British Journal ofOphthalmology 1994; 78: 185-190

Representation of the visual field in the occipitalstriate cortex

Robert McFadzean, Donal Brosnahan, Donald Hadley, Erkan Mutlukan

AbstractThe representation of the field of vision in thehuman striate cortex is based on the Holmesmap in which about 25% of the surface area ofthe striate cortex is allocated to the centrallSdegrees of vision. Foliowing the introductionof computed tomography of the brain, heaccuracy of the Holmes map was apparentlyconfirmed by clinical/radiological correlation,but a revision has been proposed by Hortonand Hoyt based on a magnetic resonanceimaging study ofthree patients with visual fielddefects due to striate lesions. They proposethat the central cortical representation ofvision occupies a much larger area. This studyreviews the perimetric and imaging findings in alarger series of patients with striate corticaldisease and provides support for the revisedrepresentation. The clinical phenomenon ofmacular sparing and its relation to representa-tion of the macula at the occipital pole is alsodiscussed.(BrJ Ophthalmol 1994; 78: 185-190)

Departments of Neuro-ophthalmology andNeuro-radiology,Institute of NeurologicalSciences, SouthernGeneral Hospital,GlasgowR McFadzeanD BrosnahanD HadleyE MudukanCorrespondence to:Mr R McFadzean,Department ofNeuro-ophthalmology, Institute ofNeurological Sciences,Southern General Hospital,1345 Govan Road, GlasgowG51 4TF.Accepted for publication22 September 1993

The representation of the visual field in theoccipital striate cortex was initially delineatedby Inouye' and subsequently by Holmes andLister2 in studies of wounded soldiers in theRusso-Japanese war (1904-1905) and the firstworld war (1914-1918).2 Thereafter Holmesdevised his original 'schema' which gained wide-spread acceptance.4 In this diagrammatic outlineofthe striate cortex Holmes demonstrated repre-sentation of the contralateral hemifield of visionin each cerebral hemisphere, with the horizontalmeridian occupying the base of the calcarinefissure and the vertical meridian demarcatingthe outer perimeter of the striate cortex. Themacular region was represented posteriorly atthe occipital pole, while the peripheral visualfield occupied the anterior striate cortex in theregion ofthe junction ofthe parieto-occipital andcalcarine fissures. It was appreciated that themacular region extended over a relatively largepart of the striate cortex and, using a planimeter,it has been calculated that 25% ofthe surface areaof the striate cortex was attributed to the central15 degrees of vision.' Following the developmentof computed tomography (CT) of the brain,several authors confirmed this original conceptwhen they found a good correspondencebetween visual field defects and the location ofstriate lesions on CT according to the Holmes'schema'.`-9 An activation study of the visualcortex using positron emission tomography(PET) scanning also supported the Holmes'schema'.'0Furthermore Holmes believed that the macula

was unilaterally represented at the occipital

pole,2 although Inouye included a small repre-sentation of the ipsilateral macula in eachoccipital lobe following the discovery of macularsparing in some clinical cases.' Such bilateralrepresentation of the macula has subsequentlybeen invoked by a number of authors in primateanimal experimental studies to explain theclinial phenomenon of macular sparing,""-15although in other studies bilateral representationof the macula in the striate cortex did notoccur.'6-18 Clinically, owing to fixational eyemovements of one to two degrees during peri-metry, there must be at least three degrees ofmacular sparing to make the finding reliableusing currently available perimetric tech-niques."" However, the bilateral representa-tion theory proposed in the above experimentalstudies is dependent on a nasotemporal overlapacross the vertical meridian which is only 0-6 to2 degrees wide."-"

Recently the traditional Holmes hypothesiswas challenged in a magnetic resonance scanningstudy5 of three patients with striate disease and arevised map of the representation of the visualfield in the human striate cortex was producedin which the area serving central vision wasexpanded and the area devoted to peripheralvision reduced. Similarities to data from closelyrelated non-human primate species were noted,in particular to electrophysiological studies ofOld World primate genera, in which centralvision occupied a large proportion of the striatecortex.'6172324 Indeed, in macaque monkeys thecentral 15 degrees of vision occupy about 70% ofthe total surface area of the striate cortex.2324Horton and Hoyt's revision of the classical

Holmes 'schema' requires confirmation ina larger series of patients and the clinicalphenomenon ofmacular sparing further elucida-tion. This paper attempts to address these twoissues.

