Optometry (2011) 82, 298-305

Transient complete homonymous hemianopiaassociated with migraine

Denise Goodwin, O.D.

Pacific University College of Optometry, Forest Grove, Oregon.

KEYWORDS Abstract

mig

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Homonymoushemianopia;

Migraine;

Aura

INTRODUCTION: Because of the transient and rare nature, objective visual and neuroimaging evalua-tion during an acute, spontaneous attack of a migrainous aura causing a complete homonymoushemianopia has not been reported.CASE REPORT: A healthy 27-year-old white woman with a history of typical aura with migraine pre-sented during an episode of no light perception in the right hemifield of both eyes. Ophthalmic testingand neuroimaging were unremarkable. The visual field defect started to resolve 1 hour after initialsymptoms, and significant improvement was seen after 4 hours. One year later, the patient had novisual field defects and had not experienced another episode of homonymous hemianopia.DISCUSSION: More than one third of migrainous patients experience visual symptoms. Typical aurawith migraine is diagnosed usually by history. Laboratory testing and neuroimaging are necessary ifan alternative cause is suspected, i.e., the aura begins after age 40 years, negative features are predom-inant, or the aura is very short or prolonged. Correct diagnosis is critical, because conditions that mimicmigrainous aura have potentially devastating consequences. Migraine with aura patients may have per-sistent visual field defects and are at an increased risk for stroke compared with nonmigraine patients.This case improves our knowledge of the nature of a transient homonymous hemianopia associatedwith migraine.Optometry 2011;82:298-305

Nearly 36% of those with a history of migraine expe-rience a visual aura.1-3 Common descriptions of visual aurainclude bright spots (42%), flashes of light (39%), blindspots (32%), foggy vision (27%), and fortification spectra(20%).4

Prolonged homonymous hemianopia associated withmigraine has been reported.5-8 Rarely, a transient and com-plete homonymous hemianopia is attributed to migraine.9,10

K€unzlberger et al.11 reported a transient right homonymoushemianopia 5 minutes after an injection of polidocanol 1%

Disclosure: The authors have no financial or other relationships that

ht lead to a conflict of interest.

Corresponding author: Denise Goodwin, O.D., Pacific University College

ptometry, 2043 College Way, Forest Grove, OR 97116.

E-mail: goodwin@pacificu.edu

9-1839/$ - see front matter � 2011 American Optometric Association. All r

:10.1016/j.optm.2010.12.012

(1% Aethoxysklerol�; Kreussler, Wiesbaden, Germany) so-lution for treatment of varicose veins that induced a vascu-lar spasm, which was felt to provoke a migraine attack. Thepatient also had prickling of the hands and feet starting onthe right side and progressing to both sides. Visual fieldsperformed approximately 90 minutes after the initial epi-sode showed an incomplete, dense right homonymous hem-ianopia. After 150 minutes, the visual field was no longerconstricted, but the patient had a left frontal headache,which resolved after 2 hours. No neuroimaging wasperformed.

Because of the transient nature of migrainous aura,objective visual testing and neuroimaging during a spon-taneous migraine attack, resulting in a complete homon-ymous hemianopia, has not been reported. This case

ights reserved.

Goodwin Clinical Care 299

describes complete visual and neuroimaging evaluationduring an episode of visual aura causing a completehomonymous hemianopia.

Case report

A 27-year-old white woman reported to our clinic at 10:00a.m. reporting that everything had gone dark on the rightside of her vision one half hour previous. She reportedrunning into walls, at which time a friend drove her to ourclinic. She reported no tingling, numbness, or weakness ofthe extremities and no nausea, diplopia, oscillopsia, tinni-tus, or headache. Her medical history was remarkable onlyfor a history of migraines with an aura that occurred 2 to 4times per week. The aura associated with previous mi-graines was described as classic scintillating lights thatstarted centrally and progressed peripherally, lasting ap-proximately 30 minutes, and occurring before a unilateral,throbbing, moderate to severe intensity headache. Theheadaches were always accompanied by nausea, photopho-bia, and phonophobia. She denied use of tobacco, alcohol,or illicit drugs, and she was taking Excedrin� Migraine(Novartis, Basel, Switzerland) when needed for migraineheadaches. Family history was negative for migraine, dia-betes, or neurologic disease.

Visual acuities were 20/20 in each eye. Ishihara pseu-doisochromatic plates showed normal color discriminationin each eye. Extraocular muscle motilities were full with nonystagmus or dysmetria. Pupils were equally reactive tolight with no relative afferent pupillary defect. Frequencydoubling technique visual field screening found a completeright homonymous hemianopia (see Figure 1), and confron-tation visual field testing found no light perception in theright hemifield of each eye.

