More complete discussions of most of these entities are found elsewhere in this text.
SUBARACHNOID HEMORRHAGE Epidemiology SAH has an annual incidence of approximately 1 per 10,000 in the United States10 and represents 1 percent of all nontraumatic headaches seen in the ED.1 However, SAH accounts for up to a quarter of all sudden severe headaches.6 SAH occurs in young people, with a median age of 50 years. Mortality rates from SAH are high; 50 percent of patients die within 6 months, and only 58 percent of survivors regain their premorbid neurologic state.22
Clinical Features At the time of presentation, almost half of patients with SAH have normal findings on neurologic examination, including normal vital signs, normal level of consciousness, and no neck stiffness.22 The headache of SAH is most commonly severe and of sudden onset, but it may also be more subtle. The most common location for the headache is occipitonuchal.8 Many presentations are atypical and may mislead the clinician. For example, sudden-onset intense neck pain may be mistakenly attributed to radiculopathy. Also, resolution of the pain even without treatment does not exclude the diagnosis. Beware of radiation of pain down along the spine, since this suggests tracking of subarachnoid blood down the spinal canal.
Diagnosis Investigation of suspected SAH usually begins with a plain CT scan of the head. Retrospective studies suggest sensitivity of newer generation CT may be in excess of 93 percent for the detection of SAH when symptom presentation is within 24 h and may be even higher if performed within 12 h of symptom onset. 23 However, no study has convincingly shown that CT alone can rule-out SAH, even within 12 h.24 CT sensitivity falls to slightly over 80 percent after 24 h and decays rapidly thereafter. Older generation CT scanners were less sensitive among patients who were alert compared to those with altered sensorium. 25 It remains unclear whether this finding holds with new generation scanners.26
Most authorities consider an LP to be mandatory following a negative CT. An alternate view suggests that LP may be unnecessary when the pretest probability is very low.27 However, this view has itself been challenged on the basis that so-called low-probability patients (isolated severe headache and absence of neurologic findings) may still have up to a 12 percent chance of SAH and that CT may be less sensitive in these patients. 28 Thus, given the potential for catastrophic outcome, it remains prudent to perform an LP on all patients suspected of SAH in whom the CT scan was negative. In fact, restricting investigations to only an LP has been proposed for patients meeting "lone acute sudden headache" criteria (acute sudden headache without neck stiffness and normal neurologic examination, vital signs and level of consciousness). However, the utility of this protocol has not been proven in clinical studies. 28
The gold standard for the diagnosis of SAH is the presence of xanthochromia in the cerebrospinal fluid supernatant. If LP is performed 12 h or longer after headache onset (sufficient time for xanthochromia to develop) and spectrophotometry is used for the cerebrospinal fluid analysis, xanthochromia is virtually 100 percent sensitive for up to 2 weeks following a bleed. Naked-eye detection of xanthochromia may lead to false-negative results in up to 50 percent of cases. 10
MENINGITIS All forms of meningitis can cause headache. In viral or bacterial meningitis, the headache may be severe and of rapid onset, and is usually accompanied by fever and meningismus. Opportunistic infections in immunocompromised patients, such as cryptococcal meningitis, may present with a more insidious onset of headache, and fever and neck stiffness may be absent. An LP is required if there is any suspicion of meningitis, and it need not be preceded by a CT scan in patients with normal findings on neurologic examination, a normal level of consciousness, and no papilledema. If the LP must be delayed for any reason and bacterial meningitis is suspected, antibiotics should be started immediately. 4
INTRAPARENCHYMAL HEMORRHAGE AND CEREBRAL ISCHEMIA About 55 percent of patients with intraparenchymal hemorrhage report headaches at the onset of their symptoms. Only 17 percent of ischemic stroke patients and 6 percent of patients with transient ischemic attacks (TIAs) complain of headache. Other neurologic signs and symptoms are present in most patients.
