Headache attributed to head trauma …

J W Wu MD

Headache & Pain

Updated 08.28.2024
Released 11.04.1993
Expires For CME 08.28.2027

Headache attributed to head trauma

Author: J W Wu MD

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Editor: Shuu-Jiun Wang MD

Headache attributed to head trauma

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Introduction

Overview

Posttraumatic headaches are a common consequence of traumatic brain injury. Research has gradually uncovered its pathophysiology. This article reviews the clinical course, diagnosis, and management of posttraumatic headache and discusses the emerging treatment options.

Key points

	• Posttraumatic headache is common following head or neck trauma.
	• The International Headache Society defines posttraumatic headache as “acute” if headache develops within the first 7 days after the accident and resolves within the first 3 months and “persistent” if headache lasts longer than 3 months.
	• Underlying pathophysiological mechanisms associated with the development and maintenance of posttraumatic headache remains uncertain and may include psychogenicity and diffuse axonal injury. Different mechanisms may be involved in posttraumatic headache of civilians and that of combat soldiers.
	• Therapeutic treatment of posttraumatic headache should be individualized and comply with the treatment options for the underlying or accompanying primary headache disorders it resembles.

Historical note and terminology

Headache following head or neck injuries has been reported for centuries. Although the proposed mechanisms for the generation and maintenance of posttraumatic headache have evolved over the years, the subject is still controversial (29).

In his book Posttraumatic Neurosis: From Railway Spine to Whiplash, Trimble traces the arguments that began in the 19th century (117). In 1882, Erichsen published a series of lectures concerning how mild head injuries or “spinal concussion” (so-called “railway brain” or “railway spine”) could result in severe disability (26). However, others casted doubt on the validity of “railway spine” incidence (103). The prevailing view in the 1800s was that headache and other sequelae of head injury were due to malingering or psychogenic or other functional disorders. Interestingly, these contradictory observations were made prior to the development and implementation of worker’s compensation and other liability laws (117). One hundred years later, in the chapter on posttraumatic headache in the Handbook of Clinical Neurology, Miller concluded that the posttraumatic syndrome was caused by compensation neurosis or psychoneurosis (83). In contrast, Symonds took an opposing position in the article “Concussion and its sequelae” (114).

In 1988, the International Headache Society Classification Committee provided the first formal definitions of acute and chronic posttraumatic headache (47). In 2004, the revised International Classification of Headache Disorders (ICHD-II) categorized “headache attributed to head and/or neck trauma” into 12 subtypes (48). The most recent update of the International Classification of Headache Disorders, 3rd edition (ICHD-3), was released in 2018 and categorized "headache attributed to head and/or neck trauma" into eight subtypes:

	• Acute headache attributed to moderate or severe traumatic injury to the head (ICHD-3 code 5.1.1, Table 1 and Table 2)
	• Acute headache attributed to mild traumatic injury to the head (ICHD-3 code 5.1.2, Table 1 and Table 3)
	• Persistent headache attributed to moderate or severe traumatic injury to the head (ICHD-3 code 5.2.1, Table 4 and Table 5)
	• Persistent headache attributed to mild traumatic injury to the head (ICHD-3 code 5.2.2, Table 4 and Table 6)
	• Acute headache attributed to whiplash (ICHD-3 code 5.3, Table 7)
	• Persistent headache attributed to whiplash (ICHD-3 code 5.4, Table 8)
	• Acute headache attributed to craniotomy (ICHD-3 code 5.5, Table 9)
	• Persistent headache attributed to craniotomy (ICHD-3 code 5.6, Table 10)

Table 1. Acute Headache Attributed to Traumatic Injury to the Head

Diagnostic criteria:
(A) Any headache fulfilling criteria C and D (B) Traumatic injury to the head has occurred (C) Headache is reported to have developed within 7 days after one of the following:
	1. The injury to the head 2. Regaining of consciousness following the injury to the head 3. Discontinuation of medication(s) that impair ability to sense or report headache following the injury to the head
(D) Either of the following:
	1. Headache has resolved within 3 months after the injury to the head 2. Headache has not yet resolved but 3 months have not yet passed since the injury to the head
(E) Not better accounted for by another ICHD-3 diagnosis

Table 2. Acute Headache Attributed to Moderate or Severe Traumatic Injury to the Head

Diagnostic criteria:
(A) Headache fulfilling criteria for Table 1 (5.1) Acute headache attributed to traumatic injury to the head (B) Injury to the head associated with at least one of the following:
	1. Loss of consciousness for more than 30 minutes 2. Glasgow Coma Scale (GCS) score of less than 13 3. Posttraumatic amnesia lasting more than 24 hours 4. Alteration in level of awareness for more than 24 hours 5. Imaging evidence of a traumatic head injury such as intracranial hemorrhage and/or brain contusion

