Post traumatic Headache
© American Psychiatric Publishing
Headache is a common problem following traumatic brain injury (TBI) as well as head or neck trauma. It is especially common in the early postinjury period but may persist for months or years thereafter. Although headache is often associated with other postconcussive symptoms, it may dominate the clinical picture in some individuals. Whether as the presenting symptom or a key comorbidity in a patient with multiple acute or persistent postconcussive symptoms, headache contributes importantly to distress and functional limitations among persons with TBI. In this chapter, we offer a brief review of posttraumatic headaches, beginning with the definition, epidemiology, and pathophysiology of this condition. We then describe the assessment and management of posttraumatic headache, with special focus on the management of headache among Veterans with polytrauma and persons with severe TBI, including those with communication impairments.
Definition
The classification system of the International Headache Society (Headache Classification Subcommittee of the International Headache Society 2004) has a distinct category for posttraumatic headaches, which encompasses headaches associated with head and neck trauma. This classification system is based on a medical model and may not fully capture the complexity of posttraumatic headaches (Zasler 1999). Posttraumatic headaches usually develop within 7 days of head trauma or return of consciousness following TBI. Occasionally, the onset of headaches may be delayed by weeks to months. The most frequent types of civilian head trauma also injure the cervical spinal cord and neck musculature. Pain can originate from both the head and the neck.
Posttraumatic headaches often have features of other headache types. The most common patterns of posttraumatic headaches resemble tension, cervicogenic, and migraine headaches. Other less common headache types that will not be further discussed include epilepsy-related headache; cluster headache; paroxysmal hemicrania; dysautonomic headache; cavernous sinus headache; carotid artery cavernous sinus fistula headache; tension pneumocephalus headache; posttraumatic sinus headache; retro-orbital headache; and other headache types associated with upper cervical pathology producing myofascial injury or occipital nerve injury (Zasler 1999). Posttraumatic headaches can have a pattern of mixed headaches, with features of more than one primary type of headache.
The majority of civilian posttraumatic headaches can be classified as tension-type or cervicogenic headaches, with the fraction of tension headaches being as high as 85% (Evans 2004). Tension headaches meet at least two of the following four criteria: 1) bilateral pain, 2) pain that is pressing or tightening but not pulsating, 3) mild to moderate pain intensity, or 4) pain that is not aggravated or is only minimally aggravated by physical activity. Tension headaches are not accompanied by nausea or vomiting. Tension headaches may be accompanied by either phonophobia or photophobia, but not both. (Note that in this chapter, we refer only to photophobia rather than photosensitivity; the latter describes an aversion to light, whereas photophobia also can include a sensation of eye pain.) During a tension headache, patients may have tenderness of pericranial muscles. Among individuals who experienced tension headaches prior to head trauma, posttraumatic tension headaches are associated with an increase in headache frequency or intensity or a change in the pain pattern following head trauma. Most headaches resolve within 3 months, but the condition will persist indefinitely for a significant minority of individuals (McCrea and American Academy of Clinical Neuropsychology 2008).
Cervicogenic pain is focused in the neck and occipital region of the head. It is often associated with palpable contraction of posterior cervical muscles and can be partially alleviated by cervical massage or heat applied to the neck. In our experience, topical treatments that may increase blood flow to skin and underlying muscle can reduce pain. Cervicogenic pain can be increased by neck movement, particularly extreme forward flexion or rotation. In contrast, tension headaches have a pattern of pain that is bandlike and temporal, or perceived as behind the eyes. Tension headaches can also be perceived as a holo-cephalic pressure or as if a belt or cap is tightening about the head. Both cervicogenic and tension headaches are usually characterized by a dull, aching type of pain. Individuals with head and neck trauma may have features of both cervicogenic pain and tension headaches.
