Indiana University
School of Optometry

Primary Headaches
Primary headaches include . . .


Tension type headaches (TTH) are also known as muscle contraction or anxiety headaches. They account for 90 percent of all headaches. Patients will complain of a bilateral, dull, bandlike tightness. No photophobia or phonophobia occurs, and a tension type headache does not worsen with physical activity. These headaches are believed to be inflammatory in nature.

Although TTH is referred to as a muscle contraction headache, EMG studies show that there is more muscle contraction with migraines. Are they really all part of the same process? One study showed maxillary alveolar tenderness (tenderness in area of upper molars) in 1026 of 1100 patient with TTH or migraines. That's 93%!

An episodic variant of TTH is associated with emotional or physical stress. Chronic type TTH is often found with depression or taking too many over-the-counter (OTC) medications for pain.

Treatment usually consists of OTC NSAIDs. Caffeine can help.

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Only 0.1% of the population has cluster headaches. Males (in their 20s to 40s) are affected twice as often as females (2:1). Patients experiencing cluster headaches report severe, excruciating, unilateral, retro-orbital or frontal pain with no aura. Nasal congestion and facial/forehead sweating are associated with these headaches. "Projectile" lacrimation and conjunctival redness and congestion also occur. Personality characteristics are described as precise, tense, conscientious, and overwrought.

These headaches tend to "cluster" into several daily attacks, lasting anywhere from 10 minutes to 2 hours. A cluster can be a period of weeks to months, often occurring at night. Cluster headaches are associated with Horner's syndrome (ptosis and miosis). This occurs as a result of vasodilation of the internal carotid causing compression of the third order sympathetic neuron.

Treatment consists of Verapamil (prophylactic) and oxygen. Sumatriptan is used for aborting.

Cluster Headache Differential Diagnosis:   Raeder's syndrome (painful Horner's with pain in V1 distribution; caused by neoplasm in and around the trigeminal nerve).

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Approximately 16 percent of population (18-22 million Americans) are affected by migraines. The most prevalent age for migraines to occur is between 25 and 55, but possible at any age. About 1 in 6 women suffer from migraines; 1 in 20 men. Three females to every 1 male experience migraines; however, the female-to-male ratio is equal before onset of menstruation. Considering that 80 percent of migraine sufferers have a family history, a definite genetic predisposition exists. Those who experience migraines as adults often have a history of childhood car sickness and/or benign vertigo.

There is a strong correlation of migraines with depression. The lowest prevalence of migraines is found in middle income groups.

Twenty percent (20%) of migrainuers experience headache attack under the age of 5. Half of all adults who get migraines experience their first episode by age 20; occurrences peak around age 45. Spontaneous remission in older adults is common and thought to be due to hardening of the arteries or hitting menopause.


Etiology

Circulation Theory: Intracerebral constriction causes hypoxia leading to extracerebral dilation of arteries. An aura is caused by ischemia secondary to vascular spasm. The headache is believed to be caused by the vasodilation. This theory has fallen out of favor!

Neural Hypothesis: The brain of migraine patients has a decreased threshold for various stimuli. When exposure to these internal or external stimuli occurs, there is "spread" of cortical depression: "cortical hyper excitability." This in turn affects the vasculature which is believed to cause pain. The somatosensory cortex is thickened in patients who suffer from migraines. It is unclear whether this is related to the cause of the migraines or is an effect of experiencing repeated attacks.

Migraine brains may be constantly low on "energy." Triggers then stress the "low energy" brain leading to headaches. What is the #1 location for pain?     . . . around the eyes! (study of 1283 patients).

Genetic Predisposition: Threshold to triggers is determined by

  • magnesium levels
  • amino acid levels
  • dopamine sensitivity
  • the hypothalamus
  • other factors

Triggers: Precipitating Factors

  • Foods
    • Tyramine (bananas, avocado, yogurt, aged cheeses, pods of broad beans)
    • Phenylethylamine (chocolate, cheese, wine)
    • Sodium nitrites (food coloring, preservatives, processed meats and fish)
    • Artificial sweeteners
    • Caffeine
    • MSG (Chinese food, processed meats, frozen dinners, canned soup)
  • Weather or air pressure
  • Bright sunlight
  • Glare
  • Fluorescent lights
  • Chemical fumes
  • Menstrual cycles (more likely during first two days of cycle)


Migraine Types in ICHD-II

  1. Migraine without aura (formerly common migraine) is experienced by 80 to 90 percent of migrainuers. These same patients may suffer from multiple subtypes at various times. A migraine without aura is usually unilateral but may be bilateral headaches. It is typically located in the temporal or occipital region. Children tend to experience bilateral, frontal, temporal or retro-orbital pain. A migraine without aura eventually works up to severe, throbbing pain that can last 24 hours (sometimes up to 72 hours).

