ESSENTIAL INQUIRIES
Age > 50 years.
Rapid onset and severe intensity (ie, “thunderclap” headache).
Fever.
Trauma.
Vision changes.
HIV infection.
Current or past history of hypertension.
Neurologic findings (mental status changes, motor or sensory deficits).
Rapid onset and severe intensity (ie, “thunderclap” headache).
Fever.
Trauma.
Vision changes.
HIV infection.
Current or past history of hypertension.
Neurologic findings (mental status changes, motor or sensory deficits).
General Considerations
Headache is a common reason that adults seek medical care, accounting for approximately 13 million visits each year in the United States to physicians’ offices, urgent care clinics, and emergency departments. A broad range of disorders can cause headache. This chapter will deal only with the approach to the acute nontraumatic headache in adolescents and adults. The challenge in the initial evaluation of acute headache is to identify which patients are presenting with an uncommon but life-threatening condition. In the emergency department setting, approximately 1% of patients seeking medical attention for acute headache will have a life-threatening condition, whereas the prevalence of life-threatening conditions in the office practice setting is considerably lower.
Regardless of the underlying cause, headache is currently believed to occur as a result of the release of neuropeptides from trigeminal nerve endings that encapsulate the blood vessels of the pia mater and dura mater, resulting in neurogenic inflammation. Because this represents a final common pathway for many etiologies, diminution of headache in response to typical migraine therapies (such as serotonin receptor antagonists or ketorolac) does not rule out critical conditions such as subarachnoid hemorrhage or meningitis as the underlying cause.
Clinical Findings
A. Symptoms
A careful history and physical examination should aim to identify causes of acute headache that require immediate treatment. These causes can be broadly classified as imminent or completed vascular events (intracranial hemorrhage, thrombosis, vasculitis, malignant hypertension, arterial dissection, or aneurysm), infections (abscess, encephalitis, meningitis), intracranial masses causing intracranial hypertension, preeclampsia, and carbon monoxide poisoning. Having the patient carefully describe the onset of headache can be helpful in diagnosing a serious cause. Report of a sudden-onset headache that reaches maximal and severe intensity within seconds or a few minutes is the classic description of a “thunderclap headache” and should precipitate workup for subarachnoid hemorrhage, since the estimated prevalence of subarachnoid hemorrhage in the setting of a thunderclap headache is 43%.
The general medical history can also guide the need for additional work-up. A new headache in a patient over the age of 50 or with a history of HIV disease under most circumstances (including a normal neurologic examination) warrants neuroimaging immediately (Table 2–8). When the patient has a medical history of hypertension—particularly uncontrolled hypertension—a complete search for criteria satisfying a diagnosis of “malignant hypertension” is appropriate to determine the correct urgency level of hypertension management (see Chapter 11). Headache and hypertension associated with pregnancy may be due to preeclampsia. Episodic headache associated with the triad of hypertension, heart palpitations, and sweats is suggestive of pheochromocytoma. In the absence of thunderclap headache, advanced age, and HIV disease, a careful physical examination and detailed neurologic examination will usually determine acuity of the work-up and need for further diagnostic testing.
Patient symptoms can also be useful for diagnosing migraine headache in the absence of the “classic” migraine pattern involving scintillating scotoma followed by unilateral headache, photophobia, and nausea and vomiting (Table 2–9). The presence of three or more of these features can establish the diagnosis of migraine (in the absence of other clinical features that warrant neuroimaging studies), and the presence of none or one of these features (provided it is not nausea) can help to rule out migraine.
B. Physical Examination
Critical components of the physical examination of the patient with acute headache include vital sign measurements, neurologic examination, and vision testing with funduscopic examination. The finding of fever with acute headache warrants additional maneuvers to elicit evidence of meningeal inflammation, such as Kernig and Brudzinski signs. Besides malignant hypertension, significant hypertension can also be a sign of intracranial hemorrhage, preeclampsia, and pheochromocytoma. Patients over 60 years of age should be examined for scalp or temporal artery tenderness.
