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Andy Jagoda, MD

Critical Questions in the EDCritical Questions in the EDManagement of HAManagement of HA

What is first line therapy for the treatment of HA

Does a response to headache pain therapypredict the underlying etiology of the HA?

Which patients with an acute headache requireneuroimaging in the ED?

What are the indications for a lumbar puncturein the patient with an acute headache?

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ED VisitED Visit Past history of migraines with aura:

scintillating lights followed by nauseaand right temporal throbbing headache

Present headache was different inintensity, onset, and location

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ED Visit #1ED Visit #1 PMH: Migranes Q-month

MEDS: Naprosyn PRN; BCP

LNMP: 7 Days prior

SH: No Tob / ETOH / drugs

FH: Mother - Migraines

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ED VisitED Visit Appearance: 32 year old female, alert,

cooperative but appeared uncomfortable,holding the top of her head

VSS: 118/76, 72, 16, 98.6

Head: Atraumatic Neck: Nontender, supple Heart: Regular, no murmurs, no clicks Lungs: Clear Abdomen: Soft, nontender

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ED VisitED Visit MS: Alert; Oriented X 3 PUPILS: Not documented CN: Intact GAIT: Normal

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A diagnosis of migraine was made. Which of the followingA diagnosis of migraine was made. Which of the followingis your drug of choice in treating acute severe migraine?is your drug of choice in treating acute severe migraine?

Opioid (Meperidine or morphine) Nonsteroidal (Ketorolac) Sumitriptan

DHE Prochlorperazine

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Migraine: PathophysiologyMigraine: Pathophysiology Common pathway for headache pain regardless of

the underlying etiology Headache pain is transmitted via the trigeminal nerve Trigeminovascular axon stimulation results in a

release of neurogenic peptides stored in the afferentC fibers innervatin cephalic blood vessels

Vasoactive neuropeptides mediate an inflammatorycascade, neurogenic inflammation

Vasodilatation and enhanced permeability of plasmaproteins result in a perivascular reaction

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Andy Jagoda, MD

Migraine: PathophysiologyMigraine: Pathophysiology Serotonin receptors modulate neurogenic

peptide release and cause vasoconstriction Goal of migraine therapy is to abort the

neurogenic peptide release

5-HT1c receptor is most involved in mediatingheadache

Drugs working at the 5-HT receptor are thepreferred therapy for headache

Narcotics cause initial pain relief but result invasodilatation with a high incidence of rebound

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Migraine TherapyMigraine Therapy First line agents: Prochlorperazine 5-10 mg IV

Metoclopramide Chlorpromazine

Second line agents: DHE .5-1 mg IM / IV or

sumatriptan 6 mg SQ Third line agent: Ketorolac Fourth line agent: Butorphanol 1 mg

intranasally

Fifth line agent: OpioidsCanadian Headache Society. Guidelines for the diagnosis and management of Migraine in clinical practice. Can Med Assoc J 1997; 156:1273-1287

US Headache Consortium. www.aan.com/public/practice guidelines

http://www.aan.com/public/practicehttp://www.aan.com/public/practice

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ED VisitED Visit Diagnosis: Migraine Treatment: Prochlorperazine Disposition: Headache resolved

HOME

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Does response to therapy predict theDoes response to therapy predict theetiology of an acute severe headache?etiology of an acute severe headache?

All headache pain is mediated by serotonin receptors Case series / case reports (Class III evidence) Seymour. Am J Emerg Med 1995. 3 patients treated with

ketorolac or prochlorperazine with resolution of headache /

Discharged / All with catestrophic outcomes Gross. Headache 1995. 3 cases of meningitis with resolutionof pain with DHE and metoclopramide

Pain response can not be used as an indicator or theunderlying etiology of an acute headache.

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Should this patient have receivedShould this patient have receiveda head CT?a head CT?

