The Representation of the VisualField in Human Striate CortexA Revision of the Classic Holmes MapJonathan C. Horton, MD, PhD, William F. Hoyt, MD

\s=b\We have tested the accuracy of Gor-don Holmes' retinotopic map of humanstriate cortex by correlating magneticresonance scans with homonymous fielddefects in patients with clearly definedoccipital lobe lesions. Our findings indi-cate that Holmes underestimated the cor-tical magnification of central vision. In arevised map of the human striate cortex,we expand the area subserving centralvision and reduce the area devoted toperipheral vision. These changes bringthe map of human striate cortex intoagreement with data reported for closelyrelated nonhuman primate species.

(Arch Ophthalmol. 1991;109:816-824)

"1 he representation of the visual fieldin the human striate cortex was

originally studied by Inouye,1 an oph¬thalmologist who treated woundedsurvivors of the 1904-1905 Russo-Japa¬nese War.1,2 He correlated visual fielddeficits with the trajectory of missilespenetrating the occiput to constructthe first retinotopic map of the striatecortex. A decade later, Holmes andLister3 examined soldiers injured inWorld War I and confirmed the essen¬tial features of Inouye's map.3J Thefamiliar Holmes map (Fig 1) has beenwidely reproduced in textbooks andstill provides the most detailed sourceof primary data concerning the repre¬sentation of the visual field in thehuman striate cortex. '

The Holmes map depicts an orderly,topographic representation of the con¬tralateral hemifield of vision in thestriate cortex. The vertical meridian isrepresented along the perimeter of thestriate cortex. The representation ofthe horizontal meridian runs along thebase of the calcarme fissure. The mac¬ula occupies the occipital pole, whilethe periphery of the visual field ismapped anteriorly. Both Inouye andHolmes realized that the central reti¬na, more densely cellular and special¬ized for best visual acuity, has a rela¬tively expanded representation in thestriate cortex. Using a planimeter, wehave examined the maps of the striatecortex published by Inouye andHolmes to calculate the area appor¬tioned to central vision. Our analysisindicates that both investigators as¬

signed 25% of the surface area of stri¬ate cortex to the central 15° of vision.

After the introduction of computedtomography, the accuracy of theHolmes map was confirmed by clinico-radiologie correlation. In a series ofpioneering studies, occipital lesionswere localized by computed tomogra¬phy in patients with visual field defi¬cits.""9 A good match was reported be¬tween the neuroradiological findingsand the location of lesions predicted bythe Holmes map. However, these ear¬

ly studies were limited by the ratherpoor resolution of early computedtomography.

The striate cortex has been carefullymapped using modern electrophysio-logic methods in a number of OldWorld primate genera: Papio, Cerco-pithecus, and Macaca.10'1" These re-

ports have shown that central visionoccupies an enormous fraction of thestriate cortex in Old World primates.For example, in macaque monkeys,the central 15° of vision fills about 70%of the total surface area of the striatecortex.1112 This figure far exceeds theproportion (25%) allotted by Holmesand Inouye to the central 15° in humanstriate cortex.

The discrepancy between the humanand monkey data suggests either thatthe Holmes map requires modificationor that human visual cortex is funda¬mentally different from monkey visualcortex in terms of the percentage ofstriate cortex devoted to central vi¬sion. Over the past year, we havecorrelated magnetic resonance imageswith visual field deficits in our patientswith occipital lobe lesions to help usdecide between these two alternatives.In this report, three typical cases are

analyzed in detail to illustrate the clini¬cal evidence we have collected to sup¬port amendment of the Holmes map.

