Headache in Older Adults

Evaluation and management of headache in older adults can present diagnostic and therapeutic challenges. Some primary headache disorders, such as migraine, may present differently in older adults; others, such as hypnic headache, may be encountered more frequently in older than in the general population. New-onset headaches in older adults are more likely to be secondary, with one study showing that 15% of people over 65 y with new headache had a serious underlying cause compared with 1.6% of people younger than 65 y.¹ When treating headache, medication choice is influenced more frequently by comorbidities and polypharmacy, with consideration of the potential for drug interactions.

Primary Headache Disorders in Older Adults

The prevalence of migraine decreases with age² and new-onset migraine in a person older than 60 y is infrequent. A large population study of headaches across different age groups demonstrated that the severity of migraine (and probable migraine) decreases with age as does the prevalence of photophobia and phonophobia.² In contrast, the prevalence of aura increases with age,² and older individuals are more likely to have aura without headache. Migraine aura without headache is not uncommon: in a study of 239 people with migraine who were older than 64 y, 13.4% of those with migraine with aura had aura without headache.³

Older individuals without a known migraine history occasionally can present with a de novo migraine aura without headache; however, this diagnosis should be a diagnosis of exclusion. The first painless migraine aura carries a differential diagnosis of transient ischemic attack (TIA), especially in older people, who are more likely to have stroke risk factors. Migraine aura is more likely to present with gradual progression of symptoms and positive phenomena, although neither of these features is sufficient to rule out TIA. Retinal pathology is in the differential diagnosis, and people with a first monocular visual event should undergo ophthalmologic evaluation. Negative monocular events raise a question of amaurosis fugax. Whereas a history of stereotyped events is reassuring, new onset of frequent episodes is not common and warrants additional evaluation for vascular pathology, such as reversible cerebral vasoconstriction, dissection, or posterior reversible encephalopathy syndrome.

Few primary headache disorders are known to be more common in older adults than in younger groups. One to consider is hypnic headache, which generally presents after the age of 50 y. Prevalence is estimated to be between 0.22% and 0.3%, and hypnic headache is diagnosed more often in women, with a ratio of 2:1.⁴ Per International Classification of Headache Disorders, 3rd edition (ICHD-3) criteria, hypnic headache is characterized as recurrent headaches that develop exclusively during sleep and generate awakening (classically at the same time each night). Supporting features for a formal diagnosis include the absence of cranial autonomic features or restlessness, duration between 15 minutes and 4 hours, and an incidence of headaches on 10 days per month for >3 months.⁵

Nocturnal headaches mimicking hypnic headache may occur in people with intracranial masses, poorly controlled obstructive sleep apnea, nocturnal hypertension, nocturnal hypoglycemia, or medication overuse or withdrawal.⁴ Nocturnal headaches also can occur in people with other causes for intracranial hypertension and occasionally with cervicogenic etiologies.

Treatment methods for hypnic headache have been determined based on data from case reports and series. Caffeine before bedtime often is advised, with most studies recommending a formulation containing between 100 and 200 mg of caffeine for greatest benefit.⁴ Caffeine is effective in around 54% and 79% of those with hypnic headache as prophylaxis and rescue therapy, respectively.⁴ In select cases, lithium may be used. Other treatments include the indomethacin 25 to 150 mg per night and melatonin 2 to 5 mg per night, which demonstrate response rates of 51% and 50%, respectively. Given the potential for adverse events and drug–drug interactions with these medications, treatment needs to be tailored to the individual patient.

Secondary Headache Disorders in Older Adults

Onset of a new headache in a person over age 50 y is considered a red flag,⁶ and the American College of Radiology considers a new headache in people >50 y to be an appropriate criterion for neuroimaging.⁷ Change in the behavior of a preexisting headache disorder warrants the same consideration. Several common etiologies for headaches that are more common in the older population are discussed in the following section, and additional etiologies, such as cerebrovascular disorders and causative medications, can be found in Table 1.

