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Acute Neurological Emergencies: Headache. Brad Bunney, MD Associate Professor Dept of Emergency Medicine. University of Illinois College of Medicine Chicago, IL.

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brad bunney md associate professor dept of emergency medicine

Brad Bunney, MDAssociate ProfessorDept of Emergency Medicine

University of Illinois College of Medicine

Chicago, IL


Michael Gerardi, MD, FAAP, FACEPVice-Chairman, Department of Emergency MedicineMorristown Memorial HospitalMorristown, New JerseyNina T. Gentile, MDAssociate ProfessorDivision of Emergency MedicineTemple University School of MedicinePhiladelphia, PADaniel G. Murphy, MD, FACEPVice Chair & Medical DirectorMaimonides Medical CenterBrooklyn, New York

the case
The Case

One hour prior to ED presentation, a 42 year old man was jogging and “hit” by the worst headache of his life. It was associated with some nausea and the feeling as if he was going to pass out. He rested for 30 minutes but the headache persisted as a diffuse, throbbing pain radiating to the base of his skull.

the case continued
The Case (Continued)

EMS was called. The patient felt as if he could not concentrate, there was no confusion, nor was there any other focal neurologic complaint.

There was no past medical history, no medications, no family history, and no significant use of alcohol, tobacco or other drugs.


If a patient presented with the worst headache of his life, what is the work-up that should be initiated?

a. Non-contrast CT

b. LP after neg. CT

c. LP without CT

d. CT, LP, and angiography

  • What is the differential of a “thunderclap headache”?
  • What is the sensitivity of neuroimaging in subarachnoid hemorrhage (SAH)?
  • What constitutes a “positive” lumbar puncture in SAH and when should it be performed?
  • Do patients with suspected SAH who have a negative CT and lumbar puncture require additional imaging to “rule-out” expanded but unruptured aneurysm?
  • 1 of 10 top presenting complaints
  • 1 to 2% of visits to ED
  • 18 million outpatient visits
  • 638 million days of work lost per year
  • 78% of women and 64% of men had experienced at least one in the prior year
  • 36% of women and 19% men suffer from recurrent headaches
  • Most have primary headache disorders
    • migraine
    • tension
  • Only a few have treatable secondary causes that threaten life, limb, brain such as subarachnoid hemorrhage
    • 1 - 4 % of headache visits
worst headache
“Worst” Headache
  • Normal exam: 12- 33% SAH
  • Abnormal exam: 25% SAH
  • Initial hemorrhage may be fatal
  • Early definitive surgery improves outcomes
  • Patients with greatest likelihood of benefiting from surgery are most likely to receive incorrect diagnosis
physicians consistently misdiagnose sah
Physicians Consistently Misdiagnose SAH

1. Failure to appreciate spectrum of clinical presentation

2. Failure to understand limitations of CT

3. Failure to perform and correctly interpret the results of LP

ed goals in headache patients
ED Goals in Headache Patients

1. Differentiate life-threatening from benign

2. Initiate prompt treatment

3. Provide prompt pain relief

4. Prevent drug seeking and refer

5. Minimize resource utilization in ED

6. Optimize patient use of ED

7. Increase pre-ED treatment and reduce ED use

medical conditions that present with headache
Medical Conditions That Present With Headache
  • Pheochromocytoma
  • Hyperthyroidism
  • SLE
  • Giant Cell Arteritis
  • Fibromyalgia
types of headaches in the ed
Types of Headaches in the ED

