Headache attributed to head trauma …

J W Wu MD

Headache & Pain

Updated 05.22.2023
Released 11.04.1993
Expires For CME 05.22.2026

Headache attributed to head trauma

Author: J W Wu MD

See Contributor Disclosures

Editor: Shuu-Jiun Wang MD

Headache attributed to head trauma

In This Article

Quick Link

Introduction

Overview

Headache is common following head injury. Most individuals recover within days, weeks, or months, but a minority of subjects may suffer from intractable posttraumatic headache despite treatment. Posttraumatic headache remains a subject of controversy concerning its pathophysiology. Litigation and medicolegal problems further complicate this issue. This article attempts to summarize current understanding of posttraumatic headache, including a brief historical review of the disease, the classification and diagnostic criteria, the epidemiology, clinical manifestations, pathophysiology, diagnostic evaluation, and management.

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 (118). 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 (104). 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 (118). 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 (84). In contrast, Symonds took an opposing position in the article “Concussion and its sequelae” (115).

In 1988, the International Headache Society Classification Committee provided the first formal definitions of acute and chronic posttraumatic headache (48). In 2004, the revised International Headache Society Classification of Headache Disorders (ICHD-II) categorized “headache attributed to head and/or neck trauma” into 12 subtypes (49).

In 2018, the International Classification of Headache Disorders, 3rd edition (ICHD-3) 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) (134). 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 common after the traumatic brain injury, which occurs in 18% to 58% of patients following head injury (28; 97; 59). Headache is the most common but not the only manifestation of the posttraumatic or postconcussion syndrome. Additional symptoms include somatic (dizziness, tinnitus, hyperacusis, photophobia, phonophobia, blurred vision, easy fatigability), cognitive (impaired concentration and memory), and psychological symptoms (depression, anxiety, irritability, apathy, insomnia) (105). Also, posttraumatic headache is an important predictor of overall outcome after concussion.

Headache attributed to head or neck trauma usually begins hours or days after the injury but may be delayed for weeks. The timing of posttraumatic headache onset is crucial because it is the requisite for diagnosis according to the ICHD-3: the onset must be within 7 days after the injury (or regaining of consciousness or discontinuation of medications that impair the ability to sense or report the headache) (50). However, the recognition of headache onset could be hindered by cognitive impairment after the injury or by concomitant orthopedic or multi-organ trauma, in which patients may focus primarily on body pain rather than headache, or by the use of pain control that may alleviate the headache.

The most common clinical phenotypes of posttraumatic headache are migraine-like or tension-type-like headaches (71). However, the percentage of headache phenotypes are different in each study (68). 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 (63). A 5-year prospective study found migraine-like headache (58%) is more common than tension-type-like headache (14%) (114). One study found posttraumatic headache frequently presenting as migraine-like headache but usually without aura (59). One observational study from 100 U.S. soldiers found more than 95% of posttraumatic headache patients fulfilled migrainous headache (27). In contrast to civilian injuries, migraines account for perhaps 58% to 75% of posttraumatic headache in soldiers (122; 116).

Rare case reports have attributed trauma to the onset of cluster headache (119), hemicrania continua (30), short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) (101; 102), short-lasting unilateral neuralgiform headache attacks with cranial autonomic features (SUNA) (55), and chronic paroxysmal hemicrania (79).

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 (127; 124). 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 (06).

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 (112). 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 (112). Cervicogenic headache may occur after head trauma: a site-locked unilateral pain starting in the neck and spreading to the fronto-ocular area (123). Myofascial pain syndrome is also common, featuring the presence of active myofascial trigger points that produce referred pain on palpation (36).

Chronic posttraumatic headache may result in pain in temporomandibular joints (19). Temporomandibular joint dysfunction may present as a decrease in the range of motion of the joints, increased pain with chewing, audible clicking, and tenderness to palpation. However, one systematic review found conflicting evidence regarding the effects of whiplash on the development of temporomandibular disorders (33).

Occipital neuralgia can follow whiplash-type injuries. Fracture of the styloid process can produce symptoms resembling Eagle syndrome: unilateral pain in the throat or neck, or referred pain in the shoulder, chest, tongue, eye, cheek, temporomandibular joint, or ear (134).

A continuous hemicranial headache that presented with continuous half-sided headache, cranial autonomic symptoms with exacerbations, and a response to indomethacin were reported after cranial surgery (38).

Other rare case reports, including an orthostatic headache after a bicycle accident that occurred five days prior to presentation due to cervical spine fracture owing to cerebral spinal fluid leak, and progressive intracranial hypertension due to superior sagittal sinus thrombosis following mild head trauma, were reported (137).

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 (66; 58).

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 (74). 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 (17). 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 (54).

