Active MS is associated with accelerated retinal ganglion cell/inner plexiform layer thinning

Abstract

Objective: To determine the effect of clinical and radiologic disease activity on the rate of thinning of the ganglion cell/inner plexiform (GCIP) layer and the retinal nerve fiber layer in patients with multiple sclerosis (MS) using optical coherence tomography (OCT).Methods: One hundred sixty-four patients with MS and 59 healthy controls underwent spectraldomain OCT scans every 6 months for a mean follow-up period of 21.1 months. Baseline and annual contrast-enhanced brain MRIs were performed. Patients who developed optic neuritis during follow-up were excluded from analysis.Results: Patients with the following features of disease activity during follow-up had faster rates of annualized GCIP thinning: relapses (42% faster, p 5 0.007), new gadolinium-enhancing lesions (54% faster, p , 0.001), and new T2 lesions (36% faster, p 5 0.02). Annual GCIP thinning was 37% faster in those with disability progression during follow-up, and 43% faster in those with disease duration ,5 years vs .5 years (p 5 0.003). Annual rates of GCIP thinning were highest in patients exhibiting combinations of new gadolinium-enhancing lesions, new T2 lesions, and disease duration ,5 years (70% faster in patients with vs without all 3 characteristics, p , 0.001).Conclusions: MS patients with clinical and/or radiologic nonocular disease activity, particularly early in the disease course, exhibit accelerated GCIP thinning. Our findings suggest that retinal changes in MS reflect global CNS processes, and that OCT-derived GCIP thickness measures may have utility as an outcome measure for assessing neuroprotective agents, particularly in early, active MS. The anterior visual pathway is frequently affected in multiple sclerosis (MS), with 94% to 99% of patients with MS demonstrating optic nerve lesions postmortem.

Relationships between quantitative spinal cord MRI and retinal layers in multiple sclerosis

“…Our findings expand on prior studies that demonstrated that retinal layers (pRNFL and GCL 1 IPL) reflect global clinical and radiologic CNS processes in MS, and that specific retinal layers may reflect differential pathologic processes, including neurodegeneration and inflammation. 27,29 Our findings suggest that not only do retinal and SC-MRI measures reflect global pathologic processes in MS that are not adequately captured by brain atrophy alone, but that the regional and global pathologic processes that SC-MRI reflect are distinct from those that are captured by retinal measures, and that these processes independently contribute to mediating clinical disability in various functional systems. These findings highlight the importance of including an assessment of multiple compartments of the CNS affected by MS to better understand both global and regional disease processes, their interplay, and how they contribute to clinical disability in various functional systems.…”

Disease-modifying therapies modulate retinal atrophy in multiple sclerosis

“…Prior studies demonstrate that OCT-derived ganglion cell 1 inner plexiform layer (GCIP) thickness has superior reliability and reproducibility and correlates better with visual function and disability in MS than peripapillary retinal nerve fiber layer thickness (pRNFL). [8][9][10] Rates of GCIP thinning are accelerated in patients with MS exhibiting inflammatory activity, 11 and correlate strongly with rates of brain, particularly gray matter, atrophy over time. 8 Despite the increasing support for OCT as an outcome for assessing neurodegeneration in MS trials, whether different DMTs differentially affect retinal atrophy in MS remains to be assessed.…”

Dynamic molecular monitoring of retina inflammation byin vivoRaman spectroscopy coupled with multivariate analysis

“…by iNOS has deleterious effects on the electron transport chain, and is a major cause of neuronal and axonal damage [14]. The pro-inflammatory cytokine TNF-a is a key component of the signaling cascade associated with the inflammatory response in nervous tissue resulting in cellular damage [29].…”