Post-traumatic Headache

Introduction

Patients with post-traumatic headache (PTH) may seem an enigma to the treating physician. Frequently, patients with a serious head injury will not complain of any headache symptoms. In contrast, patients may present with severe headaches following a minor head trauma. Post-traumatic headache accounts for approximately 4% of headache disorders. It is a common consequence of traumatic brain injury (TBI), especially, as mentioned, mild TBI (mTBI). The most common causes of TBI include traffic accidents, falls, sports injuries and violence – in that order. It has been estimated that nearly 70 million TBIs occur annually worldwide. In the United States, the CDC has estimated that there were 214,110 TBI-related hospitalizations in 2020 and 69,473 TBI-related deaths in 2021. Fortunately, mTBI (also called concussion) accounts for 80-90% of all TBI cases. Less fortunately, the cumulative 1-year incidence of PTH in patients with mTBI has been estimated at 91% (and 71% among patients with TBI in general).

It is important to differentiate between:

• Acute PTH
• Persistent PTH.

The basic distinction between acute and persistent PTH is duration: acute PTH lasts for a maximum of three months. Beyond that, PTH is classified as persistent. The ICHD-3 classification includes criteria for both acute PTH and persistent PTH caused by traumatic injury to the head, with each of these types further subdivided by TBI severity into PTH attributable to mTBI and PTH attributable to moderate/severe TBI (Table 9-1). To be classified as PTH, the headache must develop within 7 days of the TBI, regaining of consciousness after TBI, or discontinuation of any medication impairing the ability to sense or report the headache. In addition to PTH attributable to head injury, the ICHD-3 also provides diagnostic criteria for other types of traumatic injury-related headaches, including:

• Acute headache attributed to whiplash (ie, sudden acceleration or deceleration movements of the head with flexion or extension of the neck)
• Persistent headache attributed to whiplash
• Acute headache attributed to craniotomy
• Persistent headache attributed to craniotomy.

Goldstein has indicated that the term “postconcussive headache” is distinct because a blow to the head does not inherently result in a loss of consciousness. He encourages using the words “traumatic” or “concussive” to describe head injuries that precipitate headache. It is important to remember that PTH, independent of the original cause, is part of a post-traumatic syndrome.

The post-traumatic syndrome is usually associated with:

• Headache
• Dizziness
• Irritability
• Lack of concentration
• Intolerance to alcohol consumption.

The origin of PTH as a pathophysiologic or psychological response to trauma is a subject of much debate. Research in the 1940s was conducted on veterans returning from the war who had incurred head injuries. The investigators, led by Brenner, attributed the symptom complex following head injury as being related to:

• Specifics of the injury
• Personality of the injured
• Compensation elements
• Sociologic determinants.

Post-traumatic headache was common in patients with preinjury neurotic or nervous symptoms and emotional reactions to the trauma. Headache incidence was also related to laceration of the scalp. In the absence of coma or amnesia, the incidence of headache was lower.

Studies by Simons and Wolff revealed that post-traumatic headache could be attributed to excessive muscle contraction, entrapment of nerves and scar tissue, and dilated vessels. Acceleration-deceleration injuries may also result in headaches. Vijayan and Watson reported on a series of patients who did not report loss of consciousness but experienced headache at the site of injury and who suffered scarring and entrapment of sensory nerves. They concluded that headache could result from scar formation or direct injury and disordered regeneration.

