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ABSTRACT

Headaches occur more frequently in theelderly than is commonly appreciated. This articlediscusses the challenges associated with diagnos-ing and managing headache disorders in theelderly and reviews the most common primaryheadache disorders (late-life migrainous accom-paniments, tension-type headache, clusterheadache, and hypnic headache) as well as sec-ondary headache disorders (medication overuseheadache, giant cell arteritis, exploding headsyndrome, and lesional headaches). With a focuson the different presentations and etiologies ofheadache in patients older than 65 years, neu-rologists have many tools at their disposal forappropriate management. (Adv Stud Med. 2003;3(6C):S556-S561)

Headache, migraine in particular, is typi-cally considered a disorder of youngerto middle-aged adults. The prevalenceof migraine is highest between the agesof 20 and 55 years, peaking at about

age 40 years and declining thereafter.1,2 However, theprimary headache disorders exist in older populations.

Prevalence studies report that 53% of men and 64% ofwomen aged 55 to 74 years experience headache, as wellas 22% of men and 55% of women 75 years and older.3

Headache is reported to be the 10th most commonsymptom in elderly women and 14th most common inelderly men.4 The demographic landscape of headacheetiology changes over time, from predominantly primaryheadaches in younger individuals to a greater incidence ofsecondary headaches in older individuals, regardless ofsex. Yet, headache remains a significant health problemfor the geriatric population. Consider also that the elder-ly (ie, those aged 65 years and older) are the fastest grow-ing segment of the US population.5

DIAGNOSIS AND MANAGEMENT CHALLENGES

Obtaining an accurate and detailed history is essen-tial for any headache patient, but even more so withthe elderly patient. A meticulous medication history isvital, because the potential clue to the headache sourcemay lie in the medication(s) the patient is taking.

The primary headache disorders, including migraine,may either attenuate over time (reduced frequency, sever-ity and/or duration) or present in an atypical manner.6

Some patients no longer experience the positive visualdisplay but may continue to experience the ensuingheadache. Chronic daily headache may continue intoolder age. In addition, 5% to 10% of patients older than65 years first develop chronic daily headache; however,in the authors’ experience, many of these patients have ahistory of migraine.

Treatment of elderly patients with headaches is farmore challenging than in their younger counterpartsfor several reasons, including the increased frequencyof secondary headache, comorbid or coexisting condi-tions, and polypharmacy. A single diagnosis may no

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HEADACHE IN THE ELDERLY*

—

David J. Capobianco, MD†

*Based on a presentation given by Dr Capobianco at theAmerican Headache Society Scottsdale HeadacheSymposium.

†Assistant Professor, Mayo Medical School, Mayo Clinic,Jacksonville, Florida.

Address correspondence to: David J. Capobianco, MD,Department of Neurology, Mayo Clinic, 4500 San Pablo Road,Jacksonville, FL 32224. E-mail: capobianco.david@mayo.edu.

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longer link the signs and symptoms into a neat, uni-fied headache classification; thus, excluding sec-ondary or symptomatic causes of headache isabsolutely essential. Coexisting diseases complicatetreatment, both acute and preventive. Also, elderlypatients have reduced tolerance to medications dueto changes in hepatic and renal clearance.Polypharmacy is common; 12% of the population isolder than 65 years, yet they consume more than onethird of all prescription medications.5,6 It is helpful,therefore, to obtain assistance from the patient’s pri-mary care physician and/or the pharmacist for acomplete medication history. The advice to “startlow and go slow” is especially true for the elderlypatient.

Following is a summary of the major primary andsecondary headache disorders in the elderly. TheFigure provides an algorithm for differential diagnosis.

