Abstract and Introduction
Headaches that present to an ophthalmologist include migraine, facial pain syndromes, and pain associated with cranial neuropathies, orbital, and ocular disease. Some headaches are symptoms of medical emergencies, placing the ophthalmologist in the front line of their recognition and management.
Headache and ocular pain are frequent complaints in ophthalmic practice. Clinically a clear distinction between headache, facial pain, and eye pain is not always apparent, but when present, it helps in the diagnostic approach. In this update we will categorize pain syndromes into migraines, facial pain with or without Horner's syndrome, and headaches associated with other cranial nerve involvement. Intraocular findings may be manifestations of both ocular and systemic pathology. The goal is to present the most common and the most ominous headache presentations.
The most common definable headache syndromes are those designated migraine, with a prevalence of 5-25% and a marked female preponderance. In 2004, the Headache Classification Committee of the International Headache Society separated migraine syndromes into two main groups: migraine with and without aura.
Migraine without aura, or common migraine, represents more than half of migraine headaches. Most often the headache is unilateral, variable in frequency, and lasts a minimum of 4 hours.[1,2,3] Unilaterality is less common in children (approximately 20%). The pain is usually throbbing or pulsating, moderate to severe, and aggravated by physical activity, bright lights, and loud noises. A clear relationship with menstrual cycle has been established. Associated symptoms are nausea, anorexia, and photophobiathe latter possibly from irritation of the trigeminal nerve. Activation of the trigeminal autonomic reflex arc also accounts for sympathetic dysfunction during the attacks, such as delayed dilation of pupil in the darkness on the symptomatic side.[2,4,5] Patients with autonomic symptoms, such as eyelid edema, redness, lacrimation, or nasal congestion, during the migraine attacks are more likely to respond to sumatriptan, a serotonin receptor agonist. A hallmark of migraine without aura is the absence of permanent neurological deficits.
Migraine with aura, formerly called classic migraine, constitutes 10-35% of migraines and consists of aura, headache, and postheadache period. The aura is a transient cortical or brain stem dysfunction of gradual onset and less than 60 minutes duration. Cerebral blood flow reduction above ischemic threshold has been demonstated. Diagnostic criteria include a nor mal neurological examination and absence of an underlying organic disorder.[2,7]
Auras can be divided into visual and neurological with both occurring at the same time in 88%.[2,7] Neurological auras are paresthesias, numbness, motor weakness, vertigo, aphasia, alexia, and even hemiplegia.[2,7] Paresthesias in extremities are especially common with visual auras, and symptoms in the extremities are characteristically associated with visual aura. Visual auras are thought to orginate in striate cortex and range from an enlarging scintillating spot to a complete homonymous hemianopia. Scotomas may be positive or negative. The shimmering border of scintillating scotomas are colored lines forming angles and polygons to produce so-called fortification figures that usually progress from central field to the periphery. The persistence of visual aura following bilateral enucleation and its simultaneous binocular nature proves these originate in the brain, not the eye. Although recurrent transient monocular visual loss without headache and with complete recovery in young persons has been considered a variant of migraine, this phenomenon clearly must emanate from retina and optic nerve.[2,7]
Headache on the contralateral side typically follows aura and lasts for several hours. Other visual symptoms in migraine are micropsia, macropsia, diplopia or polyopia, halos, movement of stationary objects, changes in color, and even for med visual hallucinations. Migraine with aura does carry a small risk of ischemic stroke.[9,10]
Multiple mechanisms have been proposed in an attempt to explain the unique symptoms of migraine headache and to aid in management of this challenging disorder. Despite the success of conventional pharmacologic therapy of migraine with nonsteroidal anti-inflammatory drugs, caffeine, and calcium channel blockers, there are reports of treatment with botulinum toxin injections to the cranial musculature and injections of lidocaine with epinephrine to block the branches of the ophthalmic nerve.[10,11,12,13]
Lasting neurological defects, including visual field defects, should prompt neuroimaging.[2,8,9] Of particular interest to the ophthalmologist is the novel notion that there might be increased prevalence of glaucomatous visual field defects in migraineurs.[7,14]
Compr Ophthalmol Update. 2004;5(4) © 2004 Comprehensive Ophthalmology Update, LLC
Cite this: Headache and the Eye - Medscape - Jul 01, 2004.