Being able to differentiate Bell’s palsy from stroke is an essential skill for all front-line clinicians. Bell’s palsy, which is also sometimes referred to as idiopathic facial paralysis, and ischaemic stroke are the first and second most common causes of acute facial paralysis respectively.

The two conditions present very similarly, and as a consequence, they can be easily confused by the assessing clinician. For this reason, the ability to differentiate the two conditions and explain the reasoning behind the difference is very commonly assessed in medical examinations, both written and clinical (OSCEs).

To fully understand the difference between Bell’s palsy (lower motor neuron facial palsy), and the facial weakness caused by ischaemic stroke (upper motor neuron facial palsy), a sound understanding of the anatomy of the facial nerve (CN VII) is required.

The facial nerve is the seventh of the cranial nerves. It has motor, parasympathetic, and special sensory functions. The course of the facial nerve can be divided into two main parts:

  • Intracranial
  • Extracranial


The intracranial anatomy of the facial nerve

Three brainstem nuclei contribute to the facial nerve:

  • Facial nerve nucleus in the pons (motor fibres)
  • Superior salivary nucleus in the pons (secretomotor parasympathetic fibres)
  • Nucleus of the solitary tract in the medulla (sensory/taste fibres)


The facial nerve nucleus is situated in the caudal portion of the ventrolateral pontine tegmentum; its axons form the motor root of the facial nerve. The superior salivary nucleus and nucleus of the tractus solitarius combine to form the intermediate nerve, which lies between the motor component of the facial nerve and the vesitbulocochlear nerve.

The two roots leave the pons at the cerebellopontine angle, medial to the vestibulocochlear nerve. They then pass across the subarachnoid space together to enter the internal auditory meatus, within the petrous temporal bone. At this point, they lie in very close proximity to the inner ear.


The course of the facial nerve in the temporal bone (from Gray’s Anatomy)


They then pass laterally across the internal auditory meatus to reach and enter a ‘Z’ shaped structure called the facial canal.  Within the facial canal, the two roots fuse to form the facial nerve. The facial nerve then forms the geniculate ganglion (the sensory ganglion of the facial nerve). It is here that three branches originate:

  • The greater petrosal nerve
  • The lesser petrosal nerve
  • The external petrosal nerve


The facial nerve then runs posteriorly from the geniculate ganglion and passes through the tympanic segment, passing posterior to the cochleariform process, tensor tympani and the oval window, before running vertically downwards at the second genu to the mastoid segment.

The mastoid segment extends from the second genu to the stylomastoid foramen. The nerve gives off three further branches in the mastoid segment:

  • Nerve to stapedius
  • Chorda tympani
  • Nerve from the auricular branch of the vagus nerve


The facial nerve then exits the cranium through the stylomastoid fomamen, just posterior to the styloid process of the temporal bone. The stylomastoid artery also passes through the stylomastoid foramen.


The extracranial anatomy of the facial nerve

As the nerve exits the stylomastoid foramen, it gives off the posterior auricular nerve, which controls movements of some of the scalp muscles around the ear. After exiting the cranium, it runs anteriorly to the outer ear before passing between the posterior belly of the digastric muscle and the stylohyoid muscle, giving off branches to each of these muscles in the process.

It then enters the parotid gland, which it does not innervate. Lying between the deep and superficial lobes of the gland the nerve divides into its five terminal motor branches, which innervate the muscles of facial expression:

  • Temporal branch
  • Zygomatic branch
  • Buccal branch
  • Marginal mandibular branch
  • Cervical branch


A plan of the course of the facial nerve, its branches and communications (adapted from Gray’s Anatomy)


The anatomy of the chorda tympani nerve 

The chorda tympani nerve is a special sensory branch of the facial nerve that is responsible for the taste innervation of the anterior 2/3 of the tongue.

It arises in the facial canal and travels across the bones of the middle ear before exiting the cranium via the petrotympanic fissure to enter the infratemporal fossa.