Most cases of posttraumatic migraine headaches resemble migraine without aura (common migraine). The criteria for migraine are recurrent episodes of pain lasting 4–72 hours with at least two of the following four characteristics: 1) unilateral pain, 2) pulsating quality, 3) moderate or severe intensity, or 4) exacerbation caused by or causing avoidance of routine physical activity. In addition, migraines have at least one of the following characteristics: 1) nausea, vomiting, or both, or 2) phonophobia or photophobia. Among individuals who experienced migraine headaches prior to head trauma, posttraumatic migraine headaches are associated with a definite increase in headache frequency or intensity or change in the pain pattern following head trauma. In civilian populations, posttraumatic migraine headaches typically resolve within 3 months (McCrea and American Academy of Clinical Neuropsychology 2008). Mixed migraine tension headaches have features of both headache types. Headaches associated with combat-acquired TBI are often mixed migraine tension headaches in character and complicated by coexistent stress disorders, such as posttraumatic stress disorder (PTSD), depression, and sleep disorders (Ruff et al. 2008, 2009).
Epidemiology
The prevalence of posttraumatic headaches differs for TBI in a civilian setting versus TBI in a combat setting. Among civilians, 15.34% with mild TBI (mTBI) had persistent posttraumatic headache at 3 months compared to 2.2% among controls with minor non-TBI injury (Faux and Sheedy 2008). In contrast, 52%–55% of combat Veterans had headaches more than 1 year after combat-related TBI (Lew et al. 2009; Ruff et al. 2008).
Among civilians and Veterans, prevalence of pain, particularly posttraumatic headache, is inversely related to TBI severity (Theeler and Erickson 2009). Uomoto and Esselman (1993) found that 95% of individuals with mTBI reported pain, predominantly headaches, whereas only 22% of those with moderate to severe TBI did so. Patients with poor cognitive recovery may have a lower incidence of headaches because pain perception is related to the integrity of cognitive function (Formisano et al. 2009). Additionally, pain may be underrecognized in people with poor cognition. Skull fracture or meningeal laceration predisposes to headache (Clark et al. 2009; Gironda et al. 2009; Lew et al. 2009).
The character of posttraumatic headaches differs between civilian-sustained TBI and combat-acquired TBI associated with Operation Iraqi Freedom (OIF)/Operation Enduring Freedom (OEF). Posttraumatic headaches associated with mTBI acquired in a civilian setting are usually tension or cervicogenic headaches, whereas headaches following mTBI in combat have features of migraine in 60% of individuals (Ruff et al. 2008; Theeler and Erickson 2009).
Posttraumatic headache prevalence varies with time after the injury. At 1 month following injury, rates of headaches range from 31.3% (Keidel and Diener 1997) to 90% (Rutherford et al. 1979). At 3 months postinjury, which corresponds to the threshold criterion for diagnosis of chronic posttraumatic headache (Headache Classification Subcommittee of the International Headache Society 2004), the rates have been found to be as high as 78%. At 6 months, prevalence ranged up to 44% (De Benedittis and De Santis 1983). Four years following injury, 20%–24% of civilians with TBI still reported headaches (Keidel and Diener 1997). Civilians with prolonged posttraumatic headaches often have complex psychosocial problems that compromise recovery (Martelli et al. 1999).
Combat TBI differs from civilian TBI in several ways. Current combat TBI is often caused by explosions that produce injuries to multiple body areas (i.e., polytrauma). Blast-associated injuries can include sequels of pressure-wave exposure, shrapnel injuries, traumatic amputation, and physical displacement injuries. Concurrent nociceptive and neuropathic pain conditions are common (Clark et al. 2009). Nociceptive pain results from tissue injury, whereas neuropathic pain results from alterations to the central or peripheral nervous systems involved in pain transmission or modulation. Neuropathic pain can have an electric-like character. OIF/OEF soldiers injured by combat-related blasts had less improvement in pain intensity than did soldiers with other types of combat injuries or those injured in noncombat situations, despite equivalence in TBI frequency and severity (Clark et al. 2009). Additionally, combat troops who do not experience physical trauma as a consequence of blast exposure may be subjected to repeated blasts throughout their tours of duty, possibly incurring unidentified mTBIs.
