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Show Atypical Clinical Presentation of Oculomotor (III) Nerve Palsy W. W. BIXE MAN, M.D. Abstract The dtypicdl c1inicdl presentdtions of three patients with an oculomotor (III) nerve pdlsy Me outlined. The first pdtient is d ol9-yedr-old with d painful, pupilspdring ophthalmoplegid of sudden onset due to a pituitary ddenomd which had eroded into the cavernous sinus. The second pdtient is a 7-year-old with a traumatic III nerve palsy who despite full recovery of her oculomotility, has been symptomatic due to a permanent internal ophthalmoplegia. The third patient is an S-year-old who has undergone prolonged optometric therapy for an "atypical esotropia," but in fact has a congenital III nerve palsy with oculomotor synkinesis and deep amblyopia. All clinicians are familiar with the typical clinical presentation of an oculomotor (III) nerve palsy (Fig. 1). An external ophtha/moplegi(l is present with the eye in (l position of abduction. slight depression, and intorsion. Oculomotility is limited only to abduction (intact VI nerve function) and incyclotorsion on attempted downgaze (intact IV nerve function), with small degrees of depression in abduction and limited adduction which does not go to the midline. Concurrent with these features is a paralysis of the levator palpebrae resulting in ptosis of the upper lid which fortunately will relieve the patient of the incapacitating double vision. An internal ophthalmoplegia is also present as manifested by a dilated (intact sympathetic innervation), unreactive pupil and paralysis of accommodation. Depending upon the etiology of the III nerve palsy, partial or complete recovery can be expected in approximately 48% of patients. I Recovery, when it occurs, usually begins weeks to months after the onset of the palsy and may progress with varying degrees of completeness. Some cases evolve into the c1inicJI picture of "aberrant regeneration" or "mi direction syndrome." Although typically occuring JEter III nerve palsies of aneurysmal or traumatic origin (Fig. 2), other etiologies have been reported. It has recently been suggested that acquired 0 u/omotor synkinesis is a more correct term for this c1inicdl presentation2 in view of the reports of primJry 0 ulomotor synkinesis:"" and "aberrdnt regener<ltion" after migraine.~· f, This report will describe three December 1982 pdtient with either In atypical clinical presentation llr pn>gression of their III nerve palsy. Pupil-Sparing Oculomotor (III) Nerve Palsy To some clinicians, all pupil-sparing III nerv palsies are diabetic in origin and all diabetic III nerve palsies are pupil- paring. While there is an element of truth to this generalization, one should be cautioned against the indiscriminate use of such an oversimplification in the clinical setting. In Rucker's original series,~ 86% (18 of 21) of diabetic III nerve palsies were indeed pupil-sparing but the remaining 14% (3 of 21) had incomplete iridoplegia. In Cogan's series of diabetic III nerve palsies,? 77% (17 of 22) were pupil-sparing while 23% (5 of 22) had varying degrees of iridoplegia. While it may be true that diabetic III nerve palsies rarely produce a fully dilated and totally unreactive pupiV some degree of iridoplegia may be seen in approximately 20% of cases. In this instance, the near reaction should be closely checked as a concurrent light-near dissociation with denervati n hypersensitivity has been reported with a diabetic III nerve palsy.M Conversely, nondiabetic pupil-sparing III nerve palsies are uncommon, but do occur. Extradural compressive lesions in the region of the superior orbital fissure and cavernous sinus have been known to produce III nerve palsies without pupillary involvemenl.!1 The many reported cau es of nondiabetic pupil-sparing III nerve pal ies have included cavernous sinus .meurysms.'" int('rnal carotid-posterior communic.1ting .1rtery .meurysms,. 