Craig Blackwell, MD
Ophthalmology

Santa Cruz, CA
Diplomate: American Board of Ophthalmology
Fellow: American Academy of Ophthalmology

Welcome to the Website of Craig Blackwell, MD

An Ophthalmology Practice in Santa Cruz, CA

Migraine I Overview

You may be wondering why I am writing about Migraine as it is not strictly an eye topic, its origin being in the central nervous system. For many people the visual symptoms are the predominate feature that motivates them to seek attention so they come to an ophthalmologist first to check for an eye problem. Not an unreasonable place to start. The symptoms are usually so characteristic that the diagnosis can usually be arrived at after the first few sentences of history. Following is a description of Migraine mostly from the ocular perspective. Along the way there are links to follow for those who want to read more.

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Progression of migraine visual symptoms.

From: Survey of Ophthalmology Vol. 33, No. 4, p.224.

Migraine is a complex and interesting condition in which there are a number of possible symptoms sharing a common cause. The usual syndromes are as follows:

  • Common Migraine: One-sided headache, usually throbbing, may be severe, with nausea, and sensitivity to light and sound. Officially, Migraine without Aura.
  • Classic Migraine: Begins with visual symptoms of flashing lights or a sensation of watery movement that starts in one corner of vision and expands to cover half or more of vision, usually with part of the image missing, as in the illustrations. This “aura” phase lasts from 15 minutes to hours, followed by the headache phase as described above. Officially, Migraine with Aura.
  • Ocular Migraine: Visual symptoms of aura, but not followed by headache. Officially, Typical Aura without Headache.

Migraine is a surprisingly common disorder as shown in the following graph. It occurs in up to 8% of men and over 25% of women, its occurence peaking in ages 30 to 50 years.

Prevalence of Migraines by Age and Sex

From: Neurology 1993; 43(suppl 3):S6-S10

The International Headache Society (IHS) has a site with the full classification system for all types of headaches including Migraine. An excerpted version of Migraine criteria is available here.

You can read more about how migraine symptoms are distinguished from TIA and stroke symptoms in the classic Miller Fisher paper excerpted here.

Classic Mechanism of Migraine

Recent techniques for studying electrical activity and circulation in the brain have revised previous ideas about migraines.

Classic Model of Migraine Mechanism

The classic theory of migraine posited a vascular cause. First, a “trigger” event caused a narrowing of specific arteries supplying the brain thereby reducing blood flow and causing the aura phase. That was followed by reflex dilation of the arteries whereby the stretching of the artery walls was responsible for the headache pain. Medicines, like caffiene and ergotamine, were thought to reduce pain by constricting blood vessels. Until recently this was also thought to be the mechanism of action of the Triptans.

Evolving Model of Migraine Mechanism

Investigations underway since the 1980’s are modifying the entire model.

Recent Model of Migraine Mechanism

What predisposes some people to have migraines is still not known. Speculation centers on malfunctioning ion transport mechanisms that are probably inherited.

In migraine with aura the visual or sensory symptoms come from a spreading electrical disturbance on the cortex, the surface of the brain. Blood flow changes follow the electrical changes, but are probably not the primary cause of pain.

Where exactly the pain comes from is a subject of investigation and discussion. At present it is known that stimulation of the Trigeminal nerve mediates the pain pathway as well as vasodilation of cranial vessels. The pain could come from pain sensing cortex, abnormally sensitized cortex or blood vessels.

Interestingly, in patients with common migraine (no aura) there are not the spreading electrical changes on the surface. It is hypothesized they may occur under the surface or in an as of yet undetected area, but the pain is still produced from Trigeminal nerve stimulation.

Medication used to treat migraine headache pain were initially thought to work because of their ability to constrict blood vessels. That was the original target motivating the development of Triptans, like Imitrex. It was later found there are 5-HT receptors on the trigemenal nerve and that is the current site at which they are thought to act.

For a more detailed look at mechanism go to:

Mechanism of Migraine in more Detail.

Common Triggers

  1. Stress is the most common cause cited. For some the migraine comes after relief of stress.
  2. Hormonal changes, particularly surrounding menstruation.
  3. Diet. About a quarter of migraineurs can identify a particular food or chemical which can reliably trigger an attack.common examples are: Tyramine in aged cheese, sour cream, chopped liver, sausage, pork, beans, herring, and Chianti wine. Phenyalanine in chocolate. MSG and nitrates. Aspartame.

In a study of 1,207 people with migraines, 76% reported having some trigger event: 70% infrequently, 27% frequently, and 9% very frequently. The following table shows the frequency of various patient-reported triggers.

Stress

80%

Alcohol

38%

Hormones in Women

65%

Smoke

37%

Not Eating

57%

Sleeping Late

32%

Weather

53%

Heat

30%

Sleep Disturbance

50%

Food

27%

Perfume or Odor

44%

Exercise

22%

Neck Pain

38%

Sexual Activity

5%

Lights

38%

Frequency of Various Patient-Reported Migraine Triggers

From: Cephalgia 2007; Vol.27:No.5;P.394-402

Treatment

As an ophthalmologist it is not my scope of practice to treat nonocular conditions. That would fall to your medical doctor or neurologist. However, I can pass on some general comments for educational purposes. Migraine treatments are divided into three categories.

  1. Migraine Prevention. Medicine taken on a daily basis to decrease the frequency and intensity of attacks. The current recommended first line choices include: the antidepressant Elavil, anticonvulsants Valporate or Topamax, and beta-blockers like Inderal. (From Headache 2007;47 [Suppl 1]:S52)
  2. Treatment of the acute attack of migraine. Medicine taken at the beginning of an attack to decrease the severity and duration. Ergotamine was used historically, but it has been superceded by the Triptans which have a very high success rate(85-90%). Analgesics may be added for pain relief.
  3. Techniques for cognitive and behavior modification are under continuing study.

On the American Academy of Neurology (AAN) website there is a comprehensive listing of available migraine treatments with a rating of quality of evidence supporting their effectiveness. Link to AAN Migraine Treatment Guidelines

If you want to read more here go to:

Mechanism of Migraine in more Detail.

CBlackwell-Sep 2008