Materials and methodsPatients suspected of suffering from occipitalcortical disease had a full neuro-ophthalmicexamination including detailed perimetry.Goldmann dynamic and/or Humphrey's staticthreshold perimetry were used in the majority ofcases, but if there was any doubt about thefindings these were confirmed on the Bjerrumscreen in a few cases. Imaging of the visualpathways, to confirm the presence of striatecortical disease and exclude any other lesion, wascarried out using a CT tomoscan and/or 0-15Tesla magnetic resonance (MR) scan. In somepatients an initial planning scan was carried outin the sagittal plane to identify the oblique courseof the calcarine fissure, which does not of courserun in a straight line. Its oblique plane was

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Table I Pathological lesions (n=26)

No ofcases

Infarction 1 5Neoplasm 5Haematoma 3Cerebromalacia 2Arteriovenous malformation I

Table 2 Visualfield defects (n=26)

No ofcases

Complete homonymous hemianopia 17Incomplete homonymous hemianopia 5Discrete homonymous scotomas 2Bilateral altitudinal 2

Table 4 Occipital pole/operculum sparing (n= 17)

No ofcases*

Macular sparing 9/11Macular splitting 0/7

*One case demonstrated both macular sparing and splitting(case 5).

Figure I T2 weighted (SE2000180) axial magneticresonance section shows a leftoccipital infarct involvingthe anteromedial striatecortex, but sparing theposterior striate cortex.

Figure 3 Ti weighted (IR 16001401400) parasagittalmagnetic resonance sectwn shows a left occipital infarctinvolving the superior bank ofthe striate cortex (arrowhead),but sparing the posterior striate cortex.

determined by drawing a straight line on thesagittal scan joining its anterior (at the junctionwith the parieto-occipital fissure) and posterior(at the occipital pole) limits. Subsequent scanswere performed axially in the plane of thecalcarine fissure or coronally at right angles to it.The imaging changes were then compared withthe patient's visual fields and the expected visualfields according to the Holmes 'schema' andHorton and Hoyt's map.

ResultsOccipital striate cortical disease was identified in26 patients with an age range of 21-82 years(average 50 years) and a male to female ratio of11:15. The majority of patients suffered fromoccipital infarction but there were also a numberof other pathologies (Table 1). The visual fielddefects were recorded (Table 2) in which a

complete homonymous hemianopia is defined as

one which extends to within 10 degrees of centralfixation, while an incomplete homonymoushemianopia lies beyond 10 degrees from centralfixation. A blind patient presented with a

macular sparing homonymous hemianopia andthen lost the residual field a few days later due topresumed bilateral occipital infarctions.

Macular involvement - that is, within 10degrees of central fixation, occurred in 17patients, unilaterally in 16 patients, and bilater-ally in one patient (see below). These were

Figure 2 Goldmanndynamic visualfield shows aright homonymoushemianopia to within 10degrees ofcentralfixationusing I2e and I4e targets.

Table 3 Macularinvolvement (n= 17)

No ofcases

Sparing 10Splitting 6Sparing/splitting 1

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Figure 4 Humphrey'sstatic threshold central visualfield (30-2 program) shows a

right homonymoushemianopia to within 10degrees ofcentralfixation.