Giant Cell Arteritis

One of the most concerning and yet easily missed etiologies for secondary headache in an older patient is giant cell arteritis (GCA). This must be on the differential diagnosis for anyone over the age of 50 y presenting with a new or changing headache. Over 85% of people with GCA present with headache,⁸ with pain occurring anywhere in the head. Scalp tenderness and jaw claudication are common associated features. Between these, jaw claudication is the stronger predictor of a positive temporal artery biopsy and has a specificity of approximately 90%.⁹

Systemic symptoms such as fever, anorexia, and weight loss may occur. Because 40% to 60% of cases of GCA are associated with polymyalgia rheumatica,⁸ pain and stiffness of the hips and shoulders may provide additional diagnostic clues. GCA also may involve other large vessels, often the thoracic aorta and its branches, and result in limb claudication. Examination of the temporal arteries may reveal weak or absent pulses, or tenderness, hardening, or nodularity. Permanent vision loss is not uncommon: a recent population-based retrospective study of 245 people with GCA reported an 8.2% risk of permanent vision loss.¹⁰ Vision loss most often occurs suddenly and typically is painless. In a study of 170 people with GCA, permanent vision loss was preceded by amaurosis fugax 63.6% of the time,¹¹ presenting an opportunity to intervene emergently with high-dose glucocorticoids. Once vision loss occurs, it rarely is reversible, although emergent high-dose glucocorticoids are critical to prevent vision loss in the nonaffected eye.

The clinician should order laboratory tests which include erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in all patients over the age of 50 y presenting with a new or different headache. However, whereas these inflammatory markers are usually elevated—often greatly—in GCA, the combination of ESR and CRP can be normal up to 4% of the time,¹² necessitating further evaluation if the pretest suspicion is high. However, elevation of inflammatory markers is nonspecific and often coincidental to a patient’s headache. In addition to inflammatory markers, the clinician should order a complete blood count, because people with GCA often present with normochromic anemia or reactive thrombocytosis.

Patients with suspected GCA should be started on high-dose glucocorticoids while they await further evaluation. Because long-term glucocorticoids can decrease the sensitivity of temporal artery biopsy, biopsy should be performed within 2 weeks. Sensitivity of temporal artery biopsy for GCA is only 77%,¹³ with false-negative results related to inadvertent sampling of unaffected regions of the temporal arteries. Therefore, a negative biopsy should not dissuade the diagnosis if pretest suspicion is high. Temporal artery ultrasound, used in some centers, was estimated to have a sensitivity of 68% and specificity of 81% compared with temporal artery biopsy in a recent meta-analysis.¹⁴ The mainstay of treatment of GCA is high-dose prednisone followed by very slow taper as tolerated, with monitoring of inflammatory markers. Steroid-sparing agents such as tocilizumab may be used.¹⁵

Intracranial Mass

The incidence of malignant and nonmalignant brain tumors rises with age.¹⁶ These trends are particularly striking for glioblastoma multiforme and nonmalignant meningioma.¹⁶ Most systemic cancers associated with brain metastases also are increasingly common with age. Intracranial neoplasms may or may not present with headache. If they increase intracranial pressure, people may have headaches with classic features of intracranial hypertension (eg, worse in the morning or when supine, aggravated by Valsalva, associated with awakening from sleep); may have associated transient visual obscurations, pulsatile tinnitus, or abducens nerve palsies with horizontal diplopia; and may have associated papilledema on examination. More commonly, however, headaches in people found to have intracranial neoplasms are nonspecific.¹⁷ These headaches may have features similar to tension-type headache and may be worse on the side ipsilateral to the neoplasm¹⁷ or may be diffuse.⁵ In the long term, headaches are likely to be accompanied by other symptoms related to intracranial neoplasm, such as seizure or focal deficits.⁵

Coronary Artery Disease

Cardiac cephalalgia is defined as headache associated with acute myocardial ischemia and has clinical criteria defined by the ICHD-3.⁵ Cardiac cephalalgia is postulated to be a referred pain phenomenon and may occur in association with other symptoms of myocardial ischemia, such as chest pain, or, rarely, may occur alone.¹⁸ As with other anginal symptoms, it is most often provoked or aggravated by exertion and is in the differential diagnosis for exertional headache. However, a review of 30 cases of cardiac cephalalgia reported that 33% of cases occurred during rest.¹⁸

Cardiac cephalalgia may be mistaken for migraine by the unsuspecting clinician as the headache is often moderate to severe in intensity, aggravated by exertion, and associated with nausea. Differentiation is critical, as inadvertent treatment of cardiac cephalalgia with triptans or ergots could worsen myocardial ischemia. Cardiac cephalalgia may be less likely than migraine to be associated with photophobia or phonophobia. Nitroglycerin typically alleviates headache in cardiac cephalalgia and aggravates migraine. Diagnosis involves the simultaneous occurrence of headache with objective evidence of myocardial ischemia such as an abnormal stress test. For this reason, in an older patient presenting with new-onset headache provoked or significantly worsened by exertion, an ECG and stress test should be considered in addition to neuroimaging.

