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Show Journal of Neuro- Ophthalmology 19( 2): 118- 119, 1999. © 1999 Lippincott Williams & Wilkins, Inc., Philadelphia Bilateral Trochlear Nerve Palsy Associated With Cryptococcal Meningitis in Human Immunodeficiency Virus Infection Federico Sadun, M. D., Anna Maria De Negri, M. D., Paola Santopadre, M. D., and Paola Pivetti Pezzi, M. D. This is the report of a case of bilateral trochlear nerve palsy secondary to cryptococcal meningitis in a 34- year- old woman with acquired immune deficiency syndrome. Based on clinical and neuroradiologic findings, it is concluded that in the present case, a postinflammatory shrinking of the arachnoid has stretched the fourth cranial nerves at their point of emergence from the dorsal surface of the brainstem. Key Words: Acquired immune deficiency syndrome- human immunodeficiency virus infection- Cryptococcal meningitis- Diplopia- Trochlear nerve palsy. Central nervous system ( CNS) involvement in human immunodeficiency virus ( HIV) infection is found clinically in 40% to 60% of patients at sometime in the course of their disease, and in 75% to 90% of patients at autopsy ( 1). Neuro- ophthalmologic abnormalities occur as frequently as 8 of 100 patients ( 2), and include cranial nerve palsies, optic neuropathy, papilledema, nystagmus, central eye movement disorders, pupillary abnormalities, and visual field defects ( 3,4). Common causes include: CNS toxoplasmosis, cryptococcosis, lymphoma or viral encephalopathy ( implying infection by HIV, progressive multifocal leukoencephalopathy [ PML], cytomegalovirus [ CMV], and herpes viruses) ( 2). We present the case of a woman with HIV infection and bilateral palsy of cranial nerve IV, secondary to cryptococcal meningitis. CASE REPORT A 34- year- old woman with acquired immune deficiency syndrome ( AIDS) was admitted to the hospital with headache, fever, and cutaneous papular lesions. Computed tomographic scan of the head produced normal findings. The Cryptococcus neoformans serum antibody titer was 1: 32,768. Cerebrospinal fluid ( CSF) ex- Manuscript received March 26, 1997; accepted December 2, 1998. From the Institute of Ophthalmology ( F. S., A. M. D. N., P. P. P) and Department of Infectious Diseases ( P. S.), University of Rome " La Sapienza," Rome, Italy. Address correspondence and reprint requests to Paola Pivetti Pezzi, MD, Institute of Ophthalmology, University of Rome " La Sapienza," Viale del Policlinico, 00161 Rome, Italy. amination revealed a positive culture for Cryptococcus neoformans, with white blood cell count of 340/ mm3, protein level of 95 mg/ dl, glucose level of 41 mg/ dl, and nonreactive venereal disease research laboratory. A diagnosis of disseminated cryptococcosis was established, and intravenous fluconazole and amphotericin therapy was begun with progressive clinical improvement over the following 3 weeks. However, a few days before discharge, the patient gradually became aware of vertical diplopia in primary gaze and in all gaze positions except upgaze. She was referred to our institution for neuro- ophthalmologic evaluation approximately 4 weeks after discharge. At that time, the Cryptococcus neoformans serum antibody titer was reduced to 1: 1024, and the CSF culture was negative; the diplopia was subjectively unchanged from that at initial examination. Neuroophthalmologic examination showed a right and left hypertropia alternating with different gaze positions and head tilts. A Bielschowsky test and a double Maddox rod test were performed and were consistent with bilateral trochlear nerve palsy. The remaining ocular and neurologic examination was normal. The patient underwent magnetic resonance imaging of the brain with gadolinium-diethylenetriamine pentaacetic acid ( DTPA), with findings of diffuse meningeal thickening involving the skull base, without other abnormalities ( Fig 1). Based on clinical and neuroradiologic findings, a diagnosis of bilateral trochlear