    Associated symptoms and conditions include:
    • Nausea and vomiting
    • Photophobia and phonophobia
    • Anorexia
    • Improves with sleep (patient seeks a dark, quiet area)
    • Conjunctival injection and tearing
    • Associated with strokes (migraine is a risk factor for ischemic stroke--especially in women before age 50)
  2. Migraine with aura (formerly classic migraine) is experienced by 10 to 20 percent of migraine sufferers. Scotoma with shimmering, flickering borders or zig-zagging forms precedes or rarely accompanies/follows the headache. The aura is typically hemianopic and begins centrally in both eyes then spreads peripherally, leaving behind an area of impaired vision. The migraine with aura develops over 5-20 minutes and may last 20-60 minutes. This type of migraine may be associated with having a patent foramen ovale (failure of the fetal hole between the right and left atriums of the heart to close). One study showed that the incidence of PFO in people who suffer from migraines with aura was two times the normal rate.
    The aura is seen with eyes open or closed. The symptoms and associations are the same as those found in migraine without aura. The aura is an advantage for treatment purposes. When patients experience the aura, they know a headache is coming and they can take attack-aborting medication.

    Example of aura with migraine. (JAOA by Bonerman, OD)

    Clock diagrams below demonstrate classical migrainous scintillating scotoma with march and expansion of fortification figures.
    (1)   Initial small paracentral scotoma. (2)   Enlarging scotoma 7 minutes later.
    (3)   Scotoma obscuring much of central vision 15 minutes later. (4)   Break-up of scotoma at 20 minutes.

    Some patients report that their migrainous central scotoma is like "looking through a film of water."
  3. Childhood periodic syndromes that are often precursors of migraines
  4. Retinal migraine
  5. Complication of migraine


Ocular Issues with Migraines

Aura is the most common cause of transient vision loss in patients under age 45. Migraine sufferers may experience hemianopsias and rarely some are affected with Horner's syndrome. Normal tension glaucoma (NTG) is another ocular issue associated with migraines. Persistent visual field defects (VF) can occur up to weeks after an attack (no aura required). On rare occasions, VF loss can be permanent.


Older Migraine Variant Terminology

  1. Acephalgic Episode (migraine equivalent)

    The term "acephalgic" is no longer used in the classification scheme.

    An acephalgic episode is a bilateral aura with no headache. Patients may have no history of migraine. This condition usually occurs in males over age 40, but onset is often before age 40. Thirteen percent (13%) of "migraine with aura" patients will occasionally suffer an acephalgic episode.

    Some patients stop having migraine headaches but continue to have auras as they age. Scintillating scotomas are the most common indicator. Other neurological signs (including hemiparesis, paraesthesias, and dyphasias) can also occur.

    The origin of an acephalgic episode is in the occipital region. Although the event is bilateral, patients often think only one eye is involved.

    Scintillating scotomas, demographics, and history are the key to diagnosis. You must rule out amaurosis fugax or transient ischemic attacks (TIAs) from embolic sources.

  2. Ocular Migraine (currently "retinal" migraine)

    A retinal migraine occurs when there is transient (or very rarely permanent) visual disturbance in ONE eye. The event may last from seconds to hours, but usually just several minutes. The patient may experience a headache near the affected eye before or after the visual episode. It is believed to be due to an interruption in ciliary or retinal circulation from a vascular spasm. Retinal migraines are usually found in patients under age 40.

    The practitioner must distinguish from amaurosis fugax based on patient demographics and symptoms.

    The old term of "ocular migraine" is no longer in the classification scheme. It historically referred to monocular aura without a headache.

