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Show J. (lin. Nl'Ur(l-(lphth.llnwl. 2: 140-151\, 1°1\::. Crossed-Quadrant Homonymous Hemianopsia The "Checkerboard" Field Defect SHELLEY ANN CROSS. M.D. J. LAWTON SMITH. M.D. Abstract A 70-yeu-old mlln wilh II history of hy~rlensionand coronary llrtery disellse suffered lin abrupt loss of vision in June 1980, Neuro-ophthllimologic euminlltion in August 1981 revellied 20/20+ llcuity in both eyes, but qUllntillltive ~rimetry disclosed II dllssic crossed-qulldfllnt homonymous hemillnOpsia, This is known liS the "checkerboud" visual field defect; II right up~r qUlldrllntllnopsill liS well liS II left lower qUlldtllntllnopsia. A re",iew of Ihe eight pre",iously reported cases is presented. A trilll with "checkerbo<rrd" Fresnel prisms g...ve only a slight impro"'ement in ambient field in this plllient. The significllnce of thllt point is discussed. To our knowledge, this is Ihe first palienl with a "ch«kerbo<rrd" occipital lobe infuction pallern documented by compuled tomography. Crossed-quadr,mt homonymous hemianopsia, the "checkerboard" visual field defect, is the homonymous loss of two diametrically opposed quadrants of the visual field, is d rare occurrence. We report the case of a pdtient with this field defect documented by crossed-quddrdntic computed tomographic findin~s, .lAd describe eight cases from the literature in which simi!'lr fields are recorded. The c1inic.11 fl',lturt's .md anatomico-pdthological correl.ltions llf crossedquadrant homonymous hemianopsi,l ,1fl' discussed. Case Report A 70-year-old, left-handed m,m presented to thl' Bascom Palmer Eye Institute on August 27, 1981, because of difficulty with his vision. Several yeilrs earlier he suffered occ.asional transient loss of vision in the right visual fields accomp.:mied by flashing lights, but had not reported these to a physician. In June 1980, he suffered several epi- From the ~p,,"m.. nt of Ophthalmology, B.lscom r~lm('r ln~liluie, University of Miami 5C'hool of Medicin('. Mi~mi. FI"rid~. September 1982 sodes of scintill<ltions, sometimes synchronous with his pulse, covNing the entire field of vision in both eyes. One morning while shaving, he WJ.S suddenly unable to see, experienced flashing lights to the right, and had <l severe pJ.rieto-occipital headache. These complaints prompted admission to a hospital in Wilmington, Delaware. The patient hJ.d a ZO-year history of hypertension, reportedly well controlled, and he had a myocardial infarction in 1978. Physical examination recorded only a right homonymous hemianopsi<l with some left fidd loss in addition. A CT scan done at that time reportedly showed a left occipital infarction. An EEG showed decreased alpha activity on the left. The diagnosis of a posterior circulatory ischemic was made, and the patient was treated with ascriptin ,md perSJ.ntine. He appeared to recover uneventfully and at the time of discharge from the hospital on June 1·1, 1980, a right homonymous hemianopsia, denser dbove, remained. Neuro-ophthalmological consultation was performed on August 27, 1981. The patient considered thilt his visual function hild rl'm<lined st.lble since the 1980 hospitalization, but noted th<lt he frequently bumped into objects up and right i1nd down and left. He also complilined of difficulty with his memory. By this he ml'ant th.ll he could no longer give directions while his wife was driving, as strel'ts in his neighborhood always looked unfamiliar. He was vexed by the inability to recall names of friends and acquaintances, but denied difficulty with rec<111 of past events, Cillculations. right-left discrimination, reading, writing, or balancing. There was no diplopia, dysarthria, weakness, numbness, or dizziness. There had been no scintilldtions or other visual hallucinations since 1980. Examindtion revl',lled a corrected visual acuity of 20/20+4 and J-l in the right eye and 20/15-1 dnd J-l in the left eye. The blood pressure was 140/80. Visual field testing (Figs. 1-3, d and b) showed d crossed-quadrant homonymous hemianopsia, with the right upper defect extending 149 VISUAL. FIEL.DS (peripheral) I.E. R.E. 90· (Central) '0' Figure I. rcr;ph...r~1 fields to 10/330 wh"", on August 2". 1"8J (A,mdrk p<.'rimel~rJ_ !'.:Olt' Ull~CI monoculdr lower '..mpor.ol crescent in ]<:'ft eye (white Mrowhe~d). w, JUebt. Fi~ur .. 