Headache: Geriatric Headaches

Older persons have fewer headaches than younger ones. The prevalence of headaches at different ages in women and men, respectively, is as follows: 21 to 34 years, 92% and 74%; 55 to 74 years, 66% and 53%; and after age 75, 55% and 22%. Although 90% of headaches in younger patients are of the primary type, only 66% of headaches in the elderly are primary.

There is a decreasing prevalence of migraine with older age. Past age 70, only 5% of women and 2% of men still have migraine. There are many causes of new-onset headaches in the elderly, some of which can be particularly worrisome. The risk of serious secondary disorders in people ages 65 and older is 10 times higher than in younger people.

Late-Life Migraine Accompaniments

Late-life migraine accompaniments are transient visual, sensory, motor, or behavioral neurologic manifestations that are similar or identical to migraine aura. Headache is associated with only 50% of cases and may be mild. These accompaniments occur more often in men than in women. From most to least common, migraine accompaniments consist of visual symptoms such as transient blindness, homonymous hemianopsia (loss of vision on one side of one’s visual field), and blurring of vision; paresthesias (numbness, tingling, pins-and-needles sensation), or a heavy feeling of an extremity); brain stem and cerebellar dysfunction such as ataxia (clumsiness), hearing loss, tinnitus (ringing in ears), vertigo (sense of room spinning), and syncope (loss of consciousness); and disturbances of speech, such as dysarthria (slurred speech) or aphasia (loss of ability to speak).

Other causes of transient cerebral ischemia should be considered, especially when the patient is seen after the first episode or if the case has unusual aspects. The usual diagnostic evaluation for transient ischemic attacks (TIAs) or seizures is performed.

Features that help distinguish migraine accompaniments from TIAs include a gradual buildup of sensory symptoms; a march of sensory paresthesias; serial progression from one accompaniment to another; longer duration (90% of TIAs last for less than 15 minutes); and multiple stereotypical episodes.

If the episodes are frequent, preventive treatment can be considered with medications such as verapamil, topirimate, divalproex sodium, aspirin, and clopidogrel. For acute treatment, ergotamine, DHE, and triptans should be avoided because of the risk of increasing blood pressure.


Cerebrovascular Disease

Headaches commonly accompany stroke. In a prospective study of 163 patients with stroke, headache occurred in 29% with bland infarcts, 57% with parenchymal hemorrhage, 36% with TIAs, and 17% with lacunar infarcts. Women and patients with a history of prior recurrent throbbing headaches were more likely to have headaches associated with stroke. The headache began before the stroke in 60% of cases and at its onset in 25%. The quality, onset, and duration of stroke-associated headaches vary widely. The headaches are equally likely to be abrupt and to be gradual in onset. In patients presenting with what they consider to be the worst headache of their life, subarachnoid hemorrhage should be excluded.

Headache accompanying stroke is usually unilateral, focal, and of mild to moderate severity, although up to 46% of patients may have an incapacitating headache. The headache may be throbbing or nonthrobbing and, in rare cases, may be stabbing. The headache is more often ipsilateral than contralateral to the side of the cerebral ischemia (reduction in blood supply). Headache is more common in ischemia of the posterior circulation of the brain than of the anterior circulation and more common in cortical (gray matter) than in subcortical events (involving white matter of the brain.) The headache is of longest duration in cardioembolic infarcts and thrombotic infarcts, of medium duration in lacunar infarction, and of shortest duration in TIAs.

Head Trauma

Although there are numerous causes of head trauma, falls are of particular concern in the elderly. Approximately 30% of all persons older than 65 years fall at least once a year. Subdural hematomas follow approximately 1% of mild head injuries, even those involving no loss of consciousness, such as a bump on the head or riding a roller coaster. Chronic subdural hematomas occur more often in the elderly because of brain atrophy that causes stretching of the parasagittal bridging veins and a predisposition to tearing. The atrophy in an older person also permits hematomas to accumulate without symptoms for a longer period of time than it does in a younger person. Other risk factors include use of aspirin or warfarin and alcoholism.

Headaches are present in up to 90% of patients with head trauma. The headaches are nonspecific; they can range from mild to severe and from paroxysmal to constant and can be bilateral or unilateral. They may be exacerbated with coughing, straining, or exercise, and may be associated with vomiting or nausea. About 50% of patients with chronic subdural hematomas will have altered mental status. A strokelike presentation with a transient or persistent hemiparesis can also occur. Only about 50% of patients with a chronic subdural hematoma will have a history of a head injury. The history may also be inaccurate in patients with dementia.


