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Introduction

            Headache and neck pain are the most common physical complaints following concussive brain injury and are experienced early after injury by up to 70% of persons with these types of injuries (1-4). Headache also occurs after more severe brain injury however, it tends to be a less common phenomenon in this group of patients when compared with the incidence following mild traumatic brain injury (3,5,6). This may suggest that the TBI itself is probably not the primary cause of the headache because it would logically follow that if it was, one would expect more headache problems with more severe TBI, which in practice is not the case (4). Headache is also a common problem after cranial trauma, as well as spinal acceleration deceleration (i.e., whiplash) injuries (3,7,8). Headache is a hallmark co-morbidity associated with sports trauma where it has been termed sports concussion headache (SCH) (4). Post-concussive headaches do not necessarily occur due to the concussion itself but often times are the result of head impact injury and/or cervical whiplash-type injuries. The terms post-traumatic headache (PTHA) and SCH (which may be fine as “umbrella” terms) do not convey any real information of value regarding the specific headache etiology or underlying headache diagnosis, nor do they guide treatment of the headache disorder (3,9). Use of such general terms may, therefore, cause practitioners and others to misattribute the headache disorder to traumatic brain injury when, in fact, its cause may be extra-cerebral as in the case of impact injury pain, post-traumatic neuralgic or neuritic pain, and/or cervicogenic headache, among other possibilities (2-4,10).

            Often, injured persons will seek medical care following traumatic injuries only to be diagnosed with PTHA. Such a non-specific diagnosis without elaboration as to pain generator etiologies leaves treaters and others (including patients and their families) with no real information regarding the true etiology of the headache disorder, its prognosis, or the appropriate treatment regimen that should be administered to modulate or ideally cure the headache (2,9)..

            Although the majority of headaches following concussive brain injury (CBI) are most likely benign relative to these disorders and do not typically require surgical treatment, there are, on occasion, complications that occur after both CBI and more severe injury that may cause headache and require surgical intervention. Subdural and epidural hematomas (blood collecting between the brain and the skull), carotid cavernous fistulas (abnormal communication between the venous blood flow and arterial blood flow), traumatic carotid artery dissection, cavernous sinus thrombosis, as well as post-traumatic intracranial pressure (ICP) abnormalities (high versus low ICP), among other conditions can all be responsible for headaches and bring with them a potential need for surgical intervention (3,7,8). 

            The experienced clinician should be able to determine the underlying cause for the PTHA with appropriate time taken to acquire an adequate pre-injury, injury, and post-injury history, as well as conduct a careful physical evaluation (including all relevant head, neck, and upper thoracic structures) and as clinically indicated, order appropriate diagnostic testing (2-4,8). Treatment should be instituted in a holistic fashion as early as possible with the goals of maximizing the benefit/risk ratio of any particular intervention, prescribing treatment that can be optimally complied with, and educating the patient and family regarding the condition, its treatment, and prognosis to avoid the negative biopsychosocial effects of more chronic cephalalgia.

            Late onset headaches (i.e., greater than six months post-trauma) should cue the treating clinician to think of less common injury-related conditions such as seizures as a cause for the headache disorder or just as likely a non-injury related cause such as a space occupying lesion (i.e., brain tumor, colloid cyst), among other conditions (3).

Categorization

            The major types of headaches seen following trauma include musculoskeletal headache (including direct cranial trauma, cervicogenic headache, and TMJ disorders), neuromatous and neuralgic (nerve) headache, tension type headache, migraine, as well as less common causes such as dysautonomic headaches, seizures, facial and/or skull fractures, tension pneumocephalus (air in the head), cluster headaches, paroxysmal hemicrania, post-traumatic sinus infections, drug-induced headaches, medication overuse headaches (previously called rebound headache) and the surgical conditions previously mentioned (3).

Although still debated, the most frequent cause of PTHA in our experience is cervicogenic headache, which may have several different possible causes. Referred cervical myofascial pain as a consequence of cervical whiplash is a particularly common cause for this condition. One can often find activated trigger points in the suboccipital musculature, sternocleidomastoid, and/or upper trapezius muscles as common sources of referred pain into the head in patients post-whiplash (2-4). Another pain generator of cervicogenic headaches is facet dysfunction, especially in the upper cervical spine. The C2/3 segment should specifically be focused on as this segment refers into the occiput region and is commonly involved after a whiplash injury (11,12).

