eMedicine Specialties > Neurology > Neuro-ophthalmology

Migraine Headache, Neuro-ophthalmic Perspective

Author: Ronald Braswell, MD, Assistant Professor, Department of Ophthalmology, University of Alabama-Birmingham
Contributor Information and Disclosures

Updated: Sep 4, 2008

Introduction

Background

This complex, recurrent headache disorder is one of the most common complaints in medicine today. The term migraine is derived from the Greek word hemikrania. This later was corrupted into low Latin as hemigranea, which eventually was accepted by the French translation as migraine. A typical episode is characterized by unilateral head pain that may be preceded by various prodromal symptoms. Other focal neurological symptoms, collectively known as an aura, may precede or coincide with the onset of headache. Although many more headache types are listed in the International Classification of Headache Disorders¹ , the following are the most often encountered in practice, with migraine being the most challenging:

• Migraine without aura (formerly common migraine)
• Probable migraine without aura
• Migraine with aura (formerly classic migraine)
• Probable migraine with aura
• Chronic migraine
• Chronic migraine associated with analgesic overuse
• Tension-type headache
• Cluster headache
• Chronic daily headache
• Ophthalmoplegic migraine
• Retinal migraine
• Childhood periodic syndromes that may not be precursors to or associated with migraine
• Complications of migraine
• Migrainous disorder not fulfilling above criteria

For related information, see Medscape's Headache Resource Center.

Pathophysiology

Historically, migraine has been associated with fluctuations in cerebral perfusion. Investigations show areas of hypoperfusion preceding the onset of headache, followed by a period of reactive hyperperfusion and eventual normalization of flow. Current theories advocate a primarily neurogenic phenomenon related to changes in levels of neuropeptides serotonin and dopamine.

• Certain symptomatic and prophylactic agents are effective (in part) through binding at specific serotonin (5-hydroxytryptamine [5-HT]) binding sites.
• Signs and symptoms (eg, anorexia, nausea, vomiting, pallor, yawning) respond to dopaminergic antagonists.
• The concept of an altered migrainous threshold in individual patients has been advocated. Imbalances in inhibitory and excitatory neuronal pathways may sensitize the trigeminovascular system and provoke a migraine event.

Frequency

United States

Recent epidemiological studies indicate that 23 million Americans, approximately 18% of females and 6% of males, have one or more migraine headaches per year.

Migraine headaches are experienced by 64% of all female and 43% of all male sufferers of severe headache.

Mortality/Morbidity

Migraine headache continues to be a major health problem.

• In the American Migraine Study, more then 85% of women and 82% of men with severe migraine had headache-related disability.
• Estimated lost productivity is $1-13 billion dollars per year.²
• Migraineur males required 3.8 bedrest days per year; women, 5.6 days.

Race

• A recent study showed that among women, 20.4% of whites, 16.2% of African Americans, and only 9.2% of Asian Americans met IHS criteria for migraine.
• Similarly, in males, 8.6% of whites, 7.2% of African Americans, and 4.8% of Asian Americans were considered to have migraine.

Sex

In children younger than 10 years, prevalence appears to be higher in males than in females. After the onset of puberty, migraine is considerably more common in females (female-to-male ratio 3:1).

• In general, the incidence of migraine in males declines to a low rate by age 28-29 years (1 case per 1000 person-years).
• For females, the incidence of migraine with aura peaks at age 12-13 years (3-4 y before that of migraine without aura).
• Migraine prevalence among females increases sharply up to age 40 years and then declines gradually. The male peak prevalence is slightly less and decreases over a broader age range.

Age

• Incidence or age of onset of migraine with aura appears to peak at or before age 4-5 years (6.6 cases per 1000 person-years), whereas the highest incidence for migraine without aura occurs at age 10-11 years (10.1 cases per 1000 person-years).³
• Data indicate that migraine is a chronic condition, although prolonged remissions are common. One study showed that 62% of young adults were migraine free for more than 2 years, but only 40% continued to be migraine free after 30 years.
• The severity and frequency of attacks tend to diminish with increasing age. After 15 years, approximately 30% of men and 40% of women no longer have migraine attacks.