The psychosocial context in which injuries occur can affect the consequences of TBI. Comorbid psychiatric conditions, particularly PTSD, develop in association with combat TBI (Clark et al. 2009; Lew et al. 2009; Ruff et al. 2008, 2009). Comorbid PTSD occurred in about 40% of military personnel and Veterans with combat-acquired mTBI (Gironda et al. 2009; Lew et al. 2009), in contrast to about 6% of civilians with mTBI (Bryant et al. 2010). Soldiers with mTBI were more likely to report persisting headache than were soldiers with other injuries (Hoge et al. 2008). Combat TBI and PTSD challenge reintegration into society (Roberts 2008). Individuals with psychiatric conditions are known to experience higher levels of pain-related disability and poorer outcomes (Breslau et al. 2003).
Pathophysiology
The pathophysiology of headaches is poorly understood. Cervicogenic head and neck pain is associated with injuries to cervical paraspinal muscles and vertebrae (Kaniecki 2003). Posttraumatic headaches may be associated with the existence of hypersensitivity of central pain processing networks. Patients with tension headaches experience more intense pain in response to noxious stimulation to the face and have lower pain thresholds (Ashina 2004), and central sensitization is implicated at the level of the upper cervical spinal dorsal horns and trigeminal nuclei (Bendtsen 2000). Brain trauma may precipitate tension headaches by injuring the central pain modulation pathways that disrupt normal mechanisms for suppressing pain.
The impact of nervous system trauma on the genesis of pain has been most extensively studied in spinal cord injury, which may provide insight into TBI pain. Classes of neuronal sodium (Na+) channels differ in their properties. Increasing Nav1.3 channel expression causes neuronal hyperexcitability. Trauma upregulates Nav1.3 channels in thalamic neurons involved in pain transmission and pain modulation (Waxman and Hains 2006). Maintenance of pain after trauma and upregulation of Nav1.3 channels result from activation of microglia that produce prostaglandin (PGE2) (Zhao et al. 2007). Decreasing PGE2 production reduces Nav1.3 channel expression and diminishes pain (Zhao et al. 2007).
TBI may trigger or rekindle migraine due to damage to meningeal blood vessels or injury-induced neuronal hyperexcitability. Migraine is currently seen as a neurovascular disorder with the primary dysfunction in the central nervous system. Altered cerebral activity changes the activation of pain-producing intracranial meningeal structures that give rise to headache pain (Hargreaves and Shepheard 1999). Episodes of migraine are associated with trigeminal nerve activation of pain-sensitive meningeal structures (Bolay et al. 2002). TBI also may injure the meninges and alter the trigeminal communication with the meninges. By mechanisms similar to those of tension headaches, injury to excitable elements of the meninges may produce a hyperexcitable state, leading to migraine.
Migraine is also associated with cortical hyperexcitability to auditory and visual stimuli (Coppola et al. 2007). The phenomenon of cortical spreading depression entails a wave of cortical excitation moving over the cortex, followed by reduced cortical excitability (Mulleners et al. 2001). Spreading depression is most prominent in the occipital cortex. The occipital poles are particularly vulnerable to injury due to TBI, and perhaps injury-induced hyperexcitability facilitates spreading depression. Thalamocortical traffic is increased during attacks of migraine (Coppola et al. 2007). Thalamocortical activity is associated with pathological trigeminal stimulation of the meninges. The trigeminal sensory fibers release substance P, which is a small neuropeptide that is both a neurotransmitter and a pro-inflammatory agent. Meningeal inflammation contributes to migraine pain (Bolay et al. 2002).
Clinical Assessment
A diagnosis of posttraumatic headache requires a standard comprehensive clinical interview (Sherman et al. 2006). When a patient complains about headache, the history taking should focus on eliciting details about the character of the headache pain, its speed of onset, location(s), and duration, as well as factors that exacerbate or relieve it. The acronym COLDER—for character, onset, location, duration, exacerbation, and relief—may serve as a useful reminder of these elements of the headache history (Zafonte and Horn 1999). History taking also seeks to identify environmental triggers or other antecedents to the headache, prodromal symptoms, and headache-associated symptoms (e.g., photosensitivity or sonosensitivity, photophobia or sonophobia, eye pain, tearing, nausea, vomiting, dizziness, fatigue). The frequency of headaches, their course, and their relationship to TBI are noted as well.
