Post–Acquired Brain Injury Headaches

CHAPTER 10

MAURICIO F. VILLAMAR

JONATHAN H. SMITH

OVERVIEW

Headache (HA) attributed to acquired brain injury (ABI), and particularly HA attributed to traumatic brain injury (TBI), is among the most common secondary HA disorders (Headache Classification Committee of the International Headache Society, 2013). Although posttraumatic headache (PTH) can occur in isolation, it is often a component of postconcussion syndrome (PCS), an entity that includes multiple somatic, cognitive, and psychological symptoms. These may include HA, fatigue, memory and concentration deficits, sleep disturbances, mood changes, anxiety, dizziness, blurred vision, among others (Dikmen, Machamer, Fann, & Temkin, 2010) (see Chapter 1).

Interestingly, HA and other pain disorders are more frequent in milder as compared with more severe TBI (Nampiaparampil, 2008; Yamaguchi, 1992). This is thought to be secondary to damage to central nervous system (CNS) structures involved in affective pain processing seen in severe TBI (Riechers, Walker, & Ruff, 2015), or also thought to be caused by a higher likelihood of developing a sensitization effect after mild injury (Miller, 2000). However, it is also possible that pain is underrecognized in people with deficits in communication or cognition as a consequence of severe brain injury.

The presence of post-ABI HA does not necessarily imply coexistence of severe underlying anatomical abnormalities. However, HA can be a manifestation of disorders such as intracranial or extra-axial hematomas or other mass lesions, carotid–cavernous fistulas, communicating hydrocephalus, dural leaks, and/or ventriculoperitoneal shunt malfunction. In the appropriate setting, the foregoing should be considered part of the evaluation of HA.

HISTORY

HA disorders have been written about throughout the centuries, with references to sick-headaches in Sumerian poems, Egyptian papyrus, and in the writings of Hippocrates (c.460–c.370 BCE).

Hippocrates described complications of head injury, with later authors referring to the effects of commotio cerebri after trauma (McCrory & Berkovic, 2001).

PATHOPHYSIOLOGY

The pathophysiology of post-ABI HA is yet to be fully understood. The genesis of chronic pain after CNS injury appears to be related in part to the increased expression of certain sodium channel subtypes, leading to neuronal hyperexcitability, particularly in the thalamus and in other regions involved in pain processing (Waxman & Hains, 2006). Activation of microglia and production of prostaglandin E₂ perpetuates sodium channel overexpression (Zhao, Waxman, & Hains, 2007).

Episodic tension–type HA appears to be secondary to nociceptive stimuli originating from pericranial myofascial tissues. If such noxious stimuli persist over a prolonged period of time, sensitization of pain pathways in the CNS such as the spinal dorsal horn and the trigeminal nucleus may ensue, leading to HA chronification. Decreased antinociceptive activity from supraspinal structures, impairing the descending inhibition of pain, may also be a contributing factor (Bendtsen & Jensen, 2009).

Pathogenesis of post-ABI migraine-like HA is complex, and many mechanisms have been involved. These include increased cortical excitability secondary to proinflammatory and excitatory molecules leading to spreading depression; structural damage to the meninges and blood vessels; and dysfunctional activation of the trigeminal nucleus caudalis (Riechers et al., 2015).

Cervicogenic HA may develop as a consequence of injury to the cervical vertebrae and cervical paraspinal muscles. This is particularly common in acceleration–deceleration or rotational injuries affecting the head and neck (Riechers et al., 2015).

ETIOLOGY

HA may occur in the setting of multiple causes of ABI. These may all be identified through an appropriate clinical history and neurologic examination.

Traumatic Brain Injury

TBI is defined as a structural or functional lesion secondary to the effect of external forces on the head, such as blunt trauma, acceleration/deceleration movements (e.g., whiplash), penetrating injuries, blasts or explosions (see Chapters 1 and 2).

HA is among the commonest sequelae of TBI, and most of the information discussed in this chapter is centered on this topic.

Cerebrovascular Disease

HA that occurs in the setting of an acute onset, focal neurologic deficit should prompt concern for a medical emergency, such as ischemic stroke or intracranial hemorrhage.

HA that is abrupt in onset and progression (“thunderclap onset”) requires immediate emergency evaluation to screen for aneurysmal subarachnoid hemorrhage.

Meningoencephalitis/Encephalitis

HA is the commonest and often the first symptom of meningitis and encephalitis (see Chapter 5).

The diagnosis should be suspected when HA is accompanied by neck stiffness, fever, altered mental status, and/or seizures.

Early, aggressive treatment with antimicrobial agents is critical to reducing morbidity and mortality resulting from CNS infections.

Release of bacterial toxins and inflammatory mediators directly stimulate sensory terminals in the meninges. Increased intracranial pressure can occur in encephalitis and also have a role in the genesis of HA (Headache Classification Committee of the International Headache Society, 2013).

EPIDEMIOLOGY

Prevalence of HA immediately following TBI can be as high as 90% (Obermann, Keidel, & Diener, 2010). It can persist beyond 6 months in up to 44% of patients (Martelli, Grayson, & Zasler, 1999), and beyond 1 year in 18% to 33% (Lew et al., 2006).

Mild TBI has been linked to a higher risk of developing PTH as compared with moderate or severe TBI. Another significant risk factor is the preexistence of HA before injury (Lew et al., 2006). Older age appears to be protective and, although some evidence suggests a higher likelihood of developing PTH in females, there are no clear differences between genders (Lucas, Hoffman, Bell, & Dikmen, 2014).