Results of an anterior and posterior segment examina-tion were unremarkable (see Figure 2), and intraocularpressures were 16 mmHg in each eye. The patient was re-ferred for an emergent magnetic resonance imaging (MRI)and magnetic resonance angiography (MRA), which didnot show a cause for the vision loss (see Figure 3).

Figure 1 Complete right homonymous hemianopia shown with Frequen

The patient returned to our office after neuroimaging atapproximately 1:30 p.m. the same day, at which time theneuroimaging results were verified to be normal. Thepatient reported that by the time she arrived at the neuro-imaging center (approximately 10:30 a.m.) she felt hervision starting to get better; she began seeing spots ofvision on the right side. By 1:30 she could see peoplemoving on the right side of her vision. She reported reddesaturation in the lower right quadrant of each eye, andHumphrey� (Humphrey� Field Analyzer HFA II-i Series;Carl Zeiss Meditec, Inc., Dublin, California) 30-2 Sita-Fast Threshold visual field testing at this time found an in-complete right homonymous hemianopia (see Figure 4).She did not have a headache at this time. Blood pressurewas 112/65 mmHg in the right arm while sitting, and in-office blood sugar level was 72 mg/dL.

Because of her history of migraine headaches with aura,the negative neuroimaging results, and the improvement ofthe visual field deficit, the presumed diagnosis was ocularmigraine. She was asked to return for further visual fieldtesting in 48 hours unless vision did not continue toimprove or she had further symptoms. She did not returnat that time, but came back 1 week after the initial visitreporting that vision was back to normal. Humphrey 30-2Sita-Fast Threshold visual field testing results showed amild depression on the right side remaining in both eyes(see Figure 5). Humphrey 30-2 Sita-Fast Threshold visualfield testing results 1 year later were unremarkable. The pa-tient has continued to have migraine events with aura madeup of scintillating scotomas and fortification spectra but hasnot again experienced complete hemifield vision loss.

Discussion

Migraine is a common cause of headache and is rankednumber 19 among all worldwide diseases that causedisability.12 The Second Edition of The International Clas-sification of Headache Disorders (ICHD-II)12 divides mi-graine into 2 major subtypes: migraine without aura andmigraine with aura. Over one third of those with migraine

cy Doubling Technique screening visual field performed at 10:00 am.

Figure 2 Posterior pole image shows distinct disc margins without obscuration of retinal vessels. A scleral crescent is evident on both eyes. These images

are consistent with images taken 2 years previous.

300 Optometry, Vol 82, No 5, May 2011

experience visual symptoms,1,2 and approximately 30% to44% of those with migraine with aura also experienceaura without headache.2,13-15

The cause of migraine pain is not completely under-stood. Migraine headaches were previously thought to beprimarily related to vascular changes. However, sensitiza-tion of trigeminal nerve endings by surrounding vasculatureis now believed to be involved in migraine pain.12,16,17 Ad-ditionally, nitric oxide, calcitonin gene-related peptide, andserotonin are thought to play a role.12,18

The mechanism involved in an aura associated with amigraine is better understood. Clinical findings suggestoccipital involvement. There is decreased blood flow in thecerebral cortex and cortical spreading depression, with awave of depolarization beginning posteriorly and movinganteriorly. Studies have also found hyperexcitability of theoccipital cortex in migraine patients compared with con-trols.18-25 This allows external and internal stimuli to trig-ger the migraine. Migraine with aura has been associatedwith patent foramen ovale.26,27 It is thought that eithermicroemboli passing through the patent foramen ovale orhypoxic blood arriving at the brain without passing throughthe lung could cause focal cerebral ischemia, which wouldthen produce cortical spreading depression.28 Additionally,

Figure 3 Axial T1-weighted MR image with contrast at the level of the optic ra

weighted imaging (C) at the level of the optic radiations were unremarkable.

there is evidence for a genetic basis for migraine with aurawith a multifactorial inheritance pattern.29-31

Evaluation

Migraine can generally be diagnosed by a careful history.Often patients with homonymous hemianopia report mo-nocular loss of vision on the side of the hemianopia. It isimportant to differentiate these 2 conditions. Visual fieldevaluation as well as examination of the pupils, ocularmotility, and fundus is critical. Those with typical symp-toms and a previous history of migraine do not requirefurther workup. Otherwise, physical and neurologic exam-ination should be performed.