Etiology

            There are multiple sources of head and neck pain, both inside and outside of the head (2,3). The brain parenchyma itself, interestingly, is not a source of pain. Headache typically results from six major physiologic phenomena:

•           Displacement of intracranial (within the skull) structures

•           Inflammation

•           Ischemia (decreased blood flow) and/or metabolic changes

•           Myodystonia (increased muscle tone)

•           Meningeal irritation (inflammation/irritation of the thin layers of tissue “coating” the brain)

•           Increased or decreased intracranial pressure

Neuralgic and neuritic pain generators associated with surgical trauma, direct scalp contusional injury, and craniocervical acceleration/deceleration forces are often overlooked. Clinicians should understand the anatomy of the occipital nerves and their accessibility to interventional pain management techniques (see figure 1). The interconnectivity of upper cervical and cerebral pain transmission pathways (both peripheral and central) is critical to understand in the context of assessment of the pathoetiology of any PTHA presentation (see figure 2).

Examination of the Patient with PTHA

            The examination should start with taking a thorough history of the patient as related to his or her PTHA complaint (see table 1). The hands-on physical exam, which is often ignored in PTHA assessment, should take into consideration central and peripheral neurological clinical findings into consideration, as well as musculoskeletal clinical findings (2-4). The neurological evaluation should entail an elemental neurological exam of all 12 cranial nerves, funduscopic exam (to rule out papilledema), deep tendon reflexes including pathological reflexes, sensory exam with visual field testing to confrontation, motor exam and cerebellar assessment (which should also encompass measures of postural stability), assessment for meningismus, and mental status evaluation (4,13). Appropriate cognitive screening should be performed if brain impairment is suspected secondary to trauma. The peripheral neurological examination should include assessment for neuralgic and/or neuritic headache pain generators such as supra-orbital neuralgia and occipital neuralgia. The musculoskeletal exam should include palpatory assessment of the face, temporomandibular joints, head and craniocervical junction, and cervicothoracic spine at a minimum to assess for pathologic findings (2-4).

            The musculoskeletal evaluation of the patient with PTHA should emphasize function and involves inspection for body asymmetries (e.g., head tilt, shoulder droop, tilted pelvis, leg length discrepancy, or asymmetric gait), postural assessment including forward head posture, rounded shoulders, stance, pelvic alignment, and assessment for cervical and lumbar lordosis, or lack thereof. Jaw range of motion and tracking, as well as spinal range of motion, particularly at the cervicothoracic junction should be addressed in any patient with PTHA. Auscultation for bruits should be done as appropriate over the carotids, closed eyes, temporal arteries, and mastoids. The temporomandibular joints should also be auscultated, as clinically indicated, for abnormal articular sounds. Palpatory exam should include the face, head (including TMJ and masticatory muscles), shoulder girdles, and neck, which must be done in a controlled, layer by layer fashion to truly localize pathology with an eye to identifying activated trigger points and referred pain patterns (see figure 3). Neck assessment should include at a minimum assessment of vertebral somatic dysfunction, as well as testing for alar and transverse ligament integrity (2-4,14).

Treatment of PTHA

            The pharmacological management of headache after traumatic brain injury (TBI) and/or general trauma is replete with challenges due to the lack of an adequate body of evidence-based medicine examining pharmacotherapeutic agents for post-traumatic headache. The general practice trend is to approach these headache disorders as they would be treated in non-traumatic headache disorders. There are no FDA-approved drug treatments specific to post-traumatic headache whether in children or adults. General rules of pharmacological prescription in persons with TBI are to start low, go slow, minimize polypharmacy, choose effective agents that are specific to the condition being treated, reassess need for medication over time, monitor use/abuse as clinically indicated, and attempt to choose medications can be taken once to twice a day at most due to issues with likely cognitive impairments.

            Pain medications that are not specific for the particular headache subtype should usually be avoided, particularly such agents as opiates and barbiturates, which may cause a variety of long-term adverse effects including, but not limited to, medication overuse headache, endocrine effects, impairment issues that may affect safety, and addiction potential, among other reasons (3,15). There is seldom an indication for use of opiates in this group of patients, particularly for longer term use (15) Patients should only be placed on chronic opioid treatment if they demonstrate true failure to respond to a variety of other agents with less potential short and long term risks and have opiate responsive pain. Ideally, opiates should not be used long term for pain management given issues of addiction risk as well as development of tolerance, the latter requiring increasing opiate doses being prescribed to achieve historical pain control levels. Pediatric patients, those with significant Axis II issues, or those with a history of chronic substance abuse should generally not be considered candidates for such therapy.

