Headache is the cardinal symptom of the posttraumatic syndrome that follows head trauma (HT) and cervical spine whiplash injury (WI). Knowledge of the different types of posttraumatic headache (PTH) (a) guides in the choice of headache-specific treatment; (b) helps in avoiding chronification of the headache and hastening remission; and ultimately, (c) provides the basis for improving the clinical outcome of the patient (57,58). This chapter provides an overview of the definition, epidemiology, classification, pathogenesis, clinical picture, diagnosis, course, and treatment of acute PTH. Chronic PTH (80) is discussed in a subsequent chapter of this book.

The International Classification for Headache Disorders-II (ICHD-II) requires that PTH occur in close temporal relationship with HT or WI of varying severity and states that late-acquired headaches (2,16), occurring later than 1 week up to 3 months after a traumatic event, are not sufficiently validated (41).

PTH is not uniform in its epidemiology or clinical presentation. Headaches characteristic of tension-type headache, migraine, cluster headache, cervicogenic headache, headache of intracranial hemorrhage, or elevated intracranial pressure headache all have been described following HT.

The frequency of the different types of PTH is as follows: tension-type headache, 85% (27,28,34,36); postwhiplash (unilateral) cervicogenic headache, 8% at 6 weeks, 4% at 6 months, and 3% at 1 year (female:male ratio of 3:2) (24,25); and migrainelike headache, 2.5% (more common in children and teenagers) (33,97,103). The lifetime prevalence of an HT-associated migraine is 1.4% (86). The exact frequency of posttraumatic clusterlike headache is not
known but this type of headache remains rare (82,102). Basilar migrainelike PTH (36,43) and PTH associated with sexual activity (21) have been reported anecdotally. Analgesic overuse is described in 19% of all cases of chronic PTH and in 25% of chronic posttraumatic tension-type headache (36).

The incidence of head trauma is 180 to 220 per 100,000 in North America and 350 per 100,000 in Europe (30), which is comparable to that of cerebrovascular ischemia, 10 times the incidence of Parkinson’s disease (20 of 100,000), and 500 times that of myasthenia gravis (0.4 of 100,000) (55,56).

Approximately 2 million HTs occur per year in the United States, of which 80% are mild, 10% moderate, and 10% severe (46,55,56).

The frequency of PTH in HT varies between 31% and 90% (15, 20,59,68). This implies that the relative incidence of acute PTH is up to 200 per 100,000 in the United States and 315 per 100,000 in Europe (specifically, Germany). The absolute rates of newly diagnosed PTH per year are estimated as 1,800,000 in the United States and 270,000 in Germany.

The severity of the head injury is inversely proportional to the occurrence of acute PTH (72% in mild head injury, 33% in severe head injury [106]) and to chronic PTH (18). There is also an inverse relation between the duration of loss of consciousness (14) or the duration of posttraumatic amnesia (16) and the incidence of PTH.

Acceleration injuries of the cervical spine (i.e., WI) are the most common mechanisms of cervical trauma in traffic accidents (94). In one study, 88% of patients complained of headache after a mild WI (Quebec Task Force, QTF Grade II) without bony injuries or accompanying neurologic deficits (47,50,52). Other studies have indicated incidence rates of 40 to 97% (24,44,52). These wide ranges may be related partially to differences in registers used for analysis (insurance, police, hospital) and are lower in a police register (72) or an insurance register (17).

Exact figures for the incidence of PTH following moderately severe WI (with neurologic deficits; Quebec Task Force, Grade III [99]) or severe injury of the cervical spine (with osseous lesions and neurologic deficits; Quebec Task Force, Grade IV) are not available because of inadequacies in reporting the severity of the injury and difference in patient populations.

The exact pathophysiology of acute PTH is unknown. Different mechanisms of pain are likely to play a role in acute PTH because the clinical presentation could mimic migraine, tension-type headache, or other forms of primary headaches. The mechanism(s) of primary headache may help us understand the corresponding subtype of acute PTH.

Acute posttraumatic cervicogenic headache (following WI or HT combined with neck sprain) is likely the result of the multisegmental pain impulses generated from nociceptive afferents in stretched muscles, ligaments, and intervertebral disks as well as from sympathetic nerve fibers of the arterial vessels entering the cervical spinal cord via C-fibers of the C2-C5 dorsal rami (74,75). The convergence between these upper cervical roots and the spinal nucleus of the trigeminal nerve provides a pathway for referral of posttraumatic neck pain to the frontal region (and vice versa [11,53]). Rarely, direct traumatic compression of C2 fibers in the lateral atlantoaxial joint provides another explanation for cervicogenic headache as demonstrated post-mortem (9). Sympathetic vertebral nerve irritation (6) and ischemia of the vertebral artery (4,5) are other postulated, although debated (10), causes of posttraumatic cervicogenic headache.

An alteration of the antinociceptive inhibitory temporalis reflex in acute PTH of the tension type following WI suggests a transient dysfunction in central pain processing with an impairment of the serotonergic descending inhibitory pain system (48). Similar reflex abnormalities also have been described for the idiopathic tension-type headache (95). Acute PTH of tension type is accompanied by a varying degree of increase in general pain sensitivity (70,100). Subsequent chronification of the acute posttraumatic pain syndrome may be related to a windup phenomenon of central pain sensitization. The impact of the accompanying vegetative disturbances, subjective impediment, or disturbances in mood and well-being on pain intensity and duration is not fully elucidated (46,52).