1 transtentorial hemeation, 1~ temporJI 101:>(' astrocytoma/I pituitary adenoma, I~. 1'. tempor,ll arteritis, Ifi, I? ECHO virus infection,IM myasthenia gravis"!' sinusitis! meningeJI infiltration from chronic lymphocytic leukemi.1,~11,md IgG monoclon. 11 p.JrJproteinemi.1.~1 One presumes th.lt this phellllll1Cnon is prim.Hily due to the rl'lJtiv(' .111.1tomic.ll position of the snMII parasympathetic fibres in the peripheral oculomotor nerve .1nd the m.mner in which the nerve is encro'lChed upon by the p.1thology in question. Although .1 coincident ocul.lr ympathoparesis may simulate "pupil-sparing,"~~the proper diagnosis in this particular instdnce can be made with the appropriate clinical and pharmacological testing. 249 When .\ painful, pupil-sparing III ophthalmoplegia appears po toperatively after unrelated surgery. the c1ini ian is faced with a limited differential didgnosis. Patient I A 49-year-old gentleman suffered an acute inferior wall myocardial infarction on November I, 1981. Except for systemic hypertension. his background medicdl history was normal. He was left with postinfarct. severe angina decubitus, dnd on angiographic assessment had ignificant cardiac atheromatous disease. He was ddmitted to the Tucson Medical Center; on December 22, 1G8l, he underwent triple vessel, aortocoronary bypass graft surgery. On the first postoperative day, he was complaining of a severe, constant left frontal headache which required narcotic analgesia. By the fourth postoperative day, he was complaining of double vision and was noted to have limited oculomotility and a ptotic upper lid f the left eye. On examination, his vision ,·vas 20/20 in both eyes (right eye. +0.50 +0.75 cx 75; left eye, +1.50 +1.00 cx 145). Extemallv he had a total left upper lid ptosi (Fig. 3). Facial and comeal sensations were intact. There was no I.' ophthalmos or orbital bruit. Pupils were symmetrical with no anisocoria. Light and near pupillary reflexes were nonnal (4+) with no dilatation lag. Pupillary response to 4% cocaine drop was nonnal in both eyes. Oculomotilitv of the right eye was nonnal but there was I ij:urr 2. 1\ 2~·v,·",· .. ld wllh ,.",I"Ill,'I,,, '"nh.,,"'"'' :I nwnlhs ~ftrr lr~umalic right III nervI? palsy. NOlI? I\PrllI,,1 \,,,11111111.,1 "v,-Ild ,h,...urt". upr,,'r lu.t n·tr.l,,·ti,,'n in d\'\VngJle. -4 limitatic.: n of up and downgaze, and \ IIlld""h 1"'11 "I 1\1\""'1.11 n', lu ... "Co'" II~ r~) [ournal of Clinical Neuro-ophthdlmology Bixenmdn r;~u..· J. 1'.,1"'111 I (,,',. 'n') 1\ ·1~'''''."·,,ld w,th 1,.l.,J ","'rn.,1 "rhlh.lln,,'!,i<'gl,1 III Ih(· lefl ('Y". N"t,· 1.,t.\1 "I'I','r lid 1"'"'' .1".1 /'l'LII,,'" 1<'1' h,,!,"'ln'!,i... Figure 4. r~t,,,nl I (51'1' Ie II. rupil,~pJring III. IV. Jnd VI n"I'Ve palsie. ote minimal remJining sur"r,,'r rcClus mu )" function. dn obvious external ophthalmoplegid of the left eye (Fig. 4). The left globe was in d hypertropic ,md slightly exotropic position. There was minimal superior rectus function remaining which accounted for the relative hyperdeviation. Otherwise, there was no movement or torsion in dny field of gaze. Visual fields were full on confrontdtion and tangent screen examinations. A tensilon te twas negdtive. There was no ldboratory evidence of diabetes