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Headaches And Other Head Pain Health Article

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Secondary Headache Disorders

Headache may be the initial complaint in a host of central nervous system and systemic abnormalities (Table 428-1). Many of the disorders are given detailed consideration in other chapters. However, a few of the most prominent abnormalities that may result in chronic headache are discussed briefly.

GIANT CELL ARTERITIS

Giant cell arteritis (temporal arteritis;) is an inflammatory vasculitis involving branches of the temporal arteries. It most often affects individuals older than 60 years and can result in rapid and permanent loss of vision from granulomatous occlusion of the posterior ciliary or central retinal arteries. Features suggestive of temporal arteritis include orbital or frontotemporal head pain, described as dull and constant with superimposed jabbing sensations; aggravation of pain by cold temperatures; pain in the jaw or tongue pain on chewing (jaw claudication); accompanying constitutional or musculoskeletal symptoms such as weight loss, anemia, and polymyalgia rheumatica; elevated liver function tests; and decreased visual acuity, visual field cuts, pale or swollen optic disc, retinal splinter hemorrhages (i.e., anterior ischemic neuropathy) or a pale retina, and cherry-red spot (i.e., central retinal artery infarction).

The ESR, which should be measured in all suspected patients, is elevated in 95% of cases. Definitive diagnosis is made by biopsy of the temporal artery, which can be obtained within 48 hours after initiation of treatment with steroids. When the diagnosis is suspected, prompt treatment with corticosteroids is necessary to avoid visual loss, which often becomes bilateral (75% of cases) after unilateral loss.

Treatment

In patients with an elevated ESR, intravenous methylprednisolone (500 to 1000 mg every 12 hours for 48 hours) should be followed by oral prednisone (80 to 100 mg/day for 14 to 21 days), with a gradual taper over 12 to 24 months. The tapering rate should be guided by serial ESR measurements.

SUBSTANCE-INDUCED HEADACHES

Headaches may occur with acute exposure or as a result of withdrawal from many types of substances (Table 428-2).

HEADACHES ASSOCIATED WITH INCREASED INTRACRANIAL PRESSURE

Headache may occur when an alteration in intracranial pressure causes compression or traction on pain-sensitive vascular, meningeal, or neural structures in the apex or base of the brain. Most commonly, these headaches are bilateral and frontotemporal, although their location is variable. Causes of elevated intracranial pressure include mass lesion, blockage of cerebrospinal fluid (CSF) circulation, hemorrhage, hypertensive encephalopathy, venous sinus thrombosis, hyperadrenalism or hypoadrenalism, altitude sickness, tetracycline, and vitamin A intoxication. In most instances, the source of the headache and raised pressure are identifiable. Treatment of the underlying condition generally improves the headache.

INTRACRANIAL TUMOR

One of the most common concerns of patients seeking evaluation of chronic headaches is that their headache represents a space-occupying lesion such as a tumor or large vascular abnormality. Fortunately, most chronic headaches do not arise from a tumor or other structural lesion. Headaches in patients with brain tumors are usually dull and bifrontal, although they tend to be worse on the side of the tumor. The headaches are more often qualitatively similar to tension-type headaches than to migraines and tend to be intermittent and of moderate intensity; they are accompanied by nausea in about one half of cases and are usually resistant to common analgesics. Classic brain tumor headache (i.e., progressive and beginning in the morning) is not typical. Factors that should increase suspicion of an intracranial tumor include papilledema, new neurologic deficits, initial attack of prolonged headache occurring after the age of 45 years, previous malignancy, cognitive abnormality, or altered mental status.

IDIOPATHIC INTRACRANIAL HYPERTENSION

Idiopathic intracranial hypertension (pseudotumor cerebri) is a syndrome composed of headache, papilledema, and transient visual symptoms that occur in the absence of CSF abnormalities, except for elevated intracranial pressure. The syndrome is not associated with hydrocephalus or another identifiable cause. In adults, females have an 8 to 10 times higher incidence than males. The prototypic patient is an overweight woman of childbearing age. The diagnosis is made by lumbar puncture (CSF pressure higher than 250 mm Hg; normal CSF composition) after excluding a mass lesion by neuroimaging. Visual field testing often reveals an enlarged blind spot. Spontaneous recovery may eventually occur, but treatment to reduce intracranial pressure is usually indicated to prevent visual loss. Simple measures such as weight reduction should be attempted whenever appropriate. Drug therapies are usually attempted next and include medications such as acetazolamide and furosemide, which are aimed primarily at reducing CSF production. Furosemide, a potent loop diuretic, must be given with potassium supplementation and may cause hypotension. If drug treatment is ineffective, repeated lumbar punctures may sometimes be useful, although frequent lumbar puncture is not without a risk of complications, including as post-lumbar puncture headache, spinal epidermoid tumor, or infection. If other treatments fail, surgical options include optic nerve fenestration and ventricular-peritoneal shunting of CSF.