Table 3. Acute Posttraumatic Headache Attributed to Mild Traumatic Injury to the Head

Diagnostic criteria:
(A) Headache fulfilling criteria for Table 1 (5.1) Acute headache attributed to traumatic injury to the head
(B) Injury to the head fulfilling both of the following:
	1. Associated with none of the following:
		(a) Loss of consciousness for more than 30 minutes (b) Glasgow Coma Scale (GCS) score of less than 13 (c) Posttraumatic amnesia lasting more than 24 hours (d) Altered level of awareness for more than 24 hours (e) Imaging evidence of a traumatic head injury such as intracranial hemorrhage and/or brain contusion
	2. Associated, immediately following the head injury, with one or more of the following symptoms and/or signs:
		(a) Transient confusion, disorientation, or impaired consciousness (b) Loss of memory for events immediately before or after the head injury (c) Two or more other symptoms suggestive of mild traumatic brain injury: nausea, vomiting, visual disturbances, dizziness and/or vertigo, impaired memory and/or concentration

Table 4. Persistent Headache Attributed to Traumatic Injury to the Head

Diagnostic criteria:
(A) Any headache fulfilling criteria C and D (B) Traumatic injury to the head has occurred (C) Headache is reported to have developed within 7 days after one of the following:
	1. The injury to the head 2. Regaining of consciousness following the injury to the head 3. Discontinuation of medication(s) that impair ability to sense or report headache following the injury to the head
(D) Headache persists for more than 3 months after the injury to the head (E) Not better accounted for by another ICHD-3 diagnosis

Table 5. Persistent Headache Attributed to Moderate or Severe Traumatic Injury to the Head

Diagnostic criteria:
(A) Headache fulfilling criteria for Table 4 (5.2) Persistent headache attributed to traumatic injury to the head (B) Injury to the head associated with at least one of the following:
	1. Loss of consciousness for more than 30 minutes 2. Glasgow Coma Scale (GCS) score of less than 13 3. Posttraumatic amnesia lasting more than 24 hours 4. Alteration in level of awareness for more than 24 hours 5. Imaging evidence of a traumatic head injury such as intracranial hemorrhage and/or brain contusion

Table 6. Persistent Headache Attributed to Mild Traumatic Injury to the Head

Diagnostic criteria:
(A) Headache fulfilling criteria for Table 4 (5.2) Persistent headache attributed to traumatic injury to the head (B) Head injury fulfilling both of the following:
	1. Associated with none of the following:
		(a) Loss of consciousness for more than 30 minutes (b) Glasgow Coma Scale (GCS) score of less than 13 (c) Posttraumatic amnesia lasting more than 24 hours (d) Altered level of awareness for more than 24 hours (e) Imaging evidence of a traumatic head injury such as intracranial hemorrhage and/or brain contusion
	2. Associated, immediately following the head injury, with one or more of the following symptoms and/or signs:
		(a) Transient confusion, disorientation, or impaired consciousness (b) Loss of memory for events immediately before or after the head injury (c) Two or more other symptoms suggestive of mild traumatic brain injury: nausea, vomiting, visual disturbances, dizziness and/or vertigo, impaired memory and/or concentration

Table 7. Acute Headache Attributed to Whiplash

Diagnostic criteria:
(A) Any headache fulfilling criteria C and D (B) Whiplash, associated at the time with neck pain and/or headache, has occurred (C) Headache has developed within 7 days after the whiplash (D) Either of the following:
	1. Headache has resolved within 3 months after the whiplash 2. Headache has not yet resolved but 3 months have not yet passed since the whiplash
(E) Not better accounted for by another ICHD-3 diagnosis

Table 8. Persistent Headache Attributed to Whiplash

Diagnostic criteria:

(A) Any headache fulfilling criteria C and D
(B) Whiplash, associated at the time with neck pain and/or headache, has occurred
(C) Headache has developed within 7 days after the whiplash
(D) Headache persists for more than 3 months after the whiplash
(E) Not better accounted for by another ICHD-3 diagnosis

Table 9. Acute Headache Attributed to Craniotomy

Diagnostic criteria:
(A) Any headache fulfilling criteria C and D (B) Surgical craniotomy has been performed (C) Headache is reported to have developed within 7 days after one of the following:
	1. The craniotomy 2. Regaining of consciousness following the craniotomy 3. Discontinuation of medication(s) that impair ability to sense or report headache following the craniotomy
(D) Either of the following:
	1. Headache has resolved within 3 months after the craniotomy 2. Headache has not yet resolved but 3 months have not yet passed since the craniotomy
(E) Not better accounted for by another ICHD-3 diagnosis