PRIMARY HEADACHE DISORDERS

MIGRAINE AND LATE-LIFE MIGRAINOUS ACCOMPANIMENTS

Although the incidence of migraine peaks inmidlife, approximately one third of migraine patientscontinue to experience migraine headaches into olderage. The character of migraine attacks remains thesame: unilateral or bilateral temporal throbbing fre-quently associated with photophobia, phonophobia,or nausea, occurring more frequently in women. Asmall percentage (2% to 3%) experience their firstmigraine after age 50 years.7

Migraine attacks can occur with aura, yet without theensuing headache. Late-life migrainous accompani-ments, described in Table 1, are an important considera-tion for the elderly headache patient. The key feature isthe positive visual display, often beginning in one part ofthe visual field, then slowly spreading to involve 1 or

Figure. Headache in the Elderly—An Algorithm for Differential Diagnosis

Adapted with permission from Dodick DW, Capobianco DJ. Headaches. In: Sirven JI, Malamut BL, eds. Clinical Neurology of the Older Adult. Philadelphia, Pa: LippincottWilliams & Wilkins; 2002.

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both eyes, and generally lasting 10 to 15 minutes.8,9

As the positive visual display abates, the patient maythen experience positive sensory symptoms includ-ing tingling or prickling that may begin in the fin-gertips and spread to the palm or forearm, thenmove to the ipsilateral face and tongue, lasting sev-eral minutes. As the sensory symptoms resolve inthe affected extremity, the patient may then experi-ence heaviness or clumsiness that lasts several min-utes. As the clumsiness abates, difficulty in wordfinding may occur.8,9

Late-life migrainous accompaniments are oftenstereotypic attacks of short duration, lasting 20 to 30minutes. The attacks may be identical, suggesting thatthe mechanism is not cardioembolic. Patients havenormal neurological exams between attacks.Approximately one half of the patients may experiencea mild, nonspecific headache.8,9

The key to differentiating late-life migrainousaccompaniments from vascular disease (eg, a transientischemic attack) is the serial progression between onesymptom or accompaniment to another. For example,an acute left middle cerebral artery ischemic infarctwould produce abrupt onset of right hemibody weak-ness (a negative symptom), right-sided numbness (anegative symptom), and visual loss (a negative symp-tom)—all occurring simultaneously.7

Late-life migrainous accompaniments representa diagnosis of exclusion. Therefore, appropriateneuroimaging and neurovascular studies, bloodwork, and, where appropriate, cardiac studiesshould be pursued. Treatment of late-life migrain-ous accompaniments consists typically of a calci-um channel blocker (eg, verapamil). Manyphysicians may also add an antiplatelet agent.Anticonvulsant medications may also be a viableoption for some patients.

TENSION-TYPE HEADACHE

Tension-type headache is more common in elder-ly than in younger populations, with a reportedprevalence of 27% in patients older than 65 yearscompared with 20% in the entire population.10

However, it is difficult to ascertain the true epidemi-ology of tension-type headache in older personsbecause it can be confused with various disorders.

Tension-type headache can be considered a “fea-tureless headache”—dull, bilateral, or diffuseheadache of mild to moderate intensity. There is a

relative paucity of accompanying migraine features (ie,nausea, photophobia, phonophobia, worsening withmovement). Tension-type headache can easily be con-fused with structural or metabolic intracranial diseaseor depression, which are both more common in theelderly population, so careful examination for otherpotential causes is imperative.

Tension-type headache, like migraine, in theelderly should be treated with nonpharmacologictherapies, with judicious use of abortive and preven-tive antimigraine medications. Approximately 10%of individuals will develop tension-type headacheafter age 50 years; in these patients, an organic causemust first be ruled out.

