Posttraumatic Headache

Thomas K. Watanabe

GENERAL PRINCIPLES

Definition

According to International Classification of Headaches Criteria, 3rd edition (ICHD-3), headaches (HAs) that develop within 1 week after head trauma (or within 1 week of regaining consciousness) are referred to as posttraumatic headaches (PTHs). PTH that last longer than 3 months is referred to as chronic or persistent PTH [1]. This definition may not be adequate in describing the incidence and prevalence of PTH (see section “Natural History”).

Epidemiology

• HAs may develop in up to 90% of patients with traumatic brain injury (TBI) [2].

• A systematic review found an aggregate prevalence of 57.8% [3].

• Risk factors include female gender and preinjury history of HA [4].

Natural History

• 28% of PTH in a moderate-severe civilian TBI population did not report HAs until more than 3 months after injury [4].

• Only 27% of returning war veterans who developed HAs after TBI had initial complaints in the first week after injury [5].

• Overall prevalence of 71% in the first year after moderate-severe TBI [4].

• Overall incidence of 91% in a civilian mild TBI population over the course of the first year postinjury [6].

Classification

• HAs are often classified based on their clinical features.

• Most studies identify migraines as the most common type of PTH in both mild and moderate to severe TBI populations. Tension-type HA is the next most common type [6,7].

• Less common—cervicogenic HA, neuritic pain, musculoskeletal HA, dysautonomic HA, sinus HA, posttraumatic cluster HA, and medication overuse HA.

• PTH may also present as mixed or difficult to classify.

• ICHD-3 classification does not differentiate based on clinical features: [1]

A. HA attributed to trauma or injury to the head and/or neck

1. Acute HA attributed to traumatic injury to the head

a. Acute HA attributed to moderate or severe traumatic injury to the head

b. Acute HA attributed to mild traumatic injury to the head

2. Persistent HA attributed to traumatic injury to the head

a. Persistent HA attributed to moderate or severe traumatic injury to the head

b. Persistent HA attributed to mild traumatic injury to the head

3. Acute HA attributed to whiplash

4. Persistent HA attributed to whiplash

5. Acute HA attributed to craniotomy

6. Persistent HA attributed to craniotomy

Pathophysiology

Pathophysiology is poorly understood and is likely often multifactorial. There are a number of potential sources of pain after head trauma, including injury to: bones, skin, nerves, dura, muscles, joints (cervical and mandibular), ligaments, and muscles. Central mechanisms, psychological factors, vascular changes, neuroinflammation and medications (including those being used to treat HA) may also play roles in generating pain [8]. The development of PTH may be a warning sign of a serious intracranial process (see section “Diagnosis”).

DIAGNOSIS

History

• Quality of pain—COLDER (character, onset, location, duration, exacerbation, relief).

• Ask about severity, frequency, temporal associations, and postural relationships.

• Associated symptoms—Nausea, vomiting, dizziness, visual dysfunction, and auras.

• Patients with family history of HA are more likely to develop PTH [9].

Clinical Presentation (Based on International HA Society Classification of HA)

Clinical presentation often comprises a hybrid rather than falling into only one of the following categories.

• Migraine HA—Throbbing, moderate-severe intensity, aggravated by activity, unilateral, lasts 4 to 72 hours, may be associated with nausea or vomiting, photophobia, and/or photophobia, may have aura. Basilar artery migraines can occur secondary to traction on the vertebral-basilar circulation from acceleration–deceleration injury.

• Tension-type HA—Moderate diffuse nonpulsating pain in forehead or temples, mild-moderate intensity, usually bilateral, often described as pressure, or band-like, which is not typically aggravated by activity. For episodic tension-type HA, either photophonia or photophobia may be seen, but not both, and without nausea or vomiting.

• Neuritic pain—Sharp, shooting, electric pain. Most commonly originating from greater or lesser occipital nerves, with pain located periocular and radiating from back to front of head.

• Musculoskeletal HA—“Cap-like” in quality, trigger points may be present. Patient may have history of skull fracture or bruxism.

• Cervicogenic HA—Typically originates in the cervical or occipital region and radiates rostrally. Often active trigger points can be identified, palpation of which reproduces the pain pattern.

• Dysautonomic HA—Unilateral episodic throbbing pain associated with autonomic changes.

• Sinus HA—Localized to the sinuses and associated with sinus tenderness.

• Temporomandibular joint dysfunction syndrome—Typically located in the temporal region; may be exacerbated by chewing or yawning. Clicking or malocclusion of the jaw may be appreciated [1].

