Facial Palsy

Introduction
Facial palsy is due to the damage in the facial nerve that
supplies the muscles of the face.

It can be categorized into two based on the location of casual

pathology:

1. Central facial palsy- due to damage above the facial

nucleus
2. Peripheral facial palsy-due to damage at or below the
facial nucleus.

Clinically Relevant Anatomy

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 Peripheral Facial Palsy

There are several causes of Facial Palsy:

 Idiopathic or Bell's Palsy - Cause not known but likely to

be linked to Herpes Simplex infection. This is the most
common cause of facial paralysis.

 Tumour - A tumour compressing the facial nerve can

result in facial paralysis, but more commonly the facial
nerve is damaged during surgical removal of a tumour.

 Acoustic Neuroma (AKA Vestibular Schwannoma).

 Cholesteatoma,
 Hemangioma,
 Facial Schwannoma or parotid gland tumours (or the
surgery to remove them) are the cause.

 Infection
 Ramsay Hunt Syndrome - Caused by Herpes Zoster
infection = a syndromic occurrence of facial paralysis,
herpetiform vesicular eruptions, and vestibulocochlear
dysfunction. 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.
 Lyme Disease -
 Iatrogenic Facial Nerve Damage - Iatrogenic facial nerve
injury occurs most commonly in temporomandibular joint
replacement, mastoidectomy, and parotidectomy.

 Congenital

 Rare causes - These include:

 Neurosarcoidosis,
 Otitis media,
 Multiple Sclerosis,
 Guillain-Barre Syndrome etc...

 Trauma, especially temporal and mastoid bone fractures

Risk factors

 Diabetes
 Pregnancy - might be due to hypercoagulability, elevated

blood pressure, increased fluid load, virus infection and

suppressed immunity
 Infection of ear

 Upper respiratory tract infection

 Obesity

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

 Inability to close the eye

 Inability to move the lips eg. into a smile, pucker
 At rest, the affected side of the face may "droop" although
if the person is in Synkinesis, the affected side of the
mouth may sit higher than the other side
 The lower eyelid may drop and turn outward - "ectropion"

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:
 The greater petrosal nerve, derived from the facial

nerve, supplies the parasympathetic autonomic

component of the lacrimal gland. - controlling the
production of moisture/tearing in eyes.
 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

Upper Motor Neuron versus Lower Motor Neuron

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).

Medical Management

Bell's Palsy and Ramsay Hunt Syndrome are treated with

corticosteroids (prednisone), given within 72 hours of
onset,and this can be accompanied by antiviral medication

Surgical Management

Tumours such as Acoustic Neuromas and Facial

Schwannomas are frequently resected surgically .

Patients at high risk of a corneal ulcer may be offered

oculoplastic surgery to protect the eye.

For patients with dense facial palsy and no nerve function, a

number of surgical interventions may be used. These fall into
the following categories:

1. Facial reanimation surgeries which involve nerve graft

or anastomosis
2. Facial reanimation surgeries which involve muscle
transposition
3. Static surgeries, ie. plastic surgery to improve symmetry
at rest but no improvement in movement
Physiotherapy

In the early stages of facial palsy, the most important thing to

do is to check that the patient is caring for the affected eye in
an appropriate way.

As the facial nerve is responsible for production of

lubrication to the cornea, the patient is highly likely to suffer
from a Dry Eye in the early weeks and months for facial
palsy, which puts them at risk of developing a corneal ulcer,
which can lead to damage to vision in that eye.

The therapist should educate the patient in management of a

dry Eye, if this has not been done by other medical personel.
If the eye is looking red or the patient reports frequent
episodes of redness, an urgent referral to opthalmology is
required. management including taping and use of artificial
lubrication.

 Neuromuscular Retraining (NMR)-

(Neuromuscular Facial Re-education is "the process to

facilitate the return of the desired facial movement
patterns and the elimination of unwanted facial
movements and expression patterns”. It is based on
patient education and the use of extrinsic feedback to
achieve reeducation or physical learning)

 Electromyography (EMG) and mirror biofeedback

 Trophic Electrical Stimulation (TES)
 Proprioceptive Neuro Muscular Facilitation Techniques
 Kabath technique
 Mime therapy
Evidence of Physiotherapy Treatments

 According to clinical practice guidelines, physiotherapy is

recommended ("weak recommendation") in Bell's
palsy,and Neuromuscular Retraining techniques are
effective in increasing facial range of movement and
symmetry, as well as reducing/minimising Synkinesis.
 Mime therapy can improve functionality for patients with
facial palsy. The therapy consists of exercises with mirrors.
 The effect of electrical stimulation is controversial.

 One study found that PNF technique is more effective than

conventional exercises.
 One study found PNF/Kabat technique is more effective
than no exercise.
Complications/Sequelae
Synkinesis (AKA aberrant regeneration) occurs after injury to
the facial nerve.

Synkinesis develops in cases of axonotmesis damage to the

facial nerve, and is therefore a normal sequelae to facial
nerve damage.

Physiotherapy is extremely helpful in management of

synkinesis, and neuromuscular retraining techniques and
mirror feedback exercises in particular are effective in
reducing the problems of synkinesis.