Acute posttraumatic headache occurred within 24 hours after the trauma in 78% and lasted for a median of 3.0 days (74). 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 (110). 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%) (76). A systematic review on the prevalence of chronic headache after traumatic brain injury revealed a prevalence of 57.8% (90). The prevalence rate of posttraumatic headache after whiplash-type injury tends to decrease with time (22) and was 15% after two years (61). 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 (75; 45; 133; 74; 129; 132). 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 (93).

For unknown reasons, there is inadequate correlation between severity of injury (eg, depth and duration of coma, amnesia) and outcome following traumatic brain injury (131; 21; 90; 24). The advanced functional neuroimaging techniques may be useful for predicting outcome, but further studies are needed (83). Although certain serum proteins have been proposed as potential biomarkers for traumatic brain injury (51; 73), 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 (80; 128; 99). Another extreme example is developed cerebral edema, coma, and death following trivial head injury (64).

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 (75; 86; 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 (64; 117; 08). Patients with underlying migraine have a higher risk of posttraumatic migraine after concussion (77).

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 (45). 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) (34; 35). 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 (12). The elimination of compensation for pain and suffering is associated with a decreased incidence and improved prognosis of whiplash injury in Canada (18). 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 (95).

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 (135). Functional neuroimaging (PET, functional MRI, MR spectroscopy) may demonstrate subtle abnormalities (83). 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 (100).

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 (61).

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 (61). 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 (92).

Diffuse axonal injury is one of the most common and important pathologic features of traumatic brain injury (113). 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 (39). 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 (51; 73).

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 (44; 99; 109).

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; 120; 13). 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 (14). 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) (04). This finding had been replicated by another open-label study with larger sample size (05). These findings indicated that patients with persistent post-traumatic headaches are more sensitive to CGRP with a more activated trigeminovascular system (85). 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 (16). Other molecules linking posttraumatic headaches included neuropeptide substance P and the growth factor BDNF (25; 20; 89). 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 (11). 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; 78).

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 (61). 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 (74). Estimates of headache after injury to the head or neck (whiplash) range widely from 30% to 90% (96; 61). 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 (103). 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% (116).

Posttraumatic headache usually resolves over a few weeks or months, but some may develop chronic headaches (95; 61). 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 (90). A summary of four studies consisting of 1020 military survivors with traumatic brain injury also found that 35.5% had chronic headache (125; 126; 107; 53).

One study in soldiers with mild traumatic brain injury with conscious change found blast injuries were associated a higher risk of persistent headache (130). Migraine and posttraumatic headache have a bidirectional relationship (77; 108). 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% (88; 62).

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 (40). 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 (136).

There are guidelines concerning the indications of neuroimaging for mild traumatic head injury in the acute care setting (56). However, the diagnosis of posttraumatic headache depends on clinical history taking, and routine diagnostic neuroimaging or laboratory examinations have limited diagnostic value (81). CT scan remains the imaging modality of first choice in the acute phase for detecting potential sequelae of intracranial trauma or skull fracture (91), with a sensitivity of 63% to 75% (94; 121). 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 (15). 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 (65). 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 (83; 40). 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 (09; 72) or correlation with neuropsychological deficits (41), 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 (135).

Neuropsychological testing may be useful to document cognitive deficits, predict the functional outcome, or to distinguish concomitant depression, anxiety or frank malingering (75; 60; 47). Cognitive deficits after mild head injury include alterations in attention, information processing, memory, visuospatial processing, and executive functioning (07). 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 (60) 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; 46; 69). 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 (57). Cognitive-behavioral therapy and relaxation therapy provide a useful supplement to the treatment of posttraumatic headache (52; 43). However, one study showed no benefit for whiplash headache relief with physical therapy compared with education and/or activity (106).

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 (70). 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 (82). Also, intravenous metoclopramide 20 mg plus diphenhydramine 25 mg had been shown effective and 63% of patients reported sustained headache relief for 48 hours (37). 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 (111). 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 (42).

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 (10; 69). Among anticonvulsants, divalproex sodium showed mild to moderate improvement in 60% of patients with chronic posttraumatic headache (98). 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 (67).

New options of preventive therapies have been introduced for the treatment of posttraumatic headache. One randomized, placebo-controlled, crossover study showed botulinum toxin type A could effectively reduce headache frequency of posttraumatic headache by 2.24 days per week (43.3%) at the end of 16 weeks, compared with a 1.28 days per week (35.1%) increment of headache frequency (138). Because CGRP also plays a role in the pathophysiology of posttraumatic headaches, CGRP-related therapies have been tested for the treatment of posttraumatic headaches. One open-label study of erenumab for persistent posttraumatic headache found 2.8 moderate-to-severe headache days reduction (17.8%) from baseline (15.7 days) to week 9 to 12. However, only 13% patients of patients achieved at least a 50% reduction in headache frequency (03). Future randomized controlled studies analyzing the efficacy of CGRP monoclonal antibodies are undertaken to provide more solid evidence for CGRP-targeted therapies in posttraumatic headache (85).