REPORT OF CASESCASE 1.—A 30-year-old woman from In¬

dia reported several brief episodes of flash¬ing, colored lights in her right upper quad¬rant of vision. The visual acuity in each eyewas 20/20 without correction. She denied avisual field deficit, but testing at the tan¬gent screen showed a zonal scotoma in theright upper quadrant from 6° to 18° (Fig 2,inset). In the right eye the scotoma wascontiguous with the blind spot. Within thescotoma, the patient could not see a 15-mmor 30-mm white disk at a distance of 2 m,except along a fringe near the verticalmeridian. In this relative portion of thescotoma, she could detect a 15-mm whitedisk but not a 5-mm white pin. The visual

Accepted for publication December 26, 1990.From the Neuro-ophthalmology Unit, Depart-

ments of Ophthalmology, Neurology, and Neuro-surgery, University of California, San Francisco.

Reprint requests to Neuro-ophthalmologyUnit, U-125, University of California San Francis-co, San Francisco, CA 94143-0350 (Dr Horton).

field defect was also documented by map¬ping thresholds from 0° to 60° with a Hum¬phrey Field Analyzer (Allergan-HumphreyInstruments, San Leandro, Calif) (Fig 2).

A ,-weighted magnetic resonance scanshowed a sharply delineated lesion in theleft occipital lobe, abutting the tentorium(Fig 3). The relationship of the lesion to theapproximate boundaries of the striate cor¬tex is shown schematically (Fig 3, right).The patient's occipital lobe measured 56 mm

from the occipital pole to the confluence ofthe calcarme and parieto-occipital sulci(where the striate cortex ends rostrally).The lesion began 22 mm from the occipitalpole and extended anteriorly for 14 mm.

At craniotomy, a nodule filled with puru¬lent material was excised. Specimens forbacteria, fungus, and mycobacteria were

negative. Microscopic examination showeda necrotizing granuloma consistent with a

presumed tuberculoma. The patient is im¬proving on a regimen of isoniazid, rifampin,and ethambutol.

CASE 2.—A 28-year-old woman recount¬ed a history of migraine that began whenshe was a high school student. Typicalattacks started with shimmering silver linesin the left visual field, followed by a lefthomonymous hemianopia, headache, andnausea. A computed tomographic scan wasobtained when the left homonymous hem¬ianopia persisted after an unusually severe

migraine attack. It revealed a right occipi¬tal lobe arteriovenous malformation thatwas confirmed by cerebral arteriography.

When the patient was examined 5 monthslater, the visual acuity was 20/20 in eacheye. Tangent screen testing at 2 m showeda left homonymous heminanopia to 30- and5-mm white targets (Fig 4). The field defectintersected the upper vertical meridian at10°, crossed the horizontal meridian at 15°(through the left eye's blind spot), andintersected the lower vertical meridian at20°. The visual field thresholds were alsoplotted with the Humphrey Field Analyzer(Fig 4).

A magnetic resonance image obtainedbefore surgery showed a lesion replacingthe anterior portion of the right calcarmecortex (Fig 5). It began 31 mm from theoccipital tip and extended rostrally 33 mm

to terminate at the parieto-occipital sulcus.The lesion was excised successfully.

CASE 3.—A 57-year-old woman awokewith a headache and noticed some difficultywith her peripheral vision on the left side.She gashed the left side of her forehead onan open cupboard door while preparingbreakfast. A week later, after rinsing herface in a bathroom sink, she suddenly be¬came completely blind. She was admitted tothe hospital where a small island of centralvision gradually returned over the next fewdays.

When the patient was examined, thevisual acuity was 20/20 in each eye withoutcorrection. The patient was positioned ex¬actly 57 in from the tangent screen forvisual field testing. At this distance, 1 in onthe tangent screen equals 1° of visual field.Examination showed bilateral homonymoushemianopia with macular sparing in bothhemifields (Fig 6, inset). A vertical step of

Fig 1 .—The Holmes5 map (1945) showing the representation of the visual field in the humanstriate cortex (primary visual cortex, V1 ). The map underestimates the relative magnification ofcentral vision. For example, the 30° ¡soeccentricity contour (arrow) in the Holmes map isrepresented where the 12° ¡soeccentricity contour is actually located. (From Holmes5.)

1.5° could be mapped along the upper verti¬cal meridian and the lower vertical merid¬ian. The extent of macular sparing variedfrom 0.5° to 4.0°. The I2e and III4e isopterswere identical when plotted with a Gold-mann perimeter (Fig 6). The visual fielddefects in the right eye and left eye werecongruous.

