Primary Headache Disorders

Key Points

Clinicians must be aware that patients who present with orofacial pain complaints may have a primary headache disorder that needs to be addressed.

Clinicians must be alert to the potential for primary headache disorders to mimic odontogenic pain.

Clinicians must be cautioned in providing dental mechanical interventions for primary headache disorder relief.

Clinicians should consider referral to a health care practitioner knowledgeable in the management of primary headache disorders if they are in doubt of a definitive diagnosis.

Primary headaches are disorders unto themselves and are diagnosed by their symptom profile. Secondary headaches are due to an underlying condition and are classified according to their cause.¹ The International Headache Society (IHS) classification breaks the primary headache disorders into four categories:

1. Migraine

2. Tension-type headache (TTH)

3. Cluster headache and other trigeminal autonomic cephalalgias (TACs)

4. Other primary headaches

All the primary headache disorders are listed in Box 5-1. However, it is not within the scope of this chapter to discuss all of these disorders. Those that are more widely prevalent (ie, migraine, TTH, and cluster headache and related disorders) will be discussed more thoroughly. The codes from the IHS and The International Classification of Diseases, Tenth (ICD-10) and Ninth (ICD-9) Editions are presented for each disorder.

Migraine (IHS 1.x.x; ICD-10 G43. xxx; ICD-9 346.xx)

Clinical presentation and diagnosis

Migraine is a disorder of the brain and the trigeminal system with widespread effects on other bodily systems. A diagnosis of migraine may be confirmed when certain IHS diagnostic criteria are met and after organic disease is excluded: (1) Patients need to have experienced at least five attacks, each lasting 4 to 72 hours; (2) two of the following pain characteristics must be present: unilateral pain, pulsatile quality, moderate to severe intensity, and aggravation by or causing avoidance of routine physical activity; and (3) the attack must be accompanied by nausea (and/or vomiting) or photophobia and phonophobia.

Migraine attacks may occur without aura (IHS 1.1) or with aura (IHS 1.2). Aura is the presence of reversible focal neurologic symptoms that develop gradually over 5 to 20 minutes and last no more than 1 hour. Aura may also occur in the absence of a typical migraine headache (IHS 1.2.3). Aura often takes the form of positive visual phenomena that move across the visual field over minutes, migrating paresthesias, or dysphasic speech. Patients may experience premonitory symptoms hours to a day or two before a migraine attack (with aura or without aura). These include various combinations of fatigue, difficulty concentrating, neck stiffness, sensitivity to light or sound, nausea, blurred vision, yawning, food cravings, and pallor.

If migraine occurs on more than 15 days per month for at least 3 months in the absence of medication overuse, it is called chronic (IHS 1.5.1), and if it lasts for more than 3 days in succession, it is called status migrainosus (IHS 1.5.2). Serious complications of migraines are rare and include migrainous stroke (IHS 1.5.4), aura- or migraine-triggered seizures (IHS 1.5.5), and persistent aura (IHS 1.5.3).²

Epidemiology

The American Migraine Study found that the overall 1-year prevalence of episodic migraine in the United States is 17% to 18% for women and 6% for men,^3–5 increasing with age among both women and men, reaching the maximum at ages 35 to 45 years and declining thereafter.⁶ Aura symptoms may be experienced by 20% to 36% of adult migraine patients.^6,7 Before puberty onset, migraine is slightly more common in boys, with the highest incidence between 6 and 10 years of age. In females, peak incidence is between 14 and 19 years of age. Migraine prevalence is inversely proportional to income, with the low-income group having the highest prevalence. Race and geographic region are also influential factors; the prevalence is highest in North America and Western Europe and among those of European descent.⁵ Migraine with aura has a stronger genetic influence than migraine without aura.⁸ Because migraine usually affects people during their most productive years, migraine is a major burden to the patient and society. Not only does migraine affect the patient’s quality of life by impairing his or her ability to participate in family, social, and recreational activities, but it affects society in terms of direct costs (eg, medical care) and indirect costs (eg, absenteeism and reduced effectiveness at work). The American Migraine Study estimates that 23 million US residents have severe migraines. Twenty-five percent of women experience four or more severe attacks per month; 35% experience one to three severe attacks per month; and 40% experience one or less than one severe attack per month. The study also found that more than 85% of women and more than 82% of men with severe migraine had some migraine-related disability.⁷