nerve palsy secondary to cryptococcal meningitis was made. Conservative management was decided on, and prismatic spectacles were prescribed, with partial resolution of her symptoms. At 1- year follow- up her clinical status was unchanged. DISCUSSION Ocular motor nerve palsies in HIV infection have been described primarily in association with parenchymal or meningeal infections and neoplasms ( 3,5,6). The ocular motor nerve paresis may be single or multiple, unilateral or bilateral. The abducens nerve is the most frequently involved, followed by the oculomotor nerve ( 3). Trochlear nerve palsies are uncommon, although sporadic 118 BILATERAL TROCHLEAR NERVE PALSY 119 TXrn ".."" « tf***^^ 1 ' • ' ' /* J"" J • • T n w I ft J^ JI If MP 1 1 ' I K .* \ * \ V mi \ H \ ' , . i. » */ V Y .1 H;'| ^^ 1, * J J? I'' i i ; I. I fl l'| | i 1 1.1,1 U| 1 I I 1 !• SISOTflf I'l IMF S 4 - f t i = ' k - V^ ^^ 1 7> • 5 5 1 ^ ^^^ STOIil^ >&•<> ^ Tfir niF i . i!:- / j[ si. is. « t r r n* b: c. i ^ iflfaii 1 £ r* slff SSBm- iHfo i i • . i i. ' •!•*. B FIG. 1. T1- weighted gadolinium- enhanced axial ( A) and sagittal ( B) magnetic resonance images showing thickened meninges ( arrowheads) with diffuse enhancement involving the skull base. Other images of the midbrain highlighted no parenchymal abnormalities. cases have been described in association with CNS toxoplasmosis ( 5), lymphoma ( 5,6), and varicella- zoster infection ( 7). A single case of bilateral trochlear nerve palsy was reported in 1994 in a 27- year- old man with AIDS who had primary CNS lymphoma invading the dorsal mesencephalon and causing hydrocephalus ( 8). We have presented a case of bilateral fourth nerve palsy in a patient with AIDS involving cryptococcal meningitis. Cryptococcal infection occurs in approximately 10% of people with AIDS, and neuro-ophthalmologic abnormalities are found in up to 50% of these ( most frequently, retrobulbar optic neuropathy, papilledema, and cranial nerve palsies), usually because of severe meningeal involvement resulting in adhesive arachnoiditis ( 9,10). In the present case, we suggest that postinflammatory arachnoidal shrinkage stretched the nerves as they emerged from the dorsal surface of the brain stem. In support of this hypothesis are the absence of signs of dorsal midbrain syndrome or increased intracranial pressure suggesting involvement of the fourth cranial nerves in the periaqueductal area. There was no enhancement in the midbrain on magnetic resonance imaging that would suggest an intraparenchymal cause. To the best of our knowledge, this is the first report of bilateral trochlear nerve palsy caused by cryptococcal infection in AIDS. REFERENCES 1. Petito CK, Cho ES, Lemann W, et al. Neuropathology of acquired immunodeficiency syndrome ( AIDS). An autopsy review. J Neu-ropathol Exp Neurol 1986; 45: 635^ 6. 2. Nichols JW, Goodwin JA. Neuro- ophthalmic complications of AIDS. Semin Ophthalmol 1992; 7: 24- 9. 3. Miller NR. Walsh andHoyt's clinical neuro- ophthalmology. Vol 5. 4th ed. Baltimore: William & Wilkins, 1995; 4107- 56. 4. Pivetti Pezzi P. Interessamento neuroftalmologico in corso di AIDS. Boll Ocul 1991; 70: 601- 7. 5. Mansour AM. Neuro- ophthalmic findings in acquired immunodeficiency syndrome. J Clin Neuro Ophthalmol 1990; 10: 167- 74. 6. Keane JR. Neuro- ophthalmologic signs of AIDS: 50 patients. Neurology 1991; 41: 841- 5. 7. Palestine AG, Rodriguez MM, Macher AM, et al. Ophthalmic involvement in acquired immunodeficiency syndrome. Ophthalmology 1984; 91: 1092- 9. 8. Maclean H, Ironside J, Dhillon B. AIDS- related primary central nervous system lymphoma. Arch Ophthalmol 1994; 112: 269- 71. 9. Friedman DI. Neuro- ophthalmic manifestations of human immunodeficiency virus infection. Neuro- ophthalmology 1991; 9: 55- 72. 10. Freeman WR, Lerner CW, Mines JA, et al. A prospective study of the ophthalmologic findings in acquired immunodeficiency syndrome. Am J Ophthalmol 1984; 97: 133- 42. J Neuro- Ophthalmol, Vol. 19, No. 2, 1999 |
