Journal of Neuro-Ophthalmology, June 1982, Volume 2, Issue 2

Chiasmal optic neuritis.

Two patients exhibiting bitemporal hemianopia due to chiasmal optic neuritis with pathological confirmation of noncompressive lesions are presented; the first due to a chronic, idiopathic demyelinating process, and the second a result of ethchlorvynol (Placidyl) toxicity. The literature regarding chiasmal optic neuritis is reviewed, and a discussion of other noncompressive causes of bitemporal hemianopia is presented.

J. Clin. Neuro-ophtha/mo/. 2: Q3-IOI, 1982. Chiasmal Optic Neuritis WILLIAM D. REYNOLDS ). LAWTON SMITH, M.D. JOHN A. McCRARY, III, M.D. ------ ..... - _.. _. - _ .. Abstract Two patients exhibiting bitemporal hemianopia due to chiasmal optic neuritis with pathological confirmation of noncompressive lesions are presented; the first due to a chronic, idiopathic demyelinating process, and the second a result of ethchlorvynol (PIacidyl"') toxicity. The literature regarding chiasmal optic neuritis is reviewed, and a discussion of other noncompressive uuses of bitemporal hemianopia is presented. Introduction Chiasmal optic neuntls was first described by Roenne l and later Traquair2 in reference to those rare conditions involving the chiasm which are clinically and pathologically similar to acute retro­bulbar neuritis, yet produce bitemporal visual field defects resembling those due to tumors. Most of these cases are attributable to multiple sclerosis, and this relationship has been well documented,'!' 4 This condition is to be differentiated from opto­chiasmatic arachnoiditis, a chronic inflammatory disorder of the overlying leptomeninges which typ­ically involves the chiasm secondarily. This paper presents two cases of chiasmaI optic neuritis with pathological evidence of noncompressive lesions, the first due to a chronic, idiopathic demyelinating process, and the second of a toxic etiology. Case Reports Case 1 A 61-year-old white woman was in good health until April 1976, when she developed transient horizontal diplopia. One month later, she had a mild episode of right facial weakness which cleared in 24 hours. Upon hospitalization several days later, she noted blurred vision in her left eye. The visual acuity was reduced to finger-counting in the left eye, with a central scotoma and blurred disk noted on examination. Visual acuity in the right from the Bascom Palmer Eye Institute. Deputmenl of Oph. thalmology, University of Miami School of Medicine, Miami, florida. June 1982 eye was 20/15. Skull x-rays, lumbar puncture, EEG, and a right femoral arteriogram were all normal. and a demyelinizing process was sus­pected. She was treated with steroids, and vision in the left eye dramatically improved to 20/25. Visual acuity in her left eye fluctuated over the next 1112 years, and steroid therapy was adjusted accordingly. During this time she underwent two major surgical procedures for intra-abdominal ab­scess and ruptured diverticulum. In October 1977, the patient had visual acuities of 20/25 in the right eye, and 20/40 in the left. A Marcus Gunn pupil was noted on the left. Perimetry revealed only a small upper nasal island in the left visual field, with an upper temporal defect in the right eye. Visual acuity and fields stabilized over the next 2 months, and tapering of her steroid dosage was begun on December 8, 1977. Despite only a slight decrease in prednisone dosage from IS mg to 14 mg, the patient noted a profound decrease in left eye vision 3 days later. On December IS, 1977, the right eye was 20/25, but the left eye was blind. Vision remained unchanged over the next