CLUSTER HEADACHE

Cluster headaches, due to the excruciating painthey inflict, are unmistakable. Sometimes referred to as“suicide headaches,” cluster headaches are character-ized by intense, severe pain in the orbital region, peak-ing about 5 minutes after onset, and lasting anywherefrom 15 minutes to 2 hours. Robust autonomic symp-toms (eg, lacrimation, nasal congestion, ptosis, meio-sis, rhinorrhea, or conjunctival injection) occur in thevast majority (97%) of patients.7

Cluster headache is uncommon in the elderly buthas been reported in patients as old as 80 years,accounting for 4% of elderly patients presenting to a

Table 1. Diagnostic Criteria for Late-Life MigrainousAccompaniments

� Positive visual displays (eg, scintillating scotoma, fortification spectrum)

� Slow or gradual buildup of either visual or sensory symptoms

� Serial progression from one migrainous accompaniment—visual tosensory to motor—with a delay from one symptom or accompani-ment to another

� Occurrence of identical attacks

� Duration of 20 to 30 minutes

� Flurry of attacks in midlife (age 50 to 60 years) is common

� Complete resolution between attacks; a benign course without sequelae

� Headaches do not follow accompaniments in nearly 50% of cases

� Exclusion of symptomatic etiologies

Data from Fisher.8,9

headache clinic.10 Cluster headache features in theelderly are stereotypic, but diagnosis warrants imagingstudies to eliminate other possible causes, particularlywith any unusual features at presentation.

Treatment is usually with nasal oxygen, barring anycoexisting medical contraindication. Nasal oxygen isthe safest treatment for those with comorbid cardio-vascular disease. Subcutaneous sumatriptan, althoughtypically very effective, should be avoided, especially inthose with cardiovascular risk factors—a common sub-population of cluster headache patients. Prophylacticdrug therapy is the same as for younger populations,excluding methysergide.

HYPNIC HEADACHE

Hypnic headache appears to be a primaryheadache disorder distinctly of the geriatric popula-tion, with a mean age of onset of approximately 60years. This rare type of headache, also known as“alarm clock” headache, has an estimated prevalenceat the Mayo Clinic of only 0.07%.11 The key featureof hypnic headache is its nocturnal onset (Table 2).Hypnic headaches typically begin between 1:00 AM

and 3:00 AM, occurring more than 4 times per weekin two thirds of patients. Hypnic headaches are ofshort duration (<2 hours in 64% of cases) with alack of associated migrainous and autonomic symp-toms that would suggest an alternative primaryheadache disorder, such as cluster headache. Theheadaches are typically holocephalic and are of mod-erate severity. Approximately 58% of patientscomplain of a dull, nonpulsatile headache, but42% have some throbbing quality to the pain.Although initially thought to be more common inmen, as the full spectrum of the hypnic headachesyndrome has evolved, it is apparent that womenare more commonly affected.11-14

Interestingly, resting in a supine position tendsto exacerbate the pain, so many patients may paceto relieve the pain. Treatment options includelithium 300 mg daily, indomethacin, or caffeine.Lithium is often the most effective medication but,unfortunately, is not well tolerated in geriatricpopulations. Caffeine (40 mg to 60 mg) at bed-time can be helpful; our experience has been thatcaffeine at bedtime does not interrupt patients’sleep patterns. Several studies have shown thatindomethacin, taken with food at bedtime, is alsouseful.14,15

SECONDARY HEADACHE DISORDERS

MEDICATION OVERUSE

As mentioned earlier, elderly patients consume onethird of all prescription medications. Therefore, thepossibility of medication overuse or rebound headacheshould be one of the first considerations in an elderlypatient presenting with headache. As with youngerpatients, commonly overused medications by theelderly for headache include over-the-counter anal-gesics, combination medications, ergotamine-contain-ing compounds, triptans, and narcotics. It is oftenprudent to taper and ultimately discontinue medica-tions that are not absolutely necessary.16

TEMPORAL (GIANT CELL) ARTERITIS

Like hypnic headache, giant cell arteritis (GCA)appears to be a geriatric headache disorder.6,16-18

Although the temporal artery is frequently involved,GCA is a systemic granulomatous inflammatoryprocess (with multinuclear giant cells) affecting medi-um or large arteries. A necrotizing arteritis is present.Headache is the most common symptom and the mainreason patients with GCA present to a neurologist. Theprevalence of GCA in patients in their 50s is 6.8 per100 000; prevalence is 73 per 100 000 in patients intheir 80s.17 The average age of onset is 70 years, andGCA is 4 times more prevalent in women.17,18

