EEE Tonic Ocular Tilt Reaction Simulating a Superior Oblique Palsy Diagnostic Confusion With the 3-Step Test Sean P. Donahue, MD, PhD; Patrick J. M. Lavin, MD; Latif M. Hamed, MD Background: The tonic ocular tilt reaction (OTR) con- sists of vertical divergence of the eyes (skew deviation), bilateral conjugate ocular torsion, and paradoxical head tilt. The head and superior pole of both eyes are rotated toward the hypotropic eye. Objectives To describe ocular motility and torsion find- ings in 5 patients with OTRs that mimicked superior ob- lique palsies (SOPs). Results: In 5 patients, results of the 3-step test sug- gested an SOP (bilateral in 1 patient); however, no patient had the expected excyclotorsion of the hyper- tropic eye. Two patients had conjugate ocular torsion Gintorsion of the hypertropic eye and extorsion of the hypotropic eye), and 2 patients had only intorsion of the hypertropic eye. All had other neurologic features consistent with more widespread brainstem disease. Conclusions: Vertical ocular deviations that 3-step to an SOP are notalwayscaused by fourth nerve weakness. When ‘ patient with an apparent fourth nerve palsy has ocular torsion that is inconsistent with an SOP, OTR should be suspected, especially vestibular system or posterior fossa dysfunction coexists. The rules or the 3-step test foran SOP, may be fulfilled by damaging the otolithic projections cor- responding to projections ofthe contralateralanteriorsemi- circular canal. Because results of the Bielschowsky head tlt {est may be positive in patients with the OTR, the feature distinguishing OTR from an SOP is he direction of torsion. We advocate use of a fourth step—evaluation of ocular torsion —in addition (o the standard 3 steps. Arch Ophthalmol, 19995117:347-352 From the Departments of Ophthalmology (Drs Donahue and Lavin), Peatics (Dr Donahue), and Neurology (Drs Donahue and Lavin) Vanderbilt University Medical Center, Nashville, Ten; and the Florida Eye Specialist Institute, Gainesville (OrHamed) Downloaded From: https: HE 3-STEP test was estab- lished by Parks! to iden- Lily the paretic muscle re: sponsible for an acute eyelovertical strabismus. Kushner? recognized several pitfalls of the 3-step test and identified skew deviation as | disorder that can mimica fourth nerve palsy The ocular counterrolling reflex isthe basis fr the third component ofthe 3-step test. When the head is ulted to 1 side, the lower eye supraducts and intorts and the fellow eye infraducts and extorts, This re- sponse occurs because of central projec- tions from the semicircular canals and oto- liths to the ocular motor subnucle! (Figure 1). For example, head tlt to the lefLexcites the intorters ofthe lefteye (su- perior rectusand superior oblique) and ex- tortors ofthe right eye (inferior rectus and inferior oblique) while inhibi terrolling rellex is compensatory only for approximately 10° of rol; vertical and tor- sional fusional amplitudesare sulficient 10 prevent diplopia in the normal situation. A patient with a unilateral superior ob- lique palsy (SOP) develops an ipsilateral hypertropia because the depressing and in- torting functions of the superior oblique are diminished (Figure 2). When the pa- tients head is tilted toward the paretic side, the hypertropic eye supraducts because the remaining intorter—the superior rec- tus—is activated, producing elevation. Vertical semicircular canals provide phasic innervation during dynamic head tilting; ocular alignment is then tonically ‘maintained by similar signals from the de- pendent (lower) otolith. Skew deviation is 4 supranuclear o prenuclear vertical strabismus caused by dysfunction of these vertical vestibulo- ocular reflex (VOR) pathways. It occurs with posterior fossa lesions, particularly those affecting the brainstem tegmen- ‘um, cerebellum, and midbrain.*” Such lesions may be structural (stroke, trauma, or tumor), demyelinating, or neurodegen” erative, although skew has been de- scribed with idiopathic intracranial hy- pertension.”