Other conditions that may exacerbate headaches, including sleep disturbances, depression, and anxiety, among others, should be identified. Although headaches are the primary pain condition following combat-acquired TBI (Clark et al. 2009; Gironda et al. 2009; Lew et al. 2009), they commonly are accompanied by other postconcussive symptoms, such as fatigue; memory, attention/concentration, and executive functioning deficits; and emotional distress (Clark et al. 2009; Ofek and Defrin 2007). Premorbid personal and family headache histories also may be diagnostically informative.
A thorough physical examination is an essential element of the headache assessment (Zafonte and Horn 1999). The examination focuses first on observation and palpation of the head, face (including temporomandibular joints), mouth, neck, and shoulder girdle. The posture in which the head, jaw, neck, and shoulders are held is observed, and the range of motion of the head, jaw, and neck is assessed. Cranial nerve examination, including assessment of vision and hearing and all relevant reflexes, and auscultation of the blood vessels of the neck are performed. This problem-focused examination is followed by a thorough general physical and neurological examination.
Although neuroimaging or laboratory studies are commonly obtained in the evaluation of headache, they generally are not necessary (Silberstein 2000). History or examination findings suggesting headache of cervicogenic or musculoskeletal origin may be evaluated further using plain radiographs of the cervical spine. Among patients with nonacute presentations, clinical findings that increase the likelihood of abnormalities on neuroimaging studies (i.e., magnetic resonance imaging), and hence support their performance, include headaches with atypical features or characteristics that do not conform to the strict definitions of primary headache disorders; the presence of a comorbid medical condition that increases the risk for central nervous system abnormalities (i.e., immune deficiency, autoimmune disorder); rapidly increasing headache frequency; history of headache causing awakening from sleep; and, either by history or examination, unexplained focal neurological signs and/or impaired coordination (Silberstein 2000). Among patients with acute headache presentations, focal or progressive elemental neurological signs or symptoms, altered consciousness, increasing or extreme severity, nausea and/or vomiting, or nighttime occurrence suggests the need for neuroimaging evaluation (Sherman et al. 2006; Zafonte and Horn 1999).
The definitions of headache types described earlier in the section “Definition” are used to diagnose posttraumatic headache(s); Table 10- describes the characteristics of tension-like, migraine-like, and cervicogenic posttraumatic headaches. When the history and examination do not lead to a clear headache diagnosis, it may be useful for patients to develop a headache diary to record the frequency, intensity, duration, prodromal signs, and triggers of headaches. Use of this diary during treatment also should be encouraged, and individuals with cognitive deficits should be provided with assistance with this task.
Clinical Assessment Criteria for characterizing posttraumatic headaches as tension, cervicogenic, or migraine headaches
Headache type | |||
|---|---|---|---|
Headache feature | Tension | Cervicogenic | Migraine |
Pain intensity
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Mild to moderate
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Mild to moderate
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Often severe or debilitating
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Pain character
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Dull, aching, or pressure; sharp pain possibly present, but not predominant
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Similar to tension headaches
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Throbbing or pulsatile; can also be sharp/stabbing or electric-like
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Duration
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Less than 4 hours
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Less than 4 hours
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Can last longer than 4 hours
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Phonophobia or photophobia
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One but not both may be present
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Usually neither is present
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One or both often present
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Able to carry out routine activities or work
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Usually
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Usually
|
Usually not
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Location
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Bilateral—frontal, retro-orbital, temporal, or holocephalic
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Cervical and occipital
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Usually unilateral and may vary in location among episodes
|
Nausea or malaise
|
Not present
|
Not present
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May be present
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Palpable muscle tenderness
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Pericranial muscles including temporalis, masseter, pterygoid, sternocleidomastoid, splenius, or trapezius
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Posterior neck muscles
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Localized muscle tenderness not typical; possible muscle tenderness with long-duration headaches
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Note. Posttraumatic headaches can have features of more than one primary headache type.