FigureS Ti weighted (IR 16001401400) parasagittalmagnetic resonance section shows a right occipital infarctinvolving the superior bank ofthe striate cortex (arrowhead),but sparing the posterior striate cortex and the anterior striatecortex at thejunction ofthe parieto-occipital and calcarinefissures (arrow).

divided into macular sparing - that is, outside 3degrees of central fixation, and macular splitting- that is, within 3 degrees ofcentral fixation, cases(Table 3). Imaging involvement of the occipitalpole and operculum was then identified and com-pared with the perimetric abnormalities (Table4). In two elderly patients with macular sparing itwas not possible to identify precisely whether theoccipital pole was or was not involved owing tomovement artefacts on the scan.

Figure 6 Humphrey'sstatic threshold central visualfield (30-2 program) shows aleft inferior homonymousquadrantanopia to within 6degrees ofcentralfixation.

CASE ILLUSTRATIONS

Case IA 21-year-old man developed a left occipital

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infarct following a head injury (Fig 1). Accord-ing to Holmes this infarct should have produceda right homonymous hemianopia extending towithin 60 degrees of fixation, while Horton andHoyt predict a perimetric defect extending towithin 20 degrees of fixation. In fact Goldmanndynamic perimetry showed a right homonymoushemianopia extending to within 10 degrees ofcentral fixation (Fig 2).

Case 2A 35-year-old woman developed a left occipitalinfarct (Fig 3). According to Holmes such alesion would produce a right homonymoushemianopia extending to within 30 degrees offixation, while Horton and Hoyt predict a fielddefect extending to within 12 degrees of fixation.Humphrey's static threshold perimetry showed aright homonymous hemianopia extending towithin 10 degrees of central fixation (Fig 4).

Case 3A 40-year-old man developed a right occipitalinfarct affecting the superior bank of thecalcarine cortex (Fig 5). According to Holmessu~ch a lesion would produce a left inferiorhomonymous quadrantanopia extending towithin 30 degrees of fixation, while Horton andHoyt predict a field defect extending to within 10degrees of fixation. Humphrey's static thresholdperimetry demonstrated a left inferior homony-mous quadrantanopia extending to within 6degrees of central fixation (Fig 6). This patientalso demonstrated sparing of the left monoculartemporal crescent with sparing of the portion ofthe superior bank of the right calcarine cortexadjacent to the parieto-occipital fissure. (Fig 7).

Case 4A 56-year-old man developed a spontaneousright parieto-occipital haematoma without anunderlying vascular malformation and subse-quent cerebromalacia with involvement of theoccipital pole and operculum (Fig 8). Accordingto both Holmes and Horton and Hoyt such alesion would produce a left macular splittinghomonymous hemianopia, as in this case (Fig 9).

Case SA 48-year-old woman developed bilateraloccipital infarcts after a stormy course followingclipping of a ruptured anterior communicatingartery aneurysm (Fig 10). According to Holmessuch a lesion would produce a macular splittingleft homonymous hemianopia and a macularsparing right homonymous hemianopia extend-ing to within 15 degrees of fixation, whileaccording to Horton and Hoyt such a lesionwould produce a macular splitting left homony-mous hemianopia with a macular sparing righthomonymous hemianopia extending to within2-5 degrees of fixation. Charting on the Bjerrumscreen in this case showed a macular splitting lefthomonymous hemianopia and a macular sparingright homonymous hemianopia extending towithin three degrees of central fixation (Fig 11).

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Left

Figure 7 Humphrey's static threshold peri'metry (temporal crescent program) shows sparirthe left monocular temporal crescent.

Figure 8 TI weighted (IR1600140/400) oblique axialmagnetic resonance sectionparallel to the plane ofthecalcarine fissure shows _cerebromalacia ofthe right _ tuILoccipital lobe including theoperculum.

Figure 9 Humphrey'sstatic threshold central visualfield (30-2 program) shows aleft macular splittinghomonymous hemianopia.

