Headache

Rosen’s Chapters 17 and 105

November 9th, 2006

By George Filiadis

Epidemiology

• 85% of the US population had significant headaches at least once

• 3-5% of ED visits have as chief complaint headache

• 50% accounts for tension headache while only 8% of headache has a potentially serious cause

• Only 1% of headache in ED have life threatening cause(usually subarachnoid hemorrhage)

Rapid Assessment and Stabilization

• Airway, Breathing, Circulation and Mental Status assessment in all critical patients with headache.

• If there is change in mental status accompanied by headache, it must be assumed that cerebral circulation is compromised

• The main principle of cerebral resuscitation focuses on 7 causes: lack of substrate (glucose, oxygen), cerebral edema, mass lesion intracranially, endogenous or exogenous toxins, metabolic alterations(fever, seizure), ischemia, or elevated intracranial pressure.

Pivot Findings in history

• Pattern and onset of pain

• Activity at onset of pain

• History of head trauma

• History of HIV or immunocompromised state

• Character of the pain

• Location of head pain• Intensity of pain• Exacerbating or

alleviating factors• Associated symptoms

and risk factors• Prior history of

headache

Differential Diagnosis

• Subarachnoid hemorrhage

• Shunt Failure

• Migraine

• Tumor/Masses/ Subdural hematoma

• Carbon Monoxide Poisoning, Mountain Sickness

• Temporal Arteritis

• Glaucoma/Sinusitis• Tension headaches/

Cervical Sprain• Cluster • Bacterial Meningitis/

Encephalitis• Anoxic Headache/

Anemia• Hypertensive crisis

Migraine Headaches

• Accounts for 1 million visits a year in the ED

• Onset is usually in second decade of life

• More prevalent among women

• Historically thought to be due to cerebral vasoconstriction and subsequent vasodilatation

• New beliefs indicate that changes in the serotonergic activity in midbrain are precursors to migraines

• Divided in migraine with and without aura

• Precipitants are nitrates, sleep deprivation, alcohol, hormonal changes, stress, chocolate, caffeine, oral contraceptives

Migraine Without Aura (Common Migraine)

• Most common cause of migraine (80%)

• A.At least five attacks with the criteria B,C,D, and E

• B. Attack lasts 4 to 72 hours with or without treatment

• C. Has two of the following: unilateral location, pulsating quality, and moderate to severe intensity, aggravated by activity

• D. During headache associated with nausea/vomiting or photophobia/phonophobia

• E. History, physical and diagnostic tests that exclude related organic disease

Migraine with Aura (Classic Migraine)

• A. At least two attacks that fulfill criterion B• B.At least three of the four characteristics:

1)one or more reversible aura symptoms indicating focal cerebral or brainstem dysfunction 2) at least one aura develops gradually over more than 4 minutes and no single aura lasts longer than 60 minutes 3)headache begins during aura or follows with a symptom-free interval of less than 60 minutes

• C. An appropriate history, physical, and diagnostic tests that exclude related organic disease.

Clinical Features

• Most common aura is visuala)scintillating scotomas b)photopsias

c)teichopsiasd)blurred vision

• Less common auras are somatosensorya)tingling or numbness b)motor disturbances

c)cognitive disturbances

Clinical Features

• Ophthalmoplegic migraine is a rare condition associated with paresis of ocular nerves that may last days to weeks

• Hemiplegic migraine is characterized by episodic hemiparesis or hemiplegia as an aura that is slow or marching in progression and lasts 30 to 60 minutes

• Basilar artery migraine arises with an aura referable to brainstem and associated with near blindness, dysarthria, tinnitus, vertigo, bilateral paresthesias, or altered consciousness

• Status migrainosus persists longer than 72 hours and requires pain management

Treatment-AbortiveMild to Moderate Attacks

Moderate to Severe Attacks

Refractory Attack,

Status Migrainosus

Acetaminophen Aspirin

Ibuprofen Naprosyn

Dihydroergotamine(1mg IV or IM), may repeat 1 hr Sumatriptan,(6 mg SC/ 25-100mg PO) Rizatriptan, Naratriptan, Zolmitriptan,

