Chapter 41 Headache pain is one of the most common medical complaints heard by health professionals. Migraine headache pain and its accompanying symptoms vary from patient to patient. The key to diagnosis of migraine is an accurate history and categorization of the type of migraine episode. Once this has been accomplished, appropriate adjunctive testing and therapy may be started.1 A neurologist or neuro-ophthamologist should evaluate the patient referred with suspected migraine, especially when accompanied by visual and neurologic symptoms, within a week, and sooner if there are atypical features that might suggest intracranial mass, inflammation, or hemorrhage. The patient who has visual disturbances, including transient monocular visual loss, should be evaluated by an ophthalmologist to rule out ocular disease. Migraines are a frequently familial disorder characterized by recurrent attacks of headache of variable frequency, duration, and intensity. They are usually unilateral but may be holocranial, and are often associated with anorexia, nausea, and vomiting. These attacks may be preceded or accompanied by neurologic or visual symptoms. Migraines are categorized as migraine without aura and migraine with aura. The latter category also includes complicated migraines and other migraine variants.2 Migraines affect women two to three times more than men. Many migraineurs experience their first attack in their second or third decade of life, yet some may begin in childhood or less commonly in later life after the age of 50.2 Studies have shown that migraines tend to be more prevalent in lower socioeconomic groups, possibly secondary to poor diet and the stress of decreased incomes.3 Identifying precipitating factors is important to establish a treatment plan. A very common trigger for a migraine attack is an emotional, stressful upheaval in the patient’s life. Other factors include hormonal changes associated with menstruation, menopause, or pregnancy; dietary products containing certain amino acids such as tyramine or phenylalanine; alcohol; medications; bright lights; fatigue; hypoglycemia; or head trauma.1,2 A migraine headache with or without aura may have prodromal symptoms. There may be an alteration of one’s mood, including depression, euphoria, irritability, restlessness, hyperactivity, or apathy. Patients may experience nausea, stiff neck, fatigue, thirst, hunger, specific food cravings, urinary frequency, anorexia, diarrhea, and/or vomiting. Symptoms and signs of neurologic dysfunction include photophobia, phonophobia, weakness, paresthesias, aphasia, dysphasia, visual loss, and vertigo. Similar signs and symptoms may occur during or subsequent to the migraine attack.1,2 Migraine without aura, previously referred to as common migraine, represents ~60% of all migraine headache episodes. Migraine without aura lacks a well-defined, preceding set of visual symptoms. Headaches last at least 4 hours, and often persist for a day or more. The pain may be unilateral in location, described as pulsating or throbbing pain of moderate or severe intensity. Nausea with or without vomiting frequently accompanies a severe headache and may be more disabling and troubling than the headache itself. The patient may exhibit photophobia or phonophobia during the migraine attack.2 Migraine with aura, or classic migraine, is composed of an antecedent visual event, followed by a headache and a postheadache phase. The aura of a classic migraine lasts 5 to 60 minutes, but it may last longer, and may be a visual disturbance, a variety of transient neurologic symptoms, or both. The classic visual aura consists of binocular, often homonymous hemianopic scotomas described as glimmering lights, zigzag lines, or wavelike phenomena similar to heat waves rising off the pavement on a hot day. “Scintillating” scotomas have a shimmering border, and may consist of angular lines, creating a “fortification” scotoma. The visual aura may also include: • Zigzag streaks of light • Shimmering spots of light • Multicolored circles • Flashing lights • Pinwheels • Distortion of lights • Moving veils of lights Some patients may have transient complete total blindness as their visual aura. The visual changes most often precede the headache, and less commonly occur during or persist after the headache. It is believed that most of the linear, zigzag, and variably colored auras arise from the visual cortex.2 Some patients have an isolated visual aura in the absence of headache pain, classified as acephalgic migraine.4 Visual loss in migraine is most often transient; permanent visual field defects are rare. Unilateral pupillary dilation may occur prior to or during a migraine attack.5 This may be due to sympathetic overactivity or parasympathetic impairment, as in ophthalmoplegic migraine. Horner’s syndrome may accompany migraine, with a constricted pupil, but its presence should prompt evaluation for other causes of painful sympathetic dysfunction (see Chapter 36). If the retina is examined ophthalmoscopically during migraine-associated transient monocular visual loss, the retinal vessels may appear constricted.6 Otherwise the fundus is normal during a migraine attack. The following features should raise the question of alternate diagnoses:
MIGRAINES AND MIGRAINE VARIANTS
URGENCY OF EVALUATION
DIAGNOSIS
DEFINITIONS
DEMOGRAPHICS
PRECIPITATING FACTORS
SYMPTOMS
Prodromal
Migraine without Aura
Migraine with Aura
Isolated Aura
SIGNS
Visual Fields
Pupils
Retina and Optic Disc
Red Flags
Evidence of continuous progressive, severe headache pain, often with focal neurologic signs. This may represent a subarachnoid hemorrhage, vascular malformation, or ruptured cerebral aneurysm.7
Longstanding, constant, or progressive pain, associated with nausea, vomiting, and transient visual obscurations lasting seconds. This suggests intracranial pressure elevation from mass or pseudotumor cerebri. Papilledema is usually present.
New-onset severe temporal headache pain and stiff neck in a patient over age 50 with an elevated erythrocyte sedimentation rate, suggests giant cell arteritis9 (see Chapter 18).
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