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Treatment
Pharmacotherapy
Episodic tension or cervicogenic headaches
Episodic tension headaches usually respond to nonsteroidal anti-inflammatory drugs (NSAIDs). Pain treatment is more likely to be successful if the medication is taken at headache onset. Occasionally, opioid medications are required to treat severe tension headache; however, repeated use of opioid medication can lead to problems associated with dependence and may exacerbate cognitive and behavioral manifestations of TBI. Aspirin and acetaminophen are often combined with caffeine or a sedative drug in a single medication. Combination drugs may be more effective than NSAIDs or acetaminophen alone, but persistent usage may lead to rebound headaches and chronic daily headaches. Combinations of acetaminophen or aspirin and an opioid should be used with caution.
Individuals with more than three tension headaches per week may benefit from preventive treatments (Table 10-). Medications useful in reducing tension headache frequency include tricyclic antidepressants, NSAIDs, and acetaminophen; if the headaches are associated with anxiety, then anxiolytic medications also may be useful. Persistent usage of NSAIDs or acetaminophen may result in rebound headaches. Although other agents such as anticonvulsants have been used to prevent tension headaches, they have not been evaluated in controlled clinical trials. Poorly controlled tension headaches may indicate that attention should be directed to physical or psychological factors triggering headaches.
Treatments for migraine headaches include both abortive and preventive approaches. Medications used commonly for prophylaxis against recurrent migraine headaches are described in Table 10-. One of the authors of this chapter (R.L.R.) has observed β-blockers and topiramate to be the best prophylactic agents for posttraumatic migraine or mixed headaches in Veterans of OIF/OEF. These agents can improve the life quality of individuals with migraines (Garcia-Monco et al. 2007). β-Blockers are useful when headaches are associated with anxiety, and these medications typically do not impair cognition. There is anecdotal concern that β-blockers may worsen depression; however, careful analysis suggests that they do not cause depression (Huffman and Stern 2007). Because β-blockers may worsen sleep disorders and may intensify nightmares, sleep should be carefully monitored. If β-blockers are effective in reducing the frequency and intensity of headaches, but are associated with nightmares, the nightmares can be treated using prazosin (Raskind et al. 2007). Topiramate may be the first choice for Veterans with impaired sleep. The dose of topiramate needs to be increased slowly to minimize daytime somnolence and impaired cognition. Topiramate may potentiate neural repair (Follett et al. 2004). Weight loss, a potential side effect of topiramate, may benefit some patients.
Migraine-like headache Medications that may reduce the frequency of tension or cervicogenic headaches
Medication | Typical dosing | Side effects | Comments |
|---|---|---|---|
Tricyclic antidepressants
|
Amitriptyline 10–75 mg at bedtime
|
Weight gain, dry mouth, daytime somnolence
|
Most effective, but side effects limit utility
|
Nortriptyline 10–50 mg at bedtime
|
Somnolence, dry mouth
|
Fewer side effects, but may not be as effective as amitriptyline
| |
Antianxiety agents
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Lorazepam 25–50 mg twice daily
Clonazepam 10 mg two to four times daily
|
Sedation and habituation; possibility of dependency
|
Should be used on a time-limited basis for periods up to 4 weeks
|
Nonsteroidal anti-inflammatory drugs
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Choline-magnesium-trisalicylate 750 mg three times daily
Ibuprofen 400–600 mg three to four times daily
|
Potential for gastrointestinal upset
Renal damage possible from excessive use
|
Rebound headaches possible with regular usage, particularly of combination medications containing caffeine
|
Acetaminophen
|
250–500 mg three to four times daily
|
Liver damage can result from excessive use; avoid use in patients with hepatitis
|
Rebound headaches possible, particularly if agent combined with caffeine
|
Anticonvulsant medications
|
Topiramate 100–200 mg/day in two divided doses
Valproate 100–250 mg three times daily
|
Sedation, impaired cognition
Sedation, impaired cognition, and ataxia
|
Not shown to be effective for tension headaches; best used for headaches with migraine features
|
Migraine-like headache Medications used to prevent migraine headaches
Medication | Comment |
|---|---|
Amitriptyline 10–50 mg at bedtime, upper limit of 150 mg/day
|
Side effects include dry mouth, weight gain, and next-day sedation. Some side effects can be minimized by very gradually increasing the dosage.