few months. In June 1978, the patient first noted diffi­culty reading with the right eye. A CT scan and pneumoencephalogram were normal, and the CSF contained 31 mg/dL of protein. She was main­tained on 60 mg of prednisone/day. Although the right eye vision remained at 20/20, progression in the upper temporal defect was noted, and she was referred to the Bascom Palmer Eye Institute for further evaluation. Neuro-ophthalmological examination on July II, 1978, revealed best-corrected visual acuity in the right eye of 20/25, with no light perception in the left eye, The right pupil reacted 2+ to light, and the left pupil was amaurotic. Perimetry demon­strated a dense upper temporal defect in the right visual field with extension into the lower temporal quadrant noted on the tangent screen (Fig. 1). Ophthalmoscopic eX'lmination showed bil.:lteral optic dtrophy, more marked on the left than on the right. Review of previous x-ray studies produced equivocal findings in the region of the sella and left optic canal. Due to the characteristic chiasmal field defect and questionable neuroradiological findings, the patient underwent a bifrontal crani­otomy on July 14, 1978. No mass lesion was iden­tified at surgery, and because the left eye had been 93 Chi,l~I1\,11 Optic Nt'uritis NAME CASt: , I t 1.f. , ----_.------ 0.1. July 11. 1978 V.. l.. _ .......L....._ VISUAL FIELDS , .."h.." Itl. T.. I • ~Jut .......:..;1i::,.~l~,~;;.~..;;:;;;~~;.;.:;,..;";'~~"'i~r- ." "tNrk p~t'tflle["· 10/H.) 11-11 PL C( Figure 1. ase I. Perometry how a dense upper temp rol def. I ,n Ihe rlght \'lSu.1 field eXlendinlt tnlo the lower tem""..1 qUJdrdnt wIth smaller ISO pierS The left eye IS .Jmauroti. amaurotic for over 7 months. a left optic nerve biopsy was performed. Examination of the left optic nerve specimen with multiple stains demon­strated markedly reduced myelin, decreased axons, astrocytosis, and scanty inflammation consistent with a chronic demyelinating disorder (Figs. 2-4). The patient's right eye vision continued to dt>­cline despite steroid therapy, and she becdme com· pletely blind in July 1980. Steroid were subse­quently discontinued in October 1080. At follow­up communicdtion in Mdrch 1082, except for blindness and rect'nt dt'velopment of bilaterdl CM­pdl tunnel syndrome, she had absolutely no neu­rologicdl complaints. Summary. A prC'viously he,llthy b I-ye,lr-old white fem.lk experienced sudden reduction in left eye visu.ll acuity to finger-counting .lCcompanied by other si~ns of optic neuritis which resolved with ..I,·wid Irc',ltfTll'nl. ller clinlc.11 Cl)U.,e fluctuated over the next 1\<! years, necessitating continued steroid therapy, After this period of time, left eye vision stabilized at 20/40, but visual field exami­n, ltion demonstrated only a small upper nasal is­land on the left. with an upper temporal defect on the right, A modest attempt at tapering the steroid dosage was followed by a sudden, complete loss of vision in the left eye which has persisted. Diagnos­tic work-up for an intracranial mass lesion was negative. Despite maintaining good vision in the right eye, progression of the upper temporal field defect into the lower temporal quadrant over the next 7 months was noted. A bifrontal craniotomy was performed because of equivocal neuroradiol­ogical findings in the region of the left optic canal dnd sella. There was no evidence of a mass in the region of the chiasm. Because of the amaurotic left eye, an optic nerve biopsy was performed which revealed findings consistent with a chronic demye­linating disorder. Right eye vision deteriorated fur- Journal of Clinical euro-ophthalmology .' Figure 2. J!'o{' I (H &, E. wath L X 40,) Th,.. (ru~s-~{' ...tlUn \.It th(" kft l'ptu: n~r\'(' J"·n1t.lO..tr,IIt.' .. Jl>,~nl "~rllrJI myt'i1n, mJr~edly r~duc~d l'~npherJI mvelln, Jrld ,nuN-.d cellulJrll\' dut, I, • .lstr" ...