° Ocular misalignment in skew (©1909 American Medical Association, All sights reserved. jamanetwrork.com/ on 06/20/2020‘rg a try Popetens Tea Ca lente Praions @ Figure 1. Neuranatomicl pathy subsenng te vereal vestibul-oulr rel Each ofthe 3 semicteulr canals projets fo 2 etaocaar muscle sacl n each ie, eset of projections toa eyelovertcal muscle and itsconraatral yoke) seein whereas rectors ote antaganist ur canal hasan and yoke right Inenor eas. Te poster semerea cna proets ina smi fstian {othe ote 4 cjeloverea masls Otol pathways ae ss el kok Burra rc sane macs day sn pad. Fm ard Zee SA inte superior fetus 1, nea bleu, 1 iror (cts 5, sper blue esl uc fot esonar fue: 1 ocr nucleus Bc, vachiom eonlurctvuns ML, medal fongtudinal accu’ VI, vents opment pay SU, senor vestibular nuts’ Lal estou nucleus MV, med ves hile tenor vestibular mucus: Pr reposts nace’, abdceus rues: AC, ante semiciul canal PC posterior secre cana, 1nd HO, ronal semiieala aal. deviation may be comitant oF incomitant, may simulate 4 paresis of an extraocular muscle," and may alter nate with time!? or with gaze direction." The ocular tilt reaction (OTR)” is particular of skew deviation, consists ofa triad of vertical d Figure 2. The ocular countering ele tog causes a compensatory ‘jlraton of bath ees fo manta the subjective sal vera On et head it te cg eyenraduet ard exycotarts ard te fee sypraduets ndings eave othe positon of he ead and tue wert Velo soa are encoded byte semiceula eal, The eyes malian {his positon tonal because eat nuts fom te ure and sacle ‘antes fhe ove ea. Ina ght superior obgue pay ida ih, igh ee extred because fe ck a intorsian fom he parte for bigue ceased ac othe ero —the ht superior acts caees a hypertopa at worsins when mare inorsion ‘lemande yang te head tote nigh (mil et} et oct ‘eacton caused by abnormal ite vertcalestbulo-gelr telex Projections rm the le vesibl system causes af hypotonia wt biter toson ne decton of baat lower ig) For each ee, he Ine though the comea represent he lorsonal erica ans. tion, head tilt in the direction of the lower eye, and bi lateral ocular torsion in the direction of head tilt (Fig- ture 2). The amount of ocular torsion may be syrmmetri- cal or asymmetrical. Halmagyt etal! and others! noted that a tonic OTR can be produced by injury to the utricle or the vestibular nerve or by stimulating the otoliths,” utricular nerve," semicircular canals,” or midbrain.” Like other forms of skew deviation, OTR may be associated with diplopia or signs of brainstem dysfunction, stich as pendular nystagmus, Patients with OTR may also per ceive the subjective vertical as tilted. We describe 5 patients with OTRs that simulated SOPs using the 3-step test. In each patient, however, oct lar torsion was inconsistent with an SOP. We hypoth- esize that asymmetrical dysfunction ofthe otolithie ves- ular projections, corresponding to projections of the anterior semicircular canal contralateral to the eye with apparent SOP, is responsible ss ]#+_$€ CASE a old man had a history of intractable diplopia af- + 2severeclosed-head injuries sustained 3 years apart and years before evaluation. He had allt head lt of approx 10°andaslight eft face turn (Figure 3). Visual acu- ¥y was 20/40 OD and 20/60 OS. He had bilateral torsional nystagmus, worse on side gaze. His pupils were normal. ‘Ocular motility demonstrated +2 overaction of the right inferior oblique with 1 underaction of the right superior oblique (Figure 4). In primary position, he had an & prism diopter (A) right hypertropia that measured ©1999 American Medi Association, All rights reserved.12. in left gaze and 6 A in right gaze. The right hyper- twopia was 15 \ on right head ult and 5 on left head Ul. However, results of double Maddox rod testing dem- onstrated 5° of intorsion of the right eye and 5° of ex- torsion of the left eye. Results of dilated fundus examni- nation confirmed the torsional findings: the right eye was intorted 22° and the left eye was extorted 15° as measured by fundus photography (Figure 8). A small horizontal incomitancy may have explained the face wr. Because of the torsion and nystagmus, the patient was tunable to fase with press-on prisms, Baclofen use did not relieve his oscillopsia, CASE 2 A4-year-old boy had a left hypertropia noted by his par- ents for 2 years but worsening recently. His developmen- tal milestones were delayed. Visual acuity was 20/30 OD and 20/80 OS asa result of srabismic