Facial Palsy


  1. Understand the anatomy and function of the facial nerve, its branches and be able to describe its intra & extracranial route in the body. 

  2. Understand the incidence/prevalence, clinical presentations, the management and prognosis of the various causes of facial palsy.



Annual incidence of 15-30 cases per 100,000 population.

Bells palsy accounts for approximately 60-75% of cases of acute unilateral facial paralysis




There are many methods for formulating the differential diagnosis of a condition. One particularly useful method is using a surgical sieve (mnemonic). There are numerous examples of a surgical sieve the one we will use here is VITAMIN D.





V ascular                                CVA / Cerebral Aneurysm 


 I diopathic/ Iatrogenic          Post surgery / surgical accident in parotidectomy, middle ear surgery or                                                        surgery on the internal acoustic meatus.



T raumatic                              Fractured temporal bone/laceration 


A utoimmune                         Sarcoid / Multiple Sclerosis / Guillain-barré syndrome /                                                                                     Melkersson-Rosenthal Syndrome                                                         



M etabolic                             Diabetes mellitus 


 I nflammatory/ Infective       Acute suppurative otitis media, Cholesteatoma and Malignant otitis     



Ramsay Hunt Syndrome.
its correct name is Herpes Zoster Oticus this tells you the cause. In this condition a herpetic rash is seen on the pinna, EAC, face or soft palate in addition to the facial palsy. Hearing loss and vertigo may also be present.


                                                 Bell's Palsy
                                                    This accounts for more than half of cases.    

                          By definition, it is a diagnosis of exclusion and can be only be made                                    when other causes ruled out. Research suggests that it is of viral origin -                            probably herpes simplex type 1.


N eoplastic                            Facial or Vestibular Schwannomas and  Malignancy of the Parotid

                                                   (such as mucoepidermoid tumour or adenoid cystic carcinoma) are the                                                         main causes here but both are rare causes of facial weakness. Note that                                                       benign parotid tumours such as pleomorphic adenoma do not cause                                                             facial paralysis.




D evelopmental                    Moebius Syndrome / Hemifacial Microsomia


The facial nerve (VII) originates in the pons area of the brain. It forms from two separate nerves; a large motor nerve and smaller sensory root (the intermediate nerve). These nerves fuse to form the facial nerve after passing through the (IAM) internal auditory meatus and onto the facial canal. 

The geniculate ganglion is a collection of nerve cell fibres and bodies (Genu (Gk) = knee).

The facial canal is a 'Z' shaped structure which encloses the nerve as it passes through the remainder of its intra-temporal path.  

Before leaving the skull, the facial nerve gives rise to a number of branches:


Greater superficial petrosal nerve

Synapses with the sphenopalatine ganglion which provides parasympathetic nerve innervation to the lacrimal gland and the mucosal glands of the nose, palate, and pharynx.


Nerve to the stapedius

Innervates the stapedius which helps dampen excessive movement of the stapes. 


Chorda Tympani

Special sense of taste from the anterior two-thirds of the tongue.

The facial nerve passes through the stylomastoid foramen, exiting the skull to start its extracranial path.

The nerve passes anteriorly through the parotid gland where it branches to form five motor branches.

A great mnemonic to remember these branches is

"To Zanzibar By Motor Car"


These nerves innervate the muscles of facial expression as listed below.

- Frontalis, orbicularis oculi and corrugator supercilii

- Innervates the orbicularis oculi

- Innervates the orbicularis oris, buccinator and zygomaticus         muscles.

- Innervates the mentalis muscle.

- Innervates the platysma

It is only through a thorough knowledge of the underlying anatomy of the facial nerve that a good understanding of the importance of clinical findings and examination can be achieved.

Clinical examination

The first part of the examination is to establish if a facial nerve palsy exists! The level of weakness varies from dense weakness to very subtle. We do this by testing the 5 distributions and corresponding facial expression.

Temporal branch

Get the patient to raise their eyebrows. 

Maxillary branch

Ask the patient to close their eyes tightly and keep them closed against resistance.

Buccal branch

Request the patient puffs out their cheeks.

Marginal mandibular

Ask the patient to smile showing their teeth.


Harder to explain without demonstrating yourself. Get the patient to grimace, showing the platysma muscles of the neck.

Upper Vs Lower motor neurone causes

It is important to be able to distinguish an upper from a lower motor neurone weakness. Remember that muscles of the forehead have bilateral cortical representation.

Let's study the diagram below. Upper motor neurones from the two hemispheres of the cerebral cortex are represented with differing colours. The patient's left cortex are coloured red, the right cortex are represented by yellow.

In the left diagram we see that each facial nerve nuclei (grey circle) receives upper motor neurone input from both sides of the cerebral cortex (via left and right corticobulbar tract in the posterior limb of the internal capsule). As seen by the mixed red and yellow coloured lines, the temporal branch of the face receives innervation from both hemispheres. The remaining branches  of the facial nerve, however, only have single hemisphere innervation (single coloured lines).

In the middle diagram there is a lesion of the lower motor neurone (blue circle). This could be a Bell's Palsy, for example. The pathology interrupts the nervous supply of all of the facial nerve taking out both the yellow (right) and red (left) cortical nervous innervation to the facial muscles. As such there is ipsilateral weakness in all of the facial divisions on the right side of the face (pale blue coloured side).


Therefore, in lower motor neurone pathology we expect all branches of the facial nerve to be weakened.

In the right diagram the red circle represents an upper motor neurone (UMN) pathology in the left side of the patient's brain e.g. a stroke. We would expect, from our neurology anatomy, the right side of the patient's face to be weakened (dark pink side). The stroke disrupts the red nervous innervation to the face (left corticobulbar tract), however the right side of the patient's brain (yellow) still gives innervation to the upper branches of the facial nerve, through the pathway described above. 


This means that the forehead or temporal branch of the facial nerve is spared. So, we can deduce an UMN lesion clinically in a facial palsy by the sparing of the forehead muscles from weakness.

The House-Brackmann classification

It is important to be aware of the method used for classifying the severity of a facial weakness. The table below outlines this classification. There is no need to memorise this, just be aware that it exists.

Other areas to examine


A full and thorough examination must be conducted to ensure no pathology is missed and the correct diagnosis is made. Areas to specifically focus on are the parotid, the ear, oral examination, and a thorough neurological examination including cranial nerves. 

It is also important to get a baseline audiogram to help rule out an acoustic neuroma.


Below is an example of a commonly used facial palsy sticker that is completed and documented in the notes. It summarises examination and treatment nicely.