·vh.'SIS ... ." ~- ..,. " , , , ­. .' ., . .. -, . ", I•io·t. p ,. If • I~ • .~ ... - " - ".1. C""'IlIII" • ~.4,1_. ..•.•• fl•• .. ' . '. .. ..", - -. "- .. , ... ~. ., , .. '. + " .~, '- ~-.' ..' .. Figure J. (,)':0(' (H & L wlIh I 1501 ~\.ltkn·d .' ..Irmvhl""" ,...l ...."ll.lh·d with Jlftu..,· dcmyehndtion to thi .. t,lptil nC"t\fC" " ru....-..(·, tUlIl June 1982 9S Chi"'IIl.,1 ()plil N('uritis • "I· ''':. ........~" .~. ,. .'- ,., .'.'" ~ '," i' .· • '\' " ~.• .,:..,' . •e• ,• \ ~ "'l. . ". -. "'•• ,~. ~ .~, • '.,1' : :,' .J'. .. "l- .• ~ " '. '.' '" 41'. ,. ...... ' :;... , .~" ~' ".. ',\ .. ~. "'~~' ~!..' ~, ~••,. -.;.. ( " x· · · : ".---.' ':..A. - L dO' .•. , 6" ~ ~, - t'. ,.~~~ .(~ ., -:' __'I/o' ......... . ..' ~ ,,-, .. \ ,"', .,.... ~ • .J. '~. ,r...""._ '). ,,:" ••• , ..... ~"" ...'-, .':. I~ .~. "" -.•, ..rr~:,\4''.""..'.; .,J" t".,\':":"...r-.~ '. ..', ..' , ",' ,'. e.' J-• •• •• .,~ . .._.. .., t,) 0 • • • ,-~ ''',,'''~ 'III • ,.) • t~ '" .. .,,\ \...., ~t,' •, •,~ .. "'. "' , ,# ...~ ~ • ,. .. '\I:' e~ ",'.' ,\~. , ~.."".. ~ ".~ ..,..~, :'-.;.. :" \"'.~\ f 9 ? • : ,'., ~ .. _ ... \II • , • .., ". ' ~\. eO' \ ,. ..." t '" • . .~,..., .,- . "' t., . , ... ..: 4r.. ~. -. 11 .l7 -...l ,. -,.. .. . ,.. ..... • · ,~ t ,,' "1 '..... '•• " .' _ l figure 4. J>C 1 fB,.J'Jn. reduced fr,.m )( .\00 I '-<J!tcrcd. rcdud·d "curti," l.mJII. d.HJ... d\I'~1 J((" ('vldc-nl l'n lhr rl~ht "Idr \' In., \1pth. Il('t"\'(> \.(\I .... • ..('dh' O. but Jf(' .llm~'... t hllJlly Jbsent un thr Idl ~Ide There JrC' moln\, J ...... ~'lIJI d ol .. tr~'(\'tl( nudel ther until total blindness was sustained 2 years later. She hds been free of neurological complaints other than the recent onset of bilateral carpal tun­nel syndrome throughout the course of the disease. Case 2 A 37-year-old white male with a history of se­vere mij;raine headaches since age 12 requi ring Sansert and Gynergen injections experienced sud­den, profound, painless visudl loss in both eyes in January 1963. He denied any history of scintillol­lions, blurred vision, or pilresthesias Jccompanying the headaches, which characteristically stolrted with a feeling of uneasiness and occasion.ll nolU ea.•lnd progressed to a unilateral hemicrania, nH'. t (llm­monly on the right side. Past medical hi.ll1ry \\'.15 sij;nific,ml for labile hypertl.'nsion of .Ippn1'\i­mdtely 10-years duration. His vi ion rem.lined st.l­ble for 16 days, .It which lime he W.1S ('V.llu.lted .It thl' Bascom Poll mer Eyl' Institule. Neuru-ophlh.llmologic.11 ex.lmin.ltil'n on Febru­ary )5, J963, rl'vl'olkd best-clHrl'(tl'd "iSU,11 ol(uity of 20/100 in Ihl' right eye, .Ind finger'(llunting .II 10 fl in the Idt. Pupils Wl're .j mm bil.lter.llly, .md rl'.:I('ted 2-3+ 10 light, .}nd 4+ II' neM. Visu.ll fil'ld l'xolmin.:ltion demonstr,ll('d the pr('st'l1(e of bil,ller.ll ce('ucenl rol I scutumolS with definite nlldzon.ll telll­poral defe t~ (Fig. 5). t )phlh.llnlllsn'py reve.lled slight poll lor of the uptiC' disk .}l1d slight l1",rowing d thl' v('~~el~ on the I(·ft, but W.1S ,'lherwise unre­IllMk.\ blt,. Hl'c.IlI'l' uf tht, bitrlllpl'r.11 vi. u.11 field d,·r,·, I, .•m lnl LIl r"ni,I' m.l" IV." 