Ominous Symptoms That May Indicate Intracranial Pathology

• Increased intracranial pressure (ICP)—worsening and constant cephalgia, associated nausea and vomiting, decreased arousal. May be secondary to a space-occupying lesion (e.g., bleed), tension pneumocephalus, hydrocephalus, or shunt failure.

• Low ICP—HA exacerbation in upright position. Usually secondary to overshunting or CSF leak.

• Acute or delayed vascular dysfunction (see also Chapter 58):

Carotid artery injury—severe and ipsilateral pain, involving orbital or periorbital regions.

Vertebral artery injury—severe pain in cervical or ipsilateral occipital regions, ipsilateral facial dysesthesia, vertigo, nausea/vomiting.

Carotid cavernous fistula—frontal HA, facial pain, chemosis, proptosis, and diplopia [9].

Physical Examination

• Comparison to baseline (whenever possible) is key.

• Migraine or tension HA—Likely normal neurological examination, but may have transient neurological changes during initial phase of a migraine attack.

• Neuritic HA—Palpation of affected nerve may reproduce HA pain.

Greater occipital nerve—best palpated below base of skull, off midline, pain referred to vertex.

Lesser occipital nerve—best palpated behind sternocleidomastoid, one-third of muscle length from mastoid; pain often radiates to mastoid, ear, and/or lower temple.

• Sinus HA—Sinuses may be tender with palpation.

• Musculoskeletal and cervicogenic HA—Identify trigger points that may reproduce pain; palpate paracervical and/or suboccipital muscles or muscles of mastication in temporomandibular joint. Pain may also be reproduced with cervical range of motion [9].

Ominous Examination Findings That May Indicate Intracranial Pathology

• Increased ICP—Deterioration in mental status, focal neurological deterioration, and papilledema.

• CSF leak—Clear rhinorrhea, otorrhea that may worsen with Valsalva.

• Vascular injury—External evidence of neck trauma, cervical carotid bruit, ocular bruit, sensory changes, visual deficits, and Horner’s syndrome.

• Infection—Fever, nuchal rigidity, purulent drainage from wound or postsurgical site [9].

Laboratory Studies

• Limited utility—If infection is suspected, CSF may be studied.

Radiographic Assessment

• In the absence of signs of increased intracranial pressure, new or worsening focal neurological deficits, bruits or meningeal irritation cerebral imaging is generally not warranted.

• If focal neurological findings are noted, computed tomography (CT) or magnetic resonance imaging (MRI) of the brain should be considered.

• Increased ICP—CT of brain is imaging of choice because of the ease of obtaining study, and will also identify cerebral swelling and pneumocephalus. If situation is not acute, MRI is more sensitive.

• Vascular injury—MRI or MRA of neck will assess blunt carotid trauma. Ultrasound can also detect vascular lesions and vasospasm but is limited by technique. Angiography may be considered in selected cases (e.g., as a preop assessment).

• Infection—CT or MRI with contrast can identify abscesses.

• Musculoskeletal HA—Consider C-spine plain films (lateral, open-mouth, flexion-extension); C-spine MRI if disc disease is suspected and symptoms are not responsive to conservative measures.

• Sinus HA—CT can be used to evaluate for sinusitis, and anatomic or structural problems [9].

TREATMENT

Guiding Principles

• There is insufficient evidence to support any particular treatment protocol.

• Interventions should be based on HA phenotype; migraine HA is the most common type in most TBI populations.

• For HAs because of identified intracranial pathology, address the underlying pathology directly.

• Evaluate for depression or other psychological factors, including PTSD, which may contribute to HA frequency and severity [10].

• Identify and counsel patient on PTH triggers—including, for example, sleep, caffeine, stress, exercise, or diet [11].

Initial Management

• Consider the need for evaluation for acute intracranial pathology [2]

• Categorize HA phenotype

• Consider time-limited use of opioid medications for severe HA (see section “Pharmacological Treatment” for discussion of precautions with use in this patient population)

• Consider time-limited use of acetaminophen or nonsteroidal anti-inflammatory medication for mild-moderate HA

• For HA’s that meet the criteria for migraine, start with a trial of a triptan, provided there are no contraindications (e.g., complicated migraine, cardiovascular disease)

• For HA’s that are associated with cervical spine pain, consider a referral to physical therapy that may include gentle cervical range of motion exercises without resistance and modalities to decrease symptoms once structural spine pathology has been ruled out

• Identify and address existing comorbidities that may be contributing to symptoms such as sleep dysfunction, stress/anxiety, visual problems and inadequately treated pre-existing HA disorder

Ongoing Care

• Re-evaluate the need to evaluate for intracranial pathology [2]

• (Re)-categorize HA phenotype

• For HA’s that meet criteria for migraine/probable migraine, assess efficacy and frequency of use of abortive medication; consider trial of different type if not efficacious (including a different triptan if one has been trialed previously). If patient experiencing more than 8 migraine HA’s per month, initiate trial of prophylactic migraine HA medication.