Temporal Arteritis

Temporal (giant cell) arteritis (TA) is a systemic panarteritis that selectively involves arterial walls with significant amounts of elastin. Approximately 50% of patients with TA have polymyalgia rheumatica, and about 15% of patients with polymyalgia rheumatica have TA. Both conditions occur almost exclusively in patients older than 50 years, with a mean age of onset of about 70. The ratio of women to men with TA is 3:1. The annual incidence is about 18 per 100,000 population in persons older than 50 years.

Headaches are the most common symptom of TA, reported by 60% to 90% of patients. The pain is most often throbbing, although many patients describe a sharp, dull, burning, or lancinating pain. The pain may be intermittent or continuous and is more often severe than moderate or slight. For some patients, the pain may be worse at night when lying on a pillow, while combing the hair, or when washing the face. Tenderness or decreased pulsation of the superficial temporal arteries is present on physical examination in about half of all patients with TA. The location of the headache is variable and may be unilateral or bilateral. Intermittent jaw claudication occurs in 38% of cases in which one gets pain associated with talking or eating.

The diagnosis is based on clinical suspicion, which is usually but not always confirmed by laboratory testing. The three best tests are the Westergren erythrocyte sedimentation rate (ESR), the C-reactive protein (CRP) level, and temporal artery biopsy. For elderly patients, the ESR range of normal may vary from less than 20 mm/hr to 40 mm/hr. Elevation of the ESR is not specific for TA; it can be seen in any infectious, inflammatory, or rheumatic disease. TA with a normal ESR has been reported in 10% to 36% of patients. When abnormal, the ESR averages 70 to 80 mm/hr and may reach 120 or even 130 mm/hr. If the ESR is elevated at the time of diagnosis, it can be followed to help guide the use of corticosteroid treatment.


CRP is an acute-phase plasma protein from the liver. As with the ESR, elevation of CRP levels is nonspecific and can be seen with numerous disorders. The CRP level is not influenced by various hematologic factors or age and is more sensitive than the ESR for the detection of TA. The combination of ESR and CRP levels gives the best specificity (97%).

The diagnosis is made with certainty when a superficial temporal artery biopsy demonstrates necrotizing arteritis characterized by a predominance of mononuclear cell infiltrates or a granulomatous process with multinucleated giant cells. The false negative rate of temporal artery biopsies ranges from 5% to 44%.

In patients without contraindications, treatment is typically started with prednisone at a dosage of 40 to 80 mg a day. The headache will often improve within 24 hours. The initial dose is maintained for about 4 weeks and then slowly reduced over many months, depending on the clinical effect, the ESR, and the occurrence of side effects. Long-term treatment is often required. Delay in treatment of temporal arteritis can result in permanent blindness.

Trigeminal Neuralgia

Ninety percent of cases of trigeminal neuralgia (also known as tic douloreux) begin after age 40. About 80% of cases result from vascular compression of the trigeminal nerve at the root entry zone, most commonly by a branch of the superior cerebellar artery. About 5% of cases are caused by tumors. The pain is a severe, sharp, shooting, or electric shock-like sensation lasting seconds to 2 minutes. It is usually in a unilateral maxillary or mandibular trigeminal distribution and uncommonly in the ophthalmic division.

In about 90% of cases of trigeminal neuralgia, the patient has trigger zones, usually in the central part of the face around the nose and lips. Normally nonpainful stimuli in these zones can trigger pain. Stimuli can include talking, chewing, washing the face, brushing the teeth, shaving, facial movement, and cold air. After a paroxysm of pain, there is a refractory period lasting up to several minutes during which stimulation of the trigger zone will not trigger pain. Facial grimacing or spasm may accompany the pain. Between painful paroxysms, the patient is usually pain free, although dull aching may persist for a few minutes after attacks of long duration or multiple clustered attacks. Multiple attacks may occur for weeks or months. About 50% of patients with trigeminal neuralgia will have spontaneous remissions for at least 6 months. Physical examination is usually normal except for trigger zones, although up to 25% of patients will have sensory loss. Patients usually see dentists before seeking medical evaluation as they may think they have a cavity.

