how best to “label” PCHs; how- Risk factors for development of specific headache ever, consideration should be given to avoiding phenotypes may differ in different types of CBI mecha- nonhelpful generic labels such as PCH or PTHA and nisms, including assaults, vehicular, sports, whiplash, not providing further diagnostic information. Instead, and blast injury, but no methodologically sound data practitioners need to stipulate the presumed pain gener- are available yet to answer this question. Theoretically, ators (e.g., cervicogenic, migraine, tension, neuralgic, each of the aforementioned mechanisms of injury etc.), which may at times be mixed in order to 8 may put a patient at greater risk for certain types of adequately direct treatment decisions. Use of such gen- post-traumatic head pain generators than others. Addi- eral terms may also cause practitioners and others to tionally, the acute, subacute, and chronic variants of misattribute the headache disorder to traumatic brain PCH have not been studied in a manner to determine injury when, in fact, its cause may be extracerebral as differences in incidence, prevalence, etiology, diag- in the case of impact injury, post-traumatic neuralgic nostic accuracy, treatment efficacy and prognosis. Simi- or neuritic pain, referred myofascial and cervicogenic larly, risk factors for PCH and vulnerabilities for headache, among other possibilities. The phrase

Concussion. https://doi.org/10.1016/B978-0-323-65384-8.00006-7 Copyright © 2020 Elsevier Inc. All rights reserved. 59 60 Concussion

“chronic PCH” should also be avoided since a chro- any type of diagnostic testing.8 Based on symptom nicity label may only have been given due to an incor- profiling, ICHD-3 has the potential to incorrectly cate- rect diagnosis and/or treatment, which results in gorize secondary headache disorders due to trauma, persistence of the underlying pain disorder. Such labels including overdiagnosis of migraine.3,4 As noted by can only serve to negatively bias evaluating clinician Dwyer and others, no specific headache features or perspectives. It is therefore preferential to document treatment approaches accompany the definition, which the headache onset date and duration of symptoms as likely limits its usefulness in both research and clinical well as the specific presumed pain generators. practice.11 Whether classification systems, such as IHS ICHD-39 or ICD-10,12 are truly relevant to PCH and PTHA, more generally, remains to be seen. In the CLASSIFICATION CHALLENGES context of secondary headache disorders, such classifi- Use of the current IHS (International Headache Society) cation systems may have limited value and the potential International Classification of Headache Disorders to incorrectly or inadequately classify these headache (ICHD-3 and 3B) systems has its limitations with subtypes, which in turn may lead to inappropriate treat- regard to how PCHs and PTHAs in general are classified. ment being rendered and as a consequence a subopti- There is a lack of differentiation of the various causes of mal outcome. As a consequence of these concerns, PCH/PTHA and all PTHAs are categorized under section some have advocated for a more multifaceted classifica- 5 of ICHD-3 and are divided into three broad categories tion system taking into consideration the nature of the relative to headache being due to trauma to the head, brain injury and symptom-based profiles.13 neck, or secondary to craniotomy. The specific cate- gories include acute as well as persistent headache attributed to traumatic injury to the head, acute as LIMITATIONS OF EXISTING LITERATURE well as persistent headache attributed to whiplash, Historical studies assessing incidence of headache and acute as well as persistent headache attributed to subtypes post-TBI have relied on neurological head- craniotomy. Acute PTHA is defined as headache that re- ache classification systems such as ICHD and ICD solves within 3 months from the date of injury, whereas withlittleornoregardtotheoverlapofsymptoms persistent PTHA refers to headache lasting greater than of PCH with PCD (i.e. autonomic symptoms like 3 months (although this is somewhat distinct from photosensitivity and sonosensitivity), physical exam typical “chronic pain” definitions that use a timeframe correlates of underlying pain generators, and/or head- of greater than 6 months before chronicity is estab- ache pain symptom validity measures. Additionally, lished). There is additional division of the classification the role, if any, of secondary gain incentives including system based on the severity of TBI, which is dualistic litigation, worker’s compensation, and social security and divides TBI into two broad categories of mild TBI disability in headache reporting and prognosis re- and moderate/severe TBI. Onset of headache must be mains to be edified. What contribution comorbid af- within 7 days of injury (although to our knowledge fective issues including depression, anxiety, and this is empirical and not evidence-based), regaining PTSD have on headache presentation and persistence consciousness or discontinuation of medications that are also unknown. Lastly, the diagnosis of concussion might impair the ability to sense or report headache may be associated with nocebo effects and negative following the injury in question.9 The 7-day onset crite- expectancy biases as related to headache reporting rion has been shown to underestimate incidence of this and prognosis that we currently have no good disorder; specifically, PCH may have its onset after methods of assessing. 1 week post injury.10 The terminology used in ICHD The literature is highly variable in study methodolo- is confusing as brain injury and head injury appear to gies, criteria for “concussion” diagnosis, and delinea- be used interchangeably and should not be since the tion of involvement of potential secondary gain two phenomena can occur separately or conjointly. incentives that may serve to perpetuate headache com- There is no mention of the myriad other causes of plaints. For example, the study by Lane et al. found a PTHA such as migraine, tension-type headache headache persistence rate at 24 months of 70% with (TTHA), neuralgic/neuritic headache, among numerous 90% of patients meeting criteria for migraine or prob- other conditions that are categorized elsewhere but may able migraine.14 Stacey, Lucas, and Dikmen et al. present following trauma.11 Another problem with use assessed PTHA (very few with mTBI) natural history of ICHD is the fact that it is only symptom based and over 5 years and used ICHD-2 criteria and found a does not consider physical examination findings or high rate of frequent headache at 60 months (36%) CHAPTER 6 Postconcussive Headache 61 with migraine accounting for just under 60% of head- including sinuses, eye sockets, etc. The skin, nerves, ache subtypes and with close to 30% of headaches be- muscles, and periosteum of the cranium are all pain ing “unclassifiable”.15 Yet, other studies show sensitive. Cervical/cranial joint capsules (including the significantly lower rates of headache complaint persis- temporomandibular joint), cervical facets/zygapophy- tence and much lower rates for migraine-type seal joints, peripheral nerves (supraorbital, trochlear, e headaches.16 18 These disparities reinforce the calls greater occipital, lesser occipital, as well as third occipi- for further research on PCH using randomized tal nerves), and the cervical sympathetic plexus may all controlled study protocols and broadening the scope be pain generators that produce local or referred head of the assessments. pain.20,21 It should also be noted that cervical whiplash injury Given CBI injury mechanisms, it is possible to incur has been found to be associated with various auto- various types of trauma to the aforementioned struc- nomic comorbidities that may mimic postconcussive tures including but not limited to impact injuries symptomatology, which can further complicate head- (both long and short impulse), stretch injuries of ache classification. Given the complexities of these in- various tissues (both rotational and linear), penetrating juries, it would be naïve to assume that headache injuries, shearing/tearing injuries, and compression, as classification is as simple as finding one thing that is well as herniation-related forces. One of the most com- causing the headache. In most cases, there are multiple mon, yet often overlooked, sources of head pain pain generators and/or perpetuators that require holis- following CBI is referred cervical pain, which is typically tic assessment and treatment. The neck should be associated with acceleration-deceleration insults or considered a primary target for examination in the whiplash-associated disorders. Postwhiplash sequelae context of PCH assessment and yet, has historically may include referred myofascial pain emanating from received little recognition or attention. any of the four layers of the posterior cervical, as well Another significant area of concern is the nomencla- as anterolateral cervical musculature; traumatic neural- ture inconsistencies across studies as related to use of gias (as noted above), vertebral osseous somatic brain, head, and neck injury labels and criteria for the dysfunction, disc herniation and/or rupture, ligamen- same. There is often inadequate information regarding tous injury and/or facet joint trauma (with potential whether subjects truly met criteria to be diagnosed for osteoarthropathy and/or traumatic injury to the with concussion, as well as a lack of documentation medial branches of the dorsal ramus). Risk factors for on comorbid injuries to the cranium, cranial adnexal persistent postwhiplash symptoms including headache structures, and/or neck. Another common oversight is should be identified and addressed as apropos.22 These the focus on CBI as the most likely explanation for injuries can be seen in the absence of CBI or as a comor- the PCH. Headache onset after concussion does not bid feature and should always be considered in the mean that the concussion itself was necessarily the context of identifying the specific pain generators cause of the headache. Clinicians should understand contributing to the PCH even in the absence of subjec- that aside from concussion, cranial impact injuries, cra- tive complaints of cervicalgia. nial adnexal trauma, e.g., TMJ, and cervical acceleration The neurobiology of PCH following a single trau- deceleration (whiplash) injuries, among other condi- matic insult may involve cerebral/intracranial, cranial tions often cause PCH and/or contribute to it. There is as well as cranial adnexal, and cervical structures also likely a reporting bias relative to preexisting head- involved with encoding and processing of craniocervi- ache disorders as well as genetic loading risk factors, cal noxious stimuli. Pain receptors may be activated by both of which