Table 10. Persistent Headache Attributed to Craniotomy

Diagnostic criteria:
(A) Any headache fulfilling criteria C and D (B) Surgical craniotomy has been performed (C) Headache is reported to have developed within 7 days after one of the following:
	1. The craniotomy 2. Regaining of consciousness following the craniotomy 3. Discontinuation of medication(s) that impair ability to sense or report headache following the craniotomy
(D) Headache persists for more than 3 months after the craniotomy (E) Not better accounted for by another ICHD-3 diagnosis

Posttraumatic headache research has been hindered by methodological problems, most particularly the heterogeneity of patient populations. Studies may include individuals with both trivial and significant head injuries as well as patients with definite abnormalities on testing and subjects with normal investigations. Furthermore, patients with symptom onset hours after injury have been included with those whose symptoms began months after injury. The ICHD-II provided the operational diagnostic criteria for posttraumatic headache. However, the temporal criterion of the acute and the chronic forms is artificial. Some experts disagreed that onset of headache should occur within 7 days from the injury (or after regaining consciousness) (133). The ICHD-3 suggests that there is not enough evidence at this time to change this requirement. It is the hope of the International Headache Society that clinicians and researchers alike will field-test the new diagnostic criteria in both epidemiological and clinical trials.

Clinical manifestations

Presentation and course

Headache is the most common but not the only manifestation after traumatic brain injury; the prevalence ranges from 18% to 58% among patients following head injury (28; 96; 58). One prospective, longitudinal, multicenter cohort study (TRACK-TBI Study) analyzed the prevalence of headache after mild traumatic brain injury and found that 60.4% of patients have acute posttraumatic headache 2 weeks after the head injury. Posttraumatic headache persisted 3 months after injury in 52.4% of those affected.

Of note, patients might have postconcussion symptoms other than headache, including dizziness, fatigue, irritability, sleep problems, concentration problems, memory disorders, and emotion perturbations (113). According to the ICHD-3, the diagnosis of “headache attributed to trauma or injury to the head and/or neck” requires that headache must be reported within 7 days after the traumatic brain injury or within 7 days that patients are able to report their headache (49). This “rule of 7 days” is somehow arbitrary, and the ICHD-3 encourages further studies to analyze those with delayed-onset posttraumatic headache (03).

The most common clinical phenotypes of posttraumatic headache are migraine-like or tension-type-like headaches (70). However, the percentage of headache phenotypes are different across each study (67). One Danish study found tension-type-like headache accounts for about 97% of chronic posttraumatic headache patients and only 28% of patients have of migraine-like headache (62). A 5-year prospective study found migraine-like headache (58%) is more common than tension-type-like headache (14%) (112). One study found posttraumatic headache frequently presenting as migraine-like headache but usually without aura (58). One observational study from 100 U.S. soldiers found more than 95% of posttraumatic headache patients fulfilled the diagnostic criteria for migraine (27). In contrast to civilian injuries, migraines account for perhaps 58% to 75% of posttraumatic headache in soldiers (121; 115).

The phenotype of posttraumatic headache can also include trigeminal autonomic cephalalgias, although these are relatively rare. Case reports include cluster headache (118), hemicrania continua (30; 37), short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) (100; 101), short-lasting unilateral neuralgiform headache attacks with cranial autonomic features (SUNA) (54), and chronic paroxysmal hemicrania (78).

Medication overuse is common in chronic posttraumatic headache, and some authorities believe that it is the major cause of headache perpetuation. Warner argues that medication overuse headache is the most frequent cause of chronic posttraumatic headache and that stopping overuse of over-the-counter or prescription analgesics leads to headache resolution in most patients (126; 123). Baandrup reviewed the headache diaries of 53 chronic posttraumatic headache patients from the Danish Headache Center; analgesic overuse was found in 42%, but half were not improved following detoxification therapy (07).

Neck pain is more common in those who have sustained whiplash, a sudden acceleration then deceleration to the neck resulting in pain without an actual blow to the head (110). The major constituents of whiplash syndrome include neck pain and/or tenderness, restriction of neck mobility, and headache. Pain arising from the cervical spine often radiates to the occipital area but may extend to the parietal, temporal, and frontal regions. Range of motion may be limited, and palpation tenderness may be noted. Most whiplash-induced headaches tend to occur close in time with the whiplash injury, resembling tension-type headache or cervicogenic headache in phenotypes, and are often short lasting (110). Cervicogenic headache may occur after head trauma: a site-locked unilateral pain starting in the neck and spreading to the fronto-ocular area (122). Myofascial pain syndrome is also common, featuring the presence of active myofascial trigger points that produce referred pain on palpation (35).

