Oculomotor nerve (CN III) palsy is a common short case at the neurology station and it is usually evident with a distant because of unilateral complete ptosis.
As the name implies, the oculomotor nerve supplies the majority of the extraocular muscles apart from Lateral Rectus (supplied by VI nerve) and Superior Oblique (supplied by IV nerve). In addition, it supplies Levator Palpebrae Superioris muscle of upper eyelid and Sphincter Pupillae muscles which is responsible for pupillary constriction. This innervation is vital for understanding the clinical signs in III CN palsy, namely ptosis (often complete), dilated pupil and ophthalmoplegia.
There are two clinical entities, “Medical” and “Surgical” third nerve palsies. In a case of Surgical third nerve palsy, you are expected to do an extended examination to clinically locate the site of nerve compression to obtain full allocated marks.
This is obvious! You have to manually and gently elevate the upper eyelid when you carry on your examination to look for ophthalmoplegia.
Due to Medial Rectus palsy and unopposed action of Lateral Rectus supplied by the VI nerve.
In fact, the eye will be “Down & Out” because the Superior Oblique (supplied by IV nerve) is unantagonized by the paralyzed Superior Rectus, Inferior Rectus and Inferior Oblique muscles.
Impaired adduction of eye due to paralysis of Medial Rectus.
Due to the involvement of the parasympathetic nerve supply from the Edinger-Westphal nucleus. These fibers are located superficially, thus in external compression, they are affected first, making the pupil dilated.
Due to the involvement of the Ciliary muscle.
This is especially important when the pupil is affected (Surgical Third Nerve palsy) which would indicate an external compression of the Oculomotor nerve somewhere along its cause. You should do a targeted neurological examination to find out the possible location of the nerve.
Due to the involvement of Corticospinal tracts usually due to a Brainstem infarction.
Sometimes associated with tremor and involuntary movements (Benedikt Syndrome) when the red nucleus of the midbrain is involved.
It is seen without the involvement of other adjacent nerves. Here, the nerve is in close relationship with the posterior communicating artery and can be compressed with aneurysms of the above-mentioned artery.
At the cavernous sinus the oculomotor nerve is closely related to Trochlear and Abducens nerves and ophthalmic and Maxillary branches of Trigeminal nerves. Those nerves are affected together in case of Cavernous sinus thrombosis.
At the orbit, the Maxillary branch of the Trigeminal nerve is not in close relationship with the Oculomotor nerve, hence unaffected. It can occur in intraorbital cellulitis.
This patient has right complete ptosis and a divergent strabismus at neutral position. The right eye movements are impaired especially the adduction and it is fixed in down & out position. The right pupil is fixed and dilated. The accommodation reflex of the right eye is lost.
On my extended limited neurological examination, there are no associated IV or VI nerve palsies on the right side. There is no sensory deficit over the areas supplied by the maxillary and ophthalmic divisions of the Trigeminal nerve. The patient is having left hemiplegia. There are no hand tremors or involuntary movements.
So, my diagnosis is right oculomotor nerve palsy secondary to brainstem (midbrain) stroke. So, this is a case of Weber Syndrome.
It arises from the anterior aspect of the midbrain and originates from two nuclei. • Oculomotor nucleus – Originates at the level of the superior colliculus. • Edinger-Westphal nucleus – supplies parasympathetic fibres via the ciliary ganglion.
It originates at the midbrain at the level of superior colliculus —> passes between superior cerebellar and posterior cerebral arteries —> pierces the dura matter anterior and lateral to the posterior clinoid process —> transverses the cavernous sinus —> divides into two branches (Superior and inferior) at the orbit.
◦ Superior branch supplies the superior rectus and levator palpebrae superioris. ◦ Inferior branch divides into three divisions and supplies to medial rectus, inferior rectus, inferior oblique and ciliary ganglion (Sphincter pupillae & Ciliary muscle)
1. Weber Syndrome – Third nerve palsy + Contralateral Hemiplegia 2. Benedikt Syndrome – Third nerve palsy + Contralateral Involuntary Movements
1. Brainstem Tumours 2. Brainstem Strokes (Ischemic/ Haemorrhagic) 3. Brainstem Demyelination 4. Cavernous Sinus Thrombosis 5. Tentorial Herniation 6. Posterior Communicating Artery Aneurysms 7. Superior Orbital Fissure Lesions 8. Subacute Meningitis 9. Mononeuritis Multiplex (in Diabetes)
The examination of hand for neuropathies is commonly encountered at OSCE stations. Ulnar Claw-hand is a very characteristic finding in Ulnar nerve palsy.
Firstly, introduce yourself and get consent before you proceed to examine the patient.
Given below is a targeted examination for Ulnar nerve palsy. But remember to examine other nerves (Median & Radial) to exclude multiple nerve involvement.
There is marked clawing of the ring and little fingers of the right hand and there is wasting of hypothenar eminence with dorsal guttering, but the thenar eminence is not affected. The actions of palmar and dorsal interossei are impaired and Froment’s sign is positive.
The opposition of the thumb and finger extension is intact. There is an area of sensory loss over the palmar aspect of the medial side of the hand and medial one and half fingers. There is no hypopigmented patches or ulnar nerve thickening and there are no visible scars on the forearm.
So my tentative diagnosis is right-sided Ulnar nerve palsy, probably a lower lesion.
It is the hyperextension of the metacarpophalangeal joints and flexion of proximal and distal interphalangeal joints.
It is due to paralyzed Interossei and Lumbricals with unopposed action of long flexors and extensors.
The clawing is only obvious in medial two fingers (Because lateral two Lumbricals which are supplied by the median nerve are spared).
Surprisingly, high division of the ulnar nerve (anywhere hand’s breadth above the wrist) causes less clawing than the lower lesions.
In higher lesions the innervation to the medial half of Flexor Digitorum Profundus is also lost, causing less intense flexion of the fingers.
From the degree of clawing and the area of sensory involvement (see examination).
1. Flexor Carpi Ulnaris.
2. Medial half of Flexor Digitorum Profundus.
3. All Palmar Interossei.
4. All dorsal Interossei.
5. 3rd & 4th Lumbricals.
6. Adductor Pollicis
The patient tries to compensate for the ‘lost’ adduction of the thumb by flexion of it (with Flexor Pollicis Longus which is supplied by the Median nerve).
1. Leprosy (often bilateral).
2. Laceration over the wrist or anywhere along its course.
3. Fracture medial epicondyle.
4. Dislocation of elbow.
5. Cubital tunnel syndrome.
6. Degenerative arthritis.
7. Malunion of fractures of the lower end of the humerus (Tardae Ulna nerve palsy).
1. Ulnar nerve decompression.
2. Ulnar nerve anterior transposition.
3. Medial epicondylectomy.