although this was considered dn unlikely diagnosis in this case, A CT scan demonstrated deminerdliz.:ltion and/ or destruction of the dorsum sell,1 (Fig. 5), ,15 well as the middle and left side of the sellu floor. An dbnorrnal soft tissue density was pre ent in the sella which extended into the posterior ,1nd left side of the sphenoid sinus and CdYernous sinus. Superiorly, the mas extended from 4 to 5 mm into the suprasell.ar cistern (Fig. 6). Follow-up c,1rntid angiography demonstrated a vague tumor blush in the region in question. On ]anudry I, 1982, this presumed pituitary tumor was managed neurosurgically from ,l tr,ln- December 1982 sphenoiddl dpproach. A preoperative endocrine assessment had indicated normal pituit,try function. The hemorrhagic tissue which was encountered urgically was removed. The neurop.'lthologlC.l1 picture WdS consistant with hemorrh.lgic inf.Hction into d pituitdry ,tdenom.t. His postoper,ltive C(1urse wa uneventful. His he,ld.1Ches pn' l11ptly subsided. but he hds required h(lrm(ln,t1 repl,KemenL He W.lS disch.arged on ].lnU,lry 20, 1082. On office follow-up on Febru.lI"Y 10, [0:32. his best corrected vision rem,lined 20;20 in both eves. He hdd no ptosis but did h,lVe .1 residu,ll left VI nerve pJresis (-2 under,lCti,1n L-LR),l11d III nerve p.lresis (-2 under,lcti,lll L-IRl. Bec.llIse llf the l)(1n- Qmit.mt rsodevi.lti,ll) due tll his VI nerve p.He-i , he Wol .lssuming ,1 left L1("e turn in order to see singly. By MMch 15, lQ82, his oculomotility hold returned to norm,ll (Fig. 7). 11 prism-cover testing. he h,ld 46 esophQri,l ,1t dist,lOce Jnd 86 esophorid at neM. Hi visu<11 fields rem,tined full. His stereOdcuity was now normdl (TNO = 60 seconds/ arc). 251 t kllh'111l1t,'r (III) Nerve 1'.lby Figure S. P,lIient I 1'1'1' 1"'11. Al:>n"rm.\1 ",fl I",ue d('n"ly ,n ,,'ft <ode "f ,,,II.lr fl"", .lnd (','endinl: 1.l1l'r.lllv 1111" re~l( n llf (.l\,{'f1WUS ,nu, Comment This patient had a totell, unilelteral, pupil-sparing ophthalmoplegia secondary to el pituitary adenoma which had eroded into his cavernous sinus and had pre umably undergone an apoplectic. hemorrhagic event. He clinically presented with a painful. postoperative ophthalmoplegia of sudden onset with normal visual fields. What is interesting is the report by Robert et Hlturt' ... I'.1 tol'"l I 1_"" t<-,o ,\\'nMnl,,1 ,,'t! I",u(' J('nsitv (.lrrowsl ,. h'ndlJt),: 'lIp\'n"r1v Inlt..1 ... upr.h.l,lI,lr l'l~t{'rll only 4 Ill.5 ntn) olJld ,l((OuntIll~ tl~r I.h J... ill ,Ill.l"lll.d 11\\'l11\"('I11l'nt lou mal of Clinical Neuro-ophthalmology Bixenman Fi~ure 7. r.,!I('nl I (,('(' Il"" Full r('n'v('ry 01 o,-ulomotilily II w('('I-., ~ft('r 'lIr~('ry. al. l " of ophth<llmoplegia associaled with pituitary lumors. In a retrospective review of 64 patients wilh pituitary tumors, nine (14%) had an oculomotility disturbance. Seven of these nine palients had a III nerve palsy, of which three had an associaled VI nerve palsy <lnd lwo <l IV nerve palsy. The remaining two of the nine patients had an isolated VI nerve palsy. Three of their seven patients with a III nerve palsy had iI total parillysis and all hild complele iridoplegiil. Four of these seven piltients hild iI "partial" III nerve palsy and varying degrees of pupillary sparing i1S well. (These piltients with a "partial" III nerve pillsy all hild pilrtial or complete ptosis with relatively little oculomotility disturbance.) Of importance, one-third of these patients had normal visual fields and eight of the nine piltients had iI gradual and progressive onsel of lheir oculomotility disturbance. The one patient with an