Notes on Nystagmus

Notes on NystagmusFrenzel glasses disallows fixation and exaggerates nystagmus PPRF has go there neurons. Forceful. If PPRF if faulty, eyes move slowly away from sight of interest. It is responsible for saccades. Implicated in cerebellar damage SCD type 2 cannot saccadeSaccade loss of vision in between normal should be smooth pursuitCerebellar lesions cause loss of pursuit and causes saccadic eye movementsNeural integrator has stay there neurons. It fires based on the position and velocity of the eyeballs. Distributed throughout brainstem and cerebellum When seeing down-beating nystagmus, suspect cervicomedullary junction lesion or Arnold Chari malformation OR bilateral posterior SCC (central pathways of it ??)Upbeating = bilateral superior SCC

Pendular nystagmus can be divided into congenital or acquiredCongenital nystagmus features reverse OKN, nullpoint, convergence improves nystagmus, pendularCriteria for convergence involves intact vision ie. No occipital lobe lesion. Convergence also uses CN3 pathwayCauses of seesaw nystagmus Vertical/ loss of vertical gaze = PSP/midbrain lesion (rostral lesion)Questions to ask patientVertigo?DurationSingle ep or recurrentNeuro exam central/peripheral Why is the MLF a site of involvement in MS, causing INOAnswer: MLF is a highly myelinated area (to make up for inherent lag from CN 6 / CN3 pathway). MS affects myelinated areas!!