The following discussion is for general informational purposes only and is not meant to provide the reader with specific medical advice. Please consult with your personal physician, or with a neurologist, for specific advice, guidance and information regarding your particular circumstances.

Introduction

Headaches are a common health problem and one of the most frequent reasons for neurological consultation. Tension headaches are the most prevalent headache type, and are usually mild, not associated with significant disability, not lateralized, are not throbbing/pulsatile, and are responsive to over-the-counter analgesics. Migraines, on the other hand, are described as throbbing, often lateralized, intense or severe headaches, often associated with nausea, vomiting, sensitivity to light, sound or smell, and exacerbation with movement. In some cases, migraines can be preceded or accompanied by visual or sensory disturbances.

Migraine affects approximately 12% of the United States population and is, in most instances, an inherited disorder. However, they are often incorrectly diagnosed as sinus headaches, tension headaches, cluster headaches, or neck pain. Correct diagnosis is essential so that appropriate treatment can be successfully implemented and improve the patient’s quality of life.

Mechanisms of Migraine

The once popular vascular theory of migraine, which suggested that migraine headache was caused by the dilatation of blood vessels, while the aura of migraine resulted from vasoconstriction (constriction of an artery), is no longer considered accurate.  The current prevailing theory is that dysfunction in certain parts of the brain leads to a sequence of changes intracranially and extracranially that account for migraine, including the four phases of premonitory symptoms (before the onset of migraine episode), aura, headache, and postdrome (after effects of the migraine episode).

The genetic basis of migraine is likely to be complex and in some people may be based on the cumulative effect of more than one genetic source.  People prone to migraine have a genetic threshold that renders them susceptible to an acute migraine attack depending upon the balance between stimulation and inhibition in different parts of the nervous system.  Subtle dysfunction, involving membrane channels, receptor families, and enzyme systems have been linked to migraine in certain groups and individuals which are the targets of migraine therapies.

Diagnosis

Migraine is diagnosed largely based on a consistent clinical history and the absence of atypical features. However, additional testing, such an MRI and vascular imaging (carotid ultrasound and transcranial Doppler scan), may be indicated to exclude conditions that can mimic migraine. It is up to the physician to make a clinical diagnosis of migraine. Features that could cast doubt on the diagnosis include sudden onset severe headache, new onset headaches after age 50, new onset headaches with an underlying medical condition such as cancer or other systemic illness (e.g. HIV), headache with fever, or headache with other neurologic symptoms (e.g. sudden loss of vision, altered awareness, lateralized weakness). In these patients, the diagnosis of migraine should be one of exclusion. Lastly, a headache which is distinctly different from or worse than any previously experienced headache warrants immediate medical attention.

Migraine Subtypes

There are numerous well recognized subtypes of migraine, including migraine with brainstem aura, hemiplegic migraine, retinal migraine, and vestibular migraine.

Migraine with brainstem aura is an uncommon form of migraine with aura where the primary signs and symptoms are localized to the brainstem without weakness. Migraine with brainstem aura was previously called basilar-type migraine. It occurs more often in females than in males. Onset is usually between ages 7 to 20. The auras consist of some combination of vertigo, slurred speech, tinnitus, double vision, ataxia, impaired consciousness, and diminished hearing.

The most significant feature that differentiates hemiplegic migraine from other types of migraine with aura is the presence of muscle weakness as a manifestation of aura in at least some attacks. In addition to weakness during the aura phase, which is typically lateralized to one side of the body, the symptoms of hemiplegic migraine attacks may include severe headache, visual changes, numbness, tingling, and impaired speech/language. Hemiplegic migraine may occur either in families or sporadically.

Retinal migraine is a rare condition that is characterized by repeated attacks of monocular scotomata or blindness lasting less than one hour, associated with or followed by headache.  Irreversible visual loss may be a complication of retinal migraine, although the incidence is uncertain.

Vestibular migraine symptoms include episodic vertigo in people with a history of migraines or with other typical features of migraine (photophobia, phonophobia, visual aura, etc). The association of headache with vertigo is variable, even in individual patients. Other disorders, specifically Meniere disease and structural and vascular brainstem disease, must be excluded in most cases.

Treatment

Treatment of migraines falls into two broad categories: acute treatment to relieve pain from a migraine, and preventative treatment to reduce the frequency of migraine. The migraine regimen should be individualized to a specific patient's needs.

The following have been reported as common migraine triggers and should be avoided where possible:

  • Emotional stress
  • Hormones in women
  • Irregular meal times/skipped meals
  • Weather
  • Sleep disturbances
  • Odors
  • Neck pain
  • Lights
  • Alcohol
  • Smoke
  • Sleeping late
  • Heat
  • Food
  • Exercise
  • Sexual activity

However, most people with migraine ultimately require medication intervention. Mild migraine with minimal disability often responds to nonspecific over-the-counter simple analgesics including aspirin, acetaminophen and nonsteroidal antiinflammatories (NSAIDs).  Migraine sufferers who experience more disability usually require specific prescription migraine medications, such as triptans, that work by inhibiting the pain pathways in the migraine process.  The combined use of a triptan and a nonsteroidal anti-inflammatory drug (NSAID) to treat acute migraine appears to be more effective than using either drug class alone.  The newest class of medications, gepants, are small molecule calcitonin gene-related peptide (CGRP) receptor antagonists that block the CGRP receptor, inhibiting a pathway known to play a role in the pathophysiology of migraine. In people where nausea and vomiting are early prominent symptoms, there are medications available for self-injection or nasal administration that do not require gastrointestinal absorption.

