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)
Facial nerve palsy can be either UMN type or LMN type. It can be unilateral or bilateral. The most common scenario would be LMN type unilateral facial nerve palsy (Bell’s Palsy) you would encounter at the exam. LMN lesions affect both upper & lower parts of the face in contrast to the UMN lesions.
You should be thanking your destiny if you got Bell’s palsy as one of your cases at the exam because it is one of the easiest short cases you would ever get at the neurology station. Though it is a pretty straightforward case, just diagnosing Lower Motor Neuron (LMN) type of facial nerve palsy may not be enough for you to acquire higher marks. Always think about the possible aetiology & try to localize the site of the lesion whenever possible once you detect LMN type of facial nerve palsy.
The general instruction would be to “Examine the lower motor crannial erves” or “Examine the motor cranial nerves”. Always follow the instruction of the examiner.
This patient is having left side facial asymmetry involving both upper and lower parts of the face. There is absent blinking of the left eye. The mouth is deviated to the right side when an attempt to clench the teeth. There is reduced facial expressions with widened palpebral fissure and flattened nasolabial fold on the left side.
The parotid gland is not enlarged or tender. There is a vesicular rash involving the left external auditory meatus and soft palate. Other cranial nerve examination is unremarkable.
He is having left LMN type Facial nerve palsy secondary to reactivation of Varicella-Zoster Virus; that is Ramsay-Hunt Syndrome.
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.
The examination of hand for neuropathies is commonly encountered at OSCE stations. One of the most common scenarios would be carpal tunnel syndrome.
Firstly, introduce yourself and get consent before you proceed to examine the patient.
Usually, the command is to examine the hands of the patient, but sometimes you might be given a clue like “This lady presented with tingling sensation in her hands”. The disease is often bilateral.
This patient who presented with tingling sensation of hands has bilateral thenar muscle wasting but there is no wasting of hypothenar eminence or dorsal guttering. There are no visible surgical scars, suggestive of previous carpal tunnel decompression surgery. Her opposition of the thumbs is weak and the pen touch test is positive, but there is no weakness in finger adduction or extension. There is an area of sensory loss over the palmar aspect of the lateral three and a half fingers and no other areas of sensory loss. Tinel’s test and Phalen’s test are positive. So my tentative diagnosis is bilateral Carpal Tunnel Syndrome (CTS) and I would like to assess her functional disability and probable aetiology.
It is the symptomatic compression of the median nerve at the carpal tunnel where it runs deep to the flexor retinaculum (Commonest entrapment neuropathy).
Roof – Flexor retinaculum. Medial (Ulnar) – Pisiform & Hook of Hamate. Lateral (Radial) – Scaphoid and Trapezius. Palmar aspect – Transverse carpal ligament.
1. Median nerve.
2. Four tendons of Flexor Digitorum Superficialis.
3. Four tendons of Flexor Digitorum Profundus.
4. Tendon of Flexor Pollicis Longus.
5. Tendon of Flexor Carpi Ulnaris (in a separate compartment).
1. Palmar cutaneous branch of the Median nerve.
2. Ulnar nerve.
3. Ulnar artery.
4. Tendon of Palmaris Longus.
Because the palmar cutaneous branch of the Median nerve is given away proximal to the flexor retinaculum and which passes over it.
1. All thenar muscles except Adductor Pollicis.
2. Radial two Lumbricals.
Nerve conduction studies (NCS).
4. Diabetes Mellitus.
5. Rheumatoid Arthritis.
1. Cervical rib.
2. Cervical spondylosis.
3. Pancoast’s syndrome.
Carpal tunnel decompression by longitudinally dividing the flexor retinaculum in full length in a bloodless field under local anesthesia.
1. Local steroid injection.
2. Splinting of the wrist at night.
3. Treating the underlying cause.
Radial nerve palsy (Saturday night palsy) is one of the common clinical presentations. The radial nerve is one of the three major peripheral nerves of the upper limb. It supplies the extensor aspect of both arm and forearm. It innervates triceps and all the muscles in the posterior aspect of the forearm which are responsible for extension of the elbow and the wrist, fingers, and supination of the forearm.
It originates in the axilla as the terminal continuation of the posterior cord of the brachial plexus carrying its all five nerve root values from C5 to T1.
