part 9 Flashcards
where does nystagmus originate
vestublo-occular pathway
where does vertigo and dizziness originate from
vestibular cortex
nystagmus was originally defined as
sleepiness or drowsiness
nystagmus key chractersistics
involuntary, rapid rhythmic, oscillatory eye movement with at least 1 slow phase
what directions can the nystagmus be
horizontal (L,R)
vertical (up, down)
Rotary (circular)
horizontal rotary
vertical rotary
jerk nystagmus
nystagmus with a slow phase and fast phase
- typical nystagmus
pendular nystagmus
nystagmus with only slow phases
what component describes the nystagmus
fast component
ex., fast to left is a left beating nystagmus
2 types of nystagmus
- unidirectional (constant quick component- beats same direction)
- bidirectional- quick component changes in different fields. look L beating left, look R beating right
is a bidirectional beating nystagmus Central or peripheral
central
1st degree nystagmus
-mild nystagmus
only see nystagmus when look at one side (towards fast phase)
ex., look left- nystagmus, central no and right no
2nd degree nystagmus
nystagmus at fast phase and when you look ahead (Straight)
3rd degree nystagmus
most severe
-nystagmus in all directions (slow phase, fast phase and direct ahead)
attributes of nystagmus
Binocular
Conjugate
Velocity
Frequency
Wavelength
Amplitude
Temporal profile
Age of first appearance
what is temporal profile of nystagmus
how it is changing over time (better or worse)
Nystagmus categories (2)
- physiologic
- pathologic
physiologic nystagmus
occur in normal subjects
Triggered by:
vestibular induced (caloric, rotational, MRI)
visual induced (optikinetic)
extreme lateral gaze
- show normal function, if triggered something is not working correctly
pathologic nystagmus
underlying abnormality
- spontaneous
gaze evoked
triggered
* challenge is to determine if it is secondary to peripheral disorder or is it coming elsewhere
vestibular (peripheral) pathologic nystagmus characteristics
- unidirectional (constant)
- direction is horizontal, horizontal and torsional, vertical and torsional or torsional (NEVER just vertical that is CNS)
- Jerk motion (always)- quick and slow component that is inhibitory- slow phase towards site of lesion, fast towards healthy
- inhibited by visual fixation (goes away or lessens when looking at finger)
Central pathology characteristics
any direction, can change
vertical
nodes possible
not associated with true vertigo
intensity stays same or speeds up
when a vestibular system is damaged what happens to neural firing
it becomes asymmetrical. One side decreases firing rate and the healthy side now has a perceived higher firing rate, this causes the brain to think we turned our head- activating the VOR to maintain gaze (slow phase). However we didn’t move head. So now the brain quickly puts image back into target with fast movement (saccade).
explain conjugate nature of vestibular spontaneous nystagmus
present at same time in both eyes- herrings law
peripheral nystagmus follows alexander law about fast component gaze explain
fast component gaze increases with frequency and amplitude- nystagmus increase when patient looks towards fast component and decreases when looks towards slow component
alexanders law
- fast phase toward healthy ear
- nystagmus greatest when gaze directed towards healthy ear and attenuated at central gaze, absent or reduced when directed towards impaired
- augmented when vision denied- increased (moves a lot)
when are alexanders laws wrong
with excitatory nystagmus or recovery nystagmus
excitatory nystagmus
the affected side is hyperactive, so the healthy side is the one with less firing rate and the fast phase will be directed towards unhealthy ear ex., meniers
- contradicts alexanders rule#1
recovery nystagmus
too low then too high or reverse
fast phase also towards unhealthy
explain how vestibular nystagmus changes over time
CNS compensates after few days 3rd degree disappears
1-2 weeks 2nd degree will disappear then 1st
nystagmus only observed with no fixation (5-10 years later)
what is the timecourse for CNS compensation
2-4 weeks ; varies
gaze evoked nystagmus
prominent with fixation
not able to maintain eye deviation away from primary position (nystagmus when looking at side)
different from extreme lateral gaze (greater than 30 degrees)
non conjugate nystagmus
1 eye (monocular)
central disease
nystagmus is healthy side
dissociated nystagmus
type of non-conjugate nystagmus
where eyes change depending on gaze. (non yoked)
indicated CNS
hering’s law
if ears affected eyes following hering’s law moving in the same direction and same velocity
bi-directional nystagmus
quick phase of nystagmus are directed away from the primary postion of gaze in both directions (MS)
rebound nystagmus
primary postion nystagmus provoked by prolonged eccentric gaze holding (looking forward)
cerebellar pathology
bruns nystagmus
combination of nystagmus slow large amplitude (gaze paretic nystagmus) when looking towards side of lesion and rapid small amplitude (jerk nystagmus-vestibular) when looking away from lesion
i.e., CPA lesion, characterizes scwanoma
up-beating nystagmus
central
primary gaze with linear slow and fast phases
need to rule out medications (can be side effect)
downbeating nystagmus
primary gaze with upward slow phase downward fast
CNS disorder
ocular flutter
back to back series of horizontal conjugate saccades
10-25/second; 20-60 degrees amplitude
central
- not nystagmus bc doesn’t have slow phase
- paraneoplastic,para-infectious
square wave jerks
saccadic intrusions
MS or parkinsons