A magnetic resonance scan showed bilat¬eral infarcts involving visual cortex alongthe medial surface of the occipital lobe (Fig7). The posterior 10 mm of cortex along theinterhemispheric fissure appeared sparedon each side. In addition, the occipital polesand opercula were intact bilaterally (Fig 7,right).

The patient was retested 2 months afterher stroke. Her visual fields wereunchanged.

COMMENT

The visual field deficits in our pa¬tients are incompatible with theHolmes map of the striate cortex.5According to his map, in the first pa¬tient the tuberculoma should havecaused a scotoma between 20° and 40°,centered at an eccentricity of about 30°(Fig 1, arrow). In fact, the patient'sscotoma was smaller and closer to fixa-

tion: it extended from 6° to 18° and wascentered at an eccentricity of 12°. Inthe second patient, the Holmes mappredicts a field cut between 40° and90°. However, visual field testingshowed a scotoma that approachedwithin about 15° of fixation. Finally, inthe third patient, the cortical infarctsshould have resulted in sparing of thecentral 15° of vision in each hemifieklaccording to Holmes. Instead, wefound bilateral macular sparing thatreached a maximum of only 4°.

In all three patients, the Holmesmap correlates poorly with the actuallocation of the lesion imaged by mag¬netic resonance, even if one allows fornatural variation in the exact dimen¬sions and location of the striate cortexthat occurs from patient to patient.Collectively these cases demonstratethat central vision occupies a greaterproportion of the human striate cortexthan Holmes portrayed in his retinoto¬pic map. In 1952, Spalding" publisheda revision of the Holmes map based onclinical findings in wounded veteransof World War II. Although the Spai-

Fig 2.—Merged 30-2 and 60-2 full-threshold visual field tests performed by patient 1 using a Humphrey Field Analyzer. Ahomonymous, congruous scotoma was present in the right upper quadrant using a 0.43° test spot against a backgroundillumination of 31.5 apostilbs. Within the scotoma, thresholds for detection of the test spot were greater than 10 000apostilbs. Elsewhere in the visual field the thresholds were normal. Inset, Visual fields of patient 1 are mapped at the tangentscreen. The scotoma extended from 6° to 18°. 5/2000W indicates 5-mm white pin at 2000 mm; 15:30/2000W, 15- or 30-mmwhite disk at 2000 mm.

Fig 3. —Parasagittal magnetic resonance image of the left occipital lobe in patient 1. The lesion in the visual cortexproduced the visual field defect shown in Fig 2. Scale = 5 cm. Right, Note location of the lesion (cross-hatched area) relativeto the likely extent of striate cortex (stippled area). The striate cortex exposed on the lateral surface of the hemisphere is notseen in this sagittal view. The calcarine sulcus (solid arrow) and the parieto-occipital sulcus (open arrow) are marked bydots. These sulci were better visualized on parasagittal images closer to midline.

Fig 4. —Full-threshold 60° visual fields in patient 2 mapped using a Humphrey Field Analyzer. The central 15° of the lefthemifield were intact. The visual field of the left eye was tested with the blind spot monitor off (otherwise the instrumentattempts futilely to plot the blind spot). Inset, Tangent screen plot of visual fields shows that the field defect actually bisectsthe blind spot representation of the left eye. 30:15/2000W indicates 15- or 30-mm white disk at 2000 mm.

Fig 5.—

,-weighted parasagittal magnetic resonance image through the right occipital lobe inpatient 2 shows the arteriovenous malformation responsible for the visual field defect illustratedin Fig 4. The posterior margin of the lesion is situated 31 mm from the occipital tip, marking theapproximate location of the representation of the left eye's blind spot (eccentricity = 15°). Thecalcarine (curved arrow) and parieto-occipital (straight arrow) sulci are indicated. Scale = 5 cm.(From Holmes.5)

ding map assigns slightly more cortexto central vision than the Holmes map,it still fails to allocate sufficient cortexto the representation of central vision.