Nevertheless, the pathophysiology of PTH is to a large extent unknown and remains to be elucidated. Current consensus proposes five possible mechanisms: impaired descending modulation, neurometabolic changes, cortical spreading depression (CSD), CGRP-related mechanisms, and neuroinflammation (Figure 9-1). Briefly, the impaired descending modulation hypothesis (Figure 9-1a) posits that damage to the cortical and subcortical regions could prevent the normal functioning of pain modulation systems that inhibit the trigeminocervical complex responsible for the feeling of pain. The neurometabolic changes hypothesis (Figure 9-1b) suggests that mechanical damage to the head results in neuron-level damage, inducing excessive glutamate release and dysregulating the normal ion flux; restoration of ion homeostasis then depletes cellular ATP stores and causes oxidative stress, possibly causing migraine-like headache. In migraine, a self-propagating wave of neuronal and glial depolarization – CSD – is associated with disruptions of the normal ion gradients, increased neuronal excitability, and activation of the trigeminal sensory system (Figure 9-1c); there is evidence from experimental models that a similar mechanism may operate in PTH. Data from rat and mouse studies suggests that CGRP signaling in involved in PTH in a mechanism similar to that of migraine (Figure 9-1d); administration of CGRP antagonists has been shown to improve the animals’ cephalic pain hypersensitivity – an indirect measure of headache. Finally, the neuroinflammation hypothesis posits that mechanical injury activates the production and release of pro-inflammatory cytokines in glial cells, which in turn cause damage to neuronal and vascular tissues (Figure 9-1e), and activates the trigeminovascular system. It is likely that PTH results from a combination of these and other, still unknown, mechanisms.

Post-traumatic headache can present in many forms:

• Tension-type headaches (TTH)
• Migraine
• Occipital neuralgia
• Traumatic dysautonomic cephalalgia.

Post-traumatic TTH may be the most frequently occurring consequence of head injury. The clinical picture of these headaches includes:

• Continuous symptoms
• Pain described as hatbandlike, caplike, or pressure
• Not accompanied by neurologic symptoms.

Patients may also complain of associated symptoms, including:

• Vertigo
• Light-headedness
• Giddiness
• Anxiety
• Malaise
• Fatigue.

Head and neck injuries can occur together. The following injuries may trigger TTH:

• Sprain of the cervical neck
• Exacerbation of disc disease
• Exacerbation of preexisting spondylosis.

One study by De Benedittis’ group found that patients with post-traumatic, chronic TTH had higher scores on the Minnesota Multiphasic Personality Inventory (MMPI) test in the following scales:

• Hypochondriasis
• Depression
• Hysteria
• Schizophrenia.

These investigators did not find any correlation between the headaches and the patient’s:

• Age
• Neurologic deficits
• Duration of unconsciousness
• Pending litigation and compensation.

The clinical picture of post-traumatic migraine is similar to that of nontraumatic migraine. Preexisting migraine can be exacerbated by trauma. Certain physical activities, although not considered traumatic, can trigger vascular headaches. For example, the “footballer’s migraine” is precipitated by the heading of a soccer ball. If the patient had no prior history of headaches, the diagnosis of migraine may be established by a family history of this disorder. Similar symptoms may occur in rugby players (who might, for example, sustain a blow to the face during a tackle) or hockey players (who may, for example, be hit in the nose during a check). Transient global amnesia may manifest after mTBI and has been associated with trauma-induced migraine.

Autonomic dysfunction with vasomotor instability may represent a contributing cause of post-traumatic migraine. Sustained muscle contraction resulting from the injury may directly affect the extracerebral vasculature. A high familial incidence of migraine has been demonstrated in patients with post-traumatic migraine. In children with juvenile head trauma, the following symptoms, similar to those of juvenile migraine with aura, have been observed:

• Cortical blindness
• Hemiparesis
• Somnolence
• Brain stem dysfunction.

In a study by Haas’ group of 25 children with juvenile head trauma, 15 had a positive family history for migraine. They also reported a 12% incidence of transient focal neurologic abnormalities with migraine in family members.

Cluster headaches can occur after head injury. Some patients with cluster headaches will report an incidence of head injury prior to the onset of the initial series. Cluster headaches that occur post-traumatically are similar in symptomatology to the nontraumatic type.

Following fracture of the jaw or facial bones with concomitant injury to the branches of the facial nerve, patients may experience post-traumatic trigeminal neuralgia. These symptoms could also ensue after surgical trauma. As with other cases of trigeminal neuralgia, patients usually experience sensitivity to touch over the affected area and tenderness of the nerve may occur. Other post-traumatic neuralgias, such as those affecting the glossopharyngeal nerve and the greater occipital nerve, may also occur.

