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Show Journal of Clinical Neuro- ophtha[ mo[ ogy 11( 2): 96- 103,1991. Cryptococcal Optic Neuropathy in the Acquired Immune Deficiency Syndrome Karl C. Golnik, M. D., Steven A. Newman, M. D., and Brian Wispelway, M. D. © 1991 Raven Press, Ltd., New York Cryptococcus neoformans infection occurs frequently in patients with the acquired immune deficiency syndrome ( AIDS). Cryptococcal meningitis can result in optic neuropathy. Improvement in afferent visual system dysfunction has not been documented. We report three patients with AIDS who developed either unilateral ( 1) or bilateral ( 2) afferent visual system dysfunction. The bilaterally affected patients had visual field deficits compatible with chiasmal involvement. All patients had improvement in their vision following appropriate treatment with amphotericin B. Reactivation of cryptococcal infection was heralded by neuro- ophthalmic manifestations in two patients, in spite of maintenance therapy. Despite the poor overall prognosis, AIDS patients with presumed cryptococcal optic neuropathy can benefit from optimal therapy. Key Words: Optic neuropathy- Cryptococcus neoformans- Acquired immune deficiency syndrome, From the Departments of Ophthalmology ( K. CG., S. A. N.) and Internal Medicine ( B. W.), University of Virginia, Charlottesville, Virginia, U. S. A. Address correspondence and reprint requests to Dr. S. A. Newman, Department of Ophthalmology, University of Virginia, Charlottesville, VA 22908, U. s. A. 96 Cryptococcal infection of the central nervous system ( CNS) is among the most frequently recognized life- threatening infections in patients with acquired immune deficiency syndrome ( AIDS) ( 1), Neuro- ophthalmic manifestations occur commonly in this group and are often attributed to concurrent cryptococcal meningitis ( 2). Presumed cryptococcal optic neuropathy has been reported by several authors ( 3,4). Despite treatment, improvement in afferent visual system dysfunction has not been documented. We document 3 patients with AIDS, cryptococcal meningitis, and presumed cryptococcal optic neuropathy. All three patients showed improvement in visual function following appropriate treatment. CASE REPORTS Case 1 AIDS was diagnosed in a 43- year- old black man in 1986 during a hospitalization for Pneumocystis carinii pneumonia. In March 1989, evaluation for headache and fever revealed Cryptococcus neoformans in the cerebrospinal fluid ( CSF) by India ink preparation and was confirmed on culture. Cytomegalovirus ( CMV) serology was positive. Treatment with amphotericin B( 0.7 mglkg/ day) was terminated after 3 days because of acute renal failure and was restarted at a lower dose. Following an initial response, chronic maintenance amphotericin Btherapy ( 0.4 mglkg three times per week) was initiated. In August 1989, the patient's left visual acuity dropped to 8/ 200 over a 2- week interval ( acuity aD = 20/ 25). Color vision was 9110 aD and OlIO as using Hardy- Rand- Rittler ( HRR) pseudoisochromatic plates. There was a 1.5 log unit left afferent pupillary defect. Automated static perimetry showed a superior arcuate deficit aD and a central scotoma with superior arcuate deficits as CRYPTOCOCCAL OPTIC NEUROPATHY IN AIDS 97 : F +---~==~:::.: FIG. 1. Case 1: Visual fields ( 7/ 27/ 89) showed a central scotoma and a superior arcuate deficit as. ( Fig. 1). Fundus exam was normal 00, but several areas of hemorrhagic retinal necrosis were evident as ( Fig. 2). There was no significant retinal edema associated with the CMV retinitis. The remainder of the ophthalmic exam was unremarkable. A computed tomographic ( CT) scan of the head was normal. Amphotericin B was increased ( 1.0 mg/ kg/ day) to treat a presumed retrobulbar cryptococcal optic neuropathy and recrudescence of cryptococcal meningitis. Ganciclovir ( 5 mg/ kg q12h) was begun for the CMV retinitis. After two weeks of optimal therapy, vision had improved to 20/ 60 as )";" :...:...:.•.:.... :"':'. J;~:: I~;~::~ im:~; m:~ i~ jL:.: . . " ~:)-;.:.}..~..~:~.;...~~:.~...~..:.~.,..(.~..:...=..- ~-,).:~~;;:;~~;;. ;:; : ..