2. C,-"tr,,1 v'_u.,1 f;('ld, tu 70/1000 whit.. pwj<"<"tion light on August 27, 1981. Not.. nlr..me congruity in ,,,nlrdl fields will. II,.. ", ht·, ",-,1" •. ,,,1" dd.>, t (rll\ht "rP'" ljuddr.lI\IJnopsi.l .lAd It'll lower qu.dr.nIAno~i.). Not" th., extension into right lower '1""1, ,," ,,".". d.·",,·, 'h,,,, th" ""'". _"btl,> (',1('Il~;on into It'll UPP'" qu..dr.. nt. h' , d Clinical Npuro-ophth..lmo!ogy " • 0 Figurt' 301. Coldmolnn v;su,,1 firld on left eye on July 6. 1981. figurt' Jb. GoJdm<lnn visual field on right l'ye On July 6. 1961. Sj~ isoptel"S wert' plotted in uet> eye. Th.. Largest isopt"r (V41') WoIS dr.wn here, since 1II4l' and 114.. we,,- .1II'ssl'nli.. lly the same, showing th"t th .. field ddul hlod "bsolull', .nd nol sloping margins. This wdS consistent with old inf"'ction, These fil'lds were done by periml'lric technicians .nd show "pspudoincongrnity".t first glanet'. This is l'~pl.linl'd by the int.....! IOWl'T Il'mpoul c.t>SCl"nl;n It'ft eye• • nd Riddoch phenoml'non oIccounts for some diff'nences in isopt... with v<lrying spelNls of l\!'Sting kinetic fields. s1i~htly below the horizon toll meridiJn, but respcctin~ th(' v('r!iC.11 mNidiJn. SimilJTly, the left lower Jd('r! extended ,lbove th(' horizont.11 mNidi.Jn, but ,I~,lin respl'cted th(' v('rtk.l1 midline. An isthmus of p.lrti.llly int.let (entr.11 field ("onnected the two int. ll't qu,ldr.lflts. Fix.ltion Jpp('Jred to be split up .md to the ri~ht, bUI in th(' infNior hllif of the field the presenl'l' of splittin~ versus spMing WJ!< difficult 10 Jetermine, There W.lS J subtl(' MCU.lt(' dl'fect in the left urrl'r qu.ldr.ml. The monoculJr temporJI cres( ent in the lefl eye WilS spMed, On Amsler grid testing the pJtient report('d a "missing" right upper qu,ldr.mt in e.lch ey('. He did not report .lny abnormJlity in his left field. Optokinelic responses werl' 3+ lind symmetricJI with targets III ken right, Ide up, and down. Muscle b.llancl', motilily, externJI. slil IlImp, lind ophthalmoscopic examin",lions were within normal limits. Neurologiclll examin.ltion showed thllt the patient was alert and oriented. Immediate, recent, and remole m('mory were intact. Spe('ch WllS fluent and withoul ('TTors ('"(cept for momentM'Y h('sit.ltions and occasionlll inability to provide a noun in difficult nJming tasks, such as nllming the parts of a watch. The plltient provided th(' nam('s of politiclll figur('s piclured in a magllzine. Color naming, cdlculdtions, .lnd right-l('ft diSlinctions were well perform(' d. Writing ,md reading were abnormdl only for hesitation in the use of proper dnd common names. The patient's constructions included a floor plan of his house in which two rooms were reversed in position. A drawing of a clock and a map of Florida were w('11 ('xecuted. The patienl had claimed difficulty in recognizing familiar places, but this could not be demonstrated using photographs. Crani.ll nerves, molor, sensory, and cerebellar testing were normal. In particular, the palient did not extinguish on double simultaneous stimulation, and graphesthesia and stereognosis were intact. A computed tomographic scan with axial cuts and specific coronal studies of the occipilal lobes (Figs. 4-6) was performed on October 14, 1981. There was d sm.llllucency high in the right caledrine cortex, and a larger lucency was seen low in Ihe cdlcarine region dnd ddjdcent linguJI gyrus on Ih(' left. Neither of these lesions enhdnced. The findings were consistenl with old infdrctions. Be("duse the pdtient complained thai he encountered unseen objl"cts up dnd right, and down and left, we fitted his glasses with"checkerbOdCd" Fresnl'! prisms (Figs. 7 dnd 8), A JO-diopter base out Fresnt>l prism was placed in the right upper qUddrani of Ih(' right lens, and ,mother JO-diopter base out prism was pldced in the left lowl"r quadr.Jnt of the left lens. Both prisms were Irimmed so thdl they did nol encrO,Ich upon fixdtion. The patient wore th(>sl' prisms gldsses for severdl months. He W.I" nol impress('d with his .lbilily 10 ambulatl" wilh tlwlll T.lIl~('nl s("(el'n lesling, however, done ,-'- Figur~ 4. A>.,.l CT K.n m.de October 14. 1981. NOlI' hypod~ n~ lesion high In right ulurine corte>. /bl.ck .rrow}_ This .ceounts for ,he I~h lower homonymous visu.1 field d~ed in our p~tient. Figu~ S. AKi.1 CT sun m.de October t •. 