Final Diagnosis Percentage

Infection - not intracranial 39.3

Tension HA 19.3

Miscellaneous 14.9

Post-traumatic 9.3

Hypertension related 4.8

Vascular (Migraine) 4.5

No diagnosis 6.0

SAH 0.9

Meningitis 0.6

causes of headache that require specific therapy
Causes of Headache That Require Specific Therapy
  • Subarachnoid hemorrhage
  • Meningitis
  • Encephalitis
  • Cervicocranial-artery dissection
  • Temporal arteritis
  • Acute angle-closure glaucoma
  • Hypertensive emergency
causes of headache that require specific therapy1
Causes of Headache That Require Specific Therapy
  • Carbon Monoxide poisoning
  • Pseudotumor cerebri
  • Cerebral venous and dural sinus thrombosis
  • Acute stroke (hemorrhagic or ischemic)
  • Mass Lesion
    • tumor
    • abscess intracranial
    • hematoma
    • parameningeal infection
headache danger signals
Headache Danger Signals
  • Onset
    • after 40 years
    • new or different headache
    • subacute HA that worsens
    • exertion, sex, coughing, straining
  • Worst ever experienced
headache danger signals associated with neurologic change
Headache Danger Signals: Associated With Neurologic Change
  • Memory impairment
  • Ataxia
  • Drowsiness
  • Sensory loss
  • Signs of meningeal irritation
headache danger signals associated with neurologic change1
Headache Danger Signals: Associated With Neurologic Change
  • Progressive visual or neurologic change
  • Confusion
  • Weakness
  • Loss of coordination
  • Asymmetry of pupils, DTRs
headache danger signals abnormal medical evaluation
Headache Danger Signals: Abnormal Medical Evaluation
  • Fever
  • Chronic malaise
  • Arthralgia
  • HTN
  • Myalgia
  • Wt loss
  • Tender, poorly pulsatile temporal arteries
subarachnoid hemorrhage
Subarachnoid Hemorrhage
  • Incidence of 16 /100,000
    • about 33,600 cases per year
    • 54% secondary to ruptured aneurysm
  • Without treatment, 40% of aneurysm pts. have recurrent bleeding
  • Aneurysm pt who survives initial rupture and is treated conservatively:
    • 50% survival at one year
current problems in management of subarachnoid hemorrhage
Current Problems in Management of Subarachnoid Hemorrhage
  • Errors and delays in diagnosis
  • Treatment of acute effects
  • Prevention of recurrent hemorrhage
  • Prevention or treatment of vasospasm or cerebral ischemia
classic symptoms of subarachnoid hemorrhage
Classic Symptoms of Subarachnoid Hemorrhage
  • Sudden, unusually severe or “thunderclap” headache
  • Loss of consciousness
  • Pain in neck, back, eye or face
  • Nausea, vomiting, photophobia, phonophobia
classic signs of subarachnoid hemorrhage
Classic Signs of Subarachnoid Hemorrhage
  • Abnormal vital signs
    • Respiratory changes, hypertension, cardiac arrhythmias
  • Meningismus
  • Focal neurologic signs may be present
    • III nerve palsy – IC/PCA aneurysm
    • Paraparesis – ACA aneurysm
    • Hemiparesis, aphasia – MCA aneurysm
  • Ocular hemorrhages
subarachnoid hemorrhage1
Subarachnoid Hemorrhage
  • Onset: Acute
  • Location: Global
  • Ass Sx: N,V, meningismus, focal
  • Pain: Worst ever
  • Duration: Brief
  • Prior Hx: No
  • Dx tests: CT 80-90%
  • Phys ex: Focal signs, LOC, meningismus
subarachnoid hemorrhage2
Subarachnoid Hemorrhage
  • Warning leaks in 50%
  • CT misses up to 10% small leaks
  • Suspect if:
    • > 35 years
    • no previous HA
    • no fading of HA
    • came on with exertion
    • altered LOC or neuro deficits
    • stiff neck
subarachnoid hemorrhage neurologic findings
Subarachnoid Hemorrhage: Neurologic Findings
  • Sudden HA without localizing findings
  • Altered mentation
    • Confusion, lethargy
  • Bilateral extensor plantar reflex
  • Unusual to find focal deficits
causes of non traumatic subarachnoid hemorrhage
Causes of Non-Traumatic Subarachnoid Hemorrhage
  • “Berry” aneurysms
  • AVM
  • Cerebral angiomas
  • Mycotic aneurysm
  • Extension from parenchymatous hemorrhage
  • Anticoagulation therapy
causes of non traumatic subarachnoid hemorrhage1
Causes of Non-Traumatic Subarachnoid Hemorrhage
  • Systemic bleeding diathesis
  • Hemorrhagic encephalitis
  • Hemorrhagic cerebral vasculitis
  • Hemorrhage into CNS tumors or metastases
  • Unknown
warning headache
Warning Headache
  • 20 - 50% patients with SAH have HA days or weeks before index episode
    • unusually severe
    • distinct
  • “Thunderclap” headache
    • Day and Raskin 1996
    • intense, acute, peak intensity at onset
    • develop in seconds
    • maximal intensity in minutes
    • lasts hours to days
thunderclap headache
“Thunderclap” Headache
  • 25% associated with SAH
  • “Warning” headache
    • followed by SAH in 5% to 60%
  • Expansion or dissection of unruptured aneurysm
  • Cerebral venous thrombosis
  • Exertional / coital headache