Infection CNS mass lesion

Tumor, IIH, Hydrocephalus Collagen vascular disease

Temporal arteritis, vasculitis Ophthamologic etiologies

Glaucoma, optic neuritis Metabolic abnormalities Toxins Pregnancy related

Eclampsia, dural sinus thrombosis

CNS vascular event Subdural, epidural, SAH

Primary headache disorder

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Which patients with acute headacheWhich patients with acute headacherequire neuroimaging in the ED?require neuroimaging in the ED?

Neuroimaging is obtained to assess for treatable lesions: SAH, CVT, tumors,hydrocephalus (Less tangible: Patient reassurance)

Abnormal neuro exam increases the liklihoodof a positive CT 3 times (95% CI 2.3-4) Normal neuro exam is not predictive Location, vomiting, headache waking patient

up, worsening with valsalva are not predictive

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Which patients with acute headacheWhich patients with acute headacherequire neuroimaging in the ED?require neuroimaging in the ED?

Patients presenting with an acute HA and anabnormal neurologic exam should have anemergent head CT

Patients presenting with a sudden severe HA

should have an emergent head CT HIV patients with a new type of headacheshould have an urgent head CT

Patients over the age of 50 with a new type of headache should have an urgent neuroimagingstudy

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Should this patient have had aShould this patient have had ahead CT?head CT?

History: HA was sudden and severe in onset HA was different from past headaches

Physical: No neurologic exam documented:

In the HA patient, the neuro exam focuses onpupil, fundoscopy, and cranial nerves III, IV, VI

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ED Visit #2ED Visit #2

Patient returned 24 hours later withworsening of her headache

Positive findings on the physicalexamination: Papilledema Left 6th cranial nerve palsy on far lateral

gaze A noncontrast head CT was obtained

and was normal

h h i di i f i

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What are the indications for LP inWhat are the indications for LP inacute HA?acute HA?

Suspected SAH in a patient with a normal headCT CT is 90 98% sensitive for acute SAH Sensitivity decreases over time

Suspected meningitis LP without CT in patients with normal neuro examincluding normal mental status and normalfundoscopic exam

Suspected idiopathic intracranial hypertension Headache with papilledema Normal CT

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ED Visit #2ED Visit #2

Lumbar puncture: Opening pressure 280mm Hg; No cells; Normal protein andglucose Normal opening pressure < 160 mm Hg

Diagnosis of idiopathic intracranialpressure was made

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Idiopathic Intracranial Hypertension:Idiopathic Intracranial Hypertension:(Benign Intracranial Htn, Pseudotumor Cerebri)(Benign Intracranial Htn, Pseudotumor Cerebri)

Syndrome defined by signs and symptoms of high ICP without apparent intracranial mass

50% have an identifiable underlying etiology Altered absorption of CSF at the arachnoid

villus Elevated pressure within the sagittal sinus Increased resistance to drainage of CSF within the

villus

Idi hi I i l H iIdi thi I t i l H t i

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Idiopathic Intracranial Hypertension:Idiopathic Intracranial Hypertension:Physical FindingsPhysical Findings

Papilledema 100% Headache 94% Visual disturbance 80%

Transient visual obscuration 68% VI CN palsy (False localizing) 38% Decreased visual acuity 30% Blindness 10%

Giuseffi. Neurology 1991; 41:239-244

Idi thi I t i lIdi thi I t i l

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Idiopathic IntracranialIdiopathic IntracranialHypertension: TreatmentHypertension: Treatment

Correct predisposing factors Serial lumbar punctures Acetazolamide, 1-4 gms / day

Corticosteriods, 40-60 mg / day Surgery

Optic nerve sheath decompression

Lumboperitoneal shuntRadhakrishnan. Mayo Clin Pro 1994; 69:169-180

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ConclusionsConclusions Errors in management

No fundoscopic exam: Opthalmoscope was notworking

No CT: symptoms resolved and CT backed-up Lessons learned

Patients with headache require a comprehensiveneurologic exam

First line therapy for headache are drugs that workat serotonin receptors but response to therapy doesnot predict etiology

Patients with sudden severe headache require a CT;if negative followed by an lumbar puncture