Optical coherence tomography (OCT) and multiple sclerosis (MS)

Abstract

Acute optic neuritis (ON) is a common manifestation of multiple sclerosis (MS). ON is the first clinical demyelinating event in MS for about 20 % of patients. In the Optic Neuritis Treatment Trial (ONTT), the overall cumulative probability of developing clinically-definite MS, defined as a second clinical event, was 50 % by 15 years after the onset of acute ON. Furthermore, those patients with a positive brain MRI consistent with demyelination had a far greater risk of developing of MS compared to those with a normal baseline MRI (72 % vs. 25 %). The subsequent development of MRI-based diagnostic criteria for MS has led to a paradigm shift in our clinical approach to patients with ON as a first clinical demyelinating event. In those patients with MRI scans consistent with demyelination, platform MS therapies have become standard treatment for patients with clinically isolated syndromes (CIS), including ON. Our ability to diagnose MS with a single MRI scan has allowed us to more expeditiously establish the diagnosis of MS while advances in OCT (optical coherence tomography) has provided us an opportunity to better resolve the visual dysfunction that occurs in this disorder. OCT permits the correlation of structural aspects of anterior visual pathway axonal and neuronal loss with visual function in ON. It is now known that patients with MS have thinning of the retinal nerve fiber layer (RNFL, axons) and ganglion cell/inner plexiform layer (GCL+IPL, neurons) even in the absence of a history of acute ON. Such patients have clinically meaningful worsening of vision and quality of life (QOL). Furthermore, OCT is useful in patients with MS for distinguishing macular disease from ON, and for monitoring patients for macular edema associated with use of fingolimod. In this chapter, we summarize the data and current concepts for use of OCT in the evaluation and monitoring of patients with MS. Importantly, we will highlight how OCT has expanded our thinking about the pathogenesis of visual pathway dysfunction, and how RNFL and GCL+IPL thickness may serve as structural markers for monitoring disease in our patients.