Misdiagnosis of SAH

  • 217 patients from 4 institutions
  • 54 (25%) were initially misdiagnosed
  • 121 patients initially presented in good clinical condition
  • 46 (38%) were initially misdiagnosed

Stroke 1996;27:1558-63

misdiagnosis of sah
Misdiagnosis of SAH

Outcome of Patients with Good Initial Presentation in Misdiagnosed and Correctly Diagnosed Patients With SAH

Outcome Misdiagnosis (n=45) Correct Diagnosis (n=75)

Excellent/good 24 (53)* 68 (91)*

Fair 5 (11) 4 ( 5)

Poor/vegetative/dead 16 (36)* 3 ( 4)*

Values are number (%) in each clinical grade category.

  • P<.001

Stroke 1996;27:1558-63


Misdiagnosis of SAH

Rebleeds and Deteriorations Before Treatment in Misdiagnosed and Correctly Diagnosed Patients With SAH

Misdiagnosis (n=54) Correct Diagnosis (n=163)

Rebleeds 21* 4

Deteriorations 5 0

Total 26 4

*12/21 of misdiagnosed and 3/4 of correctly diagnosed patients rebled within 5 days of presentation.

Stroke 1996;27:1558-63

sah but not classic
SAH…But not “Classic”
  • Roughly half have minor bleeding with atypical features
  • Nonstrenuous activities (34%)
  • Sleep (12%)
  • HA in any location (localized, generalized, mild)
  • May be relieved by non-narcotic analgesics
  • Diagnosed as migraine, tension-type, sinusitis
sah most patients have
SAH: Most patients have...
  • Abrupt onset of severe, unique headache, or neck pain
  • Abnormal findings on neurologic examination
  • Subtle meningismus or ocular findings
international headache society
International Headache Society
  • A first episode of severe headache cannot be classified as migraine:
    • more than 4 episodes
  • nor as tension-type headache:
    • more than 9 episodes
  • First or worst headache requires evaluation
    • as do qualitatively different headaches
can a ct scan safely rule out sah
Can a CT Scan Safely “Rule Out” SAH?
  • First diagnostic study
  • Thin cuts ( 3 mm) through base of brain
  • Blood on CT function of Hgb
    • Hgb < 10: blood isodense
  • Sensitivity decreases over time from onset of symptoms
sah ct findings
SAH CT Findings
  • High density hemorrhage injury
    • (1) Interhemospheric fissure
    • (2) Inferior frontal sulci
    • (3) Third ventricle
    • (4) Ambient cistern
    • (5)Sylvian fissure
sah ct sensitivity sames acad emerg med jan 1996
SAH: CT SensitivitySames: Acad Emerg Med Jan 1996
  • 181 patients; aged 13-86 with SAH
    • Sensitivity 91.2%
      • pain < 24 hrs 93.1%
      • pain > 24 hrs 83.8%
  • LP 100% sensitive if neg CT
  • “A normal NGCT does not reliably exclude the need for LP”
sah diagnosis lp needed sidman acad emerg med sep 1996
SAH Diagnosis: LP NeededSidman: Acad Emerg Med Sep 1996
  • 140 patients; aged 10-88
  • Sensitivity of CT
    • < 12 hrs 80/80 100%
    • > 12 hrs 49/60 81.7%
  • Overall, 11/140 had (-) CT and (+) LP
    • overall sensitivity 92.1%
Morgenstern LB, et al:Worst headache and SAH: Prospective, modern CT and spinal fluid analysis.Ann Emerg Med Sept 1998.
  • 38,730 patients over 16 months, prospectively screened for “worst HA”
  • Blinded neuroradiologists
    • Neg CT LP
      • cell count x 2
      • visual and spectrophotometric detection of xanthochromia
      • CSF D-dimer assay
morgenstern et al ann emerg med 1998
Morgenstern, et al: Ann Emerg Med 1998
  • 455 headaches & 107 “worst headache”
  • CT: 18 of 107 (17%): (+) SAH
  • (-) CT/ (+) SAH: Only 2 (2.5%)
    • (95% CI, 0.3%to 8.8%)
  • Modern CT is sufficient to exclude 98% of SAH in patients
morgenstern et al ann emerg med 1998 107 worst ha s
Morgenstern, et al: Ann Emerg Med 1998 (107 “Worst HA’s)