Acute treatments optimally should not be used more than two days per week. With more frequent use, there is the risk of transforming episodic migraine into a pattern of chronic migraine or chronic daily headache. Sometimes if a patient has entered that cycle, abstinence from analgesics is required.

For some migraine patients, a daily preventative medication is required. These medications are typically used in people who have frequent migraines, or long-lasting severe migraines that cause significant disability. These medications include blood pressure medications, anticonvulsants, certain antidepressants, and the newest class of medications which are calcitonin gene-related peptide (CGRP) inhibitors. Botox injections, which are given every 3 to 6 months, can also be very effective for treatment of migraines that are refractory to the standard preventative therapies.

People with migraines often report a lower quality of life, increased emotional distress, difficulty sleeping, and miss days from work or school due to the migraines. There are now numerous options for treatment of migraines, many of which have minimal side effects. The goal in treatment is to prevent or reduce migraines and their associated disability, and to improve the migraine sufferer’s quality of life.

Treatment is individualized based on many considerations and different physicians within and outside of our practice have different preferences and prioritization for different treatments.

Listed below are commonly prescribed acute treatments for migraine attacks and the most commonly associated side effects:

Triptans

  • Eletriptan: mild dizziness and nausea
  • Naratriptan: mild dizziness and nausea
  • Sumatriptan (oral, nasal spray, nasal powder, and subcutaneous) chest pressure or heaviness, flushing, weakness, drowsiness, dizziness, malaise, a feeling of warmth, and paresthesias
  • Rizatriptan: dizziness, asthenia/fatigue, nausea, and somnolence; in one study these effects were dose dependent
  • Zolmitriptan: (oral and nasal): nausea, dizziness, somnolence, paresthesia, fatigue, and tightness in the throat or chest
  • Almotriptan: nausea and dizziness
  • Frovatriptan: nausea and dizziness

Triptans have proven to be safe and effective for most patients with migraine.  All triptans should be limited to no more than 10 days of use per month to avoid medication overuse headache. Based on limited evidence, it is still recommended that triptans be avoided in patients with hemiplegic migraine, basilar migraine, ischemic stroke, ischemic heart disease, Prinzmetal's angina, uncontrolled hypertension, and pregnancy. 

Lasmiditan (Reyvow) is a selective serotonin 1F receptor agonist that lacks vasoconstrictor activity. It is probably best suited for people with relative contraindications to triptans due to cardiovascular risk factors.  Side effects include dizziness; other relatively frequent adverse events are paresthesia, somnolence, fatigue, and nausea.

CGRP Blockers

  • Rimegepant (Nurtec): nausea, somnolence, and dry mouth
  • Ubrogebant (Ubrelvy): nausea, somnolence, and dry mouth

Ergots

  • Dihydroergotamine: Chest tightness and dizziness
  • Ergotamaine: May worsen the nausea and vomiting associated with migraine and chronic use can increase risk of valvular heart disease.  Ergots should be avoided in people with coronary artery disease because they cause sustained coronary artery constriction, peripheral vascular disease, hypertension, and liver or kidney disease.

Other non-pharmacologic options for acute migraine treatment:

Neuromodulation

  • Transcutaneous supraorbital nerve stimulation (Cefaly)

Nerve Blocks

  • Occipital nerve block
  • Sphenopalatine Ganglion Block

Some indications for preventative therapy:

  • Frequent or long lasting migraine headaches
  • Migraine attacks that cause significant disability or diminished quality of life despite appropriate acute treatment
  • Contraindication to acute therapies
  • Failure of acute therapies
  • Serious adverse effects of acute therapies
  • Risk of medication overuse headache
  • Menstrual migraine

Listed below are commonly prescribed preventative treatments for migraine attacks and the most commonly associated side effects (in parentheses):

Beta Blockers: (light headedness, dizziness, low blood pressure, low heart rate, sexual dysfunction)

  • Metoprolol
  • Atenolol
  • Propranolol

Calcium Channel Blockers: (constipation, light headedness, dizziness)

  • Verapamil

Anti-depressants: (dry mouth, sedation, constipation, weight gain, palpitations)

  • Amitriptyline
  • Nortriptyline
  • Lexapro
  • Venlafaxine

Anticonvulsants:

  • Valproate (weight gain, tremor, hair loss)
  • Topiramate (tingling/parethesia, fatigue, anorexia, diarrhea, weight loss, hypesthesia/reduced sensation, memory difficulty, language problems, difficulty with concentration, nausea, and taste changes)
  • Gabapentin (sedation, dizziness)

CGRP antagoniststs (brand name in parentheses as generics not available):

  • Eerenumab (Aimovig)
  • Fremanezumab (Ajovy)
  • Galcanezumab (Emgality)
  • Eptinezumab (Vyepti)

Non-pharmacologic preventative therapies:

  • Transcutaneous supraorbital nerve stimulation
  • Botulinum Toxin (e.g. Botox)

Useful links:

American Headache Society