Daniel and Whitteridge" publishedthe first complete map of macaquestriate cortex based on microelectroderecordings. They invented the termlinear magnification factor to refer tothe millimeters of cortex representing1° of visual field at any given eccentric¬ity. Their data showed a ratio of morethan 40:1 in linear magnification factorbetween the fovea (0° eccentricity) andperiphery (60° eccentricity). The arealmagnification factor

—

millimeterssquared of cortex/degree squared—hasa ratio of more than 1000:1 betweenthe fovea and 60°. Van Essen andcolleagues12 have also studied the rep¬resentation of the visual field in themacaque striate cortex. Their map is inclose agreement with the findings re¬

ported by Daniel and Whitteridge. Be¬tween 55% and 60% of the surface areaof the striate cortex is occupied by therepresentation of the central 10° ofvision.

A Revised Map of theHuman Striate Cortex

The findings in our patients suggestthat the relative magnification of cen-

Fig 6.—Visual fields of patient 3 plotted using a Goldmann perimeter show bilateral homonymous hemianopia with bilateralmacular sparing. In the right hemifield, the macular sparing is slightly greater. Because the visual field defects (right and lefteyes) were perfectly congruous, they are drawn on a single field chart. Inset, Magnified plot of residual visual fields of patient3 tested at the tangent screen (note scale marker). The steps across the upper vertical meridian and the lower verticalmeridian each measured 1.5°. Macular sparing ranged between 0.5° and 4°.

trai vision in the human striate cortexagrees more closely with the laborato¬ry data obtained from macaque mon¬

keys than with the clinical data report¬ed originally by Inouye and Holmes. Arevision of the Holmes map, scaled tothe cortical magnification found in themacaque striate cortex,1112 is presentedin Fig 8. The foveal representation islocated at the occipital pole, where thestriate cortex usually extends about 1cm onto the lateral convexity of theoccipital lobe (operculum). The ex¬

treme periphery of the visual field isrepresented anteriorly, at the junctionof the calcarine and parieto-occipitalfissures. Only a small portion of thestriate cortex, containing the repre-

sentation of the vertical meridian, isexposed on the medial surface of theoccipital lobe (Fig 8, top right). Most ofthe striate cortex is actually buriedwithin the depth of the calcarine fis¬sure (Fig 8, top left), making it diffi¬cult to depict the coordinates of themap directly on the cortical surface. Abetter view of the visual field map canbe obtained by schematically unfoldingand flattening the visual cortex to arti¬ficially create a planar surface (Fig 8,bottom left). The striate cortex con¬tains a topographic but highly distort¬ed representation of the contralateralhemifield of vision (Fig 8, bottomright).

In artificially flattened maps of ma-

caque monkey visual cortex, the stri¬ate cortex appears as an ellipse ap¬proximately twice as long as wide." 12

The average surface area of macaquestriate cortex is 1200 mm2.12 Estimatesof the total surface area of humanstriate cortex range considerably, re¬

flecting natural variation from speci¬men to specimen and technical differ¬ences from laboratory to laboratory.The most detailed study reports amean area of 2134 mm2 in formalde¬hyde solution-fixed brains.15 Allowingabout 15% for shrinkage caused byfixation, the average human striatecortex measures about 2500 mm2. As¬suming that the configurations of hu¬man and macaque striate cortex are

Fig 7.—Axial proton density-weighted magnetic resonance image through the occipital lobes in patient 3 shows brightsignal in the calcarine cortex along the interhemispheric fissure that represents a recent infarct. Scale = 5 cm. R indicatesright; P, posterior. Right, Note location of lesions (cross-hatched areas) and approximate location of striate cortex (stippledareas). Intact striate cortex is indicated by the dashed occipital lobe border. In the left occipital lobe, about 2 cm of the striatecortex was preserved posteriorly, accounting for 2.5° of macular sparing in the right visual hemifield.

similar, the human striate cortex isshaped like an ellipse measuring about80 40 mm (Fig 8, bottom left).

