Background: Brain atrophy, which is associated with cognitive impairment and retinal nerve fiber layer (RNFL) atrophy, is the main biomarker of neurodegeneration in multiple sclerosis (MS). However, data on the relationship between inflammatory markers, such as oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF), and cognition, RNFL atrophy, and brain atrophy are scarce. The aim of this study was to assess the influence of RNFL thickness, brain atrophy markers, intrathecal OCBs, and the immunoglobulin G (IgG) index on cognitive decline over a 5-year period in patients with MS.Methods: This prospective, single-center, observational cohort study included 49 patients with relapsing MS followed up over 5 years. At baseline, the patients underwent brain magnetic resonance imaging (MRI). Cognitive evaluation was performed using the Brief International Cognitive Assessment for MS (BICAMS), and RNFL thickness was assessed using optical coherence tomography (OCT). OCBs and IgG levels in the CSF were evaluated at baseline. The BICAMS, OCT, and MRI findings were re-evaluated after 5 years.Results: A significant reduction in information processing speed, visual learning, temporal RNFL thickness, the Huckman index, and third ventricle mean diameter was found in all 49 patients with relapsing MS over the observation period (p < 0.05). Of the patients, 63.3% had positive OCBs and 59.2% had elevated IgG indices. The atrophy of the temporal segment and papillomacular bundle and the presence of OCBs were significantly related to a decline in information processing speed in these patients (p < 0.05). However, brain atrophy markers were not found to be significant on the general linear models.Conclusions: RNFL atrophy and the presence of OCBs were related to cognitive decline in patients with MS over a 5-year follow-up period, thereby suggesting their utility as potential biomarkers of cognitive decline in MS.
Purpose The aim of the study was to assess changes of macular thickness after trabeculectomy and compare them in respect to the usage of preoperative prostaglandins and status of diabetes mellitus. Methods The prospective observational study included 93 glaucomatous eyes (90 patients) that underwent trabeculectomy. 81 (87.1%) patients were on prostaglandins treatment preoperatively. 5 (5.38%) patients had type 2 diabetes. The foveal and sectoral macular thicknesses were measured preoperatively, 1 week, 6 months and 12 months after the surgery using spectral domain optical coherence tomography. Retinal thickness was compared across the follow‐up visits and in respect to the preoperative use of prostaglandins and diabetes. Results There was a reduction in mean ± SD intraocular pressure of 18.5 ± 8.6mmHg 1 week, 15.4 ± 7.9 mmHg 6 months and 14.4 ± 8.3 mmHg 12 months after trabeculectomy (p < 0.001). 1 week postoperatively retinal thickening was observed in all macular subfields (p < 0.001); the central macular thickness increased from 267.23 ± 19.20 μm at baseline to 271.12 ± 19.59 μm. 6 months postoperatively macula remained slightly thicker in central, nasal, inner superior and outer temporal sectors (2.10 ± 5.97 μm, p < 0.001 in central subfield). 12 months after trabeculectomy retina showed thinning in the outer nasal and superior subfields (‐3.54 ± 8.57 μm; ‐1.94 ± 7.02; p < 0.01, respectively). There were no differences in the changes of macular thickness when compared in respect to preoperative prostaglandins (p > 0.05). The retinal changes did not differ between diabetic and nondiabetic patients (p > 0.05). Conclusions Trabeculectomy induced mild macular thickening, more pronounced in the early postoperative period. Neither diabetes nor the use of prostaglandins before surgery had impact on these changes regardless their potency to increase vascular permeability.
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