According to the ICHD-II,12 migraine headaches are re-current and typically last from 4 to 72 hours. They shouldhave at least 2 of the following characteristics: unilateral,pulsating, moderate to severe intensity and worseningwith physical activity. Nausea/vomiting or photophobiaand phonophobia should be present during the headache.Additionally, the migraines must not be attributable to an-other disorder, such as trauma; sinus, vascular, or intracra-nial disease; medication or other substances; infection;disruption of homeostasis; or psychiatric disorders.

diations (A). MR angiography showing the circle of Willis (B) and diffusion-

Figure 4 Humphrey 30-2 Sita-Fast Threshold visual field shows incomplete right homonymous hemianopia approximately 4 hours after onset (right eye on

right, left eye on left).

Goodwin Clinical Care 301

The ICHD-II describes typical aura with migraine head-ache as a migraine headache accompanied, and usuallypreceded, by reversible focal neurologic symptoms(see Table 1).12 The neurologic symptoms typically developgradually over 5 to 20 minutes and last less than 60 minutes.Visual phenomena associatedwith amigraine can be negative,such as scotomas, or positive, such as photopsias or scintillat-ing scotomas. Frequently, scintillating scotomas accompanyfortification spectrum, a zigzag design that starts near fixationand spreads peripherally to form a C-shaped figure with ashimmering border and an accompanying absolute or relativescotoma. Visual symptoms are usually homonymous, butcentral vision may be affected. Less commonly, a visualaura includes blurring, metamorphopsia, or hemianopia.

Although visual illusions are the most common phe-nomena associated with migraine,13-15,30,32-34 other mani-festations, including sensory (31% to 54%) and speech(9% to 32%) problems, typically occur in succession or co-exist with visual symptoms.2,13-15,32,34 Sensory symptoms,such as tingling or numbness, should be unilateral and

Figure 5 Humphrey 30-2 Sita-Fast Threshold visual field 1 week after complet

greater than right eye (right eye on right, left eye on left).

spread up or down the limbs. Speech difficulties are typi-cally in the form of dysphasia. Vertigo is also a commonfinding associated with migraine aura.

Four to 58 percent of those who experience aura neverget a migrainous headache.14,15,35 Of those with a typicalaura and migraine headache, 30% to 44% occasionally ex-perience an aura without a migraine headache.2,14,15 It isunusual to have sensory symptoms other than visual symp-toms in a typical aura without a headache.14,15,36

Laboratory testing and neuroimaging are generally notneeded to make the diagnosis of migraine. However, thesemay be necessary for an atypical or complicated migraine.Laboratory testing should be performed if an inflammatory,infectious, metabolic, or hematologic cause is suspected. Ifaura begins after age 40 years, if negative features such asscotomas are predominant, or if the aura is very short orprolonged, a cause other than migraine should be sus-pected. The widespread use of neuroimaging, particularlyMRI and MRA, has allowed more definitive testing to helprule out other causes of transient homonymous hemianopia.

e homonymous hemianopia shows mild loss in the right hemifield, left eye

Table 1 ICHD-II criteria for diagnosing typical aura withmigraine headache.12

A. At least 2 attacks fulfilling criteria B through DB. Aura consisting of at least one of the following but no

motor weakness1. Fully reversible visual symptoms including positive fea-

tures (e.g., flickering lights, spots, or lines) and/ornegative features (i.e., loss of vision)

2. Fully reversible sensory symptoms including positivefeatures (i.e., pins and needles) and/or negative fea-tures (i.e., numbness)

3. Fully reversible dysphasic speech disturbanceC. At least 2 of the following:1. Homonymous visual symptoms and/or unilateral sensory

symptoms2. At least 1 aura symptom develops gradually over R5

minutes and/or different aura symptoms occur in suc-cession over R5 minutes

3. Each symptom lasts R5 and %60 minutesD. Headache fulfilling criteria for migraine without aura be-

gins during the aura or follows aura within 60 minutesE. Not attributed to another disorder

302 Optometry, Vol 82, No 5, May 2011

Although MR images, including diffusion weightedimages, apparent diffusion coefficient, and MRA, aretypically normal in migraine cases,8,37-39 reversible abnor-malities on diffusion weighted images and fluid attenuatedinversion recovery sequences have been reported in patientswith a prolonged aura.8,40 Isolated case reports have alsodescribed narrowing of the posterior cerebral artery, revers-ible white matter enhancement, and T2 hyperintensity dur-ing the headache phase of typical aura with migraine.10,41

Additional neuroimaging characteristics in those with typi-cal aura with migraine include subclinical infarcts and deepwhite mater lesions.28,42,43 Changes in perfusion imaging,represented by decreased blood flow in the cortex contralat-eral to the hemifield affected by the aura, have been docu-mented before and after the aura.37,44,45

Differential diagnoses

A migraine is typically diagnosed by history; however,because many conditions have potentially devastating conse-quences, conditions that mimic migraines must be ruled out.