'lI~l'r(led, .md he was promptly hospitalized for diagnostic work-up. Skull -rays, bilateral carotid angiography, and pneumoencephalogram were all normal. Lum~ar puncture produced clear CSF with normal opelllng pressure. one white blood cell, and 83 mg/dL of protein. Three days after admission, the patient became disoriented, with visual and auditory hal­lucinations and generalized muscle twitches. It was leolmf'd that he had been taking Placidyl for 2 to 3 vt'drs. often as many as 5-6 capsules a night. An EEG revealed no localizing abnormalities. His men­tal stoltus gradually improved over the ne t several davs. Follow-up e ami nation 2 weeks later revealed significant improvement in visual acuity to 20/25 in both eves. Central field examination showed bilaterJI c~cocentral scotom<lS extending towards fixation with sharp temporal borders and reduction of the bitemporal defect noted earlier (Fig. 6). The pJtient continued to improve over the next 2 months, with vision returning to 20/20 in the right eve olnd 20/25 in the left. and the visual fields were c~mpletely normal. Apprl)ximoltely 3 months later, the patient was found dead in his apartment, with hundreds of b.nbiturJte and other sedative containers scattered llll the premises. Autopsy performed by the Dade County Medical Examiner revealed a grossly nor­m. ll brain with no mass lesion. Death was attrib­uted to drug overdose. Summary. A 37-year-old white male with 25­ye. lr history of severe migraine headaches experi- Journal of Clinical Neuro-ophthalmology _______ O.h. h·" ....... tv I'. 1~1,1 T.. , ottlut. II no whll,' O.tl hH "I' Al_r" Iwr 1"""1 1'1 VISUAL. FIELDS Qle.lp".,,!J yhl •• !O/I(Jil _ lAf' ". Figure 5. Cd (> 2~ Bil~u."rdl cecoce-ntTdl '!io(otl,JmJ~ (l)t,tendin~ lnlO bllemplHoll mllJz,-""n.l1 defects enced sudden, profound, painless visual loss in both eyes and bitemporal visual field defects. Com­plete diagnostic work-up was negative for a com­pressive intracranial mass lesion. While in thl? hospital, the patient exhibited frank signs of sub­stance withdrawal, and it was then learned that he had been chronically abusing Placidyl, taking up to 6 capsules per night. After abstinence from the drug, his visual acuity and fields dramatically im­proved to an essentially normal state Approxi­mately 3 months later, the patient was found dead of apparent drug overdose, and autopsy revl?alt>d a grossly nonnal brain and confirmed the absence of a mass lesion. Discussion Bitemporal hemianopia is the hallmark of chias­mal disease. Its presence invariably prompts a search for a surgical lesion, since by far the most common cause is a compressive intracranial mass June 1982 lesion. As Roenne colorfully phrased it, "Most physici<lns no doubt feel inclined to vote for the presence of .I hypophyseal tumor as soon as an <lffliction of the chi<lsm h<ls been e t.lblished.":· On occ<lsion, however, the ophthalmologist may en­counter bitemporal hemi.lnopi.l which, .lfter e...­haustive neuroradiologic<ll studies, m.lY not be at­tributable to dn extrdchi<lsmdl compressive lesion. <lnd the possibility of other etiologies intrinsic to the chidsm dnd its supporting tissues must be considered. The noncompressive causes of bitem­pordl hemianopi<l are listed in Table l. Primary chidSnlal neuritis W<lS first described by Roennc in 1912,' dnd Idterconfirmed by Trdqudir,~ in reference to several C<lses char<lcterized by dcute dfft>ctions of d fairly rdpid course giving rist> to chi<lsm<ll-hemianopic visual field defects. This en­tity was noted to be similar to acute retrobulbar neuritis both in pathological features and clinical characteristics, such as age- and sex-incidence, on­set and course, and prognosis for recovery.