1. Adam Quick, MD Assistant Professor of Neurology adam.quick@osumc.edu
Headache Emergencies
Adam Quick, MD
Assistant Professor of Neurology

2. 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.
of the module, you should be able to accomplish each of these objectives.”

3. Learning Resources
Headache Articulate module from Part 1
Finseth Review
Neurology Blueprints
USMLE World

4. 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

5. 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

6. Initial Evaluation Primary Headache Disorder
Key Decision Point
Primary Headache Disorder
Secondary Headache Disorder

7. 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

8. 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

9. 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

10. 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

11. 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
Fever may suggest meningitis or less commonly encephalitis, brain abscess or temporal arteritis
Hypertensive headaches occur if SBP>180, DBP>110 or there are other findings consistent with malignant hypertension

12. 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

13. 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

14. 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

15. 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

16. Clinical Presentations of Several Important Acute Emergencies

17. 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

18. 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

20. 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

21. Intraparenchymal Hemorrhage
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
Intraparenchymal hemorrhage originating in the basal ganglia of a 57 year old man with poorly controlled hypertension

22. 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

23. Acute Subdural Hematoma
Head CT scans showing right sided subdural hematomas at different ages. In the acute setting (left image) the hyperdense signal is easily seen. In the subacute setting (right image) the subdural may become isodense and is easier to miss.

24. 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

25. 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

26. 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
Kernig's sign positive when the thigh is bent at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful
Brudzinski's sign is involuntary lifting of the legs when the head is raised from supine position

27. 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

28. 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

29. Spontaneous Intracranial Hypotension
Subdural fluid collections
Diffuse Dural Enhancement

30. 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

31. 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

32. 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

33. Primary Headaches in the ER

34. 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

35. 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

36. 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

37. 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

38. 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 hours

39. 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

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