amblyopia. Lid and pupil examination findings were normal, and he was not dysmorphic. He had an intermittent right head tlt Results of an ocular motility examination demon- strated a +3 overaction of the left inferior oblique with a =3 undersction ofthe elt superior oblique. He had a comi- tant 35-A esotropia and a o-A left hypertropia in pri- mary position that increased to 12 A on right gaze and to 20 A on left head tlt (Rable 1). The left hypertropia measured 18 on up and right and down and right gaze Atnear, he had a 12-A left hypertropia in addition to 35 \ of esotropia. He had no right hypertropia on up and left gaze. Cycloplegic refraction was normal. Dilated fun- ue we (me oe NA NLS ashi stir dus examination findings were normal except for mod- erate intorsion of the left fundus, There was no signifi cant extorsion of the right fundus. A magnetic resonance image of the brain demonstrated old diffuse white ma ter lesions. Genetic investigation revealed an XXY karyo- type (Klinefelter syndrome). Strabismus surgery consist- ing of bimedial rectus recession and left superior rectus recession brotight the eyes into monofixation range and climinated the objective fundus torsion, CASE 3 A To-yeat-old man developed vertical diplopia after sub- ‘occipital craniotomy for a posterior fossa meningioma that had caused imbalance and incoordination. His sual acuity was 20/50 OD and 20/25 OS. He had bila Figure yep 2 mot easements orp 7. RT nda ght Figure 3. fundus photography reveals moderate intron of se () and dere eosin oh i hypertope ft ee (btn) pat ‘Table 1. Summary of Patients Devaion on Devan wih ‘side onze eae rt amary positon “rugat tat’ "Rignt ett allot no. Hebd Tuk Hypertopla Gaze Gaze Ti TMK OTR_—_—_Torlon Diagnosis 1 v ERAT GRA T2RWT ISAT SRT LP incylo QD, Closed head vauna 15" rye 0S 2 a GIMT LNT GAT 12LMT20LAT nein 0S, Kinatetar syndrome wit ater ease 3 a SLM 16LAT MLAT 12LHT18LHT —-Rxcjclo 0D; arbor mass iyo OS 4 a AUNT GUAT ALT 2 RAT 10LAT —Rngyelo 0S Demjlnating dees Tesionsin the ova rita 5 Na TRAT 0 2RHT 10RHT Lot quaied Faia paride ataxia “OTR nactes ecu ttreacon: ef Right RET ight hyperopia: LT. hyperropi: nd NA, not appeal (©1909 American Medical Association, AU rights reserved, jamanetwrork.com/ on 06/20/2020Figure 0. T-veighed magnetic resonance nage athe lover bainstem {naten 3). Hyperntense lesion consistent wt demyelinating disease are resent ear te vestibular nck eral cataracts, more dense on the right. Results of his pu- pil examination were normal The man had a moderate right head ult. Results of orthoptic examination demonstrated a left hypertropia rmeasuiring 14 in primary position that increased on right ¥ ad ult (Table 1). He did not complain of subjective image ult but reported 4° of excyclodeviation, in the right eye when tested with a double Maddox rod. Results of indirect ophthalmoscopy demonstrated mod- erate incyclodeviation of the left fundus and moderate excyclodeviation of the right fundus, Magnetic resonance imaging demonstrated a left infratentorial mass that extended anteriorly tothe leltcer- cllopontine angle and around anteriorly to the brain- stem. The mass effect enhanced and extended through- out the left cerebellar hemisphere, suggesting tumor infiltration. Extra-axial compression of the brainstem and midline shift were present. CASE 4 ‘A 35-year-old man awoke with dizziness and blurred vi. sion 6 weeks before examination, His dizziness improved in 2 weeks, but his blurred v double vision that varied with gaze. He had unsteadiness| anda drunken feeling, slurred speech, and transient dif culty swallowing. He had 2 previous episodes of similar di ziness 3 104 years earlier, each lasting only a few days. His visual acuity was correctable to 20/15 OU with, normal color vision and confrontation visual fields, His pupil responses were mildly sluggish, with an equivocal left relative alferent pupillary defect and mild light-near dissociation, Versions were full. cular motility demonstrated a 22 A comitant eso- twopia with a left hyperteopia that fullilled the 3-step criteria for a left SOP (Table 1). He had a right hyper- tropia on right head tilt suggesting a bilateral SOP, but jon became frank vertical idox rod. General neurologic