|
Timolol 10–30 mg/day or propranolol 20–160 mg/day
|
Side effects include fatigue, lightheadedness, insomnia, bradycardia or exercise intolerance, depression, and sexual dysfunction. Agent should be avoided in patients with asthma, severe cardiovascular disease, insulin-dependent diabetes mellitus, and Raynaud disease. In Veterans with PTSD, ″-blockers may worsen nightmares. These agents are particularly useful when headache onset is associated with episodes of anxiety. Some literature suggests that ″-blockers can worsen depression, but more recent data suggest that ″-blockers do not trigger or worsen existing depression.
|
Topiramate 50–150 mg/day
|
Side effects are similar to those of divalproex, but in our experience, topiramate is better tolerated by Veterans with TBI. Side effects can be minimized by starting with 25 mg/day and increasing by 25 mg/day at weekly intervals up to 50–100 mg twice daily or until headaches are controlled.
|
Divalproex sodium 125–200 mg/day
|
Side effects of potential cognitive impairment and tremor can limit acceptability of this medication.
|
Methysergide 4–8 mg/day
|
Agent is rarely used due to concern about the side effect of retroperitoneal fibrosis. This side effect can be avoided if the medication is stopped for 1 month after 11 months of use. Advantage of this agent is that it is well tolerated aside from the potential serious side effect of retroperitoneal fibrosis.
|
Note. Medications are presented on the basis of evidence of their medium to high efficacy and mild to moderate side effects. PTSD = posttraumatic stress disorder; TBI = traumatic brain injury.
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Migraine-like headache Acute migraine interventions
Type of intervention | Specific agents used | Comment |
|---|---|---|
Medications
|
NSAIDs alone or combined with caffeine, isometheptene, or a sedative
|
These can be useful for moderate-intensity infrequent headaches. Repeated use may lead to rebound headaches.
|
Triptans
|
These are currently the first-line acute treatment, with several different preparations available. They may be combined with an antiemetic.
| |
Ergotamines (includes dihydroergotamine)
|
Some individuals get good response from injectable ergotamine.
| |
Tramadol
|
This agent is a mild agonist of the … opioid receptor. It is not a controlled substance. Sedation can limit utility. Some individuals respond well to tramadol alone or combined with acetaminophen.
| |
Oxygen inhalation
|
Typically provided as 2–4 L/minute via nasal prongs or mask
|
This is an effective intervention for some people with migraine. It is safe and has few side effects and will not induce rebound or overuse headaches. The limitation is that the individual may not have access to oxygen when a headache starts.
|
Note. In general, medications should be provided orally whenever possible. In cases of nausea and/or vomiting, medication administration via injection, suppository, or orally dissolving preparation is appropriate. NSAID = nonsteroidal anti-inflammatory drug.
| ||
Migraine-like headache Rescue interventions for migraine
Type of intervention | Specific agents used | Comment |
|---|---|---|
Medications
|
Ketorolac
|
Gastric protection against ulceration should be used because ketorolac can cause gastric ulceration.
|
Triptans or ergotamines
|
These agents are available in parenteral formulations, but may be ineffective for an advanced migraine attack.
| |
Tramadol
|
The side effect of sedation can be useful because migraine attacks can abate with sleep.
| |
Divalproex sodium
|
Intravenous administration of 500 mg can break a migraine.
| |
Butorphanol
|
The nasal inhalation formulation may abort a migraine attack.
| |
Opioids
|
Morphine sulfate 2–4 mg (or comparable dose of another parenteral opioid) can be useful in breaking a migraine attack. Regular usage can lead to habituation. These are restricted medications.
| |
Oxygen inhalation
|
Typically provided as 2–4 L/minute via nasal prongs or mask
|
This treatment can be given in conjunction with other interventions.
|
Note. In general, medications should be provided orally whenever possible. If nausea and/or vomiting are present, then medication administration via injection, suppository, or orally dissolving preparation is appropriate.
| ||
Effective abortive treatment (Table 10-) requires that individuals recognize their own headache warning signs. These may include a classic aura or prodromal symptoms such as changes in mood, onset of fatigue, sensory sensitivity, and difficulty with attention or concentration. Abortive treatment is more successful if treatment begins at headache onset. Prompt initiation of acute treatment also reduces the need for opioid medications to “rescue” patients from severe pain. If acute treatment is not effective, rescue treatments may be required to break the migraine (Table 10-). If rescue therapy is required on a regular basis, then prophylactic treatment is needed.