            The following brief review will attempt to summarize the most common PTHA variants and their drug treatments.

Migraine

            There are three basic approaches to pharmacotherapeutic management of post-traumatic migraine. These include prophylaxis, abortive therapy, and symptomatic therapy. Migraine prophylactic therapy should be aimed at improving quality of life, decreasing abortive drug therapy usage, as well as complications, and reducing attack frequency, severity, and/or duration. There are generally considered to be three broad classes of medications currently endorsed for migraine prophylaxis. These include anti-epileptic drugs (AEDs), antihypertensives, and antidepressants.  Botulinum toxin A has also been FDA approved for use in chronic migraine management. AEDs are commonly used in migraine prophylaxis; however, only divalproex sodium and topiramate are FDA approved. Physicians prescribing such medications need to be aware of drug monitoring requirements as well as drug/drug interactions. Tricyclic antidepressants (TCAs) are good alternatives because of their overall efficacy and relatively good tolerance when given at the low doses needed for headache pain management. Amitriptyline and nortriptyline are the most commonly prescribed TCAs due to the extant headache literature examining their efficacy but are not FDA approved for migraine (and may exacerbate cognitive impairment at higher doses in persons with TBI due to their anticholinergic effects). Antihypertensives such as propranolol and timolol are the only two beta-blockers approved by the FDA for migraine prophylaxis, but caution should be taken with geriatric patients or those with other medical comorbidities such as depression, diabetes, or thyroid problems. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and calcium channel blockers have all been shown to be effective, at least to some extent, for migraine prevention but are generally not used as first-line agents (15).         

            Naturopathic agents such as feverfew and butterbur should also be considered as prophylactic anti-migraine alternatives with the latter agent being available commercially as Petadolex®, which is a patented, standardized CO2 rhizome root extraction. Other agents including magnesium, riboflavin, and coenzyme Q10 have been touted as also being beneficial with empirical data being best for magnesium supplementation.            

            Over-the-counter medications such as Advil® Migraine, Excedrin Migraine®, and Motrin Migraine®, which are all FDA approved, should be considered first-line migraine abortives and are often times quite effective if not over used. Prescription abortive medications include ergot derivatives, dihydroergotamine derivatives, and triptans, as well as combination medications such as Treximet®. Dihydroergotamine-containing compounds such as DHE-45 can be given intravenously, typically with concurrent administration of metoclopramide (Reglan), for expedient abortive management of migraine. Dihydroergotamine is also available as a nasal spray, marketed as Migranal®. Ergotamine formulations include oral medications such as Cafergot®, as well as ergotamine tartrate with caffeine, in addition to Ergomar® sublingual tablets and Migergot® suppositories. Parenteral atypical antipsychotics may also be used for abortive purposes (15).

            Generally, pain medications that are not specific for migraine management such as opiates and barbiturates should be avoided unless no diagnosis-specific drugs have been effective and the headache disorder is in fact felt to be organic in etiology, due to the long-term side-effects of these drug classes. Nonsteroidal antiinflammatory drugs can be used for both prophylaxis and abortive therapy, the latter including menstrual migraine. Midrin®, which is an acetaminophen-containing compound (acetaminophen-isometheptene-dichloralphenazone) has also been used for migraine headache management, but typically works better for tension type headaches (2,3,15).  

            Symptomatic medications are typically used for decreasing symptoms associated with nausea and emesis that may accompany migraine headaches. Traditionally, the drugs that are used for symptomatic management include prochlorperazine (Compazine) and promethazine (Phenergan), which may be given orally or via other route such as rectal suppository. Metoclopramide (Reglan) and domperidone (Motilium) are also used as adjutants either orally or intravenously for symptomatic control and will also facilitate intestinal drug absorption.