  3. Ophthalmoplegic "Migraine"

    The onset of an Ophthalmoplegic "Migraine" occurs in childhood; usually age 10 and up with history of typical migraine. Ophthalmoplegia ipsilateral to periorbital headache. Ophthalmoplegia can persist for days to weeks (even months). It affects CN III over CN VI 10:1; very rarely is CN IV affected. Ptosis and pupil dilation are common. CT-scans and MRI are normal. The condition can become permanent after years of attacks. It is no longer classified as a migraine, instead it is a cranial neuralgia which is often inflammatory in nature.

    Be sure to rule out diabetes mellitus, aneurysm, CNS infiltrative or infectious disease, Tolosa Hunt syndrome (painful ophthalmoplegia), and orbital pseudotumor.


Benign episodic pupillary mydriasis is seen in women with a history of migraine. Pupillary dilation lasting from minutes to one week, with an average of 12 hours, occurs. Pupil may or may not react to light.


Treatment of Migraines

  • Prophylactic (Preventive) Treatment

    Consider prophylactic (preventive) treatment if patient suffers from 2 or more migraines per month.

    • Beta blockers--Inderal, Lopresssor, Tenormin
    • Antidepressants
      • Selective Serotonin Reuptake Inhibitors (SSRIs)--Paxil, Prozac, Zoloft
      • Tricyclics--Amitriptyline (Elavil, Endep), Nortriptyline
      • MAO inhibitors--Nardil, Parnate
    • Epilepsy medication--Depakote, Topamax. (Topamax has an FDA warning about causing angle closure)
    • Lithium
    • Calcium channel blockers--Verapamil. To prevent intracranial vasoconstriction; often don't work well
    • Botox (botulinum toxin). Anecdotal evidence: believed to block pain receptors. Need injections every 2-3 months. Expensive!
    • Natural Prophylaxes
      • 400 mg riboflavin (Vitamin B) daily = 60% decrease in headaches
      • Butterbur root 150mg/day = 60% decrease
      • Magnesium 800mg/day: must take calcium to prevent stomach upset
      • Co-enzyme Q-10 300mg/day

  • Attack-Aborting Treatment

    • Cerebral Vasoconstrictive Agents
      • Ergotamine tartrate (Ergomar): alpha adrenonergic antagonist--vasoconstrictor
      • Dihydroergotoamine (Migranal, DHE45)--It is theorized that dihydroergotoamine selectively binds to 5-HydroxyTryptamine (5-HT) receptors on intracranial blood vessels which leads to their constriction &nbps; OR &nbps; the drug binds to 5-HT receptors on the peripheral trigeminal nerve which results in blocking the inflammatory (pain) response. Dihydroergotoamine treats the entire migraine complex--nausea, vomiting, photophobia, and phonophobia.
    • Serotonin Agonists: Selective 5-HT receptor agonists
      • Sumatriptan Succinate--Imitrex (injection, tabs, nasal spray, wafer)
      • Zolmitripan (zomig), Relpax (eletriptan), Frovatriptan, Rizatriptan, Naratriptan (Amerge)
    • Non-Constrictive Abortive Agents
      • Narcotic injections
      • Stadol NS (nasal spray)--opiod analgesic
    • Antiemetic Drugs (Phenergan): treatment for nausea, dizziness, and vomiting
    • General Pain Management
      • Narcotic analgesics--codeine, percodan, demerol, methadone, tylox
      • Non-narcotic analgesics--Midrin, Fliorinal
      • Over-the-counter (OTC) analgesics are usually not useful

  • Non-Drug Alternatives

    • Feverfew leaf--thought to prevent the spasms of blood vessels in head
    • Vitamin B2--possibly reduces the number of migraines experienced by patients
    • Magnesium--mixed support; studies contradict each other; consider 400mg as part of preventive treatment for migraine
    • Petasites hybridus (butterbur root)--50mg capsule twice a day; available under the name Petadolex; used for prophylaxis treatment
    • Biofeedback, acupuncture, stress management

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Go to:   [Headaches CE table of contents]   [Online CE main page]


URL: http://www.opt.indiana.edu/ce/headache/primary.htm
Revised: December 5, 2007

IU Optometry home page: http://www.opt.indiana.edu/
Comments (content): Dr. Brad Sutton
Comments: Web Administrator
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