Dexamethasone And MethylPrednisolone In Treatment Of Indirect Traumatic Optic Neuropathy
Kitthaweesin K, Yospaiboon Y
J Med Assoc Thai 2001 May;84(5):628-34
Khon Kaen University, Faculty of Medicine, Department of Ophthalmology, Thailand
A randomized, double blind study was carried out to compare the efficacy of Dexamethasone and MethylPrednisolone in the treatment of indirect traumatic Optic Neuropathy.
Twenty-one patients, 20 male and 1 female, were diagnosed as having suffered from indirect traumatic Optic Neuropathy. The time from injury to treatment was within 7 days.
The average age was 26.38 +/- 11.89 years. The most common cause of injury was Motor Vehicle Accident (MVA). Associated head and MaxilloFacial injury were reported 43.48 and 34.78 per cent, respectively.
Before treatment, no light perception was detected in 19.05 per cent of the participants. Treatments were randomized: ten patients received Dexamethasone intravenously for 72 hours and 11 MethylPrednisolone.
The Best Corrected Visual Acuities (BCVA) were determined using the Snellen Chart before and 1, 2, 3, 7, 14 and 60 days after treatment.
Three or more lines of improvement of the BCVA, were found in 70 and 67 per cent of patients treated with Dexamethasone, and 45.45 and 33.33 per cent of patients treated with MethylPrednisolone, at 2 weeks and 2 months, respectively.
There were no significant differences in age, cause of injury, injury to treatment interval, initial BCVA and Visual improvement between the two groups.
Size-Selective Neuronal Changes In The Anterior Optic Pathways Suggest A Differential Susceptibility To Injury In Multiple Sclerosis
Evangelou N, Konz D, Esiri MM, Smith S, Palace J, Matthews PM
Brain 2001 Sep;124(Pt 9):1813-20
University of Oxford, Centre for Functional Magnetic Resonance Imaging of the Brain, UK
Axonal damage is found in both acute and chronic lesions of Multiple Sclerosis. Direct Axon counting in post-mortem tissue has suggested that smaller Axons might have a greater susceptibility to damage, but methodological limitations have precluded unequivocal interpretation.
However, as Neuronal and Axonal sizes are linked and Neuronal changes would be expected with Retrograde or TransSynaptic Degeneration following Axon injury.
We hypothesized that an alternative strategy for studying this phenomenon would be to define Multiple Sclerosis-associated changes in Neurons.
To test this hypothesis, we measured both Axonal Loss and Neuronal size changes in the Anterior Optic Pathway [including the Optic Nerve (ON), Optic Tract (OT) and Lateral Geniculate Nucleus] of the Brains of eight patients who died with Multiple Sclerosis and in eight control Brains.
The ONs and OTs in Brains from the Multiple Sclerosis patients showed a trend to smaller mean cross-sectional areas (ON, Multiple Sclerosis = 6.84 mm(2), controls = 9.25 mm(2); and OT, Multiple Sclerosis = 6.45 mm(2), controls = 7.94 mm(2), P = 0.08).
And, had reduced Axonal densities (ON, Multiple Sclerosis = 1.1 x 10(5)/mm(2), controls = 1.7 x 10(5)/mm(2); and OT, Multiple Sclerosis = 1.4 x 10(5)/mm(2), controls = 1.8 x 10(5)/mm(2), P = 0.006).
Estimated total Axonal counts were reduced by 32 (OT)-45% (ON) in the patients relative to controls (ON, Multiple Sclerosis = 8.1 x 10(5) Axons, controls = 14.8 x10(5), P = 0.05; and OT, Multiple Sclerosis = 9.1 x 10(5), controls = 13.3 x 10(5), P = 0.02).
The size distributions of the MagnoCellular Cells in the Lateral Geniculate Nucleus were similar for the two groups, but in Multiple Sclerosis Brains the ParvoCellular Cells were significantly smaller.
(Mean sizes: Multiple Sclerosis = 226 microm (2), controls = 230 microm(2), P < 0.001) and had a larger variation in size, suggesting a greater proportion of Atrophic Neurons.
Axon Loss in the Optic Nerves of Multiple Sclerosis patients correlated strongly with measures of increased dispersion of cell sizes in the ParvoCellular layer (r = 0.8, P < 0.04).
These data demonstrate that both Atrophy and decreased density contribute to the substantial Axonal Loss in the Anterior Visual Pathway of these patients.
This appears related to a relatively selective Atrophy of the smaller Neurons of the ParvoCellular layer in the Lateral Geniculate Nucleus, supporting the hypothesis that smaller Axons may be preferentially susceptible to injury in Multiple Sclerosis.
Pokroy R, Modi G, Saffer D
Eye 2001 Aug;15(Pt 4):469-73
University of Witwatersrand, Department of Neurology, Baragwanath Chris Hani Hospital, Johannesburg-Soweto, South Africa
To describe the clinical profile of Idiopathic Optic Neuritis in South African blacks.
South African black patients with acute isolated idiopathic Optic Neuritis, treated and followed for at least 3 months at a large medical center, were studied.
Exclusion criteria were other causes of Optic Neuropathy (such as Ischaemic Optic Neuropathy, Toxins or Leber's Hereditary Optic Neuropathy); all causes of Optic Neuritis (such as HIV, NeuroSyphilis, Sarcoid or Connective Tissue Disease); Neurological Disease outside of the Optic Nerves; and any race other than South African black.
Patients underwent extensive Ophthalmic, Neurological, Radiological, CerebroSpinal Fluid and blood assessment.
Eighteen eyes of 10 patients were studied. The mean age was 35.7 years and 9 patients were female. Only 2 patients had truly UniLateral Optic Neuritis, the other 8 having either BiLaterally simultaneous or consecutive disease.
Presenting Visual Acuity (VA) was less than 6/60 in 17 of 18 Eyes, with severe DysChroMatopsia in all Eyes. Fifteen Eyes had Optic Disc swelling. All patients were treated with CorticoSteroids.
After at least 3 months follow-up only 6 Eyes recovered VA of 6/12 or better, with only 3 Eyes recovering Color Vision of 10/13 or better on Ishihara plate testing. No patient had Multiple Sclerosis (MS) on presentation, nor developed MS on follow-up.
Idiopathic Optic Neuritis in black South Africans differs from that in whites.
The higher prevalence of BiLateral cases and of Optic Disc swelling, the weaker association with MS and the extremely poor Visual outcome distinguish Optic Neuritis in black South Africans.