exami- nation findings revealed absent abdominal reflexes, hyperteflexia of the left upper limb with finger-nose ataxia on the left, a wide-based unsteady gait, and an {inability to perform tandem gait “Magnetic resonance imaging demonstrated hyper- intense lesions in the lower brainstem, near the region of vestibular nuclei and suggestive of demyelinating dis- case (Figure 6). CASES 47-year-old man complained of inter sn vertical dip lopia, progressively worsening, for 5 years. He also noted cyclodiplopia, intermittent oscllopsia, poor balance, and vertigo. He had no history of trauma. Medical history in- cluded childhood polio that had recovered fully. His mother had vertigo, ataxia, nystagmus, and other cerebellar find- ings, suggesting dominant spinocerebellar ataxia, Visual acuity was 20/15 OU. Color vision and con- frontation fields were normal. The pupils were normal. ‘cular motility was full, He had gaze-evoked nys- ugmus in all directions. On right and left wgmus had a torsional and downbeating component. A small right hypertropia in primary position increased on left gaze and with right head tilt (Table 1). The right hy- pertropia was greatest in up and lelt gaze. Saccadic dys- ‘metria was present, and addueting saccades were slowed bilaterally. Results of double Maddox rod testing dem- onstrated no eyelotorsion, We did not evaluate the fundi the nys- for objective torsion because we were unaware of a r lation between skew deviation, ocular torsion, and SOPs when this patient was first seen, Resulls of general neurologic examination demon- strated incoordination of both upper limbs with finger- nose alaxia, dysdiadochokinesta, and difficulty with dem gait. Vestibulo-ocular reflexes were tested by ‘meastring visual acuity during head shaking at | Hz and, \were markedly impaired. Dilated fundus examination find- ings were normal Infrared eye movement recordings demonstrated pri- ‘mary position upbeat nystagmus that increased on up gize Recordings also demonstrated small-amplitude lelt- beating nystagmus primary position and gaze-evoked hori- zontal nystagmus. Saceades were hypermetric with re- bound nystagmus. “Magnetic resonance imaging of the posterior fossa demonstrated marked midline cerebellar atrophy that was ‘most pronounced in the superior vermis, a AlL5 patients had orthoptic measurements suggest aan SOP, but the fundus torsion was inconsistent with that diagnosis in the 4 patients in whom it was evaluated. P jents with a true SOP have extorsion of the hypertropic (Our patients had intorsion of the hypertropic eye oF extorsion of the hypotropic eye. Surgery for SOP (el- ther a weakening procedure for the antagonist inferior oblique or a strengthening procedure for the paretic su- perior oblique) would aggravate torsion in these pa- feof ©1999 American Medi Assoc on, AU rights reserved,tients, and therefore, other surgical methods of address- ing torsion should be considered. Thus, determining the direction and pattern of ocular torsion is erucial to es- lablishing the correct diagnosis, UR PATIENTS also had other neurologic signs, although subtle, which were at- tributable to posterior fossa disease, sug- ‘gesting that the strabismus was not the result of an isolated fourth nerve palsy. Patients 3, 4, and 5 had poor coordination and balance. Patients 1 and 5 had torsional nystagmus, Thus, findings from a careful history and clinical examination are also im- portant when evaluating ocular moulity disorders. The relationship between skew deviation and oct lar torsion is well dacumented.* In 1984, Trobe" pro- posed that patients with skew deviation do not have oct- lar torsion and that this feature distinguishes them from patients with SOP. However, he exclided patients with positive Bielschowsky head tit test results, which prob- ably biased the resulls by excluding those patients with ‘ocular torsion. Halmagyi and Hoyt” and others" re- ported that patients with the OTR may have positive head llts and torsion, Brandt and Dieterich reported some degree of ocular torsion inall their patients with skew de- Viation, in whom torsion was toward the hypotropic eye when evaluated with fundus photography. Unilateral oF bilateral torsion is now considered to