References

01: Aaseth K, Grande RB, Kvaerner KJ, Gulbrandsen P, Lundqvist C, Russell MB. Prevalence of secondary chronic headaches in a population-based sample of 30-44-year-old persons. The Akershus study of chronic headache. Cephalalgia 2008;28:705-13. PMID 18498398
02: Andrasik F, Wincze P. Emotional and psychosocial aspects of mild head injury. Semin Neurol 1994;14:60-6. PMID 8029561
03: Ashina H, Iljazi A, Al-Khazali HM, et al. Efficacy, tolerability, and safety of erenumab for the preventive treatment of persistent post-traumatic headache attributed to mild traumatic brain injury: an open-label study. J Headache Pain 2020a;21(1):62. PMID 32493206
04: Ashina H, Iljazi A, Al-Khazali HM, et al. Hypersensitivity to calcitonin gene-related peptide in post-traumatic headache. Ann Neurol 2020b;88(6):1220-8. PMID 32959458
05: Ashina H, Iljazi A, Al-Khazali HM, et al. CGRP-induced migraine-like headache in persistent post-traumatic headache attributed to mild traumatic brain injury. J Headache Pain 2022;23(1):135. PMID 36253732
06: Baandrup L, Jensen R. Chronic post-traumatic headache--a clinical analysis in relation to the International Headache Classification 2nd Edition. Cephalalgia 2005;25:132-8. PMID 15658950
07: Babikian T, Freier MC, Ashwal S, Riggs ML, Burley T, Holshouser BA. MR spectroscopy: predicting long-term neuropsychological outcome following pediatric TBI. J Magn Reson Imaging 2006;24:801-11. PMID 16941608
08: Barros J, Damasio J, Tuna A, et al. Cerebellar ataxia, hemiplegic migraine, and related phenotypes due to a CACNA1A missense mutation: 12-year follow-up of a large Portuguese family. JAMA Neurol 2013;70(2):235-40. PMID 23407676
09: Belanger HG, Vanderploeg RD, Curtiss G, Warden DL. Recent neuroimaging techniques in mild traumatic brain injury. J Neuropsychiatry Clin Neurosci 2007;19:5-20. PMID 17308222
10: Bell KR, Kraus EE, Zasler ND. Medical management of posttraumatic headaches: pharmacological and physical treatment. J Head Trauma Rehabil 1999;14:34-48. PMID 9949245
11: Bigal ME, Walter S, Rapoport AM. Calcitonin gene-related peptide (CGRP) and migraine current understanding and state of development. Headache 2013;53(8):1230-44. PMID 23848260
12: Binder LM, Rohling ML. Money matters: a meta-analytic review of the effects of financial incentives on recovery after closed-head injury. Am J Psychiatry 1996;153:7-10. PMID 8540596
13: Bree D, Levy D. Development of CGRP- dependent pain and headache related behaviours in a rat model of concussion: implications for mechanisms of post-traumatic headache. Cephalalgia 2018;38(2):246-58. PMID 27899434
14: Bree D, Stratton J, Levy D. Increased severity of closed head injury or repetitive subconcussive head impacts enhances post-traumatic headache-like behaviors in a rat model. Cephalalgia 2020;40(11):1224-39. PMID 32600065
15: Brown CV, Zada G, Salim A, et al. Indications for routine repeat head computed tomography (CT) stratified by severity of traumatic brain injury. J Trauma 2007;62:1339-45. PMID 17563645
16: Bukovics P, Czeiter E, Amrein K, et al. Changes of PACAP level in cerebrospinal fluid and plasma of patients with severe traumatic brain injury. Peptides 2014;60:18-22. PMID 25017241
17: Carroll LJ, Cassidy JD, Peloso PM, et al. Prognosis for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med 2004;(43 Suppl):84-105. PMID 15083873
18: Cassidy JD, Carroll LJ, Cote P, Lemstra M, Berglund A, Nygren A. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000;342:1179-86. PMID 10770984
19: Chibnall JT, Duckro PN, Greenberg MS. Evidence for construct validity of the TMJ scale in a sample of chronic post-traumatic headache patients. Cranio 1994;12:184-9. PMID 7813031
20: Corrigan F, Vink R, Turner RJ. Inflammation in acute CNS injury: a focus on the role of substance P. Br J Pharmacol 2016;173(4):703-15. PMID 25827155
21: Couch JR, Bearss C. Chronic daily headache in the posttrauma syndrome: relationship to the extent of head injury. Headache 2001;41:559-64. PMID 11437891
22: Crutebo S, Nilsson C, Skillgate E, Holm LW. The course of symptoms for whiplash-associated disorders in Sweden: 6-month followup study. J Rheumatol 2010;37:1527-33. PMID 20472922