Tension Headaches

            Acute pharmacotherapy of tension-type headaches should include non-steroidal anti-inflammatory drugs (including acetylsalicylic acid) sometimes in conjunction with caffeine, sedatives, and/or tranquilizers. There is no scientific evidence to support the use of muscle relaxants. Prophylactic pharmacotherapy for tension-type headache is more diversified and without any FDA-approved drugs currently endorsed. Tricyclic antidepressants, tizanidine, botulinum toxin, and venlafaxine (the latter a SNRI) have all shown at least some benefit, with TCAs having the best evidence basis (15).

Neuritic and Neuralgic Headache   

            Drug management of post-traumatic neuritic and neuralgic pain tends to emphasize focal injection therapies and topical agents. Secondary interventions may include enteral medications, such as non-steroidal antiinflammatory drugs, tricyclic antidepressants, SNRIs, such as duloxetine, or anticonvulsants, such as carbamazepine, gabapentin, and pregabalin. For focal post-traumatic neuropathies involving larger nerves of the face, scalp and/or craniocervical junction, focal injection therapy remains the mainstay of treatment, although serial injections may be necessary to abate the pain generator. With more diffuse, neuritic pain associated with scalp injuries such as post craniotomy pain or local blunt trauma neuritic scalp pain, compounded topical formulations should be considered. Such topical agents, typically applied as an ointment or gel, generally need to be applied three to four times per day to be optimally effective. Topical agents for neuropathic pain may include TCAs, local anesthetic, NSAIDs, AEDS such as gabapentin, clonidine, and ketamine hydrochloride, among other agents (2,3,15). For information on local and/or regional compounding pharmacies see http://www.pcab.info/find-a-pharmacy.shtml.

Myofascial Pain-Related Headaches

            Pharmacologic interventions for myofascial pain, although traditionally not first-line treatment, include non-steroidal antiinflammatory drugs, tricyclic antidepressants, and possibly, muscle relaxants. Muscle relaxants have no proven efficacy, although some resemble TCAs in their structure and clinical effect and may contribute to treatment efficacy. Antispasticity drugs are seldom used for myofascial pain, although tizanidine may have some theoretical benefit over other traditional antispasticity agents due to its antinociceptive properties garnered through its effect on blocking of substance P (3,15).

Medication Overuse Headache

Medication overuse headache (MOH) may be seen from excessive use of a variety of analgesic and/or abortive headache agents including ergotamines, opiates, caffeine, triptans, and/or barbiturates.  Overuse of these medications may lead to development of increased headaches and even chronic daily headache. Patients may become dependent on these symptomatic headache medications. Drug withdrawal, particularly when abrupt, normally results in worsening of headache. Alternatively, if MOH is a concern, the offending medication should be slowly weaned with concurrent alternative headache management options prescribed.  Headache medication overuse may also make headaches refractory to prophylactic headache medication and the affected person more sensitive to headache triggers (3,15).

Conservative treatment options can also be especially useful for managing post-traumatic headaches that have a cervicogenic component. Physical therapy, chiropractic, osteopathic, and craniosacral therapies have all shown efficacy at reducing cervicogenic headache frequency and intensity in appropriately selected patients (3,13,16,17).

Natural History, Prognostic Factors, and Outcome

            There are inadequate evidence-based studies to stipulate the natural history, prognostic factors and long term outcomes of PTHA, in part, because PTHA is not one single pathophysiological disorder but rather a symptom descriptor that may involve multiple pain generators/causes including psychogenic ones. Additionally, there are major methodological flaws including an absence of pain-reporting validity measures of any kind, lack of identification of secondary gain incentives and a relative over-reliance on using the International Headache Society (IHS) headache classification system as the only method to categorize headache subtypes (9,18).

            The relative lack of prospective, controlled, and blinded studies only further challenges our collective ability to accurately diagnose and treat this group of patients. There are also multiple methodological challenges in studying an impairment that is predominantly based on subjective patient reporting, including issues of misattribution bias (on the part of the patient as well as the assessing clinician), patient recall bias, nocebo effects of the diagnosis, and potential response bias relative to symptom amplification as well as minimization (depending on incentives) regarding pain reporting and/or associated pain related disability, among other issues (2,19).  

            Any study of chronic PTHA must also address the inherent co-morbidities of the psychological and medical effects of chronic pain (and the associated stress) on not only the patients reporting of their pain but also on a myriad of other aspects of function including cognition, behavior, and sleep (13,19). The majority of the studies to date have not based conclusions on comprehensive physical assessments that integrate neurological and musculoskeletal assessment. Additionally, studies have not linked specific exam findings with current headache classification systems (the latter which have been criticized relative to their lack of applicability and relevance to this particular population) (2,9).