be a necessary and sullicient condition for diagnosing OTR" The double Mad- ddox rod, indirect ophthalmoscopy, fundus photography, and evaluation of the subjective visual vertical” are all re liable methods of detecting ocular torsion, In our experience with these patients, the double Maddox rod gives reproducible measurements (within 3°) of subjective ocular torsion. We place the rods at ‘oblique angles and ask the patient to make the rods parallel to each other and to the horizon, ‘Objective measurements of acular torsion are dilf- ‘cult o make because of variability in the normal relation- ship between the optic dise and fovea. Extorsion may often ‘be overlooked because the healthy fundus typically has the fovea lower than the center of the dise by 2° to 7°." How- ‘ever, clear intorsion of the hypertropic eye was evident in 4 of our patients, The fifth patient had subjective torsion, that was not quantified. Objective torsion using funds pho- ography was measured only in patient 1 We believe that all 5 patients had an OTR caused by unilateral damage to the vertical VOR pathways that subserve the normal ocular countertolling reflex. These pathways originate in the vestibular end organ (utriele, saccule, and semicircular canals) and travel through the brainstem to the cyclovertical ocular motor subnuclet in the midbrain (Figure 1); their injury causes skew devia- ion” Bach vertical semicircular canal has an exeit- alory projection to 1 eyclovertical extraocular muscle sub- nucleus for the ipsilateral eye and to the corresponding yoke muscle subnucleus for the fellow eye (Figure 1); inhibitory projections travel o the corresponding cyclo- vertical antagonist muscles." (The horizontal canals project only to the horizontal rect and therefore, ate not Involved in the vertical VOR.) Projections [rom the oto- liths (utricle and saceule) converge with the semicireu- larcanal pathways atthe vestibular nuclei and ascend to- gether.® Otoliths and semicircular canals together provide {information for the dynamic VOR, whereas the otoliths alone predominantly affect the static VOR. Disruption of the semicircular canal inputs to the eyclovertical extraocular muscle subnuclet will produce an OTR that is phasic and associated with nystagmus, Be- cause all our patients had sustained OTRs, the respon- sible lesions must have involved the otolithic projec- ions—predominantly the utricular component—that parallel those ofthe semicircular canals but mediate static vestibular input. Thus, we hypothesize that OTR in our patients resulted from asymmetrical or unilateral dam- age to the otolithic-oeular projections In 1904, Brandt and Dieterich damage to the anterior semicircular pathways could produce intorsion, but they did not address the mecha- nism by which it could mimic an SOP. We postulate the following mechanism to explain how, using the 3-step test, OTR could produce an apparent SOP. Step 1: A patient with right-sided otolithic projection damage will have decreased tonic excitatory input to the right supe- rior rectus and left inferior oblique (Figure 1) that results in a right hypotropia (left hypertropia) with incyclotorsion of the left eye. Disinhibition of projec- ions to the right inferior rectus and left stiperior oblique will worsen the right hypotropia and left incy- clotorsion. Step 2: The left hypertropia increases in right gaze becatise this is the field of action of affected rectus muscles, Step 3: Left head tlt stimulates the left luricle and its excitatory projections to the left superior oblique, left superior rectus, contralateral right inferior oblique, and right inferior rectus.” In the absence of compensatory effects from the damaged right utricular projections, a large left-over-right vertical skew (the OTR) occurs, as is seen experimentally with left-sided uutricular nerve stimulation.” The left eye supraducts and intorts and the right eye infraducts and extorts, worsening the right hypotropia and paradoxical torsion Right head ult fails to excite the damaged right otolithic projections, causing the vertical deviation to be less than with left head tilt. Thus, the net motility distur- bance isa left hypertropia that fulills the 3-step criteria for a left SOP