Headache is a common complaint that affects nearly everyone at some time in life. In the vast majority of cases, headaches do not reflect a serious underlying disorder and are not of sufficient sever-ity or frequency for the individual to seek medi-cal attention. However, as with other complaints of pain, the possibility of a clinically significant underlying disorder should always be considered. The practitioner should solicit other associated symptoms or clinical findings that suggest serious underlying pathology. Table 47–10 lists impor-tant causes of headache. Disorders in which the primary complaint is headache are considered in the following discussion. As will become apparent, there is significant variability in clinical presen-tation and overlap in the symptoms of the major headache syndromes, particularly between tension and migraine headaches.
Tension headaches are classically described as tight bandlike pain or discomfort that is often associated with tightness in the neck muscles. The headache may be frontal, temporal, or occipital, more often bilateral than unilateral. Intensity typically builds gradually and fluctuates, lasting hours to days. They may be associated with emotional stress or depres-sion. Treatment is symptomatic and consists of NSAIDs.
Migraine headaches are typically described as throb-bing or pounding and are often associated with photophobia, scotoma, nausea and vomiting, and localized transient neurological dysfunction (aura). The latter may be sensory, motor, visual, or olfactory. Classic migraines by definition are preceded by an aura, whereas common migraines are not. The pain is usually unilateral but can be bilateral with a fron-totemporal location and lasts 4–72 h. Migraines pri-marily affect children (both sexes equally) and young adults (predominantly females). A family history is often present. Provocation by odors, certain foods (eg, red wine), menses, and sleep deprivation is com-mon. Sleep characteristically relieves the headache. The mechanism is complex and may include vaso-motor, autonomic (serotonergic brainstem systems), and trigeminal nucleus dysfunction. Treatment is both abortive and prophylactic. Rapid abortive treatment includes oxygen, sumatriptan (6 mg sub-cutaneously), dihydroergotamine (1 mg intramus-cularly or subcutaneously), intravenous lidocaine (100 mg), nasal butorphanol (1–2 mg), and sphe-nopalatine ganglion block. Other abortive options include zolmitriptan nasal spray, dihydroergotaminenasal spray, or an oral serotonin 5-HT 1B/1D-receptor agonist (almotriptan, frovatriptan, naratriptan, rizatriptan, eletriptan, or sumatriptan). Prophylactic treatment may include β-adrenergic blockers, cal-cium channel blockers, valproic acid, amitriptyline, and onabotulinumtoxinA (Botox) injections.
Cluster headaches are classically unilateral and periorbital, occurring in clusters of one to three attacks a day over a 4- to 8-week period. The pain is described as a burning or drilling sensation that may awaken the patient from sleep. Each episode lasts 30–120 min. Remissions lasting a year at a time are common. Red eye, tearing, nasal stuffiness, pto-sis, and Horner’s syndrome are classic findings. The headaches are typically episodic but can become chronic without remissions. Cluster headaches primarily affect males (90%). Abortive treatments includes oxygen and sphenopalatine block. Lithium, a short course of steroid medication, and verapamil may be used for prophylaxis.
Temporal arteritis is an inflammatory disorder of extracranial arteries. The headache can be bilateral or unilateral and is located in the temporal area in at least 50% of patients. The pain develops over a few hours, is usually dull in quality but may be lancinating at times and worse at night and in cold weather. Scalp tenderness is usually present. Temporal arteritis is often accompanied by polymyalgia rheumatica, fever, and weight loss. It is a relatively common disorder of older patients (>55 years), with an incidence of about 1 in 10,000 per year and a slight female predomi-nance. Early diagnosis and treatment with steroids is important because progression can lead to blindness through involvement of the ophthalmic artery.
Trigeminal neuralgia (or tic douloureux) is classically unilateral and usually located inthe V2 or V3 distribution of the trigeminal nerve. It has an electric shock quality lasting from seconds to minutes at a time and is often provoked by contact with a discrete trigger. Facial muscle spasm may be present. Patients are middle-aged and elderly, with a 2:1 female to male ratio. Common causes of tri-geminal neuralgia include compression of the nerve by the superior cerebellar artery as it exits the brain-stem, cerebellopontine angle tumor, or multiple sclerosis. The drug of choice for treatment is carbam-azepine although it carries a risk of agranulocytosis. Phenytoin or baclofen may be added, particularly if patients do not tolerate the required doses of car-bamazepine. More invasive treatments for patients who do not respond to drug therapy include glycerol injection, radiofrequency ablation, balloon com-pression of the gasserian ganglion, and microvascu-lar decompression of the trigeminal nerve.