Ocular Palsies Flashcards
Lesions of the Ocular Motor Nuclei or Nerves weaken
or paralyse the EOM(s) they supply usually causing a
triad of which symptoms?
- Deviation of the eye from the primary gaze position in the opposite direction(s) of the muscle’s normal actions (strabismus)
- Double vision (diplopia)
- Limitation of eye movements in the muscle’s normal direction(s) of action (external ophthalmoplegia)
What are the three conditions needed to satisfy a ‘classical’ nerve palsy?
It needs to be:
- Complete (i.e. all the nerve’s function needs to be affected)
- Isolated (no other brain region or nerves can be involved)
- Unilateral ( It must affect one nerve and one eye only)
Why are we concerned with ‘classical’ nerve palsies?
They are relatively common
What are some potential Oculomotor damage sites?
True or False- ‘Classical’ nerve palsies can be both acquired and congenital
True
What does it mean if a palsy is mixed?
It does not satisfy the conditions needed to be a classical palsy e.g. it may be bilateral or not all of the nerve is affected or maybe other structures are involved.
What are potential acquired sites of damage and causes of palsies (both classical and mixed)?
Defect of Nuclei in the Brainstem (often part of a syndrome):
- Because other brainstem structures are involved
- Vascular infarct, tumours, inflammation
- e.g., Multiple sclerosis (demyelination affecting oligodendrocytes)
Intra-Cranial Nerve affected (most common ‘classical’ causes):
- Something wrong in the Sub-arachnoid spacen(because the 3 Nerves are widely separated here hence classical cause)
- Ischaemic Micro-Vascular Neuropathy (associated with maturity-onset, type 2 diabetes)
- Trauma (skull fractures)
- Tumours (1o arachnoid meningiomas; 2o metastases)
- Arterial aneurysms
Intra-Cranial Nerve (mixed, multiple nerve involvement):
- Usually in or near Cavernous Sinus, since all 3 Nerves are close together here
- Inflammation (Tolosa-Hunt), thrombosis, ICA (Internal Carotid Artery) aneurysm, Pituitary adenoma
What is the subarachnoid space and when does the oculomotor nerve encounter it?
It is the space between the Arachnoid mater and the pia mater. The oculomotor nerve encounters it as it gets to the mid brain.
What are causes of acquired Adult Palsies?
What is External Ophthalmoplegia and what does it result in?
Paralysis of EOMs
Limited/no adduction or elevating eye movements
What is Internal Ophthalmoplegia and what does it result in?
Paralysis of inner eye muscles
Dilated & unreactive pupil; loss of accommodation
What are 3 clinical features of ‘Classical’ 3rd Nerve Palsy?
- Ocular Deviation: Complete abduction (exotropia) & some depression (hypotropia)
- External Ophthalmoplegia: Limited/no adduction or elevating eye movements
- Internal Ophthalmoplegia: Dilated & unreactive pupil; loss of accommodation
- Complete or Partial Ptosis: so no/little diplopia!
Why does a px with classical 3rd nerve palsy have weakened/no adduction (and that outwards and downward appearance)?
When the third nerve is damaged:
All adductors (MR,IR,SR) & elevators (SR,IO) are paralyzed
thus
The two abductors (LR,SO) & 1 depressor ( which the SO acts as) work unopposed.
[Think RADSIN to know which muscles adduct]
Why does a px with classical 3rd Nerve Palsy have a dialted (mydriasis) and unresponsive pupil?
Due to third nerve damage the constricting (sphincter) muscle is paralyzed and so the dilator muscle works unopposed.
[3rd Nerve has a parasympathetic role -Pupillomotor 3rd Nerve Axons drive the pupil to constrinct]
Why does a px with classical 3rd Nerve Palsy experience ptosis?
Because due to third nerve damage the LPS muscle is paralyzed, and so the orbicularis oculi operates unopposed
What is a common cause of classical third nerve palsy and why?
Posterior Communicating Artery Aneurysm due to its close proximity with the third nerve thus it is succeptible to compression.
What are the key clinical features of classical 6th nerve palsy?
Ocular Deviation: Complete adduction (esotropia)
External Ophthalmoplegia: Limited/no abduction eye movements
the main abductor (LR) is paralyzed, with all adductors (MR, SR, IR) unopposed (‘over-acting’)
Horizontal Diplopia: worsening with gaze towards the affected side & at ‘Far’
What abnormal head posture is a compensatatory strategy for diplopia caused by LEFT classical 6th nerve palsy?
- Turn head (left) towards affected eye & direct gaze to the right
- Can reduce or even eliminate the diplopia
Define Avulsing
Fancy way of saying ruptured
What are common causes of sixth nerve palsies?
What are clinical features of classical fourth nerve palsy?
Ocular Deviation: Extorsion, some hypertropia & esotropia
External Ophthalmoplegia: Limited/no abduction, especially on ‘Near’ Gaze
the main intorter (SO) is paralyzed, with the main extorter (IO) unopposed, and with other opposing muscles ‘over-acting’ for up (SR) or in (MR)
Torsional & Vertical Diplopia: worse when looking down in ‘Near’ Gaze
[Px’s really complain about their SO palsy when attempting to read or walk down stairs, because….In adduction, the SO normally becomes a major - even ‘pure’ - depressor!]
What is the compensatatory abnormal head posture (AHP) for fourth nerve palsy?
): Head tilt away from affected eye
(reduces vertical & torsional components of diplopia)
What are common causes of fourth nerve palsy?
Common causes:
Frontal Head Trauma, ‘Whiplash’
Brainstem tumours, that push the brain backward or forward
These displacements can rupture (avulse) the nerve, as it is long, thin & unprotected by dura as it curves around the midbrain in the sub-arachnoid space