abrupt onset presented with bilateral total III nerve palsies and pituitary disfunction, typical of pituitary apoplexy. Sev('n of these nine pdtients with an oculomotility disturbdnce had full recovery within 6 months. In comparing the pattern of pupillary involvement with the oculomotility disturbance in cases of III nerve pillsies due to cilvernouS sinus dneurysms and meningeomas,'" lhe degree of pdr.lsympilthoparesis paralleled the degree of involvement of the inferior division of lhe III nerve. Mdrked pdrilsympathoparesis was <lSsociilted wilh los of adduction (medial rectus) <lnd depression (inferior rectus), while lilck of parasympilthetic involvemenl was associated with full <ldduction and depression. This of course, would be the expected finding, knowing the route of the pdrJsymp.1thetic supply to the eye. The reported p<ltient is unique in Ih.1t hI.' h.ld virtually a total external ophth<llmoplegi'l with in- December 1982 volvement of cranial nerves III, IV, i1nd VI; however, he had spilred parilsympathetic supply of the involved eye. From the clinical stilndpoint, one USUJlly assumes that spared pupillary function indiciltes the an<ltomical integrity of the III nerve, regilrdless of the degree of the associated external ophthillmoplegiil. One is more optimistic, therefore, thaI full function<ll recovery will ensue. To dale, there hilS been no reported cilse of i1cqui red synkinesis (misdirection syndrome) i1ppe•.uing after a pupil-sparing III nerve palsy. Persistent Internal Ophthalmoplegia The integrity of the parasympathetic supply to the eye frequently is overlooked during the clinical follow-up and management of III nerve palsies. This is not surprising, as the external ophthalmoplegia is dramatic and the incapacitating diplopia is the p<ltient's primilry concern. One assumes that i1ny subsequent recovery from the pal v will equ<llly involve all components of III nerve' function, with the accommodative ,md pupillt)mOk)r recovery p<ualleling that of lhe ml)h)r .lspect. Although generally the case, one 1ll.1Y see p.1tients where a slight mydri.lsis is the ,)nly residuum of .1 previous III nerve palsy.~:l Ht)wevl"r. the slate of the accommod<ltive mech.lI1ism is seldom addressed. Patient 2 A 7-yc.1r-old girl W.1S initi.llly e"\,llllined t)n July 13, I Q81. in the intensivl' C.Ht> unil t)f the Tu(st)n Medic.ll Center. Lulier thdl d.ly, she h.ld bt>en in .1 twO-(.)f collision .lnd h.1d sllsl.lined .1 closed head injury with concussion. On ex.1min.ltion, she had an isol.ltl.'d, llllal right III Ilerve palsy. The remainder of her neu rologic.ll and neuro-ophthalmic examin. llions were unrem.ukable. Her b<lckground ocul.u .1Ild medic.11 hi tory were negative. 253 Fil:ure 1\. 1'.'tll'lll 2 1'<'1' 11"11 A 7,vI'"r."ld w,th t,~um~t" right III nl'rvl' p"J,y I h"", ""I'''''~ 1,,11", IlVII' p.lrll.ll n,'lt.very. By her first follow-up office visit on August 4, 1081. there alreddy WdS improvement of her oculomotility and ptosis (Fig. B). She had a dilated. 5.5-mm right pupil which was unreC!ctive tIl both light dnd neM responses. Her vision was right eye. 20/50-2, being unable to read 1B print; and left eye, 20/20- I. reading 11 print with ea e. Her best corrected vision was right eye, 20/25+2 (+1.50 +0.75 cx 100); and left eye, 20/20-1 (+ 1.50 +0.25 cx BO). On follow-up on September 3, 1°81, .he wa complaining of headache while reading .1t school. Her mother had n ticed that she would close her right eye while reading or watching televi ion. On examination, her uncorrected vision was un· changed-right eye, 20/50-2; and left eye, 20/201. Her