~ These 97 Ld't Right, TABL[ I. oncomp,essi"e Causes of Bitempo,al Hemianopia o h,asmal LesIOns I Chid mJI up" n('untt.. A 1nn~lmmJh.'ry I. Muh,pll' "INClS" 2. Neun1mYl"'lItis ~lnd (,thtr dt'myC'hnJIIn~ dl~l'rdC'rt;, -,_ Id,,'p.lIhlc B Tv"c I. [,hcl",vvnl'l (PlaCldvl', ~. Phen,pra~lnc ICat,on ') II l)ph,... hIJc;,m.1tlt.•HJc:hn"ldlti... A P{\sUr.1UmJtll B. Postm('clitlu ... I. Local d. NJlI;l'ph.Hvn, . .. i~'u ...{'~ b aliI" Syc;,t<.'mll .1 ~vrhllt, b Tubt·null1"." , Oln." findin~~ ,u~~('sted th.ll the romnll'n nmJililll1 ,If retrobulb.lf llplit" nC'uritis rould 011 ,lrr.l~i,\O pr,'~· re'~ to, llr ('ven Mbe fwm. the chi,bm-prllJlIl'in~ h.lr,lrtni,tir Illr.llizin~ 5i~Il~. An illlp,'rl,lI1t fl'.1turl' llf th{' fll'ld Jefl'cl~, .IS m.leJ bv R,'enlH'. W.l~ ,1 tendenry III wJnd('r fwm llile p.;rt l.f Ihe flelJ I,l .111 lit her, wllh rapId Improvement llf prevl1l1l51y inv"lv{'d pllrti(ln~. Chl.,~m,ll llplic Il('urili~ i~ nlllsi l',lmlllllllly dUl' 1<1 mullirl!' 'rkn'~I' Thi~ ,1~~,l"'.lli"1l Ius III ,1St rn ('lIllv bl'I'1l rq'''rll'd ny S.lr"~ .111.1 Mcll?n, , ,1I1J "1"" I"r '" ,11 I fhe- 1,'lIl'r .1lIthllr_ l'i1l'J thl' Ji5p.1fitv -' Ncb,al d Menlnli:1t1S b Enccphaltl's C P,'>lhcmorrhJ!l1C o Inflamm.llN...- I Multiple de','sls E Id",path" III Va.cula, Jbnormaltl,es A Int,aeh'Jsmal hemJIC1ma B. Giant (ell artenll 1\' rl,.",fotlrJurnJII( <hl.J~mJI 5\'ndr mC' \' t'IIJsn'l.ll r.l\hl"nPl-r\.'~I~ ()rtl\. Nerve;" Lr"'h.'Ins I Tilled "pi'" d.. ~, '" II hl,emel\' l'nlJ'lled blind Sp,'IS III BdJIE"rJI ..:C'...·ll(E'ntrJI SCl"ltl"mJS R..'1In.,1 lC'~ll'ln~ ChloHl\.julne fetm...'pJth,,"" II S('ch,lr r("tamil, rl~m,mh.'1sJ belwef'n Ihl? frequent involvl:'ment of the optic l'hi.lsm by demyelination as seen on neuropatho­1,1~ j(,11 examination and the paucity of clinical re­p, lrts of chi.1sm,11 visUJI fil:'ld defects in multiple scleH'sis p,1tients. They suggested that careful vis­u, 11 field I?x,1mination of the asymptomatic eye, as well .1S screl:'ning of the central fields, could more freljuently detect chiasm.al involvement. Histopdthological examination of the left optic nerve of the patient presented in case 1 confirmed lhe presence of a demyelindting disorder. Clinical finGings, however, were not suggestive of multiple lou mal of Clinical Nl:'ur -ophthdlmology sclerosis in that, other th,ln .1 tr,lnsil'nt, mild hem­ifacial weakness prior to the onset of ViSlhll im­pairment and the recent devl'IClpn1l'nt of bil.ltN.11 carpal tunnel syndrotlH:', no llther nl'urologir.ll findings have been ,lpp.ul'tlt thn,ughl,ut till' 5-Yl'.H course of the dise.lse. It is thl'rC'fllrl' unlikely th.lt this represents .l C.lse Clf multiple sclerosis. Chiasmal demydin.ltion (.In .llsll bl' sel'n in neuromyelitis Clptic.l. Sever.ll c1inic.ll fl'.lturl'S of this dise.lse were 11l1t seen in this p.ltient. ~u(h .1S spinal cord invllivement with p.u.lplegi.l, ViSU.ll loss which r.lpidlv becomes bil.lter.ll, .lnd .lffliction typically of Yllu~ger p.ltients.; Oemyelin.ltil)J1 llf the chiasm and optic nerves may also llCCur in enceph.llt1meningomyelitis, but ag,lin, these pa­tients show significant neurologic.ll imp.lirnwnl.M In summ.lry of case I. therefore, we havl' a 51­year- old female with an aggressive, blinding, de­myelinating disorder which has not manifested any signs of generalized neurological involvement. This disease is not chardcteristic of multiple scierClsis or Clther demyelin.lting conditions, and thus is diag­nosed as idiopathic chidsmal optic neuritis. Toxic factors may also give rise to chidsmdl optic neuritis. The association between ethchlorvynol (Placidyl~), a synthetic sedative, dnd toxic ambly­opia hds been reported in two patients by Hdining and Beveridge,H and Brown and Meyer. llI Both cases demonstrated bilaterdl