1981. On this cut. which is lower th.n th.t s«n in Fig. 4, • luger hypodensity is sl'l'n in I~ft occipit~l lobe (..rowhuds). This .ceounts for th~ right upper homonymous visu.l field d~ert in Our p.tient. 'emni'l of CHnical Neuro-ophthalmology Cross. Smith Fip~ 6. Coron<ll CT SC<ln mJde October 14. 1961 The right upper ulcJrine inFJrction (single "rrowl "nd the I"rger lower left c.lurine inf"rrtion (doubl" Jrrows), show the "checkerboJrd" In<llomic,,,1 correl"le to the visu<ll field defl.'<"ts. Fig....... 6. "CheckerboJrd" Fresnel prism glJss"s, d"s('f view. N"le' pJli"nl is r.,ein" th" r.,mer,' ,lOd holding the gl<lsSf's "s h" w.....'s th ...m. September 1982 153 CWSSf'd-Qu4.dr",nl Homonymous Hl"miolnopsiol without the glasses, and with the prism glasses on, showed th4.t the field in the blind qUddrdnts was increolSt"d by 10-1S d~n.·es from the vertical meridioln when wearing Ihl" glolsses. It WclS thought th.:Jt thl" intclct monocul.u t('mporoll crescent in the left eye dnd the presence of Ihe Riddoch phenomenon in this pdtient probdbly olccounted for the fdCI that he did not clpprt'Ciate a more dramoltic improvement from the Frrsnel prisms. Comment. This 7O-yedf-old man wilh a history of hypertension and atherosclerosis may have suffered loss of som(' of the right ViSUdl field several years before his presentdtion, as simple hallucinations and intennittent visual loss had occurred in that field. However, calastrophic visual loss occurred at the time of the 1980 hospitollization, when he suffered ,ln occipitdJ he,ld,lche and more h,llJucinations. The right visudl field W,lS significanlly dffected, ,l new anomi,l W,lS present, and the left field loss along with right parietal deficils probably ,llso dated from that hospitalization. Severoll char,lcterislics of the poltient's visu,ll field dU' of interest. Only the right field loss was specifically nott'd by the poltient. The missing quadrants respected the vertical meridian, but encroached upon areas on the opposite sides of their resp«tive horizontal meridians. An isthmus of relatively intact field connected the two intact qU,ldrants. Tht' "intact" areas of field showed subtle deficits. The monocular temporal crescent in the left eye was spared. Nonnal optokinetic responses favored an occipitoll loc,ltion for the lesions. Liter..ture Review A search of the liter,llure revealed that only eight cases of crossed-quadrant homonymous hemianopsi.-. h.-.ve bet'n reported. Many of these c.-.ses suffer from inadequate clinical descriptions dnd lolck of pathologic correloltion. However, some of the reports contain clinical observations which are relevant to the problems we will discuss, and are recorded here in as much detail .IS was availdble. Case I In 1891, Groenouw· reported the cast' of.-. patient who had suffert'd a left hemiplegi.-. and .-. left homonymous hemi,mopsi<1. Ten months I.-.ter, he hold <1 st'Cond apopledic cltt<llck from which <lI crossed-qu.-.drant hemi<llnopsi<ll W<llS discoverE'd. ThE' field cut W<llS not clbsolute. Comment. If this p<lltient's initi<ll[ deficits <lire to be E'xpl<llined by <lI singlt' lesion, tht' most likt'ly loc<lltion would bt' in the region of the right intemoll c<llpsult' <lind optic radicltion. W<,ymJnn's roltient~ hold syphilis and .-. violent \'pnt inutlu" h<'old,lche. AftN oln dbrupt col1dpse with loss of consciousness, a right hemiplegia and a cTOSsed-quadrant hemianopsia were found. The scomat<ll were not absolute, and they did not change <lifter <lIntiluetic therapy. Comment. In this case, the quadrantanopsias seem to hdve had simultaneous onset. luetic vasculclr disease was their cause. Proximal posterior cerebral olrtery occlusion is likely, but deep parietal involvement, possibly in the middle cerebral artery, is dlso possible. Case J Felix·1 reported the Cdse of a 63-year-old man who hold atherosclerosis and cardiac disease. He awoke one morning completely blind, but unconcerned about his plight. Over several days his vision improved so that he could see large objects "ciS in a mist." Four months after the initial event, he complolined that he could see small photographs more easily than Idfge ones, and that reading was impossible. Examination of the visual fields revealed a crossed-quadrant hemianopsiol. "The left upper scotomata take not only the left upper quadrclnts but also rather more than one-third part of the nexl lower qUoldrants (left lower quadrants). The right lower scotomata