Acute migraine treatment must be used prudently to avoid inducing overuse or rebound headaches. Overuse headaches are typically tension-like. Overuse of opioid medication may contribute to the transformation from episodic to chronic migraine (Bigal and Lipton 2009). Treatment of medication-overuse headaches requires stopping daily use of acute treatments, which often results in withdrawal symptoms that include rebound headaches. In many cases, patients fall into a pattern of continued medication overuse in an effort to avoid rebound headaches. Headache diaries may reveal overuse. When patients are caught in a pattern of medication overuse, headaches are usually refractory to preventive medications. In most cases, headaches improve after an analgesic washout period. It is important to educate patients that acute migraine medication should be limited to three treatments per week.
Psychological and Behavioral Interventions
Tension and cervicogenic headaches
Tension and cervicogenic headaches associated with TBI may be resistant to medication alone. Patients may achieve better pain relief if medication is coupled with other treatments. Cognitive-behavioral interventions such as relaxation training and biofeedback can help individuals learn to identify tension and relax the muscles contributing to the tension headache. Physical therapy can be used to exercise neck muscles and maintain appropriate range of motion. Physical activity can reduce the frequency and intensity of tension headaches. Improving other psychiatric conditions, including depression and PTSD, also may reduce the frequency and/or perceived severity of headaches (Fann et al. 2000; Griffith 2009; Peterlin et al. 2009).
Cognitive-behavioral interventions for headache conditions produce headache relief comparable to that from medication (Holroyd et al. 2009). Education regarding headaches and wellness may help to correct pain-related cognitive distortions, encourage proactive self-management, and promote an increased sense of control over the headache conditions. Finally, because individuals with recent onset of posttraumatic headache are at risk for transformation to treatment-resistant chronic daily headache conditions, patients should be educated about analgesic overuse.
Spinal manipulation can be used to treat cervicogenic pain if the neck is mechanically stable. A review of nine studies that tested spinal manipulative therapy for tension headaches concluded that spinal manipulation is comparable in benefit to medications used for the prevention of tension headaches (Bove and Nilsson 1998).
Migraine headaches
Effective treatment for posttraumatic migraine headaches typically requires the use of a combination of acute and preventive medications and nonpharmacological prevention strategies, including lifestyle regulation, stimulant reduction, and trigger avoidance. Cognitive-behavioral migraine intervention should include a focus on identification and avoidance of migraine triggers. Common headache risk factors and triggers include sleep disruption; increased time between meals; stress; and specific foods, beverages, and odors. Other nonpharmacological treatments commonly employed are extracranial pressure and cold compresses. Regular exercise, sleep, and meal schedules are also an important part of the treatment regimen. Oxygen inhalation can also be used to abort an acute migraine or as a migraine rescue treatment (see Tables 10- and 10-).
Sleep problems
Obtaining deep, restful sleep may be particularly important for individuals with posttraumatic headache. Sleep disorders commonly develop after TBI. For individuals with moderate to severe TBI, sleep disorders include hypersomnia, insomnia, and impaired breathing during sleep, including sleep apnea (Orff et al. 2009). Individuals with mTBI may suffer from interrupted sleep in association with posttraumatic stress reactions, including PTSD (Ruff et al. 2009). Prazosin successfully blocks nightmares and other sleep interruptions caused by PTSD (Raskind et al. 2007). In an observational study of OIF/OEF Veterans with mTBI due to combat explosions, prazosin treatment combined with sleep hygiene counseling was able to reduce headache frequency and severity (Ruff et al. 2009). Healthy sleep patterns facilitate synaptic homeostasis (Tononi and Cirelli 2003) and other processes that contribute to cerebral plasticity (Jha et al. 2005), which will enhance the ability of the brain to adapt after traumatic injury.
