Anatomy clinical correlates: Facial (CN VII) and vestibulocochlear (CN VIII) nerves

The facial nerve is all about supplying those facial muscles and allowing for the whole range of facial expressions that they create. But don’t just judge a nerve by its face; ‘cause that’s not all it can do! The facial nerve is also involved in salivating, secreting tears, and it even plays a role in taste.

On the other hand, the vestibulocochlear nerve is the cranial nerve that helps you hear your favorite song, so then you can use your facial nerve to smile when you hear it. And it also plays a role in balance, so you can dance along without tipping over! Understanding the anatomy of the facial and vestibulocochlear nerves is important, as damage to these nerves can cause significant impairments when it comes to facial expression, hearing and balance, among several other functions!

Let’s start with the general anatomy of the facial nerve. Remember that there are two facial nerves, one on each side, and each of them is primarily responsible for providing motor innervation to the muscles of facial expression. The facial nerve also innervates the stapedius muscle in the middle ear; gives parasympathetic innervation to the lacrimal glands, nasal glands, palatal mucosal, submandibular, and sublingual salivary glands; and also carries the special sensory information of taste from the anterior two-thirds of the tongue and the palate.

It is also involved in the corneal reflex, also known as the blink reflex, which causes involuntary blinking when the cornea is stimulated to protect the eye from foreign bodies like sand. In this reflex, the trigeminal nerve is the sensory or afferent pathway, while the facial nerve serves as the motor or efferent pathway.

Now, the clinical presentation of facial nerve damage is called facial nerve palsy. If the entire facial nerve is damaged, all of its functions are affected. Without motor innervation, facial muscles become weak or impaired. This means the affected individual will have trouble when trying to smile, frown, raise their eyebrows, puff their cheeks, or whistle.

Paralysis of these muscles can also cause the face to look different on the affected side; for example, there can be loss of the characteristic nasolabial fold or less wrinkling in the forehead when compared to the unaffected side. Because the orbicularis oculi muscle is affected, the lower eyelid can become everted, and they can’t close the affected eye. Because the sphincter and dilator muscles of the mouth are affected, the corner of the mouth droops. There is also decreased tear secretion, decreased salivation and loss of taste due to loss of innervation to the lacrimal glands and submandibular glands.

Since the stapedius muscle normally acts on the stapes to dampen down excessive vibrations, when it loses its innervation and becomes paralyzed, increased sensitivity to certain sound frequencies can result, which is called hyperacusis. Finally, if you stimulate the cornea by lightly touching it with a piece of cotton, you will notice that the corneal reflex is absent, meaning that there is no involuntary blinking.

The facial nerve can be injured in many ways. If the fibers above the facial nucleus are damaged, it is referred to as an upper motor neuron lesion or central facial palsy. Common causes include stroke, trauma, multiple sclerosis, and brain tumors.

Remember that the facial nucleus has a dorsal and a ventral part. The dorsal region controls the muscles of the upper face. It receives innervation from upper motor neurons from both the right and left hemispheres of the brain, meaning it is under bilateral control. So, if upper motor neuron fibers from one side of the brain are damaged, they still receive innervation from the upper motor neuron in the other hemisphere, so the muscles of the upper face won’t be affected with a unilateral upper motor neuron lesion of either facial nerve.

On the other hand, the ventral part of the facial nucleus, which controls the muscles of the lower part of the face, only receives innervation from the upper motor neurons of the contralateral hemisphere. Therefore, an upper motor neuron lesion will result in contralateral dysfunction of the muscles of the lower face. This is because the upper motor neuron fibers decussate right before synapsing with the lower motor neuron, so symptoms of upper motor neuron lesions will appear on the contralateral side. A good way to remember this is to think of the phrase ‘Upper spares Upper’, meaning an upper motor neuron lesion will spare the muscles of the upper face, and will only affect the muscles of the lower face on the contralateral side.

A lower motor neuron lesion, or peripheral facial palsy refers to any injury that affects the facial nerve from the facial nucleus up until it gives off its terminal branches. Things are a bit different now. There is no dual innervation here, and fibers travel through the lower motor neuron to the ipsilateral side. Also, information from both the dorsal and ventral parts of the nucleus are together at this point in the nerve. So, these lesions will affect all muscles of facial expression, both of the upper face and the lower face, on the same side as the lesion.

Ok, that was a lot of information. Can you tell the difference between central and peripheral facial nerve palsy?

Great! Now let’s look into Bell palsy, which is the most common cause of peripheral facial palsy. The cause of this condition hasn’t been established yet, but it is thought to be caused by the reactivation of the herpes simplex virus. In addition to unilateral facial paralysis, those with Bell palsy may also have hyperacusis, decreased tear production and loss of taste to the anterior two-thirds of the tongue.