The prevalence of PTH differs between civilian and military populations. Among civilians, HA has been reported to persist for more than 3 months in 15% of mild TBI patients (Faux & Sheedy, 2008). This contrasts with a prevalence of 52% to 55% among Operation Iraqi Freedom and Operation Enduring Freedom veterans 1 year after suffering mild combat TBI (Lew et al., 2009; Ruff, Riechers, Wang, Piero, & Ruff, 2012). This may be related, at least in part, to differences in brain injury mechanisms. For instance, exposure to blasts is much more frequent in the latter population, and has been associated with neuronal dysfunction even in the absence of obvious structural lesions (Kato et al., 2007). Likewise, the concurrent presence of mental health conditions (e.g., depression and posttraumatic stress disorder), which is higher in military populations, may play a role.

CLINICAL PRESENTATION

Clinical presentations of PTH are variable. Multiple HA subtypes have been described, including those with characteristics of tension-type HA, migraine, cervicogenic HA and, more rarely, cluster HA, hemicrania continua, and chronic paroxysmal hemicrania (Finkel, Yerry, Scher, & Choi, 2012).

In civilians, tension-type HA appears to be the most frequent semiology (37%–85% of all PTH) (Evans, 2004; Lew et al., 2006), although some studies suggest that migraine may be the predominant type (Lucas, Hoffman, Bell, Walker, & Dikmen, 2012). Cervicogenic HA is less common, and approximately 10% of PTH cannot be classified as a diagnosable syndrome (Lucas et al., 2014). Among military populations, as well as in children, most PTH (55%–78%) are described as migraine-type (Kuczynski, Crawford, Bodell, Dewey, & Barlow, 2013; Theeler & Erickson, 2009; Theeler, Flynn, & Erickson, 2010).

The most common semiologies of post-ABI HA are characterized by the following features:

Migraine phenotype: Location preferentially unilateral, but can change sides. Pain described as throbbing or pulsating. Frequently associated with nausea, vomiting, or dizziness. Tends to worsen with exertion and exposure to loud sounds or bright lights. Can be preceded by transient neurologic symptoms (i.e., aura). Moderate to severe intensity.

Tension-type phenotype: Location bilateral, predominantly occipital, although commonly holocephalic, helmet- or band-like. Pain typically dull, pressure-like, pulling, or dragging but not pulsating. Absence of associated nausea or vomiting, and less frequent environmental sensitivities as compared to migraine. Not worsened by physical activity. Mild to moderate intensity.

DIAGNOSTIC CONSIDERATIONS

A careful clinical assessment is essential in the evaluation of HA. HA diaries are also critical in establishing HA characteristics, triggers, premonitory signs, severity, frequency, and duration.

Brain imaging studies are not ordered routinely in all patients with post-ABI HA. However, certain signs and symptoms can suggest the presence of intracranial lesions or elevated intracranial pressure that warrant neuroimaging. These may include HA that awakens the patient from sleep, HA that worsens with Valsalva maneuver or when lying down, or the concomitant presence of double vision, seizures, gait difficulty, or papilledema (optic disk swelling). Any abnormality on the neurologic examination should prompt further investigation.

If symptoms develop acutely after the injury, a CT scan of the head is the initial test of choice, particularly to evaluate for hemorrhagic complications. When evaluating the patient days, weeks, or longer after the injury, MRI is of much higher yield.

Traumatic Brain Injury

According to the third edition of The International Classification of Headache Disorders (ICHD-3), HA is arbitrarily attributed to traumatic injury if it develops within 7 days of either (a) head injury, (b) regaining consciousness following head injury, or (c) discontinuation of drugs that impair ability to sense or report HA following injury (Headache Classification Committee of the International Headache Society, 2013).

Temporal relation is easy to establish when HA occurs shortly after trauma. However, in a study of civilians with mild to moderately severe TBI, approximately 28% of new HA had its onset 3 or more months after the injury (Hoffman et al., 2011). Among war veterans, only 27% of HA had its onset within the first 7 days of injury (Theeler & Erickson, 2009), all of which complicates the diagnosis of post-ABI HA.

Temporal classification of HA attributed to TBI:

Acute: if HA duration is less than 3 months.

Persistent: if HA continues for more than 3 months after injury and cannot be better explained by another ICHD-3 diagnosis.

When HA following trauma becomes persistent, the possibility of medication-overuse HA should be considered.

Cerebrovascular Disease

HA with acute onset neurologic deficits requires emergency room evaluation with CT scan of the head to screen for intracranial hemorrhage.

The clinical history of a thunderclap HA (rapidly peaking, typically within 1 minute) requires a standard emergency room approach with a CT, sometimes followed by a lumbar puncture to screen for a ruptured aneurysm.

Meningoencephalitis/Encephalitis

The classic triad of HA, fever, and neck stiffness seen in meningitis is relatively uncommon, although the presence of two of these features is relatively sensitive for the diagnosis (Attia, Hatala, Cook, & Wong, 1999).

The diagnosis requires empiric treatment with intravenous antimicrobials, along with blood cultures and spinal fluid evaluation. Patients who are older (>60), immunocompromised, and/or have an abnormal neurologic examination should undergo CT imaging of the head before lumbar puncture out of concern for precipitating brain herniation.