Prochlorpethazine

Metaclopromide

Ketorolac, Meperidine

Dihydroergotamine

Steroids

Treatment-Prophylactic

• More than 2-3 episodes a month, prolonged attacks, severe and debilitating

*b-blockers like propanolol*calcium channel blockers

*tricyclic antidepressants *depakote

*monoamine oxidase inhibitors

New thoughts for treatment of Migraines-Haldol

• Monzilo PH, Nemoto PH.Acute treatment of migraine in emergency room: comparative study between dexamethasone and haloperidol. Arq Neuropsiquitr. 2004 june:62: 513-8

-29 patients who met HIS criteria formigraine: 14 pt received Haldol 5mg and 15 pt received decadron 4 mg . Conclusion. Pt who received haldol

reached 50% reduction in pain in 30 min, while patients who received decadron reached the

same level of anesthesia at 2 hrs.

New thoughts for treatment of Migraines-Haldol

• Honkaniemi, Jari, Liimatainen Suvi, Rainesalo(2006) Haloperidol in the Acute Treatment of Migraine: A Randomized, Double-Blind, Placebo-Controlled Study. Headache: The Journal of Head and Face pain. 46 (5), 781-787

-40 patients were enrolled in a double-blind, placebo-controlled study. 80% of patients who were fiest treated with haldol showed significant relief while 79% of the patients treated with placebo first and subsequently with haldol felt significant pain relief.

Cluster Headache

• More common in men• Associated with several episodes over 24

hrs that can last minutes up to 2 hrs• Clinical features include

-unilateral sharp stabbing pain in eye -involves the distribution of CN V -30% of patients have partial Horner’s -eye is often injected, tearing

Cluster Headache-Treatment

• High flow oxygen of 7-10 l/min

• Sumatriptan, DHE

• Prednisone tapering dose

• Sphenopalatine nerve anesthesia with intranasal cocaine or lidocaine-controversial

Tension Headache

• Most common type of headache• Higher prevalence in middle aged women• Usual frequency is 5 episodes per month• Clinical features include -

tight, band-like discomfort around the head -intensity of pain is not severe and thus not debilitating -headache does not worsen with physical activity -coexisting anxiety and depression are common

Tension headache-Treatment

• Aspirin, acetaminophen, NSAIDs

• Exercise program

• Nonpharmacologic regimen like massage, mediation, and biofeedback

• Psychotherapy

Brain Tumor

• In elderly, brain tumor is usually metastatic from lung or breast carcinoma.

• Primary brain tumor are more common in adults younger than 50 years

• HA is caused either by direct pressure on the brain or elevated ICP

• Typical presentation is headache that worsens over over weeks to months

• HA is usually present on awakening initially, then it becomes continuous.

Brain Tumor

• HA is often worse with sneezing, bending, coughing.

• Diagnostic tools include CT with IV contrast or MRI(best test)

Subarachnoid Hemorrhage (SAH)

• Extravasation of blood in subarachnoid space activates meningeal nocireceptors causing occipital pain and meningismus.

• SAH accounts for 10% of all strokes and is most common cause of death from a stroke.

• Causes are saccular aneurysms (80%), blood dyscrasias, arteriovenous malformations, mycotic aneurysms, cavernous angiomas.

• Risk factors include increased age,hypertension, smoking, excessive alcohol consumption and sympathomimetic drugs.