are somewhat larger than the quadrants there (extending into the right upper quadrants). Tht' quadrant scotomata show a sparing of the macula and are absolute. The left lower quadrants of the visual fields are color blind. In the centre and in the right upper quadrants, which show a peripheral rrstriction, colours are recognized till about ISO-outside this there is colour blindness." Comment. This patient had total occipital blindness which, upon recovery, resolved into a crossedquadrant hemianopsia. The seeing fields were abnonndl. First, the quadrantic defects extended into them. Second, perception of colors was abnormal within them. There was some sparing of central vision. Case 4 In 1896, Allyn" recorded the case of a 49-yearold mdn with bilatercll homonymous hemianopsia. The poltient suffered two episodes of loss of vision. each one resulting in a homonymous field defect. The first occurred. while he was standing at his desk. The sight of both eyes left him and he remarked to a friend thdt he was blind. After a few minutrs a slow and incomplete recovery commt: nced. Three weeks later, on formal field testing. 01 left homonymous hemianopsia was discovered. There was sparing of SO around fixation. No other neurological deficits were noted. Six months later the patient suddenly fell to the floor clnd remained unconscious for 2 hours. Within 36 hours, the vision in both eyes began to loumal of Clinical Neuro-ophthalmology / fail rapidly and the patient was unabll' to Sl'l' bcl's or find his way about a room. For a fl'w hours, his speech was "thick." His wifl' thought th,lt his hearing had been ,1ffectl'd. One week ,lfter his collapsl', the visual ,1cuity was hand motions. The fundi Wl"Tl' norm,l!. The patient complained of visu,ll h,lllucin,ltions. For example, he thought th,lt his wifl"s nose was painted red. Anothl'r time, the p,ltil'nt thought that burglars were bre,lking into thl' housl'. In thl' subsequent months. his vision improV('d steadily. Serial ViSU,ll field testing, hampl"Ted by the patient's inabilitv to see the fix,ltion target. showed ,1 slowly improving crossed-quadr'lI1t hemianopsia. One year after the illness. central vision had significantly recovered, ,1nd crossed-quadrant hemianopsia r~mained. Comment. The patient's first illness resulted in bilateral occipital blindness which resolved into a left homonymous hemianopsia. The second episode is suggestive of a basilar embolus which caused transient brain stem ischemia and then occipital cortex infarction. The hallucinations imply either posterior parietal ischemia or posterior limbic ischemia with peduncular hallucinosis. Case 5 Traquair" illustrated field defects found 10 weeks after an attack of necrotizing ependymomyelitis. Damage to the walls of the lateral ventricles had been ascertained by ventriculography. Impairment of memory was present, but dysphasia and other signs of cortical involvement were absent. On the right side, the upper quadrant and the superior part of the lower quadrant were affected. On the left side, the lower quadrant was affected. An isthmus of intact field connected the intact quadrants. In addition, there was general depression of the fields. The optic discs appeared normal. The vision in both eyes was 20/20. Comment. This case, documented by ventriculography, again shows the development of a crossed-quadrant homonymous hemianopsia secondary to deep lesions in the radiations. The defects extended across the horizontal meridian, and central field was preserved. Case 6 Walsh and Hoyt" showed the field of a 70-yearold woman with basilar artery disease. Quadrantic defects were found in the right upper field and the left lower field with a narrow congruous isthmus near fixation. The left temporal crescent was spared and there were incongruities along the upper vertical meridian and the right horizontal meridian. Comment. This case suggests that incongruity may occur in occipital defects. This question will be addressed in detail later. Central vision was relatively well preserved. September 1982 Cross, Smith Case 7 Janssens and Berthelon' reported two cases. The first was that of .1 65-yedr-old woman who was admittC'd to hospital for Whdt appeared to be total blindnC'ss dnd dmnesia. She hdd .1 history of mitral valvC' diseasC' dnd a congC'nital hemolytic anemia. The vision was 20/25 in both C'yes. Confrontation