1. Recognize the “red flags” for headaches that require further evaluation.

2. Distinguish the various types of “common” headaches.

3. Discuss the reasons for missing the diagnosis of SAH.

4. Recommend appropriate testing for diagnosis of SAH.

5. Discuss the treatment options for stroke.

Nontraumatic Headaches
James (Trey) Morris, MD, MPH, Assistant Professor, Department of Emergency Medicine, Texas A&M University College of Medicine, and Scott & White Memorial Hospital, Temple, TX

Diagnosis: history and physical examination still most useful tools; in certain cases, neuroimaging, blood tests, and cerebrospinal fluid (CSF) analysis helpful; tests not typically performed in emergency department (ED) but useful for continued inpatient investigation include carotid Doppler ultrasonography, cerebral angiography, magnetic resonance imaging (MRI), MR angiography (MRA), and rarely, electroencephalography (EEG)

“Red flags” for headaches: sudden onset (benign thunderclap headache possible); altered mental status or abnormal neurologic examination; study found that 95% of patients with life-threatening headaches had abnormality on neurologic examination; age >50 yr; worsening of headache over short period (minutes to hours); new-onset headache (different in pattern) in immunocompromised patient; any “first” or “worst” headache; if accompanied by seizure

Features that categorize headaches: time course (sudden vs gradual onset); acute, subacute, chronic, or recurrent; important to ask about prodromal symptoms (eg, scotomata), constitutional symptoms, and concurrent symptoms; temporal association (whether headaches worsen with activity or come on with certain activities; association with menses; relationship to medications); location; quality (eg, throbbing, lancinating); obtain—medical, occupational, and family history; ask patient—reason for presenting to ED; how patient arrived at ED (patient arriving by emergency medical services [EMS] significantly more likely to have subarachnoid hemorrhage [SAH]); how present headache compares to previous ones; last time patient had headache so severe

Physical examination: vital signs—presence of fever, hypertension, or hypotension; funduscopic examination—any abnormality (eg, papilledema, absence of spontaneous venous pulsations, hemorrhages) changes probability of SAH; neck examination useful if concerned about SAH or meningitis; jolt examination—patient asked to turn head rapidly to side 3 times; considered positive if headache worsens; bruits raise concern for artery dissection; cardiac examination—not specific but may point to ischemic cause of headache; head, eyes, ears, nose, and throat (HEENT) examination—palpate scalp, particularly if tenderness reported; for eyes, check for pupillary response, whether cornea clear or cloudy, presence of injected conjunctiva, and ecchymosis; check for abnormalities on nasal examination; examination of ears useful if positive; examine skin for rashes; neurologic examination—record mental status and level of consciousness (be specific); test for cranial nerve deficits; thorough testing of motor strength, reflexes, and sensation; assess for Babinski and Hoffman reflexes, depending on degree obtunded; cerebellar function and gait; study—found that 3 features significant independent predictors of serious pathology; include age >50 yr (likelihood ratio [LR] 2.34), sudden onset (LR 1.74), and abnormal neurologic examination (LR 3.56); presence of any 1 of 3 features had sensitivity of ≈99%; negative LR ratio very low

Neuroimaging: computed tomography (CT)—most common and most useful; particularly helpful in suspected mass lesion, early presentation of SAH, and stroke; MRI and MRA—better at detecting mass lesions than noncontrast CT; better for detecting vascular anomalies and aneurysms not apparent on angiography; also for acute strokes; angiography—only indication suspected aneurysm with absence of blood on CT, but present on lumbar puncture (LP); useful in venous thrombosis, but more likely detected by MRI or MRA; diagnosis of arterial dissection made more by MRI or MRA than angiography; indications for head CT—patient who presents with worst or first headache; decreased level of consciousness or altered mental status; abnormality present on neurologic examination; new headache in individual >50 yr of age, immunocompromised patients, or those with progressive worsening of subacute headache; in presence of meningismus and fever, normal neurologic status, and absence of other factors, head CT not useful and may delay definitive care; persistent vomiting with headache indication for head CT

Common headaches: migraine without aura—“common” migraine; probably most frequent; lasts 4 to 72 hr; diagnosed after 5 attacks that meet criteria (2 of following, unilateral location, pulsing quality, moderate or severe intensity, and aggravation by physical exertion); also requires 1 of following, nausea and/or vomiting, photophobia and/or phonophobia; migraine with aura—classic migraine; characterized by fully reversible focal cerebrocortical or brainstem dysfunction; some patients unconscious during aura, have profuse vomiting, or paralysis; by definition, aura lasts 5 to 60 min; headache follows within 60 min after symptom-free interval; common auras include scotomas, blind spots, zigzag lines, fortification (images of castle ramparts), photopsia (flashes of light), visual and auditory hallucinations, paresthesias, and metamorphopsia (everything changing shape); atypical migraines—basilar migraine (unconsciousness, drop attacks, vomiting, and other cranial nerve symptoms); ophthalmic migraine—presents with temporary visual field defect; more common in pregnancy; ophthalmoplegic migraine; familial hemiplegic migraine; abdominal migraine— uncommon in adults; more common in children; presents as periumbilical vague abdominal pain; with or without headache; etiology unknown; also associated with one of migraine precursors in children that causes recurrent vomiting; chronic migraine—defined as headaches occurring >10 days/mo for >3 mo; status migrainosus—persists for >72 hr; persistent aura without infarction or migrainous infarction possible (symptoms last >60 min and result in permanent neurologic damage); small subset of population susceptible to migraine-triggered seizures