            Based on the available studies, headache tends to improve in the months following trauma, whether to the brain, head, or neck. Appropriate and timely treatment shortens the period of impairment, associated disability, lost work hours, and pain and suffering (20,21).  

            At least some evidence indicates that ongoing litigation has little effect on the persistence of headache complaints (22). Specifically, studies have shown that patients still continue to report significant symptoms even after litigation has ended. The work in this area is limited and further research to confirm the findings of prior studies is recommended. A small number of patients will develop intractable, severe post-traumatic headache; however, this group of patients has been poorly studied and the influence of non-organic and/or psychogenic factors in such patients remains unclear (3,21). When properly diagnosed and treated, most PTHAs are able to be cured (particularly when addressed earlier than later), or substantively modulated. Most PTHA will not likely be disabling over the long term, and work disability due to PTHA is very uncommon in the hands of a sophisticated practitioner with a good treatment team, unless there are secondary gain incentives at work.

            PTHA prognosis must be based on an exact understanding of headache etiology (based on history and focused examination), overlay as relevant of psychogenic factors (including patient pre-injury characterological issues) and secondary gain incentives, response to appropriate historical treatment, and consideration of whether the correct treatment for the pain generator was ever instituted at all.

Patient Education

            Patients, as well as significant others/caretakers, need to understand the goals of pharmacotherapy. Education should be provided regarding all relevant aspects of treatment including expected outcomes, potential drug interactions, as well as side-effects, importance of medication compliance, and adequate trial duration, among other issues. Clinicians should remain accessible for questions or concerns.

Conclusions

            PTHA is ultimately a symptom and not a diagnosis. This complex disorder has multiple potential causes, and, as a result, has multiple potential ways to address the pain that is associated with the underlying pain generators. Assessing and treating PTHA is a process that requires adequate time commitment and knowledge by the treating clinician. Some will consider this “a pain” and if that is the case, then those clinicians should defer treatment to others who make it their business to assess and treat these types of patients. Pejorative and potentially self-prophesising labels such as “chronic PTHA” are often a misnomer due to the fact that the actual pain generators were never diagnosed correctly in the first place. Ideally, such labels should be avoided. There is in fact hope for those with PTHA regardless of how long they have suffered from pain. The challenge is finding clinicians who understand the disorder and have experience in holistic assessment and treatment of patients who have been traumatized including those with TBI, cranial trauma, and whiplash injuries.

Figure 1.

Anatomy of the upper posterior cervical region with specific reference to C2 terminal branches of the greater and lesser occipital nerves.

Reprinted with permission from Zasler, ND, Katz, DI, Zafonte, RD (eds): Brain Injury Medicine: Principles and Practice, Second Edition, Demos Medical Publishing, 2013.

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 with permission from Zasler, ND, Katz, DI, Zafonte, RD (eds): Brain Injury Medicine: Principles and Practice, Second Edition, Demos Medical Publishing, 2013.

Figure 3.

Referred myofascial pain patterns from activated trigger points in the cervical and shoulder girdle musculature

Sternocleidomastoid

Upper Trapzius

Multifidi

Splenius Capitis and Cervicis

Reprinted and modified with permission from Zasler, ND, Katz, DI, Zafonte, RD (eds): Brain Injury Medicine: Principles and Practice, Second Edition, Demos Medical Publishing, 2013.

Table 1.

PTHA headache historical points for inquiry.

  • 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 (e.g., pain faces).
  • “COLDER” mnemonic – character of pain, onset, location, duration, exacerbation, and relief.
  • 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 genetic loading risk factors for PTHA/PCH such as 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.

Reprinted and modified with permission from Zasler ND: Sports concussion headache: A Review. Brain Injury. 2014. Oct 7:1-14. [Epub ahead of print]

References

1.     Lucas S, Hoffman JM, Bell KR, Dikmen S. A prospective study of prevalence and characterization of headache following mild traumatic brain injury. Cephalalgia. 2014;34(2):93-102. doi:10.1177/0333102413499645.

