Part 13 Flashcards
what are saccades
rapid eye movements that bring target into focus on fovea
what is the latency of saccades
200ms
abnormal saccades
over or undershoot or slow
procedure for testing saccade
hold indexes 15 degrees to side of nose, alternate fast left and right (non-rhymtically), horizontal vertical and diagonally
abnormalities in saccades are due to
brainstem or cerebellar pathology (central)
excitatory burst neurons (EBN)
8-12 ms before saccade
silent during fixation and slow movements
inhibitory burst neurons
inhibit antagonist OMN
omnipause neurons (OPN)
maintain stable fixation
- stops firing before saccade and starts immediately after saccade ends
Long lead burst neurons
40-100ms before saccade
synchronize onset and end of saccades
inhibit and hold opn
smooth pursuit eye movement (tracking)
ability to track a target image and stabilize on fovea
what does smooth pursuit depend on
visual information
predictive
brainstem output
when does smooth pursuit decline and what happens
with age it becomes saccadic and choppy
smooth pursuit impairment disease
Parkinsons
Progressive supranuclear palsy
cerebellar disorders
large cerebral lesions
smooth pursuit procedure
follow moving target which moves 10-20 degrees L R and up down at slow speed (0.2-0.8Hz)
with smooth pursuit what are we looking for
smooth conjugate eye movement
what does abnormalities in smooth pursuit show
brainstem or cerebellar abnormality
what are the abnormalities of smooth pursuit
catch up saccades (eyes fall behind target)
back up saccades (eyes faster than target, congenital nystagmus, latent nystagmus, maldevelopment of cortical tracking system)
optikinetic reflex
allows eyes to follow objects in motion when the head remains stationary (e.g., looking out car window)
hypermetria
overshoot
when are OKN present
normally present
what does OKN comprise of
smooth eye movements interspersed by saccades
OPN procedure
ask patient to follow fast changing repetitive image
think iPad example during class
abnormal OKN
absent OKN
unilateral vestibular deficit will show slow OKN on what side
same side as vestibular deficit
fixation
gaze holding, neural integrator makes fixation possible but fixation itself is high eye level control
abnormal fixation
when nystagmus present
fixation procedure
hold patient head with. one hand and have them follow finger 30 degrees to L R up down and pause in each position
VOR supression
ability of vestibulocerebellar system to surpress a vestibular signal
VOR supression procedure
patient in chair, hold out arms with thumbs in front of eyes, fixate on thumbs, patient rotated side to side in chair
VOR supression procedure abnormal
if VOR suppression abnormal almost always sign of cerebellar brainstem
VOR suppression look for
patients ability to maintain visual fixation or if the patient makes saccadic eye movements