Additionally, one case report describes a patient who developed orthostatic headaches following a head injury, with diagnostic tests later confirming a spinal CSF leak (136). This case emphasizes the importance of a thorough evaluation in posttraumatic headache cases.

The rate of posttraumatic stress disorder was higher (97.9%) among U.S. soldiers with comorbid chronic posttraumatic headache attributed to head injury, but only 9.3% among military personnel in Iran (65; 57).

Prognosis and complications

The different types of head injury play an important role for the prognoses. The prognosis is favorable for most patients with mild head injury (73). The children usually recover well with quick resolution of symptoms and few residual deficits. For adults, cognitive deficits and symptoms are common in the acute stage, and the majority would recover within 3 to 12 months (18). Patients with moderate to severe traumatic brain injury may have an extended recovery time. Strong predictors for 6-month outcome after moderate to severe traumatic brain injury include the Glasgow Coma Scale, midline shift on CT scan, subdural hematoma, and pulsatility index on transcranial Doppler (53).

Acute posttraumatic headache occurred within 24 hours after the trauma in 78% and lasted for a median of 3.0 days (73). One month after mild head injury, 30% to 90% of patients have headache; one year after injury, headache prevalence ranges from 8% to 35%, based on different definitions and methodologies (108). A prospective study found a 91% 1-year cumulative incidence of new or worsened headaches in patients with mild traumatic brain injury after vehicle-related crash and this study showed that up to 49% of patients met the criteria for migraine or probable migraine, followed by tension-type headache (40%) (75). A systematic review on the prevalence of chronic headache after traumatic brain injury revealed a prevalence of 57.8% (89). The prevalence rate of posttraumatic headache after whiplash-type injury tends to decrease with time (22) and was 15% after two years (60). Risk factors associated with chronic posttraumatic headache include female gender, increasing age, mechanical factors such as position of head and neck at the time of trauma, prior headache history, multiple traumatic brain injuries, premorbid psychological status, and presence of headache at the emergency room (74; 44; 132; 73; 128; 131). Preexisting facial pain, lack of confidence to recover completely, sore throat, medication overuse, high Neck Disability Index, hopelessness/anxiety, and depression predict the develop of chronic headache (92).

For unknown reasons, there is inadequate correlation between severity of injury (eg, depth and duration of coma, amnesia) and outcome following traumatic brain injury (130; 21; 89; 24). The advanced functional neuroimaging techniques may be useful for predicting outcome, but further studies are needed (82). Although certain serum proteins have been proposed as potential biomarkers for traumatic brain injury (50; 72), their roles in posttraumatic headache are uncertain.

Clinical vignette

A 33-year-old woman developed chronic daily headache and other postconcussive symptoms following an automobile accident. She was an unrestrained passenger in a midsize car that rear-ended a bus. It was estimated that the car she was traveling in collided with the bus while traveling at approximately 35 mph. There was significant damage restricted to her car’s front bumper. The patient struck her head against the dashboard or windshield. The patient lost consciousness for less than five minutes. In the emergency department, she had anterograde amnesia for several hours following the accident and complained of diffuse headache. CT scan of her head was normal. She was observed for eight hours and discharged.

Over the ensuing 48 hours, she developed dizziness, tinnitus, and headache. The headache was bilateral, located in the occipital-nuchal region and radiated to her temples. It was a dull, constant pressure. She had photophobia and phonophobia, but there were no gastrointestinal or trigeminal autonomic features. Approximately once a week it would intensify and resemble the migraine headaches that she had suffered as an adolescent. She attempted to return to her job as a customer service representative but noted difficulty with distractibility, concentration, and memory. She sought relief through physical therapy, chiropractic manipulation, massage therapy, and naturopathic treatments with only modest, transient benefit. Her symptoms gradually improved over the following months, but her daily headache persisted. Six months post-injury she was evaluated by a neurologist; her examination was unremarkable, and she was educated regarding the good prognosis for her symptoms. She was started on amitriptyline 25 mg and titrated to 50 mg. Additionally, she was referred for biofeedback and relaxation therapy and encouraged to participate in a physical fitness program. At her 2-month follow-up, she was much improved, and headaches were occurring once weekly with minimal associated disability.

