Headache Emergencies
Adam Quick, MD
Assistant Professor of Neurology
adam.quick@osumc.edu
Learning Objectives








Recognize the clinical presentation and describe the acute management of
subarachnoid hemorrhage.
Recognize the clinical presentation and describe the acute management of
meningitis/encephalitis.
Recognize the clinical presentation and describe the acute management of
temporal arteritis.
Describe the pathophysiology, clinical presentation, differential, diagnostic
considerations, and basic management of headache.
Describe the pathophysiology, clinical presentation, differential, diagnostic
considerations, and basic management of central nervous system infection.
Describe the pathophysiology, clinical presentation, differential, diagnostic
considerations, and basic management of brain tumors.
Differentiate among the clinical syndromes associated with headache, and
the methods of evaluation for further work up the diagnosis.
Recognize acute hemorrhage and ischemic stroke on CT of the brain.
Learning Resources
 Headache Articulate module from
Part 1
 Finseth Review
 Neurology Blueprints
 USMLE World
Overview
 Basic Concepts
 Approach to headache




Distinguishing primary from secondary headaches
Patient history
Physical exam
Diagnostic testing
 Differential diagnosis of common and emergency
headaches
 Treatment approaches to common headache scenarios
Basic Concepts
 Headaches are an extremely common problem



Most people will experience a headache of some sort during their lifetime
Perhaps over 300 causes – most are benign
Primary headache disorders are headache syndrome that are not caused by
another medical problem – the headache syndrome IS the disorder
 Headache accounts for 3.3 million ER visits/year
 4th most common reason adults seek care
 Vast majority of patients presenting to the ER with headache are
going to have one of the primary headache disorders such as:



Migraine
Tension
Cluster
 About 10% will have a secondary headache (these are the ones you
don’t want to miss!)
 First purpose of history and examination is to distinguish benign
recurrent or primary headaches from secondary headaches that
suggest the possibility of a life-threatening event or condition
Initial Evaluation
Key Decision Point
Primary Headache Disorder
Secondary Headache
Disorder
History Taking




Age of onset
Frequency – single vs recurrent
Onset, rate of progression
Character of pain: pressure, stabbing,
throbbing, pounding
 Location of pain
 Severity of pain
 Duration
Additional Headache history
 Premonitory symptoms - auras
 Associated symptoms







Nausea, vomiting
Photophobia, phonophobia
Tearing, rhinorhea
Ataxia
Visual disturbances
Numbness, weakness, other focal neurologic symptoms
Neck pain/stiffness
 Provocative and ameliorative measures
 Important medications: oral contraceptives, analgesic
medications, anti-platelet agents and anticoagulants
 Mood or sleep disturbances
Symptoms Suggestive of Primary HA Disorder
 Stable pattern of headache over time…even if the
current headache is a little atypical
 Follows pattern of a defined primary headache
 Positive family history

Most common with migraine
 Headache improves with sleep
 Headache worsened during or just prior to menses in
women
 Normal physical and neurological examinations
Headache Warning Signs
 First or worst headache of life
 Abrupt new headache symptoms or clear change in
headache pattern
 New onset headache after age 50
 Headache that disrupts sleep or is present upon
awakening
 Headache brought on by exertion or coughing
 Headache with a significant positional component
 New headache following head trauma
 Signs/symptoms of systemic illness: fever, night sweats,
weight loss
 Neck stiffness
 Alterations in personality, behavior or consciousness
 Abnormal neurologic exam
Physical Exam and Headache
 Vital signs
 HEENT: assess temporal artery pulse, look for
conjunctival erythema and ptosis, occipital
tenderness
 Neck: check range of motion, tenderness, muscle
spasm (remember that neck pain is present in
approx. 75% of migraine patients)
 Neurological Exam: Extraocular movements,
fundiscopic exam, facial sensation, coordination,
Romberg testing
Diagnostic Testing
 Labs that may be useful include




CBC to assess for infection
ESR screens for malignancy, collagen
vascular disease and may help establish
the diagnosis of temporal arteritis
TSH may be useful in screening for
thyroid disorders which may sometimes
exacerbate headaches
Toxicology if drug use is suspected
Lumbar Puncture
 Crucial in several clinical situations