Clinical

History

The migraine headache is typically a unilateral and throbbing pain, but the features often vary. Migraineurs often experience a bilateral event. The pain can be felt anywhere around the head or neck.

• Prodrome is experienced by 60% of patients.
  • Forewarning of a migraine may occur hours to days before a headache event.
  • Although the specific features of the prodrome vary, they tend to be consistent for a given individual. They may include the following:
    • Neurological symptoms (eg, photophobia, phonophobia, osmophobia)
    • Lethargy
    • Mental and mood changes (eg, depression, anger, euphoria)
    • Polyuria
    • Meningismus
    • Anorexia
    • Constipation or diarrhea
• Aura is experienced by 10-20% of patients.
  • Aura is defined as focal neurological symptoms that evolve over a period of 5-15 minutes and generally last approximately 1 hour.
  • In most cases, the headache follows the aura. However, the 2 events can occur simultaneously, or the aura may develop after the headache is in progress.
  • Visual symptoms, including the following, are most common:
    • Negative scotomata or negative visual phenomena, such as homonymous hemianopic or quadrantic field defects, central scotomata, tunnel vision, altitudinal visual defects, or even complete blindness
    • Positive visual phenomena or scintillating scotomata, the most common consisting of an absent arc or band of vision with a shimmering or glittering zigzag border: This often is combined with photopsias or visual hallucinations, which may take various shapes. This is a highly characteristic syndrome that always occurs prior to the headache phase of an attack and is pathognomonic of a classic migraine. It is called a "fortification spectrum" because the serrated edges of the hallucinated "C" resemble a "fortified town with bastions around it."
    • Photophobia
    • Photopsia (uniform flashes of light) or simple forms of visual hallucinations that occur commonly with positive visual phenomena
• Motor symptoms may be observed.
  • Hemiparesis
  • Aphasia
• Headache characteristics typically include the following:
  • Unilateral (60-70%)
  • Gradual onset, lasting 4-72 hours
  • Described as a throbbing or pulsatile type of pain but can evolve into a chronic ache or bandlike pattern
• Associated symptoms include the following:
  • Anorexia
  • Nausea
  • Vomiting
  • Blurred vision
  • Skin pallor
  • Photophobia
  • Phonophobia
  • Light-headedness

Physical

Evidence of autonomic nervous system involvement can be helpful, although most patients with migraine exhibit few or no findings. Serial neurologic examinations are recommended.

• Possible findings
  • Cranial/cervical muscle tenderness
  • Horner syndrome (ie, relative miosis with 1-2 mm of ptosis on the same side as the headache)
  • Conjunctival injection
  • Tachycardia/bradycardia
  • Hypertension/hypotension
  • Hemisensory or hemiparetic neurological deficits (ie, complicated migraine)
  • Adie type pupil (ie, poor light reactivity with light-near dissociation)
• Pertinent physical examination negatives
  • Dim scotoma lasting a few seconds to several minutes (ie, amaurosis)
  • Temporal artery tenderness in the elderly
  • Meningismus
  • Increased lethargy (unrelated to medication use)
  • Mental status changes

Causes

• Family history
• Stress
• Excessive or insufficient sleep
• Medications - Vasodilators, oral contraceptives
• Smoking
• Foods and food additives - Alcohol, caffeine, chocolate, artificial sweeteners (aspartame, saccharin), monosodium glutamate (MSG), citrus fruits, meats with nitrites, salt
• Foods containing tyramines - Aged cheese, yogurt, sour cream, chicken livers, sausages, bananas, avocados, canned figs, raisins, peanuts, soy sauce, pickled fish, fresh-baked breads, pork, vinegars, beans
• Exposure to bright or fluorescent lighting
• Strong odors (eg, perfumes, colognes, petroleum distillates)
• Hormonal changes - Menstruation (common association), pregnancy, ovulation
• Head trauma
• Weather changes
• Metabolic or infectious diseases
• Physical exertion or fatigue
• Motion sickness
• Cold stimulus (ice cream headaches)

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