SUBDURAL HEMATOMA A history of remote trauma in a patient with a headache should raise suspicion of a subacute or chronic subdural hematoma. A low threshold for initiating investigations is appropriate for high-risk patients, including patients on anticoagulants, chronic alcoholics, and the elderly, in whom there may be no clear history of trauma.4
BRAIN TUMOR Up to 70 percent of patients with brain tumors complain of headache at the time of diagnosis, and only about 8 percent have normal findings on neurologic examination.12 The headache may be unilateral or bilateral, intermittent or continuous. The classic headache of brain tumors (worse in the morning, associated with position and nausea and vomiting) occurs in only a few. If headache is suspected of being due to a tumor and 24-h follow-up can be ensured, a reliable patient with normal findings on neurologic examination, including no papilledema, can be investigated as an outpatient. 412
TEMPORAL ARTERITIS Epidemiology Temporal arteritis (TA) occurs almost exclusively in patients over 50 years of age. In this age group, there is an annual incidence rate of 15 to 30 cases per 100,000 persons, and it occurs more commonly in women.29
Pathophysiology TA is a systemic panarteritis that selectively involves arterial walls with significant amounts of elastin. 12
Clinical Features Headache is the most common symptom of TA, reported in 60 to 90 percent of patients. The headache is most often severe, throbbing, and usually located over the frontotemporal region. Other strongly suggestive features include jaw claudication or evidence of polymyalgia rheumatica, with which TA is strongly associated. The involved temporal artery may be nonpulsatile or tender, or have a diminished pulse. The most serious complication is loss of vision, usually due to ischemic optic neuritis.1229
Diagnosis The diagnosis is established by fulfilling three of the five following criteria: age over 50 years, new-onset localized headache, temporal artery tenderness or decreased pulse, erythrocyte sedimentation rate over 50 mm/h, and abnormal arterial biopsy findings. 29
Treatment In order to prevent loss of vision, treatment should begin immediately with 40 to 60 mg/day prednisone when TA is clinically suspected. Patients should be referred urgently for definitive diagnosis and follow-up.29
OPHTHALMIC DISORDERS Acute glaucoma may present with headache, and in other eye disorders, such as iritis or optic neuritis, some patients may describe eye or supraciliary pain as headache. These conditions can usually be distinguished by a careful history and eye examination, including measurement of intraocular pressure when necessary.4
HYPERTENSION Hypertension may cause headaches, with higher diastolic pressures generally associated with more severe headaches. Physicians should be cautious prior to making this diagnosis, however, since hypertension may also occur as a sign of other secondary headache conditions (e.g., stroke, pheochromocytoma, or preeclampsia) or may simply be secondary to the pain and anxiety associated with a primary headache syndrome.4 When other secondary causes of headache, including hypertensive emergency (see Chap, 53), have been ruled out, reduction of the blood pressure should result in improvement or resolution of the headache. While some consider isolated headache associated with hypertension as evidence of possible end-organ involvement, most such patients can be discharged following complete resolution of symptoms and blood pressure reduction if follow-up in the next 24 to 48 h can be arranged.
SINUSITIS Infection of the sinuses may result facial pain or headache. Maxillary sinusitis, by far the commonest type, causes pain over the anterior aspect of the face, rather than headache. Involvement of other sinuses can cause headache: frontal sinusitis over the forehead, ethmoid sinusitis behind and between the eyes, and sphenoid sinusitis a diffuse headache. The headache frequently varies with head position. Symptoms predictive of sinusitis include colored nasal discharge, maxillary toothache, and poor response to decongestants, while reliable signs include purulent nasal discharge and abnormal transillumination (not easy to do properly in the ED). Regardless of plain sinus x-ray findings, patients with four or more of the abovementioned features have a very high likelihood of sinusitis, while those with fewer than two features are very unlikely to have sinusitis.
DRUG-RELATED AND TOXIC OR METABOLIC HEADACHES Various drugs, such as nitrates, MAOIs, or chronically used analgesics, may cause headache. Such metabolic conditions as hypoxia, hypercapnia, and hypoglycemia and such toxins as monosodium glutamate and carbon monoxide may cause headache as well. Withdrawal from alcohol may also result in headache. Such headaches can be identified either in the history or through appropriate laboratory testing. 4
BENIGN INTRACRANIAL HYPERTENSION (PSEUDOTUMOUR CEREBRI) A rare entity, benign intracranial hypertension (BIH) should be considered in a young, obese patient presenting with long-standing headaches. Nausea, vomiting, and visual disturbance may also be present. While its cause is unknown, BIH has been linked to the use of oral contraceptives, vitamin A, and tetracycline and to thyroid disorders. BIH is characterized by papilledema, a normal level of consciousness, normal CT scan findings, and markedly elevated cerebrospinal fluid pressure on LP. The only serious adverse outcome is the potential for visual loss. Initial treatment is usually with acetazolamide or steroids. When these fail, repeated LPs to drain cerebrospinal fluid or surgery (cerebrospinal fluid shunts or optic nerve sheath fenestration) may be tried.
INTERNAL CAROTID AND VERTEBRAL ARTERY DISSECTION While rare, dissection of the internal carotid or vertebral artery is frequently associated with headache. Dissection may be spontaneous or the result of trauma and generally occurs in younger patients (median age, 40 years). Internal carotid artery dissection may be suspected in a patient with unilateral anterior neck pain or headache, usually around the eye or frontal area. Most patients present with or eventually develop neurologic signs, such as TIA, stroke, Horner syndrome, transient monocular blindness, or cranial nerve palsies. Vertebral artery dissection typically presents with marked occipital or posterior neck pain associated with signs of a brainstem TIA or stroke. Diagnosis is usually made by angiography. Duplex scanning and MRI may also identify vessel abnormalities. SAH may be caused by dissection through the adventitia of the vessel, and this must be ruled out prior to initiating anticoagulant therapy.
POST-LUMBAR PUNCTURE HEADACHE Between 10 and 36 percent of patients who undergo LP develop a headache within 24 to 48 h due to a persistent cerebrospinal fluid leak from the dura. The incidence of post-LP headaches can be minimized through the use of smaller-bore needles with noncutting tips in order to spread, rather than cut, dural fibers.30 Patients who present to the ED with a post-LP headache may respond to simple analgesics, but, if this treatment fails, a blood patch may be required. This procedure involves an epidural injection of autologous blood at the level of the LP in order to "patch" the cerebrospinal leak. 31
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