In the infratemporal fossa, the chorda tympani joins the lingual nerve, a branch of the mandibular division of the trigeminal nerve. The lingual nerve carries with it the taste fibres from the anterior 2/3 of the tongue.

The chorda tympani also carries presynaptic parasympathetic fibres to the submandibular ganglion, providing secretomotor innervation to the submandibular and sublingual glands and to the vessels of the tongue.


The chorda tympani nerve (from Gray’s Anatomy)


The function of the facial nerve 

The facial nerve has motor, parasympathetic, and special sensory functions:

  • Motor supply – innervates the muscles of facial expression, the posterior belly of digastric, stylohyoid, and stapedius.
  • Parasympathetic supply – supplies several glands of the head and neck, including the submandibular and sublingual salivary glands, nasal, palatine, and pharyngeal mucous glands, and the lacrimal glands
  • Special sensory supply – taste sensation to the anterior 2/3 of the tongue


The muscles of facial expression are sometimes innervated by more than one of the branches of the facial nerve. The muscles innervated by each of the branches are shown in the table below:


Branch of the facial nerveMuscles innervated
Temporal branchFrontalis
Orbicularis oculi
Corrugator supercilli
Auriculares anterior
Auriculares superior
(also acts as efferent limb of the corneal reflex)
Zygomatic branchOrbicularis oculi
Buccal branchOrbicularis oris
Levator labii superioris
Levator labii superioris alaeque nasi
Depressor septi nasi
Marginal mandibular branchMentalis
Depressor labii inferioris
Depressor anguli oris
Cervical branchPlatysma


Examining the facial nerve

The examination of the facial nerve involves the assessment of:

  • Motor supply to the muscles of facial expression
  • Taste on the anterior 2/3 of the tongue


The motor supply to the muscles of facial expression can be tested by asking the patient to crease their forehead by raising their eyebrows, keep their eyes closed against resistance, puffing out their cheeks, and showing their teeth.

Taste to the anterior 2/3 of the tongue can be assessed by, in turn, placing sweet, salty, bitter, and sour tasting solutions on one side of tongue with a cotton bud. The patient should rinse their tongue between each test and each side of the tongue should be tested in turn.


Lesions of the facial nerve

The causes of isolated facial nerve lesions should be separated into upper and lower motor neuron lesions.

Isolated upper motor neuron facial nerve lesions can be caused by:

  • Stroke
  • Intracranial tumours
  • Multiple sclerosis
  • Syphilis


Isolated lower motor neuron facial nerve lesions can be caused by:

  • Bell’s palsy
  • Otitis media
  • Skull fracture
  • Cerebellopontine angle tumours
  • Parotid tumours
  • Herpes zoster (Ramsey Hunt syndrome)
  • Lyme disease


Differentiating lesions of the facial nerve

In cases of upper motor neuron facial nerve lesions the upper facial muscles are partially spared because of the alternative pathways situated in the brainstem. The patient will be able to wrinkle their forehead and the ‘sagging’ of the face that is generally seen with lower motor neuron lesions is not as prominent. Stroke also usually weakens voluntary movement, but often spares involuntary movements, such as spontaneous smiling. For this reason, it has been postulated that there are different pathways for voluntary and emotional movement.

In cases of lower motor neuron facial nerve lesions the facial paralysis is complete and there is no sparing of the forehead muscles because the final common pathway has been damaged. In these cases, the lesion is situated outside of the brainstem. 80% of cases of isolated sudden onset lower motor neuron facial palsies are attributed to Bell’s palsy. It is postulated that this is caused by swelling of the facial nerve within the petrous temporal bone secondary to a latent herpes virus, specifically HSV-1 and HZV.


A patient demsonstrating the complete facial weakness associated with a Bell’s palsy Wikipedia
Courtesy of Dr. James Heilman CC BY-SA 3.0



Header image used on licence from Shutterstock

Thank you to the joint editorial team of for this article.