Contributions
Abstract: 99
Type: Oral
The anterior visual system presents several advantages for testing neuroprotection because the effects of treatment on its structure and function can be measured with increasingly sensitive noninvasive techniques including optic nerve MRI, optical coherence tomography and visual evoked potentials.
Several recent optic neuritis trials have tested the neuroprotective potential of drugs such as erythropoietin, and inhibitors of voltage gated sodium channels, glutamate receptors, and acid-sensing ion channels. Proof of concept of neuroprotection, indicated by preservation of the retinal nerve fibre layer and/or the area of the optic nerve, has been suggested in trials using phenytoin, memantine and erythropoietin. In the phenytoin trial, treatment from a mean of 8 days after onset of visual loss, and continued for 3 months, prevented 30% of the loss of thickness of the retinal nerve fibre layer, and 34% of the loss of macular volume, when measured after 6 months.
Interestingly, preservation of structure in the active arms of these trials has not been associated with a significantly better visual outcome, measured using high and low contrast acuities, suggesting that more effective therapies (or combinations of drugs targeting different mechanisms of injury), and more sensitive structural and visual outcomes, may be required. Some of these issues are being investigated in ongoing work comparing the utility of different visual outcomes, and comparing measurements of the thickness of the retinal nerve fibre layer with the thickness of individual segmented layers of the macula.
Recent progress encourages the view that optic neuritis could serve as model for testing therapies which prevent neurodegeneration in acute inflammatory lesions. However, the relevance of the model to neuroprotection in other relapses of MS, and to progressive MS, remains uncertain, and will depend considerably on the extent to which the mechanisms of neuronal injury are shared in these different situations.
Disclosure: Supported by the US National Multiple Sclerosis Society, the Multiple Sclerosis Society of Great Britain and Northern Ireland, the National Institute for Health Research Clinical Research Network, and University College London Hospitals Biomedical Research Centre.
Abstract: 99
Type: Oral
The anterior visual system presents several advantages for testing neuroprotection because the effects of treatment on its structure and function can be measured with increasingly sensitive noninvasive techniques including optic nerve MRI, optical coherence tomography and visual evoked potentials.
Several recent optic neuritis trials have tested the neuroprotective potential of drugs such as erythropoietin, and inhibitors of voltage gated sodium channels, glutamate receptors, and acid-sensing ion channels. Proof of concept of neuroprotection, indicated by preservation of the retinal nerve fibre layer and/or the area of the optic nerve, has been suggested in trials using phenytoin, memantine and erythropoietin. In the phenytoin trial, treatment from a mean of 8 days after onset of visual loss, and continued for 3 months, prevented 30% of the loss of thickness of the retinal nerve fibre layer, and 34% of the loss of macular volume, when measured after 6 months.
Interestingly, preservation of structure in the active arms of these trials has not been associated with a significantly better visual outcome, measured using high and low contrast acuities, suggesting that more effective therapies (or combinations of drugs targeting different mechanisms of injury), and more sensitive structural and visual outcomes, may be required. Some of these issues are being investigated in ongoing work comparing the utility of different visual outcomes, and comparing measurements of the thickness of the retinal nerve fibre layer with the thickness of individual segmented layers of the macula.
Recent progress encourages the view that optic neuritis could serve as model for testing therapies which prevent neurodegeneration in acute inflammatory lesions. However, the relevance of the model to neuroprotection in other relapses of MS, and to progressive MS, remains uncertain, and will depend considerably on the extent to which the mechanisms of neuronal injury are shared in these different situations.
Disclosure: Supported by the US National Multiple Sclerosis Society, the Multiple Sclerosis Society of Great Britain and Northern Ireland, the National Institute for Health Research Clinical Research Network, and University College London Hospitals Biomedical Research Centre.