23: Daiutolo BV, Tyburski A, Clark SW, Elliott MB. Trigeminal pain molecules, allodynia, and photo- sensitivity are pharmacologically and genetically modulated in a model of traumatic brain injury. J Neurotrauma 2016;33(8):748-60. PMID 26472135
24: Dobscha SK, Clark ME, Morasco BJ, Freeman M, Campbell R, Helfand M. Systematic review of the literature on pain in patients with polytrauma including traumatic brain injury. Pain Med 2009;10:1200-17. PMID 19818031
25: Elliott MB, Oshinsky ML, Amenta PS, Awe OO, Jallo JI. Nociceptive neuropeptide increases and periorbital allodynia in a model of traumatic brain injury. Headache 2012;52(6):966-84. PMID 22568499
26: Erichsen JE. On concussion of the spine: nervous shock and other obscure injuries of the nervous system in their clinical and medico-legal aspects. London, England: Longmans, Green and Company: 1882.
27: Erickson JC. Treatment outcomes of chronic post-traumatic headaches after mild head trauma in US soldiers: an observational study. Headache 2011;51(6):932-44. PMID 21592097
28: Evans RW. Post-traumatic headaches. Neurol Clin 2004;22:237-49. PMID 15062537
29: Evans RW. Persistent post-traumatic headache, postconcussion syndrome, and whiplash injuries: the evidence for a non-traumatic basis with an historical review. Headache 2010;50:716-24. PMID 20456159
30: Evans RW, Lay CL. Posttraumatic hemicrania continua. Headache. 2000 Oct;40(9):761-2.
31: Faul M, Xu L, Wald MM, Coronado VG. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention National Center for Injury Prevention and Control, 2010:1-71.
32: Faux S, Sheedy J.A prospective controlled study in the prevalence of posttraumatic headache following mild traumatic brain injury. Pain Med 2008;9:1001-11. PMID 18266807
33: Fernandez CE, Amiri A, Jaime J, Delaney P. The relationship of whiplash injury and temporomandibular disorders: a narrative literature review. J Chiropr Med 2009;8:171-86. PMID 19948308
34: Ferrari R, Constantoyannis C, Papadakis N. Cross-cultural study of symptom expectation following minor head injury in Canada and Greece. Clinical Neurol Neurosurg 2001a;103:254-9.
35: Ferrari R, Obelieniene D, Russel AS, et al. Symptom expectation after minor head injury. A comparative study between Canada and Lithuiania. Clin Neurol Neurosurg 2001b;103:184-90. PMID 11532561
36: Freund B, Schwartz M. Post-traumatic myofascial pain of the head and neck. Curr Pain Headache Rep 2002;6:361-9. PMID 12207849
37: Friedman BW, Babbush K, Irizarry E, White D, John Gallagher E. An exploratory study of IV metoclopramide + diphenhydramine for acute post- traumatic headache. Am J Emerg Med 2018;36(2):285-9. PMID 29074068
38: Gantenbein AR, Sarikaya H, Riederer F, Goadsby PJ. Postoperative hemicrania continua-like headache - a case series. J Headache Pain 2015;16:526. PMID 25968100
39: Gilkey SJ, Ramadan NM, Aurora TK, et al. Cerebral blood flow in chronic post traumatic headache. Headache 1997;37:583-7. PMID 9385758
40: Gladstone J. From psychoneurosis to ICHD-2: an overview of the state of the art in post-traumatic headache. Headache 2009;49:1097-111. PMID 19583599
41: Govind V, Gold S, Kaliannan K, et al. Whole-brain proton MR spectroscopic imaging of mild-to-moderate traumatic brain injury and correlation with neuropsychological deficits. J Neurotrauma 2010;27:483-96. PMID 20201668
42: Griesbach GS, Tio DL, Nair S, Hovda DA. Recovery of stress response coincides with responsiveness to voluntary exercise after traumatic brain injury. J Neurotrauma 2014;31(7):674-82. PMID 24151829
43: Gurr B, Coetzer BR. The effectiveness of cognitive-behavioural therapy for post-traumatic headaches. Brain Inj 2005;19(7):481-91. PMID 16134736
44: Haas DC, Lourie T. Trauma-triggered migraine: an explanation for common neurologic attacks after mild head injury. J Neurosurg 1988;68:181. PMID 3276835
45: Ham LP, Andrasik F, Packard RC, Bundrick CM. Psychopathology in individuals with post-traumatic headaches and other pain types. Cephalalgia 1994;14:118-26. PMID 8062349
46: Ham LP, Packard RC. A retrospective, follow-up study of biofeedback-assisted relaxation therapy in patients with posttraumatic headache. Biofeedback Self Regul 1996;21:93-104. PMID 8805960
