supranucelar shit Flashcards
what is skew deviation
think of diagnosis if their is a newly acquired vertical diplpina
usually associated with horizontal and vertical deviation
it = concomitant hypertropia in pt with posterior fossa disease (eye = up)
due to brainstem or cerebellar lesion
r skew deviation would produce
right hypertropia
and incylotorison
if torsion = towards the hypertrophic eye = skew
differentiating between skew and a 4th
skew - higher eye is intorted
in superior oblique higher eye is extorted
in 4th nerve their is ipsilateral eyxclytorsion
upright supine test
in a 4th nerve palsy when pt is lying down vs sitting up their isn’t much difference in thyopermetropia in skew hypermetropia singifcantkly decreases (if it decreases indicates otolith dysfunction which is associated with skew)
ateiology of a skew deviation
posterior fossa lesion
in Arnold chiari malformation
trauma
abscess
haemorrhage
management for skew
usually transient , treat conservatively for 6 months afterwards
5 step test for skew
pct in primary postion
pct in side gaze
pct on tilt
upright supine
pct on maddox rod
difference between a 4th and skew deviation
incyclotrosion of higher eye in skew in 4th nerve eyxlotrsion excyclotrosion of higher eye
other neuro signs
usually are present e.g. gaze evoked nystagmus
skew typically associated with other neuro signs such as gaze evoked nystagmus and gaze palsies
what is an internuclear opthalmolplegia
defective adduction in ipsilateral side of lesion
own shows reduced adduction saccades
VOR
OKN
ALSO can be affected
dissociated nystagmus of contrlateral eye
contralateral abducting nystagmus
saccades typically slow and hypsometric
convergence and INO association
posterior INO = convergence is intact
Anterior INO= convergence is reduced
ateiology of INO
deymyleination in younger patents
brain ishchameia in older patients
Arnold chiari malformato meningitis
bilateral INO
in primary position eyes are usually straight
e.g. if looking to the right, right eye might have a weak adduction and when you look to the left their Weill be a dissociated horizontal abducting nystagmus
due to lesion for 6th nerve nucleus has to talk to contralateral 3rd nerve nucleus
structure = medial longitudinal fasiculus
adduction weakness
abducting nystagmus in both eyes
asymmetric
no associated skew deviation
management of INO
resolution documented in 50% of pts
medication (same for nystagmus)- gabapentin , baclofen , memantine
MRI
differential diagnosis for INO
Myasthenia Gravis
but convergence is often affected in MG
what causes an ino
lesion at the site of the medial longnituddinal fasiculus
when to think of an ino diagnosis
ino with or without exotropia if their is an adduction problem only , no ptosis no up and down gaze plays, no up and down movement to suggest third nerve palsy
++++ especially if pp = straight
in a young person you should be thinking of demyelinating disease
in older could be stroke and pseudo ino - most commonly caused my Myasthenia Gravis
quick ino features
adduction defects
dissociated horizontal abducting nystagmus
if in. with directions = bilateral
if exotropic = EBINO
MRI of mlf to ensure not stroke or demyelinating disease at the level of the medial longntiudinal fasiculus
1 and a half syndrome is….
a condition where one eye is completely paralysed for horizontal movements and the other can only move outwards
contralateral exo and ipsilateral gaze palsy
e..g left 1 and a half syndrome
left eye will be unable to adbuct and adduct and right eye will be unable to adduct but will be able to abduct
e..
ateiology of one and a half syndrome
ms
pontine lesion
brain stem infarction
arteriovenous malformation
myasthenia gravis the mimic
lesion in the 6th nerve palsy produces a
horizontal gaze palsy
ateiology of parinauds
pineal gland tumour
vascular accident in the dorsal midbrain
lsesion in the Sylvia aqueduct
obstructive hydrocephalus
signs of parinauds
light near dissociation
pupils react to near but not to light
on attempted upgazelid retraction. and convergence retraction nystagmus
dorsal midbrain syndrome = so loss oof upgaze
lid retraction of down gaze colliers sign
convergence weakness/spasm
sun setting sign if associated with hydrocephalus
progressive suprnuclear palsy
defective vetrtical saccades up gaze and downgaze
progressivve loss of visual movement
smooth pursuit and VOR
symptoms due to poor muscle tone and posture - difficulty swallowing
ateiology = extreme brainstem degernation of reticular formation
ocuclocrgyric crisis -
looss of balance presents in 6th decade
bells phenomena affected = eye dosnt close and is seen going up
]]may have complete opthalmoloplegia
signficicant decline appears year after year
differentials for parkisonsn
defective upwards and slow vertical saccades
Huntingtons dorea
should be differentiated from other basal ganglia diseases
double elevator palsy
one eye cannot look up
nad in pp /// hypotropia of affected eye
ateiology = supranuclear lesion in dorsal midbrain
differentials = browns -limitation of upgaze in adduction
duanes - globe reraction in downgaze
usually congenital
usually unilateral
pseudo ptosis
gaze palsies
vertical gaze palsy - due to lesions in the posterior commissure
rostral intestinal nucleus of the NFL
bells phenomena = vertical dolls head should be intact
lesion in the basal ganglia - Parkinson’s disease
unilateral lesion
oculocygruc crisis = eyes roll into the back of the head
lesion at the dorsal midbrain
horziontal gaze palsy
fibres descend from the FEF though basal ganglia and then deccuate before going to the PPRF
lesion before decussation
loss of conjugate gaze to contractural side
lesion below decussation - loss of conjugate movement to ipsilateral side
oculomotor apraxia
reduced induced horizontal saccades
selective horizontal plasy
absent voluntary horizontal gazer
vertical gaze nroammly
benign
bilateral FEF lesions
corpus callosium lesion
