HEADACHE

Headache is such a common complaint and can occur for so many different reasons that its proper evaluation may be difficult. Headaches of acute onset are discussed in Common Symptoms. Chronic headaches are commonly due to migraine, tension, or depression, but they may be related to intracranial lesions, head injury, cervical spondylosis, dental or ocular disease, temporomandibular joint dysfunction, sinusitis, hypertension, and a wide variety of general medical disorders. Although underlying structural lesions are not present in most patients presenting with headache, it is nevertheless important to bear this possibility in mind. About one-third of patients with brain tumors, for example, present with a primary complaint of headache.
The intensity, quality, and site of pain—and especially the duration of the headache and the presence of associated neurologic symptoms—may provide clues to the underlying cause. Migraine or tension headaches are often described as pulsating or throbbing; a sense of tightness or pressure is also common with tension headache. Sharp lancinating pain suggests a neuritic cause; ocular or periorbital icepick-like pains occur with migraine or cluster headache; and a dull or steady headache is typical of an intracranial mass lesion. Ocular or periocular pain suggests an ophthalmologic disorder; band-like pain is common with tension headaches; and lateralized headache is common with migraine or cluster headache. In patients with sinusitis, there may be tenderness of overlying skin and bone. With intracranial mass lesions, headache may be focal or generalized; in patients with trigeminal or glossopharyngeal neuralgia, the pain is localized to one of the divisions of the trigeminal nerve or to the pharynx and external auditory meatus, respectively.
Inquiry should be made of precipitating factors. Recent sinusitis or hay fever, dental surgery, head injury, or symptoms suggestive of a systemic viral infection may suggest the underlying cause. Migraine may be exacerbated by emotional stress, fatigue, foods containing nitrite or tyramine, or the menstrual period. Alcohol may precipitate cluster headache. Temporomandibular joint dysfunction causes headache or facial pain that comes on with chewing; trigeminal or glossopharyngeal neuralgia may also be precipitated by chewing, and masticatory claudication sometimes occurs with giant cell arteritis. Cough-induced headache occurs with structural lesions of the posterior fossa, but in many instances no specific cause can be found.
The timing of symptoms is important. Headaches are typically worse on awakening in patients with sinusitis or an intracranial mass. Cluster headaches tend to occur at the same time each day or night. Tension headaches are worse with stress or at the end of the day.
The onset of severe headache in a previously well patient is more likely than chronic headache to relate to an intracranial disorder such as subarachnoid hemorrhage or meningitis. The need for further investigation is determined by the initial clinical impression.
A progressive headache disorder, new onset of headache in middle or later life, headaches that disturb sleep or are related to exertion, and headaches that are associated with neurologic symptoms or a focal neurologic deficit usually require cranial MRI or CT scan to exclude an intracranial mass lesion. Signs of meningeal irritation and impairment of consciousness also indicate the need for further investigation (cranial CT scan or MRI and examination of the cerebrospinal fluid) to exclude subarachnoid hemorrhage or meningeal infection. The diagnosis and treatment of primary neurologic disorders associated with headache are considered separately under these disorders.
Tension Headache
Patients frequently complain of poor concentration and other vague nonspecific symptoms, in addition to constant daily headaches that are often vise-like or tight in quality and may be exacerbated by emotional stress, fatigue, noise, or glare. The headaches are usually generalized, may be most intense about the neck or back of the head, and are not associated with focal neurologic symptoms.
When treatment with simple analgesics is not effective, a trial of antimigrainous agents (see Migraine, below) is worthwhile. Techniques to induce relaxation are also useful and include massage, hot baths, and biofeedback. Exploration of underlying causes of chronic anxiety is often rewarding. Local injection of botulinum toxin type A is sometimes helpful, has few systemic adverse effects, and requires only infrequent administration.
Depression Headache
Depression headaches are frequently worse on arising in the morning and may be accompanied by other symptoms of depression. Headaches are occasionally the focus of a somatic delusional system. Antidepressant drugs are often helpful, as may be psychiatric consultation.
Migraine
Essentials of Diagnosis



Headache, usually pulsatile.



Nausea, vomiting, photophobia, and phonophobia are common accompaniments.



May be transient neurologic symptoms (commonly visual) preceding headache of classic migraine.