HEADACHE ASSOCIATED WITH DECREASED INTRACRANIAL PRESSURE

Decreased intracranial pressure (<50 to 90 mm H 2 O), which is usually caused by a decrease in CSF volume, is commonly associated with dull, throbbing, sometimes severe headaches that are probably caused by reduced brain buoyancy and subsequent traction on pain-sensitive meningeal and vascular structures. Low-pressure headaches often become more intense on standing or sitting upright and may be relieved by lying down. The headaches may be accompanied by dizziness, visual symptoms, photophobia, nausea, vomiting, and diaphoresis. Although low-pressure headaches may begin spontaneously, they most commonly follow lumbar puncture. Other possible etiologies include intracranial surgery, ventricular shunting, trauma, and various systemic medical conditions such as severe dehydration, postdialysis status, diabetic coma, uremia, or hyperpnea. If the headache is prolonged, the possibility of a persistent CSF leak may be investigated by radioisotope cisternography or computed tomographic myelography. Post-lumbar puncture headaches can be caused by excessive leakage of CSF through a dural tear caused by the lumbar puncture needle. Headaches follow 10 to 30% of lumbar punctures and occur twice as frequently in women as in men. The headache may begin minutes to several days after the lumbar puncture and can persist up to 2 weeks.

Treatment strategies include corticosteroids, oral fluid or salt intake, intravenous fluids, CO 2 inhalation, methylxanthines such as theophylline (200 mg three times daily), caffeine (500 mg IV), or intrathecal autologous blood patch.

HEAD AND FACIAL PAIN ASSOCIATED WITH DISORDERS OF CRANIAL NERVES

Trigeminal neuralgia, also known as tic douloureux, usually occurs in older patients. The sharp, often electric shocklike pain of trigeminal neuralgia occurs in a rapid series of jabs (lasting seconds to minutes) in one or more divisions of the trigeminal nerve. The volleys of jabbing may be provoked by stimulation of areas on the face quite discrete from the site of pain and are usually followed by brief refractory periods. When trigeminal neuralgia occurs in persons younger than 40 years, a specific cause can often be found, such as demyelination (e.g., multiple sclerosis, especially when bilateral) and compression by vascular abnormalities or tumors (e.g., myeloma, metastatic carcinoma, cholesteatoma, chordoma, acoustic neuromas, trigeminal neuromas). In the elderly, trigeminal neuralgia has a prevalence of 155 per million and a female-to-male ratio of 3:2. Among older individuals with trigeminal neuralgia, microvascular compression of the trigeminal nerve root is often present. Because of the association with structural lesions (i.e., demyelinative or neoplastic), the initial evaluation should include MRI studies, which detail the cerebellopontine angle and the entry foramen (e.g., V 1 superior orbital fissure, V 2 foramen rotundum, V 3 foramen ovale). In the absence of a structural cause, treatment usually consists of drugs such as carbamazepine (400 to 1200 mg), valproate (500 to 1500 mg), phenytoin (200 to 500 mg), baclofen (40 to 80 mg), or clonazepam (2 to 6 mg). Therapy with any of these agents must be initiated slowly. Patients who fail to respond to medication should be considered for microvascular decompression surgery.

Glossopharyngeal neuralgia is characterized by paroxysmal pain within the distribution of the vagus and glossopharyngeal nerves. The pain is paroxysmal, unilateral, and sudden in onset, and it has a jabbing or briefly persistent (square wave) quality. The pain is most often felt in or around the ear, tongue, jaw, or larynx, and it can be triggered by swallowing, talking, chewing, clearing the throat, yawning, or tasting spicy food or cold liquids. Although pain is usually followed by a brief refractory period, attacks may occur more than 20 times per day and may awaken sufferers from sleep. The intermittent pain may be superimposed on a dull, constant pain in the same area. Rarely, the pain of glossopharyngeal neuralgia is followed by bradycardia, syncope, or asystole, presumably resulting from the intense glossopharyngeal outflow and vagal efferent discharge. The usual cause of glossopharyngeal neuralgia appears to be microvascular compression, although abscess and tumor are sometimes associated. Medical treatment is similar to that for trigeminal neuralgia and includes slow introduction of carbamazepine (400 to 1200 mg), gabapentin (900 to 1800 mg), or baclofen (40 to 80 mg). Cases refractory to adequate medical treatment often respond to microvascular decompression.