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DiscussionThese cases and the others reviewed in this seriesclearly demonstrate that Horton and Hoyt'sconcepti of an expanded area serving centralvision with a reduced area devoted to peripheralvTision can be confirmed in a larger series ofpatients. Although there are considerable varia-tions in the surface area and extent of the striatecortex in humans, the findings from the presentstudy indicate that the central 10 degrees ofvisual field are represented by at least 50-60% ofthe posterior striate cortex. Cases 1 and 2 clearlvdemonstrate that at least 50% of the posterior

75~ striate cortex is devoted to the central 10 degreesof visual field. The field defect in case 3 extendsto within 6 degrees of fixation while a similarlylarge area of posterior striate cortex is preserved,and in addition, sparing of the monoculartemporal crescent corresponds to sparing of thestriate cortex adjacent to the parieto-occipital/calcarine fissure junction. Case 4 illustratesmacular splitting dependent on involvement ofthe occipital pole and operculum. while in case 5sparing of the left occipital pole and operculumresults in sparing of the right central threedegrees of vision, but involvement of the rightoccipital pole and operculum causes loss of the

g of' left central three degrees of vision. The lattercase clearly demonstrates both macular sparingand macular splitting dependent on the integrityof the occipital pole and operculum.

Indeed these cases suggest that Horton andHoyt may have slightly underestimated theextent of the central 15 degrees of vision on theposterior striate cortex, although variations inlocal anatomy might to some extent account forthis. Our findings in the human striate cortexare compatible with microelectrode recordingsin macaque striate cortex- 24 in which studies oflinear and areal magnification factors concludedthat the central 10 degrees of vision was repre-sented by between 55-60% of the surface area ofthe striate cortex. In addition the pattern shiftvisual evoked potential is largely a reflection ofmacular vision26 with 60% of the amplitude of thewaveform being generated by the central eightdegrees of vision. Such a finding is compatiblewith the concept that a large part of the occipitalpole, from which most of the visual evokedpotential recording is derived, represents centralvision.

It may seem surprising that the originalHolmes 'schema' was confirmed by CT and PETstudies.6'0 The CT scans, however, were carriedout in the customary orbito-meatal plane whichslices through the calcarine fissure obliquely andtherefore does not give an accurate representa-tion of the local anatomy. An activation study ofthe visual cortex using PET scanning" wascarried out in the anterior/posterior commissuralline and was therefore subject to similar morpho-logical misinterpretation. The calcarine fissure,although taking a variable course, does runobliquely in an anterosuperior direction from theoccipital pole to the junction of the parieto-occipital and calcarine fissures. Therefore aninitial sagittal planning MR scan, as in thisstudy, to identify the orientation of the calcarinefissure with sequential scans axial and coronal tothe plane of the calcarine fissure give a much

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Representation ofthe visualfield in the occipital striate cortex

Figure 10 T2 weighted(SE 2000/80) axialmagnetic resonance sectionshows bilateral occipitalinfarcts, involving theoccipital pole and operculumon the right side but sparingthese structures on the leftside. In addition there arerightfrontal and temporalinfarcts.

better impression of the local anatomy. Never-theless, it is important to be cautious in relatingthe anatomical extent of a lesion on an MR scanto the functional perimetric findings, as theformer simply outlines disturbances of watercontent and distribution within tissues withoutnecessarily implying neuronal death, while thelatter is a subjective determination ofvariation infunction at one point in time. Clearly patho-logical verification of the imaging/perimetricfindings is essential before precise determina-tions can be made, but an approximate evalua-tion can be obtained from the cases reported hereand by others.

Indeed, based on the imaging findings, it isnow possible clinically to classify striate lesionsinto anterior, intermediate, and posterior.Anterior lesions lie adjacent to the parieto-occipital fissure and affect the monoculartemporal crescent of the contralateral visualfield. This area has been shown to constitute lessthan 10% of the total surface area of the striate

9O0

cortex.27 Posterior lesions are located in theposterior 50-60% of the striate cortex, includingthe occipital pole and operculum, and affectmacular vision - that is, the central 10 degrees inthe contralateral hemifield. Intermediate lesionslie between the anterior and posterior confinesand affect from 10 to 60 degrees in the contra-lateral hemifield.The clinical phenomenon of macular sparing

has generated much discussion since Inouye andHolmes's original publications.' 2 The findings inthis study clearly demonstrate that macularsplitting occurs when the occipital pole andoperculum are involved by the lesion andmacular sparing occurs when there is sparing ofthese structures. Unfortunately, in two of ourelderly patients with macular sparing it was notpossible to come to a definite decision aboutinvolvement of the occipital pole on imagingowing to movement artefacts during scanning.