Treatment: triptans—most commonly prescribed; not often used in ED; better as abortive therapy than rescue therapy; less favorable side effect profile (use with caution); antiemetics—most commonly used; although serotonergic antiemetics effective at relieving vomiting in migraines, not effective at relieving headache; dihydroergotamine (DHE)—gold standard; several contraindications; use with caution in hypertensive patients, those with severe coronary artery disease, and pregnant women; avoid if patient used triptans in past 24 hr; valproic acid—not as commonly used; effective; given 500 mg intravenously (IV); nonsteroidal anti-inflammatory drugs (NSAIDs)—should not work in pure migraine; since most patients have mixed headache, effective as adjunct; corticosteroids—more effective as longer-term agents in helping to prevent rebound headaches; no acute effect (due to slow onset of action); IV fluids—help dehydrated patients feel better faster; study data—show haloperidol (Haldol) effective in people for whom other therapies not successful; magnesium and propofol also found effective; speaker’s protocol—typically starts with 10-mg dose of metoclopramide (eg, Reglan; akathisia and extrapyramidal side effects possible, so he preemptively treats with IV diphenhydramine and saline); if no improvement after 20 to 30 min, another dose of metoclopramide given with dexamethasone (eg, Decadron) and ketorolac (Toradol; discontinued); if no good relief after 1 hr, consider DHE; next step haloperidol or narcotics (not effective in terminating migraine, but put patients to sleep)

Subarachnoid Hemorrhage
Kevin Klauer, DO, Clinical Assistant Professor, Department of Internal Medicine and Osteopathic Medicine, Michigan State University College of Osteopathic Medicine, Lansing, MI; Director, Quality and Clinical Education, Emergency Physicians, Ltd, and Director, Center for Emergency Medical Education, Canton, OH

Introduction: incidence—23,000 to 28,000 cases annually in United States; patients with “run of the mill” headache do not present to ED; associated with atypical or mild presentation; failure to recognize severity and/or acuity issue; reasons for claims—failure to initiate diagnostic work-up; mistaken reliance on physical examination and reliance on pain medications; failure to obtain head CT; mistaken reliance on head CT; reluctance to perform LP; misinterpretation of results; reluctance to consult neurosurgeon; inadequate follow-up plan and work-up; costs—diagnostic delays lead to increased bleeding or rebleeding, with resulting morbidity and mortality; missed diagnosis of SAH leads to rebleeding and death or significant neurologic sequelae; peak age 55 to 60 yr; cost of medical and custodial care; estimated malpractice cost of missed SAH ≈$126,000 (probably higher now)

Diagnosis: history—symptoms, eg, headache, neck pain, nausea, vomiting; risk factors, eg, polycystic kidney disease; recognize spectrum of presentations (Hunt and Hess classification); patient may present with unusual symptoms and no headache; classic presentation warning headache (“thunderclap” headache); headache that develops during exertion; syncope with headache SAH until proven otherwise; important to determine whether meningeal signs or neurologic changes present with headache; classic presentation occurs in ≈50% of patients; with headache in any location, secondary head injury possible; hypertensive emergencies may be due to SAH; avoid thrombolytics (patient might have pseudoinfarct pattern on electrocardiography [ECG]); increased intracranial pressure (ICP) and injuries in brain cause diffuse pseudo-ST elevations; physical examination—vital signs; funduscopic examination critical (look for papilledema); good neurologic examination; testing—CT without contrast good (but not great); LP (presence of xanthochromia specific but not sensitive; visual inspection usually used to determine xanthochromia); differentiate between traumatic LP and SAH; no threshold for number of red blood cells (RBCs) in SAH; MRA has 5% false-negative rate; neither CT angiography (CTA) nor MRA can detect aneurysms reliably if <5 mm; negative noncontrast CT with negative LP has excellent negative predictive value

