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The adult neuro-ophthalmologist may see patients presenting for the first time with symptoms and signs classically associated with paediatric conditions. Therefore a literature review combined with case descriptions from the author's clinic is presented here, divided into problems of the optic nerve, ocular motility or visual function. Though such a review cannot be comprehensive nor cover every paediatric condition that has ever presented to an adult clinic, the authors hope that it will provide some useful insights and interesting clinical vignettes to assist clinicians in their own practice. [ABSTRACT FROM AUTHOR]

Vision in the mesopic range is affected by a number of inherited and acquired clinical disorders. We review these conditions and summarize the historical background, describing the clinical characteristics alongside the genetic basis and molecular biological mechanisms giving rise to rod and cone dysfunction relevant to twilight vision. The current diagnostic gold standards for each disease are discussed and curative and symptomatic treatment strategies are summarized. [ABSTRACT FROM AUTHOR]

The article cites a case of a 25-year-old female secretary who was diagnosed of acute optic neuritis. The patient complained a blurry vision in her right eye and experienced color blindness. White matter abnormalities were found by magnetic resonance imaging. The patient undergone a course of intravenous corticosteroids followed by the initiation of interferon beta-1a therapy.

General neurologists and stroke specialists are regularly referred cases of visual disturbance by general practitioners, emergency doctors and even ophthalmologists. Particularly when the referral comes from ophthalmologists, our assessment tends to focus on the optic nerve; however, retinal conditions may mimic optic neuropathy and are easily missed. Their diagnosis requires specific investigations that are rarely available in a neurology clinic. This article focuses on how a general neurologist can identify retinal problems from the clinical assessment and how to proceed with initial investigations. The following cases were all referred to a consultant neurologist (GTP) from ophthalmology services as optic neuropathies or other neurological disorders. Part A of the summary describes the presentation and findings in the neurology clinic; part B describes the subsequent specialist assessment in the neuroophthalmology/ eye clinic. [ABSTRACT FROM AUTHOR]

Bilateral optic neuropathy in Dar es Salaam is now considered endemic and is estimated to affect 0.3–2.4% of young adults. The condition is characterized by a subacute bilateral loss of central vision of unknown aetiology. Findings of spectral domain optical coherence tomography have not previously been reported for these patients. All patients diagnosed with endemic optic neuropathy over a 2-year period at the Muhimbili National Hospital underwent spectral domain optical coherence tomography macular imaging. Scans were graded qualitatively for severity of retinal nerve fibre layer loss as well as the presence of microcystic macular changes, which have not previously been described in this condition. Of the 128 patients included (54.7% male; median age 20 years), severe retinal nerve fibre layer loss was found in 185 eyes (74.0%). There was full concordance in retinal nerve fibre layer thickness between the two eyes in 113 (91.1%) patients. Microcystic macular spaces were found in 16 (12.5%) patients and were bilateral in nine (7.0%) individuals. These changes were typically more prominent in the nasal than the temporal macula, predominantly involving the inner nuclear layer, and often occurred in an annular configuration that was evident on en face infra-red imaging, though not discernible on colour fundus photography or clinically. All patients with microcystic macular changes had severe thinning of the retinal nerve fibre layer (P = 0.02). Four patients in whom cystic spaces were demonstrated had sequential scans, and there was no detectable alteration in the configuration of these changes over a period of up to 16 months. This is the first study to document optical coherence tomography findings in endemic optic neuropathy. We have observed symmetrical severe loss of the caeco-central projection (papillomacular bundle) with otherwise well-preserved macular architecture. Also, we have observed microcystic retinal changes in a significant proportion of patients, which were associated with severe retinal nerve fibre layer loss. Similar changes have recently been reported from optical coherence tomography images of patients with multiple sclerosis, relapsing isolated optic neuritis, dominant optic atrophy, Leber’s hereditary optic neuropathy and a patient with a chronic compressive optic neuropathy, supporting the hypothesis that this may be a non-specific phenomenon secondary to ganglion cell death. The correspondence of the changes to an annulus discernible on infra-red en face imaging, but not using other conventional retinal imaging techniques highlights the potential usefulness of this modality. [ABSTRACT FROM PUBLISHER]

Three patients on haemodialysis presented with acute painless visual loss. From each, a comprehensive medical and ophthalmic history was taken and each underwent a complete ophthalmic examination. Visual evaluation was carried out by recording Snellen visual acuities, Ishihara colour test scores, the presence of a relative afferent pupillary defect (RAPD) and visual fields with either Goldmann or Humphrey perimetry. Review of renal case notes was performed and appropriate laboratory investigations including imaging were carried out to investigate the cause of disc swelling in all cases. All cases presented with acute painless visual loss, a RAPD, disc swelling, impaired colour vision and a visual field defect. All cases had a history of post-dialysis hypotension. In 2 cases, post-dialysis hypotension was documented just prior to the development of anterior ischaemic optic neuropathy (AION) suggesting a causal relationship. Falls in mean arterial pressure (MAP) of 31 and 22 mmHg were recorded. None of the cases had other well documented risk factors for AION such as diabetes or hypercholesterolaemia. One case had crowded discs. Two cases had bilateral involvement. Two cases were treated with corticosteroids and 1 with aspirin. Visual improvement was noted in 1 case coincident with corticosteroid treatment. Common risk factors in all 3 cases were anaemia and post-dialysis hypotension. In conclusion, patients undergoing haemodialysis may be at risk of AION particularly if they are anaemic and develop post-dialysis hypotension. They should be informed of a small and unpredictable risk of visual loss. [ABSTRACT FROM AUTHOR]