Because the most common symptom is headache,GCA should be considered in any elderly person with

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Table 2. Diagnostic Criteria for Hypnic (“Alarm Clock”)Headache

� Occurs only in older or elderly populations (>60 years)

� Headache awakens the patients from sleep at a consistent time, usual-ly between 1:00 AM and 3:00 AM (63%)

� Identical headaches also can occur during daytime naps

� Headache frequency often occurring >4 nights/week

� Headache resolution within 2 hours in most patients

� Neurologic examination, laboratory studies, and brain imaging areunrevealing

� Headache severity remains unchanged or attenuates over time; fre-quency may vary in either direction

Data from Dodick et al.11

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either new-onset headache or change in a previouslystable headache pattern.17,19,20 There is no specificheadache pattern or characteristic in GCA. In onestudy of GCA, the headache occurred outside the tem-poral region in 25% of cases.20 The headache may waxand wane in intensity but is usually dull, althoughthrobbing may occur with bending or stooping. Scalptenderness, especially near the temporal or occipitalarteries, is sometimes present.

Polymyalgia rheumatica, malaise, and fatigue occurin more than one half of GCA patients and may be theinitial symptoms in 20% to 40% of patients.21 Visualsymptoms, including amaurosis, diplopia, and perma-nent visual loss, are some of the most serious symp-toms of GCA. Visual loss can be unilateral or bilateral;untreated unilateral vision loss can evolve into bilater-al visual loss within 1 to 2 weeks. Visual loss is usuallysudden, but Lipton et al have reported gradual visualloss with recovery after treatment.22 The incidence ofvisual loss ranges from 8% to 20%, approaching 40%in untreated patients.

On examination, the affected artery may be tenderor nodular to palpation.16,18 The best screening test forGCA is the erythrocyte sedimentation rate; althoughadmittedly nonspecific, sedimentation rates are elevat-ed in the vast majority of cases. Typical values for GCAare greater than 50 mm/hour; normal values varyamong laboratories but are typically less than 30mm/hour.23-25 However, the sedimentation rate may befalsely low early in the disease course if the patient istaking corticosteroids or other anti-inflammatorymedications; in patients with sickle cell or low fibrino-gen states; and in patients in whom the blood workwas not properly processed (ie, blood was allowed tosit for more than 2 hours after being drawn).26 Otherlaboratory abnormalities may include an anemia ofchronic disease, elevated platelet counts, alkaline phos-phatase, C-reactive protein, factor VIII/vonWillebrand’s factor, fibrinogen, alpha-2-globulin, andinterleukin-6, as expected with vasculitis.27

Temporal artery biopsy may not be technically nec-essary but prudent; on occasion, one may uncover analternative diagnosis.28 Typically, biopsies are per-formed unilaterally on the side of the tender orindurated blood vessel. An appropriate segment is 3cm to 5 cm, multiply sectioned, given that GCA is amultifocal vasculitis with skip lesions.24,25,27,28

The treatment of choice for this disorder is pred-nisone (40 mg–80 mg starting dose) and should be

initiated immediately if GCA is suspected.24,25 Patientstaking corticosteroids should be biopsied within 24 to48 hours of the steroid dose, but a biopsy can be per-formed up to 2 weeks later. Once improvement ismaintained for 2 weeks, the steroids can be taperedgradually over weeks to months. Any relapse is usuallydue to incomplete suppression of the inflammatoryresponse, not an exacerbation. As with any long-termsteroid use, patients should be monitored for potentialcomplications, such as hypertension, osteoporosis,peptic ulcer disease, diabetes, and cataracts.7,21,25

EXPLODING HEAD SYNDROME

Exploding head syndrome is rare and occurs morecommonly in women than in men. In general, patientswith exploding head syndrome are older than 50 years,although no age group is spared. It is not a headache perse, but a cephalic sensation. As patients are falling asleep,they may awaken with the sensation of a loud noise or abang in their head. These sensations may occur severaltimes per night, and then may remit for several months.There are no associated autonomic symptoms thatwould suggest cluster headache. The mechanism is notunderstood but may represent a sleep-related disorder.Treatment, as suggested by Pearce, who characterizedthis syndrome, is reassurance.29,30

LESIONAL HEADACHES

The incidence of lesional headaches increases withage as the incidence of intracranial disease increases.The elderly are more prone to the development of sub-dural hematomas because of the associated cerebralatrophy that puts the bridging veins at risk of tearing,even with trivial trauma.

