Migraine Headache

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Original Editors - Katie Elder from Bellarmine University's Pathophysiology of Complex Patient Problems project.

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Definition/Description

Migraine is a chronic, episodic primary headache.  Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).

Symptoms typically last 4 to 72 hours and may be severe. Pain is often but not always unilateral, throbbing, worse with exertion, and accompanied by autonomic symptoms (eg, nausea; sensitivity to light, sound, or odors).  Fortification spectra and other transient focal neurologic deficits occur in a few patients, usually just before the headache, also known as aura. Diagnosis of migraine can usually be made by history alone.  Treatment includes lifestyle changes (diet, exercise, sleeping habits), medications including NSAIDs, analgesics, serotonin receptor agonists, beta blockers, calcium channel blockers, and antiemetics.

Prevalence

Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches at some point. Lifetime prevalence is 18% for women and 6% for men in the US.  It most commonly begins during puberty or young adulthood, waxing and waning in frequency and severity over the ensuing years and usually diminishing after age 50. In 90% of migraineurs, the first attack generally develops before the age of 40 years.  In women the frequency of headaches is highest during their reproductive years, when estrogen levels are higher, and decreases to some extent after menopause. About 45% of cases of migraine emerge during childhood or adolescence. Migraine with aura is more likely to develop at an earlier age than migraine without aura.

Characteristics/Clinical Presentation

Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).

Associated Co-morbidities

• Allergies
• Meniere's disease
• Systemic lupus erythematosus
• Epilepsy
  • Although studies vary, individuals with either migraine or epilepsy are more than twice as likely to have the other disorder. 5 Possible causes for comorbidity: (1) Migraine could cause epilepsy by inducing brain ischaemia and injury. (2) Epilepsy could cause migraine by activating the trigeminovascular system, in which we would expect an excess risk of migraine after, but not before, the onset of epilepsy. (3) Shared environmental risk factors because the risk of migraine is significantly increased in people with idiopathic or cryptogenic epilepsy, known environmental risk factors cannot account for all of the comorbidity. (4) Shared genetic risk factors might account for comorbidity. (5) Ottman and Lipton proposed that an altered brain state (increased excitability) might increase the risk of both migraine and epilepsy and account for comorbidity, a hypothesis that draws support from therapeutic similarities.
• Stroke:
  • The migraine-stroke association is mostly apparent for young women with migraine with aura. Although there are several hypotheses about the biologic link between migraine with aura and ischemic stroke, the precise mechanisms remain unclear. However, because the absolute risk of stroke is low in patients with migraine with aura, and migraine without aura is likely not associated with ischemic stroke, most migraine patients will not experience a stroke event..
  • According to large series, migrainous infarcts account for 0.5-1.5% of all ischaemic strokes and 10-14% in young patients. Migraine itself might cause spasm or even hyperplasia, it is unlikely to be the cause of embolism or among other disorders. dissection. Migrainous infarcts, due to severe hypoperfusion during an attack are rare and mostly involve the posterior-cerebral-artery territory and are more common during attacks of migraine with aura than without aura. The precise mechanism of this severe hypoperfusion is unknown. Increased risk due to treatments used in migraine, particularly vasoconstrictors, is supported by the increase in white-matter abnormalities and in mortality found in patients taking ergotamine, but two recent studies found no increase in severe vascular events with triptans. Drugs widely used in migraine, such as aspirin and non-steroidal antiinflammatory drugs, decrease the risk of cerebral ischaemic events.
  • Migraine headache can occur as a comorbidity of ischaemic stroke, carotid or vertebral artery dissection, arteriovenous malformations, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL syndrome), or platelet disorders (eg, thrombocytosis).

Medications

According to Clinical Neurology (6th ed), the following medications are generally used:

1. Acute Treatment:

Simple Analgesics

• Aspirin
• Naproxen Sodium
• Ibuprofen
• Acetominophen

Comments: May cause gastric pain or bleeding and rebound headache if used frequently.

