CHAPTER 51

Headache

Tracey Kramar, MS, PA-C • Christine Lazaros Amendola, MS, PA-C, NY-SAFE

Headache is a challenging symptom for both patients and providers. Etiologies are varied and include idiopathic and specific conditions, with prognoses ranging from benign to life threatening. Furthermore, depending on the nature of the headache syndrome, the impact on the patient and on society may be minimal or major. Nearly 45 million people suffer from chronic headaches, and headache is a common cause for primary care visits (Kunkel, 2010). According to the World Health Organization, migraine headaches are the 19th most common disease causing disability worldwide. Thus, it is important to recognize serious secondary causes of headache and manage the benign yet potentially disabling primary headaches.

The primary headache syndromes are those headaches that are considered idiopathic, including migraine, tension-type headache (TTH), and cluster headache. Secondary headache syndromes usually can be found to have a treatable cause, which will result in “cure” of the headache. These headaches may be caused by a wide variety of conditions, from the relatively rare brain tumor and subarachnoid hemorrhage to the more common and benign systemic viral syndromes. Diagnostic classifications of headaches are discussed in this chapter, using the updated and revised version of the International Headache Society (IHS) criteria (International Headache Society, 2004). As per the IHS, headaches are divided into two categories: primary and secondary.

ANATOMY, PHYSIOLOGY, AND PATHOLOGY

The symptom of headache arises when pain is referred to the surface of the head from either intra- or extracranial sources. Although the anatomy and pathophysiology of all headache syndromes have not been fully elucidated, certain structures and contributing physiology are understood and aid the provider in both diagnosis and treatment.

Anatomic Sources for Headache

Intracranial structures that are implicated in some headaches include the periosteum, the dura at the base of the skull, the venous sinuses, the anterior and middle meningeal arteries, and the upper cervical nerves and cranial nerves V, VII, IX, and X. Pain from intracranial sources above the tentorium is usually referred via cranial nerve V to the frontal, orbital, and temporal regions. Pain originating below the tentorium and in the posterior fossa is typically transmitted via the facial, glossopharyngeal, and vagus nerves and the upper cervical nerves to the ear, nose, throat, and occiput. The brain parenchyma and bony skull themselves are almost completely insensitive to pain, as are certain cranial nerves (I, II, and VIII).

Extracranial structures that can give rise to headache include the skin, fascia, muscles, extracranial vasculature, ears, nasal mucosa, eyes, teeth, and cervical spine (Goroll, May, & Mulley, 1995); pain referred from these structures usually directly overlies the structure.

Pathophysiological Mechanisms

Several types of stimuli affect these structures and become detected as pain. Dilatation of intra- and extracranial vasculature occurs in migraine, giant-cell arteritis, malignant hypertension, eclampsia, transient ischemic attacks, arteriovenous malformation, and alcohol or drug withdrawal. Contraction or tension of cranial and cervical muscles is implicated in TTH, temporomandibular joint dysfunction, and head or neck trauma.

Distention, stretching, or displacement of the dura or cranial nerves may be associated with an increase or decrease in intracranial pressure, mass lesions, or mass effect from bleeding. Inflammation of the meninges, as in meningitis or meningoencephalitis, or of cranial or spinal nerves, as in trigeminal neuralgia, mass lesions, and cervical radiculopathy, also can cause headache. Iritis and angle-closure glaucoma may yield headache along the trigeminal nerve (cranial nerve V, first division), in addition to eye pain (Wyngaarden, Smith, & Bennett, 1992).

The known pathophysiology of the primary headache syndromes reveals complex neurohormonal and neurochemical contributors. Migraine, for example, involves both vascular and neurologic factors. Vascular changes include constriction of branches of the carotid artery, causing the prodromal symptoms, followed by arterial dilation, causing the pain, and ending with arterial wall edema, which accounts for the sometimes protracted pain. However, regional blood flow does not explain all aspects of migraine. A neurologic component may be mediated by a phenomenon called cortical spreading depression, which decreases the excitability of central neurons to neurochemical transmitters.

Primary headaches are a common problem in the United States. In the United States, head pain was the fifth most common complaint reported by patients presenting to the emergency department, and approximately 1.2% of patients seek outpatient care for headaches (Smitherman, Burch, Sheikh, & Loder, 2013). According to the International Classification of Headache Disorders-II (ICHD-II), TTHs are the most common headache reported, with a lifetime prevalence as high as 78%. Approximately 12% of the adult population in the United States reports being affected by migraine headaches; most of these occur in early adulthood, but they can start as early as elementary school age. Migraine headaches are more common in women than men (~6% men and ~18% females) (Gillmore & Michael, 2011). Cluster headaches are the least common primary headache. These affect less than 1% of the population, with men approximately five to eight times more likely to suffer than women (Kunkel, 2010). The predominance of headaches not only causes poor quality of life among sufferers, but in the working class it also creates financial issues due to absences from or poor performance at work (Taylor, 2013). Table 51.1 shows typical prevalences for the primary headache syndromes.

Among secondary headache syndromes, many of the relatively benign types are highly prevalent. The more serious secondary headache syndromes are, fortunately, relatively rare.