likely get underreported either due to tissue injury and neuroinflammation and mediated by recall bias or lack of knowledge.19 Lastly, there has bradykinin, serotonin, substance P, histamine, leuko- been inadequate study of the potential role that pre- trienes, cytokines, and prostaglandins.23,24 Addition- scription drugeinduced headaches, and more impor- ally, it seems clear that there are likely both tantly, medication overuse headaches (MOHs) play in peripheral and central mediators of PCH. Acutely, it the PCH population. is more likely that peripheral mechanisms account for pain mediation rather than central or supraspinal causes. Cranial mechanical hyperalgesia likely related PCH PATHOETIOLOGY to peripheral structure injury to blood vessels, nerve fi- Anatomic sources of head pain that may be relevant in bers, and osseous structures, as well as the inflamma- the assessment of a patient presenting with PCH tory cascade, likely serve as sources of peripheral include the dura, venous sinuses, and cranial cavities, pain sensitization and PCH. The aforementioned 62 Concussion would suggest that earlier more aggressive treatments generators and/or mechanisms are involved in both during the acute phase could prevent secondary chron- the origin of PCH and its promulgation. ification through central sensitization mechanisms. Some have speculated that central mechanisms are involved in persistent allodynia related to somatosen- PCH CLINICAL PRESENTATIONSdAN sory cortex injury. Mechanisms of central sensitization OVERVIEW are still being explored; however, it appears that Headache and neck pain are the most common physical abnormal neuronal excitability may lead to altered complaints following CBI and are experienced early af- processing of sensory stimuli causing cortical ter injury in a very large percentage of patients and, in a spreading depression and trigeminal activation. There smaller percentage, longer term (however, the latter are numerous pathways in the neuromatrix that literature is not as strong methodologically). The major when damaged may lead to centrally mediated pain. types of headaches seen following trauma include Central sensitization contributes to both acute allody- musculoskeletal headache (including direct cranial nia and headache persistence. Sensitization, whether trauma, cervicogenic headache, and TMJ disorders), peripheral and/or central, is not just relevant to post- neuromatous and neuralgic (nerve) headache, TTHA, traumatic migraine but may be seen in cervical whip- migraine, as well as less common causes such as lash injury, traumatic temporomandibular disorder, dysautonomic headaches, seizures, facial and/or skull among other conditions. Repetitive concussions may fractures, cluster headaches, paroxysmal hemicrania, promote trigeminal sensitivity and microglial prolifer- post-traumatic sinus infections, drug induced head- ation, astrocytosis and neuropeptide release in the tri- aches, MOHs, and the surgical conditions previously geminovascular system further exacerbating the mentioned. There remain controversies regarding the underlying headache disorder.25 occurrence and causal relationship of trigeminal auto- Nitric oxide synthase and calcitonin geneerelated nomic cephalgias such as cluster and paroxysmal hemi- peptide have been implicated as at least potentially cranias with concussion. The overlap in headache contributory to mediating allodynia in migraineurs subtypes as related to cervicogenic, referred myofascial, following concussion, which has been linked with tri- migraine, and tension headache cannot be overempha- geminal neuroplastic changes.26 Others have speculated sized in the context of both assessment and treatment that the pathophysiology of PTHA is shared with the implications.28 pathophysiology of brain injury itself relative to inflam- The majority of headaches following CBI are most matory responses. These inflammatory responses could likely benign and do not typically require surgical treat- persist beyond timeframes for actual beneficial physio- ment; although, there are, on occasion, complications logical effect leading to secondary injuries due to alter- that occur after both CBI and more severe injury that ations in neuronal excitability, axonal integrity, central may cause headache and require surgical intervention. processing, as well as other changes.27 Subdural and epidural hematomas, carotid cavernous A key anatomic entity that must be appreciated in fistulas, traumatic carotid or vertebral artery dissection, the pathobiology of PCH is the convergence of upper cavernous sinus thrombosis, as well as post-traumatic cervical and trigeminal nociceptors through the trigem- intracranial pressure (ICP) abnormalities (high vs. low inal nucleus caudalis (TNC). Nociceptive input from a ICP), among other conditions can all be responsible variety of sources in the neck can activate the TNC via for headaches and bring with them a potential need occipital and cervical afferents (whether from muscles for surgical intervention. Readers are referred to more or joints). This phenomenon may account for improve- comprehensive sources for details on the aforemen- ments seen in postconcussive migraine and tension tioned less common etiologies of PTHA.3 headache when cervical nociceptive afferent inputs, if PCH is best evaluated with time taken to acquire an present, are appropriately identified and treated, lead- adequate preinjury, injury, and postinjury history and ing to decreased or negated nociceptive afferent input in that context, a detailed history of the presenting into the TNC. Such treatment can also help modulate headache symptoms. Equally important, but often peripherally sensitized trigeminal branches such as the ignored, a headache physical examination (including supraorbital nerves.4 relevant neurological and musculoskeletal elements) Lastly, the disparate findings on the correlation be- should be performed. As clinically indicated, other diag- tween injury severity parameters and type, frequency, nostic testing, including imaging, psychoemotional, severity, and duration of PTHA seemingly begs the and/or pain assessments, among other examinations, question of whether other non-CBI-related pain may be necessary/helpful. One of the most frequent CHAPTER 6 Postconcussive Headache 63 areas of concern is whether the patient with suspected physical therapy, and/or psychological management. CBI requires brain/head imaging. In general, such imag- The clinician should get as much information as ing is not necessary except in cases where there are wors- possible about injury mechanisms to understand risk ening headaches, medically unresponsive headaches, factors for particular PCH pain generators such as might and/or protracted headaches after injury. The main be associated with brain injury itself, cranial impact in- physical findings that justify considering neuroimaging juries, and/or cervical whiplash. Lastly, clarification of in head trauma as well as CBI include eye swelling or the functional consequences of PCH is important and pupil abnormalities, diplopia or vision loss, and/or may include limitations in physical activity, including focal neurological findings.29 exercise and sexual activity, work or school pursuits, Late-onset headaches (i.e., greater than 2 months sleep quality, and mood alterations, among other fac- post trauma) should cue the treating clinician to think tors to explore. Use of headache questionnaires to of less common injury-related conditions such as a assess disability from same such as MIDAS or HIT-7, slowly expanding extra-axial collection as a cause for headache diaries, and tracking tools/applications for the headache disorder or just as likely, a noninjury- smartphones (e.g., Curelator, Headache Diary Lite related cause such as a space-occupying lesion (e.g., Pro, iHeadache, Migraine Buddy, MigrainePal and My brain tumor, colloid cyst, subsequent injury), among Migraine Triggers), although none have been validated other conditions3; although, late-onset headaches for PCH, may further complement the information apportionable to the initial injury can happen even garnered during history taking.4 Given the existing liter- years post insult. ature on the accuracy, or limits thereof, of histories pro- vided by people with brain injury, it is important to interview corroboratory sources as well due to potential THE PCH HISTORY limitations in patient insight and memory. The examination should start with taking a thorough history from the patient as related to their PCH complaint. One of the most important pieces of infor- THE PCH PHYSICAL EXAMINATION mation to acquire in this context is to determine if the The hands-on physical examination, which is often patient had any type of headache complaints preemp- ignored in PTHA assessment, should take into consider- tory to the injury in question and if so, whether the ation central and peripheral neurological clinical find- headache presentation has changed. In that context, it ings, as well as musculoskeletal clinical findings. The is also important to determine if there are genetic neurological evaluation should entail an elemental loading risk variables for headache such a migraine in neurological examination of all 12 cranial nerves, fun- the patient’s family.30 Important information to garner duscopic examination (to rule out papilledema), deep in the context of the history taking is the timing of head- tendon reflexes including pathological reflex testing, ache onset relative to the traumatic event. Clarifying the sensory examination including visual field confronta- frequency and severity of pain is also of paramount tional testing, motor examination and cerebellar assess- importance and ideally should include use of standard- ment (which should also encompass measures of ized pain rating scales and/or headache questionnaires. postural stability), assessment for meningismus, and A nice mnemonic to assist in taking a headache history mental status evaluation. Appropriate cognitive is “COLDER”.character of pain, onset, location, dura- screening should be performed as clinically indicated. tion, exacerbation, and relief. Understanding how the The peripheral neurological examination should headache has evolved post injury is also important as include assessment for neuralgic and/or neuritic head- is acquisition of a treatment history relative to what spe- ache pain generators such as supraorbital neuralgia, cific treatments were prescribed and what the patient’s temporoauricular neuralgia, and occipital neuralgia. response was to the same. As it relates to prior drug The musculoskeletal examination should include pal- treatment, it is important to note that the clinician patory assessment of the face, temporomandibular should edify both the dose of the medicine as well as joints, head and craniocervical junction, cervicothoracic the duration that the medicine