Abstract
Cryptococcal induced visual loss is a devastating complication in survivors of cryptococcal meningitis (CM). Early detection is paramount in prevention and treatment. Subclinical optic nerve dysfunction in CM has not hitherto been investigated by electrophysiological means. We undertook a prospective study on 90 HIV sero-positive patients with culture confirmed CM. Seventy-four patients underwent visual evoked potential (VEP) testing and 47 patients underwent Humphrey's visual field (HVF) testing. Decreased best corrected visual acuity (BCVA) was detected in 46.5% of patients. VEP was abnormal in 51/74 (68.9%) right eyes and 50/74 (67.6%) left eyes. VEP P100 latency was the main abnormality with mean latency values of 118.9 (±16.5) ms and 119.8 (±15.7) ms for the right and left eyes respectively, mildly prolonged when compared to our laboratory references of 104 (±10) ms (p<0.001). Subclinical VEP abnormality was detected in 56.5% of normal eyes and constituted mostly latency abnormality. VEP amplitude was also significantly reduced in this cohort but minimally so in the visually unimpaired. HVF was abnormal in 36/47 (76.6%) right eyes and 32/45 (71.1%) left eyes. The predominant field defect was peripheral constriction with an enlarged blind spot suggesting the greater impact by raised intracranial pressure over that of optic neuritis. Whether this was due to papilloedema or a compartment syndrome is open to further investigation. Subclinical HVF abnormalities were minimal and therefore a poor screening test for early optic nerve dysfunction. However, early optic nerve dysfunction can be detected by testing of VEP P100 latency, which may precede the onset of visual loss in CM.
Highlights
Cryptococcal meningitis (CM) and other opportunistic infections in HIV infected patients continue to be a burden in developing countries despite established antiretroviral drug treatment programmes [1]
Rex et al have suggested a dual mechanism of early optic neuritis and late papilloedema resulting from optic nerve infiltration and raised intracranial pressure respectively [7]
Flash light emitting diode (LED) goggles visual evoked potential (VEP) was done for 6 patients who could not fixate due to severe visual loss or inattention
Summary
Cryptococcal meningitis (CM) and other opportunistic infections in HIV infected patients continue to be a burden in developing countries despite established antiretroviral drug treatment programmes [1]. Rex et al have suggested a dual mechanism of early optic neuritis and late papilloedema resulting from optic nerve infiltration and raised intracranial pressure respectively [7]. Conflicting reports of the optic neuritis, papilloedema and the more recent compartment syndrome models abound in the literature [8,9,10,11]. A definitive model is still lacking but the compartment syndrome occurring along the nerve or at the optic canal level seems most plausible [12,13]. A better understanding of the pathogenesis of cryptococcal induced visual loss will certainly provide better guidance to management and prevention of blindness in this group. The likelihood of optic nerve infiltration and the benefit of corticosteroids have not been entirely excluded as treatment option as demonstrated pathologically by Corti et al that fungal infiltration of the optic nerve does occur and by De Schacht et al of the benefit of corticosteroids especially in the setting of immune reconstitution [17,18]
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