Then it passes posterior to the axillary artery to enter the anterior compartment of the arm crossing the inferior border of the teres major muscle. After a short course, radial nerve leaves the anterior compartment of the arm accompanying the profunda brachii artery to enter its posterior compartment. Here the nerve directly lies on a diagonal groove on the shaft of the mid humerus (Spiral Groove) running from medial to lateral.
Reaching the lateral side of the arm, it pierces the lateral intramuscular septum to re-enter the anterior compartment of the arm in between brachialis and brachioradialis muscles. Then it enters the forearm passing anterior to the lateral epicondyle of the humerus and immediately divides into two branches, namely deep branch and superficial branch.
The deep branch of the radial nerve enters the posterior compartment of the forearm piercing the supinator muscle where it is termed posterior interosseus nerve for the remainder of its course.
Out of the four sensory branches of the radial nerve, three of them arise in the upper arm descends downwards. They are namely, lower lateral cutaneous nerve of the arm, posterior cutaneous nerve of the arm and posterior cutaneous nerve of the forearm. The fourth branch is the terminal continuation of the radial nerve itself as the superficial branch of the radial nerve which is the only branch of radial nerve crosses which the wrist joint.
The radial nerve itself innervates all three heads of the triceps in the arm and extensor carpi radialis longus and brachioradialis muscles. It supplies the supinator muscle while piercing through it and the remainder of the muscles are innervated by the posterior interosseous nerve.
Cutaneous branches of the radial nerve supply the skin of the lower lateral arm, dorsal aspect of the arm, forearm and the lateral three and a half fingers. However, there is a significant overlap of sensory innervation from the adjacent nerves except in the dorsal aspect of 1st webspace of hand.
The clinical presentation of radial nerve palsy is different depending on the site of the lesion. It is susceptible to injury commonly at four sites.
Due to its close relationship to proximal humerus and shoulder joint, the radial nerve is liable for injury in axilla by shoulder dislocation and fractures involving the proximal humerus. It may also be damaged falling asleep one’s hand hanging over the arm of a chair compressing the radial nerve at axilla for a prolonged duration (Saturday night palsy) or by a badly fitting crutch (Crutch palsy).
The extension of the forearm at the elbow is totally lost as the triceps is denervated completely when the nerve is damaged at the axilla. Obviously, the wrist extensors in the forearm are also paralyzed resulting in wrist drop due to unopposed activity of intact flexor muscles.
As all four of the sensory branches are affected in this case, there will be a widespread sensory loss affecting the lateral aspect of the arm, posterior aspect of arm and forearm and the dorsal aspect of lateral three and a half fingers of the hand and palm.
Here the nerve lies directly on the humerus as it winds around it and susceptible for damage in fractures involving midshaft of the humerus.
The forearm extension is only weakened (in contrast to total paralysis) due to triceps’ partially intact innervation. The branches for long head & lateral head of the muscle are given off proximal to the spiral groove resulting in incompletely denervated muscle. Only its medial head loses the nerve supply. There will be wrist drop deformity owing to loss of motor supply to wrist extensors as the deep branch of the radial nerve is affected.
Since the sensory branches to arm & forearm are given off in the upper arm, they remain intact. The only branch to be affected is the superficial branch of the radial nerve which in turn results in sensory loss over the dorsal surface of the lateral three and a half fingers which is more marked over the 1st webspace.
Here the nerve lies close proximity with the radial neck and can be easily damaged in posterior dislocation of elbow joint and fractures involving the head & neck of the radius.
Even though most of the muscles in the posterior compartment of the forearm are affected which are innervated by the deep branch of the radial nerve, surprisingly the wrist drop deformity does not occur. It is due to intact extensor carpi radialis longus which is innervated by the main branch of the radial nerve itself before its division hence unaffected in the injury. This muscle alone can maintain the wrist in extension though there is some degree of weakness.
As the superficial branch of the radial nerve is unaffected there will be no sensory loss.
The superficial branch of the radial nerve can be damaged due to direct trauma causing soft tissue injuries in the forearm such as stabs or lacerations.
The only branch may be involved is the superficial branch of the radial nerve which is purely sensory. The patient will have no motor weakness and there will be sensory loss over the lateral three and a half finger of the affected hand