~::~~:~:~:: ::; _ ••• 4 ••• _, FIG. 3. Case 1: Visual fields ( 8/ 16/ 89) showed diminution of the central scotoma and superior arcuate deficit OS. and the left central scotoma had diminished ( foveal sensitivity increased from 10 to 26 dB) ( Fig. 3). The amphotericin B was decreased to maintenance levels ( 0.7 mg/ kg three times per week). In January 1990, 5 months later, vision dropped rapidly to 3/ 100 ( aS), and the patient died 2 weeks later. Autopsy was denied. Case 2 A 36- year- old HIV- positive black man presented with P carinii pneumonia in April 1989. In May FIG. 2. Case 1: Optic discs were normal OU, but an area of hemorrhagic necrosis was present as ( arrows). J Clin Neuro- ophthalmol. Vol. 11, No. 2, 1991 98 K. C. GOLNIK ET AL. 1989 he developed persistent headache and fever. Lumbar puncture revealed an opening pressure of 440 mm water, and cryptococci were seen on India ink preparation. Laboratory studies for Toxoplasma gondii were negative, as were CMV serology and CSF VORL. Several days later, development of binocular horizontal diplopia prompted ophthalmic evaluation. Visual acuity was 20/ 30 00 and 20/ 25 as. Color vision was OlIO au using the HRR plates. There was no afferent pupillary defect, but a complete right sixth cranial nerve palsy and bilateral hypometric saccades were present. Auto- .:;~ fll~ w~ . f{;; j; U:; · , . ::'-:':~.'>:':".'.;:":~'.:: I .~":~' ,;.::,~:••• :-.~;•• ::•• :: .:•• ~~. :;: L: · ,; · ; 1.'; A~~;, ...................... ,.... '~; AA:.,,~~.~ q:;~, · ~. 4s~? j~ B: l .. • " - t, .... i •••• mated static perimetry showed normal foveal sensitivities and primarily central bitemporal deficits ( Fig. 4). The remainder of the ophthalmic exam was normal. CT scan of the head was normal. Amphotericin B therapy ( 0.7 mg/ kg/ day) was begun to treat the cryptococcal meningitis and presumed cryptococcal chiasmaI involvement. Three weeks later the visual field deficits had resolved ( Fig. 5). The sixth cranial nerve palsy gradually improved. In August, 5 months later, while on maintenance amphotericin B therapy ( 0.4 mg/ kg three times per week), the patient's vision suddenly decreased to FIG. 4. Case 2: Visual fields ( 5/ 11/ 89) showed central bitemporal deficits with normal foveal sensitivities. . - . ... .. -• .. I - , . ., •• 0 I . .. - . .. .. . , : : .... , I .. : :: : : ~ : : : ~ ~ : ~ : • • •• : : : : : : : I : : ~ .. : • ~ : .... I ... ; ; : ; ~ ; : : : ~ ~ : " . o •• I ••••••••• , •• - 0' • '. 0 •.••. _•..•• _.... , ... -'-'." .. ' ,.,",., 1._', -., ••••• .. .. • • .. i ~ ~ • ~ ; •• : ••••• t, • , JClin Neuro- ophlhalmol.. Vol. 11, No. 2, 1991 . to, , •••._ -; : : ~ : : : : : ! ; ~ : : ; : ;, : : : ; : : ~: ::: ~ .•.. ". " 0' " •• , ... .. . . . .. - . . .. .. .. ':. CRYPTOCOCCAL OPTIC NEUROPATHY IN AIDS 99 10/ 200 00 and 3/ 200 OS. Visual fields had worsened, demonstrating central scotomas and a bitemporal character ( Fig. 6). Lumbar puncture revealed cryptococci on India ink preparation and culture associated with an increase in CSF cryptococcal antigen. Amphotericin B therapy was considered a failure, and fluconazole treatment ( 400 mg/ day) was begun. The patient remained stable until June 1990, when he presented with a oneweek history of headache, vomiting, stiff neck, weakness, and blurred vision. The patient was aware of decreasing visual acuity within hours of not feeling well. Repeat lumbar puncture demonstrated cryptococcal organisms and an elevation in the cryptococcal antigen titer from 1: 1617 ( October 1989) to 1: 1892. In addition, protein test values had risen from 54 to 161 %. The patient was treated with intravenous ( i. v. mg%) fluconazole, and systemic symptoms improved over 3 days. He was discharged while using an increased dosage of oral fluconazole. Visual acuity remained stable, although automated perimetry revealed the onset of a new superior arcuate defect on the left. .. .~.-..~ ., -" ~ - .. -.. ----,..... --,... .. - •• -.. • I - _ ... - • - I - .. ~ ~ " .. .-.... · ,- · .' ,--'-- 1""-,-,, .. , .. , .. ,,.-., ::.: : : ~ : : : : I I : : : : ~ •• -". -. -.' 101 ., ... , .11" ", : ••: .. ,1 II .••. "': 1_ to 01 ,., ,., " ......... ". i'.'" ,',. ~ ~:: ~ ~ : : : ~ : = : : : : ~ ~ : : : : - '. : ~ : : : ~ : : . :: :: - =~ ~ ~ :', : :~., ~-- ~ -. '.. .