الفهرس | Only 14 pages are availabe for public view |
Abstract M ultiple sclerosis is an inflammatory demyelinating disease that affects CNS. It is thought that it is caused by multiple factors like immunological factors, vitamin d deficiency, vitamin b12 deficiency or infection by EBV or HHV6. It has a lot of ocular manifestations as optic neuritis, diplopia, oscillopsia, nystagmus and ophthalmoplegia. RRMS is treated by fingolimod which is the first approved oral drug for RRMS, it cause macular edema after 4 months of use as a side effect. In our work we did a full ophthalmological examination, visual acuity testing, anterior segment examination by slit lamp bio-microscopy, IOP measurement by goldmann applanation tonometer, indirect fundus examination by 90D lens, OCT macula at the first assessment and OCT macula and electrophysiological tests after 4 months of treatment by fingolimod to 15 patient of RRMS who were candidate for fingolimod treatment. We found that the mean best corrected visual acuity change after treatment slightly decreased but this was non-significant. IOP measurements were not changed after treatment. Despite the changes in visual acuity; fingolimod associated macular edema did not develop. Among 15 patients (30 eyes), 11 eyes have slightly increased MT, 5 eyes have stable MT and 14 eyes have slightly decreased MT. Regarding amplitude in MfERG in ring 1, and it happened without development of macular edema (ME), as 50% of patients had MfERG changes in spite of absence of ME. Also we found that 4 eyes affected in PERG test in form of decreased P50 amplitude and delayed latencies. So we recommend doing electrophysiological tests (MfERG and PERG) in follow up protocol of fingolimod treatment. |