Headaches Related to Aberrations in Blood Pressure

Whereas the relationship between headache and chronic hypertension is controversial, an acute rise in blood pressure to a systolic blood pressure ≥180 mm Hg or diastolic blood pressure ≥120 mm Hg may present with rapid-onset, bilateral, and throbbing head pain.¹⁹ Per ICHD-3 criteria, causation can be established by the presence of a temporal relationship between the rise in blood pressure and the headache, with headache developing, worsening, or improving in parallel with the blood pressure.⁵ Older adults may be at higher risk for orthostatic hypotension related to medications, dehydration (related to decreased sense of thirst), or neurodegenerative disorders that affect autonomic function. Hypotension may be associated with a “coathanger” headache syndrome, which commonly involves associated diffuse pain in the neck and upper trapezius regions.

Acute Angle-Closure Glaucoma

The incidence of acute angle-closure glaucoma rises with age. Given some shared clinical features, acute angle-closure glaucoma may be confused with migraine if a high index of suspicion is not maintained. Both acute angle-closure glaucoma and migraine may cause severe orbital or retroorbital headache associated with photophobia, nausea, and vomiting.²⁰ Diagnosis may be more challenging in people with a longstanding migraine history. The physical examination is critical, as people with angle-closure glaucoma may present with a mid-dilated pupil with poor light reactivity, conjunctival injection, or corneal clouding. If available, slit-lamp examination may reveal a shallow anterior chamber. Acute angle-closure glaucoma is an ophthalmologic emergency.

Classic Trigeminal Neuralgia

Classic trigeminal neuralgia, or trigeminal neuralgia related to neurovascular compression, is more common in older populations, with one study reporting an average age at onset of 52.9 y.²¹ A diagnosis of trigeminal neuralgia requires that facial pain be limited to the trigeminal nerve territory; that it be paroxysmal, severe, and neuropathic in quality; and that it be triggered by stimuli in the trigeminal nerve territory that would normally be innocuous (such as chewing, talking, or light touch).⁵ Severe numbness or objective sensory loss is not seen in classic trigeminal neuralgia; if present, numbness may instead suggest a neuropathy of the trigeminal nerve. Classic trigeminal neuralgia must be distinguished from secondary causes, and MRI of the brain with and without contrast is mandatory unless contraindicated.

Carbamazepine or oxcarbazepine are first-line treatments. Second-line agents may include gabapentin, baclofen, or lamotrigine. If medical management fails, people can be sent to a specialty center for consideration of microvascular decompression, gamma knife therapy, or destructive trigeminal nerve procedures. If the individual has only intraoral triggers and no cutaneous triggers on the face, dental pathology should be considered. If there is prominent allodynia and a history of rash or erythema, herpes zoster infection involving the trigeminal nerve may be possible. GCA sometimes may present as facial pain.

Migraine Treatment Considerations in Older Adults

Standard available guidelines for migraine treatment apply to older as well as general populations, although there are several additional factors to consider in older patients.²² When treating migraine in older adults the clinician should ask about lifestyle factors that may aggravate migraine, such as poor sleep and limited diet. Older patients are more likely to have comorbidities that present contraindications to specific acute or preventative migraine medications or that may require adjustments of medication dosage. For instance, a recent narrative review outlined medication use in the setting of kidney disease and hepatic disease,²³ both of which are more common in older adults. Older adults are more prone to side effects from medications such as tricyclic antidepressants. Coronary artery disease and history of stroke, both more common in older adults, are strict contraindications to treatment with triptans and ergots. Some noninvasive neuromodulation devices are contraindicated in people with pacemakers or defibrillators.²⁴ Older adults are more likely to be taking multiple medications, presenting the risk of potential drug interactions. Given heightened risk of side effects in older adults, medications should be started at a low dose and titrated slowly.²²

Older age alone does not present a contraindication to migraine-specific medications. For example, triptans do not need to be withheld from the healthy older individual who does not have contraindications or drug interactions. Calcitonin gene-related peptide inhibitors have not been studied in the elderly but are not contraindicated in this population. Treatments such as onabotulinumtoxinA often are used in the setting of chronic migraine, given the favorable side effect profile and lack of drug interaction. In addition, peripheral nerve blocks may be a safe option for use in this population.²⁵

Conclusion

Older adults warrant a special set of considerations for the diagnosis and management of headaches, with an expanded differential diagnosis, a higher incidence of secondary headache, and a more frequent need for medication adjustment because of comorbidities or polypharmacy.