Definition
A.Diffuse pain in some part of the head or pain located above the orbitomeatal line of the head.
B.The International Headache Society divides headaches into primary and secondary headaches.
1.Primary: Benign headaches without any abnormal pathology. More than 90% of headaches are primary. Three types are recognized.
a.Migraine: Characterized by attacks of moderate to severe throbbing headaches that are often unilateral in location, worsened by physical activity, and associated with nausea and/or vomiting, photophobia, and phonophobia. Migraine headaches may last from 4 to 72 hours.
i.Classic migraine: Migraine with aura—the aura usually only lasts up to 60 minutes.
ii.Common migraine: Migraine without aura.
iii.Status migrainosus: Migraine lasting more than 3 days.
b.Tension-type headache: Most common form of headache that can last from 30 minutes to 7 days. Characterized by bilateral mild to moderate nonthrobbing pressure such as pain, without associated symptoms. Mostly described as tight band around the head.
c.Cluster headache: Less common. Brief episodes of severe unilateral throbbing pain, mostly in the retro-orbital area that usually last from 15 minutes to 3 hours. Ipsilateral autonomic symptoms such as eyelid edema, nasal congestion, and lacrimation may be present.
2.Secondary: Malignant headaches caused by structural lesion or organic pathology. Less than 10% of headaches are secondary.
a.Examples include headaches due to brain tumor, meningitis, substance withdrawal, and intracerebral hemorrhage.
Incidence
A.Many headache sufferers do not seek medical attention.
B.An estimated 23 million Americans and 240 million people worldwide have migraine headaches each year.
C.Migraine headaches occur in a 3:1 female-to-male ratio.
D.Episodic tension-type headaches are present in about 46% of the U.S. population.
E.Chronic tension-type headaches are present in approximately 2% of the U.S. population.
Pathogenesis
A.The exact mechanism involved in the development of primary headaches is unknown.
B.Headaches usually result from vasodilation/constriction of blood vessels.
C.Migraine headaches are thought to result from activation of meningeal and blood vessel nociceptors, combined with a change in central pain modulation.
D.Activation of trigeminal system results in release of neuropeptides, which, in turn, causes neurogenic inflammation and increase in vascular permeability and local dilation of blood vessels, causing pain and associated symptoms via the trigeminal pathway.
E.Decrease in levels of serotonin (5-hydroxytryptamine [5–HT]) have shown to induce migraine.
Predisposing Factors
A.Foods containing tyramine (aged cheeses, pickled foods), nitrites (cured meats), monosodium glutamate, or sulfites.
B.Alcoholic beverages, especially red wine and beer.
C.Emotional factors such as stress, anxiety, and depression.
D.Hormonal fluctuations.
E.Decreased sleep or sleep deprivation.
F.Medications: Estrogen, nitroglycerine, or ranitidine.
G.Physical fatigue.
H.Environmental: Weather, odors, sound, bright lights, and barometric changes.
Subjective Data
A.Common complaints/symptoms (red flag symptoms).
1.Every headache evaluation should begin with a search for certain signs and symptoms. The presence of any of these red flag
symptoms warrants an urgent extensive workup.
2.Systemic symptoms (fever, weight loss) or secondary risk factors (HIV, systemic cancer).
3.Neurologic symptoms or abnormal signs (impaired alertness or consciousness, confusion, weakness, visual loss).
4.Onset: Sudden, abrupt, or split-second.
5.Increased age: New-onset and progressive headache, especially in middle age (>50 years [giant cell arteritis]).
6.Previous headache history: First headache or different headache (marked change in attack, frequency, severity, or clinical features).
B.Diagnostic criteria.
1.The gold standard for diagnosis of headache is a detailed interview and clinical examination.
2.Headache onset (age, sudden or gradual onset, factors associated with onset such as exercise, sexual activity, Valsalva maneuver, febrile illness).
3.Location of pain: Unilateral, bilateral, global.
4.Duration (see section “Definition” for details).
5.Frequency.
6.Quality: Throbbing, squeezing, band like, stabbing.
7.Severity (at onset, at peak, and duration from onset to peak).
8.Associated symptoms such as nausea, vomiting, blurred vision, nasal congestion, mood swings, and so forth.
9.Presence or absence of an aura: Visual scotomas, flashing lights, or facial numbness.
10.Aggravating and relieving factors: Body position or darkness.
C.History.
1.Medication history: Contraceptives, hormonal therapy, vitamins, herbals, and painkillers.
2.General medical history.
3.Family history of headaches.
Physical Examination
A.Perform a complete general examination with focus on the head and neck and a full neurological examination. Generally, these are normal, with no neurological deficits in primary headaches. A focal neurological deficit with acute headache predicts central nervous system (CNS) pathology.
B.Observe the body habitus. Patients with pseudo tumor cerebri tend to be obese.
C.Perform a funduscopic examination to rule out papilledema as in pseudo tumor cerebri or diseases with increased intracranial pressure (ICP).
