Migraine Headache is the 2nd most common primary headache disorder that can present with or without aura.
- Affects more women than men.
- Peak prevalence 25-45 years of age
- Risk of migraine headache increases in patients with positive family history of migraines.
- Two types: Migraine With Aura (Classic Migraine) affects 85% of patients and Migarine Without Aura (Common Migraine) affects 15% of patients.
- Two theories exist regarding pathogenesis.
- Vasogenic theory: intracranial vasoconstriction is responsible for the aura symptoms and the headache results from a rebound dilation and distention of cranial vessels and activation of peirvascular nociceptive axons.
- Neurogenic theory: identifies the brain as the generator of the headache and the vascular changes that occur during the migraine are a result rather than the cause of the attack.
PERTINENT HISTORICAL FINDINGS/ CLINICAL SYMPTOMS
- Both types of migraines can present with prodromol symptoms that begin 24-48 hours before attack: hyperactivity, mild euphoria, lethargy, depression, craving for certain foods, fluid retention.
- Aura: Transient episodes of focal neurologic dysfunction appearing 1-2 hours before the onset of headache and resolving within 60 minutes.
- Aura symptoms: homonymous visual disturbance, expanding scotoma, unilateral paresthesias and or numbness affecting distal ends of the extremities or perioral region of face; unilateral weakness and dysphagia.
- Sometimes aura symptoms localize to brain stem causing vertigo, dysarthria, tinnitus, fluctuating hearing loss, diplopia, bilateral weakness, ataxia, bilateral paresthesias, & decreased level consciousness.
- Headache phase consists of 4- 72 hours of unilateral, throbbing head pain that is moderate to severe in intensity and worsened by routine physical exertion and associated with nausea, photophobia, phonophobia.
PERTINENT PHYSICAL EXAM FINDINGS
- No significant findings on exam other than the neurologic findings described as part of the aura or prodromal symptoms.
- Transient ischemic attacks
- Cerebrovascular accident
- Subarachnoid hemorrhage
- Brain tumors/masses
- Post-traumatic headache
- Routine labs are done to rule out other concurrent disorders but no specific lab or imaging studies are diagnostic.
- Non-pharmacological therapy: behavior modification, biofeedback, relaxation training, establish regular meal schedule, avoidance of trigger factors, consistent sleeping schedule.
- Mild attacks: analgesics (acetaminophen), NSAIDs (aspirin, ibuprophen, naproxen).
- Moderate attacks: combination of acetaminophen, isometheptene mucate, and dichloralphenazone; butalbital combined with caffeine, aspirin or acetaminophen.
- Moderate to severe attacks: dihydroergotamine, 5-HTB/D receptor agonist (sumatriptan), 2nd generation sumatriptan-like drugs (naratriptan, zolmitriptan, rizatriptan), ergotamine.
SURGICAL MANAGEMENT (when applicable)
- Not applicable
EMERGENCY MANAGEMENT (when applicable)
- Severe attacks may be treated with: Dihydroergotamine administered subcutaneously or intravenously; Meperidine, intramuscularly; Intravenous neuroleptics for severe, unresponsive, or prolonged attacks.
PATIENT EDUCATION/ MAINTENANCE – PREVENTION
- Avoid triggers such as tyramine-containing foods, meats preserved with nitrites, chocolate, MSG, sleep deprivation, strong odors, stress, menses, fasting, caffeine, red wine, smoking, some oral contraceptives.
- Preventive/ Prophylactic therapy is recommended if headaches limit work or normal daily activity 3 or more days per month.
- Β-adrenergic blockers: propranolol, atenolol, nadolol, timolol, metoprolol.
- NSAIDs: aspirin, naproxen, ketoprofen.
- Tricyclic antidepressants: amitriptyline, nortriptyline.
- Calcium channel antagonists: verapamil, flunarizine.
- Anticonvulsants: divalproex sodium, topiramate, gabapentin, topiramate.
- Serotoninergic drugs: methysergide, cyproheptadine.
- Monoamne oxidase inhibitor: phenelzine.
- Angiotensin II receptor blocker: candesartan.
Dr. Zachary Lahlou