fields disclosed a left homonymous hemianopsia dnd on the following day, a right hemianopsia. Two days after admission, ophthalmological examination revealed a left homonymous hemianopsia which WdS "very incongruent." Fifteen days later, a congruent homonymous crossed-quadrantic hemianopsia was discovered. A final visual field, performed I! months after the initial examination demonstrated essentially full recovery of the inferior quadrant defect. Neurological examination was normal. Comment. This case again raises the question of incongruity in the visual field in these lesions. A tenable explanation for the apparent abrupt change in the side of the hemianopsia is that both hemifields were initially involved and the Riddoch phenomenon was notably present. Case 8 The second of Janssens' and Berthelon's cases' was that of a 51-year-old man who complained of a black spot in his right visual field. A few days later he noted a defect in the right visual field accompanied by the sensation of light and paresthesias of the hands and the right side of the mouth. Three weeks later, when first examined by an ophthalmologist, the patient had a visual acuity of 20/200 on the right and 20/40 on the left. There was a congruous partial bilateral homonymous hemianopsia involving the right hemifield, particularly superiorly, and the left upper quadrant. Neurological examination disclosed a left facial weakness and right hemihypesthesia involving the trunk as well as the limbs. Stereognosis was diminished in the left hand. Examination 1 week later revealed an acuity of 20/20 in both eyes. The field defect persisted. Arteriography of both carotid arteries and the right vertebral artery showed multiple thromboses in the terminal segments of the right sylvian branches, a probable thrombosis in the terminal segment of the right posterior cerebral artery, and a new thrombosis of the middle third of the left posterior cerebral artery. Comment. This patient was reported to have had numerous thrombotic central nervous system lesions. Their distal locations suggest that they might actually have been embolic in origin. Discussion Crossed-quadrant homonymous hemianopsia is a rare occurrence. In our survey of the literature, 155 C..ussed -Qu.ld...lnt Humunymuus H('m i.llll.psi.1 including discussions focusing eln occipitJI visUJI Illss llf .111 types, thert' wert' only ('ight reported l-.lSl'S. Our C.1S(' is th(' ninth. Although clinicJI deslTiptions .H(' incompiC'le, th(' d.lt.l .lv.liIJbl(' do indicll(' som(' import.lIlt f('.ltures of the It'sions and resulting visu.ll field deficits .lIld .1ssllCiated Jbnorm. llities. On(' C.1S(' W.1S sludied by v('ntriculography (C.1St' 5) .lIld on(' by .1rteriogr.lphy ((.15(' 8). Our l-.lse W.1S investig.lted by CT se.lIlning. No autopsy m.lteri.ll is .1V.lil.lble. The vi5u.ll fields in (.lS('5 of crossed-quadrantic deft'cts h.1V(, s('v('r.ll interesting chJfac!eristics: I) The ,'nset of till' defect<, m.1Y be in twu .,imultan('ou., Lju.ldr.1I1t.lnopsi.1'>, two sUllc",ive homunymous hemi. lIWpsi.1S edch resolvll1g into .1 ljuadrdntanupsia, or simultaneuus bilater.ll helnwnymous hemi.1I10p.,las re""lving into crosscd-qu.ldr.lntic defeds. 2) Thc Ljuddrdntic defect., usually extend auoss the horizont.ll meridi.1I1 while the vertical meridian is alw.lys respected. This meridian may appear to be viol.lted when there are defects in the seeing fields. In order to demonstrate its integrity, it., entire extent must sometimes be explored in detail. 3) Central vision is rel.ltively well preserved, with an isthmus of intact field connecting the two intdCt quadr. 1I1ts. 4) The monucul.H temporal crescent may be spared. 5) The "intact" quadrants are not necessarily normal. Sm.lll targets may not be detected in them The Riddoch phenomenon may be present. Color vision may be abnormal. The defective .Heas of field may encroach upon the intact quadrants. Simple or complex hallucinations may appear in either the blind or in the seeing fields. The question of incongruity in homonymous crossed-quadrantic field 1055 was raised by case b and CJse 7. Incongruity may be either apparent or true. There are two importJnt fJctors that must be considered in occipitJI lobe field defects that can cause an apparent incongruity (ur "pseudoincongruity") in the field. These are the Riddoch phenomenon and the presence of the monocular