Attempts to explain the clinical phenomenonof macular sparing on the basis of bilateralrepresentation of the macula with a naso-temporal overlap"'" found in electrophysio-logical studies in non-human primates, areunsatisfactory, as the extent of the overlappingretinal ganglion cells would allow only one to twodegrees of macular sparing. In practice, becauseoffixational eye movements ofone to two degreesduring perimetry'9-" it is necessary to detect atleast three degrees of macular sparing in order toconfirm the clinical phenomenon.The explanation for the clinical phenomenon

ofmacular sparing is almost certainly to be foundin a consideration of the blood supply of theoccipital pole and operculum which lie in awatershed zone between the posterior andmiddle cerebral arteries. There is a considerablevariation in the course and distribution of thearteries supplying the striate cortex28 but in 50%of normal brains the calcarine branch of theposterior cerebral artery supplies the entirestriate cortex. In the remainder, the occipitalpole and operculum are supplied by the posteriortemporal or parieto-occipital branch of theposterior cerebral artery or an occipital branch ofthe middle cerebral artery. In the former situa-tion a calcarine artery infarct would result in amacular splitting homonymous hemianopia butin the latter a similar infarct would allow a

Figure 11 Bjerrum centralvisualfield shows a macularsplitting left homonymoushemianopia and macularsparng right homonymoushemianopta usingS and 10mm white target at 2 metres. LE

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macular sparing homonymous hemianopiaowing to a collateral circulation from theposterior temporal or parieto-occipital branch ofthe posterior cerebral artery or an occipitalbranch ofthe middle cerebral artery. This simpleanatomical explanation has been borne out inclinical practice in this series and confirmsHolmes' original hypothesis that the macula wasunilaterally represented.

Although Holmes's original concept of therepresentation of the visual field in the occipitalstriate cortex was simply a 'schema', subsequentstudents of this subject have failed to seeksatisfactory clinicopathological correlations ofhis early observations. Modem imaging tech-niques permit perimetric-imaging comparisons,but the requirement for histological confirma-tion of the anatomical extent and effects ofclinical striate lesions remains. The advent ofactivation studies of the occipital cortex by echoplanar imaging may provide further spatialresolution of the central visual field representa-tion.29 30

ConclusionThis study confirms Horton and Hoyt's revisedmap ofthe representation ofthe visual field in theoccipital striate cortex with the central 10degrees occupying at least 50-60% of the striatecortex posteriorly and the more peripheral visualfield a correspondingly reduced area. Thesefindings are compatible with electrophysio-logical studies in Old World primates. Lesions ofthe striate cortex can now be classified intoanterior, intermediate, and posterior locationsbased on imaging findings and the correspondingvisual field defects identified an perimetry. Theexplanation for the clinical phenomenon ofmacular sparing lies in the variations in the bloodsupply of the occipital pole and operculum and itis not necessary to invoke bilateral representa-tion of the macula to explain this clinical finding.This paper is based on an oral presentation at the IXInternational Neuro-ophthalmology Symposium, Williamsburg,Virginia, 28 June-3 July 1992.The authors wish to thank their consultant neurological and

neurosurgical colleagues at the Institute of Neurological Sciencesfor referring these patients, Ms Alison Buchanan, head orthoptist,for assistance with the perimetry, Mrs June Cunningham, medicalphotographer, for the illustrations, and Mrs Rosemary Tracey,secretary, for careful preparation of this manuscript.

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