Medications that may be effective against trigeminal neuralgia, alone or sometimes in combination, include carbamazepine, oxcarbazepine, baclofen, phenytoin, clonazepam, divalproex sodium, topirimate, lamotrigine, gabapentin, and pimozide. About 30% of patients are nonresponsive to medical treatment but may respond to one of the many surgical approaches available.


Postherpetic Neuralgia

Although herpes zoster most commonly occurs in the thoracic region, the second most commonly involved area is a trigeminal distribution, usually in the ophthalmic division (herpes zoster ophthalmicus), which occurs in 23% of cases. The zoster is almost always unilateral. The incidence of postherpetic neuralgia (PHN) (i.e., the persistence of pain for more than 1 month after the initial outbreak) greatly increases with older age, to about 1,000 per 100,000 population for those 80 years of age or older. PHN develops in 50% of persons older than 50 years and in 80% of those older than 80 years. Zoster involving the face nearly doubles the risk of developing facial PHN, which lasts longer than PHN in other locations.

Typically, the vesicles crust, the skin heals, and the pain resolves within 3 to 4 weeks after the onset of the rash of herpes zoster. PHN involves three types of pain: a constant burning or deep aching; an intermittent spontaneous pain with a jabbing or lancinating quality; and a superficial, sharp, or radiating pain or itching provoked by light touch (allodynia), which is present in 90% of persons with PHN and often interferes with sleep. The type of pain experienced varies from patient to patient.

Oral corticosteroids (e.g., prednisone, starting at 60 mg/day and tapering off over 2 weeks) may reduce acute pain in herpes zoster but do not lower the risk of PHN. One week of therapy with famciclovir (500 mg every 8 hours) or valacyclovir (1,000 mg every 8 hours), ideally started within 72 hours after onset of acute zoster, mildly reduces the risk and duration of PHN.Numerous treatments of varying efficacy are available for PHN, including tricyclic antidepressants (amitriptyline, nortriptyline, and desipramine), gabapentin, topical agents (capsaicin, lidocaine, aspirin, and NSAIDs), opioids, and tramadol. Unfortunately, PHN persists for 1 year or more in over 20% of patients.

Cardiac Ischemia

In rare cases, cardiac ischemia can cause a unilateral or bilateral headache brought on by exercise and relieved by rest. The headache can occur alone or can be accompanied by chest pain. Angina is generally believed to be caused by afferent impulses that traverse cervicothoracic sympathetic ganglia, enter the spinal cord via the first to the fifth thoracic dorsal roots, and produce the characteristic pain in the chest or inner aspects of the arms. Cardiac vagal afferents, which mediate anginal pain in a minority of patients, join the tractus solitarius. A potential pathway for referral of cardiac pain to the head would be convergence with craniovascular afferents.


Hypnic Headache

Hypnic headache is a rare disorder that occurs in men and women from 40 to 79 years of age. The headache occurs only during sleep and awakens the sufferer at a consistent time. Nausea is infrequent, and autonomic symptoms are rare. The headache can be unilateral or bilateral, throbbing or nonthrobbing, and mild to severe in intensity. The headaches can last 15 minutes to 6 hours and can occur frequently, as often as nightly, for many years. Medications reported to be effective include caffeine (one or two cups of caffeinated coffee or a 40 to 60 mg caffeine tablet before bedtime), lithium carbonate (300 mg at bedtime), indomethacin, atenolol, melatonin, cyclobenzaprine, prednisone, and flunarizine (not available in the United States).

The diagnosis is one of exclusion. Secondary causes of nocturnal headaches that must be ruled out include drug withdrawal, temporal arteritis, sleep apnea, oxygen desaturation, pheochromocytoma, primary and secondary neoplasms, communicating hydrocephalus, subdural hematoma, and vascular lesions. Migraine, cluster, and chronic paroxysmal hemicrania are other primary headaches that can cause awakening from sleep. Migraine typically has associated symptoms and very uncommonly occurs only during sleep. Cluster headaches have autonomic symptoms and may occur during the day as well as during sleep. Chronic paroxysmal hemicrania occurs both during the day and at night, lasts for less than 30 minutes, and occurs 10 to 30 times a day.

WebMD Medical Reference from WebMD Scientific American Medicine Reviewed by William Blahd, MD on April 23, 2016


The author is a consultant or a member of the speakers' bureaus of GlaxoSmithKline, AstraZeneca, Merck & Co., Inc., Pharmacia & Upjohn, Pfizer, Inc., Elan Corp., and Ortho-McNeil Pharmaceutical, Inc.

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