47: Hanks RA, Millis SR, Ricker JH, et al. The predictive validity of a brief inpatient neuropsychologic battery for persons with traumatic brain injury. Arch Phys Med Rehabil 2008;89:950-7. PMID 18452745
48: Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia 1988;8(Suppl 7):1-96.
49: Headache Classification Committee of the International Headache Society. International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004;24(Supp1):1-160.
50: Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38:1-211. PMID 29368949
51: Hergenroeder GW, Redell JB, Moore AN, Dash PK. Biomarkers in the clinical diagnosis and management of traumatic brain injury. Mol Diagn Ther 2008;12:345-58. PMID 19035622
52: Hickling EJ, Blanchard EB, Silverman DJ, Schwarz SP. Motor vehicle accidents, headaches and post-traumatic stress disorder: assessment findings in a consecutive series. Headache 1992;32(3):147-51. PMID 1563947
53: Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA. Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med 2008;358:453-63. PMID 18234750
54: Husson EC, Ribbers GM, Willemse-van Son AH, Verhagen AP, Stam HJ. Prognosis of six-month functioning after moderate to severe traumatic brain injury: a systematic review of prospective cohort studies. J Rehabil Med 2010;42:425-36. PMID 20544152
55: Jacob S, Saha A, Rajabally Y. Post-traumatic short-lasting unilateral headache with cranial autonomic symptoms (SUNA). Cephalalgia 2008;28:991-3. PMID 18513261
56: Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med 2008;52:714-48. PMID 19027497
57: Jensen OK, Nielsen FF, Vosmar L. An open study comparing manual therapy with the use of cold packs in the treatment of post-traumatic headache. Cephalalgia 1990;10(5):241-50. PMID 2272094
58: Jouzdani SR, Ebrahimi A, Rezaee M, Shishegar M, Tavallaii A, Kaka G. Characteristics of posttraumatic headache following mild traumatic brain injury in military personnel in Iran. Environ Health Prev Med 2014;19(6):422-8. PMID 25216772
59: Kamins J, Charles A. Posttraumatic headache: basic mechanisms and therapeutic targets. Headache 2018;58(6):811-26. PMID 29757458
60: Kay T. Neuropsychological diagnosis: disentangling the multiple determinants of functional disability after mild traumatic brain injury. In: Horn L, Zasler N, editors. Rehabilitation of Postconcussive Disorders. Philadelphia: Hanley & Belfus, 1992:109-27.
61: Keidel M, Ramadan NM. Posttraumatic headache. Olesen J, Tfelt-Hansen P, Welch KM, editors. The Headaches. Philadelphia: Lippincott Williams & Wilkins, 2000:765-80.
62: Kirk C, Nagiub G, Abu-Arafeh I. Chronic post-traumatic headache after head injury in children and adolescents. Dev Med Child Neurol 2008;50:422-5. PMID 18422678
63: Kjeldgaard D, Forchhammer H, Teasdale T, Jensen RH. Chronic post-traumatic headache after mild head injury: a descriptive study. Cephalalgia 2014;34(3):191-200. PMID 24045573
64: Kors EE, Terwindt GM, Vermeulen FL, et al. Delayed cerebral edema and fatal coma after minor headache trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine. Ann Neurol 2001;49:753-60. PMID 11409427
65: Kou Z, Wu Z, Tong KA, et al. The role of advanced MR imaging findings as biomarkers of traumatic brain injury. J Head Trauma Rehabil 2010;25:267-82. PMID 20611045
66: Kozminski M. Combat-related posttraumatic headache: diagnosis, mechanisms of injury, and challenges to treatment. J Am Osteopath Assoc 2010;110(9):514-9. PMID 20876836
67: Kuczynski A, Crawford S, Bodell L, Dewey D, Barlow KM. Characteristics of post-traumatic headaches in children following mild traumatic brain injury and their response to treatment: a prospective cohort. Dev Med Child Neurol 2013;55(7):636-41 PMID 23560811
68: Labastida-Ramírez A, Benemei S, Albanese M, et al. Persistent post-traumatic headache: a migrainous loop or not? The clinical evidence. J Headache Pain 2020;21(1):55. PMID 32448142
69: Lane JC, Arciniegas DB. Post-traumatic headache. Curr Treat Options Neurol 2002;4:89-104. PMID 11734106
70: Larsen EL, Ashina H, Iljazi A, et al. Acute and preventive pharmacological treatment of post-traumatic headache: a systematic review. J Headache Pain 2019;20(1):98. PMID 31638888
71: Lew HL, Lin PH, Fuh JL, Wang SJ, Clark DJ, Walker WC. Characteristics and treatment of headache after traumatic brain injury: a focused review. Am J Phys Med Rehabil 2006;85:619-27. PMID 16788394