centrdl scotomdS and decreased visual acuity, with dyschromatopsia in one. Discontinuation of the drug was followed by gradual return to essentially normal visual status. Bilateral paracentral scotomas, reduced visual acu­ity, overshoot nystagmus, and slight macular de­generation was noted in another patient with chronic Placidyl abuse, which also resolved with discontinuation of the drug. IT Diplopia and nystag­mus have been seen in several other patients taking large quantities of Placidyl.l~-lr. In the patient pre­sented in case 2, it is reasonable to suspect a syndrome of chiasmal optic neuritis secondary to Placidyl abuse for several reasons. First, he ex­hibited typical signs of Placidyl withdrawal, char­acterized by appedrance after at ledst 3 days of confusion, disorientation, visual and auditory hJI­lucinations, and involuntary movements. 11 Second, his visual status improved over the next 2 months, with eventual return to normal visual acuity Jnd fields. Third, autopsy fdiled to reveal .In intracra­nial mass lesion or other gross processes that could account for the bitemporal hemianopia ob l'rved. Pheniprazine (Catron), a monoamine uxidasl' in­hibitor no longer available, was Jlso associatl'd with bitemporal visual field def" t . as wl'1I .IS other visual disorders."" I; Bitemporal hemianopid may on llCc.lsion b" the result of a chronic localizl'd infldmmatory prllCl'SS affecting the leptomeninges surroundlllg the chiasm and intracranidl optic nl'rvl's. This nllldi- June 1982 Rl'yn"ld~, mith, MlCr.HY tion, known as optochiasmatic arachnoiditis, was fir t describl'd by BalJdo and Satanowsky in IQ 2Q,'M Cushing in 1930/' and subsequently by numerous authors. Whether it is purely a se und­. lry response to .1 mort' generalized process or llCl"Jsionally .1 disease SU; i{l'ner;s .1S proposed by some r('mdin' cuntrov('rsial. From a liniCdl stand­point, however, is is sufficient to state that dS a consequence of various disease processes, such as infection and trdUmJ, d meningeal inflammatory rl'dction in the region uf the chiasm can occur, t.lking the form of constrictive fibrous adhesions, thickened arachnoid sheaths, and compressive cys­tic collections of subarachnoid fluid. These patho­logical ch.mges can subsequently produce damage to the visual system by compression or ischemia. Optochiasmatic arachnoiditis has been reported in association with head trauma.~I1·:1 locdlized infections of the nasopharynx and sinuses/! systemic infections such as syphilis~' ~.I-::. and tu­berculosis,~';-~ M cerebral infections such as menin­gitis and encephalitis,:!!I subarachnoid hemor­rhage,:~ l. '" and many other disease entities. Its re­lation to retrobulbar neuritis and chiasmal optic neuritis was noted by Hdrtmann, who found that constriction or compression of the optic nerves and chiasm by scarring was often moderate in contrast to the abnormal, atrophic appedrance of the nerves, suggesting that optochiasmatic arachnoiditis may not simply be a disease of the arachnoid with secondary mechanical damage to the nerve fibers, but an inflammatory process of both tissues in variable proportions."