D.Auscultate the skull and orbits for bruits as heard in arteriovenous malformation and fistulas.
E.Palpate and tap the sinus for tenderness in sinus inflammation.
F.Arteries may be tender and harder to palpate in temporal arteritis.
G.Palpate both temporomandibular joints for tenderness and crepitus while the patient opens and closes the jaw.
Diagnostic Tests
A.The diagnosis of primary headache is usually made on the basis of headache history, physical examination, and neurological examination. No specific diagnostic tests are available.
B.The diagnosis of secondary headache involves the following.
1.Complete blood count (CBC), chemistry panel, urinalysis, liver function test, and thyroid profile.
2.Sedimentation rate and C-reactive protein: Elevated in temporal arteritis.
3.Neurological imaging, which should be considered in patients with any of the following findings.
a.Thunderclap headache/worst headache of life.
b.Altered mental status.
c.Meningismus.
d.Papilledema.
e.Acute neurological deficit.
f.New onset headache after age 50.
g.History of cancer or HIV or immunocompromised state.
4.CT of head: Best to rule out acute injury and bleed.
5.CT of paranasal sinuses: To rule out sinusitis.
6.MRI of brain (more sensitive than CT): Useful to rule out space occupying lesions, demyelinating lesions, ischemia, and abscess.
7.Magnetic resonance angiography (MRA): Helpful in identifying vascular abnormalities such as aneurysms and arteriovenous malformation.
8.Lumbar puncture: Useful in diagnosing infections, malignancy and subarachnoid hemorrhage, and idiopathic intracranial hypertension.
9.Tonometry: If symptoms suggest acute narrow angle glaucoma (visual halos, corneal edema, shallow anterior chamber).
Differential Diagnosis
A.Differential diagnosis.
B.Brain tumor.
C.Brain hemorrhage.
D.Seizure.
E.Meningitis.
F.Dissection.
G.Cerebral aneurysm.
Evaluation and Management Plan
A.Migraine headache.
1.General interventions.
a.Lifestyle modifications and trigger prevention should be emphasized.
b.Analgesics such as aspirin, acetaminophen, ibuprofen, and naproxen can be used in mild headache. Opioids are generally avoided in primary headaches.
2.Acute migraine: Abortive treatment in inpatient or ED setting.
a.Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids: Caution necessary in patients with hepatic or renal impairment, diabetes, or gastritis. One of the following drugs can be used.
i.Ketorolac 30 mg IV.
ii.Methylprednisolone 100 to 200 mg.
iii.Dexamethasone 10 to 40 mg.
b.Neuroleptics: Can be used alone and as pretreatment to ergot derivatives to offset nausea.
i.Diphenhydramine 25 to 50 mg, lorazepam 0.5 to 1 mg, and/or benztropine 1 mg is often given before neuroleptic to prevent akathisia.
ii.ECG: Check and avoid neuroleptics if QTc is prolonged.
c.Anti-nausea medications can be used to alleviate the sense of nausea, but are also effective in controlling migraines in select patients.
i.Metoclopramide 10 to 20 mg IV.
ii.Prochlorperazine 10 to 20 mg IV, IM.
iii.Droperidol 0.625 to 2.5 mg IV or IM.
iv.Chlorpromazine 12.5 to 100 mg PO, IV (up to 50 mg only).
d.Dihydroergotamine 0.5 to 1 mg IV push: Migraine-specific but also helpful in cluster headache. This drug must not be administered if a triptan has been taken in the preceding 24 hours, and it is contraindicated in patients with a history of, or at high risk for, myocardial infarction (MI), or stroke.
e.Anticonvulsants: Can be useful; given as rapid infusions (over 10–20 minutes).
i.Valproic acid: 500 to 1,000 mg; can also be useful for cluster headache.
ii.Levetiracetam: 1,000 to 2,000 mg, maximum recommended dose is 3,000 mg/d.
f.Magnesium sulfate: 1 to 2 g IV piggyback.
g.Serotonin (5-HT) receptor agonists: Sumatriptan 6 mg SC or 10 mg intranasal.
3.Migraine prophylaxis: Used when attacks exceed two per month or when acute attacks are refractory. One of the following drugs can be used.
a.Beta adrenergic blockers: Propranolol—drug of choice.
b.Tricyclic antidepressants: Amitriptyline 25 to 125 mg PO hs.
c.Serotonin antagonists: Methysergide 1 to 2 mg PO TID.
d.Calcium channel antagonist: Verapamil 40 to 80 mg TID.
e.Anticonvulsant: Valproic acid total 250 mg BID or TID.
B.Tension-type headache.
1.Usual abortive treatment can be any simple analgesic.
2.Drug of choice for prophylaxis is amitriptyline 50 to 150 mg/d.
3.Concurrent depression or anxiety disorder needs to be addressed if present.
C.Cluster headache.