In head injury, a variety of posttraumatic neurochemical, neurohumoral, and neuroelectrical changes are described (107). They include elevated extracellular K⁺ and intracellular Na⁺, Ca⁺, and Cl⁻, reduced intracellular and total brain Mg, influx of extracellular Ca²⁺ (in axolemmas), accumulation of platelet-derived 5-hydroxytryptamine in the central nervous system, increased release of excitatory amino acids (e.g., glutamate), cortical spreading depression, increased levels of endogenous opioids, and increased nitric oxide activity (73,107). Some authors consider this altered neurochemical environment to be responsible for the acute manifestation of PTH or aura, and suggest a mechanistic cascade for the syndrome that is similar to primary migraine (73,107,108).

Animal models and functional brain imaging studies in HT and WI show various structural, blood flow, and metabolic changes, which do not necessarily translate into mechanisms of acute PTH. Factors likely to be involved in the pathophysiology include:

1. Referred pain from nociceptive input caused by lesions of musculoskeletal, discoligamentous, and other soft-tissue structures (including vessels, perivessel sheets, and nerves)

2. Activation of meningeal nociceptive afferents due to traumatic epidural, subdural, and subarachnoidal bleeding

3. Stretching of pain-sensitive intracranial structure from increased intracranial pressure

4. Intracranial hypotension (79,81)

5. Activation of the trigeminovascular system by posttraumatic sinus venous thrombosis

The IHS diagnostic criteria (5.1.1) for acute PTH attributed to moderate or severe head injury (Headache Classification Committee, 2004) (40) are as follows:

A. Headache, no typical characteristics known, fulfilling criteria C and D

B. Head trauma with at least one of the following:

1. Loss of consciousness for >30 minutes

2. Glasgow Coma Scale (GCS) <13

3. Posttraumatic amnesia for >48 hours

4. Imaging demonstration of a traumatic brain lesion (cerebral hematoma, intracerebral and/or subarachnoid hemorrhage, brain contusion and/or skull fracture)

C. Headache develops within 7 days after head trauma or after regaining consciousness following head trauma.

D. One or other of the following:

1. Headache resolves within 3 months after head trauma.

2. Headache persists but 3 months have not yet passed since head trauma.

The IHS diagnostic criteria (5.1.2) for acute PTH attributed to mild head injury (1) (Headache Classification Committee, 2004) (40) are as follows:

A. Headache, no typical characteristics known, fulfilling criteria C and D

B. Head trauma with all the following:

1. Either no loss of consciousness or loss of consciousness of <30 minutes’ duration

2. Glasgow Coma Scale (GCS) = 13

3. Symptoms and/or signs diagnostic of concussion

C. Headache develops within 7 days after head trauma.

D. One or other of the following:

1. Headache resolves within 3 months after head trauma.

2. Headache persists but 3 months have not yet passed since head trauma.

The IHS diagnostic criteria (5.6.1) for acute headache attributed to other head and/or neck trauma (Headache Classification Committee, 2004) (40) are as follows:

A. PTH, no typical characteristics known, fulfilling criteria C and D

B. Evidence of head and/or neck trauma of a type not described above

C. Headache develops in close temporal relation to, and/or other evidence exists to establish a causal relationship with, the head and/or neck trauma.

D. One or other of the following:

1. Headache resolves within 3 months after the head and/or neck trauma.

2. Headache persists but 3 months have not yet passed since the head and/or neck trauma.

The IHS diagnostic criteria (5.3) for acute headache attributed to whiplash injury (Headache Classification Committee, 2004) (40) are described elsewhere in the book.

Headache (with or without accompanying neck pain) is the cardinal symptom of the posttraumatic syndrome (108). Direct HT and WI cause a similar syndrome. In the acute phase, it is characterized by vegetative symptoms (dizziness, nausea, vomiting, orthostatic dysregulation, and thermodysregulation), a neurasthenic depressive syndrome (subjectively reduced cognitive performance sometimes with overt neuropsychologic deficits, mood alteration, nervousness, and irritability), and a sensory syndrome characterized by excessive sensitivity to light and noise (49).

Following WI, the PTH is associated with a feeling of heaviness of the head in almost half of the patients. It usually follows a complaint-free interval of a few hours to 1 day (52). The headache is mainly occipital, dull pressing, or dragging and reaches maximum intensity in the evening (47,49,50). Headaches of the tension type following head or neck injury (i.e., WI) have similar features (36,50,52). Some patients with the posttraumatic stress disorder (PTSD) report headache shortly after the trauma (a mild or trivial head injury in some cases) but the DSM-IV diagnostic criteria for PTSD do not include headache as a prominent symptom (3). Furthermore, acute PTH and PTSD are distinct in temporal profile despite the overlap in vegetative symptomatology. Acute PTH usually resolves within 3 weeks (47,49,52). In contrast, PTSD is only diagnosed safely when symptoms persist for more than 2 months.

The clinical features of PTH overlap with those of the primary headache disorders (i.e., migraine, cluster, tension, etc.) (see Table 105-1). Posttraumatic tension-type headache (90%) is characterized by a dull-pressing, dragging, or pulling pain, which is mainly holocephalic, bandor helmetlike, usually nucho-occipital, seldom episodic, and often continuous (101). Tension-type PTH must be differentiated from posttraumatic cervicogenic headache (8% after WI [24,25]), which is mainly occipitonuchal and typically dragging. The pain of posttraumatic cervicogenic headache radiates from occipital to frontal. It is not holocephalic, strongly unilateral without side change, and commonly associated with limited mobility of the cervical
spine. The pain can be triggered by turning the head, sometimes in a position resulting in pressure on the occipital nerve entry points. The diagnosis is confirmed by a trauma-related bony injury of the cervical spine and by pain relief after local anesthetic infiltration of the tender greater occipital nerve or C2 root (75).