7.1 Cranial Nerve III (Oculomotor) Palsy
7.2 Cranial Nerve IV (Trochlear) Palsy
7.3 Cranial Nerve VI (Abducens) Palsy
7.4 Cranial Nerve VII (Facial) Palsy
7.5 Optic Nerve Function
7.6 Visual Fields to Confrontation
7.8 Horner’s Syndrome
7.10 Neuro-Ophthalmic Differential Diagnoses and Aetiologies
Cranial nerve III palsies may be associated with potentially life-threatening conditions - GCA, cerebral aneurysm, pituitary apoplexy - although these are generally not found in person in exams! However, these cases may be given as vignettes so it is important to be familiar with them. Most importantly, the examiner is looking for you to demonstrate that you can exclude these conditions. It is essential that the candidate look carefully for signs of a “surgical” cause - the pupillary exam is crucial.
+ Aberrant Regeneration?
+ CNIV Palsy?
NB: If all that is seen in failure of adduction, this might be an INO instead of a CNIII – so look for abducting nystagmus of the contralateral eye.
Aberrant regeneration of the third cranial nerve, or oculomotor synkinesis, refers to the abnormal response to firing of the oculomotor nerve causing paradoxical co-contraction of muscles. It is typical a result of an aneurysm or tumour in the cavernous sinus but can be seen following trauma to the third cranial nerve. The third cranial nerve supplies the superior rectus, inferior rectus, medial rectus, inferior oblique, the parasympathetically innervated pupil sphincter and levator palpebrae muscles. In aberrant regeneration after injury to the oculomotor nerve, fibres grow to supply other muscles, leading to co-contraction of these muscles (extraocular muscles, lid or pupil) on firing of the nerve.
Move the eye from full abduction (where there is no CNIII activation) to midline and then into adduction to see the full extent of the lid or pupil changes:
This can occur in the absence of other CNIII signs!
Aberrant regeneration doesn’t occur with “medical” causes (because the nerve sheath hasn’t been breached).
Right Cranial Nerve III Palsy with Aberrant Regeneration
A. Patient looking in primary position. Note the mild right upper lid ptosis and slightly dilated right pupil, consistent with a compressive cause.
B. Patient looking to the left (adduction). Note that the right pupil constricts (due to co-contraction of the parasympathetic fibres going to the pupillary sphincter). The right upper lid demonstrates prominent elevation (from co-contraction of the levator palpebrae). The adducting saccadic velocity of the right eye is reduced from incomplete recovery of the medial rectus function.
C. Patient is looking to the right (abduction). Note that right pupil is again slightly dilated and the right upper lid demonstrates mild ptosis, the same as they were in primary position (since there is no longer any firing of the oculomotor nerve).
D. Patient is looking up. The right pupil constricts and the upper lid elevates more than the left upper lid.
E. Patient is looking down. The right pupil constricts and the upper lid elevates more than the left upper lid.
Look for a concomitant CNIV palsy:
Look for intorsion (by observing the movement of the vessels on the conjunctiva) during attempted depression in abduction
Check fundus to see if fovea is still (normally) below the optic disc (SO / CNIV and SR / CNIII intort the eye. Loss of intorters will cause fovea to be above the optic disc).
NB: This is only helpful in a complete CNIII palsy. If it is a partial CNIII palsy with SR still functional, this does not apply as the SR will still intort and hence the fovea will not necessarily be above the optic disc.
Don’t miss: GCA, Aneurysm, Pituitary apoplexy, cavernous sinus thrombosis.
HT, Cholesterol, DM, smoking
GCA, Vasculitis, Sarcoidosis
Posterior communicating artery aneurysm (assume this unless proven otherwise), ICA aneurysm, Subarachnoid haemorrhage, carotico-cavernous fistula, cavernous sinus thrombosis, pituitary apoplexy
Glioma, meningioma, nasopharyngeal carcinoma
IOID (Tolosa-Hunt syndrome)
Meningitis / encephalitis / abscess
Trauma / Surgical
Subarachnoid, extradural haemorrhage → uncal herniation
NB: Pain does not distinguish between ischaemic microvascular disease and a compressive lesion.
MRA has extremely high sensitivity for all causes of CNIII, no radiation and gives the added benefit of looking for demyelination BUT must requires a 3 Tesla magnet (difficult to get urgently) and patients may become claustrophobic. CTA is much more sensitive for detection of posterior communicating aneurysms, gives more “anatomic” detail than MRA (for neurosurgeons), is easier to obtain and is quicker. Digital angiography can be used if CTA / MRA is not possible.
See Li Q, Lv F, Li Y, Luo T, Li K, Xie P. Evaluation of 64-section CT angiography for detection and treatment planning of intracranial aneurysms by using DSA and surgical findings. Radiology. 2009;252(3):808‐815. doi:10.1148 / radiol.2523081911 for more information.
Treat the underlying cause (e.g. aneurysm, diabetes, hypertension).
Indications for treatment:
(no duction, poor saccade, poor forced generation test)
E.g. Occlusion of perforating branches of PCA.
Contralateral hemiplegia (corticospinal tract in cerebral peduncle)
Tremor (red nucleus)
Contralateral ataxia (superior cerebellar peduncle)
Tremor (red nucleus) + Contralateral ataxia (superior cerebellar peduncle)
All rights reserved. No part of this publication which includes all images and diagrams may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the authors, except in the case of brief quotations embodied in critical reviews and certain other noncommercial uses permitted by copyright law.
Vitreoretinal Surgery Online
This open-source textbook provides step-by-step instructions for the full spectrum of vitreoretinal surgical procedures. An international collaboration from over 90 authors worldwide, this text is rich in high quality videos and illustrations.