-. '.- 1-' . _ " 1' . ., ... - ---,..-._. - - - - ~ . .. .. .. . . .. . .. .. .. .. .. ~ ."-._"-"_, .. .. .-.... - I · • • • _ .. - - ... , ..... _-,..-. ... I •••• ,11.,' FIG. 5. Case 2: Visual fields ( 5/ 30/ 89) showed near resolution of pretreatment deficits. 30';:) • _ I I .... 1 - - ... - •• ~ • , ••• 4 •• s ~ , •• , •• - • • .. , •• , , .. _ • _ ~ • s , , - - - - • , , f ' .... - - •• .,.... ,, '''' , ,,, , .. . , . - .. ~ .. , , " , ... " •••• ., ~ 4 • ..... , .. .. -- ' .. I Clin Neuro- ophthalmol. Vol. 11, No. 2. 1991 100 K. C. GOLNIK ET AL. IFIG. 6. Case 2: Visual fields ( 10/ 8/ 89) worsened after 5 months of maintenance amphotericin B therapy. ~ ~ •• I I •••••• ::;::~ ;;;::.: :"'::'" r~ :.~ :::;::;:::-. :<'.::'.::', : : :: : ~ : : ~ ~ : : : : :: : ~: I :::::: ~ : : :: : :: :. ;:~: .:~ ~ .. .. "., _. ~... . .. , , _. " :~~ ::::.:~:~~: :-:', ::::::~:~:::~: ;:: . . ~ .... . .. . -. . . , ~ . - _. - .."- ~ • • • • • • "•• 1 ,• •• - - ••• - ,• . I • " .,., • • • • I • • • • .. .. • ~ ~ - • , • •• ~ ... -", ,- - . ............. - - ••••••••• 0 • .• •.•. e .•.•. •- • i -",. l , ~ Case 3 A previously healthy 32- year- old black man presented in February 1989 with headache and progressive horizontal diplopia. Two days later, bilateraI loss of vision occurred over a I- hour period. On examination there was no light perception OU and both pupils were 7 mm and unreactive to light. A right gaze palsy, left abduction deficit and bilateral seventh and eighth cranial nerve palsies were present. The remainder of the examination, including the optic nerve heads, was normal. A CT scan of the head was normal. Lumbar puncture revealed an opening pressure of 400 mm of water and cryptococci on India ink preparation and culture. Western blot for human immunodeficiency virus ( HIV) was positive. Laboratory studies for T gondii as well as CMV serology and CSF VDRL were negative. Amphotericin B ( 0.7 mglkg/ day) and flucytosine ( 52 mglkg/ day) were initiated. After 2 weeks, vision had improved to hand motions OU, and bitemporal visual field deficits were present to confrontation. Amphotericin B was reduced to maintenance levels ( 0.4 mg/ kg three 1Clin NeuriKlphllull"", I, Vol. ii, No. 2. 1991 CRYPTOCOCCAL OPTIC NEUROPATHY IN AIDS 101 times per week) and the afferent visual system stabilized. Optic nerve head atrophy developed after several months, although vision had improved to 3/ 200 00 and 11200 as. Ten months after initial presentation, while the patient was on maintenance amphotericin B, CSF was India ink and culture negative. COMMENTS The increasing incidence of AIDS necessitates familiarity with previously uncommon opportunistic infections and their ophthalmic manifestations. The hemorrhagic retinal necrosis caused by cytomegalovirus ( CMV) infection is now well recognized because of its prevalence in the AIDS population ( 2,5). Although less common than CMV retinitis, ophthalmic manifestations due to varicella zoster ( 6), herpes simplex ( 7), T gondii ( 8), Candida ( 9), and P carinii ( 10) are now being seen in association with AIDS. Recently C neoformans infection of the CNS was identified as the most likely etiology of neuro- ophthalmic pathology in AIDS patients ( 2). Cryptococcus neoformans is a ubiquitous, encapsulated, yeastlike fungus that preferentially infects the CNS of immunocompromised individuals ( 11). The incidence among AIDS patients ranges from 7 to 13% and thus is the fourth most frequently lifethreatening infection in this group ( 1). The CNS predilection may be due to the lack of serum anticryptococcal factors ( 12) or complement activity ( 13) in the cerebrospinal fluid. Central nervous system involvement may manifest as focal granulomata ( toruloma) or more typically as a meningitis ( 11). Intraocular involvement is either a chorioretinitis ( 14) or uveitis ( 15) and is unusual. Neuroophthalmic manifestations are most frequently reported, in particular papilledema, optic atrophy, and cranial nerve palsies ( 2,16,17). Internal ophthalmoplegia ( 18), internuclear or supranuclear ophthalmoplegia ( 19), and Horner's syndrome ( 