anisocoriC! and unreactive right pupil were unchanged. She had no ptosis. Her duct ions and versions were full except for a residual weaknes in the right inferior rectus (-3 under.lCtion). On prism-cover testing, she manifested b~ X (T) .It distance and near with .1 small A-pattern present. With full pectacle correction of hN hypermeIropic refractive error, she re.1d 20/25+ I wilh her righl eye, and with .1 + 1.50 add, she re.1d 'I print. Her near point of accommod.1110n (NPA) with full spectacle orrection W.1S 1.5 dioptres wilh hcr right l'ye .Ind 12.5 dioptrc~ with h('f left. Withl11lt spcc· 1.1 Ie orrl'rtion her Sler('ll.lCuity W.1~ pl,,'r (T 0 = 480 "1',·ol1lb/.lfl) but improved signifir.lntlv with corrl'rlilln (TNO = 120 serllllds/.nl). . It W.l~ llbvlllus Ih.1t despite .1111111St full fl'C,'VCrv llf the molor romponC'nl of III nerve functil1n, sh~ h.ld .1 virtu.llly complete intern.11,'phlh.lll1111plC'gi.1 with .1 mydri.llic unre.KtivC' pupil .md .m .1lT,lm· mllJ.ltivl' p.ll"y. RI'.IJing gl.lsscs were pfl'scribedright eye, +3.00 +0.75 r\ 100; I£'ft I'Vl" + 1.00 +0.25 n. 80. (Hifol·.llll1rrl·rtilln W.IS rdlls~d bv b"th rhild .1I11J p,nl'nh.) . -. I On follow-up on October 23, 198L she had full recovrrv of her oculomoldity (Fig. 9). She now had minima'l right upper lid retraction in levodeorsumver ion as the only sign of an acquired synkinesis (Fig. 10). Her internal ophthalmoplegia remained unchanged. There was no evidence of synkinetic pupillary reaction. On prism-cover testing, she was orthophoric at distance and manifested 6.l exophoria at near. Convergence was nonnaI (no miosis "f right eye, howeverl. Her ductions and versions were fuJI with no A- or V-pattern. Her stereoacuitv was normal with correction (TNO = 30 seconds/ arc) but reduced without her glasses (TNa = 240 seconds!drC). On subsequent follow-up visit ver the next b months, her presentation has remained unchanged. Her internal ophthalmoplegia has demonstrated no sign of recovery and whenever an attempt has been made to we.tn her off her glasses, her headaches and monocular eyelid closure return, Cllmment Thi!' child i. fl'lrtunate to have made such a dr.1m.1tic reC'l\'er\'. as onlv 38% of traumatic III nerve p.llsies den~,)nstrate impnwement. 1 She has, however.•1 perm.1nent internal ophthalmoplegia with mydri.1sis .1Ild accommodative palsy, which 10 nwnths later ha. as yet demonstrated no sign of re«'Very. Thi!' uncommon presentation is not addressed in the st.lIldard textbooks of neuro-ophthalmology, but "bvi"usIY C.111 be a source of patient complaint. Without the proper spectacle correction, this child was symptomatic with asthenopic headaches and volitional eyelid closure. With correction, she has remained symptom-free and has enjoyed nonnal stereopsis. Journal of Clinical Neuro-ophthalmology Bixenm.1n Figure 10. PJllCnl ~ (,ee tC'l). Nlllc right uppcr lid rclrJclilln In d"wl1-left gJzc. (n traumatic III nerve palsies, one typically finds on pathological examination either avulsion of the emerging rootlets at the ventral midbrain surface, contusion necrosis of the proximal III nerve trunk or intraneural and perineural hemorrhag s at the level of the superior orbital fissure.