temporal crescent. The first of these was reported in 1917 by Riddoch," who described dissociation of visual perceptions in patients with occipital injuries. The ten patients studied fell into three groups. Those in the first group h.ld homonymous hemianopsias with preservation of the ability to detect moving-but not st.lIic-t.Hgets in the blind field. Some had preservation of the monocular temporal crescent (to be discussed later). .lnd in some of these movement could be detected in the crescent only, and not more centrally. In some cases, an object could actually be identified when seen in the crescent, but the identity would then be lost until it appeared in the intact hemifield. The second group of patients h.ld homonymous hemi.lIlopsi.ls which showed recovery. Field 1055 for st.ltie t.Hg('ts W.1S Jlw.lys gre.lter in extent than fil'ld loss for moviny, targets. The ability to detect n1ll1 ion in .111 ,H('.l of field preceeded the ability to see static test objects. The third group of patients had homonymous field defects in which there was no dissiciation between detection of movmg and static targets. Benton et al.~ have emphasized that preservation of the monocular temporal cres~~nt often correlates with striking spanng of the abilIty to perceive moving stimuli. Riddoch's observatio.ns argue for the importance of testing patlen~s WIth both static and kinetic targets when mappIng the visual fields resulting from occipital lesions_ It also provides one explanation for apparent inco~gruity, if a different velocity is used when testmg Isopters in the different eyes. A second reason for apparent incongruity in the fields lies in the existence of the monocular temporal crescent itself. The crescent is that part of the visual field which represents unpaired peripheral nasal fibers. It is in the extreme temporal periphery, outside the field of binocular representation. When it is spared, the fields simply look incongruous. The unwary observer may map the temporal side on the perimeter as being full when only the crescent is present, or when the field central to the crescent is defective. Conversely, when only the central 30° of field is examined, as on the tangent screen, the presence of an intact crescent may be overlooked. In some cases of crossed-quadrantic homonymous hemianopsias, the fields may be truly, not just apparently, incongruous. The associated neurological deficits of memory loss, right and left parietal defects such as anomia and spatial disorientation, motor weakness, and thalamic type sensory changes indicate that the lesions extend forward into the parieto-occipital white matter and the posterior perforated substance. A few of the lesions, in fact. may lie in the distal territory of the middle cerebral artery or the anterior perforators. The incongruity of the fields in these few cases may be accounted for by anterior optic radiation involvement. However, it should be emphasized th,lt the crossed-qu.ldrant hemianopsia is nearly alw.lys an occipital lobe sign. The origin of bilateral hemianopsias, of which the crossed-qu.ldrant homonymous hemianopsias .He .1 subset, .md the determination of whether the deficits Me simultaneous or successive, has been .\lid ressed .It length by Symonds and MacKenzie. 1O M.lteri.ll derived from 58 cases (29 with postmortem) is discussed by these authors. In their cases, the 1055 of vision was either sudden or gradual and bl)th half-fields could be affected simultaneously or in succession. Simultaneous loss was more common. Frequent prodromal symptoms were attacks of vertigo and transient episodes of visual impairment. The pattern of field loss was often such that the central 10° was preserved. In the more peripheral parts of the field the sectors adjacent to the vertical meridians were not infrequently spared. Selective Journal of Clinical Neuro-ophthalmology /r central visual loss was r.u(', but it did occur. Oisorders of higher function including sp,lti,ll disorientation, visual ,lgnosi,l, and deni.llof blindness; visual hallucinations were inconstantly present, but sometimes conspicuous. In cases in which the ViSU,ll loss in the two h.llffields was simult,lI1eous, the most frequent c.lse was embolization of the c.llc.uine .uteries, with the source of th(' emboli ,uising in the b.lsil.H or vertebral drt('ries (a fr('ljuent finding) ~)r thrombi .1Ssociated with valvul.lr