Facial nerve palsy

Question 1

Facial Nerve Anatomy

Where does the facial nerve exit?

What does it pass through?

Branches

Answer 1

The facial nerve exits the brainstem at the cerebellopontine angle.

On its journey to the face it passes through the temporal bone and parotid gland.

It then divides into five branches that supply different areas of the face:

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

Question 2

Function

Answer 2

Motor: Supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.

Sensory: carries taste from the anterior 2/3 of the tongue.

Parasympathetic: it provides the parasympathetic supply to the submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).

Question 3

UMN vs LMN lesion

Answer 3

Each side of the forehead has upper motor neurone innervation by both sides of the brain. Each side of the forehead only has lower motor neurone innervation from one side of the brain.

In an upper motor neurone lesion, the forehead will be spared and the patient can move their forehead on the affected side.

In a lower motor neurone lesion, the forehead will NOT be spared and the patient cannot move their forehead on the affected side.

Question 4

Causes of upper motor neuron lesions

Unilateral vs bilateral

Answer 4

Unilateral upper motor lesions occur in:

• Cerebrovascular accidents (strokes)
• Tumours

Bilateral upper motor neurone lesions are rare. They may occur in:

• Pseudobulbar palsies
• Motor neurone disease

Question 5

Ramsay Hunt Syndrome

Cause

Clinical Features

Treatment

Answer 5

Ramsay-Hunt syndrome is caused by the herpes zoster virus. It presents as a unilateral lower motor neurone facial nerve palsy.

Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior 2/3 of the tongue and hard palate.

Treatment should ideally be initiated within 72 hours.

Treatment is with:

Prednisolone
Aciclovir
Patients also require lubricating eye drops.

Question 6

Bell’s Palsy

Pathophysiology

Clinical Features

Management

Answer 6

Bell’s palsy is a relatively common condition.
PATHOPHYSIOLOGY
It is idiopathic, meaning there is no clear cause.

CLINICAL FEATURE
It presents as a unilateral lower motor neurone facial nerve palsy.

The majority of patients fully recover over several weeks but recovery may take up to 12 months. A third are left with some residual weakness.

MANAGEMENT
If patients present within 72 hours of developing symptoms, NICE guidelines recommend considering prednisolone as treatment, either:
- 50mg for 10 days
- 60mg for 5 days followed by a 5 day reducing regime of 10mg a day

• Patients also require lubricating eye drops to prevent the eye on the affected drying out and being damaged.
• If they develop pain in the eye they need ophthalmology review for exposure keratopathy.
• Tape can be used to keep the eye closed at night.

Question 7

Other causes of lower motor neuron facial nerve palsies

Answer 7

Infection:

• Otitis media
• Malignant otitis externa
• HIV
• Lyme’s disease

Systemic disease:

• Diabetes
• Sarcoidosis
• Multiple sclerosis
• Guillain–Barré syndrome

Tumours:

• Acoustic neuroma
• Parotid tumours
• Cholesteatomas

Trauma:

• Direct nerve trauma
• Damage during surgery
• Base of skull fractures

Question 8

Pseudobulbar Palsy

Pathophysiology

Answer 8

A pseudobulbar palsy is caused by a bilateral lesion affecting the corticobulbar tracts (running from the motor cortex to the motor nuclei of cranial nerves 9, 10, and 12 in the medulla).

Note that a bilateral lesion is required as the cranial nerve motor nuclei have bilateral cortical representation (except the motor nuclei of the lower half of cranial nerve 7).

A pseudobulbar palsy can be thought of as an ‘upper motor neurone’ lesion of speech and swallow.

Question 9

Pseudobulbar palsy

Clinical Features

Answer 9

Clinical signs include a:

• spastic tongue
• a slow thick (“hot-potato”) speech
• a brisk jaw jerk reflex, and emotional lability.

Other upper motor neurone features in the limbs may be present e.g. spastic hypertonia, pyramidal weakness, and hyper-reflexia.

Question 10

Bulbar Palsy

Pathology

Causes

Answer 10

Damage to the medullary nuclei of CN 9, 10, 12 (Glossopharyngeal Nerve, Vagus nerve, Hypoglossal Nerve)

Bulbar Palsy is a LMN lesion of speech and swallow

Causes:

• Motor Neurone Disease
• GBS
• Lateral medullary Syndrome
• Myasthenia gravis

Question 11

Bulbar palsy

Clinical Features

Answer 11

Quite nasal voice

Absent Jaw Jerk

Absent Gag reflex