Eye Movements and Gaze week 6 Flashcards
What kind of visual impairment does lesion of CN VI cause? What makes this worse?
What other nucleus is often damaged with a CN VI lesion?
What is fascicular damage of CN VI often associated with?
How else can this nerve be damaged? What is it particularly susceptible to?
- Supplies the ipsilateral lateral rectus muscle
- Causes horizontal binocular diplopia, worse when looking to side of lesion
- Can be subtle with apparently full ductions
- Nuclear
- Ipsilateral horizontal gaze palsy, not overcome with VOR
- Frequently with 7th CN
- Fascicular
- Frequently associated with other brainstem signs
- Subarachnoid
- False localizing sign with increased ICP!
- Has intimate contact with meninges, edge of tentorium
- More susceptible to increased ICP, meningeal processes
- Remember that CN VI (along with III, IV, V1-opthalmic and V2-maxillary)
What kind of visual issue does lesion of the trochlear nerve cause?
What eye movements do patients have difficulty with?
What is hypertropia and why do pts with CN IV issues get it?
How do these pts hold their heads at rest and why?
- Oblique/ vertical diplopia
- Difficulty looking down and in towards the nose
- Ipsilateral HYPERtropia (one eye is higher up than the other), worse when looking to the opposite side and when tilting head to same side
- Will frequently have resting contralateral head tilt
What causes lesions to the trochlear nerve?
The 4th nerve nucleus supplies the (contralateral/ipsilateral) superior obliquie muscle.
- Most common causes are trauma and decompensation of a congenital 4th
- Microvascular can also occur frequently
- Same causes as 6th (damage in cavernous sinus, increased ICP, meningeal processes)
- The 4th nerve nucleus supplies the CONTRAlateral superior oblique muscle
- Frequently associated with ipsilateral Horner’s syndrome
- Decussates immediately after leaving brainstem so a lesion of the nerve is ipsilateral to the muscle
What are the symptoms of damage to the oculomotor nerve?
What may cause compressive 3rd nerve palsy?
What may new 3rd nerve palsy without any other symptoms be indicative of?
Symptoms
▪ Ocular muscle weakness (SR, IR, IO, MR)
▪ Loss of pupil constriction
▪ Ptosis (weakness of levator palpebrae)
▪ “Down and Out”
- ICA, Pcomm, basilar and PCA aneurysms can cause compressive 3rd nerve palsies (also uncal herniation)
- New 3rd nerve palsy without other symptoms can be the herald sign of aneurysm rupture
What symptoms are present with a right 3rd nuclear lesion? How and why are they different from compression of the fibers of CN III?
Right nuclear third lesion
▪ Complete right third nerve palsy
▪ Bilateral ptosis. Note inattached pic that there is only one levtator palpebrae superioris nucleus. Damage to the 3rd nucleus will cause bilateral ptosis
▪ Bilateral elevation deficit. The nuclei of superior rectus innervates the contralateral muscle so that amage to one of the 3rd nuclei will cause elevation deficit on the contralateral eye. The ipsilateral eye is also affected because the fibers from the contralateral superior rectus nucleus decussate so that these fibers end up being damaged as well.
Explain the attached diagram.
What eye movement is this pathway responsible for?
The FEF (frontal eye fields) in the frontal cortex and the secondary visual cortices (18 & 19) synapse in the PPRF (paramedian pontine reticular formation). The PPRF relays to the nucleus of CN VI. CN VI (of course) innervates the ipsilateral lateral rectus but also sends fibers via the MLF (medial longitudinal fasciulus) to innerate the oculomotor nucleus.
This pathway is for horizontal eye movement (conjugate gaze). This coordinates the movement of the eyes when looking horizontally in either direction. When you look laterally (abduct), the other eye must adduct (medial rectus, hence innervation of CN III nucleus).
What is internuclear opthlamoplegia?
What is it caused by? What kind of disease is it often seen in?
What symtoms are present and why?
Internuclear opthalmoplegia is a lesion of the medial longitudinal fasciculus-innervation of oculumotor nucleus by abducens nucleus.
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Adduction Deficit on side of lesion
- May only be seen on adducting saccades
- May be overcome by convergence
- Abducting Nystagmus. This is due to overfiring of CN VI attempting to stimulate CN III.
- May have associated skew deviation
Internuclear opthalmoplegia is often seen in pts with demyelinating diseases such as MS. The MLF is highly myelinated because communication must be quick so the eyes can move together. Also seen in strokes.
What nuclei are involved in vertical gaze?
riMLF: rostral interstitial nucleus of the MLF. responsible for upward gaze
interstitial nucleus of Cajal: responsible for downward gaze
do not know as much about vertical gaze as we do horizontal gaze. just know these nuclei
What is dorsal midbrain syndrome?
What are the symtoms/exam findings?
What is the commonly cause dorsal midbrain syndrome?
▪ Supranuclear vertical gaze paresis (unable to look up)
▪ Convergence Retraction Nystagmus: when pt attempts to look up, have nystagmus where eyes move medially. look up a video
▪ Lid Retraction (Collier Sign)
▪ Pupillary light-near dissociation: pupils constrict with accommodation but not with light stimulation
- Initially decreased ability to look up, typically accompanied by slow vertical saccades
- Eventually can involve horizontal eye movements
- Typically with lid retraction, decreased blink rate.
- Overcome with oculocephalic reflex
- Classically seen in neurodegenerative disease with midbrain pathology, especially progressive supranuclear palsy. Can also see with pineal tumor/cyst compression of structures in midbrain responsible for vertical gaze
What is smooth pursuite?
What are saccades?
What areas of the brain are responsible for each?
smooth pursuit: eyes are fixated on moving object and eyes move along with object. fairly involuntary
saccades: more voluntary. ability to intentionally look in different places
FEF responsible for saccades.
striate cortex (primary visual cortex): smooth pursuit
What is optokinetic nystagmus?
How may it be tested?
If optokinetic nystagmus is present, what does this tell you?
Optokinetic nystagmus is a normal physiologic nystagmus. It is a test of smooth pursuit and saccades-striate cortex and FEF respectively. If have optokinetic nystagmus, these areas are intact
When a subject views a rotating striped drum, his or her eyes involuntarily follow a stripe with a “slow eye movement” (smooth pursuit), then return with a fast eye movement (saccade) to fixate on a new stripe. The whole cycle can be repeated indefinitely as long as the subject views the moving drum.
Where is the lesion? What is this called?
- Right and Left Eyes
- Adduction deficit on right
- Abduction deficit on left
- Left Gaze palsy
- Localizes
- Left abducens nucleus
- Left PPRF
- Right FEF