20) occur less often. Without treatment cryptococcal meningitis is uniformly fatal. The mainstay of therapy is amphotericin B, a broad- spectrum polyene that binds fungal cell membranes, causing lysis of cellular contents ( 21). Recommended dosage is 0.4- 0.6 mglkg of body weight per day i. v. 5- Fluorocytosine ( flucytosine) is a fluorinated pyrimidine that is deaminated to 5- fluorouracil and inhibits DNA synthesis. Flucytosine lacks efficacy as a single agent ( 22), but in combination with amphotericin B it may be more effective than amphotericin alone ( 21). Dosage is 37.5 mglkg of body weight every 6 hours orally. Experience with treatment of cryptococcal meningitis in the AIDS patient has produced new therapeutic considerations. The bone marrow suppression caused by flucytosine is tolerated poorly, especially with concurrent azidothymidine ( AZT) use, and therefore is seldom used in AIDS patients ( 23). Additionally, an increase in amphotericin B dosage ( 0.8- 1.5 mg/ kg/ day) has been found more efficacious. Initial therapy is continued until a 1.0 gram minimum has been given ( 23). Unfortunately, the immunosuppression of AIDS cannot yet be corrected. Presumably, this continued immunosuppression is responsible for the cryptococcal meningitis relapse rate of 50% in 6 months for previously treated AIDS patients ( 24). Therefore, a weekly amphotericin B maintenance regimen is recommended ( 23). Amphotericin's requisite i. v. administration and renal toxicity compounded by the need for perpetual maintenance therapy has renewed interest in alternate antifungal agents. Fluconazole, an oral triazole, is administered in doses of 50- 200 mg/ day orally. Two studies have shown a decreased relapse rate of cryptococcal meningitis in AIDS patients when fluconazole is used following initial amphotericin B therapy ( 25,26). Recently, a controlled trial was completed comparing fluconazole ( 200 mg/ q. d.) with amphotericin B ( 1 mg/ kg/ wk) as maintenance therapy for cryptococcal meningitis ( Sixth International Conference on AIDS, unpublished data). Fluconazole was found to be at least equally effective as- or perhaps better than- the amphotericin regimen, with lower associated toxicity. Our three patients had AIDS, cryptococcal meningitis, and retrobulbar optic neuropathy. Two patients had presumed cryptococcal chiasmal involvement. Case 1 had CMV retinitis as well. Although CMV optic neuropathy cannot be absolutely ruled out, we feel the pattern of visual loss, lack of peripapillary CMV retinitis and absent disc edema were more compatible with a cryptococcal etiology. These neuro- ophthalmic signs were the first indications of cryptococcal meningitis recrudescence. They occurred despite maintenance therapy and improved after increasing the amphotericin B dose. Case 2 had bilateral afferent visual system involvement manifest by normal foveal sensitivities and central bitemporal visual field deficits ( Fig. 4). We felt this to be due, at least in part, to chiasmal involvement. The patient improved with initial amphotericin therapy ( Fig. 5) but while on maintenance therapy complained of decreased vision. His repeat spinal tap revealed evidence of relapsed cryptococcal meningitis. Amphotericin therapy was felt to have failed and fluconazole was ] Clin Neuro- ophthalmol, Vol. 11, No. 2, 1991 102 K. C. GOLNIK ET AI. substituted. The patient then stabilized, but 10 months later cryptococcal recrudescence was again heralded by visual symptoms. Case 3 improved after amphotericin B treatment despite initial subacute bilateral visual loss to no light perception. Visual fields were consistent with chiasmal involvement. These patients had unilateral ( 1) or bilateral ( 2) presumed cryptococcal optic neuropathy. In two patients neuro- ophthalmic findings were the initial signs of recurrent cryptococcal meningitis. To our knowledge, these patients are the first reported to benefit from optimizing amphotericin B therapy. Previous reports of presumed cryptococcal optic neuropathy in the AIDS patient are limited. Winward et al. reported a patient with AIDS and cryptococcal meningitis who developed bilateral visual loss and choroidal