First or worst headache of the patient’s life
Headache associated with altered mental status or fever
Progressively worsening headache
Postural headache
An atypical chronic and intractable headache
 Generally in a patient presenting with headache it is
reasonable to get imaging (CT) prior to LP
Indications for Neuroimaging
 Any unexplained objective abnormality
on neurological exam
 Rapidly increasing headache frequency
 History of being awakened by headache
 New headache in patients with cancer or
immune deficiency
 H/O IV drug use
 Recent head trauma or history of falls
(especially in elderly)
 New-onset HA after age 50
 HA precipitated by coughing, sexual
activity, exercise
 Fever, personality changes or altered
level of consciousness
 Strongly consider MRI imaging in the
setting of trigeminal neuralgia or other
cranial neuralgia syndrome
 Head CT has about a 95% chance of
finding sub-arachnoid hemorrhage within
the first 24 hours
Differential Diagnosis of Secondary Headache
 Infection: meningitis,
sinusitis, encephalitis
 Structural abnormality
 Cerebrovascular
ischemia
 Intracranial hemorrhage:
subarachnoid or
parenchymal
 Head trauma
 Venous sinus
thrombosis
 Malignant hypertension
 Vasculitis
 Altered intracranial
pressure
 Carotid/vertebral
dissection
 AV malformation or
aneurysm
 Intraocular disease
 TMJ disorders
 Dental disease
 Cervical spine disease
 Congenital
malformations: Chiari
Type-1, arachnoid cysts
 Metabolic and toxic
causes: noxious and
poisonous gases
 Cranial/upper cervical
neuralgias
Clinical Presentations of Several
Important Acute Emergencies
Sudden Onset Severe Headache
“Thunderclap Headache”




Subarachnoid hemorrhage
Cerebral Venous Thrombosis
Cervical Arterial Dissection
Spontaneous Intracranial
Hypotension
 Pituitary Apoplexy
 Benign Exertional Headache




Ischemic Stroke
Hypertensive Crisis
Third Ventricle Colloid Cyst
Call-Fleming Syndrome
[reversible cerebral
vasoconstriction syndrome]
 Primary Thunderclap
Headache
 Benign Orgasmic
Headache
Subarachnoid Hemorrhage
 Sudden onset first or worst headache.
 HA usually generalized and associated with neck stiffness,
loss of consciousness, nausea, vomiting, photophobia.
 Blood pressure often rises significantly
 Fever may result from meningeal irritation
 1/3 of patients may have early symptoms of more mild HA,
neck stiffness, nausea, vomiting, syncope or visual change
often attributed to “sentinel bleeds/headaches”
 Usually results from ruptured aneurysm or arterial-venous
malformation (80%)
 Risk factors for rupture: size, smoking, evidence of cranial
nerve compression, ETOH use, female gender, hypertension
and exposure to sympathomimetics, increasing age
 Focal neurologic signs are uncommon and suggest AVM or
parenchymal hemorrhage
 Diagnosis is usually with non-contrast head CT
 Lumbar puncture (if CT (-) but clinical suspicion high)
demonstrates elevated pressure, gross blood, xanthochromia
Intraparenchymal Hemorrhage
 Sudden onset headache pain that is often similar in
quality to that seen in SAH
 Differentiating factors: focal neurologic signs, and more
localized head pain
 Etiology most commonly is uncontrolled hypertension
which produces structural changes to the walls of
penetrating arteries- lipohyalinosis
 Most common sites include: putamen, thalamus, pons,
cerebellum and lobar
 Other potential etiologies include vascular
malformations, tumor, amyloid angiopathy
Intraparenchymal Hemorrhage
Intraparenchymal hemorrhage
originating in the basal ganglia
of a 57 year old man with poorly
controlled hypertension
The scan on the left shows bleeding
from an AVM in a woman in her 20’s.
On the right is a post-op scan
Acute Subdural Hematoma
 Elderly and alcoholic patients with cerebral atrophy
 Usually there is a history of prior head trauma
(although this may not clearly be present in elderly)
 Venous source with blood filling the potential space
between the dura and arachnoid membranes
 Location: lateral cerebral convexities, around
tentorial membrane, under the temporal lobes,
posterior fossa
 Presenting signs: headache, confusion, drowsiness,
focal neurologic signs (sometimes false localizing
signs), seizures
Acute Subdural Hematoma
Internal Carotid or Vertebral Dissections
 Headache associated with these may be gradual or
sudden in onset
 It is usually ipsilateral to the site of dissection and may
involve the face and periorbital area
 Often there are focal neurologic signs (usually related to
stroke or TIA) but these may be delayed in onset
 In carotid dissections Horner’s syndrome may be
present
 Pulsatile tinnitus is also a classic symptom
 Often there is a history of recent head or neck trauma
(including chiropractic manipulation)
 Diagnosis is via MRA or CTA
On fat-suppressed T1 MRI
carotid dissection may be seen
as a crescent shaped signal
abnormality when mural
thrombus is present
MRA showing the presence of internal
carotid artery dissection
Bacterial Meningitis
 Classically presents with
headache, fever, stiff neck and
subacute alterations in
consciousness without focal
neurologic signs
 Kernig and Brudzinski signs have
very low sensitivity
 LP should be done in any patient
with new onset headache
associated with fever
 Clinically may be differentiated
from encephalitis patients by the
absence of seizure or focal
neurological deficit
Cerebral Venous Thrombosis
 Requires a high index of
suspicion
 Predisposing conditions:
pregnancy/peripartum,
OCPs, obesity,
dehydration,
hypercoagulable states,
infection
 Symptoms: headache,
seizures, stupor,
papilledema, vision loss,
hemiplegia
 Oculomotor and abducens
palsies may be present
 Diagnosis is usually by MR
venogram
Arrows showing filling defects due
to superior sagittal thrombosis on
MRV
CSF Hypotension
 The classic presentation of this is postural related HA
that worsens in the upright position and disappears
within about 30 minutes when supine
 Often bifrontal or holocephalic with associated nausea,
vomiting, tinnitus and sometimes cranial nerve palsies
 Most common cause is persistent CSF leak following
lumbar puncture
 MRI may show slit like ventricles, prominent dural
sinuses, subdural collections, downward displacement of
the pons and cerebellar tonsils and diffuse dural
enhancement
 Lumbar puncture shows low CSF pressure and high
protein
 Treatment: fluid replacement, IV caffeine infusion,
epidural blood patch
Spontaneous Intracranial Hypotension
Subdural fluid collections
Diffuse Dural Enhancement
Brain Tumors
 It is rare for brain tumors to
present with headache in
isolation
 Usually there are seizures,
focal deficits, cognitive or
speech impairments
 Classically the headaches
associated with intracranial
masses will wake patients from
sleep or are present in the
mornings
 Bending or straining may
worsen or produce the
headache
Temporal Arteritis
 Consider in any patient over 50 with new onset
headache
 Usually there are some associated symptoms of jaw
claudication, transient vision loss or disturbance, fevers,
fatigue or polymyalgia rheumatica
 There may be a tender, erythematous, nodular temporal
artery
 ESR is usually greater than 60
 Diagnosis is by temporal artery biopsy
Idiopathic Intracranial Hypertension
 Typical symptoms are transient visual obscurations or
sometimes complete vision loss caused by papilledema
from increased intracranial pressure
 Diplopia from CN6 palsy sometimes occurs
 Headache is usually generalized frontal but may be
unilateral.
 Most commonly affects obese women of childbearing
age
 Diagnosis is confirmed by lumbar puncture with CSF
pressures usually >25cm H2O
Primary Headaches in the ER
Reasons Migraineurs Come to the ER
 Unusual sudden onset of headache
 Associated intractable vomiting and dehydration
 Onset of headache during unusual circumstances:
exertion, sexual intercourse
 Headache is refractory to usual measures
 Unusual features such as hemiplegic migraine,
migrainous vertigo
 Drug seeking
Treatment
 General measures
Dehydration should be assess and treated as a first step
Placement in dark quiet rooms
Anti-emetics are often useful both for the nausea and
sometimes the headache
Avoidance of opioid medications