2.     Zasler ND, Martelli MF, Jordan B. Post-concussive headache. In: Textbook of Concussion and Traumatic Encephalopathy. Cambridge University Press; In Press.

3.     Horn LJ, Siebert B, Patel N, Zasler ND. Post-traumatic headache. In: Zasler ND, Katz D, Zafonte RD, eds. Brain Injury Medicine : Principles and Practice. 2nd ed. Demos, New York: Demos Medical Publishing, LLC; 2013:932-953.

4.     Zasler ND. Sports concussion headache. Brain Inj. 2015;29(2):207-220.

5.     Dobscha SK, Clark ME, Morasco BJ, Freeman M, Campbell R, Helfand M. Systematic Review of the Literature on Pain in Patients with Polytrauma Including Traumatic Brain Injury. Pain Medicine. 2009;10(7):1200-1217.

6.     Walker RL, Clark ME, Nampiaparampil DE, et al. The hazards of war: blast injury headache. J Pain. 2010;11(4):297-302.

7.     Zasler ND. Post-traumatic pain. In: Zollman FS, ed. Manual of Traumatic Brain Injury Management. 1 edition. New York, NY: Demos Medical Publishing; 2011.

8.     Russo A, D’Onofrio F, Conte F, Petretta V, Tedeschi G, Tessitore A. Post-traumatic headaches: a clinical overview. Neurol Sci. 2014;35 Suppl 1:153-156.

9.     Zasler ND: Post-traumatic headache, caveats and controversies. Journal of Head Trauma Rehabilitation. 1999;14(1):1-8.

10.   Becker WJ. Cervicogenic headache: evidence that the neck is a pain generator. Headache. 2010;50(4):699-705.

11.   Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of chronic cervical zygapophysial joint pain after whiplash. Spine. 1995;20(1):20-25; discussion 26.

12.   Aprill C, Mb ADB, Mb NBB. Cervical Zygapophyseal Joint Pain Patterns II: A Clinical Evaluation. Spine. 1990;15(6):458-461.

13.   Zasler N, Martelli MF, Nicholson K. Post-traumatic pain disorders: Medical Assessment and Management. In: Zasler ND, Katz DI, Zafonte RD, eds. Brain Injury Medicine: Principles and Practice. 2nd ed. Demos, New York: Demos Medical Publishing, LLC; 2013:954-973.

14.   Steilen D, Hauser R, Woldin B, Sawyer S. Chronic neck pain: making the connection between capsular ligament laxity and cervical instability. Open Orthop J. 2014;8:326-345.

15.     Zasler ND. Pharmacotherapy and post-traumatic cephalalgia. J Head Trauma Rehabil. 2011;26(5):397-399.

16.   Racicki S, Gerwin S, Diclaudio S, Reinmann S, Donaldson M. Conservative physical therapy management for the treatment of cervicogenic headache: a systematic review. J Man Manip Ther. 2013;21(2):113-124.

17.   Liu L, Huang Q-M, Liu Q-G, et al. Effectiveness of Dry Neeedling for Myofascial Trigger Points Associated with Neck and Shoulder Pain: A Systematic Review and Meta-analysis. Arch Phys Med Rehabil. 2015. doi:10.1016/j.apmr.2014.12.015.

18.   Monteith TS, Borsook D. Insights and advances in post-traumatic headache: research considerations. Curr Neurol Neurosci Rep. 2014;14(2):428.

19.   Martelli M, Zasler ND. Post-traumatic pain disorders: Psychological Assessment and Management. In: Zasler ND, Katz D, Zafonte RD, eds. Brain Injury Medicine: Principles and Practice. 2nd ed. Demos, New York: Demos Medical Publishing, LLC; 2013:974-989.

20.   Hoffman JM, Lucas S, Dikmen S, et al. Natural history of headache after traumatic brain injury. J Neurotrauma. 2011;28(9):1719-1725.

21.   Packard RC, Ham LP. Posttraumatic headache: determining chronicity. Headache. 1993;33(3):133-134.

22.   Packard RC. Post-traumatic headache: permanency and relationship to legal settlement. Headache. 1992;32(10):496-500.

Websites of Interest

American Council for Headache Education. www.achenet.org

National Headache Foundation. www.headaches.org

The American Council for Headache Education provides a listing of on-line and local support groups. www.achenet.org

An online headache diary is available at http://www.achenet.org/your/diary1.php