Headaches caused by brain tumor are not easilyidentified because the classic cardinal features original-ly taught in medical school (ie, severe headache, worsein the morning with associated vomiting) do not holdtrue in the majority of patients with a brain tumor. Infact, many are mistaken for tension-type headache.31

Most are mild and nondescript.7

The majority of patients with brain tumor and asso-ciated headache have a history of migraine in theiryounger years, underscoring the importance of followingup on any slight change in the quality of headache orassociated features, including slowed mentation. Signs orclues to brain tumor as the cause of headache includeincreased headache frequency, paroxysmal headaches(with sudden onset and peaking within seconds), and

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associated neurologic signs and symptoms. Magnetic res-onance imaging with gadolinium is the imaging methodof choice.

CONCLUSION

Diagnosing and managing headache in the elderlypresents numerous challenges unique to this popula-tion. Establishing the correct diagnosis is essential toimplementing the appropriate treatment plan. Anychange in the medication schedule should be reviewedwith the referring primary care physician given thelarge number of prescription medications this popula-tion consumes.

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2. Lipton RB, Stewart WF, Diamond S, Diamond ML, Reed M.Prevalence and burden of migraine in the United States:data from the American Migraine Study II. Headache.2001;41(7):646-657.

3. Waters WE. The Pontypridd headache survey. Headache.1974;14(2):81-90.

4. Hale WE, Perkins LL, May FE, Marks RG, Stewart RB.Symptom prevalence in the elderly. An evaluation of age,sex, disease, and medication use. J Am Geriatr Soc.1986;34(5):333-340.

5. Katzman R, Rowe JW. Principles of Geriatric Neurology:Philadelphia, Pa: FA Davis Company; 1992

6. Edmeads J. Headaches in older people. How are they differ-ent in this age group? Postgrad Med. 1997;101(5):91-100.

7. Dodick DW, Capobianco DJ. Headaches. In: Sirven JI,Malamut BL, eds. Clinical Neurology of the Older Adult.Philadelphia, Pa: Lippincott Williams & Wilkins; 2002.

8. Fisher CM. Late-life migraine accompaniments—furtherexperience. Stroke. 1986;17(5):1033-1042.

9. Fisher CM. Late-life migraine accompaniments as a causeof unexplained transient ischemic attacks. Can J Neurol Sci.1980;7(1):9-17.

10. Solomon GD, Kunkel RS Jr, Frame J. Demographics ofheadache in elderly patients. Headache. 1990;30(5):273-276.

11. Dodick DW, Mosek AC, Campbell JK. The hypnic (“alarmclock”) headache syndrome. Cephalalgia. 1998;18(3):152-156.

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25. Caselli RJ, Hunder GG. Giant cell (temporal) arteritis andcerebral vasculitis. In: Johnson RT, Griffin, eds. CurrentTherapy in Neurologic Disease. 4th ed. St. Louis, Mo: BCDecker; 1993:196-201.

26. Wong RL, Korn JH. Temporal arteritis without an elevatederythrocyte sedimentation rate. Case report and review ofthe literature. Am J Med. 1986;80(5):959-964.

27. Lee AG, Brazis PW. Arteritic anterior ischemic optic neu-ropathy and giant cell arteritis. In: Lee AG, Brazis PW, eds.Clinical Pathways in Neuro-ophthlalmology. New York, NY:Thieme; 1998:67-91.

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