Pendular Nystagmus and Ocular Motor Signs in MS

𝗢𝗿𝗶𝗴𝗶𝗻𝗮𝗹 𝗗𝗲𝘀𝗰𝗿𝗶𝗽𝘁𝗶𝗼𝗻: This is a 30-year-old man with a 15 year history of multiple sclerosis. For the last 12 months, he experienced horizontal oscillopsia. On examination, there were ocular motor abnormalities including gaze-evoked nystagmus, saccadic smooth pursuit, and hypermetric saccades which were attributable to his posterior fossa demyelinating disease. Additionally, there was horizontal pendular nystagmus, and this abated briefly with the termination of saccades and with blinks, both of which commonly suppress pendular nystagmus (albeit transiently). His vision was 20/100 OU with 0/10 HRR plates OU with temporal pallor OU. Because pendular nystagmus is commonly seen in MS patients, it has been suggested that the nystagmus might result from a prolonged response time for visual processing, supported by the fact that nystagmus is commonly more intense in the eye with poorer vision. However, pendular nystagmus doesn't change with visual feedback removed, and inducing visual delays by itself is not capable of causing the oscillations seen in MS. Therefore, it's likely that instability in the neural integrator (gaze holding machinery) plays a significant role in many cases, and his severe posterior fossa disease was likely to have contributed to neural integrator dysfunction. 𝗡𝗲𝘂𝗿𝗼-𝗼𝗽𝗵𝘁𝗵𝗮𝗹𝗺𝗼𝗹𝗼𝗴𝘆 𝗮𝗻𝗱 𝗡𝗲𝘂𝗿𝗼-𝗼𝘁𝗼𝗹𝗼𝗴𝘆 𝗧𝗲𝘅𝘁𝗯𝗼𝗼𝗸 𝗟𝗲𝗴𝗲𝗻𝗱: This patient had a 15 year history of MS, and for the last 12 months, he experienced horizontal oscillopsia. On examination, there were central ocular motor abnormalities including gaze-evoked nystagmus, saccadic smooth pursuit, and hypermetric saccades which were attributable to his posterior fossa demyelinating disease. Additionally, there was horizontal pendular nystagmus, and this abated briefly with the termination of saccades and with blinks, both of which commonly suppress APN (albeit transiently). His vision was 20/100 OU with 0/10 HRR plates OU with temporal pallor OU. Because pendular nystagmus is commonly seen in MS patients, it has been suggested that the nystagmus might result from a prolonged response time for visual processing, supported by the fact that nystagmus is commonly more intense in the eye with poorer vision. However, pendular nystagmus doesn't change with visual feedback removed, and inducing visual delays by itself is not capable of causing the oscillations seen in MS. Therefore, it's likely that instability in the neural integrator (gaze holding machinery) plays a significant role in many cases, and his severe posterior fossa disease was likely to have contributed to neural integrator dysfunction. https://collections.lib.utah.edu/ark:/87278/s6nc9v0z