Vitreo-retinal traction, carotid artery disease, and amau-rosis fugax will cause monocular transient visual distur-bances. In addition, a retinal migraine affects the anteriorvisual pathway resulting in monocular visual loss that lastsless than 30 minutes. Transient constriction of retinalarteries may also be observed during a retinal migraine.46

A homonymous hemianopia is typically caused by aretro-chiasmal lesion. The most common cause of a homon-ymous hemianopia in adults is stroke.47,48 A typical aurawithout a headache can be difficult to distinguish from astroke or a transient ischemic attack (TIA). Stroke or TIAshould be considered if risk factors for stroke are presentor if the patient is older than 40 years with new-onset

aura. TIA typically has a more abrupt onset and shorter du-ration (3 to 10 minutes) compared with migraine aura. Ad-ditionally, TIA symptoms are more likely to be static andnegative in nature. An aura can generally be distinguishedfrom a stroke by a migraine’s gradual onset and resolution,presence of both positive and negative features, and shortduration. Although symptoms of a migraine are similar tothose of a stroke, 99% of those with nonvisual symptoms as-sociated with a migraine will also experience a visual auraeither at the same time or prior to nonvisual symptoms.13-15

A diagnosis of stroke is confirmed with neuroimaging.Other causes of homonymous hemianopia include

trauma, tumor, hemorrhage, demyelination, infection, in-flammation, radiation damage, and migraine. Other thanmigraine, causative findings are usually evident on neuro-imaging. Creutzfeldt-Jakob disease, Alzheimer disease,subtle occipital ischemia, and nonketotic hyperglycemiahave also been reported to cause a homonymous hemiano-pia without detectable changes on MRI.49 Creutzfeldt-Jakob disease, Alzheimer disease, and subtle ischemiaresult in a permanent loss to the visual field. Because non-ketotic hyperglycemia may present with positive as well asnegative visual phenomena,50-53 diabetes mellitus should beconsidered when a sudden-onset homonymous hemianopiaoccurs. Visual field loss with nonketotic hyperglycemiaresolves with treatment of the hyperglycemia.49-53

Some medications have been reported to cause transienthomonymous hemianopia. Cohen et al.54 reported a tran-sient left homonymous hemianopia after treatment with cis-platinum, vinblastine, and bleomycin for testicularcarcinoma. The hemianopia began to improve after 48 hours,had a small residual scotoma in the superior quadrant at 4days, and essentially full visual fields at 2 weeks. Foroozanand Buono55 presented a patient with incongruous homony-mous hemianopia after taking topiramate for 6 weeks. Thevisual field defect slowly improved over 8 to 12 weeks afterdiscontinuation of the medication. K€unzlberger et al.11 re-ported a transient right homonymous hemianopia 5 minutesafter injection of polidocanol 1% solution for treatment ofvaricose veins. Visual fields performed approximately 90minutes after the initial episode showed an incomplete,dense right homonymous hemianopia. After 150 minutes,the visual field was no longer constricted.

Tumors of the occipital lobe can cause photopsias thatresemble an aura. However, these are typically persistentand stationary. Rarely, an internal carotid artery dissec-tion56 or vertebral artery dissection57 produces bilateralphotopsias and a migrainous-type headache that can bemistaken for typical aura with migraine.

Although occipital seizures can result in both positive andnegative visual symptoms, visual patterns differ between thisand migrainous episodes. Occipital seizures tend to havemore centrally located positive phenomenon and diffusenegative symptoms, whereas the symptoms with migrainepatients are more peripherally located.58 The patients seecolored, circular patterns that develop quickly.59 The dura-tion of hallucinations associated with occipital epilepsy is

Goodwin Clinical Care 303

shorter, most lasting 5 to 30 seconds.59 Occipital seizureshave been reported to cause homonymous hemianopia.60