The lifetime prevalence for headaches secondary to head trauma is 4% and in those who suffer from medication overuse it is at a low range of 0.7 to 1.7%. While those patients who report headaches from an intracranial hemorrhage constitute approximately 50% of secondary headaches, the lifetime prevalence of headache is much lower in this population (Perkins, 1998).

Age

Primary headache syndromes can have their onset at any age, but typical patterns are seen. Migraine headaches tend to present in the second and third decade. The peak prevalence of migraines occurs at approximately 40 years of age (Ebell 2006), whereas TTHs peak in the third decade for both men and women and decrease slightly with age (Bendtsein et al., 2010).

In contrast, vascular and other secondary headaches are more prevalent in the elderly, necessitating close attention to the presentation, or change in pattern, of headache in the elderly.

Gender

Among the primary headache syndromes, migraine and TTH disproportionately affect women. The 1-year prevalence of migraines is 6% in men and 18% in women. The gender differences are further accentuated by age and subtype of headache, as shown in Table 51.2.

Source: Bajwa and Sabahat, 2013; Chawla, 2013; Millea, 2002.

Source: Kunkel, 2010; Lipton et al., 2004.

Cultural Factors

The IHS classifies headaches according to their unique definition or pathological basis (Table 51.3). The IHS system then provides a list of diagnostic criteria that characterize each headache syndrome by its specific features—its history, pattern of recurrence, and known contributing factors.

Clinical use of the IHS system, therefore, relies on the ability of the provider to elicit a sound and complete history. Indeed, because primary headaches have no physical markers, the history is the provider’s prime tool for diagnosis. The physical examination and laboratory workup are used selectively to detect other illnesses or specific treatable entities when indicated.

HISTORY AND PHYSICAL EXAMINATION

Approximately half of headache sufferers, depending on the type of headache, do not seek care or obtain a formal diagnosis. Those who do seek care may have already had headaches for some time; others come in very early, at the first sign of headache. In general, the secondary headache syndromes present more acutely or can have more serious consequences, whereas the primary headache syndromes often have a benign prognosis but can be quite limiting if not well diagnosed or treated. It is important to look for “red flags” when getting a detailed history from a patient with the complaint of headache.

The headache history (Table 51.4) should be used to characterize the headache and discern any acute or serious features. Unusual symptoms should be assessed: headache that flares during coughing, sneezing, or physical exertion (including sex); headache described as the “worst ever”; ongoing neurologic symptoms and signs during or after the headache; seizures or syncope; red eye; and others (see “Referral Points and Clinical Warnings” section). Headache that awakens the patient from sleep is another feature that should alert the provider to possible intracranial mass.

Additional essential elements of the history include:

The physical examination is used to find any secondary causes of headache and to screen for warning signs of serious etiologies. A general examination, including a complete neurologic examination, is essential. Fever, abnormal mental status, restricted range of motion on neck examination, hypoxia, purulent nasal discharge, and clicks on jaw movements may all point to secondary causes of headache. Warning signs of neurologic compromise include persistent visual field defects, focal weakness or sensory loss, seizures, orbital bruits, change in mental status (confusion, drowsiness), asymmetrical pupillary response, and papilledema. Any unusual finding on the history or physical examination should prompt the provider to consider a more sophisticated workup, which may include immediate consultation with a neurologist or infectious disease specialist or referral to the emergency department.

Primary Headache Syndromes

MIGRAINE HEADACHES

Both migraine without aura (common migraine, Table 51.5) and migraine with aura (classic migraine, Table 51.6) are typically recurrent, unilateral, throbbing, or pulsating headaches accompanied by nausea or vomiting, or by photophobia and phonophobia. They tend to last 4 to 72 hours if untreated. The site, intensity, and features can vary from headache to headache.

Patients can often identify certain precipitating factors that seem to trigger the headaches. Common triggers include excess or lack of sleep, irregular eating habits, and certain foods or food additives. Women may find that headaches occur with menstrual periods. The so-called menstrual migraine commonly arises during the few days before the onset of menses and resolves at menstruation.

Source: Adapted from the International Headache Society, 2004.

^a See also Table 51.5.
Source: Adapted from the International Headache Society, 2004.

Some patients also notice premonitory symptoms 1 to 2 days before the headache, which can include hyper- or hypoactivity, depression, cravings, and repetitive yawning. Such symptoms are distinct from a true aura. Migraines with aura are further characterized by typical neurologic symptoms shortly preceding the headache: visual scotomata (flashing lights), visual field defects (hemianopsia, quadrantopsia), fortification scintillations (zigzag lines or waves), vertigo, and (rarely) aural or olfactory hallucinations. Typically, the symptoms of an aura cease soon after the headache begins and leave no permanent sequelae.

Migraine variants exist. Occasionally, a patient notes a typical aura that is not followed by a headache, considered a migraine equivalent. In complicated migraines, the neurologic symptoms or focal deficits of the aura persist through the headache and may leave neurologic impairments. Other causes for lasting deficits (stroke, intracranial bleeds, vascular malformations, or brain tumors) must be excluded before this migraine variant is diagnosed. Ophthalmoplegic, hemiplegic, and basilar artery migraines are rarer forms with more unusual focal neurologic symptoms and signs such as ocular palsies, persistent weakness or sensory losses, or symptoms suggestive of basilar artery involvement (vertigo, ataxia, tinnitus, diplopia, and disturbed consciousness).

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