Subarachnoid Hemorrhage(SAH)

• There is familial association of cerebral aneurysms with several diseases -autosomal dominant polycystic kidney

disease-coarctation of the aorta-Marfan’s syndrome-Ehlers-Danlos Syndrome type IV

• 1 to 4% of all ED patients with headache have SAH with 50% associated morbidity and mortality

Clinical Features of SAH

• Sudden “thunderclap” headache

• Can be associated with exertional activities

• Nausea/vomitng-75%• Neck stiffness-25%• Seizures-10%

• Meningismus-50%• Subhyloid or retinal

hemorrhages• Oculomotor nerve

pulsy with dilated pupil

• Restlessness and altered level of consciousness

Prognosis

• It depends on neurological status at the time of presentation

• Hunt and Hess scale

• Grades I and II have good prognosis

• Grades IV and V have

grave prognosis

Grade Condition

0 Unruptured Aneurysm

I No symptoms or minimal headache

II Moderate/Severe HA, nuchal rigidity, no neuro deficit other than CN pulsy

III Drowsiness, confusion, or mild focal deficit

IV Stupor, severe hemiparesis

V Deep coma, decerebrate

Diagnostic Studies

• Emergent CT scan of head

• CT is greater than 90% sensitive for acute bleeding-less than 24 hr

• Sensitivity decreases to 50% by the end of the first week

Diagnostic Studies

• When CT is negative a lumbar puncture should be performed

• The CSF should be spun and the supernatant fluid should be observed for xanthochromia (develops after 12 hrs)

• CSF xanthochromia with negative CT is diagnostic

• Xanthochromia by spectophotometry is more sensitive

Diagnostic Studies

• Patients with persistent bloody CSF without xanthochromia should go vascular imaging

• Up to 90% of patients with SAH have cardiac arrhythmias or EKG findings suggestive of ischemia

• Typical EKG changes include ST-T wave changes, U waves, and QT prolongation

Treatment

• Airway, breathing, circulation and neurosurgical consultation.

• Patients with Grade III SAH usually require endotracheal intubation

• Nimodipine 60 mg PO or NG to lessen the chance of ischemic stroke due to vasospasm

• Anticonvulsants for patients with evident seizure

Giant Cell Arteritis

• Systemic inflammatory process of small and medium size arteries.

• Mean age of onset is 71 years, rare before 50

• Headache is intermittent, worse at night or on exposure to cold

• Associated symptoms include jaw claudication, fever, anorexia, pain and stiffness in joints aka polymyalgia rheumatica

• On exam there is tenderness of temporal artery.

• It’s a medical emergency because long term sequelae is permanent visual loss.

• Diagnostic tests include ESR, CRP, LFTs, platelet count

• Definite diagnosis is by temporal artery biopsy

• Treatment is prednisone 60-120mg daily.

Carotid and Vertebral Artery Dissection

• Most common cause of stroke in persons younger than 45 years.

• Associated with sudden neck movement or trauma following neck torsion, chiropractic manipulation, coughing, minor falls, MVA.

• The pathologic lesion is an intramural hemorrhage in the media of the arterial wall that can be subtle in the early phase leading to thrombus formation over time with emboli or significant enough to occlude the vessel.

• Patients can present with stroke symptoms days to years after dissection.

Carotid artery Dissection

• Classic triad includes unilateral headache, ipsilateral partial Horner’s syndrome, and contralateral hemispheric findings like aphasia, neglect, visual disturbance or hemiparesis.

• Older age, occlusive disease, stroke on initial presentation has worse prognosis

• Diagnosis is via CT angio, MRI/MRA

Vertebral Artery Dissection

• Unilateral posterior headache, and neurological findings like vertigo, ataxia, diplopia, hemiparesis, and unilateral facial weakness, tinnitus

• Diagnosis is same as in carotid dissection

• Treatment includes early anticoagulation followed by antiplatelet therapy

Idiopathic Intracranial Hypertension

• Also known as Pseudotumor Cerebri.

• Commonly seen in young obese women o

• Predisposing factors include anabolic steroids, oral contraceptives, tetracyclines, Vitamin A

• Caused by increased brain water content and decreased CSF ouflow.

• Most common symptom is generalized headache.

• Eye movement, bending forward or Valsava may worsen headache

• On exam patients have papilledema and visual defects, including an enlarged blind spot followed by loss of peripheral lesion.

Idiopathic Intracranial Hypertension(IIP)

• Treatment-stop offending

med -lower CSF production with acetazolomide andfurosemide.-steroids-repeat LPs-ventricular shunt

if with impending visual loss.