Foster drug dependence

Less effective than migraine-specific treatments
Higher risk of rebound and analgesic overuse
effect

Antidopaminergic Agents
 Initially thought to only be useful for nausea/vomiting
associated with migraine
 Have evidence for efficacy in aborting migraine pain
 Side effects




Somnolence
Akathisia
Acute dystonia
Prolonged QT interval- needs EKG
 Options include metaclopramide, prochlorperazine or
chlorpromazine mgIV
DHE
 Available in multiple formulations
 Signficant vasoconstrictive effects





Contraindicated in pregnant patients
Peripheral vascular disease
Coronary artery disease
Cerebrovascular disease
Uncontrolled hypertension
 Typical dose is 1 mg IV preceded by antiemetic such as
prochlorperazine or metaclopramide +/diphenhydramine
 Lower potential for headache recurrence than many
other treatments
NSAIDS and Steroids
 IV ketorolac given alone or in combination with
antidopaminergic medications may be effective in
patients failing triptans
 Randomized trials of steroids have had mixed results
 Meta-analyses have indicated modest benefit when
steroids added to other abortive agents
 May be most effective in reducing HA recurrence rates at
24-72 hours
Valproate and Magnesium
 Both have limited evidence for significant efficacy
 IV depacon (500 – 1000 mg) via rapid infusion




Lack of cardiovascular effects
No interaction with triptans
No sedation
Lack of dependence
 IV magnesium 2 grams


Minimal side effects
Safe in pregnancy
Thank you for completing this module
Questions? Contact me at:
adam.quick@osumc.edu
Survey
We would appreciate your feedback on this module. Click on the
button below to complete a brief survey. Your responses and
comments will be shared with the module’s author, the LSI
EdTech team, and LSI curriculum leaders. We will use your
feedback to improve future versions of the module.
The survey is both optional and anonymous and should take
less than 5 minutes to complete.
Survey