Review of literature: article from 2000 reported that reasons for misdiagnosis include failure to appreciate spectrum of disease, failure to understand limitations of CT, and failure to perform LP; incorrect interpretation of CSF; xanthochromia (crenated RBCs) takes 12 hr to develop in CSF in test tube; study (JAMA 2004)—482 patients with SAH at tertiary referral center; looked at outcome measures; found 12% misdiagnosed on first visit, with ≈50% in ED; median time to establish correct diagnosis 4 days; diagnostic error not performing CT most of time, misinterpretation of LP in 11%, and performing CT without LP in 7%; risk factors for misdiagnosis—include good clinical grade, right-sided aneurysm, smaller hemorrhages, history of sentinel bleeding, and fewer signs and minimal symptoms; grades 1 and 2 in Hunt and Hess classification have mortality rates of 45% (because patients often sent home, rebleed in 48 hr, and more likely to die); study—1996; looked at 217 patients with SAH; 25% misdiagnosed at initial evaluation; 48% had delayed rebleeding and deteriorated; LP still needed, even if CT normal; sensitivity of CT ≈100% if done in <12 hr, 81% in >12 hr, poor at >24 hr; patients still undiagnosed at >24 hr require LP; newer CT scanners minimally better for diagnosis of SAH; study by Morgenstern—set standard of 25% reduction in xanthochromia from tube 1 to tube 4 to qualify as “traumatic tap”; data weak, and standard arbitrarily set; case illustrations—indefensible missed SAHs

Recommendations: have low threshold for ordering unenhanced CT; if normal, perform LP; give anxiolytic (not conscious sedation); consider “worst” headache, neurologic signs, neck pain, syncope, and family history; atypical presentations key; if patient has “unusual” headache, consider work-up for SAH; time-frame for CT and LP and interpretation of results important; consultation for significant number of RBCs; gold standard cerebral angiography; ensure discharge instructions given to responsible party; avoid aspirin if SAH suspected

Stroke
Dr. Klauer

Introduction: varied presentations; transient ischemic attack (TIA) must be recognized as potential stroke in evolution; debilitating and often causes death; no consensus in medical community that thrombolytics beneficial for stroke (not standard of care by legal definition)

Evaluation: if giving thrombolytics, patient’s consent necessary; consent form must present issues in unbiased fashion; determine speed and time of onset and distribution of symptoms (vascular distribution); comorbidities; ask about transient loss of consciousness (LOC), visual changes, and gait changes; assess vital signs; perform funduscopic examination; check for bruits; screen for conditions that mimic stroke, eg, migraine, Bell’s palsy

Vascular distribution: lesion in anterior cerebral artery—results in contralateral weakness (greater in leg than in arm) and speech problems; middle cerebral artery—contralateral weakness and numbness (face and arm greater than leg); posterior cerebral artery—cortical blindness; basilar artery syndrome—locked-in syndrome; patient awake but unable to talk; cerebellar infarct—many symptoms, including vertigo occasionally; drop attacks—8% due to central nervous system (CNS) ischemic events

Testing: CT most important; early finding hyperdense sign at interface of gray and white matter

Treatment: aspirin—irrefutable for myocardial infarction (MI) and stroke; heparin—used if able to document embolic phenomenon as cause of stroke (otherwise, likely to convert ischemic infarct into hemorrhagic infarct); fibrinolytics— false standard of care; in patient with ischemic stroke, if treating with tissue plasminogen activator (tPA), ensure that patient within time window and fits specific criteria; have stroke policy in institution

Review of literature: National Institute of Neurological Disorders and Stroke (NINDS) trial—624 patients; tPA given within 3 hr; 30% more likely to have minimal or no disability at 90 days, sustained for 1 yr; symptomatic intracerebral hemorrhage (ICH) rate 6.4%; asymptomatic ICH rate 4%; ICH rate 10.8%; did not exclude TIAs; JAMA 2000 article— reported on Cleveland Clinic experience of applying NINDS trial; trial stopped because of too many deaths; had ICH rate of 17% and symptomatic ICH rate of 15.7%

Hypertension: reducing blood pressure (BP) in ischemic stroke likely worsens it (area of injury depends on BP and cerebral perfusion pressure); hypertension in stroke transient phenomenon (resolves on own in hours to days; do not treat); 2001 article in American Journal of Hypertension states that hypertension in stroke neuroprotective (brain attempting to provide more perfusion to injured area)

Use of tPA: registry shows that 13% of those eligible, and 1.7% of all stroke victims received tPA; national study of inpatients (1999-2002) showed that only 1% of ≈250,000 patients admitted with ischemic stroke received tPA; mortality rate for tPA recipients 11.4% (non-tPA recipients, 6.8%); improvement seen in patients admitted in stroke centers because of ancillary treatment (eg, pulmonary hygiene, physical therapy, speech therapy)

Transient ischemic attacks (TIAs): acute neurologic deficit that resolves in 24 hr; most resolve in 5 to 10 min; 25% of patients report previous TIA; treat as “unstable angina” of brain; JAMA 2000 article—of patients discharged from ED with diagnosis of TIA, 10.5% returned with stroke at 90 days and 50% returned within 48 hr; predictive factors include age, speech, weakness, diabetes, and prolonged symptoms (more likely to return)

Recommendations: stroke policy should be institutional; involve patient and family in decision-making; check patient before discharge; document specific risks; consider transfer to stroke center; patient with diagnosis of new-onset TIA should not be discharged