was given to assure spine, and upper thorax at a minimum to assess for that an adequate trial was provided. As far as nonphar- pathologic findings. macological treatments are concerned, the clinician The musculoskeletal evaluation of the patient with should establish that there were adequate interventions PCH should be holistic in nature as the entire body utilized to address the underlying pain generators as should be screened, not just the cervical spine. Sitting might be the case with osteopathic, chiropractic, and standing postures should be noted, preferably 64 Concussion without the patient’s awareness, so that the clinician can sternocleidomastoid, and/or upper trapezius muscles obtain a realistic view of postural habits. Details such as as common sources of referred pain into the head in forward head, increased kyphosis in the thoracic spine, such patients. and increased or flattening of the lordotic curvature in Neuralgic and neuritic pain generators associated the lumbar and cervical spines are important to note with surgical trauma, direct scalp contusional injury, as well as scapular positioning. A closer inspection for and craniocervical acceleration/deceleration forces are body asymmetries (e.g., head tilt, shoulder droop, often overlooked. Clinicians should understand the rotated or tilted pelvis, and leg length discrepancy) are anatomy of the peripheral nerves innervating the face also important to note as these asymmetries may be and scalp including but not limited to the occipital contributing to ongoing cervical dysfunction and pain nerves as well as their ability to be treated through inter- complaints. Jaw range of motion and tracking is an ventional pain management techniques. The intercon- often overlooked but important assessment as TMJ is- nectivity of upper cervical roots and brainstem sues commonly refer pain into the head and have trigeminal centers through the trigeminocervical com- been associated with both facial trauma and cervical plex is critical to keep in mind as previously noted whiplash injuries.3,4 The temporomandibular joints and to understand in the context of PCH assessment should also be auscultated, as clinically indicated, for when there is comorbid cervical whiplash injury.33 abnormal articular sounds. Migraine and tension headache have also been Cervical spine range of motion can provide valuable shown to not uncommonly be associated with insights into dysfunction (e.g., limited right rotation abnormal musculoskeletal examinations of the head and side-bending can indicate a right cervical facet andneck.Giventhisfact,cliniciansshouldalways dysfunction and rotation less than 45 can indicate assess these structures even if the diagnosis of PCH dysfunction at C2).31 Auscultation for bruits should falls in the migraine tension spectrum.34 It is also be done as appropriate over the carotids, closed eyes, important to note that patients may have had neck in- temporal arteries, and mastoids for assessment of arte- juries and be unaware of that fact and even deny pain riovenous fistulas. Palpatory examination should complaints referable to the same but still have patho- include the face, head (including TMJ and masticatory logical findings on neck examination. In patients with muscles), shoulder girdles, and neck musculature. This new-onset headache, examiners must also ascertain must be done in a controlled, layer-by-layer fashion to that they are not tender over the temporal arteries or truly localize pathology with an eye to identifying acti- demonstrating signs of nuchal rigidity, the latter which vated trigger points and referred pain patterns. Com- may be associated with a pathologic meningeal mon special tests that should be included in the process such as meningitis. musculoskeletal examination are the cervical flexion rotation test, to assess for C2 dysfunction; Spurling’s test, to assess for cervical facet dysfunction; alar liga- PCH TREATMENT PRINCIPLESdAN ment stress test, anterior shear test, Sharp Purser test, OVERVIEW and the tectorial membrane test to assess for upper cer- Treatment should be instituted in a holistic fashion as vical instability. When assessing facets, the examination early as possible with the goals of maximizing the focus should be on the first three cervical levels as these benefit/risk ratio of any particular intervention, pre- levels can directly refer pain into the head through noci- scribing treatment that can be optimally complied ceptive inputs into the trigeminocervical nucleus; with and educating the patient and family regarding although there remains some debate about whether the condition, its treatment, and prognosis in a coordi- referral of pain can occur below the C3 level. A system- nated attempt to minimize risk for longer term PCH atic review of physical examination tests for screening complaints and disability as well as improve quality for cervicogenic headache found that the cervical of life and pain adaptation.35 Ideally, treatment should flexion-rotation test exhibited the highest reliability be interdisciplinary and multipronged as clinically war- and strongest diagnostic accuracy.32 Referred cervical ranted with the most essential team members being the myofascial pain as a consequence of cervical whiplash physician, physical therapist, and psychologist. is a particularly common cause of PCH. This fact should The pharmacological management of PCH is replete emphasize the importance of a good musculoskeletal with challenges due to the lack of an adequate body of examination in any patient presenting with PCH evidence-based medicine examining the efficacy of including, of course, the neck. One can often find acti- pharmacotherapeutic agents in this population.36 The vated trigger points in the suboccipital musculature, general practice trend is to approach these headache CHAPTER 6 Postconcussive Headache 65 disorders as they would be treated in primary headache Once central sensitization is suspected to have taken disorders.37 There are no FDA-approved drug treat- place, the prognosis becomes more guarded for com- ments specific to pediatric or adult PCH or for that mat- plete pain resolution; however, clinicians must be ter PTHA more generally. General rules of familiar with methodologies for modulating this type pharmacological prescription in persons after concus- of complication in the context of PCH. A multipronged sion are to start low, go slow, minimize polypharmacy, approach has been shown to have the best results by choose agents that will likely be effective given the spe- focusing on specific targets for desensitization including cific condition being treated (as such may be available), both bottom-up and top-down strategies such as oral reassess need for medication over time, monitor use/ medications, topical analgesic therapies, as well as abuse as clinically indicated, and attempt to choose metabolic and neurotrophic factors all with the goal medications that can be taken once to twice a day at of decreasing hyperexcitability in the central nervous most to optimize compliance.38 system.45 Treatment approaches should emphasize conserva- tive measures first as possible as interventional treat- ments lack methodologically sound evidence.39 Such PCH: COMMON PRESENTATIONS AND interventions may include physical modalities, lifestyle RECOMMENDED TREATMENT changes, postural education, and behavioral therapy APPROACHES among other treatments.40 Knowledge regarding psy- The following will summarize the clinical presentation chological assessment and behavioral therapies in these and treatment of the most common PCH variants. types of pain patients is essential to holistic manage- Please see Table 6.1 for an overview of headache sub- ment as is clinical acumen on methods to ascertain types, typical symptom presentation, examination find- pain reporting response biases and pain ings, and treatment options. e catastrophizing.41 43 Interventional procedures such as facet, peripheral nerve, as well as sphenopalatine gan- Migraine glion blocks should be considered as clinically appro- Clinical presentation priate.44 With the advent of a number of different As per ICHD-3, migraine is defined based on clinical his- types of neuromodulation treatments, clinicians have tory. The patient must have at least five headache attacks more treatment choices particularly for post-traumatic that lasted for a duration of 4e72 h, with the headache migraine and certain neuralgias although these inter- having at least two of the following characteristics: uni- ventions have yet to be studied in this patient group. lateral (nonside alternating), location, pulsatile quality, Pain medications that are not specific for the partic- pain intensity that is moderate or severe, and pain aggra- ular headache subtype should usually be avoided, vated by activity or pain that limits activity.9 It should be particularly such agents as opiates and barbiturates, noted, however, that more than 50% of people who suf- which may cause a variety of long-term adverse effects fer from migraines report nonthrobbing pain at some including, but not limited to, MOH, adverse endocrine time during the attack. During the headache there must effects, drug tolerance over time, impairment issues that be at least one of the following reported: nausea or may affect safety for driving and/or equipment use, and emesis, and/or photophobia/phonophobia (also addiction, among other risks.4,37 There is seldom an referred to his photosensitivity and sonosensitivity). indication for prescribing opiates in this group of pa- There must not be any other explanation for the head- tients, particularly for longer term use. Additionally, ache to classify it as migraine. Of note, migraine attacks not all pain is opiate responsive, and clinicians should commonly occur during waking hours but less therefore use caution when prescribing such agents. Pa- commonly may awaken a person from sleep. tients should only be placed on chronic opioid treat- ment if they demonstrate true failure to respond to a Treatment variety of other pharmacotherapeutic agents with less There are three basic approaches to pharmacotherapeu- potential short- and long-term risks, have opiate tic management of post-traumatic migraine. These responsive pain, and are not candidates for neuromo- include prophylaxis, abortive therapy, and symptom- dulation, interventional pain management procedures, atic therapy. Successful treatment of migraines may be and/or surgery. Pediatric patients, those with significant paradoxically achieved by reducing medication use. In Axis II issues, or those with a history of chronic sub- medication overuse, headache worsening typically oc- stance abuse should generally not be considered candi- curs because of the overuse of abortive pain dates for opioid therapy. medications. TABLE 6.1 66 Postconcussive Headache Subtypes, Symptoms, Examination, and Treatment.