72: Lewine JD, Davis JT, Bigler ED, et al. Objective documentation of traumatic brain injury subsequent to mild head trauma: multimodal brain imaging with MEG, SPECT, and MRI. J Head Trauma Rehabil 2007;22:141-55. PMID 17510590
73: Li J, Li XY, Feng DF, Pan DC. Biomarkers associated with diffuse traumatic axonal injury: exploring pathogenesis, early diagnosis, and prognosis. J Trauma 2010;69:1610-8. PMID 21150538
74: Lieba-Samal D, Platzer P, Seidel S, Klaschterka P, Knopf A, Wober C. Characteristics of acute posttraumatic headache following mild head injury. Cephalalgia 2011;31(16):1618-26. PMID 22116940
75: Lishman WA. Physiogenesis and psychogenesis in the "post-concussional syndrome." Br J Psychiatry 1988;153:460-9. PMID 3074853
76: Lucas S, Hoffman JM, Bell KR, Dikmen S. A prospective study of prevalence and characterization of headache following mild traumatic brain injury. Cephalalgia 2014;34(2):93-102. PMID 23921798
77: Lucas S, Hoffman JM, Bell KR, Walker W, Dikmen S. Characterization of headache after traumatic brain injury. Cephalalgia 2012;32(8):600-6. PMID 22623761
78: Martelli MR, Grayson RL, Zasler ND. Posttraumatic headache: neuropsychological and psychological effects and treatment implications. J Head Trauma Rehabil 1999;14:49-69.
79: Matharu MS, Goadsby PJ. Post-traumatic chronic paroxysmal hemicrania with aura. Neurology 2001;56:273–5.
80: Matthews WB. Footballer’s migraine. Brit Med J 1972;2(809):326-7. PMID 5022042
81: May A. Hints on diagnosing and treating headache. Dtsch Arztebl Int 2018;115(17):299-308. PMID 29789115
82: McBeath JG, Nanda A. Use of dihydroergotamine in patients with postconcussion syndrome. Headache 1994;34:148-51. PMID 8200788
83: Metting Z, Rodiger LA, De Keyser J, van der Naalt J. Structural and functional neuroimaging in mild-to-moderate head injury. Lancet Neurol 2007;6:699-710. PMID 17638611
84: Miller H. Posttraumatic headache. In: Vinken PJ, Bruyn GW, editors. Handbook of Clinical Neurology. Amsterdam: North-Holland, 1968;5:178-84.
85: Mitsikostas DD, Moskowitz MA. Making headway - a role for CGRP in post-traumatic headache. Nat Rev Neurol 2021;17(3):133-4. PMID 33199891
86: Mittenberg W, DiGiulio DV, Perrin S, Bass AE. Symptoms following mild head injury: expectation as aetiology. J Neurol Neurosurg Psychiatry 1992;55:200-4. PMID 1564481
87: Molnár C, Simon É, Kazup Á, et al. A single preoperative dose of diclofenac reduces the intensity of acute postcraniotomy headache and decreases analgesic requirements over five postoperative days in adults: A single center, randomized, blinded trial. J Neurol Sci 2015;353(1-2):70-3. PMID 25899314
88: Moscato D, Peracchi MI, Mazzotta G, Savi L, Battistella PA. Post-traumatic headache from moderate head injury. J Headache Pain 2005;6:284-6. PMID 16362688
89: Mustafa G, Hou J, Tsuda S, et al. Trigeminal neuroplasticity underlies allodynia in a preclinical model of mild closed head traumatic brain injury (cTBI). Neuropharmacology 2016;107:27-39. PMID 26972829
90: Nampiaparampil DE. Prevalence of chronic pain after traumatic brain injury: a systematic review. JAMA 2008;300:711-19. PMID 18698069
91: National Institute for Health and Clinical Excellence. Head injury: triage, assessment, investigation and early management of head injury in infants, children and adults. Available at: https://www.nice.org.uk/guidance/cg56 2007.
92: Neely ET, Midgette LA, Scher AI. Clinical review and epidemiology of headache disorders in US service members: with emphasis on post-traumatic headache. Headache 2009;49:1089-96. PMID 19583598
93: Obermann M, Nebel K, Riegel A, et al. Incidence and predictors of chronic headache attributed to whiplash injury. Cephalalgia 2010;30(5):528-34. PMID 19673910
94: Orrison WW, Gentry LR, Stimac GK, Tarrel RM, Espinosa MC, Cobb LC. Blinded comparison of cranial CT and MR in closed head injury evaluation. AJNR Am J Neuroradiol 1994;15:351-6. PMID 8192085
95: Packard RC. Posttraumatic headache--permanency and relationship to legal settlement. Headache 1992;32:496-500. PMID 1468907
96: Packard RC. Epidemiology and pathogenesis of posttraumatic headache. J Head Trauma Rehabil 1999;14:9-21. PMID 9949243