Our revised map (Fig 8) can be usedto localize more accurately a lesion inthe striate cortex that creates a deficitin the visual field. Conversely, from a

magnetic resonance image of sufficientresolution, the coordinates of a scoto¬ma produced by a lesion in the striatecortex can be predicted.

Figure 9, top, shows the lesion inour first patient, inferred by plottingthe visual field deficit (Fig 2) on themap of the human striate cortex (Fig8, bottom left). The lesion involves 378mm2 of tissue, or about 15% of themean surface area of the striate cor¬tex. This figure was determined bymeasuring directly the shaded area inFig 9, top, with the aid of a planime-ter. The match between the dimen¬sions and location of the lesion derivedfrom the cortical map (Fig 9, top) andthe actual dimensions and location im¬aged by magnetic resonance (Fig 3) isexcellent.

The right visual field deficit in ourthird patient is plotted in Fig 9, cen¬ter. Planimetrie analysis indicates that564 mm2 of tissue in the left striatecortex remained intact after thestroke, corresponding to 22% of themean striate surface area. The mag¬netic resonance data also fits the corti¬cal map well. The patient's scan (Fig 7)shows sparing of 1 cm of the striatecortex at the posterior end of the cal¬carine fissure and sparing of another 1

cm of the striate cortex on the exposedoperculum. This magnetic resonance

image provides the first illustration ofthe neuroradiologic findings in a pa¬tient with macular sparing.

Macular SparingThis latter case helps to dispel some

of the mystery surrounding the age-oldproblem of macular sparing. Inouye1discovered macular sparing in some ofhis wounded soldiers. Therefore, in hismap he included a small representationof the ipsilateral macula in each occipi¬tal lobe.1 Although Holmes'' droppedthis feature from his map (Fig 1),bilateral representation of the maculais frequently invoked to explain macu¬lar sparing. According to this notion,macular vision may be preserved aftercomplete destruction or removal of one

occipital lobe because the macula isdually represented in the fellow occipi¬tal lobe. This explanation is obviouslyuntenable in our second patient, whosuffered bilateral occipital infarcts.Moreover, experiments in the ma¬

caque monkey have unequivocallyruled out any substantial bilateral rep¬resentation of the macula in the striatecortex.1"1316 Dow et al13 report that inthe foveal representation, no striatereceptive field centers are found morethan 5 minutes (1/12 of ) into theipsilateral visual field.

A nasotemporal overlap across thevertical midline about 1° wide in thecentral retina occurs in ganglion cellprojections to the brain.1'"2" This imper-

feet decussation has been advanced bysome authors as an explanation formacular sparing.1" If correct, macularsparing should also occur after lesionsof the optic chiasm or optic tract. How¬ever, in the experience of most clini¬cians, macular sparing is a corticalphenomenon. Moreover, this theorycould account at best for only 1° to 2° ofmacular sparing. In practice, macularsparing often extends well beyond an

eccentricity of 2°.The extremely high cortical magnifi¬

cation of the macula provides the keyto understanding the phenomenon ofmacular sparing. In most patients, thevascular supply to the striate cortex isprovided entirely by branches of theposterior cerebral artery. Therefore, a

macula-splitting hemianopia ensues af¬ter infarction of the posterior cerebralartery. However, in a considerable mi¬nority of patients, the occipital polestraddles the vascular territories ofthe posterior cerebral artery and themiddle cerebral artery.21 In these pa¬tients, the occipital pole remains intactafter posterior cerebral artery infarc¬tion due to perfusion by the middlecerebral artery. Because the represen¬tation of the central visual field is so

magnified in the caudal half of thestriate cortex, preservation of any por¬tion of this region after posterior cere¬bral artery occlusion will spare cortexdevoted exclusively to macular vision(Fig 8, bottom left). Relatively largevariations in the amount of survivingcortex from patient to patient will