~·' The reason for the selective la k of recovery of parasymp.lthetic innervation in this case is peculative. Agdin, one can only assume that it i the anatomical location of the parasympathetic fibres in the peripheral III nerve trunk and the manner in which the nerve is injured which produces this unique presentation. An "Unusual Esotropia" in Childhood The clinical presentation of the "misd i rection syndrome" is so typical that the features ,He virtually pathognomonic. Problems aris(' wh('re th£> diagnosis is missed and inelppropriate m.lnelgement is undertaken. Patient 3 An 8-year-old girl was reviewed on December 1, 1981, for assessment of eln "unusual esotropi.l." December 1982 Historicellly she was the product of a full-term, uneventful gestation and atrdumati forceps deliver. No known history of birth or neonatal trauma is available. A crossing of her right eye was ncted by the parents shortly elfter birth. Her growth and development were normal there.lfter. The crossed right eye remained unch.lIlged with age. In her e.lrly childhood he W.15 reviewed bv dn optometrist who di.lgm)sed .1Il "unu_ u.ll child'hood esotropia." No tre.ltment IV.1S .ldvised .It th.lt age. At .lge 6 ye.Hs, "in-depth VisU.11 tr.lining," "hand-eye cl)ordin.ltion e ercises:' .md of Cl)UrSe, spectacle correction were .lll begun. She failed Il) respond to this treatment progr.lm despite ll~ years of effort. The child's p£>di.ltri i.1I1 requested J second opinion. On rx.lmin.ltilHl, her visillil W.1S .1Il unimpnwablr 20/200 in thr right rye .lnd 20/20 in the left. Thrre W.1S no signific.11lt .lnisl)metnlpi.l present (right eye, + 1.00 +0.75 ex 00; left eyf?, +0.50 +0.50 cx (0). Fix.ltion with hf?r right eye was wandering .lnd unste.ldy. In prim.lry position, she m.lI1ifested approximately 20~ esotropid elnd 15~ right hypertropia (Krimsky corneal reflex testing). Pupils were equally reactive (4+) without anisocoria or afferent 255 figure II. 1','11<,,,1 ,\ (,,'t' h"" 1\11 ,~'V."tr."IJ w,th • "nl:,'n,I,oI fll:ht III n"I"\' 'pJI", :-,;,,1' dJ"'lJI ft'Jlurc" l'( "n"... dlt(" (11..111 ,\,Ildrlllllt' .. I iJ.;ur~ f~_ ~.llnl- p.III'·IH.h In ll,t;. .2 .\fkt .,It.lbt~mll:- "ult:.l,'r~ ~l.llh,:nl Jl.l=- "In~n.· \1"'1"·,, III prlln..HY r\...~Il1\ln .lnd ('\- tO~ tl' ('Ither ...,de \' \h.ll1~t." In ..lb,,'rr..1I1l tnn,,·r\'..1lh..ln.l1 r.ltl('rn l,f l'Ve' Tlh'l\"('nll'nt--. pupillary def ct. Motility of the ll?ft eye W.1S full Jnd unrem,Hbble while th,ll of the ri~ht eye \\'JS defi nitely Jnom,llous (Fig, I I), H,lrizont,ll e,\(tl rsion of the right eye were full ,1lth,lugh she developed ,1 10- f 26 right hyperdevi,lli,'n in rlghl gJZ(', Although n,l ph1sts W,l~ present in prim,lr:.' p,,~iti'll1, ~hl' dcvel,'ped ,I 2 t,l 3-111111 right upper lid pto... i~ in full 1,1ter,11 g.l?C Itl either sid,', SIll' \\'.lS un,lbll' tlll'll'v,lle her ri~ht eYI' ,1ny llwre th,m ,1 fclV degr('('~ ,lbllV(' h,'rizl'ntJI ,lIld ,my ,1tlempt .It upgaZl' wlluld l'licit ,In .Iddu,tilln nwvrnll'nl. O,llVng, IZI' W.l!'> ... illlil.lrly limiled ,md 1V.15 ,lSS11,i.lled with ,I p,lr.1Jllxir.ll right upper lid rl'tr.llli,ln, Thl' rl'll1"inJer "f her IlculM .lIlt! lH'llr,,-,lphth,llmil I'X,lll1ll1,ltilln" were 11l1rlll,11. Her p,Hellls deIlilwd "llrgll.11 .1Iognl1H'nl I'l this ('s"tr,lpi,l eye, ~lll>"'I'Ljul'nt ,lltl'mph ,It 1ll',lu.. illll ther,lpy h.1\'<.' been unsu,cessful due t,l b th p.lfenl ,md patient ct1mpli.lI1ce, Cllmment This child h.ls the typicJI clinical features of the "ll1isdirecli,ln syndwme," presum,lbly of congenil. ll 'Irigin. This c1inic,ll picture when fully develI) ped .l~ in her C.be, is permanent and obviously will ntlt respl)nd It) .my form of optometric "visual IrJining" ,)r "e'\ercise program," It is gener.llly fell th.lt virtually all congenital III nel\'(' p,llsies demonstrate varying degrees of oculllnllll,' r syn \...inesis,~:·'~.; Infrequently, one can obI. lin ,1 histtlfy of birth trauma or forceps injury to suggest thJt this clinical picture is one of an acquired ,)culomotor synkinesis secondary to a traum, ltic III nerve pJlsy.2h Otherwise, one is uncertain Journal of Clinical euro-ophthalmology whether or not such .1 "misdirection ~vndrtlln(''' is nuclear or infr.lIlude.H in origin.