Headache

Rosens 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/phonoph obia 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 visual a)scintillating scotomas b)photopsias c)teichopsias d)blurred vision Less common auras are somatosensory a)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-Abortive
Mild to Moderate Moderate to Severe Attacks Attacks Acetaminophen Aspirin Ibuprofen Naprosyn Refractory Attack,

Status Migrainosus

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

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 for migraine: 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, DoubleBlind, 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 Horners -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 -Marfans 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
Grade Condition

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

0 I II

Unruptured Aneurysm No symptoms or minimal headache Moderate/Severe HA, nuchal rigidity, no neuro deficit other than CN pulsy Drowsiness, confusion, or mild focal deficit

III

IV

Stupor, severe hemiparesis

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. Its 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 Horners 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 and furosemide. -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 betablockers 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
Severe HA, nuchal rigidity, HA is common meningismus complaint in meningitis, Encephalitis HA, confusion, brain abscess, fever, change of encephalitis or AIDS mental status, Diagnostic tools include seizures CT of head and LP Brain HA, vomiting, focal Abscess neurological signs, depressed level of consciousness AIDS Toxoplasmosis, CMV, Cryptococcus Meningitis

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, barbiturateanalgesic 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 doesnt rule out SAH-need LP. If CT and LP are negative think of temporal arteritis if older than 50 years, and CO poisoning. Dont forget the eyes!