Facial Palsy

Original Editor - Wendy Walker.

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Topic Expert - Wendy Walker

Clinically Relevant Anatomy

For more detail on the anatomy of the facial nerve, please see the Facial Nerve page.

The VIIth cranial Nerve has its nucleus in the Pons, and takes a rather winding route before exiting the skull through the stylomastoid foramen. It then passes through the parotid gland, splitting into 5 branches: Temporal, zygomatic, buccal, mandibular and cervical.

Causes of Facial Palsy:

• Idiopathic

Bell's Palsy - cause not known  but likely to be linked to Herpes Simplex infection 

Bell’s palsy accounts for approximately 60 per cent of all cases of sudden onset facial paralysis. It affects between 20 to 40 per 100,000 people per year.

Ramsay Hunt Syndrome - linkied to Herpes Zoster infection   = a syndromic occurrence of facial paralysis, herpetiform vesicular eruptions, and vestibulocochlear dysfunction. Patients presenting with Ramsay Hunt syndrome generally have a greater risk of hearing loss than do patients with Bell palsy, and the course of disease is more painful. Moreover, a lower recovery rate is observed in these patients.

• Tumour

A tumor compressing the facial nerve can result in facial paralysis, but more commonly the facial nerve is damaged during surgical removal of a tumour. The most common tumour to result in facial palsy during surgical removal is the Acoustic Neuroma (AKA Vestibular Schwannoma). Less commonly, cholesteatoma, hemangioma, Facial Schwannoma or parotid gland tumours are the cause.

• Lyme Disease

Infection with Borrelia burgdorferi via tick bites is another cause of facial paralysis. Of patients affected with Lyme disease, 10% develop facial paralysis, with 25% of these patients presenting with bilateral palsy. 

• Rare causes include

Neurosarcoidosis, ototis media, Multiple Sclerosis, Moebius Syndrome, Melkersson-Rosenthal syndrome, Guillain-Barre Syndrome

Trauma, especially temporal bone fractures

Millard-Gubler Syndrome AKA Ventral Pontine Syndrome

Lesion in the ventral pons leading to the damage of the fascicles of the abducent , facial and corticospinal eventually leads to the development of the millard gubler syndrome. In this syndrome there is:
1. Facial paralysis - on the ipsilateral side that is usually of peripheral type
2. Paralysis of lateral rectus on the ipsilateral side due to the involvement of the abducent nerve
3. Hemiplegia develops on the contralateral side due to involvement of the corticospinal tract

Foville Syndrome AKA Inferior Medial Pontine Syndrome 

If the lesion occurs in the pontine tegmentum, it will cause the damage to the fascicles of the facial nerve, corticospinal tract and along with these it also causes the destruction of the paramedian pontine reticular formation. This syndrome is presented by : 

1. Facial paralysis on the ipsilateral side that is usually of peripheral type
2. Conjugate gaze is also affected on the same side of lesion
3. Hemiplegia develops on the contralateral side as there is the involvement of the corticospinal tract

Eight and a half Syndrome 

If the lesion is present in the dorsal tegmentum of the caudal pons, then it will cause damage to the paramedian pontine reticular formation , nucleus of abducent nerve, medial longitudinal fasciculus and also the facial nerve nucleus and the fascicle of the facial nerve. This syndrome presents with:
1. Internuclear ophthalmoplegia and there will be horizontal gaze palsy along with this ophthalmoplegia
2. Facial paralysis in the ipsilateral side and this type of paralysis is of lower motor neuron type.

Clinical Presentation

Paralysis of the muscles supplied by the Facial Nerve presents on the affected side of the face as follows:

Appearance and range of movement:

Inability to close the eye

Inability to move the lips eg. into smile, pucker

At rest, the affected side of the face may "droop"

Functional effects:

Difficulty eating and drinking as lack of lip seal makes it difficult to keep fluids and food in the oral cavity

Reduced clarity of speech as the "labial consonents" (ie. b, p, m, v, f) all require lip seal 

Dryness of the affected eye

Somatic effects:

The facial nerve  supplies the lachrymal glands of the eye, the saliva glands, and to the muscle of the stirrup bone in the middle ear (the stapes). It also transmits taste from the anterior 2/3 of the tongue. Facial palsy often involves:

• Lack of tear production in the affected eye, causing a dry eye, with risk of corneal ulceration.

