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Notes on Nystagmus

Frenzel 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 saccade

Saccade loss of vision in between normal should be smooth pursuit

Cerebellar lesions cause loss of pursuit and causes saccadic eye movements

Neural 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 acquired

Congenital nystagmus features reverse OKN, nullpoint, convergence improves


nystagmus, pendular

Criteria for convergence involves intact vision ie. No occipital lobe lesion. Convergence
also uses CN3 pathway

Causes of seesaw nystagmus

Vertical/ loss of vertical gaze = PSP/midbrain lesion (rostral lesion)

Questions to ask patient

Vertigo?

Duration

Single ep or recurrent

Neuro exam central/peripheral

Why is the MLF a site of involvement in MS, causing INO

Answer: MLF is a highly myelinated area (to make up for inherent lag from CN 6 /
CN3 pathway). MS affects myelinated areas!!

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