~ In 1975, Bell et al. reported a case of pdthologically confirmed multiple scle­rosis associated with optochiasmatic arachnoiditis. in which histiological examination demonstr.ated the presence of extreme demyelination and fibrosis of the chidsm and optic nerves. with evidence of long-term inflammation of the surrounding me­ninges."" They interpreted this as .l nonspecific meningeal response to adjdcent areas of inflJm­mJtilln .lnd concluded that progressive seclmd.H)' sCdrring of the leptomeninge may follow bl)th intraneural (e.g., retrobulb..H neuritis) and e\tr.l­neural (e.g., basilar meningiti ) inflamm.ltory pro­cesses. Optochiasmatic ,uachnoiditis remains a diJgm'­sis of e elusion, .lIld one whirh must be confi rmed surgicJlIy. Sincl' tr.ldition.ll neufllr.ldiologic.ll tech­niques cannot .1bsolutl'ly l'st.lblish this di.l~nl)sis. .1 neg.llivl' nl'urllr.ldiologic.ll invl'stig.lti\'n shou Id nllt prl'c1udl' ch iasl1l.11 explor.ltion in some l·.lses:" Other rMl' chl.l~mal causes of bitempor.ll hemiJnl)­pi. l include V.lsl·ul.lr lesilll1s, such .1S intr.lChi.lsm.ll hematomJ:,r , .lIld gi.lOt cell .uteritis,'''· the posttr.lU­mJtic rhiJsmal syndr me:l~ .lnd chi<lsmal r.ldione­cn, ·is."" In summ.1tion, the ophthJlmologist may OCCJ­sion. llly encounter bitemporJI hemi.lIl0pia in 99 Chi.lsm.II Uplit' Nt'urilis whi h evell the most (,.Hnest sl'.Hch for .1 compres­sive m,ISS is unsuccessful. Under these circum­st, mcl's, in ,lddilion to such entities as oploch i,IS­m. ltie .lr,Khnoiditis, thl' synd rome of ch i.lsm,ll optic neuritis should bl' onsidC'rcd. References I. RO('I1IH'. H.: U('b('r d.l~ vorkomm(,11 ('ilw~ h('mi.lnll­pi~ l'h('n z('ntrdlcn skol\lm~ bei Ji~~('minicrler ~c1('­f\ lSl' und rl'trobulb.lfN n('urili~. Klin. MI"l.. l.~bl. Au­~(' n/l('il/..d. 50: 440-448, 1'112. ., T r.14u.lir. H.M.: Acul(' rt'trobulb", n('uritis .IHe ting the llptk ,hidsma ,1Ild tr<lCI. Br. /. Ophth,llnwl. 9; 433-450, 1°25. 3. S.lCks. LG., and ME'!ell, .: Bilt'mporal visu.ll fi ....ld defe ts in prE'sumed multipl(' ~d ....ro i~. I.A.M.A. 234: 1:>0-72. 1075. 4. Spellllr, R.H., G),lser, '.5., .Ind Schatz, N.L: DemyE'­linoltiv.... chi'lsmall....sions. Arch. Neuro/. 37: 757-702, 1980. 5. RIW1111('. H.: On nlm-hypophyseal affection~ of thl' chiasmol. Acta Ophthellmol. 6: 332, 343, 1'128. 1:>. Traqudir, H.M.: Clinicell Perimetry. Henry Kimpton Medicdl Publisher & BooksellE'r, London, 1'157, p. 244. 7. Walsh, F.B. and Hoyt, W.F.: Clinic-ell Neufl'-oph­th, l/mo!tlgy, Vol. I prd ed.). Williams & Wilkin Co., Bolltimore, 1°1:>°. pp. 995-1000. 8. Gartner, S.; Optic neuropathy in multiple sclerosis. Arch. Ophthellmol. 50; 718-720, 1953. 9. Haining, W.M.• and Beveridge, G.W.: Toxic ambly­opia in a patient receiving ethchlorvynol as d hyp­notic. 8r. f. Ophtha/mol. 48: 598-600, 1'104. 10 Brown, E., and Meyer, G.G.. Toxic amblyopid dnd peripheral neurop,lthy with elhchlorvynol .lbusf:'. Am. f. Psychidtr. 126: 882-884, 1969 II. Flemenbaum, A., and Gunby, B.: Ethchlorvynco/ (pla­cidyl) abusf:' and withdrdw,,1. Dis. NE'n'. Sysl. 32: 188-192, 1071. 12. Hudson, H.5., "nd Walker, H.I.: Withdrawal symp­toms following ethchlorvynol dcpendenc!". Am. I. P ychiatr. 118: 361, 1°0 I. 13. Millhouse, )., DaviE'S. D.M., and Wr,'ith. S.R.: hroni< ethchlorvynol intoxic.ltion. Llll,et 2: 1251-1252, 1960. 14. Garzd·Perez, r.. L11, S., ,lOd Lopez, E.: Addi,lil'n llt ethchlorvynol: A replnt of tWI) l".l~('S. Me(/, Sen'. I. CJnJd,1 23: 775-778, 1%7. /5. Ropper. A.H.: Unusuol! nyst,lgmus "ft('r ('Ih ..-h Il,n'\'­nul use. /L('lt('r.) I.A.M.A. 232: 1.107. 11.175. 10. Wabh, F,B., ,Ind Hoyt. W.F.: Clillil'"l Nt'ur"-lll'h. th"lnwl.lgy, Vtl/. J. Willi,lnb & Will-.ill~ CII.. R"lti­mor('. 101:>0, p. 2588. 17. Ylteborg, I.: Optil" IH'unlp,lthy during tn',ltllwnt with (.Jtron. All.! (lphth.l/llwl. (KI'benh,lVnl olol: :177-37". /0('1:>. 11\. H,ll"d(l. M.. ,lnJ Solt.lIWW~"Y, P.: Tr.,I.lmil'nh' qui­rurgin l JI' 1,1 .ltnlfi,1 Je /,1 r"l'il,t. Arch. Ar,<:l'llt. Nl'lIrtl/. 4: 71, 1°2°, JLl ·u..hlng, I I.: Thr rh ••,..m.d ~ynJrlln1l' "I' prim'lf)' tlptil .Itrophy ,'nd bih'mpnr,11 fll'ld drfech In .,dults With ,I IHlrm.11 ",,11.1 Illn il.1. ,\r'dl. l )l'hth,'11l1l11. 