In Facial Nerve palsy there are 2 problems which contribute towards making the eye dry:
1. The greater petrosal nerve, derived from the facial nerve, supplies the parasympathetic autonomic component of the lacrimal gland. - controlling production of moisture/tearing in eyes.
2. The zygomatic branch of the Facial Nerve supplies Orbicularis Oculi, and the resulting paralysis causes inability(or reduced ability) to close the eye or blink, so the tears (or indeed artificial lubrication in the form of drops, gel or ointment) are not spread across the cornea properly.

• Hyperacusis = sensitivity to sudden loud noises
• Altered taste sensation

Differential Diagnosis, UMN versus LMN:

If the forehead is not affected (ie the patient is able to raise fully the eyebrow on the affected side) then the facial palsy is likely to be a result of a lesion in the Upper Motor Neuron (UMN). Paralysis which includes the forehead, such that the patient is unable to raise the affected eyebrow, is a Lower Motor Neuron (LMN)lesion.

However, caution is advised in using preservation of forehead function to diagnose a central lesion. Patients may have sparing of forehead function with lesions in the pontine facial nerve nucleus, with selective lesions in the temporal bone, or with an injury to the nerve in its distribution in the face. It is worth remembering that a cortical lesion that produces a lower facial palsy/paresis is usually associated with a motor deficit of the tongue and weakness of the thumb, fingers, or hand on the ipsilateral side.

Diagnostic Procedures

Laboratory investigations include an audiogram, nerve conduction studies (ENoG), computed tomography (CT) or magnetic resonance imaging (MRI), electromyography (EMG).

Management / Interventions

Medical Management

Bell's Palsy and Ramsay Hunt Syndrome are treated with corticoteroids (prednisone), given within 72 hours of onset, and this can be accompanied by antiviral medication.

Physiotherapy

• Neuromuscular Retraining (NMR) 
• Electromyography (EMG) biofeedback 
• Trophic Electrical Stimulation (TES) 
• Proprioceptive Neuro Muscular Facilitation Techniques

Complications/Sequelae:

Synkinesis  (AKA aberrant regeneration) occurs after injury to the facial nerve. 

Key Evidence

jama.jamanetwork.com/article.aspx Combined corticosteroid and antiviral treatment for Bell palsy: a systematic review and meta-analysis.  de Almeida JR, Al Khabori M, Guyatt GH, Witterick IJ, Lin VY, Nedzelski JM, Chen JM.

onlinelibrary.wiley.com/doi/10.1002/14651858.CD001942.pub4/abstract Cochrane Review: Corticosteroids for Bell's palsy (idiopathic facial paralysis)  Rodrigo A Salinas, Gonzalo Alvarez, Fergus Daly, Joaquim Ferreira

onlinelibrary.wiley.com/doi/10.1002/14651858.CD006283.pub3/abstract Cochrane Review: Physical therapy for Bell's palsy (idiopathic facial paralysis)  Lázaro J Teixeira1, Juliana S Valbuza, Gilmar F Prado

Resources

www.qvh.nhs.uk/our_services/plastic_surgery_and_burns/facial_palsy.php UK NHS Facial Palsy Service, Queen Victoria Hospital, East Grinstead

www.cmft.nhs.uk/royal-eye/our-services/facial-function-clinic.aspx UK NHS Facial Function Clinic, Central Manchester University Hospitals, Manchester

www.facialpalsy.org.uk/ Charity for Facial Palsy from any cause

bellspalsy.org.uk/links.html Bell's Palsy Association, Charity

www.nhs.uk/Conditions/Bells-palsy/Pages/Introduction.aspx Information web-site on Bell's Palsy

Case Studies

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Recent Related Research (from Pubmed)

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References

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