97: Packard RC. Current concepts in chronic post-traumatic headache. Curr Pain Headache Rep 2005;9:59-64. PMID 15625027
98: Packard RC. Treatment of chronic daily posttraumatic headache with divalproex sodium. Headache 2000;40(9):736-9. PMID 11091292
99: Packard RC, Ham LP. Pathogenesis of posttraumatic headache and migraine: a common headache pathway. Headache 1997;37:142-52. PMID 9100398
100: Peskind ER, Petrie EC, Cross DJ, et al. Cerebrocerebellar hypometabolism associated with repetitive blast exposure mild traumatic brain injury in 12 Iraq war Veterans with persistent post-concussive symptoms. Neuroimage 2011;54(Suppl 1):S76-82. PMID 20385245
101: Piovesan EJ, Kowacs PA, Werneck LC. S.U.N.C.T. syndrome: report of a case preceded by ocular trauma. Arq Neuropsiquiatr 1996;54:494-7. PMID 9109998
102: Putzki N, Nirkko A, Diener HC. Trigeminal autonomic cephalalgias: a case of post-traumatic SUNCT syndrome. Cephalalgia 2005;25:395-7. PMID 15839855
103: Rasmussen BK, Olesen J. Symptomatic and nonsymptomatic headaches in a general population. Neurology 1992;42:1225-31. PMID 1603351
104: Rigler J. Ueber die Folgen der Verletzungen auf Eisenbahnen Insbesondere der Verletzungen des Ruckenmarks. Berlin: G Reimer, 1879.
105: Ryan LM, Warden DL. Post concussion syndrome. Int Rev Psychiatry 2003;15:310-16. PMID 15276952
106: Scholten-Peeters GG, Neeleman-van der Steen CW, van der Windt DA, Hendriks EJ, Verhagen AP, Oostendorp RA. Education by general practitioners or education and exercises by physiotherapists for patients with whiplash-associated disorders. A randomized clinical trial. Spine (Phila Pa 1976) 2006;31(7):723-31. PMID 16582844
107: Schwab KA, Ivins B, Cramer G, et al. Screening for traumatic brain injury in troops returning from deployment in Afghanistan and Iraq: initial investigation of the usefulness of a short screening tool for traumatic brain injury. J Head Trauma Rehabil 2007;22:377-89.
108: Seifert T, Sufrinko A, Cowan R, et al. Comprehensive headache experience in collegiate student-athletes: an initial report from the NCAA headache task force. Headache 2017;57(6):877-86. PMID 28480575
109: Signoretti S, Vagnozzi R, Tavazzi B, Lazzarino G. Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications. Neurosurg Focus 2010;29:E1. PMID 21039135
110: Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. Martin Dunitz, 2002.
111: Silberstein SD, Liu D. Drug overuse and rebound headache. Curr Pain Headache Rep 2002;6:240-7. PMID 12003696
112: Sjaastad O, Fredriksen T, Bakketeig L. Headache subsequent to whiplash. Curr Pain Headache Rep 2009;13:52-8. PMID 19126372
113: Smith DH, Meaney DF, Shull WH. Diffuse axonal injury in head trauma. J Head Trauma Rehabil 2003;18:307-16. PMID 16222127
114: Stacey A, Lucas S, Dikmen S, et al. Natural history of headache five years after traumatic brain injury. J Neurotrauma 2017;34(8):1558-64. PMID 27927072
115: Symonds C. Concussion and its sequelae. Lancet 1962;279:1-5.
116: Theeler BJ, Flynn FG, Erickson JC. Headaches after concussion in US soldiers returning from Iraq or Afghanistan. Headache 2010;50(8):1262-72.
117: Tottene A, Pivotto F, Fellin T, Cesetti T, van den Maagdenberg AMJM, Pietrobon D. Specific kinetic alterations of human CaV2.1 calcium channels produced by mutation S218L causing familial hemiplegic migraine and delayed cerebral edema and coma after minor head trauma. J Biol Chem 2005;280(18):17678-86. PMID 15743764
118: Trimble M. Posttraumatic Neurosis From Railway Spine to Whiplash. New York: John Wylie & Sons, 1981.
119: Turkewitz LJ, Wirth O, Dawson GA, Casaly JS. Cluster headache following head injury: a case report and review of the literature. Headache 1992;32(10):504-6. PMID 1468909
120: Tyburski AL, Cheng L, Assari S, Darvish K, Elliott MB. Frequent mild head injury promotes trigeminal sensitivity concomitant with microglial proliferation, astrocytosis, and increased neuro- peptide levels in the trigeminal pain system. J Headache Pain 2017;18(1):16. PMID 28176234
121: van der Naalt J, Hew JM, van Zomeren AH, Sluiter WJ, Minderhoud JM. Computed tomography and magnetic resonance imaging in mild to moderate head injury: early and late imaging related to outcome. Ann Neurol 1999;46:70-8. PMID 10401782