Ergot Preparations

• Ergotamine/caffeine (Cafergot)

Comments: May cause nausea and vomiting (N/V); contraindicated by pregnancy or coronary or peripheral vascular disease (PVD)

• Dihydroergotamine

Comments: Use with metoclopramide (antiemetic)

Narcotic analgesics

• Codeine/aspirin
• Codeine/aspirin/acetominophen
• Meperidine
• Butorphanol

5-HT agonists (Serotonin Receptor Agonists)

• Sumariptan (Imitrex)
• Rizatriptan (Maxalt)
• Zolmitriptan (Zomig)
• Naratriptan (Amerge)
• Almotriptan (Axert)
• Frovatriptan (Frova)
• Eletriptan (Relpax)

Comments:10% incidence N/V; contraindicated by pregnancy or coronary or PVD, and with monoamine oxidase inhibitors (MAOI)

Other Agents

• • Caffeine/butalbital/aspirin (Fiorinal)
• Prochlorperazine

Comments: Can cause hypotension and drug-induced dystonia

2. Prophylactic Treatment

Antiinflammatory agents: 

• Aspirin
• Naproxen Sodium

Comments: May cause gastric pain or bleeding

Tricyclic Antidepressants

• Amitriptylline
• Nortriptyline
• Protriptyline
• Doxepin

Comments: May cause dry mouth, urinary retention, and sedation; contraindicated in glaucoma or prostatism

Beta Blockers

• • Nadolol
• Atenolol
• Timolol
• Metoprolol

Comments: Listed in descending order of efficacy; symptomatic bradycardia may occur at high doses; contraindicated in asthma and congestive heart failure; not to be used with calcium blockers

Ergot Alkaloids

• Methergine

Comments: Occurrence of retroperitoneal fibrosis with urethral obstruction and mediastinal fibrosis, although uncommon, should be monitored withe creatinine, ultrasonography, or intravenous urograms, and chest x-rays every 6 months; a drug holiday every 6 months is prudent

Cyproheptadine Comments: Drowsiness common early in treatment

Anticonvulsants

• Phenytoin
• Valproic acid
• Topiramate
• Gabapentin

Calcium Channel Antagonists

• Verapamil
• Nicardipine
• Flunarizine

Comments: Contraindicated by severe left ventricular dysfunction, hypotension, sick sinus syndrome without artificial pacemaker, or second- or third-degree AV nodal block; constipation is most common side effect; not for use with beta blockers

3. Other Agents

• Prochlorperazine
• Hydroxyzine
• Metoclopramide

Comments: Adjunct to treatment; improves enteric drug absorption and reduces nausea; dystonia and akathisia may occur and respond to IV benedryl

Diagnostic Tests/Lab Tests/Lab Values

Diagnosis is based on characteristic symptoms and a normal physical (including neurologic) examination. Typical cases without worrisome findings do not require CNS imaging. Patients requiring very urgent CT or MRI to look for hemorrhage, increased intracranial pressure, and other structural causes of headache include those with:

• Sudden-onset thunderclap headache*
• Altered mental status, including seizure
• Focal neurologic deficits
• Papilledema**
• Severe hypertension

• Thunderclap headache: is an abrupt severe headache that may be a sign of bleeding in the brain and requires immediate medical attention.
• Papilledema: an optic disc swelling that is secondary to elevated intracranial pressure.
  

Causes

Common causes include: 

• Vasodilators (eg, Nitroglycerin)
• Skipping meals
• Weather changes
• Sleep deprivation
• Stress
  
• Excessive afferent stimuli (eg, flashing lights, strong odors)
• Head trauma, neck pain, or temporomandibular joint dysfunction can trigger or exacerbate a migraine
• Hormonal factors: fluctuating estrogen levels are a potent migraine trigger. Many women have onset of migraine at menarche, severe attacks during menstruation (menstrual migraine: appear to be more frequently in migraine with aura) and worsening migraine during menopause. Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura. Pregnancy can either exacerbate or relieve migraine attacks.
• Certain foods can precipitate a migraine attack (including, but not limited to):
  
  • Tyramine-containing chesses
  • Meat, such as hot dogs or bacon, with nitrate preservatives
  • Chocolate containing phenylethylamine but not chocolate alone
  • Food additives such as monosodium glutamate, a commonly used flavor enhancer
  • Coffee and alcohol (especially red wine)
  • Sugar (in vulnerable individuals)
• Genetics: There is a positive family history of migraine in about 60% of cases, which suggests a hereditary factor. All twin studies done so far (comparison of concordance rates between monozygotic and dizygotic twins) show that migraine has a genetic component in addition to environmental factors. Familial hemiplegic migraine (FHM), a rare type of migraine with aura, is the only form in which a monogenic mendelian ode of inheritance has been clearly established.

Systemic Involvement

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Medical Management (current best evidence)

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Physical Therapy Management (current best evidence)

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Alternative/Holistic Management (current best evidence)

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Differential Diagnosis

Due to the complexity of the pathophysiology and signs and symptoms attributed to migraine headaches, differential diagnosis is crucial for determining whether the headache is a medical emergency or a non-life threatening headache from other causes.  The following is a criteria developed by the International Headache Society classifying each type of headache into either primary, secondary, or other causes of headache with subclasses for each category for specific diagnosis. 

