It’s a common situation amongst eye care providers. The office phone rings; on the line––a concerned, anxious patient reporting a sudden visual disturbance. “Doctor,” the conversation typically begins, “I’m frightened. My vision has become very distorted during the last 15 minutes. It’s clear around the edges, but in the middle it’s hard to see detail. And there are these wavy, pulsating lines all around the center of my vision. Am I going blind? What should I do?”
Despite the angst in this patient’s voice, you remain calm. You’ve heard this same scenario play out a dozen times before. You suspect that you know exactly what this is. The patient is experiencing her first migraine episode. Perhaps she has a family history of the disease, which would further solidify your presumptive diagnosis. You reassure her. “Everything’s going to be okay. It sounds like a migraine. I want you to sit down and relax. I’m going to call you back in a half hour, at which point your vision will likely be just fine. But, I want you to know that you may develop a substantial headache after this, so please be prepared for that. Once everything is back to normal, we’ll arrange to see you so that we can make sure your eyes are healthy and talk a little more about this condition.”
An Overview of Migraines
The disorder that we call migraine represents a group of chronic, episodic neurological conditions chiefly heralded by headache, but also characterized by a specific group of signs and symptoms. Migraine affects women about two to three times as often as men, and the peak incidence is between the ages of 35 and 45.1 The condition often begins in the teens or early 20s, and may persist throughout life. About 70% of migraine sufferers––called “migraineurs”––have a family history of the disorder or another form of vascular headache (e.g., cluster headaches) in a first-order relative.2
In a classic migraine, the episode initiates with an “aura,” a complex of neurological symptoms that occur antecedent to or sometimes concurrent with the headache. About one-third of migraineurs experience these phenomena.3 Auras typically develop for five to 10 minutes, and persist less than one hour.1 They may present as visual, sensory or motor phenomena, or they may occur in combination. The classic visual aura is described as a “scintillating scotoma,” which begins as a small blurry area of vision near fixation that slowly expands to a large hemifield defect surrounded by a shimmering, undulating border of light. Patients who cannot articulate the visual aura may simply report flashing lights and/or distortion of vision.
Non-visual auras may include paraesthesias (i.e., progressive numbness or tingling in the extremities or face), generalized motor weakness, speech/language disturbances (e.g., aphasia), hearing disturbances or even olfactory hallucinations.
About 60% of migraineurs will also observe a “prodrome,” a premonitory sensory experience that occurs hours or even days before the headache. Prodromes may represent little more than a change in mood, behavior or general feeling of malaise.1 The actual migraine headache can be severe, pulsatile and often incapacitating. Symptoms typically associated with the attack include nausea, vomiting, photophobia and phonophobia. Other non-specific symptoms consist of vertigo, anxiety, nasal stuffiness, pupillary mydriasis, tearing, confusion and syncope. Rare neurological complications may include motor dysfunctions, such as hemiplegia, ophthalmoplegia or apraxia.
The pathophysiology of migraine is actually rather complex. The prevailing neurovascular theory suggests that the migraineur’s brain remains in a constant state of neuronal hyperexcitability––a condition that may be due, in part, to diminished intracellular magnesium and elevated lactic acid levels.4 When challenged by certain conditions or stimuli, a neurochemical imbalance ensues. Patients may perceive this imbalance as a prodrome. Ultimately, as conditions persist within the cortex, a depolarizing wave of neuronal depression is generated. This wave moves forward across the brain from the occipital cortex, activating sensory nerves within the face and head. Neuropeptides are released from the trigeminal nerve, triggering platelet aggregation and serotonin release.5 Serotonin causes vasoconstriction, which may contribute to the migraine aura. Neuropeptides (including substance P and calcitonin gene-related peptide) stimulate inflammation of the meningeal arteries, which is believed to potentiate the headache and other symptoms associated with the migraine attack.5
The International Headache Society (IHS) describes numerous forms of migraine, although the two most frequently encountered are “migraine with aura” (i.e., classic migraine) and “migraine without aura” (i.e., common migraine).6-8 As a subclassification of the former category, patients may rarely experience the aura of migraine with no ensuing headache.9 (See “International Headache Society Criteria for Migraine,” above.)
Treatment of migraine involves first making an accurate diagnosis. Although the case above illustrates how easily we can identify the typical migraine presentation by patient history, confirmatory evaluation by a neurologist is warranted to rule out more sinister etiologies (e.g., impending stroke, aneurysm or intracranial mass) and to conduct a disability assessment.10 Therapeutic management is stratified and tailored to the severity of symptoms. Mild cases may be addressed using oral, non-narcotic analgesics (e.g., acetaminophen, ibuprofen or propoxyphene), if taken within 15 minutes of the onset of headache when the pain is still minimal.
Patients with more severe symptoms typically require migraine-specific medications. Ergot alkaloids and triptans are indicated for abortive migraine therapy. The ergot alkaloids consist of ergotamine (Cafergot, Sandoz) and dihydroergotamine (Migranal, Valeant). Triptans are potent serotonin receptor agonists that include sumatriptan (Imitrex, GlaxoSmithKline), zolmitriptan (Zomig, AstraZeneca), naratriptan (Amerge, GlaxoSmithKline), rizatriptan (Maxalt, Merck), almotriptan (Axert, Ortho McNeil Janssen), eletriptan (Relpax, Pfizer) and frovatriptan (Frova, Endo Pharmaceuticals). Treximet (GlaxoSmithKline) is another recently approved medication for migraine; it combines sumitriptan with naproxen sodium and has proven to be very effective in clinical trials.11
Patients who experience a migraine attack that lasts longer than 24 hours, have more than two attacks monthly, or whose attacks are so severe as to compromise their daily activities are candidates for prophylactic therapy.12 The three classes of medication for migraine prevention include antihypertensives (e.g., propanolol, verapamil or clonidine), antidepressants (e.g., amitriptyline) and antiepileptics (e.g., divalproex sodium [Depakote, Abbott] and topiramate [Topamax, Ortho McNeil Janssen]).12-14
The final step in migraine management is identifying and avoiding “triggers” that can initiate the migraine attack. Common triggers include certain foods, such as caffeinated drinks, cheese, chocolate, monosodium glutamate (MSG), nuts, smoked meats, red wine and some artificial sweeteners; strong smells, such as perfumes and cigarette smoke; glaring or flickering lights; fatigue; lack of sleep; and emotional stress.
While there is no cure for migraine, affected patients can lead full and productive lives by utilizing appropriate behavioral and pharmaceutical therapy. The road to successful management begins with detection, an area where optometry can play a crucial role.
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