Variables CT-/LP- CT+ CT-/LP+

Photophobia 45 28 50

Stiff neck 26 37 100

Nausea 65 36 100

Lethargy 17 40 50

Time < 24 h 58 75 50

Migraine 20 11 0

Headache 48 27 0

what about lp first
What about LP First?
  • Duffy et al; 1982: 55 patients who underwent LP as initial w/u
    • Condition deteriorated immediately in 7 patients
  • Hillman et al; 1986: 4 alert patients with SAH who deteriorated after lumbar puncture
  • Both studies:
    • clots on CT or a dilated pupil
traumatic taps
Traumatic Taps
  • 20% of LPs
  • 0.5% and 6% has incidental intracranial aneurysm
  • Impression or “3-tube” method not reliable in detecting traumatic tap
  • Erythrocytes disseminate rapidly
  • Released Hgb oxyhemoglobin

xanthochromia bilirubin

  • Bilirubin, enzyme-dependent process, is diagnostically more reliable but:
    • takes up to 12 hours
  • Timing is important
  • CSF should be centrifuged and examined promptly so RBCs don’t undergo lysis in vitro, causing xanthochromia from oxyhemoglobin
xanthochromia vs erythrocytes
Xanthochromia vs. Erythrocytes
  • Xanthochromia
    • primary criterion for SAH if neg CT
    • advocates: spectrophotometry
  • Erythrocytes
    • considered more accurate by some
    • used visual inspection which can miss discoloration in up to 50%
timing the tap
Timing the Tap
  • With spectrophotometry, and waiting 12 hours after onset of headache: very accurate
    • traumatic tap done earlier does not lead to xanthochromia and confusion
  • Waiting:
    • prolongation of ED stay
    • risk “ultra-early” rebleeding
normal ct persistently bloody csf
Normal CT & Persistently Bloody CSF ???
  • Not prudent to delay LP
  • Without xanthochromia and clinical suspicion is high?
    • Vascular imaging
  • Xanthochromia present and clinical suspicion is high?
    • Vascular imaging