Biological basis

Etiology and pathogenesis

Acute posttraumatic headaches result from physical trauma to the head or neck. Trauma may trigger a new headache or may exacerbate existing primary headache disorders. Minor head trauma is an accepted trigger for attacks of migraine; footballer’s migraine (migraines triggered by “heading” the ball in soccer) is an example (79; 127; 98). Another extreme example is developed cerebral edema, coma, and death following trivial head injury (63).

On the other hand, the persistence of posttraumatic symptoms may be related to other factors, including psychogenicity, poor psychosocial support, cultural background and base rate misattribution, expectation, chronic pain, compensation or litigation, and malingering (74; 85; 29). There are some predisposing factors. For example, studies found FHM1- and FHM2-related gene mutation associated with higher neurologic response to minor head trauma (63; 116; 09). Patients with underlying migraine have a higher risk of posttraumatic migraine after concussion (76).

Similar symptom complexes among posttraumatic headache, psychiatric diseases, and posttraumatic stress disorders suggest a common psychogenic origin of these disorders. Pretraumatic neurosis and psychopathology are more common in chronic posttraumatic headache patients than in patients with low back pain or chronic tension-type headache (44). Studies of symptom expectation in normal, healthy subjects show that North Americans are more likely to expect chronic headache following a mild head injury than their counterparts in Greece or Lithuania (where rates of chronic posttraumatic headache are lower) (33; 34). The relationship between compensation and posttraumatic symptoms remains controversial. A meta-analysis of 2523 subjects following closed-head injury concluded that more abnormalities and disability were seen in patients with financial incentives (13). The elimination of compensation for pain and suffering is associated with a decreased incidence and improved prognosis of whiplash injury in Canada (19). Others have argued that compensation is not a significant factor in the perpetuation of posttraumatic headache, as the symptoms typically persist and do not improve following legal settlement (94).

Advocates for a purely neurogenic mechanism point out that patients with mild head injury have more pathologic, radiologic, and electrophysiologic abnormalities than normal controls. However, the majority of patients with persistent symptoms do not necessarily have objective abnormalities on CT, MRI, or SPECT (134). Functional neuroimaging (PET, functional MRI, MR spectroscopy) may demonstrate subtle abnormalities (82). For example, one study showed that veterans with mild traumatic brain injury had decreased cerebral metabolic rate of glucose in the cerebellum, vermis, pons, and medial temporal lobe and exhibited subtle impairments in verbal fluency, cognitive processing speed, attention, and working memory (99).

No unitary hypothesis can account for the wide spectrum of headaches that can occur following head injury. Although physical factors likely play the major role in headaches that begin hours or days following head or neck trauma, a purely neurogenic theory is unlikely to account for the range of late-onset persistent headaches that occur following minor nonconcussive injury. Chronification is most likely due to a combination of organic and psychosocial factors (60).

Keidel and Ramadan suggest the following factors may be involved in the pathogenesis of acute posttraumatic headache: (1) referred pain from nociceptive input caused by lesions of musculoskeletal, discoligamentous, and other soft-tissue structures (including vessels and nerves); (2) activation of meningeal nociceptive afferents due to traumatic epidural, subdural, and subarachnoid bleeding; (3) stretching of pain-sensitive intracranial structures from increased intracranial pressure; (4) intracranial hypotension; and (5) activation of the trigeminovascular system by posttraumatic sinus venous thrombosis (60). In cases of military traumatic brain injury or blast injury, different mechanisms may be involved: (1) an under-pressure followed by over-pressure wave during the blast; (2) penetrating injury from flying debris; (3) structural environment collapse or the body being thrown a distance; and (4) small-particle pollutants (91).

Diffuse axonal injury is one of the most common and important pathologic features of traumatic brain injury (111). It results from shearing forces between different parts of the brain that stretch, distort, or rupture parenchymal axons and may cause neuronal damage or death. It may be caused by angular acceleration of the head and can arise without increased intracranial pressure or hypoxia. Abnormal cerebral hemodynamics have been demonstrated following traumatic head injury (38). Several serum proteins, such as BB isozyme of creatine kinase, glial fibrillary acidic protein, myelin basic protein, neuron-specific enolase, and S-100B, are elevated during diffuse axonal injury and could be used as the biomarkers (50; 72).

After traumatic head injuries, there is a cascade of biochemical changes that are similar to the migraine biochemical milieu: neuronal depolarization, excessive release of excitatory amino acids and neurotransmitters, abnormalities in serotonin neurotransmission, changes in endogenous opiates, increased nitric oxide activity, alterations in cerebral metabolic activity, and cerebral hemodynamic instability (43; 98; 107).