Headache Pain Generator Presenting Symptoms Physical Examination Caveats Treatment Recommendations Concussion Migraine Unilateral location, pulsatile/ Potential for associated Consideration of prescription pharmacotherapeutic throbbing pain character, pain musculoskeletal examination interventions involving symptomatic, abortive, and/ intensity that is moderate to severe abnormalities of the head and neck or prophylactic medications including medications and aggravated by activity. which may compound and/or such as botulinum toxin. Can also consider use of Classically associated with nausea perpetuate trigeminovascular naturopathic agents and over-the-counter or emesis and or photo- and/or instability. medications including agents with caffeine. phonosensitivity. Typically occurs Interventional procedures including sphenopalatine during waking hours. ganglion blocks, occipital nerve blocks, and neuromodulation should all be considered as clinically appropriate/lifestyle changes and behavioral interventions including cognitive behavioral therapy (CBT) with stress management training, biofeedback, and relaxation training among other interventions should also be utilized as apropos. Physical therapy referral may be appropriate to treat concurrent abnormal musculoskeletal findings. Tension-type Pain is usually bilateral and Potential for associated Consideration of prescription pharmacotherapeutic headache (TTHA) occipitofrontal in location with a musculoskeletal examination interventions for abortive as well as prophylactic “tight band” feeling that may have a abnormalities of the head and neck. therapy. Avoid use of muscle relaxants. Consider throbbing quality and is usually nonpharmacologic treatments including CBT, gradual in onset with duration being biofeedback, relaxation therapy, massage, stress highly variable with a more constant inoculation treatment, and exercise among other quality but generally with mild to interventions. Physical therapy referral as moderate pain intensity. Typically appropriate to treat concurrent abnormal not aggravated by physical activity. musculoskeletal findings. May be associated with photo- and/ or phonosensitivity. Typically made worse by lack of sleep and stress. Cervicogenic Headaches tend to be unilateral and Assess for upper cervical vertebral Physical modalities including manual therapies and nonalternating as far as laterality somatic dysfunction, cervical physical therapy interventions with consideration of although they can on occasion be instability (i.e., ligamentous), facet- focused exercise therapies and in some cases bilateral. Pain described typically is mediated pain, neuralgic pain interventional pain management procedures. Rarely nonthrobbing, nonlancinating with generators such as occipital surgery. moderate to severe pain intensity neuralgia and/or activated with episodes of varying duration. myofascial trigger points in the neck May see a variety of comorbid and or upper shoulder girdles that autonomic symptoms associated may refer into the head. with these types of headaches (i.e., blurry vision, dizziness). Neuralgia/Neuritic Variable presentations based upon Assess for dysesthetic areas on the Treatment consideration should include enteral, nature of nerve dysfunction from scalp, positive Tinel’s signs over topical, and injected medication therapies. dysesthetic more diffuse pain major nerves (i.e., supraorbital, Additionally, cryoneurolysis, radiofrequency symptoms to very focal point greater occipital) or their branches, ablation, and neuroablation can be considered, tenderness to shooting or nerve tenderness, as well as referred although newer techniques involving lancinating-type pain with referral. pain. neuromodulation may provide more conservative yet Location will be variable depending effective management. upon the nerve affected. Duration can be episodic or constant. Medication overuse Typically presents as a holocephalic, Likely to find parallel physical Discontinuation of offending medication with headache throbbing headache which can be examination abnormalities as seen replacement with alternate treatment for the persistent. They tend to occur daily with migraineurs or patients with suspected background headache disorder which to nearly every day and may awaken TTHA. should be initiated either during or immediately a person in the early morning. Tend following withdrawal. Nonpharmacologic therapies to improve with pain relief such as biofeedback and targeted physical therapy medication and will return as may also be indicated. Support groups and medication wears off. May be behavioral techniques have also been found to associated with nausea, enhance success of treatment in some patients. restlessness, behavioral changes, and cognitive difficulties. HPE 6 CHAPTER otocsieHeadache Postconcussive 67 68 Concussion

Migraine prophylactic therapy should be aimed at alternatives with the latter agent being available improving quality of life, decreasing abortive drug ther- commercially as Petadolex, which is a patented, stan- apy usage, as well as complications, and reducing attack dardized CO2 rhizome root extraction. Although butter- frequency, severity, and/or duration. There are generally bar has been used for many years, it has recently been considered to be three broad classes of medications shown to have potential for serious hepatotoxicity. currently endorsed for migraine prophylaxis. These Other agents including magnesium, riboflavin, and co- include antiepileptic drugs (AEDs), antihypertensives, enzyme Q10 have been touted as also being beneficial and antidepressants.46 Botulinum toxin A has also with empirical data being best for magnesium supple- been FDA approved for use in chronic migraine man- mentation. Further studies are required to address agement and is typically reserved for patients who persistent questions about efficacy, optimal dosing have failed three preventive medications and are experi- ranges, and parameters for choosing one drug over encing chronic migraine per aforementioned criteria. another in a particular patient. The most recent guidelines for the prevention of Over-the-counter medications such as Advil episodic migraines by the American Headache Soci- Migraine, Excedrin Migraine, and Motrin Migraine, ety/American Academy of Neurology, the Canadian which are all FDA approved, should be considered Headache Society, and the European Federation of first-line migraine abortives and are oftentimes quite Neurological Societies were published in 2012. The effective if not overused. Prescription abortive medica- medications with the highest level of evidence for tions include ergot derivatives, dihydroergotamine de- migraine prevention were sodium valproate, butterbur, rivatives, and triptans, as well as combination topiramate, propranolol, timolol, and metoprolol.47 medications such as Treximet. Dihydroergotamine- Although the aforementioned guidelines included containing compounds such as DHE-45 can be given only studies published up to 2009, more recent studies intravenously, typically with concurrent administration have confirmed most of the findings of previous system- of metoclopramide (Reglan), for expedient abortive atic reviews. management of migraine. Dihydroergotamine is also Several “migraine-specific” prophylactic drugs have available as a nasal spray, marketed as Migranal. Ergot- recently been developed, including CGRP receptor an- amine formulations include oral medications such as tagonists (abortive use) and monoclonal antibodies tar- Cafergot, as well as Ergotamine tartrate with caffeine, geting CGRP (prophylactic use). These medications in addition to Ergomar sublingual tablets and Migergot target known migraine pathophysiological mecha- suppositories. Parenteral atypical antipsychotics may nisms. Several oral CGRP receptor antagonists are also be used for abortive purposes. now on the market and have shown promising efficacy Nonsteroidal anti-inflammatory drugs (NSAIDs) in treating migraine with superiority to placebo and can be used for both prophylaxis and abortive ther- comparability to triptans. Some trials have been discon- apy, the latter including menstrual migraine. Midrin, tinued because of the concerns of hepatotoxicity after which is an acetaminophen-containing compound taking the drug for multiple consecutive days. Four (acetaminophen-isometheptene-dichloralphenazone) monoclonal antibodies targeting CGRP or the CGRP re- has also been used for migraine headache manage- ceptor have been tested in humans for the prevention of ment but typically works better for TTHAs. migraine: galcanezumab, eptinezumab, erenumab, and Symptomatic medications are typically used for fremanezumab. Another major breakthrough in the decreasing symptoms associated with nausea and treatment of migraine has been the development of 5- emesis that may accompany migraine headaches. Tradi- hydroxytryptamine 1F (5-HT1F) receptor agonists, tionally, the drugs that are used for symptomatic man- such as lasmiditan, which are similar to triptans but agement