Mitochondrial encephalomyopathy, lactic acidosis, andstrokelike episodes (MELAS) presents with recurrent, pul-satile headaches with vomiting that resemble amigraine. Thestrokelike episodes can result in reversible visual fielddefects, aphasia, or deafness. The condition manifests itselfduring a similar age range as a migraine. MELAS can startbetween ages 2 and 60 years, but nearly 70% of patients haveinitial symptoms between 2 and 20 years of age.61 Serum orcerebral spinal fluid analysis shows lactic acidosis, and amuscle biopsy results show ragged red fibers. Seizures arenearly always present in this condition.61 Lesions that mimicischemic stroke are seen with MRI. However, the lesions donot correspond to vascular territories, as occurs with stroke,and are transient.61,62

Cerebral autosomal dominant arteriopathy with subcorti-cal infarcts and leukoencephalopathy (CADASIL) commonlypresents as amigrainewith an aura followed later in the courseof the disease by recurrent ischemic events and dementia.63,64

This inherited vasculopathy manifests itself in midadult lifeand has characteristic neuroradiologic findings, such as whitematter abnormalities and small subcortical infarcts.

Management

An aura usually does not require treatment. However,treatment may be desired because a reduction in migraineaura may result in fewer migraine headaches. There are fewmedications that aim to decrease the aura associated withmigraine. Isoproterenol, a beta-agonist inhaler, or sublin-gual nitroglycerin may shorten the aura. Nonsteroidal anti-inflammatory drugs, such as meclofenamate and naproxen,can be used to abort attacks.65 Verapamil or antiepilepticmedications, including valproic acid, gabapentin, and topir-amate, have been effective for aura prophylaxis. GinkgolideB, an extract from biloba tree leaves modulates glutamatein the central nervous system, has been shown to reducethe frequency and duration of an aura.66

Tonabersat, currently in clinical trials, has been shown tostop cortical-spreading depression. This safely reduces thenumber of aura attacks and the number of aura attacksfollowed by a headache, but it has no effect on the numberof nonaura migraine headache days.67

Some have suggested that the closure of a patentforamen ovale may aid in migraine aura control.27 How-ever, at this time, evidence is insufficient to suggest thatclosure of a patent foramen ovale should be used to treata migraine with aura.28

Prognosis

Migraine headaches tend to decrease in frequency andseverity with age and may cease completely in 11% to 36%of patients.15,30,68,69 The median age of cessation is 40years.68 As patients get older, headaches often decrease,but the aura remains,30 and 77% continue to have aura

without headache.15 Men tend to have a more favorableprognosis than women.30,68

Persistent visual field defects are common in migrainesufferers. Between 29% and 35% of migraine patients havesome visual field loss indicating permanent changes to thevisual system.70,71 The majority have general depression ofthe visual field.70,71 Other visual defects include arcuate, alti-tudinal, temporal sector, nasal steps, hemianopic, and isolatedscotomas. Some have suggested an association betweenmigraine and normal-tension glaucoma as a cause of somevisual field defects.72-74 Other studies have found no associa-tion between normal-tension glaucoma and migraines.75,76

Prolonged hemianopia has been associated with mi-graine.5-8 Persistent aura without infarction is defined bythe ICHD-II as an aura symptom that persists for morethan 1 week without radiographic evidence of infarction.12

Other prolonged visual field defects and aura phenomenaassociated with normal laboratory and neuroimaging resultshave been reported. These include bilateral inferior visualfield loss that spontaneously resolved after 4 months39

and a woman who experienced scintillating scotomas bilat-erally that lasted 35 days.77

Severe, extended migraine attacks are associated withstroke resulting in permanent neurologic sequelae, includ-ing permanent hemianopia.78-83 The risk of a stroke is morethan double in those with migraine with aura comparedwith those without migraine.28,84,85 This risk furtherincreases in women, those less than 45 years old, smokers,and those who use oral contraceptives.28,84 These patientswill have an infarct that is visible on neuroimaging.83,85

Although the absolute risk of stroke in these patients is stillvery low, they should be examined regularly for cardiovas-cular risk factors. Additionally, cessation of smoking anduse of low-estrogen birth control, if needed, should berecommended.28,82

Conclusion

This is the first report of objective visual testing andneuroimaging during an acute, spontaneous attack of atypical migrainous aura causing a complete homonymoushemianopia. Results of neuroimaging tests, including MRIand MRA, were unremarkable. The visual field defectbegan to resolve approximately 1 hour after onset. Fourhours after onset, the visual field had improved signifi-cantly. One week after onset the visual defect was furtherresolved, and the patient has not had a recurrence ofcomplete hemianopia in 1 year. This case improves ourknowledge of the nature of a transient homonymoushemianopia associated with migraine.

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