Diagnostic Criteria for IIP

Increased intracranial pressure(>200mmHg) measured by lumbar puncture

Signs and symptoms of increased ICP, without localizing signs

No mass lesions or hydrocephalus on imaging

Normal or low CSF protein

No clinical or neuroimaging suspicion of venous sinus thrombosis

Posttraumatic Headache(PTHA)

• Estimated that 30-50% of 2 million closed head injuries per year develop headache.

• Associated with dizziness, fatigue, insomnia, irritability, memory loss, and difficulty with concentration.

• Acute PTHA develops hours to days after injury and may last up to 8 weeks.

• Chronic PTHA may last from several months to years.

• Patients have normal neurological examination and imaging

• Treatment for acute PTHA is symptomatic while for chronic PTHA, adjunct therapies include beta-blockers and antidepressants.

Acute Glaucoma

• Sudden onset of eye pain radiating to head, ear, teeth, and sinuses.

• Visual symptoms include blurriness, halos around lights, and scotomas.

• Nausea and Vomiting

• Due to congenital narrowing of the anterior chamber angle that leads to elevated intraocular pressure (IOP)

• Medications that elevate IOP include mydriatics, sympathomimetics

Acute Glaucoma

• Physical exam shows a red eye with a fixed middilated pupil and shallow anterior chamber (separates it from cluster HA)

• IOP in the range of 60 to 90 mmHg ( not found in iritis)

• Treatment includes topical miotics, b-blockers, carbonic anhydrase inhibitors, optho consult

Postdural Puncture Headache

• Most common complication following lumbar puncture (up to 40%)

• Most common in 18 to 30 year old patients

• It can last up to 5 days

• Bilateral throbbing HA that worsens with upright position

• Thought to be due to persistent leak of CSF that exceeds its production

• Treatment includes rest, fluids, and blood patch, caffeine or theophylline for persistent HA

Intracranial Infection

• HA is common complaint in meningitis, brain abscess, encephalitis or AIDS

• Diagnostic tools include CT of head and LP

Meningitis Severe HA, nuchal rigidity, meningismus

Encephalitis HA, confusion, fever, change of mental status, seizures

Brain Abscess

HA, vomiting, focal neurological signs, depressed level of consciousness

AIDS Toxoplasmosis, CMV, Cryptococcus

Hypertensive Headache

• Elevated blood pressure is not as important in HA as the rate by which the blood pressure increases

• Nonetheless, HA with severe HTN is well documented especially in hypertensive encephalopathy

• Treatment is directed at lowering blood pressure slowly

• HA may last for days until brain edema has resolved

Medication-Induced Headache

• Medication use, abuse or withdrawal s the cause.

• Common in patients with chronic headache disorders like migraine or tension-type.

• Most common meds include ASA, NSAIDs, Tylenol, barbiturate-analgesic combinations, caffeine, and ergotamine

• Patients build tolerance to the meds and subsequently require higher doses for symptomatic relief.

• Treatment includes withdrawal of the overused medications

Carbon Monoxide Poisoning

• Usually gradual, subtle, dull, nonfocal throbbing pain associated with nausea, chest pain.

• Symptoms may wax and wane as patients may enter and leave the area of carbon monoxide

• Exposure to engine exhaust, old or defective heating systems, most common in winter months.

• Non focal neurological exams.• Diagnosis is made by elevated carboxyhemoglobin• Treatment is oxygen

High Altitude Headache

• Main symptom of Acute Mountain Sickness• Can occur at altitudes higher than 5000 feet

in unacclimatized individuals.• HA is throbbing, located in temporal or

occipital area and worsens at night or early in the morning.

• Treatment includes supplemental oxygen and descent to a lower altitude.

Key Concepts

• HA is a challenging yet common complaint in ED• Diseases that we cannot afford to miss are SAH,

CO poisoning, temporal arteritis, bacterial meningitis/encephalitis

• Be liberal with use of CT• Remember CT doesn’t rule out SAH-need LP.• If CT and LP are negative think of temporal

arteritis if older than 50 years, and CO poisoning.• Don’t forget the eyes!