Abstract
Multiple sclerosis (MS) commonly causes eye movement abnormalities that may have a significant impact on patients’ disability. Inflammatory demyelinating lesions, especially occurring in the posterior fossa, result in a wide range of disorders, spanning from acquired pendular nystagmus (APN) to internuclear ophthalmoplegia (INO), among the most common. As the control of eye movements is well understood in terms of anatomical substrate and underlying physiological network, studying ocular motor abnormalities in MS provides a unique opportunity to gain insights into mechanisms of disease. Quantitative measurement and modeling of eye movement disorders, such as INO, may lead to a better understanding of common symptoms encountered in MS, such as Uhthoff’s phenomenon and fatigue. In turn, the pathophysiology of a range of eye movement abnormalities, such as APN, has been clarified based on correlation of experimental model with lesion localization by neuroimaging in MS. Eye movement disorders have the potential of being utilized as structural and functional biomarkers of early cognitive deficit, and possibly help in assessing disease status and progression, and to serve as platform and functional outcome to test novel therapeutic agents for MS. Knowledge of neuropharmacology applied to eye movement dysfunction has guided testing and use of a number of pharmacological agents to treat some eye movement disorders found in MS, such as APN and other forms of central nystagmus.
Highlights
Multiple sclerosis (MS) is a common disorder of the central nervous system (CNS) that affects more than 2 million people worldwide
As the physiology and underlying anatomical network of eye movement control is well known from animal models and studies in humans [6], eye movement abnormalities are highly localizing to CNS structural lesions
The latter can result from a lesion of the abducens nucleus and the adjacent medial longitudinal fasciculus (MLF) or, less commonly, from a bilateral internuclear ophthalmoplegia (INO) combined with a unilateral abducens nerve palsy
Summary
Multiple sclerosis (MS) is a common disorder of the central nervous system (CNS) that affects more than 2 million people worldwide. Once thought to be predominantly an autoimmune inflammatory disease, MS is regarded as a complex entity characterized by inflammatory demyelinating events and a significant component of neurodegeneration that manifests as neuronal and axonal loss since the early stages of the disease. Our understanding of the disease has evolved dramatically over the years and, while MS was typically considered an immune disease targeting the white matter and due to T-cells dysfunction, it is clear that the pathological process targets both the gray and white matter and is enacted by complex involvement and dynamics of multiple cells, including T and B-cells, macrophages, mast cells, etc. The typical variability of phenotype and disease course observed in MS, spanning from relapsing to primary or secondary progressive clinical scenarios, is probably due to different extent and combination of inflammatory and neurodegenerative processes involving various CNS areas
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