3: SO;;·551. ,'1,10 ~O I" .. I. (,.. 1'"11"",,, M .....llhlim.Jrr.l. A...lIld finn·.l .: Posllrdumatic optochiasmdtic ardchnulditiS. Ann. Ophtha/mol. 8: 1313-1328, 1976, 21. Heuer, G.,., dnd Vail, D.T,; Chroni CIsternal arach­noiditis producing symptoms of involvement of the optic nerves and chiasm. Arch. Ophthalmol. 5: 334-349,1931. 22. Vail, D.: Optochiasmatic i1fachnoiditis: Importance of d mixed type of atrophy of the optIC nerve as a diagnostic sign. Arch. Ophtha/mol. 20: 383-394, 1938. 23. Hausman, L., Syphilitic ar<lChnoiditis of the optic chi.l m. Arch. Neurol. Psychiatr. 37: 929-958. 1937. 24. Ii VE' r. M. BE'lIer, A.I., and Behar, A.: ChiasmaI drdchnoiditis as a manifestation of generalized <lr<lChnoiditis in systemic vasculdr disease. 8r. }. Ophthd/mo/. 52: 227-235, 1968. 25 SChdUb. C.F.: Syphilitic optico-chiasmatic arach­noiditis. Am. /. Ophtha/mol. 24: 1313, 1941. 26. Scott, R.M.. Sonnldg. VK.H., Wilcox. L.M., Adel­mdn, L.S., and RockE'I, T.H.: Visual loss from opto­chiasmatic dfachnoiditis dfter tuberculous meningi­tis. /. Neurosurg. 46; 524-526, 1977. 27. Coyle, J,T.: Chiasmdtic ardchnoidilis: A Cdse report and review. Am. }. Ophthalmol. 68: 345-349, 1969. 28. FE'ld, R.. and Sicard. J.: Sur deux CdS de tubercule du chldsma. Rev. Neurol. 79: oo~-ooo. 19~7, 20. CraIg. W.M.. and L,lIie. W.1.: Chiasmdl syndrome produced by chronic locdl drdchnoiditis, Arch. Oph­tha/ mol. 5: 558-574, 1931. 30. McFadzean, R.M.. and Gow"n. M.E.: Optochiasmal ar<lchnoiditis after rupture of dn anterior communi­cating <lrtery dneurysm. Tran Ophtha/mol. Soc. u.K. 98: 490-493. 1978. 31 Lindenberg, R.. Walsh. F.B.. and Sacks. '.G.: Neu­ropJthology of Vision: An AtldS. Lea & Febiger. Philddf:'lphia. 1973. p. 24~. 32 Hartmann. E.: Optochiasmatic drdchnoiditis. Arch. Ophthalmol. 33: 08-77. 19~5. :13. Bell. R.A .. Robf:'rtson. D.M.. RosE'n. D.A., and Kerr. A. W.: Optochiasmatic ar"chnoiditis in multiple sclE" rosis. Arch. Ophtha/m0/. 93; 10 1-1°3, 1075. 3~. [r.l(i. G.. G.llligll'ni. F.. Gerllsa. M.. 5E'cchi, A.G.. Fiore, D., Zampieri. P.. Rigobello, L.. TomaZloli, L., PardoltS(her. K.. Marin. •.. and Scattolin. R.: Opto­chia matic dfdchnoiditis: A review of traditional neuroradiologicaJ diagnosis (l:"\2 cases, /951-1976). Al"t.1 !\Ipuro,hirurgil".l -l8: 151-170. 1979, 35. M.lill,md. CG, Abiko, 5 .. Hoyt. W.F., Wilson. C.B., .md Ol-..lmur,l, T.: ChiJsmoll olpoplexy: Report of four (.15es. /. Neufl1surg. 56: 118-122. 1°82. 3t,. W.llsh, F.B.. and H..,yt. W,F.: Clinic.il NE'uro-oph­th, llm,'!<l'>:\', \'(l/. 3. Willi.lms & Wilkins, Baltimore, (000 , pr. 2381-2383. :17. W.Ilsh. F.B., ,md Hoyt, W.F.: Clinicdl Neuro-oph­th, l/nHl!<lgy. Vol. 2. Williolms & Wilkins, Baltimore, 1°1:'0, p. 1883. 38. Wollsh, F.B.• and Hoyt. W.F.: Clinical Neuro-oph­th. llnl<l/,'gy, \',,1. J. WiIIi,lms & Wilkins, Bdltimore, 1°0°, pp. 2~07-2~q8. 3Ll Odl,md. M.: Bitemporal defects of the visual fields duE' to .momdlies of the optic discs. Act,) Neural. Sf,lnd. 43: 030-039, 1967. ~O. Coldh.lIl1lT:er, Y, and Smith, J.L.: Bitemporal hemi­olnopi. l in chloroquine retinopathy. NE'uro/ogy 24: 1135-1138,1974. Journal of C1inicdl Neuro-ophthalmology Acknowledgments Gr.\teful .\cknowledgml'nt is ~ivl'll tl' Dr. NI,rm.1I1 Jaffe for referring ,-.151' Z. to Dr. "'~('ph I'.HI.-l'r ("I' 1ll'1I­ropathology in C,lS(' I. Dr. a.lsi! Y,ltl'S f.'r llpl'f.ltll1g ,",hl' June 1982 RI'Ylwld~, Smith, Me rMy I, Or. Ill~('ph D,lVis fllr JutllpSy information, clnd Miss B.HbMJ Frl'neh for photllgrJphic Jssi~tclncl'. Wrile h'r reprints Ill: /.L. Smith, M.D., P.O. Box OIN\I'IO, Mi.llni, F111rid.! 33101. 101