Fig 8. —Revised map of the representation of the visual field in the human striate cortex. It is important to emphasize thatconsiderable variation occurs among individuals in the exact size and location of striate cortex. This new map provides thebest fit for our data. Top left, Note view of the left occipital lobe with the calcarine fissure opened, exposing the striate cortex.Dashed lines indicate the coordinates of the visual field map. The representation of the horizontal meridian runs

approximately along the base of the calcarine fissure. The vertical lines mark the ¡soeccentricity contours from 2.5° to 40°.The striate cortex wraps around the occipital pole to extend about 1 cm onto the lateral convexity, where the fovea isrepresented. Top right, Note view of the left occipital lobe showing the striate cortex, which is mostly hidden within thecalcarine fissure (running between arrows). The boundary (dashed line) between the striate cortex (V1) and extrastriatecortex (V2) contains the representation of the vertical meridian. It is usually located along the exposed medial surface of theoccipital lobe as shown, but variation occurs in specimens. Bottom left, Schematic map shows the projection of the rightvisual hemifield (bottom right) on the left visual cortex, by transposing the map illustrated in the top left onto a flat surface.The striate cortex is an ellipse about 80 40 mm, measuring roughly 2500 mm2 (40 mm 20 mm ir = 2500 mm2). The rowof dots indicates where the striate cortex folds around the occipital pole: the small region between the dots and the fovealrepresentation is situated on the exposed lateral convexity of the occipital lobe. The black oval marks the region of the striatecortex corresponding to the visual field coordinates of the contralateral eye's blind spot. This region of cortex receives visualinput only from the ipsilateral eye. HM indicates horizontal meridian. Bottom right, Right visual hemifield (of one of us

[J.C.H.]) shows the V4e isopter plotted with a Goldmann perimeter (by W.F.H.). The stippled region corresponds to themonocular temporal crescent that is mapped within the most anterior 8% to 10% of the striate cortex (see stippled region ofmap in bottom left).

Fig 9.—Top, The tuberculoma in patient 1 (Fig 3) diagrammed on the cortical map is locatedmore anteriorly than predicted by the Holmes map. Note that the lesion must cross the V1/V2frontier because the patient's scotoma bordered the vertical meridian. Center, Diagram of rightvisual field defect in patient 3 is plotted on the map of the left visual cortex (shaded regionindicates infarcted cortex). Macular sparing reached 2° along the upper vertical meridian, 2.5°along the horizontal meridian, and 4° along the lower vertical meridian (see Fig 6, inset). Theamount of intact cortex is considerably greater than the Holmes map indicates. Bottom, Theintegrity of most of the striate cortex (shaded area) is tested by examining only the central 30° ofvision, because the representation of central vision is so highly magnified.

manifest clinically as modest differ¬ences in the precise number of degreesof macular sparing.

Our revision of the Holmes map alsohelps to explain why the pattern-shiftvisual evoked potential is essentially afunction of macular vision. Accordingto Yiannikas and Walsh,22 the central8° generates more than 60% of theamplitude of the evoked potentialwaveform (P100). This finding has puz¬zled clinical electrophysiologists famil¬iar with the Holmes map. In practice,the actual magnitude of the visualevoked potential depends on many fac¬tors, including the surface area of thecortex stimulated and its orientationwith respect to the recording elec¬trodes. Our map is in good accord, atleast qualitatively, with the observa¬tion that stimulating beyond the cen¬tral 10° or 15° of visual field contrib¬utes little to the amplitude of thevisual evoked potential.

Our modification of the Holmes maphas implications for computerized visu¬al field testing. The acquisition ofthreshold data using these automatedinstruments is so time-consuming thattesting is often restricted to the cen¬tral 24° or 30° of vision. Failure to testthe visual field beyond 30° raises theworry that some cortical lesions mayescape detection. Fortunately, thehigh magnification of central visionmitigates this danger. For example, a30° visual field examination actuallytests the function of 83% of the striatecortex (Fig 9, bottom). A mere 24°field examination (which approaches30° in the nasal hemifield when per¬formed using a Humphrey Field Ana¬lyzer) covers 80% of the cortical sur¬face area.