include prochlorperazine (Compazine) and without their vascular side effects. This drug class binds promethazine (Phenergan), which may be given orally more specifically to the serotonin 1F receptor than do or via other routes such as rectal suppository. Metoclo- triptans, which are less specific and bind to other vaso- pramide (Reglan) and domperidone (Motilium) are constricting subtypes of serotonin receptors. Still in also used as adjutants either orally or intravenously phase III trials, this drug class may be valuable for an ag- for symptomatic control and will also facilitate intesti- ing population that is no longer eligible for triptan ther- nal drug absorption. apy because of cardiovascular and cerebrovascular risk Newer treatment interventions can also be consid- factors.46 ered in the context of migraine management, including Naturopathic agents such as feverfew and butterbar sphenopalatine ganglion and/or greater occipital nerve can be considered as prophylactic antimigraine blocks as well as neuromodulation modalities such as CHAPTER 6 Postconcussive Headache 69 transcutaneous magnetic stimulation (TMS) with the Treatment eNeura SpringTMS, transcutaneous direct current stimu- Acute pharmacotherapy of TTHA should include lation (tDCS) of the supraorbital nerves with Cefaly or NSAIDs (including acetylsalicylic acid) sometimes in vagal nerve stimulation with gammaCore, among other conjunction with caffeine, sedatives, and/or tranquil- developing methodologies.48 These modalities may be izers. There is no scientific evidence to support the use helpful in both prophylaxis and abortive treatment of of muscle relaxants. Prophylactic pharmacotherapy for migraine. TTHA is more diversified and without any FDA- Biobehavioral interventions have also been found to approved drugs currently endorsed. Tricyclic antidepres- be effective for migraine management and may include sants, tizanidine, botulinum toxin, and venlafaxine (the cognitive behavioral therapy (CBT) with stress manage- latter an SNRI) have all shown at least some benefit, ment training, biofeedback, and root relaxation training with TCAs having the best evidence basis.52 Nonphar- among the most common. Ideally biobehavioral inter- macological treatments for tension headache include ventions should be used in conjunction with pharma- CBT, stress inoculation treatment, biofeedback, relaxa- cotherapeutic approaches. tion therapy, massage, trigger point therapy, exercise, e and acupuncture.52 54 Modalities may also play a role Tension Headaches in modulating TTHA including hot or cold packs, ultra- Clinical presentation sound, electrical stimulation, postural education, By ICHD criteria, tension headaches are divided into trigger point injections, occipital nerve blocks, manual either episodic (frequent or infrequent) or chronic medicine treatment, and stretching among other inter- and further categorized by whether or not they are asso- ventions.55 Proper diet, regular exercise, and restorative ciated with pericranial muscle abnormalities. These sleep are crucial in any headache patient including types of headaches comprise the most common primary those with tension headache. headache disorder.49 Episodic tension headache is usu- ally associated with heightened motions and/or stress Neuritic and Neuralgic Headache and tends to be of moderate intensity with a self- Clinical presentation limiting course. Episodic tension headache tends to be These types of headaches may present in variable pat- responsive to over-the-counter medications although terns depending upon the nature of the peripheral nerve prescription medications are sometimes necessary. injury. Small nerve fibers in the scalp may be injured in Chronic tensionetype headache (CTTH) on the other the context of penetrating injuries, surgical intervention hand recurs daily and has been shown to be correlated such as craniotomies, as well as by direct impact injury with abnormalities in the pericranial and cervical mus- resulting in scalp dysesthesia, significant tender points, cle examinations. Genetic factors seem to be more and/or positive Tinel’s sign over the affected region. important in the pathogenesis of CTTH.50 This type of When upper cervical distal nerve roots are involved headache is usually bilateral and occipitofrontal in loca- such as greater, lesser, or third occipital nerve, the tion. Pain onset can have a throbbing quality and is pain may be localized and noted on compression over usually more gradual than the onset seen in migraine. the nerve or when more severe may radiate into the sen- Duration tends to be more highly variable than other sory distribution of the nerve. In more severe cases, headache disorders such as migraine with a more con- there will be ipsilateral radiation into the frontotempo- stant quality but lower degree of severity. The headache ral scalp and occasionally retro-orbitally.both of tends to be felt as a tightening around the head (“tight which will be described as painful by the patient. Pe- hat syndrome”) (although location can vary) and is ripheral nerve injuries to larger nerves, whether in the typically described as nonpulsatile. TTHA is not classi- face or scalp, such as the supratrochlear, supraorbital, cally aggravated by physical activity.50 They are typically infraorbital (face), and/or auriculotemporal nerve may made worse by lack of sleep and stress. These types of present with localized as well as referred pain and headaches are typically not associated with nausea or may be due to peripheral nerve injury as well as central vomiting although photosensitivity and sonosensitivity sensitization. Clinicians must be familiar with the gen- can be seen but must be differentiated from postconcus- eral anatomic location of all the aforementioned nerves sive impairments of the same nature as well as as well as their associated sensory distributions. migrainous phenomena.51 There is very little under- stood about TTHA pathoetiology in primary headache Treatment or secondary headaches such as PCH but it is likely Drug management of post-traumatic neuritic and multifactorial. neuralgic pain tends to emphasize focal injection 70 Concussion therapies and topical agents. Secondary interventions pain that can be perceived as headache. The headache may include enteral medications such as NSAIDs, tricy- may be localized or more diffuse depending on the clic antidepressants, SNRIs such as duloxetine or anti- number and location of the aforementioned trigger convulsants such as carbamazepine, gabapentin, and points. The patient may be misdiagnosed as having ten- pregabalin. For post-traumatic neuralgias involving sion headache with bilateral referred cervical myofascial larger nerves of the face, scalp, and/or craniocervical pain unless an appropriate musculoskeletal examina- junction, local injection therapy with corticosteroids tion is performed and even then, the conditions can and local anesthetic remains the mainstay of treatment. be comorbid and in such cases, both need to be Serial injections may be necessary to abate or modulate addressed from a treatment standpoint. It should be the pain generator. Greater and lesser occipital neural- further noted that such myofascial trigger points can gia treatment approaches may include segmental blocks be seen in association with headache due to whiplash, at C2 and C3, cryoneurolysis, radiofrequency (RF) abla- migraine, and tension headache.57,58 tion, and neuroablation; although, newer noninvasive strategies such as neuromodulation are now showing Treatment some promise.56 Additionally, RF lesioning as well as Treatment should focus on an understanding of myo- surgical interventions do not necessarily guarantee reso- fascial pain disorder triggers, as well as perpetuating fac- lution as there is a relatively high recurrence rate. Inter- tos. Myofascial therapies are the mainstay of such estingly, blocks of afferent cervical nociceptive inputs treatment and should include specific stretching exer- have been shown to modulate trigeminal nerve pain cises, deep soft tissue work, and myofascial techniques as well as neurogenic inflammation28 such as trigger point acupressure, and dry needling, Diffuse neuritic pain associated with scalp injuries among other techniques as clinically indicated.57,58 such as postcraniotomy pain or local blunt trauma Postural reeducation can be a very important compo- should be addressed with compounded topical formu- nent of holistic MPD treatment since incorrect posture lations. Such topical agents, typically applied as an oint- (i.e., forward head position or upper crossed syndrome) ment or gel, generally need to be applied 3 to 4 times may perpetuate referred headache pain. Manual tech- per day to be optimally effective. Topical agents for niques to restore proper mobility and alignment, mus- neuropathic pain may include TCAs, local anesthetics, cle strengthening, and individualized exercise programs NSAIDs, AEDS such as gabapentin, clonidine, and/or should all be considered in the context of such ketamine hydrochloride, among