There is strong evidence showing that calcitonin gene-related peptide (CGRP) plays a primary role in migraine and therapies targeting CGRP showed treatment efficacy in migraine patients. In posttraumatic headaches, animal models showed elevated CGRP level after head trauma; the level was associated hyperalgesia and photosensitivity (25; 23; 119; 14). Also, repetitive administration of CGRP monoclonal antibodies could prevent periorbital and cutaneous allodynia, as well as central sensitization in a mouse model of posttraumatic headache (15). Moreover, Ashina and colleagues conducted a CGRP infusion study in patients with persistent posttraumatic headaches, and their study found patients who received CGRP infusion were more likely to develop migraine-like headaches than those who received the placebo (70% vs. 20%, p< 0.001) (05). This finding had been replicated by another open-label study with larger sample size (06). These findings indicated that patients with persistent post-traumatic headaches are more sensitive to CGRP with a more activated trigeminovascular system (84). Of note, although the CGRP is important in the pathophysiology of posttraumatic headaches, the CGRP seems not to be the only driver for migraine-like headaches in patients with posttraumatic headaches. For example, one study showed elevated PACAP level in cerebrospinal fluid and plasma after severe traumatic brain injury (17). Other molecules linking posttraumatic headaches included neuropeptide substance P and the growth factor BDNF (25; 20; 88). The transient biochemical abnormalities following acute trauma may cause recurrent or chronic headaches through the development of peripheral and central sensitization. Trauma may trigger the first attack, which could then set the process in motion in predisposed patients. The CGRP release at nerve terminals causes vasodilation and headache, followed by activation of CGRP receptors in the brainstem and central sensitization (12). Another hypothesis is axonal injury, which may lead to dysregulation of brainstem nociceptive pathways. The stress from work-related disability, ongoing litigation, and a reduced capacity to participate in familial and social activities may be an ongoing trigger for the maintenance of chronic headaches (02; 77).

Epidemiology

Annually, as many as 1.7 million individuals in the United States suffer a closed-head injury (31). Of those injuries, 80% are mild, 10% moderate, and 10% severe (60). The common causes of head injury include falls (35%), motor vehicle or traffic accidents (17%), a person being struck by or against something (16%), and assaults (10%) (31).

Headache is the most common symptom following head injury, but the epidemiology of posttraumatic headache is hard to determine due to differences in definitions and difficulties with case ascertainment. The prevalence of acute posttraumatic headache in acute mild head injury was 66% according to the diagnostic criteria of ICHD-2 (73). Estimates of headache after injury to the head or neck (whiplash) range widely from 30% to 90% (95; 60). A population-based survey in Norway reported a prevalence of posttraumatic headache of 0.2% in a population aged 30 to 44 years (01). An investigation of the lifetime prevalence of posttraumatic headache in Denmark found the prevalence was 4.7% in men and 2.37% in women (102). In one study of returning U.S. Army soldiers who had one or more concussions while serving in combat zones in the Middle East, the prevalence was 37% (115).

Posttraumatic headache usually resolves over a few weeks or months, but some may develop chronic headaches (94; 60). One study in Australia found 15.34% of those who had visited an emergency room for minor head injury continued to complain of persistent posttraumatic headache 3 months later (32). A meta-analysis of 12 studies including 1670 civilians with traumatic brain injury revealed that 57.8% suffered from chronic headache (89). A summary of four studies consisting of 1020 military survivors with traumatic brain injury also found that 35.5% had chronic headache (124; 125; 105; 52).

One study in soldiers with mild traumatic brain injury with conscious change found blast injuries were associated a higher risk of persistent headache (129). Migraine and posttraumatic headache have a bidirectional relationship (76; 106). Genetic predisposition may influence the development of posttraumatic headache. One study found adolescents with a family history of migraine were more likely to developed posttraumatic headache with migrainous features after concussion. In the pediatric head injury population, the prevalence rates of chronic posttraumatic headache ranged from 3.2% to 6.8% (87; 61).

Diagnostic workup

Taking a detailed history and performing a thorough neurologic examination remain pivotal in evaluation of posttraumatic headache patients. The exact mechanism of the trauma, the area and extent of the injury, and the immediate post-injury symptoms should be queried. Determining the timing of headache onset following injury is required for diagnosis. However, the recognition of headache onset could be difficult in patients with moderate to severe traumatic brain injury or major trauma. The characteristics of headache after trauma, functional disability, and psychiatric comorbidities as well as current treatment and the use of symptomatic analgesics all should be assessed. The patients should be queried about the presence and status of any ongoing litigation or work-related disability claims (39). During the neurologic examination, any focal symptoms or signs should be evaluated. A complaint of significant unilateral neck pain may portend dissection. A history of postural headache may signify intracranial hypotension. An orbital bruit and conjunctival injection suggest carotid-cavernous fistula (135).