• For any HA type, if there is evidence of muscle tension or cervicogenic component, initiate physical therapy including cervical flexibility, strengthening and endurance exercises, manual therapy, neuromuscular re-education, home exercises, and aerobic conditioning.

• Consider behavioral therapy interventions.

Nonpharmacological Treatment

• Cognitive behavioral therapy, relaxation, education, and biofeedback have shown favorable results in uncontrolled studies [2].

• Physical therapy may be useful if the PTH is caused by musculoskeletal or biomechanical dysfunction [2]. Myofascial pain can be addressed with trigger point injections [11].

• Neuritic pain may respond to local anesthetic block of the affected nerve, most commonly the greater occipital nerve [12].

• Acupuncture has been shown to be effective as both an abortive and a prophylactic management approach for migraine HAs and for tension HA [13,14].

Pharmacological Treatment

Abortive Agents

• NSAIDs—can be effective for musculoskeletal HA, migraine HA, and tension HA [11,15–18].

• Muscle relaxants—use not supported; may worsen concomitant cognitive deficits.

• Acetaminophen—effective for musculoskeletal and tension HA.

• Opioids—consider time-limited use for severe, functionally disabling pain, with caution due to high-abuse potential and risk of sedation/cognitive impairment.

• Vasoactive medications—serotonin receptor agonists (triptans) and ergotamine derivatives are first line for migraine HA pain, provided that no cerebrovascular or cardiovascular contraindications are present. A positive response to these medications also helps confirm the diagnosis of migraine HA.

Prophylactic Agents

• β-Blockers (propranolol, metoprolol)—Primary choice for migraine prophylaxis in patients who do not have cognitive impairment due to TBI. Exercise caution in the setting of cognitive impairment

• Calcium channel blockers (verapamil)—Most evidence for efficacy pertains to cluster HA

• Antidepressants—Tricyclic antidepressants (nortriptyline, amitriptyline) and selective serotonin reuptake inhibitors (venlafaxine) are frequently used for migraine prophylaxis

• Anticonvulsants (valproate, topiramate) also may be beneficial in migraine prophylaxis

Other Agents

• Pulsed corticosteroids—May abort an attack of intractable migraine

• Inhalation of 100% oxygen for cluster HA (not a typical posttraumatic HA presentation)

• Antiemetics—Can be considered for patients with severe nausea who cannot ingest other medications

• Botulinum toxin—FDA approval for chronic migraine; some evidence for tension-type and cervicogenic HA

Outcome Measures

• Use of a HA log is recommended to accurately assess frequency and severity of HAs and to determine treatment efficacy.

• Quality of life measures, for example, Migraine Disability Assessment (MIDAS) and HA Impact Test (HIT-6), are also useful tools to evaluate impact of HA on activity and participation and to help determine the need for alterations in the treatment plan [19].

Treatment Controversies

• There may be an inverse correlation between TBI severity and the presence of PTH.

• Many patients with PTH have pending litigation; there is a possibility that secondary gain may interfere with response to treatment [20].

• Inadequacy of current ICHD criteria, including rigidity of definition of PTH (development within one week of trauma) and lack of differentiation of HA type [1].

Additional Considerations

PTH and Sport Concussion

• HA is the most common symptom after sport concussion, with rates as high as 85% being reported [21].

• HAs can also be a manifestation of physical exertion in the absence of head trauma, making the diagnosis of persistent postconcussive symptoms on the basis of exertional PTH problematic [22].

• One needs to consider other conditions that may provoke or exacerbate HAs in athletes, including dehydration, sleep disruption, stress, and use of analgesic medications.

• Postconcussion migraine HA has been shown to be associated with a more protracted recovery from concussion in young athletes [23,24].

• Management of sport concussion HA does not differ significantly from the aforementioned recommendations regarding PTH in general.

Pediatric PTH Management

• Children may be more susceptible to sequelae of concussion, including HAs.

• Treatment generally follows recommendations for treating primary HA disorders in children; note that only a few triptans are FDA-approved for pediatric use (almotriptan, rizatriptan, and sumatriptan/naproxen sodium).

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