other agents. There treatment.58 are often challenges getting insurance coverage for com- Pharmacologic interventions for myofascial pain, pounded topical pain medications. For information on although traditionally not first-line treatment, include local and/or regional compounding pharmacies see NSAIDs, tricyclic antidepressants, and possibly, muscle https://www.achc.org/pcab-accredited-providers.html. relaxants. Muscle relaxants have no proven efficacy, although some resemble TCAs in their structure and Myofascial Pain Related Headaches clinical effect and may contribute to treatment efficacy. Clinical presentation Antispasticity drugs are seldom used for myofascial Myofascial pain typically presents with pain in the neck pain, although tizanidine may have some theoretical and upper back/shoulders with potential to refer into benefit over other traditional antispasticity agents due the base of the skull in the head in general. Myofascial to its antinociceptive properties garnered through its ef- pain is associated with development of painful active fect on blocking of substance P. For chronic intractable trigger points (as opposed to latent trigger points which myofascial pain, some have advocated for use of botu- do not replicate the patient’s pain complaint pattern). A linum toxins although there are inconclusive data to myofascial trigger point (sometimes just called a trigger support this use in the head and neck regions. point) is a tight knot located within a taut muscular band. The knot or nodule can be distinctly felt under- Cervicogenic Headache neath the skin and is tender when pressed. In addition, Clinical presentation when pressure is applied to the knot, the taut muscular The clinical presentation may be confounding due to band which holds the knot contracts. This creates a the overlap of symptoms with other possible primary twitching of the muscle that can be felt or visually as well as secondary headache disorders, including ten- observed, the so-called “twitch response.”57,58 sion headache, migraine, and greater occipital neuralgia When a trigger point is located in the neck, shoulder, headache. In part, this confusion occurs because even and/or head muscles, it can cause referred or spreading the aforementioned headaches tend to be associated CHAPTER 6 Postconcussive Headache 71 with complaints of neck pain and/or with pathological family about the risks of MOH if medications are not cervical physical examination findings in the absence of taken as prescribed.68 cervicalgia. Headaches tend to be unilateral and not alternating side to side although they can be Treatment e bilateral.59 61 Headaches are typically nonthrobbing, Although withdrawal and reduction of abortive medica- nonlancinating, and associated with moderate to severe tions is considered to be the treatment of choice, there is pain with episodes of varying duration. To further no standard practice recommended as related to with- complicate things, cervicogenic headaches have also drawal at this time. Drug withdrawal, particularly been noted to be associated with sono- and photosensi- when abrupt, normally results in worsening of head- tivity, nausea, dizziness, unilateral blurred vision, ache. Alternatively, if MOH is a concern, the offending among other symptoms.62 It is critical to differentiate medication should be slowly weaned with concurrent cervicogenic headaches from other headache etiol- alternative preventative headache management options ogies63 and recognize that afferent nociceptive input prescribed with evidence based on randomized studies into the trigeminocervical complex can aggravate or best for topiramate and onabotulinumtoxin A.50,68 perpetuate migraine as well as tension headache. What role some of the newer generation migraine med- ications may have is yet to be determined. Detoxifica- Treatment tion can be done as an outpatient, in a day hospital, Conservative treatment options should be tried first, or in an inpatient setting depending on the severity of including physical therapy and manual therapies the MOH and the comorbidities of the specific case. (manipulation with or without mobilization), whether chiropractic, osteopathic, or craniosacral.54,64,65 Low load endurance craniocervical and cervicoscapular exer- PCH NATURAL HISTORY, PROGNOSIS, cises have also been shown to have a role in ameliora- AND OUTCOME tion.54 Exercise including postural and strengthening There are inadequate evidence-based studies to stipu- can play a key role in ameliorating/modulating such late the natural history, prognostic factors, and long- headaches.66 In more intractable cases, interventional term outcomes of PCH, in part, because PCH is not pain management procedures such as anesthetic blocks one single pathophysiological disorder but rather a of the upper cervical joints can be helpful in both assess- symptom descriptor that may involve multiple pain ment and treatment.67 generators/causes including psychogenic ones. The rela- tive lack of prospective, controlled, and blinded studies Medication Overuse Headache that adequately consider variables associated with head- Clinical presentation ache cause, treatment, and secondary complications MOH is defined as a headache occurring at least 15 days only further challenges our ability to understand its nat- per month in patients with preexisting headache disor- ural history and provide opinions regarding prognosis. ders and with concurrent use of either simple analgesic There are also multiple methodological challenges in agents such as ibuprofen or naproxen at least 15 days studying an impairment that is predominantly based per month or other analgesic agents such as triptans on subjective patient report including issues of misattri- or ergotamines 10 days per month for at least bution bias (on the part of the patient as well as the 3 months.68 MOH may be seen from excessive use of assessing clinician), patient recall bias, nocebo effects a variety of analgesic and/or abortive headache agents, of the diagnosis, cultural influences on pain perception including ergotamines, opiates, caffeine, triptans, and/ and reporting, and potential response bias relative to or barbiturates.69 Overuse of these medications may symptom amplification as well as minimization lead to development of increased headaches and even (depending on incentives.which may be subcon- CDH. Patients may become dependent on these symp- scious, conscious, or some combination of both) tomatic headache medications. The headache tends to regarding pain reporting and/or associated paine present as holocephalic and throbbing.70 Headache related disability, among other issues. medication overuse may also make headaches refrac- Any study of chronic PCH must also address the tory to prophylactic headache medication and the inherent comorbidities of the psychological and medi- affected person more sensitive to headache triggers. Un- cal effects of chronic pain (and the associated stress) fortunately, most patients are unaware of MOH, so pro- on not only the patient’s reporting of their pain but viders should be diligent in evaluating the frequency of also on a myriad of other aspects of function, including medication use and educating patients as well as their cognition, behavior, and sleep. Studies to date have not 72 Concussion integrated data from focused headache physical assess- confirmed. Kjeldgaard et al. studied “chronic PTHA” ments that take into consideration neurological and in a group with “mild head injury” and found a high musculoskeletal findings nor have they included mea- correlation with unemployment and interestingly sures of response bias, pain validity reporting, or anal- TTHA was the most common headache subtype noted ysis of the potential influence of secondary gain with over 30% of patients having a mixed headache pic- factors in headache reporting. Additionally, studies ture.73 Also of note in the Kjeldgaard study was the fact have not linked specific examination findings with cur- that over 50% of the chronic PCH group was involved rent headache classification systems (the latter of which in litigation. Dumke found that headache severity was have been criticized relative to their lack of applicability strongly correlated with a poorer prognosis for return and relevance to this particular population). Impor- to work; yet, based on the study it is unclear whether pa- tantly, historical studies have not attempted to assess tients were appropriately diagnosed and treated.74 the accuracy of the PCH-related diagnoses nor their his- When properly diagnosed and treated, most pa- torical response to treatment. Without knowing what tients, in our experience, are able to achieve substantive the specific PCH pain generators are in a population headache improvement, if not cured, particularly when and/or how they were treated, we cannot make determi- PCH is addressed earlier rather than later. Good out- nations of the true incidence of “chronic” PCH. Any comes depend to a great extent on patient education such conclusions would furthermore be