No preceding aura is common.
General Considerations
The pathophysiology of migraine probably relates to the neurotransmitter serotonin. Headache may result from release of neuropeptides acting as neurotransmitters at trigeminal nerve branches, leading to an inflammatory process; another possible mechanism involves activation of the dorsal raphe nucleus. Imaging studies have revealed changes in brainstem regions involved in sensory modulation, suggesting that migraine relates to a failure of normal sensory processing.
Clinical Findings
Classic migrainous headache is a lateralized throbbing headache that occurs episodically following its onset in adolescence or early adult life, although not all headaches that are throbbing in character are of migrainous origin. Moreover, in many cases the headaches do not conform to this pattern, although their associated features and response to antimigrainous preparations nevertheless suggest that they have a similar basis. In this broader sense, migrainous headaches may be lateralized or generalized, may be dull or throbbing, and are sometimes associated with anorexia, nausea, vomiting, photophobia, phonophobia, and blurring of vision. They usually build up gradually and may last for several hours or longer. They have been related to dilation and excessive pulsation of branches of the external carotid artery. Focal disturbances of neurologic function may precede or accompany the headaches and have been attributed to constriction of branches of the internal carotid artery. Visual disturbances occur quite commonly and may consist of field defects; of luminous visual hallucinations such as stars, sparks, unformed light flashes (photopsia), geometric patterns, or zigzags of light; or of some combination of field defects and luminous hallucinations (scintillating scotomas). Other focal disturbances such as aphasia or numbness, tingling, clumsiness, or weakness in a circumscribed distribution may also occur.
Patients often give a family history of migraine. Attacks may be triggered by emotional or physical stress, lack or excess of sleep, missed meals, specific foods (eg, chocolate), alcoholic beverages, menstruation, or use of oral contraceptives.
An uncommon variant is basilar artery migraine, in which blindness or visual disturbances throughout both visual fields are initially accompanied or followed by dysarthria, disequilibrium, tinnitus, and perioral and distal paresthesias and are sometimes followed by transient loss or impairment of consciousness or by a confusional state. This, in turn, is followed by a throbbing (usually occipital) headache, often with nausea and vomiting.
In ophthalmoplegic migraine, lateralized pain—often about the eye—is accompanied by nausea, vomiting, and diplopia due to transient external ophthalmoplegia. The ophthalmoplegia is due to third nerve palsy, sometimes with accompanying sixth nerve involvement, and may outlast the orbital pain by several days or even weeks. The ophthalmic division of the fifth nerve has also been affected in some patients. Ophthalmoplegic migraine is rare; more common causes of a painful ophthalmoplegia are internal carotid artery aneurysms and diabetes.
In rare instances, the neurologic or somatic disturbance accompanying typical migrainous headaches becomes the sole manifestation of an attack ("migraine equivalent"). Very rarely, the patient may be left with a permanent neurologic deficit following a migrainous attack.
Treatment
Management of migraine consists of avoidance of any precipitating factors, together with prophylactic or symptomatic pharmacologic treatment if necessary.
SYMPTOMATIC THERAPY
During acute attacks, many patients find it helpful to rest in a quiet, darkened room until symptoms subside. A simple analgesic (eg, aspirin, acetaminophen, ibuprofen, or naproxen) taken right away often provides relief, but treatment with extracranial vasoconstrictors or other drugs is sometimes necessary. Cafergot, a combination of ergotamine tartrate (1 mg) and caffeine (100 mg), is often particularly helpful; one or two tablets are taken at the onset of headache or warning symptoms, followed by one tablet every 30 minutes, if necessary, up to six tablets per attack and ten tablets per week. Because of impaired absorption or vomiting during acute attacks, oral medication sometimes fails to help. Cafergot given rectally as suppositories (one-half to one suppository containing 2 mg of ergotamine) or dihydroergotamine mesylate (0.5–1 mg intravenously or 1–2 mg subcutaneously or intramuscularly) may be useful in such cases. Alternatively, prochlorperazine administered rectally (25 mg suppository) or intravenously (10 mg) may be prescribed. Ergotamine-containing preparations may affect the gravid uterus and thus should be avoided during pregnancy.
Sumatriptan, which has a high affinity for serotonin1 receptors, is a rapidly effective agent for aborting attacks when given subcutaneously by an autoinjection device. It can also be taken in a nasal form, but absorption is limited, and an oral preparation is available. Zolmitriptan, another selective serotonin1 receptor agonist, has high bioavailability after oral administration and is also effective for the acute treatment of migraine. The optimal initial dose is 5 mg, and relief usually occurs within 1 hour. A newly developed nasal formulation has a rapid onset of action. A number of other triptans are available, including rizatriptan, naratriptan, almotriptan, frovatriptan, and eletriptan. Eletriptan (up to 80 mg over 24 hours) is useful for acute therapy and frovatriptan, which has a longer half-life, may be worthwhile for patients with prolonged attacks (up to 7.5 mg over 24 hours). Triptans may cause nausea and vomiting. They should probably be avoided in women who are pregnant and in patients with risk factors for stroke (such as hypertension, prior stroke or transient ischemic attack, diabetes mellitus, hypercholesterolemia, obesity). Triptans are contraindicated in patients with coronary or peripheral vascular disease. When used with selective serotonin reuptake inhibitors (SSRIs) or serotonin/norepinephrine reuptake inhibitors (SNRIs), triptans may precipitate the potentially fatal serotonin syndrome (agitation, confusion, fever, incoordination, vomiting, tachycardia, and alterations in blood pressure).
The neuroleptic droperidol is also helpful in aborting acute attacks. Metoclopramide given intravenously may be helpful and is being studied. Narcotic analgesics are needed in rare instances, such as meperidine (100 mg intramuscularly) or butorphanol tartrate by nasal spray (1 mg/spray in one nostril, repeated after 3 or 4 hours if necessary). Intravenous propofol in subanesthetic doses may help in intractable cases.
PROPHYLACTIC THERAPY
Prophylactic treatment may be necessary if migrainous headaches occur more frequently than two or three times a month. Some of the more common drugs used for this purpose are listed in Table 24–1. Their mode of action is unclear and may involve both an effect on extracerebral vasculature and a cerebral effect, eg, by stabilizing serotonergic neurotransmission. Several drugs may have to be tried in turn before the headaches are brought under control. Once a drug has been found to help, it should be continued for several months. If the patient remains headache-free, the dose can then be tapered and the drug eventually withdrawn. Botulinum toxin type A is also effective for migraine prevention in some patients; it has few systemic side effects and need only be given at intervals of several months. Although acupuncture has been widely used in the prophylaxis of migraine, a randomized controlled trial failed to show any difference between it and sham acupuncture.