There are guidelines concerning the indications of neuroimaging for mild traumatic head injury in the acute care setting (55). However, the diagnosis of posttraumatic headache depends on clinical history taking, and routine diagnostic neuroimaging or laboratory examinations have limited diagnostic value (80). CT scan remains the imaging modality of first choice in the acute phase for detecting potential sequelae of intracranial trauma or skull fracture (90), with a sensitivity of 63% to 75% (93; 120). However, an initially normal CT does not preclude brain injury and is of limited prognostic value. A repeated CT scan is warranted in case of neurologic deterioration (16). Compared with CT, MRI is more sensitive in detecting subtle brain abnormalities (diffuse axonal injury, nonhemorrhagic contusion, small subdural hematoma, etc.), especially diffusion-weighted imaging and diffusion tensor imaging (64). MRI is the technique of choice for patients with persistent symptoms in the subacute phase of head injury and during follow-up, or those with ongoing litigation (82; 39). Some clinical symptoms should guide further neuroimaging procedures: orthostatic headache requires an MRI with gadolinium to look for pachymeningeal enhancement characteristic of intracranial hypotension, and focal neck pain and Horner syndrome necessitate a Doppler ultrasound or MRA to look for carotid artery dissection.

Functional neuroimaging tools (SPECT, PET, functional MRI, MR spectroscopy, and magnetoencephalography) may help to demonstrate subtle abnormalities (10; 71) or correlation with neuropsychological deficits (40), but these tools have their limitations in resolution and availability. Neurophysiologic studies (eg, EEG, evoked potentials) are frequently abnormal, but their diagnostic, prognostic, and medicolegal values are negligible (134).

Neuropsychological testing may be useful to document cognitive deficits, predict the functional outcome, or to distinguish concomitant depression, anxiety or frank malingering (74; 59; 46). Cognitive deficits after mild head injury include alterations in attention, information processing, memory, visuospatial processing, and executive functioning (08). Most objective deficits resolve within 3 months, but subjective complaints may persist and appear to have a pathophysiologic and nonneurologic basis. Abnormal neuropsychological test performance should not automatically be interpreted as proof of neuropsychological impairments (59) because anxiety, depression, physical pain, or medication can impair performance.

Management

Because most patients with posttraumatic headache have varied disability in physical, cognitive, and emotional symptoms, management should be individualized, and multidisciplinary approaches are often necessary--eg, physical therapy, relaxation therapy, biofeedback, coping skills training, individual or family therapy, and appropriate pharmacologic management (02; 45; 68). The manual therapy on the neck could reduce the headache compared to ice packs therapy, but this effect was largely lost by eight weeks after treatment (56). Cognitive-behavioral therapy and relaxation therapy provide a useful supplement to the treatment of posttraumatic headache (51; 42). However, one study showed no benefit for whiplash headache relief with physical therapy compared with education and/or activity (104).

A thorough clinical evaluation and judicious use of neuroimaging studies can exclude serious brain injury and provide reassurance needed to the patient. Patients need realistic expectations regarding the time necessary for full recovery; unrealistic expectations may intensify anxiety and depression. Psychiatric evaluation and treatment are warranted in patients with significant depression, anxiety, or phobias.

There is a lack of high-quality studies in the acute and preventative treatments for posttraumatic headache (69). Therefore, treatment of posttraumatic headache should follow the guidelines for the primary headache disorder that it phenotypically resembles. Like the treatment of other primary headaches, posttraumatic headache management can be divided into acute and preventive treatment.

Acute treatments. The acute treatment options could be divided into acute treatment for “acute posttraumatic headache” and “acute attack of persistent or chronic posttraumatic headache.” For acute posttraumatic headache, an early study found repetitive infusions of intravenous dihydroergotamine with metoclopramide can break the headache cycle and diminish associated symptoms in patients with postconcussion headache (81). Also, intravenous metoclopramide 20 mg plus diphenhydramine 25 mg had been shown effective and 63% of patients reported sustained headache relief for 48 hours (36). For abortive treatment for chronic posttraumatic headache, one retrospective study with 100 military personnel found triptans had a higher responder rate (70%) than nontriptans (42%) for headache relief in two hours (27). Codeine and butalbital-containing analgesics should be restricted to refractory patients with contraindications to the aforementioned medications. Patients must be questioned directly about their daily and weekly consumption of over-the-counter and prescription analgesics. Use of abortive agents should be restricted to two days per week to avoid medication overuse headache. If medication overuse headache is present, withdrawal of the overused substances is recommended, and outpatient or inpatient detoxification may be necessary (109). Nonpharmacological options include exercise, neuromodulation, and cognitive/behavioral approaches. The benefit of exercise may due to the exercise-induced release of BDNF but the best timing of exercise after head injury remains unknown (41).