h('.ut dis('.lse, .ltri.ll fibrillation, or myoc.udi.ll inf.uction. Although th('re is no C.1S(' ~)f crossed-qu.ldrantanopsi. l with postmortem m.lteri.ll, th(' cases r('corded hl'r(" ('xcept for Traqu.lir's C,lS(" app('.H to belong to an infrequently occurring subset of bilateral homonymous h('mianopsi.l occurring with either thrombotic or embolic dise,lse. Only Tr.lquair's case W.1S the result of an ep('ndymomeningitis with ddmage to the optic rddiations dround the posterior horns of the lateral ventricles. A few cases, especially those in which there was a hemiparesis, may have had vascular lesions possibly in the middle cerebral drtery territory. Several radiologic studies have been undertaken to identify the relationship between visual field defects and arterial occlusion in the posterior circulation. 1 J. I~ Kaul et al. ll compared the extent and severity of visual field 1055 in 14 patients, the occlusions of whose posterior circulations were verified angiographically. Atheroma, embolism, and migraine were the most common types of underlying disease. Occlusion of the main trunk of the posterior cerebral artery was associated with severe and permanent visual 1055 often with central sparing due to collateral blood supply from the middle cerebral artery territory. Single or multiple occlusions of main branches of the posterior cerebral artery caused variable amounts of field loss sometimes with considerable recovery. Occlusions of smaller branches of the calcarine artery caused loss of central vision which was usudlly severe. Hoyt and Newton'~ recorded the dngiographic changes seen in the occlusion of drteries thdt supply the visual cortex. Atheromatous emboli, tumor emboli from atrial myxoma, posterior cerebral artery aneurysm, focal vasculitis, and spasm after subarachnoid hemorrhage were the most common causes of abnormal findings. Most proximal occlusions of the posterior cerebral artery were embolic. More distal occlusions of the posterior cerebral artery were related to uncal herniation with compression of the artery as it passes over the tentorial edge. True narrowings of the artery occurred with subarachnoid hemorrhage, occipitdl contusions, migraine, and arteritis. Cortical branch occlusions were also usually the result of emboli, but cortical complications of migraine and polyarteritis also caused such occlusions. Angiographic findings were sometimes normal, even in the pres- September 1982 Cross, Smith ('nce of a field defect, and they were occasionally .lbnormal with normal visual fields. The requirement for significant infarction seemed to be multiple emboli. CT SC,ln findings have been correlated with visual field dl'fects in vascular lesions of the posterior visual pathways. McAuley and Russell l ' studied 39 patients with various types of homonymous hcmianopsias. Most cases had low-density lesions within the distribution of the posterior cerebral .utery. Most of the lesions were situated posteriorly .1Ild involved visual cortex or posterior radiations. In two piltients the lesions spared this posterior .Hea .lnd involved only the anterior radiations. In both of these cases the defects were quadrantic only, and may have been within middle cerebral artery territory. In general, lesions giving rise to quadrantic defects were smaller than those causing total hemianopsias. Lower quadrantic defects tended to occur with superior CT lesions, and vice versa. Macular sparing was associated with survival of the occipital pole in some instances. Bilateral cases had a higher prevalence of associated neurological defects. Our case had crossed-quadrantic CT findings consistent with the patient's visual field loss and in agreement with the above observations. Visual rehabilitation of patients with crossedquadrant homonymous hemianopsias depends upon the extent of the deficits. One important factor is the ability to detect the presence of objects in the peripheral field. The advantage of preservation of the temporal crescent, and with it the ability to detect movement, has recently been documented in detail.~· I~ Some patients, however, are seriously disturbed by the perception of movement in the blind field. M One means of improving peripheral vision is by the use of mirrors or prisms. There are several reports in the literature!:;-I, describing the use of mirrors attached to patients' spectacles and fixed at such an angle that objects in the blind half ~)f the visuill field are reflected by the mirror Sll .1S to be imaged on seeing retin.l. There .He .lls~) repllrts of the use of prisms to increase function.ll peripheral vision. 