Differentiate Between

Traumatic LP and SAH

CSF characteristic

Traumatic tap

True SAH

Color gets lighter with subsequent tubes



RBC count in first & last tube

count decrease

stay constant

Clotting of blood in CSF



present withi4 hrs of SAH, max at 1 wk, persists for about 3 weeks

Xanthochromia in supernatant

rare with RBC count less than 200,000

thunderclap headache nl ct nl lp vascular imaging
Thunderclap Headache: NL CT & NL LP Vascular Imaging?
  • Wijdicks et al; Lancet, 1988
    • Retrospective evaluation 71 patients
    • no SAH in 3.3 years f/u
    • Half dx’d with migraine or tension HA
  • Markus 1991; Linn 1994; Harling 1989
    • 117 patients
    • no SAH, no sudden deaths
  • Occurs in 70% of patients with SAH
  • Appears after 3-4 days, peaks at 7-10 days, and resolves over 2-4 weeks
  • Can be localized or involve several arteries
  • Caused by factors released at time of bleeding that induce vasoconstriction and reduced blood flow
calcium channel blocking drugs
Calcium Channel Blocking Drugs
  • Drugs that limit transmembrane fluxes
    • Vascular smooth muscle contraction
    • Cell ischemia
    • Platelet aggregation
  • Selective cerebrovascular effects
  • Cross blood-brain barrier
  • Limited cardiovascular effects
clinical trials of nimodipine
Clinical Trials of Nimodipine
  • Nimodipine improves survival and functional recovery after SAH
  • Benefits are due to its antihypertensive and neuronal protective effects
the case continued1
The Case (Continued)

The patient had labs drawn, was given 5mg of morphine and sent off to CT scan.

The CT scan revealed an acute SAH. The neurosurgeon ordered an angiogram which revealed an aneurysm.

The patient went to the OR that day and was release with a normal neurological status 4 days later.

first ed visit late friday night
First ED Visit: Late Friday Night
  • 24 yo female with headache for 2 weeks, worse over the last 2 days
  • 104/76, 80, 18, 98.1F
  • Right frontal forehead, sharp, non-radiating, constant but waxing/waning, worse when she moved.
  • (+) nausea
  • (-) fever, photophobia, neck pain or visual changes
past medical social history
Past Medical/Social History
  • No recent trauma
  • Smoker 1 PPD
  • Social drinker
  • No hx of headaches, except for last 2 weeks
  • No allergies
  • No meds except ibuprofen and acetaminophen recently – not helpful
  • Worked as a part-time sales clerk
exam first visit
Exam: First Visit
  • Alert, oriented, looked well except for discomfort of headache
  • Face normal, Perrl, EOMI, fundi normal, TMs normal, mastoids non-tender, neck supple, motor neuro exam normal, normal gait, mental status normal
ed therapy and work up
ED Therapy and Work Up
  • Prochlorperazine 10 mg, by vein Acetaminophen 325/Oxycodone 5, orally
  • CBC, Chem 7, UCG, CT Head without contrast
ed diagnostic results visit 1
ED Diagnostic Results: Visit 1
  • WBC count 12.4K
  • CT head reviewed by ED attending and radiology resident as negative
ed disposition visit 1
ED Disposition: Visit 1
  • Patient’s pain responded to medications
  • Patient discharged with prescription for acetaminophen/butalbital/caffeine = Fioricet
radiology over read monday am 2 5 days since 1 st ed visit
Radiology Over-Read: Monday AM(2.5 days since 1st ED visit)
  • Opacification of the right ethmoid and right sphenoid sinuses with expansion of the sphenoid septations toward the left.
  • No intracranial disease
ed discrepancy procedure
ED Discrepancy Procedure
  • Patient was contacted by phone and informed of sinus problem on CT
  • Patient went to her PMD that afternoon
  • PMD discharged her with prescription for levofloxacin
2 nd ed visit tuesday morning 3 5 days after 1 st ed visit
2nd ED Visit: Tuesday Morning(3.5 days after 1st ED visit)
  • New onset swelling and severe pain around left eye
  • Continued, worsening right-sided headache
  • Slept poorly, confused, hallucinating?
  • 100/80, 96, 18, 101.9F
morning exam 2 nd visit
Morning Exam: 2nd Visit
  • Left peri-orbital edema, erythema, proptosis, chemosis, severe pain with EOMs. Left pupil reacted to light.
  • Ambulated in with normal gait. No obvious motor deficits.
  • Awake. Followed simple commands, but mildly confused, answering slowly or incorrectly, with difficulty concentrating.
  • (+) Nuchal rigidity
ed therapy work up
ED Therapy & Work Up
  • 2 grams ceftriaxone by vein after cultures
  • Repeat CT of brain and sinuses with contrast
  • LP
  • ID and ENT consults; vancomycin and metronidazole given by vein
  • Admitted to MICU
afternoon exam 2 nd visit
Afternoon Exam: 2nd Visit
  • Deteriorating mental status.
  • Mild left sided weakness left upper and left lower extremities.
ed admitting diagnoses
ED Admitting Diagnoses
  • Orbital Cellulitis
  • Meningitis
  • Rule out Cavernous Sinus Thrombosis
septic dural sinus thrombosis suppurative intracranial thrombophlebitis
Septic Dural Sinus ThrombosisSuppurative Intracranial Thrombophlebitis
  • Infected venous thrombosis of cortical veins or sinuses
  • From meningitis, subdural empyema, epidural abscess, infection in the skin of the face, paranasal sinuses, middle ear, mastoid, maxillary teeth or neck.
  • Iatrogenic cases have been associated with rhinoplasty, hip surgery and oral/dental surgery.
non septic dural sinus thrombosis
Non-Septic Dural Sinus Thrombosis
  • Dehydration from vomiting
  • Hypercoagulable states
  • Immunologic abnormalities, including the presence of circulating antiphospholipid antibodies
septic dural sinus thrombosis
Septic Dural Sinus Thrombosis
  • Rare; 155 reported cases since 1940
  • Cavernous Sinus Thrombosis (CST) is the predominant subset (62%?)
  • Fulminant, aggressive disease: mortality CST =30%, superior sagittal sinus thrombosis =78%
  • Morbidity CST: 50% cranial nerve deficit; 17% visually impaired
infected thrombus pathogens
Infected Thrombus Pathogens
  • CST: Staphylococcus aureus, other gram-positive organisms, and anaerobes.
  • Lateral Sinus (otitis media and/or mastoid infection) Proteus species, Escherichia coli, S. aureus, and anaerobes.
  • Superior Sagittal Sinus (meningitis or air sinus infection) - Streptococcus pneumoniae, S. aureus, other streptococci, and Klebsiella.
ed presentation superior sagittal sinus thrombosis
ED Presentation: Superior Sagittal Sinus Thrombosis