based on the and avoidance of nocebo, iatrogenic, and lexigenic ef- assumption or confirmation that the headache condi- fects of the injury. Additionally, work disability due to tion(s) was/were appropriately diagnosed and treated. PCH, in and of itself, is very uncommon in the hands That being said, there is no literature to the authors of a sophisticated practitioner with a good treatment knowledge regarding the natural history of untreated team, unless there are significant comorbidities PCH. including mental health issues and/or secondary gain Based on the available studies, headache tends to incentives. improve in the months following trauma, whether to PCH prognosis must be based on an exact under- the brain, head, or neck. How much improvement is standing of headache etiology (based on history and seen will be dependent on injury severity, preinjury focused examination and questionably headache classi- physical and psychoemotional status, presence of fication systems), overlay as relevant of psychogenic fac- complicating factors such as nocebo effects, secondary tors (including patient preinjury characterological gain incentives, resilience, among other factors, as well issues) and secondary gain incentives, response to as appropriate diagnosis of the underlying pain genera- appropriate historical treatment, and consideration of tors and subsequent optimal treatment for same. whether the correct diagnosis and treatment for the Appropriate and timely treatment shortens the period pain generator was made from the initial of impairment, associated disability, lost work hours, assessment.4,75 as well as pain and suffering. There is very limited evi- dence regarding the impact of ongoing litigation on PATIENT AND FAMILY EDUCATION the persistence of headache complaints but that which Patients, as well as significant others/caretakers, need to exists suggests that patients still continue to report sig- be educated so that they understand the relevant diag- nificant symptoms even after litigation has ended.71 noses, treatment plan, and prognosis. Education should Further research to confirm prior findings is strongly also be provided regarding the importance of compli- recommended. ance with recommended treatments and in particular A small number of patients will develop intractable medication use as related to avoidance of MOH, poten- and sometimes severe PCH; however, this group of pa- tial drug side-effects, and drug interactions among other tients has been poorly studied and the influence of issues. Clinicians should remain accessible for ques- other factors including inappropriate headache catego- tions or concerns.4,5 rization and treatment, MOH, secondary gain incen- tives, cultural factors, preinjury genetic loading risk variables, as well as psychogenic factors in such patients CONCLUSIONS remains unclear. The first prospective controlled study PCH is ultimately a symptom and not a diagnosis. This examining PCH persistence found that approximately complex disorder has multiple potential causes and as a 15% of patients continued to complain of headache result, has multiple treatments to address the headache at 3 months post injury72; however, accuracy of diag- disorder that is associated with the underlying pain gen- nosis and appropriateness of treatment were not erator(s). Assessing and treating PCH is a process that CHAPTER 6 Postconcussive Headache 73 requires adequate time commitment and knowledge by Practical Pain Management, Migraine tracking apps the treating clinician.some will consider this “a pain” for smartphones: https://www.practicalpainmanage and if that is the case, then those clinicians should defer ment.com/patient/resources/pain-self-management/9- treatment to others who make it their business to assess apps-tracking-your-migraine-days. and treat these types of patients and conditions. Pejora- The American Council for Headache Education (pro- tive and potentially self-prophesizing labels such as vides a listing of on-line and local support groups): “chronic PCH” are often a misnomer due to the fact www.achenet.org. that the actual pain generators were never diagnosed fi correctly in the rst place and should be avoided. There ACKNOWLEDGMENTS is in fact hope for those with PCH regardless of how We thank John Leddy, MD, FACSM, FACP, for his input long they have suffered from pain. The challenge is on this work. finding clinicians and treatment teams who understand the diversity of this class of disorders and have experi- ence in holistic assessment and treatment of patients REFERENCES who have had concussions, cranial trauma, and/or 1. Dobscha SK, Clark ME, Morasco BJ, Freeman M, whiplash injuries. Campbell R, Helfand M. Systematic review of the literature on pain in patients with polytrauma including traumatic e RESOURCES OF INTEREST FOR PATIENTS brain injury. Pain Med. 2009;10(7):1200 1217. 2. Evans RW. Persistent post-traumatic headache, post- AND PRACTITIONERS concussion syndrome, and whiplash injuries: the evidence ACHC: Pharmacy Compounding Accreditation Board for a non-traumatic basis with a historical review. Head- (PCAB): https://www.achc.org/pcab-accredited-pro- ache. 2010;50(4):716e724. viders.html. 3. Horn LJ, Siebert B, Patel N, Zasler ND. Post-traumatic American Council for Headache Education: www. headache. In: Zasler N, Katz D, Zafonte R, eds. Brain Injury achenet.org. Medicine. 2nd ed. New York: Demos; 2013:932e953. American Headache Society: https://americanhead 4. Zasler ND, Leddy JJ, Etheredge S, Martelli MF. Post- achesociety.org. traumatic headache. In: Silver JM, McAllister TW, Arciniegas D, eds. Textbook of Traumatic Brain Injury.3rd American Migraine Foundation: https://american ed. Washington, D.C: American Psychiatric Publishing, migrainefoundation.org. Inc.; 2019:471e490. BIAA (PTHA webinar): https://shop.biausa.org/ 5. Zasler ND, Martelli MF, Nicholson K, Horn L. Post- product/BOB092216CD/20160922-post-traumatic- traumatic pain disorders: medical assessment and headache-recorded-webinar. management. In: Zasler N, Katz D, Zafonte R, eds. Brain Brainline. Post-traumatic headache: https://www. Injury Medicine: Principles and Practice. 2nd ed. New York: brainline.org/article/post-traumatic-headache-after-tbi. Demos Publishers; 2013:954e973. Chiropractic Canada. Clinical practice guideline for 6. Iverson GL, Gardner AJ, Terry DP, et al. Predictors of clin- the management of headache disorders in adults: ical recovery from concussion: a systematic review. Br J e http://ccpor.ca/wp-content/uploads/CPG-for-the-Man Sports Med. 2017;51:941 948. 7. Terry DP, Huebschmann NA, Maxwell BA, Cook NE, et al. agement-of-Headache-Disorders-in-Adults-2012.pdf. Pre-injury migraine history as a risk factor for prolonged National Headache Foundation: www.headaches.org. return to school and sport following concussion. Ontario Neurotrauma Foundation. Guideline for J Neurotrauma. August 2, 2018. Epub ahead of print. concussion/mild traumatic brain injury & persistent 8. Zasler ND. Post-traumatic headache, caveats and symptoms. Third edition (for adults over 18 years of controversies. J Head Trauma Rehabil. 1999;14(1):1e8. age). Post-traumatic headache. HTTPS://BRAININ 9. Headache Classification Committee of the International JURYGUIDELINES.ORG/CONCUSSION/INDEX.PHP? Headache Society. The international classification of head- ID¼135&TX_ONFADULTS_ADULTDOCUMENTS%5B ache disorders, 3rd edition (beta version). Cephalalgia. e THEME%5D¼6&TX_ONFADULTS_ADULTDOCUM 2013;33(9):629 808. ENTS%5BACTION%5D¼SHOW&TX_ONFADULTS_ 10. Hoffman JM, Lucas S, Dikmen S, et al. Natural history of ¼ headache after traumatic brain injury. J Neurotrauma. ADULTDOCUMENTS%5BCONTROLLER%5D e ¼ 2011;28(9):1719 1725. THEME&CHASH 036827A60A01AE94FC9382FE19 11. Dwyer B. Post-traumatic headache. Semin Neurol. 2018;38: B89508. 619e626. 74 Concussion