1M. HI We have employed p.lst('-on Fresnel prisms in more recent years, and h.1\'e found them more practical in prilctice than hemi.lIlopic mirrors. A 30-diopter Fresnel prism is p!.lced with the base tow.uds the hemianopic side of the patient's glasses. The prisms are trimmed so that they do not interfere with fixation. In a patient with a total left homonymous hemianopsia, a 30-diopter Fresne( prism is placed base out (base left) on the temporal half of the patient's left spectdcle lens. An example is seen in Figure 9. Our patient was inconvenienced in ambulation by a tendency to bump into objects up and to the right, and down dnd to the left. We fitted him with Fresnel prisms in a "checkerboard" pattern. Only 157 CrossC'd-Qu.ldrant Homonymous HC'mi.mopsiJ Figure 9. ConventionJI hemiJnopic Fresnel prism JS used in J pJtient with a total left homonymous hemianopia. Patient is holding glasses and the 30-diopter Fresnel prism is base left on left lens. modest visual improvement was noted in our patient with these prisms, probably because of the integrity of the monocular temporal crescent in the left eye and also because of the Riddoch phenomenon. To our knowledge, this is the first case in which a "checkerboard" field defect has been documented by "checkerboard" CT findings, and in which "checkerboard" Fresnel prisms have been prescribed. References 1. Groenouw, A.: Uber doppelseitige hemianopsie centralen ursprungs. Arch. Psych. Nervenkr. 23: 339-366, 1891. 2. Weymann, M.P.: A case of quadrisectoral homonymous hemianopsia. Am. f. Ophthalmol. 11: 289-293, 1894. 3. Felix, CH.: Crossed quadrant hemianopsia. Br. f. Ophthalmol. 10: 191-195, 1926. 4. Allyn, G.W.: A case of bilateral homonymous hemianopsia. Arch. Ophthalmol. 25: 206-212, 1896. 5. Scott, G.!.: Traquair's Clinical Perimetry (7th ed.). CV. Mosby Co., St. Louis, 1957, pp. 277-278. 6. Walsh, F.B., and Hoyt, W.F.: Clinical Neuro-ophthalmolagy, Vol. 1 (3rd ed.). Williams and Wilkins Co., Baltimore, 1969, p. 93. 7. Janssens, C, and Berthelon, S.: Quadranopsie homonyme croisee. Bull. Soc. Beige d'Ophthalmol. 165: 376-381, 1973. 8. Riddoch, G.: Dissociation of visual perceptions due to occipital injuries, with especial reference to Jppreciation of movement. Brain 40: 15-57, 1917. 9. Benton, S., Levy, I.. and Swash, M.: Vision in the temporal crescent in occipital infarction. Brain 103: 83-97, 1980. 10. Symonds, c., and MacKenzie, !.: Bilateral loss of vision from c('n-bral infarction. Brain 80: 415-455 1~~ , 11. Kaul, S.N., DuBoulay, G.H., Kendall, B.L, and Ross RusselL R. W.: Relationship between visual field defect and arterial occlusion in the posterior cerebral circulation. f. Neural. Neurosurg. Psychiatry 37: 1022-1030,1974. 12. Hoyt, W.F.. and Newton, TH.: Angiographic changes with occlusion of arteries that supply the visual cortex. N. Z. Med. f. 72: 310-317,1970. 13. McAuley, D.L., and Ross Russell, R.W.: Correlation of CAT scan and visual field defects in vascular lesions of the posterior visual pathways. f. Neurol. Neurosurg. Psychiatry 42: 298-311, 1979. 14. Meienberg, 0.: Sparing of the temporal crescent in homonymous hemianopia and its significance for visual orientation. Neuro-ophthalmol. 2: 129-134, 1981. 15. Walsh, TJ., and Smith, J.L Hemianopic spectacles. Am. f. Ophthalmol. 61: 914-915, 1966. 16. Mintz, M.J.: A mirror for hemianopia. Am. f. Ophthalmol. 88: 768, 1979. 17. Bums, TA., Hanley, W.J., Pietri, J.F., and Welsh, LC: Spectacles for hemianopia. A clinical evaluation. Am. f. Ophthalmol. 35: 1489-1492, 1952. 18. Weiss, N.J.: An application of cemented prisms with severe field loss. Am. f. Optom. 49: 261-264, 1972. 19. Smith, J.L., Weiner, I.G., and Lucero, A.J.: Hemianopic Fresnel prisms. f. Clin. Neuro-ophthalmol. (In press.) Acknowledgments Grateful acknowledgement is given to Drs. John Clarkson. and Singh Pannu for referring the patient reported III thiS paper. The authors are also indebted to Miss Barbara French for photographic help, and to Mrs. Reva Hurtes for library help. Write for reprints to: J. Lawton Smith M.D., P. O. Box 016880, Miami, Florida 33101. ' Journal of Clinical Neuro-ophthalmology |
