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Aim: To investigate whether retinal changes in children with severe malaria affect visual acuity 1 month after systemic recovery. Methods: All children with severe malaria admitted to a research ward in Malawi during one malaria season were examined by direct and indirect ophthalmoscopy. Visual acuity was tested in those attending follow up by Cardiff cards, Sheridan-Gardiner single letters, or Snellen chart. Results: 96 (68%) children attended follow up, of whom 83 (86%) had visual acuity measured. Cardiff cards were used in 47 (57%) children, and Sheridan-Gardiner letters or Snellen chart in 29 (35%). There was no significant difference in the mean logMAR visual acuity between groups with or without macular whitening (0.14 versus 0.16, p = 0.55). There was no trend for worse visual acuity with increasing severity of macular whitening (p = 0.52) including patients in whom the fovea was involved (p = 0.32). Six (4.2%) children had cortical blindness after cerebral malaria, and all six had other neurological sequelae. Ophthalmoscopy during the acute illness revealed no abnormalities in four of these children. Conclusion: Retinal changes in severe malaria, in particular macular whitening, do not appear to affect visual acuity at 1 month. This supports the hypothesis that retinal whitening is due to reversible intracellular oedema in response to relative hypoxia, caused by sequestered erythrocytes infected by Plasmodium falciparum. Impaired visual functioning after cerebral malaria is not attributable to retinal changes and appears to be a cortical phenomenon.

A 35 month old child was referred for electrophysiology testing with pendular nystagmus, corresponding head oscillations and reduced vision. Flash visual evoked potential (VEP) revealed large responses at the right occiput (but not the left occiput) from the right eye and similar large responses at only the left occiput from the left eye, indicating absent/deficient crossover at the chiasm. A magnetic resonance imaging (MRI) scan subsequently confirmed absence of the optic chiasm. There was no other evidence of midline brain defects. Her subsequent development to age 11 has been followed. The nystagmus has remained mainly horizontal but a torsional component was noted from age 5 years and described as see-saw at age 6 years. A small right esotropia was noted at 6 years and spectacles prescribed for low hypermetropic refractive error. Bilateral superior rectus recessions at age 7 years produced an improved head posture. Her visual acuity has remained stable at around 6/24 from age 4 years. No binocularity nor stereopsis has been demonstrated over subsequent visits.

We aimed to investigate the visual evoked potential (VEP) in children unconscious with Plasmodium falciparum malaria, a common cause of death in Africa. Flash VEPs were carried out in Malawi during one peak malaria season. Children were included in the study if they had P. falciparum malaria and reduced consciousness ? Blantyre Coma Score (BCS) 4 or less out of 5. Initial VEPs were performed after stabilising the patient and commencing treatment. To investigate optimal VEP protocols, varying stimulus parameters were tested. Where possible, VEPs were repeated daily until the child recovered full consciousness (BCS 5). The initial traces of 40 children were included in the study and serial traces were obtained in 30 of these. Mean VEP latency was greater on admission than either on day 1 or at BCS 5 (paired t-test, P < 0.05) for all test protocols. There was a positive correlation between VEP latency on admission and parasite count and a negative correlation with blood glucose on admission (Spearman's rank correlation, P < 0.05 for all test protocols). Children with severe P. falciparum malaria have delayed VEP responses and recovery occurs in parallel with return to normal consciousness. VEP recordings are quick and reproducible and may find a place in assessing levels of coma and cerebral function in severe malaria.