Headache Management in Patients With Communication Impairments
The assessment of pain in patients with communication impairments is challenging (Weiner and Herr 2002). Patients with impaired cognition and communication due to TBI may not be able to convey pain complaints. The interaction between pain and cognitive symptoms may exacerbate functional impairments and impede response to treatment (Ivanhoe and Hartman 2004). Pain assessment in patients with severe brain injury has received little attention. One may adopt assessment techniques used to assess pain in people with dementia (Collett et al. 2007).
Initial effort should be directed toward determining whether a patient can use some form of self-report to communicate the existence of pain and its intensity. Neuropsychological and speech-language testing can be used to assess a patient’s abilities to provide self-report, to identify specific deficits to consider in the assessment, and to recommend strategies for obtaining valid information. Patients with mild to moderate cognitive impairment often can respond reliably to standard measures of pain intensity (Chibnall and Tait 2001). Reliability of self-report scales can improve with practice. Clinicians should question patients specifically about headaches because patients may not report having headaches when asked only about their experience of “pain.”
Behavioral observation can validate a patient’s self-report and help assess pain when the patient is unable to reliably provide self-report information. Family members or caregivers familiar with the patient’s behavior can recognize behavioral changes that indicate pain (Weiner and Herr 2002). Behavior patterns include facial expressions, verbalizations or vocalizations, body movements, changes in interpersonal interactions, changes in activity patterns or routines, and mental status changes.
Empirical trials of analgesic medication can be used to assess pain. These trials should be done in conjunction with other methods of assessment to evaluate whether the behaviors indicate appreciable pain (Gallagher et al. 2006). Some analgesics can negatively impact cognitive status, and this risk should be evaluated throughout the course of a trial to minimize effects on overall treatment. Unfortunately, no consensus exists on the best pain assessment tools to use for individuals with cognitive impairment.
Conclusion
Posttraumatic headaches are among the most common acute and chronic problems experienced by persons with TBI. These headaches may be associated with other postconcussive symptoms or may be the principal feature of the patient’s clinical presentation. Posttraumatic headaches contribute importantly to distress and functional limitations among persons with TBI, and are an important focus of treatment. Clinical assessment includes detailed history taking and headache characterization. Examination of the head, neck, and shoulder regions is complemented by physical and neurological examination and, in selected cases, neuroimaging and other laboratory studies. The treatment of posttraumatic headaches is organized according to their clinical phenotypes, the most common of which are tension, cervicogenic, and migraine headaches. Treatments include pharmacotherapy as well as psychological and behavioral interventions that target headaches and associated comorbidities (e.g., depression, anxiety, PTSD, sleep disturbances). The assessment and management of posttraumatic headaches may require modification to meet the needs of individuals with polytrauma as well as persons with severe TBI.
Key Clinical Points
- Posttraumatic headaches represent a secondary headache disorder developing with a temporal relationship to head trauma, and may have the typical clinical features of tension headache, cervicogenic headache, migraine headache, or a mixed type including features of different headache syndromes.
- Epidemiological studies have demonstrated that posttraumatic headaches have a higher incidence in Veteran populations compared with civilian injured populations; regardless of the setting of injury, headaches are more common after mild TBI than moderate or severe TBI.
- The pathophysiologies of posttraumatic headaches are not fully elucidated; however, peripheral mechanisms (e.g., injury to cervical paraspinal muscles) and central mechanisms (e.g., altered vascular reactivity, increased expression of hyperexcitable sodium channels in the thalamus) are suspected.
- Selection of the appropriate pharmacological agent to treat posttraumatic headaches is guided by the clinical characteristics of the headache (e.g., migraine, tension-type, cervicogenic). Care must be taken to avoid excessive use of headache-abortive agents, which may precipitate analgesic rebound headache.
- Cognitive-behavioral therapies for patients with posttraumatic headache focus on education about lifestyle factors affecting headaches, evaluation and identification of triggers, addressing stress and its impact on headaches, and, perhaps most importantly, addressing sleep hygiene issues.
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