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Headache Emergencies Adam Quick, MD Assistant Professor of Neurology

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1 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.

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 Key Decision Point Primary Headache DisorderSecondary 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

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

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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 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 Intraparenchymal Hemorrhage

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

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

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

40 Thank you for completing this module Questions? Contact me at:

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