IHS Classification of Headaches

This classification is hierarchical and you must decide how detailed you want to make your diagnosis. This can range from the first-digit level to the fourth. First one gets a rough idea about which group the patient belongs to. Then one obtains information allowing a more detailed diagnosis. The desired detail depends on the purpose. In general practice only the first- or second-digit diagnoses are usually applied whilst in specialist practice and headache centres a diagnosis at the third- or fourth-digit levels is appropriate.

Part I: The Primary Headaches

1. Migraine

   1.1. Migraine without aura

   1.2. Migraine with aura

          In younger patients, several unusual disorders can mimic migraine with aura:

• Dissection of the carotid or vertebral artery
• Antiphospholipid antibody syndrome
• Cerebral vasculitis
• Moyamoya disease
• CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
• MELAS (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) syndrome

         In older patients, migraine with aura can be mistaken for a transient ischemic attack, especially when the aura occurs            without headache. 

   1.3. Childhood periodic syndromes that are commonly precursors of migraine

   1.4. Retinal migraine

   1.5. Complications of migraine

   1.6. Probable migraine

2. Tension-Type Headache (TTH)

   2.1. Infrequent episodic tension-type headache

   2.2. Frequent episodic tension-type headache

   2.3. Chronic tension-type headache

   2.4. Probable tension-type headache

3. Cluster Headache and Other Trigeminal Autonomic Cephalgias

   3.1. Cluster headache

   3.2. Paroxysmal hemicrania

   3.3. Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

   3.4. Probable trigeminal autonomic cephalgia

4. Other Primary Headaches

Part II: The Secondary Headaches:

5. Headache attributed to head and/or neck trauma

   5.1. Acute post-traumatic headache

   5.2. Chronic post-traumatic headache

   5.3. Acute headache attributed to whiplash injury (S13.4)

   5.4. Chronic headache attributed to whiplash injury (S13.4)

   5.5. Headache attributed to traumatic intracranial haematoma

   5.6. Headache attributed to other head and/or neck trauma (S06)

   5.7. Post-craniotomy headache

6. Headache attributed to Cranial or Cervical Vascular Disorder

   6.1. Headache attributed to ischemic stroke or transient ischemic attack

   6.2. Headache attributed to non-traumatic intracranial hemorrhage (I62)

   6.3. Headache attributed to unruptured vascular malformation (Q28)

   6.4. Headache attributed to arteritis (M31)

   6.5. Carotid or vertebral artery pain (I63.0, I63.2, I65.0, I65.2 or I67.0)

   6.6. Headache attributed to cerebral venous thrombosis (CVT) (I63.6)

   6.7. Headache attributed to other intracranial vascular disorder

7. Headache attributed to non-vascular intracranial disorder

8. Headache attributed to a substance or its withdrawal

9. Headache attributed to infection

10. Headache attributed disorder of homeostasis

11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures

12. Headache attributed to psychiatric disorder

Part III: Cranial Neuralgias, Central and Primary Facial Pain and Other Headaches

13. Cranial Neuralgias and Central Causes of Facial Pain

14. Other Headache, Cranial Neuralgia, Central or Primary Facial Pain

Pathologic Conditions Causing Headache:

• Subdural Hematoma: Mild to severe, intermittent headache; neurologic symptoms include fluctuating consciousness
• Subarachnoid Hemorrhage: Sudden onset, severe and constant headache; elevated BP; can cause change in consciousness
• Increased Intracranial Pressure (ICP): Mild to severe headache; neurologic symptoms include hemiparesis, visual changes, and brainstem symptoms, such as vomiting, altered consciousness
• Meningitis, viral and bacterial: Severe headache with radiation down neck; acute illness and fever; positive Kernig's sign
• Brain abscess: Mild to severe headache; local or distant infection; fever may not be present; neurologic signs consistent with local site of infection
• Central nervous system: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
• Central nervous system neoplasm: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
• Toxicity: Generalized headache, pulsating; other signs of toxicity may be present
• Sinusitis: Frontal or dull headache, usually worse in the morning; increased pain in cold damp air; nasal discharge
• Otitis media, mastoiditis: Feeling of fullness in ear, stabbing pains in head, vertigo, and tinnitus
  

Case Reports

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Resources

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Recent Related Research (from Pubmed)

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References

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