Preventive treatments. The goal of prophylactic therapy is to convert daily headache into a more manageable episodic form. The tricyclic antidepressants (amitriptyline, nortriptyline, doxepin) are most often used for chronic posttraumatic tension-type headaches for their effect on the associated symptoms of irritability, dizziness, depression, and insomnia. Nortriptyline has fewer sedative and anticholinergic effects and may be preferable for patients who are older or more sensitive to these effects. The value of serotonin-specific reuptake inhibitors is unclear. The first-line prophylactic treatment options for chronic posttraumatic migraine include tricyclic antidepressants, beta-blockers, and anticonvulsants (11; 68). Among anticonvulsants, divalproex sodium showed mild to moderate improvement in 60% of patients with chronic posttraumatic headache (97). Another study found topiramate appears to be an effective headache prophylactic therapy, whereas low doses of tricyclic antidepressants appear to have little efficacy in military troops with chronic posttraumatic headache (27). One retrospective study analyzed the efficacy of preventive pharmacological treatments and found that 72% of patients under amitriptyline and 75% under melatonin achieved 50% or more of a reduction in headache frequency (66).

Options of preventive therapies have been introduced for the treatment of posttraumatic headache. A randomized, placebo-controlled, crossover study demonstrated that botulinum toxin type A effectively reduced the frequency of posttraumatic headache by 2.24 days per week (43.3%) over 16 weeks, compared to an increase of 1.28 days per week (35.1%) in the placebo group (137). Given the role of CGRP in the pathophysiology of posttraumatic headaches, CGRP-related therapies have also been explored. An open-label study on erenumab for persistent posttraumatic headache observed a reduction of 2.8 moderate-to-severe headache days (17.8%) from baseline (15.7 days) to weeks 9 to 12. However, only 13% of patients achieved at least a 50% reduction in headache frequency (04). Future randomized controlled trials are needed to provide more robust evidence for the efficacy of CGRP-targeted therapies in posttraumatic headache (84).

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

J W Wu MD

Dr. Wu of Taipei Veterans General Hospital has no relevant financial relationships to disclose.
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Editor

Shuu-Jiun Wang MD

Dr. Wang of National Yang-Ming University and Taipei Veterans General Hospital has no relevant financial relationships to disclose.
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Former Authors

Kenneth L Moore MD
Jonathan P Gladstone MD FRCPC
Shiang-Ru Lu MD
Kai-Chen Wang MD

Patient Profile

Age range of presentation: 1 month to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Acute post-traumatic headache: G44.880

Chronic post-traumatic headache: G44.3

Headache: R51

Migraine: G43

Postconcussional syndrome: F07.2

Tension-type headache: G44.2
ICD-11: Acute headache associated with traumatic injury to the head: 8A84.0

Persistent headache associated with traumatic injury to the head: 8A84.1

Other specified secondary headache: 8A84.Y

Secondary headache, unspecified: 8A84.Z

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Headache attributed to head trauma

Differential Diagnosis

carotid-cavernous fistula
CSF leaks
cerebral artery dissection
cerebral venous sinus thrombosis
skull fracture
- cervicogenic headache
- temporomandibular joint dysfunction
- cranial nerve injury
- epidural hematomas
- primary headache disorders
- subdural hematomas
- medication overuse headache

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Cluster headache
Migraine
Minor closed head injury
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Severe closed head injury
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Headache attributed to head trauma

Introduction

Overview

Key points

Historical note and terminology

Table 1. Acute Headache Attributed to Traumatic Injury to the Head

Table 2. Acute Headache Attributed to Moderate or Severe Traumatic Injury to the Head

Table 3. Acute Posttraumatic Headache Attributed to Mild Traumatic Injury to the Head

Table 4. Persistent Headache Attributed to Traumatic Injury to the Head

Table 5. Persistent Headache Attributed to Moderate or Severe Traumatic Injury to the Head

Table 6. Persistent Headache Attributed to Mild Traumatic Injury to the Head

Table 7. Acute Headache Attributed to Whiplash

Table 8. Persistent Headache Attributed to Whiplash

Table 9. Acute Headache Attributed to Craniotomy

Table 10. Persistent Headache Attributed to Craniotomy

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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