~ . Wh.lt is unftlrtun.ltC' in this ('.ISt' is th.lt the profound str.lbisrnic ,unblyt1pi,1 h,IS bl'{,ll ll'ft un" ttended ttl thn1ught'llt her childhtlod. ~h-r pfllgnosis fl'r ,my dC'gl't'l' tlf visu.1i l'l'h,lbilit,ltioll ,It this pt,int is pt'lll' ftll' IlI.lIIY I't'.lStlllS. The incidence tlf .1Inblyllpi.1 in thl' p,ll'l'l il' l'y~' ill t",lS('S tlf t·llllg~·llit.11 III Ilt'rve p.lbY is Sll higll~:' ,IS to be ,llnwst inevit.\blC'. R.lrely, the child m.IY p.H.Ido\ ic.lllv fi\.lte with the p.H('tiC l'yl' .1Ild tkvclllp ,m .1Inblytl pi,1 in the Iwnp.H('tic (,yl'.'7 Thl' c1inici,ln wht) de.lls with poH.\lytic str.lbisrnlls ill ,'hildhtl'ld must never lWt'rllll'" till ptlssibility tIl' sellsory ,Idapt.llit)ns (by suppressitlll, ,lmblyopi.l, .1Ilt! .lntmlaltlllS I'('tin.ll Ctlrrl'SpllnJ('nce). wh ich m.1Y ,wersh"t!tl\V .my subscqu(,llt recov('ry. M,lIl"l;;t:. ment in these difficult c.lses shtluld be left in the h,mds tlf the pedi.ltric tlphth,llmllltlgist who is experienced in h.1I1dling the sen, ory .lspects tlf childht) t)d str,lbiSl11l1s. _ urgic.llly, ')Il(,'S go,ll is limited tt' ,Khieving t'cubr .Ilignment in primary position [Fig. 12), ,15 the .lberr.1I1t mt)ti lity p.lltern C.1I1 abvit'usly not be ,\Itered. Summary Clinicians are familiar with the typical presentation of III nerve palsie in the elinicill setting. The purpose of this report was to outline three cases which were unusual in either theil' presentation or progression. Most pupil-sparing III nerve palsies are diabetic in origin and the progno is f I' rec very is excellent.' ·: Nondiabetic causes are uncommon. but have been reported.~-::I Most of these cases seem to have in common, involvement of the III nerve in or around the cavernous sinus or superior orbital fissure. As in patient 1, pituita ry adenomas seem to have a propensity to produce this eli nical presentation. ll. I:, The chance of recovery from a III nerve p,llsy depends upon the etiology in question.' When it ensues, recovery may b(' variable <1nd inc mplete. The status of the accommodative mechanism is not often addressed but as in patient 2, J persi tant intemal ophthalmoloplegia may be iI source of asthenopic symptoms. As opposed to paralytic str<1bismus in <1dults, children run the ri k of sensory adJpt<ltions to thei I' motor misalignment. This is puticul<lrly a problem with congenital III n('rve pdlsi('s.'" As in patient 3, a profound strabismic amblyopiJ m.ly develop if appropriate management is not undertaken .1l .In early enough age or if the di<1gnosis is mi%ed. References 1. Rush, ).A., and Young(', B.I<.: I'.lr.llysis of a,lIli.11 nerves III, IV, and VI. Arch. (Jphth,l/mpl. 99: 7,'-7Q • 1981. December 1982 Bixenmdn Z. Lqlllfl', FL, ,wd C1,lsl'r, 15.: Misdirection revisih ·d-A nilit"l ,lppr.lisJI of ,Kquir('d oculomotor nl'rvl' synlo.inl'sis.Arch. Ophth.l/nwl. 98: 2206-2209, I ()1l0. J. ~lh.II7.. N.I .. ~.Ivin(l. ".f., Jnd Curbptl, I.J,: Primary ,I [",rr,lIl I "I ullHnlltor rl'g{'ner.llion: A sign of intra(. IVNn(lUs nwning{'oll1.1. Ar ·h. N{'urol. 34: 29-32, IQ77. oj. to', T.A .. WlirstN. f.H., .Ind (;odfrl'y, W.A.: Prim, Irv .Il",rr.lnt <ll ulpmutor l'('g{'lwratiun due to Intrdl r.1Ili.1I .1IlC'lIrysm. Arth. Nr·ur"l. 36: 570-571, 197 5. ll'l ),ly, I., Hillson, F., ,H,d King. I.: Ophlhalmoplq~ic llligr,linp .1Ild .l[wrr.lnt l'('gt'nC'rJtl(l11 of oculomotor nNW. Br. J. ('phth.llmo/. 