Headache

From High Risk Emergency Medicine, sponsored by the University of California, San Francisco, School of Medicine, Department of Emergency Medicine, and Emergency Department, San Francisco General Hospital

Jonathan Edlow, MD, Associate Professor of Medicine, Harvard Medical School, and Vice Chair of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA

Educational Objectives

The goal of this program is to improve the management of headaches. After hearing and assimilating this program, the clinician will be better able to:

1.   Review the various conditions that can cause headache.

2.   Describe possible presentations of subarachnoid hemorrhage (SAH).

3.   Discuss the importance of epidemiologic context in determining the cause of headache.

4.   Explain the limitations of testing in the diagnosis of SAH.

5.   Recognize the importance of measuring opening pressure on lumbar puncture.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any per­sonal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, Dr. Edlow and the plan­ning committee reported nothing to disclose.

Acknowledgments

Dr. Edlow was recorded at High Risk Emergency Medicine, held May 21-23, 2009, in San Francisco, CA, and spon­sored by the Emergency Department at San Francisco General Hospital, and Department of Emergency Medicine, University of California, San Francisco, School of Medicine. The Audio-Digest Foundation thanks Dr. Edlow and the sponsors for their cooperation in the production of this program.

Introduction: American College of Emergency Physicians (ACEP) guidelines  —  issue as to whether standard of care to be followed at all times; difficult to determine patients to whom guidelines apply; headache  —  chief complaint in »2% of patients (serious condition in 3%-5%; subarachnoid hemorrhage [SAH] in 0.7%-0.9%); epidemiologic con­text important

Migraine: lifetime incidence 12% to 15% and higher in women than in men; International Headache Society guide­lines require 5 previous episodes for diagnosis (10 episodes for tension headache); triptans  —  not specific for mi­graine; common biochemical pathway for head pain that triptans treat; response to medication not diagnostically useful  

Subarachnoid hemorrhage: typically presents with abrupt onset of “worst” headache; may also present with neuro­logic deficits; recent study showed diagnosis missed in 12% (5% in Canadian study); least ill patients most com­monly misdiagnosed, with worse outcomes; focusing on onset, severity, quality, and associated symptoms help determine which patients require work-up (no prospective trial to determine best diagnostic algorithm); history  —compare previous headaches to current one; risk factors  —  binge drinking; cigarette smoking; hyper­tension (HTN); family history

Physical examination (PE): helpful when abnormal; neurologic examination normal in »40% of patients with aneu­rysmal SAH; subhyaloid hemorrhage (due to increase in intracranial pressure [ICP]) possible finding on exami­nation of fundi; results in bleeding between layers of retina); usually seen in more adversely affected patients with other findings; unruptured aneurysm  —  can present as seizure focus, mass lesion, or ischemia from clot in aneurysm that migrates distally and causes transient ischemic attack (TIA) or stroke; palsy of third cranial nerve (CN)  —  most common mass lesion; presents as ptosis; third CN close to posterior communicating artery (PCOM); seen in 10% to 15% of patients with SAH or aneurysms because most aneurysms in anterior circula­tion; 2 types include microvascular infarct (seen in diabetics, hypertensives, and smokers) and compressive type (usually from PCOM aneurysm); due to peripheral location of pupillary constrictor fibers of third CN (more likely to sustain damage from external compression); pupil blown in aneurysmal third nerve palsy, as opposed to microvascular infarct in vasa nervorum (stops extraocular motions but does not affect pupil)

Diagnostic tests: all have limitations, including computed tomography (CT); CT  —  beneficial in early stages when significant bleeding present (opposite seen with cardiac biomarker); patients with small hemorrhage most likely to have negative CT and to feel significantly better with analgesia; therefore, if SAH suspected, perform com­plete work-up; errors in interpretation of CT  —  technical factors becoming less important in newer scanners; SAH more difficult to determine on CT in anemic patients (hematocrit of £30%; blood isodense with brain, even with acute hemorrhage); due to errors in interpretation, must follow up negative CT with lumbar puncture (LP); retrospective study found overall sensitivity of CT 93%; 1 in 10 SAHs missed if normal CT not followed with LP; LP  —  recognition of xanthochromia one of pitfalls; in SAH, visual inspection effective; study showed signif­icant false-positives with spectrophotometry; need to distinguish traumatic LP from true SAH (measuring open­ing pressure helpful); pressure elevated in two-thirds of patients with SAH; also beneficial in diagnosis of pseudotumor cerebri and cerebrovenous sinus thrombosis; study showed blood present in cerebrospinal fluid (CSF) in 100% of patients presenting at <12 hr; xanthochromia  —  almost never seen in LP within first 4 hr; pres­ent in »60% at >6 hr; seen with visual inspection in patients who present >12 hr

When to stop work-up: symptomatic aneurysms rare in patients with severe headache and negative CT and LP, al­though acute expansion of aneurysm, acute thrombosis within aneurysm, or dissection within wall of aneurysm possible; in 7 studies with >800 patients, no SAHs and deaths seen at 6-mo to 1-yr follow-up; opening pressure also beneficial in diagnosis of spontaneous intracranial hypotension (SIH)

When to pursue work-up: in patients with elevated pretest risk (eg, smoker with family history of SAH), speaker would perform neurovascular imaging study; if patient presents >2 wk after onset of symptoms, CT almost al­ways normal and CT angiography (CTA) should be considered; if ambiguity in results of CT and LP, if patient re­fuses LP, or if LP unobtainable, pursue noninvasive imaging; aneurysm present in 2% to 4% of population; speaker does not believe CTA alone sufficient to diagnose SAH