After head or facial trauma, symptoms similar to temporomandibular joint disorder may occur. Myofascial pain dysfunction syndrome may manifest in patients who incur jaw injuries with stretching and tearing of the ligamentous structures of the jaw joint.

Vijayan described a new form of post-traumatic headache in 1977 – traumatic dysautonomic cephalalgia – which results from a soft tissue injury to the anterior neck structures surrounding the carotid vessels. The trauma was due to either blunt, nonlacerating or stretch injuries. The symptoms included:

• Unilateral throbbing headache (ipsilateral to the injury side)
• Excessive sweating
• Pupillary dilation
• Photophobia
• Blurred vision
• Nausea.

Between headaches, the patient may experience unilateral miosis and ptosis. The cause of the headaches was attributed to b-sympathetic overactivity. A clinical sign is the positive response to therapy with propranolol.

Trauma-related neck injuries may also cause headaches. Pain may be noted in the neck, suboccipital, and occipital areas. Acceleration-extension injuries, more commonly known as whiplash, are frequently the culprit in these headaches. These injuries are dependent on the velocity of the respective vehicles. Restraints, such as seat belts and head rests in the appropriate position, will prevent forceful hyperextension of the neck. The origins of the pain may be due to trauma of:

• Muscle
• Ligaments
• Discs
• Bones
• Nerve roots.

The pain may be focal or suboccipital-occipital, or it may radiate to involve all areas. Associated neck and scalp muscular contraction may precipitate the pain or exacerbate preexisting pain.

Post-traumatic headache may also be associated with unusual complications, and the headache may not conform to a standard clinical picture, thus posing a diagnostic dilemma. Post-traumatic complications include:

• Daytime sleepiness
• Otogenic pneumocephalus
• Tension pneumocephalus
• Post-traumatic hydrocephalus.

Symptoms of normal-pressure hydrocephalus may be present. Headache has also been associated with hematoma of the corpus callosum. Trauma may also cause:

• Visual abnormalities
• Monocular or binocular blindness
• Optic nerve injuries with anterior visual pathway damage due to sphenoid bone fractures
• Associated carotid cavernous sinus fistulas.

Traumatic dissection of the extracranial carotid artery may have a delayed manifestation as headache, occurring months to years after the original trauma. Symptoms include:

• Focal cerebral ischemia
• Oculosympathetic paresis and bruit.

It is essential that the patient experiencing headaches following a head or neck injury undergo a thorough workup, with appropriate diagnostic testing. The use of computed tomography (CT) scanning, magnetic resonance imaging (MRI), and plain skull films can greatly facilitate the diagnostic process. Cervical spine X-rays may also be indicated. Whether there is a family history of similar headaches should be determined during the interview. Psychological and psychiatric factors should also be investigated. Trauma can greatly impact work productivity and daily activities. The MMPI may be an important tool in the workup and delineate the presence of anxiety, somatization and conversion mechanisms.

The treatment of post-traumatic headache disorders is usually similar to that of nontraumatic headaches. Management of post-traumatic TTH and migraine utilizes conventional forms of therapy for these disorders. Pharmacologic options that do not cause cognitive changes or fatigue (e.g., anti-CGRP antibodies, onabotulinumtoxinA, and local anesthetic-based nerve blocks) are often more suitable for the treatment of PTH than other pharmacologic agents. In addition to pharmacologic agents, patients with post-traumatic headaches may benefit from physical measures such as biofeedback and physical therapy, including the use of transcutaneous electric nerve stimulation (TENS). A cervical collar and orthopedic pillow may provide some relief from the pain. Psychological counseling may be required for patients with chronic headaches following head injury.

In treating acute headaches, nonhabituating analgesics should be employed and the quantities consumed carefully monitored. Standard abortive agents should be used; the available prophylactic therapies have been discussed in previous sections. It is essential that the treatment be individualized, with a comprehensive approach to the headache problem.

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