122: Vargas BB. Posttraumatic headache in combat soldiers and civilians: what factors influence the expression of tension-type versus migraine headache. Curr Pain Headache Rep 2009;13:470-3. PMID 19889289
123: Vincent MB. Cervicogenic headache: a review comparison with migraine, tension-type headache, and whiplash. Curr Pain Headache Rep 2010;14:238-43. PMID 20428974
124: Warner JS. Posttraumatic headache – a myth. Arch Neurol 2000;57:1778-80. PMID 11115247
125: Walker WC, Seel RT, Curtiss G, Warden DL. Headache after moderate and severe traumatic brain injury: a longitudinal analysis. Arch Phys Med Rehabil 2005;86:1793-800. PMID 16181945
126: Warden D. Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 2006;21:398-402. PMID 16983225
127: Warner JS, Fenichel GM. Chronic post-traumatic headache often a myth. Neurology 1996;46:915-6. PMID 8780063
128: Weiss H, Stern B, Goldberg J. Posttraumatic migraine: chronic migraine precipitated by minor head or neck trauma. Headache 1991;31:451-6.
129: Wilk JE, Herrell RK, Wynn GH, Riviere LA, Hoge CW. Mild traumatic brain injury (concussion), posttraumatic stress disorder, and depression in U.S. soldiers involved in combat deployments: association with postdeployment symptoms. Psychosom Med 2012;74(3):249-57. PMID 22366583
130: Wilk JE, Thomas JL, McGurk DM, Riviere LA, Castro CA, Hoge CW. Mild traumatic brain injury (concussion) during combat: Lack of association of blast mechanism with persistent postconcussive symptoms. J Head Trauma Rehabil 2010;25(1):9-14. PMID 20051900
131: Yamaguchi M. Incidence of headache and severity of head injury. Headache 1992;32:427-31. PMID 1446984
132: Yilmaz T, Roks G, de Koning M, et al. Risk factors and outcomes associated with post-traumatic headache after mild traumatic brain injury. Emerg Med J 2017;34(12):800-5. PMID 28689194
133: Young WB, Khoury JB, Ramadan NM. Headaches associated with head trauma (postconcussion headache). In: Goadsby PJ, Dodick D, Silberstein SD, editors. Hamilton, Ontario: B.D. Decker Inc, 2005:185-97.
134: Young WB, Packard RC. Posttraumatic headache and posttraumatic syndrome. In: Goadsby PJ, Silberstein SD, editors. Headache. Boston: Butterworth-Heinemann, 1997:253-78.
135: Young WB, Silberstein SD. Imaging and electrophysiologic testing in mild head injury. Semin Neurol 1994;14:46-52. PMID 8029559
136: Zafonte RD, Horn LJ. Clinical assessment of posttraumatic headaches. J Head Trauma Rehabil 1999;14:22-33. PMID 9949244
137: Zimmerman JD, McCarthy DM. Cervical spine fracture presenting as an orthostatic headache secondary to cerebral spinal fluid leak. J Emerg Med 2015;49(3):e73-7. PMID 26099907
138: Zirovich MD, Pangarkar SS, Manh C, et al. Botulinum toxin type A for the treatment of post-traumatic headache: a randomized, placebo-controlled, cross-over study. Mil Med 2021;186(5-6):493-9. PMID 33241323

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.
See Profile

Editor

Shuu-Jiun Wang MD

Dr. Wang of the Brain Research Center, National Yang-Ming University, and the Neurological Institute, Taipei Veterans General Hospital, has no relevant financial relationships to disclose.
See Profile

Former Authors

Kenneth Moore MD (original author), Jonathan P Gladstone MD, Shiang-Ru Lu MD, and 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-9: Headache: 784.0

Migraine: 346.9

Postconcussion syndrome: 310.2

Tension headache: 307.81
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

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

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

Also Relevant

Cluster headache
Migraine
Minor closed head injury
Neuroimaging of headache
Severe closed head injury
- Sports activities: neurologic complications
- Tension-type headache

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

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Acupuncture

Migraine: pathogenesis and pathophysiology

New daily persistent headache

Headache associated with cervical spine dysfunction

Interventional options for cervicogenic headache

Pain

Ulnar neuropathy at the elbow

Vestibular migraine

This is an article preview.
Start a Free Account
to access the full version.