Where to treat: 4 studies show that outcomes better if patient transferred to centers with experience in SAH and neurovascular procedures; better outcomes attributed to neurosurgeons having more experience, availability of coiling and neurologic critical care, and radiologists having more experience in obtaining high-quality images

Spontaneous intracranial hypotension (SIH): suspect in patients with previous spinal surgery who present with headache of increasing severity; similar to post-LP headache; diagnosed by performing LP and obtaining low CSF pressure; if source spinal and diagnosed by nuclear imaging, patch similar to blood patch may be placed

Chronic hemorrhage: chronic subdural hemorrhage  —increasingly common in older patients (can result from mini­mal trauma); isodense on CT; epidural hematoma  —older patients usually present with more atypical symptoms; case  —  patient had headache and gait problems; CT normal, but MRI showed posterior inferior cerebellar stroke; CT not ideal test in acute stroke and for posterior circulation in general

Tumors: negative neurologic examination seen even with large lesions in brain, if growth slow or accommodated due to atrophy; pituitary apoplexy  —  usually occurs in women with nonhormone-secreting pituitary tumors; slow-growing; presentation asymptomatic because of lack of hormonal manifestations; lesion in chiasm may grow sig­nificantly and result in bitemporal hemianopsia; bleeding into tumor may result in thunder-clap headache; visual field symptoms may be present

Idiopathic intracranial HTN (pseudotumor cerebri): sixth CN has longest intracranial course, making it more sus­ceptible to meningeal inflammation or irritation or increased or decreased ICP; palsy of sixth CN also seen in SIH; should decrease ICP to slightly above normal; headache usually improves after ICP decreased; funduscopic examination  —  focus on presence of venous pulsations; look centrally at disc where vessels go backward; presence of venous pulsations highly correlated with normal ICP

Cerebrovenous sinus thrombosis: elevated CSF pressure seen in majority of patients; measuring opening pressure important part of LP

Brain abscess: if MRI unavailable, contrast CT provides more definition to lesions; frontal lobes often “silent” (ab­sence of symptoms), even in young patient without atrophy

Carotid dissection: Horner’s syndrome may be present in patient with asymmetric pupils; larger pupil not always ab­normal; in general, abnormal pupil not as briskly reactive as normal one; when other signs present (eg, ptosis), gen­erally appear ipsilaterally to abnormal pupil; if headache also present, abnormal pupil and headache ipsilateral; bilateral symmetric abnormalities rare; »10% of patients present with headache of varying nature only; usually uni­lateral; interval usually present from onset of pain to diagnosis; some patients present with neurologic deficit due to ischemia as result of dissection; headache almost always different from previous headaches

Carbon monoxide (CO) poisoning: clustering of cases often seen during winter; often see nonspecific headache or flu-like presentation; present with confusion if CO levels sufficiently high; common O₂ saturation monitors under­estimate carboxyhemoglobin level (must measure directly); ACEP policy about hyperbaric O₂ therapy controversial

Hypertensive encephalopathy: sometimes lowering blood pressure (BP) more harmful than no treatment; defined as end-organ damage resulting from HTN; maintenance of constant cerebral blood flow over wide range of BPs nor­mal physiologic function; should lower BP if end-organ damage present; labetalol and nicardipine increasingly used over nitroprusside; should not lower BP too much or too rapidly; bring down »25% from peak level; close monitoring and CT necessary to rule out bleeding

Temporal arteritis: most patients >60 yr of age (median age 75 yr in one study); juvenile pattern not as severe as typical pattern; temporal artery tenderness seen in large percentage of patients; look for jaw claudication and scalp tenderness; erythrocyte sedimentation rate (ESR) usually elevated (in one study, >100 mm/hr in 42% of cases, 70-100 mm/hr in 44%, and <70 mm/hr in 15%); visual loss seen in 13% of cases; treated with prednisone; perform temporal artery biopsy within 1 wk (histologic changes take ³1 wk to improve); should start corticosteroids as soon as possible to preserve vision; start with high dose (³60 mg) of steroids; one study suggested intravenous methyl­prednisolone better than oral prednisone (unproven)

Acute narrow angle-closure glaucoma: on inspection, eyes frankly abnormal, with swelling, haziness or smokiness of cornea from edema, and redness; asymmetry between eyes; one study showed average age of patient 54 yr; head­ache often intermittent; measure opening pressure; pupils typically mid position and poorly reactive

Suggested Reading

Church CR et al: Clinical Inquiries. What are effective medical treatments for adults with acute migraine? J Fam Pract 55:530, 2006; Clinch CR: Evaluation of acute headaches in adults. Am Fam Physician 63:685, 2001; Dupont SA et al: Thunderclap headache and normal computed tomographic results: value of cerebrospinal fluid analysis. Mayo Clin Proc 83:1326, 2008; Edlow JA et al: American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute head­ache. Ann Emerg Med 52:407, 2006; Hankey GJ et al: Easily missed? Subarachnoid haemorrhage. BMJ 339:b2874, 2009; Mathew NT et al: Coexistence of migraine and idiopathic intracranial hypertension without papilledema. Neu­rology 46:1226, 1996; Nusser J et al: Clinical inquiries. Which clinical features and lab findings increase the likeli­hood of temporal arteritis? J Fam Pract 57:119, 2008; Togha M et al: Warning signs and symptoms of subarachnoid hemorrhage. South Med J 102:21, 2009; Wakai S et al: Pituitary apoplexy: its incidence and clinical significance. J Neurosurg 55:187, 1981; Woo D et al: Smoking and family history and risk of aneurysmal subarachnoid hemorrhage. Neurology 72:69, 2009; Zaatreh M et al: Spontaneous intracranial hypotension. South Med J 95:1342, 2002.