12. ICD-10. Available at: http://apps.who.int/classifications/ cervicogenic headache responsive to third occipital nerve icd10/browse/2010/en#/G44.3. Accessed December 15, radiofrequency ablation. Pain Med. 2014;15:473e478. 2018. 29. Rau JC, Dumkrieger GM, Chong CD, Schwedt TJ. Imaging 13. Lucas S, Ahn AH. Post-traumatic headache: classification post-traumatic headache. Curr Pain Headache. 2018;30; by symptom-based clinical profiles. Headache. 2018;58: 22(10):64. 873e882. 30. Bendtsen L, Birk S, Kasch H, et al. Reference programme: 14. Lane R, Davies P. Post-traumatic headache in a cohort of diagnosis and treatment of headache disorders and facial UK compensation claimants. Cephalalgia. 2018. Epub pain. Danish Headache Society, 2nd edition, 2012. ahead of print. J Headache Pain. 2012;S1:S1eS29. 15. Stacey A, Lucas S, Dikmen S, et al. Natural history of head- 31. Hutting N, Scholten-Peeters GGM, Vijverman V, et al. ache five years after traumatic brain injury. J Neurotrauma. Diagnostic accuracy of upper cervical spine instability 2017;34(8):1558e1564. tests: a systematic review. Phys Ther. 2013;93(12): 16. Lew HL, Lin P-H, Fuh J-L, Wang S-J, Clark DJ, Walker WC. 1686e1695. Characteristics and treatment of headache after traumatic 32. Rubio-Ochoa J, Benitez-Martinez J, Lluch E, Santacruz- brain injury: a focused review. Am J Phys Med Rehabil. Zaragoza S, Gomez-Contreras P, Cook CE. Physical 2006;85(7):619e627. examination tests for screening and diagnosis of cervico- 17. Lucas S, Hoffman JM, Bell KR, Dikmen S. A prospective genic headache: a systematic review. Man Ther. 2016;21: study of prevalence and characterization of headache 35e40. following mild traumatic brain injury. Cephalalgia. 2014; 33. Watson DH, Drummond PD. The role of the trigeminocer- 34(2):93e102. vical complex in chronic whiplash associated headache: a 18. Nordhaug LJ, Hagen K, Vik A, et al. Headache following cross sectional study. Headache J Head Face Pain. 2016; head injury: population-based longitudinal cohort study 56(6):961e975. (HUNT)). J Headache Pain. 2018;19(1):8. 34. Watson DH, Drummond PD. Head pain referral during ex- 19. Silverberg ND, Iverson G, Brubacher JR, et al. The nature amination of the neck in migraine and tension-type and clinical significance of pre-injury recall bias following headache. Headache. 2012;52(8):1226e1235. mild traumatic brain injury. J Head Trauma Rehabil. 2016; 35. Bell KR, Kraus EE, Zasler ND. Medical management of 31(6):388e396. posttraumatic headaches: pharma-cological and physical 20. Walker W. Pain pathoetiology after TBI: neural and non- treatment. J Head Trauma Rehabil. 1999;14(1):34e48. neural mechanisms. J Head Trauma Rehabil. 2004;19(1): 36. Watanabe TK, Bell KR, Walker WC, Schomer K. Systematic 72e81. review of interventions for post-traumatic headache. Phys 21. Zasler ND, Etheredge S. Post-traumatic headache: knowl- Med Rehabil. 2012;4:129e140. edge update. The Pain Practitioner. 2015;25(2):19e22. 37. Zasler ND. Pharmacotherapy and post-traumatic 22. Walton DM, Macdermid JC, Giorgianni AA, cephalalgia. J Head Trauma Rehabil. 2011;26(5):397e399. Mascarenhas JC, West SC, Zammit CA. Risk factors for 38. Zasler ND. Pain management in persons with traumatic persistent problems following acute whiplash injury: up- brain injury. In: Zollman F, ed. Manual of Traumatic Brain date of a systematic review and meta-analysis. J Orthop Injury Assessment and Management. 2nd ed. New York: Sports PhysTher. 2013;43(2):31e43. Demos Medical; 2016:299e307. 23. Elliott MB, Oshinsky ML, Amenta PS, et al. Nociceptive 39. Conidi FX. Interventional treatment for post-traumatic neuropeptide increases and periorbital allodynia in a headache. Curr Pain Headache Rep. 2016;20:40. model of traumatic brain injury. Headache. 2012;52(6): 40. Fraser F, Matsuzawa Y, Lee YSC, Minen M. Behavioral treat- 966e984. ment for post-traumatic headache. Curr Pain Headache Rep. 24. Mayer CL, Huber BR, Peskind E. Traumatic brain injury, 2017;21:22. neuroinflammation, and post-traumatic headaches. Head- 41. Martelli MF, Nicholson K, Zasler N. Psychological assess- ache. 2013;53(9):1523e1530. ment and management of post-traumatic pain. In: 25. Tyburski AL, Cheng L, Assari S, et al. Frequent mild head Zasler N, Katz D, Zafonte R, eds. Brain Injury Medicine. injury promotes trigeminal sensitivity concomitant with 2nd ed. New York: Demos; 2013:974e989. microglial proliferation, astrocytosis and increased neuro- 42. Minen M, Jinich S, Vallespir EG. Behavioral therapies and peptide levels in the trigeminal pain system. J Heache Pain mind-body interventions for post-traumatic headache and Dec. 2017;18(1):16. post-concussive symptoms: a systematic review. Headache. 26. Mustafra G, Hou J, Tsuda S, et al. Trigeminal neuroplastic- December 1, 2018. Epub ahead of print. ity underlies allodynia in a preclinical model of mild 43. Martelli MF, Nicholson K, Zasler ND. Assessing and closed head traumatic brain injury (cTBI). Neuropharma- addressing response bias. In: Zasler N, Katz D, Zafonte R, cology. 2016;107:27e39. eds. Brain Injury Medicine: Principles and Practice. 2nd ed. 27. Moye LS, Pradhan AA. From blast to bench: a translational New York: Demos; 2013:1415e1436. mini-review of post- traumatic headache. J Neurosci Res. 44. Ashkenazi A, Blumenfeld A, Napchan U, et al. Peripheral 2017;95(6):1347e1354. nerve blocks and trigger point injections in headache man- 28. Giblin K, Newmark JL, Brenner GJ, Wainger BJ. Headache agement - a systematic review and suggestions for future plus: trigeminal and autonomic features in a case of research. Headache. 2010;50(6):943e952. CHAPTER 6 Postconcussive Headache 75

45. Nijs j, Malfliet A, Ickmans K, Baert I, Meeus M. Treatment 60. Becker WJ. Cervicogenic headache: evidence that the neck of central sensitization in patients with unexplained is a pain generator. Headache. 2010;50(4):699e705. chronic pain: an update. Expert Opin Pharmacother. 2014; 61. Bogduk N. The neck and headaches. Neurol Clin. 2014; 15(12):1671e1683. 32(2):471e487. 46. Ong JJY, Wei DY, Goadsby PJ. Recent advances in pharma- 62. Blumenthal A, Siavoshi S. The challenges of cervicogenic cotherapy for migraine prevention: from pathophysiology headache. Curr Pain Headache Rep. 2018;22:47. to new drugs. Drugs. 2018;78(4):411e437. 63. Vincent MD. Cervicogenic headache: a review comparison 47. Loder E, Burch R, Rizzoli P. The 2012 AHS/AAN guidelines with migraine, tension type headache and whiplash. Curr for prevention of episodic migraine: a summary and com- Pain Headache Rep. 2010;14:238e243. parison with other recent clinical practice guidelines. 64. Garcia JD, Arnold S, Tetley K, et al. Mobilization and Headache. 2012;52(6):930e945. manipulation of the cervical spine in patients with cervico- 48. Puledda F, Shields K. Non-pharmacological approaches to genic headache: any scientific evidence? Front Neurol. migraine. Neurotherapeutics. 2018;15:336e345. 2016;7:40. 49. Jensen RH. Tension type headache- the normal and most 65. Racicki S, Gerwin S, Diclaudio S, Reinmann S, prevalent headache. Headache J Head Face Pain. 2018; Donaldson M. Conservative physical therapy management 58(2):339e345. for treatment of cervicogenic headache: a systematic 50. Jay GW, Barkin RL. Primary headache disorders e Part 2: review. J Man Manip Ther. 2013;21(2):113e124. tension-type headache and medication overuse 66. Dunning JR, Butts R, Mourad F, et al. Upper cervical and headache. Disease-a-Month. 2017;63:342e367. upper thoracic manipulation versus mobilization and ex- 51. Kahriman A, Zhu S. Migraine and tension-type headache. ercise in patients with cervicogenic headache: a multi- Semin Neurol. 2018;38:608e618. center randomized clinical trial. BMC Muscoskelet Disord. 52. Ghadiri-Sani M, Silver N. Headache (chronic tension 2016;17:64. type). BMJ Clin Evid. 2016:1205. 67. Fernandez-de-las-Penas C, Cuadrado ML. Therapeutic op- 53. Alonso-Blanco C, de-la-Llave-Rincón AI, Fernández-de-las- tions for cervicogenic headache. Expert Rev Neurother. Peñas C. Muscle trigger point therapy in tension-type 2014;14(1):39e49. headache. Expert Rev Neurother. 2012;12(3):315e322. 68. Diener HC, Holle D, Solbach K, Gaul C. Medication- 54. Varatharajan S, Ferguson B, Chrobak K, et al. Are non- overuse headache: risk factors, pathophysiology and invasive interventions effective for the management of management. Nat Rev Neurol. 2016;2(10):575e583. headaches associated with neck pain? An update of the 69. Katsarava Z, Obermann M. Medication overuse headache. bone and joint decade, task force on neck pain and its Curr Opin Nueorl. 2013;26(3):276e281. associated disorders by the Ontario protocol for traffic 70. Kristoffersen ES, Lundquist C. Medication-overuse head- injury management collaboration. Eur Spine J. 2016; ache; epidemiology, diagnosis and treatment. Ther Adv 25(7):1971e1999. Drug Saf. 2014;5(2):87e99. 55. Posadzki P, Ernst E. Spinal manipulations for tension-type 71. Packard RC. Post-traumatic headache: permanency and headaches: a systematic review of randomized controlled relationship to legal settlement. Headache. 1992;32(10): trials. Complement Ther Med. 2012;20(4):232e239. 496e500. 56. Choi I, Jeon SR. Neuralgias of the head: occipital neuralgia. 72. Faux S, Sheedy J. A prospective controlled study on the J Korean Med Sci. 2016;31(4):479e488. prevalence of post-traumatic headache following mild 57. Do TP, Heldarskard GF, Kolding LT, Hvedstrup J, Schytz H. traumatic brain injury. Pain Med. 2008;9(8):1001e1011. Myofascial trigger points in migraine and tension-type 73. Kjeldgaard D, Forchhammer H, Teasdale T, Jensen RH. headache. J Headache Pain. 2018;19(1):84. Chronic post-traumatic headache after mild head injury: 58. Donnelly JM, Fernandez-de-las-Penas C, Finnegan M, a descriptive study. Cephalalgia. 2014;34(3):191e200. Freeman JL. Myofascial pain and dysfunction. In: Travell, 74. Dumke HA. Post-traumatic headache and its impact on re- Simons, Simons, eds. The Trigger Point Manual. 3rd ed. turn to work after mild traumatic brain injury. J Head Philadelphia, PA: Wolter Kluwer; 2019. Trauma Rehabil. 2017;32(2):E55eE65. 59. Packard RC. The relationship of neck injury and post- 75. Packard RC, Ham LP. Post-traumatic headache: deter- traumatic headache. Curr Pain Headache Rep. 2002;6: mining chronicity. Headache. 1993;33(3):133e134. 301e307, 2002.