Migraine Headache

Introduction

Migraine, a common, recurrent, primary headache of moderate to severe intensity, interferes with normal functioning and is associated with gastrointestinal (GI), neurologic, and autonomic symptoms. In migraine with aura, focal neurologic symptoms precede or accompany the attack.

• Activation of trigeminal sensory nerves triggers the release of vasoactive neuropeptides, including calcitonin gene-related peptide, neurokinin A, and substance P from perivascular axons. Vasodilation of dural blood vessels may occur with extravasation of dural plasma resulting in inflammation.
• Twin studies suggest 50% heritability of migraine, with a multifactorial polygenic basis. Migraine triggers may be modulators of the genetic set point that predisposes to migraine headache.
• Specific populations of serotonin (5-HT) receptors appear to be involved in the pathophysiology and treatment of migraine headache. Ergot alkaloids and triptan derivatives are agonists of vascular and neuronal 5-HT1 receptors, resulting in vasoconstriction and inhibition of vasoactive neuropeptide release.

Clinical Presentation and Diagnosis

• Migraine headache is characterized by recurring episodes of throbbing head pain, frequently unilateral.
• Approximately 12% to 79% of migraineurs have premonitory symptoms (not to be confused with aura) in the hours or days before headache onset. Neurologic symptoms (phonophobia, photophobia, hyperosmia, and difficulty

concentrating) are most common, but psychological (anxiety, depression, euphoria, irritability, drowsiness, hyperactivity, and restlessness), autonomic (e.g., polyuria, diarrhea, and constipation), and constitutional (e.g., stiff neck, yawning, thirst, food cravings, and anorexia) symptoms may also occur.

• A migraine aura is experienced by approximately 25% of migraineurs. Aura evolves over 5 to 20 minutes and lasts less than 60 minutes. Headache usually occurs within 60 minutes of the end of the aura. Visual auras can include both positive features (e.g., scintillations, photopsia, teichopsia, and fortification spectrum) and negative features (e.g., scotoma and hemianopsia). Sensory and motor symptoms such as paresthesias or numbness of the arms and face, dysphasia or aphasia, weakness, and hemiparesis may also occur.
• Migraine headache may occur at any time but usually occurs in the early morning. Pain is usually gradual in onset, peaking in intensity over minutes to hours and lasting 4 to 72 hours. Pain is typically in the frontotemporal region

and is moderate to severe. Headache is usually unilateral and throbbing with GI symptoms (e.g., nausea and vomiting) almost invariably accompanying the headache. Other systemic symptoms include anorexia, constipation, diarrhea, abdominal cramps, nasal stuffiness, blurred vision, diaphoresis, facial pallor, and localized facial, scalp, or periorbital edema. Sensory hyperacuity (photophobia, phonophobia, or osmophobia) is frequent. Many patients seek a dark, quiet place.

• Once the headache pain wanes, a resolution phase characterized by exhaustion, malaise, and irritability ensues.
• A comprehensive headache history is essential and includes age at onset; frequency, timing, and duration of attacks; possible triggers; ameliorating factors; description and characteristics of symptoms; associated signs and symptoms; treatment history; and family and social history.
• Neuroimaging should be considered in patients with unexplained abnormal neurologic examination or atypical headache history.
• Onset of migraine headaches after age 50 suggests an organic etiology, such as a mass lesion, cerebrovascular disease, or temporal arteritis.

TREATMENT

• Goals of Treatment: The goal is to achieve consistent, rapid headache relief with minimal adverse effects and symptom recurrence, and minimal disability and emotional distress, thereby enabling the patient to resume normal daily activities. Ideally, patients should be able to manage their headaches effectively without emergency department or physician office visits.
• Limit use of acute migraine therapies to fewer than 10 days per month to avoid development of medication-misuse headache. Nonpharmacologic Treatment
• Apply ice to the head and recommend periods of rest or sleep, usually in a dark, quiet environment.
• Identify and avoid triggers of migraine attacks.
• Behavioral interventions (relaxation therapy, biofeedback, and cognitive therapy) may help patients who prefer nondrug therapy or when drug therapy is ineffective or not tolerated. Pharmacologic Treatment of Acute Migraine
• Administer acute migraine therapies (Table 54–2) at the onset of migraine.
• Pretreatment with an antiemetic (eg, metoclopramide, chlorpromazine, or prochlorperazine) 15 to 30 minutes before oral or nonoral migraine treatments (rectal suppositories, nasal spray, or injections) may be advisable when nausea and vomiting are severe. In addition to its antiemetic effects, metoclopramide helps reverse gastroparesis and enhances absorption of oral medications.
• Frequent or excessive use of acute migraine medications can result in increasing headache frequency and drug consumption known as medication-overuse headache. This occurs commonly with overuse of simple or combination analgesics, opiates, ergotamine tartrate, and triptans. Limit use of acute migraine therapies to 2 or 3 days per week.

Analgesics: Acetaminophen (Panadol) 1,000 mg at onset; repeat every 4–6 hours as needed

Acetaminophen 250 mg/aspirin 250 mg/ caffeine 65 mg, 2 tablets at onset and every 6 hours

Disprin (Aspirin) 500–1,000 mg every 4–6 hours

Naproxen sodium (Neprox) 550–825 mg at onset; can repeat 220 mg in 3–4 hours

Dosing of Prophylactic Migraine Therapies

Propranolol (Inderal) 10/50 mg/day in divided doses

Amitriptyline (Amyline) 10 mg at bedtime

Ibuprofena (Brufen) 400–1,200 mg/day in divided doses