Careful assessment of visual acuity, ocular gaze, visual fields, pupillary defects, the optic disk, and retinal vein pulsations is crucial. Diminished visual acuity is suggestive of glaucoma, temporal arteritis, or optic neuritis. Ophthalmoplegia or visual field defects may be signs of venous sinus thrombosis, tumor, or aneurysm. Afferent pupillary defects can be due to intracranial masses or optic
neuritis. Ipsilateral ptosis and miosis suggest Horner syndrome and in conjunction with acute headache may signify carotid artery dissection. Finally, papilledema or absent retinal venous pulsations are signs of elevated intracranial pressure—findings that should be followed by neuroimaging prior to performing lumbar puncture (Table 2–8).
neuritis. Ipsilateral ptosis and miosis suggest Horner syndrome and in conjunction with acute headache may signify carotid artery dissection. Finally, papilledema or absent retinal venous pulsations are signs of elevated intracranial pressure—findings that should be followed by neuroimaging prior to performing lumbar puncture (Table 2–8).
Mental status and complete neurologic evaluations are also critical and should include assessment of motor and sensory systems, reflexes, gait, cerebellar function, and pronator drift. Any abnormality on mental status or neurologic evaluation warrants emergent neuroimaging (Table 2–8).
C. Diagnostic Studies
Guidance on when to perform neuroimaging is summarized in Table 2–8. Under most circumstances, a noncontrast head CT is sufficient to exclude intracranial hypertension with impending herniation, intracranial hemorrhage, and many types of intracranial masses (notable exceptions include lymphoma and toxoplasmosis in HIVpositive patients, herpes simplex encephalitis, and brain abscess). When appropriate, a contrast study can often be ordered to follow a normal noncontrast study. A normal neuroimaging study does not sufficiently exclude subarachnoid hemorrhage and should be followed by lumbar puncture. In patients for whom there is a high level of suspicion for subarachnoid hemorrhage or aneurysm, a normal CT and lumbar puncture should be followed by angiography within the next few days (provided the patient is medically stable). Lumbar puncture is also indicated to exclude infectious causes of acute headache, particularly in patients with fever or meningeal signs. Cerebrospinal fluid tests should routinely include Gram stain, white blood cell count with differential, red blood cell count, glucose, total protein, and bacterial culture. In appropriate patients, also consider testing cerebrospinal fluid for VDRL (syphilis), cryptococcal antigen (HIV-positive patients), acid-fast bacillus stain and culture, and complement fixation and culture for coccidioidomycosis. Storage of an extra tube with 5 mL of cerebrospinal fluid is also prudent for conducting unanticipated tests in the immediate future. Consultation with infectious disease experts regarding local availability of polymerase chain reaction tests for specific infectious pathogens (eg, herpes simplex 2) should also be considered in patients with evidence of centralnervous system infection but no identifiable pathogen.
In addition to neuroimaging and lumbar puncture, additional diagnostic tests for exclusion of life-threatening causes of acute headache include erythrocyte sedimentation rate (temporal arteritis; endocarditis), urinalysis (malignant hypertension; preeclampsia), and sinus CT or radiograph (bacterial sinusitis, independently or as a cause of venous sinus thrombosis).
Treatment
Treatment should be directed at the cause of acute headache. In patients in whom migraine or migraine-like headache has been diagnosed, early treatment with NSAIDs or triptans can often abort or provide significant relief of symptoms. The effectiveness of NSAIDs and triptans appears to be equivalent, although combination sumatriptan-naproxen appears to provide a greater sustained response (2–24 hours) compared with monotherapy with either agent alone. Nonoral medication administration is often necessary for patients with significant nausea and vomiting, in which case nasal and subcutaneous triptans and intramuscular ketorolac are therapeutic options. Other causes of acute headache, such as subarachnoid hemorrhage, intracranial mass, or meningitis, usually require emergent treatment in the hospital.
When to Refer
• Frequent migraines not responsive to standard therapy.
• Migraines with atypical features.
• Chronic daily headaches due to medication overuse.
• Migraines with atypical features.
• Chronic daily headaches due to medication overuse.
When to Admit
• Need for repeated doses of parenteral pain medication.
• To facilitate an expedited work-up requiring a sequence of procedures and neuroimaging.
• Monitoring for progression of symptoms and neurologic consultation when the initial emergency department work-up is inconclusive.
• Pain severe enough to impair activities of daily living or limit partic
• To facilitate an expedited work-up requiring a sequence of procedures and neuroimaging.
• Monitoring for progression of symptoms and neurologic consultation when the initial emergency department work-up is inconclusive.
• Pain severe enough to impair activities of daily living or limit partic
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