Pathogenesis

Many mechanisms and theories explaining the causes of migraine have been proposed, although the full picture is still elusive. A strong familial association and the early onset of the disorder suggest a strong genetic component. Typical migraine is believed to be polygenic, but several monogenic forms of migraine have been identified. Familial hemiplegic migraine (FHM) is a monogenic form with hemiparesis as aura. To date, mutations in three different ion channels or ion pumps have been found as causative for FHM.⁹ Migraine aura itself correlates with the cerebral cortical event of cortical spreading depression (CSD), a slowly propagating wave of depolarization, hyperpolar-ization, and vascular changes. CSD has been shown in animal models to lead to trigeminovascular activation, resulting in the release of neuropeptides, neurogenic inflammation, increased vascular permeability, and dilation of blood vessels.¹⁰ Whether these vascular changes are necessary for the full expression of migraine symptoms including headache is still unresolved. Human positron emission tomography (PET) studies have indicated that a region of the midbrain periaqueductal gray may be particularly activated or dysfunctional in migraine attacks.¹¹ Multiple neurotransmitters and modulators, including serotonin, calcitonin gene–related peptide, nitric oxide, dopamine, and glutamate, have been implicated in migraine pathophysiologic mechanisms.^12,13 It has recently been recognized that central sensitization producing allodynia and hyperalgesia is an important clinical manifestation of migraine.¹⁴

Treatment

Pharmacologic treatment of migraine may be abortive/symptomatic or prophylactic. Patients who experience frequent severe migraine attacks often require both approaches. The choice of treatment should be guided by the frequency of the attacks. Individuals with fewer than 4 headache days per month and no impairment, or those with no more than 1 headache day per month regardless of the impairment, can be treated with abortive medications.³ Individuals with more frequent attacks, such as those with 6 or more migraine days per month with normal functioning, 4 or more migraine days with some impairment, or 3 or more migraine days with severe impairment, should be considered for treatment with prophylactic medications.³ If there is a comorbid illness, a prophylactic agent that can treat both should be used when possible, and agents that might aggravate a comorbid illness should be avoided. Nonpharmacologic methods, such as biofeedback, relaxation techniques, acupuncture, and other behavioral interventions, can be used as adjunctive therapy.¹⁵ Patient preferences should also be considered.

Several medications are used for acute migraine treatment, including selective 5-HT_1B/D (serotonin) receptor agonists, analgesics, nonsteroidal anti-inflammatory drugs (NSAIDS), dopamine-antagonistic antiemetics, ergot alkaloids, and corticosteroids. Opioid analgesics play a limited role in management because of enhanced risks of medication-overuse headache (“rebound”). Drugs with proven statistical and clinical benefit according to the American Academy of Neurology are listed in Box 5-2 and should be given as first-line treatment.¹⁶ Prophylactic treatments include a broad range of medications,^17,18 recently analyzed in an evidence-based practice guideline^19,20 (Box 5-3). Beta-blockers (eg, metoprolol, propranolol, timolol) and anticonvulsants (eg, divalproex, topiramate) have the strongest evidence of benefit for migraine prevention. These medications are started at low doses and titrated to the desired effect to minimize side effects and arrive at the minimal dose needed. In more refractory cases, polypharmacy may be necessary. While a number of NSAIDS are included in the practice guidelines as showing efficacy for prevention of episodic migraine, caution must be exercised about daily use because of concerns about induction of chronic daily headache due to analgesic overuse.¹⁹ Botulinum toxin type A (onabotulinum toxin A) has been cleared by the FDA for the preventive treatment of chronic migraine, in which headaches occur at least 15 days per month and at least 4 hours per day.²¹ For the treatment of menstrually related migraine, perimenstrual use of frovatriptan is recommended. Probably effective for this type of migraine are naratriptan and zolmitriptan.¹⁹ Emerging abortive and prophylactic treatments include selective 5-HT_1F agonists, calcitonin gene–related peptide antagonists, nitric oxide synthase inhibitors, and glutamate receptor antagonists.²²

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