64: 534-53b. I Q80. l'. RlIllo.l'r. CW.. I'.lr.llysis of third, fourth, dnd ixlh ·r.lIli.,1 Nl'rvl's. Am. /. Ophth,l/nwl. 46: 787-7°4, 1%1\. 7. C"ldstpin. f.E.. .lnd Cogan, D.C.: DiJbeti ophthalmople! 4i.1 with ~P{'Ci.ll rdpren(' to the pupil. Ar h. Ophth.l/n10/. 64: SQ2-600. IQ60. 1\. ilmore, P.c.. and edrlow, T).: Di.lbell 0 ulomotor paresis with pupil fixed to light. Neurology 30: 12291230, 1080. 0. Ct g,ln, D.C.: Neurology of the 0 u/<Jr Muscle (2nd ed.). harles C Thomas, Spnngfleld. III., 1956. p. 15b. 10. Trobe, ).0., Cia er, ).5., and Post,/.D.: Meningi0mas and aneurysms of the dvernous sinu . Ar h. Oph/ hdlmol. 96: 457-467, 1978. II. Kdsoff, I.. and Kelly, D.L.: Pupillary spdring in ocu10motof pdlsy from internal cdrotid dneurysm. I. Neurosurg. 42: 713-717, IQ7S. IZ. Keane, I.R.: Ocu) motor poll y with pupilld~' paring in subdurdl hem<1toma. TW0 .lses With documented tentori,ll hernedtion. Mt. S;nd; I. Med -tl: 101-lb5. 1974. 13. a,S. ., Leiguarda, R.C., and H.lnkinson. I.: PupilI'lry sparing in oculomotor palsy from tempor.ll I,lbe dstrocytomd. Report of two cases. Act.1 Neurl,l. Latinodner. 22: 27-30, 1071:1. 14. Mead0ws. S.P.: Unu_ual liniell fe.lture.•llld modes f pres ntdtion in pitUItary adent'm,l, Including pituitary ap0plexy.ln Neun')-Ophth.llmtllt'g~·(.lIh ed.). I.L. Smith. Ed. C.V. Mt')sby Co.. _t. Louis. lOcoS. p. 178-170. 15. Robert, .V.. Fei!4 nb,lum, I.A .. •lnd St rn. W.E.· culM p.llsv t)t"curin~ with pituit.l~' tunh'rs. I. Neurl" lIrg. 38: 17-lll. 11l7J. It,. Me.ldlwvs, S.P.: T('mpl'r.ll IH ~i.ll1t (l'lI ,Ht('ntl~) phth.1Jmic Aspe(15. In clIrl'-l)phth.l/nlllJ.I~~· (.nh ed.). 1.L. Smith. Ed. C. V. Mosby II.. St. LOUIS. IOt,g. pp.14g-IS7. 17. Cr,lh,lm, E.. Hl'lI.md, A., A\'/:'~,. A.. et ,11.: Prll~IW"5 in ~i.IrlI-(eIlMtt'ritis. Br. Mtd 1.282: 2t,Q-271. logl. 11\. Hertenstein, I.R., S,lrn.l!. H.B.. ,Ind L)' 11ll1wr. n.M.: Acut,· unil,ltt'f,d llClllt'nwhlf p,llsy .15St)(i.lted With E 'Hl)- III vi r,11 il1ft't'til'I1~. I. ['ed,.ltr. 89: 711_g I. Il17l'. I'}. L)~I)('r, R.H.: MY,'51Iwni<: '\lcull'm"lllr" p,llsv. Ann. ()l'h/h.1111ll11. II: J I-.q. 1'17ll. zoo Smith, H.I'., Bill,'r, I .. ,1I1d Kelly, D.L.: L)(UltllllOtl)r p,llsy with pupill.lry spMing. Ctllncidl'nt,,1 ,1IlPurvsm ,md ,'hn>ni, Iymphllt"ytic mcnin~t·.11 infiltr,ltion. Stlrg. N('unll. It>: 2,'-2'), Ill8 I. ZI. RlI~~I('s. K.H...mel M.15. ey, E. W.: Pupil-sparing oc"(,, mollH p.,15y '"C m"nodon.ll pJr,lproteinemia. Ann. l )l'hth,JI'lIl,l. 13: 875-87l', 1981. 257 2S. 23. I{,'lll.lll- .1111PP", C., .\Ild Ldw.1rd .., ".R.: 1'.lIl1lul "phi h.ll111"hlpk~i.l:t ),'UI"I1H",'r Ill·rv,· p.,I ..y wllh"ul 111vdn.",,,, dul' hI "'lllpn·.... Il.1l by .11H'lIry"l11. f 1".Il/- .Il Ill' I~: ·jJ-.Jt'. 1"7<). W.,I ..h, r.II., .1I1d H"yl. W.I.: ( III,;, .11 "un.-ophIh. llllh'/"J.:\, (. I'd ,·d.). Wof',.llll" & Wof""h (omp.1I1 . II.ofllll",r... '<'I,Q. p. 25" 2·1 11<-111/1'. I.: ('1'.,",." ,wrVI' ,lVlIl"oll ,1I1d "th.. r '1£'111'." Injun,·.. ill nud ,lI·,·,d"I1I ... M,·d. I All../' 2: I24t" I ll",l.) , Vil hII', n.l.: Tlw Ji.lpw".. " '"111(('11110.11 untl.ll('r.,1 third IWrv.. 1'.II..v. BI',IIIl 99: 71 1-7ftl, IQ70. 20. HJrley, R.D.: PMalytic strabismu in ch"dren-EtiIlugi in idence and management of the third, rourth and sixth nerve palsies. Ophthalmol. 87: 2443, J980. 27. Ko.IzMidn, LL., clnd Flynn, J.T.: Congenital third ,1('rv(' pdlsy with ,amblyopia of the contr,aJ,ateral eye. I. l'e-J;,,'r. Ophthalmol. 5trdb. 15: 366-367, 1978. Write- or reprints to: W. W. Bixenm,an, M.D., 1500 North Wilmot ROcld, Suite 130-A, Tucson, Arizona 115712. Journ,al of Clinical Neuro-ophthalmology |