Headache, nausea and vomiting, confusion, and focal or generalized seizures.

  • Rapid development of stupor and coma.
  • Weakness of the lower extremities with bilateral Babinski signs or hemiparesis is often present.
ed presentation transverse sinus thrombosis
ED Presentation: Transverse Sinus Thrombosis
  • Headache and earache.
  • Gradinego's syndrome: otitis media, sixth nerve palsy, and retro-orbital or facial pain.
  • Sigmoid sinus and internal jugular vein thrombosis may present with neck pain.
ed presentation cavernous sinus thrombosis
ED Presentation: Cavernous Sinus Thrombosis
  • Sinusitis, midface infection for 5-10 days.
  • Fever, headache, malaise, retro-orbital pain and diplopia, which generally precede…..
  • Ptosis, proptosis, chemosis, eyelid edema, peri-orbital edema and extraocular dysmotility due to deficits of cranial nerves III, IV, and VI.
  • Hypo- or hyperesthesia of the ophthalmic and maxillary divisions of V, decreased corneal reflex. dilated, tortuous retinal veins and papilledema.
  • Meningeal signs: nuchal rigidity, Kernig and Brudzinski signs.
diagnostic studies
Diagnostic Studies
  • CBC, diff, cultures
  • Sinus Films, CT, MR, MR Venography, Venous phase cerebral angiogram
  • LP
ed management
ED Management
  • Antibiotics: S aureus is the usual cause, broad-spectrum coverage for gram-positive, gram-negative, and anaerobic organisms also, pending cultures.
  • Drain primary source of infection, if feasible (eg, sphenoid sinusitis, facial abscess).
  • Anticoagulation in carefully selected cases of septic cavernous-sinus thrombosis, not other forms of septic dural-sinus thrombosis.
  • Urokinase or rtPA?
  • Corticosteroids?
  • ENT
  • Neurology
  • ID
  • Intensive Care
outcome of case
Outcome of Case
  • Day 1: Seizure, worsening deficit, intubated
  • Day 2: Heparinized, transient neuro improvement then relapse.
  • Day 5: Sinuses drained
  • Day 6: Brain dead
  • Day 19: Demise

Acute Headache

Questions ?