but has paradoxical incyclotorsion of the hypertropic eye. In fact, the “paretic” left superior oblique actually “overacts,” because of the unopposed left-sided utricular excitation, to cause paradoxical intorsion, Related disturbances might cause vertical deviations that mimic inferior oblique palsies or pattern strabismus; we believe we have seen stich patients Injury to the vertical VOR projections that cause such a skew deviation can occur anywhere [rom the vestibu- lar end organ to the ocular motor subnuclel in the mid- brain, Four of our patients had posterior fossa or brait- stem pathology that produced such lesions, but the lesions were widespread and had poor localizing value An alternative explanation for the pattern of motil- lay defects in our patients could be a midbrain lesion in- volving the VOR projections and the adjacent trochlear nuicleis. An isolated midbrain skew deviation would pro- duce a relatively comitant vertical deviation, with the hy- yostulated that (©1909 American Med Association, All rights reserved.‘Table 2. Findings in Ocular Tit Reaction (OTR) and ‘Superior Oblique Palsy (SOP) om ‘oF inpertona ve Ye Head tt Tolower ye Tolower aye (avay tom (ay tom “parti” os) parece) Torsion Blslea eter Unita exeyeotorsen (Geen of conugatstoward of hypertopic ey toward suptior pole lower ee Nore each ye) pertropic eye on the side of the lesion.” Because the fourth nerve crosses to the other side as it leaves the midbrain, extension of such lesion into the trochlear nucleus would produce an SOP in the hypotropic eye, but it would be ‘masked” and, with the 3-step test, seem to be in the hy pertropic eye. (We doubt that this is the mechanism re- sponsible for most masked bilateral SOPs, however.) An- other alternative explanation in the patient with trauma (patient 1) isa traumatic skew deviation with a separate tuaumatic SOP in the hypotropic eye This report demonstrates that objective assess- ment of ocular torsion with indirect ophthalmoseopy, the double Maddox rod, or fundus photography is neces- sary to differentiate SOPs from the OTR because both dis- ‘orders have similar hypertropias and head tlts (fale 2). Patients with bilateral conjugate ocular torsion toward the lower eye oF ineyelodeviation in the hypertropic eye probably have skew deviation (Figure 2, lower right) rather than an SOP (Figure 2, middle right). Careful as- sessment for brainstem signs such as nystagmus is im- perative in patients suspected of having an SOP, Objec- live assessment of ocular torsion should become the {fourth step” to complement the 3-step test. Surgically weakening the inferior oblique (or strengthening the superior oblique) may be contraindicated in these pa- tients because the procedure will have a paradoxical effect on ocular torsion. Whether this iatrogenic wors- tening of torsion will he tolerated after surgery is un- known, Surgical treatment based on weakening rela- ively “overacting” cyclovertical muscles should theoretically be more helpful and was successful in 1 of| ‘our patients, Accepted for publication October 23, 1998. ‘Supported in part by a grant from Research to Pre- vent Blindness Inc, New York, NY. Corresponding author: Sean P. Donahue, MD, PhD, Vanderbilt University Medical Center, 1215 21st Ave S, Eighth Floor, Medical Center East, Nashville, TN 37232- ) 8808 (e-mail: sean.donahue@memail vanderbilt. (©1909 American Medical Ass ‘Downloaded From: https:/jamanetwork.com/ on 06/20/2020 — }-— 1. Pars MM sted esol muscle ply, Ach Qphtalmat. 195860: farts, 2 shoe Erorsin tive tp stint daprsis af erica statism Ophtalmol 08896127182 8 Ligh 28 OS Te eurigy Ee Movements 2 ed Pind, Pa Fave Go Publisher: 00: hap 2 4 ane cua sa dein: nabs of 100 cases, Ach Nero. 1975.32 ‘est. 5 Kea rasa 6 an, Detrich ML Skew deiton with cea tsion: «vee ban z ® 8 0 JR. Aerating show devatin: 47 patents. Neurology. 185:35: ftemign tpegapbe dagresi van, url 0083528 S08, Dateich Manat lens same teptin.ciedsuan. and ‘ubjeve sul erica tsi ats, Ao Mawel 198231 30-08, Horan 3, Hamagy ML Paral oer ecto ao unl cobelar Tesi Naw 107404-093 Ban, Dt Pali hnd coordination ino treeaarst "anton in marocapae and mean ston. Bran 108716. 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