infiltrates with normal discs ( 3). This presumed retrobulbar cryptococcal optic neuropathy developed despite amphotericin B treatment and did not improve. Lipson et al. reported two patients with AIDS and bilateral presumed cryptococcal optic neuropathy ( 4). One patient had a history of treated CMV retinitis and poor vision but developed sudden loss of light perception. Investigation revealed cryptococcal meningitis; despite treatment visual acuity did not improve. The second patient presented with optic neuropathy 4 months after initial treatment for cryptococcal meningitis. Further treatment and course were not discussed. The mechanism( s) by which cryptococci cause optic nerve dysfunction is unclear. Possible etiologies include chronically increased intracranial pressure ( ICP), direct optic nerve invasion by the cryptococci, and restrictive arachnoiditis. Papilledema is the most frequently observed ophthalmic manifestation in patients with cryptococcal meningitis ( 16). Optic neuropathy will occur with persistently increased ICP, but this is usually slowly progressive and spares central visual acuity until late in the course. Our patients' pattern of visual loss was either acute or subacute loss of central vision. Therefore, we doubt that increased ICP caused this ophthalmic pathology. Several authors have demonstrated cryptococcal invasion of the visual pathways ( 16,27). Kupfer and McCrane found a positive correlation between visual loss and extent of optic nerve invasion ( 27). No similar autopsy data is yet available from AIDS patients. Finally, constrictive optic nerve arachnoiditis that compromises the neural vascular supply could produce optic neuropathy. This has been described in toxoplasmic meningitis ( 28). Ofner and Baker reported a non- AIDS patient with cryptococ- 1Clin Neuro- ophllullmtll, VOl. 11, No. 2, 1991 cal meningitis and visual loss. They found cryptococci in the optic nerve meninges ( 29). One patient, reported by Lipson et al., had heterogenous signal intensity of both optic nerves on magnetic resonance imaging ( 4). The authors felt this was consistent with arachnoiditis. Maruki et al. reported a non- AIDS patient who developed bilateralloss of vision while being treated with amphotericin Band flucytosine for cryptococcal meningitis ( 30). Chiasmatic arachnoiditis was suspected after metrizamide CT cisternography showed late opacification of the chiasmatic cistern. At surgery the " perioptic arachnoid was thick, yellowish, and adhesive." After dissection of the arachnoidal adhesions the " rudimentary surface blood vessels dilated" and one year later there were no " visual problems." Thus, cryptococcal meningitis may produce optic neuropathy via several mechanisms. Autopsy material may provide the definitive answer. Our patients are the first reported with AIDS and presumed cryptococcal optic neuropathy who have improved following optimal amphotericin B therapy. In two of our patients, afferent visual system pathology was the initial evidence that cryptococcal disease had recurred, and in one of those two a third episode of CNS cryptococcal recrudescence was heralded by further visual symptoms. Thus, periodic neuro- ophthalmic examination is essential in AIDS patients with a history of cryptococcal meningitis. The recognition of cryptococcal optic neuropathy and the institution of optimal therapy can restore or prolong vision. REFERENCES 1. ~ ng RHK, , Bishburg E, Smith SM, Kapila R. CryptococcaJ infectIons In patients with acquired immune deficiency syndrome. Am JMed 1986; 81: 19- 23. 2. Jabs DA, Green WR, Fox R, Polk BF, Bartlett JG. Ocular manifestations of acquired immune deficiency syndrome. Ophthalmology 1989; 96: 1092- 9. 3. Winwar. d KE, ~ amed LM, Glaser JS. The spectrum of optic nerve disease In human immunodeficiency virus infection. Am JOphthalmoI1989; 107: 373- 80. 4. Lipso~ BK, Freeman WR, Beniz J, et al. 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Loss of vision due to cryptococcal optochiasmatic arachnoiditis and optocurative surgical exploration. Neural Med Chir ( Tokyo) 1988; 28: 695- 7. JClin Neuro- ophthalmol, Vol. 11, No. 2, 1991 [VBmeningitis] |