Our amended map is also consistentwith the paucity of reported cases de¬scribing visual field deficits confinedentirely to the monocular temporalcrescent. The temporal crescent is rep¬resented at the rostral end of the stri¬ate cortex. It lacks ocular dominancecolumns because input is received onlyfrom the contralateral eye.23 In humanstriate cortex this region has beenidentified and measured directly.24 Itconstitutes less than 10% of the totalsurface area of the striate cortex. Thetemporal crescent representation iscompressed into a much smaller area ofthe striate cortex than Holmes appre¬ciated (compare Figs 1 and 8). Theareas devoted to the representation ofthe central 1° of vision and the entiretemporal crescent are roughly equal inthe human striate cortex. This ex¬

plains why visual field deficits of corti¬cal origin limited strictly to the tempo¬ral crescent are so rare. Few lesions

are likely to fall precisely within thediminutive confines of the temporalcrescent representation in the striatecortex. Most lesions involving the tem¬poral crescent representation will alsoinvolve the optic radiations or periph¬eral binocular cortex, thereby result¬ing in bigger field defects.

Human Cortical Magnification Factor

The linear magnification factor(Miij^J in the striate cortex is inverselyproportional to eccentricity (E).2SThere is no universal agreement on thecorrect equation for linear magnifica¬tion factor (millimeters of cortex/de¬gree of visual field) in macaque striatecortex. The following expression is areasonable approximation, based on

published formulas1213·16·23'26'27:12Monkey: Mu,linear

# + 0.75,where E is eccentricity in degrees.This equation applies to the macaquestriate cortex, which has a mean sur¬face area of 1200 mm2. 12 The humanstriate cortex averages 2500 mm2,greater in area by a factor of 2.08.

If our revision of the Holmes map iscorrect, the magnification formula forthe macaque striate cortex can beadapted to the dimensions of the hu-

man striate cortex. A correction factorof 1.44 (2.081'2) must be incorporated inthe expression for linear cortical mag¬nification factor in the human striatecortex:

17 3Human: Mine„= - E+ 0.75.

This formula gives a value for linearcortical magnification of 9.9 mm/de¬gree at 1° eccentricity, 3.0 mm/degreeat 5°, and 1.6 mm/degree at 10°. Thesefigures are in good agreement withestimates of the human cortical magni¬fication factor obtained by positronemission tomography2" and by mappingphosphenes evoked by direct electricalstimulation.29'30

If we assume that human linear cor¬tical magnification is isotropie (seeTootell et al16 for a detailed discussionof this issue), the above formula can besquared to yield an expression for are-al cortical magnification factor (milli¬meters squared/degree squared):Human: M„eal = 300/(£ + 0.75)2.

Integration of this formula over thevisual field coordinates of any scotomawill provide the size in millimeterssquared of the corresponding corticallesion. In practice, it is easier to obtainthis information by referring directly

to the map shown in Fig 8, bottom left.When Inouye and Holmes published

their original maps, little was knownabout the cortical representation of thevisual field in nonhuman primate spe¬cies. When judged in this context,their maps were remarkably accurate.It would be surprising if their maps,based on clinical data collected duringthe early part of this century, did noteventually require some modification.With the advent of magnetic resonance

imaging, a technique with sufficientresolution is finally available to permitdirect validation of the Inouye andHolmes maps. Our analysis indicatesthat their maps underestimated themagnification of central vision in thestriate cortex. We suggest a revisedmap based on visual field-magneticresonance correlation that brings thehuman map into agreement with pub¬lished data obtained from laboratoryinvestigations in closely related OldWorld primate species.

This investigation was supported by the HeedOphthalmic Foundation and the Richard G. Sco-bee Memorial Fellowship (J.C.H.), Chicago, 111.

Joan Weddell provided exceptional help prepar¬ing the illustrations. Michael P. Stryker, PhD,and Roger B. H. Tootell, PhD, gave comments on

the manuscript.

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