Contributors:Elizabeth Nixon-Shapiro, MSMI, CMI, Alaina Mueller, Sam Gillespie, BSc, Maria Emfietzoglou, MD, Kimberly Clay BSN, RN
Now, let’s quickly review the anatomy and physiology of facial innervation. The 12 pairs of cranial nerves are peripheral nerves, also called lower motor neurons, that emerge from the brain or brainstem. The seventh cranial nerve is the facial nerve, which emerges from the brainstem,
and then enters the temporal bone where it travels through the facial canal. The facial nerve then exits the skull through a tiny hole called the stylomastoid foramen.
From there, it branches off to innervate different facial muscles that control facial expression ipsilaterally, so on the same side. The facial nerve also innervates the lacrimal glands, as well as the sublingual gland and submandibular salivary glands, and the mucous membranes of the nose, mouth, and nasopharynx. In addition, the facial nerve also carries sensory information about taste from the anterior ⅔ of the tongue. Finally, the facial nerve innervates the stapedius muscle in the ear, which helps dampen loud noises.
If we look back, the facial nerve receives information from a region of the brain called the motor cortex, which has upper motor neurons that send information to the brainstem nuclei of the facial nerve, and then the facial nerve gives rise to two lower motor neurons, one to innervate the lower side of the face, and one for the upper side. Now, the lower motor neuron that innervates the upper side of the face receives information from both sides of the motor cortex, so both from an upper motor neuron coming from the ipsilateral side, as well as an upper motor neuron coming from the contralateral or opposite side that crosses in the midline. On the other hand, the lower motor neuron that innervates the lower side of the face only receives information from the contralateral motor cortex, so from an upper motor neuron that crosses in the midline.
Now, Bell palsy is caused by damage to the facial nerve. Although the precise cause of the damage is unknown, risk factors include history of viral infections, such as herpes simplex virus or HSV, Epstein-Barr virus or EBV, and varicella-zoster virus or VZV; as well as bacterial infections, such as Borrelia burgdorferi, which causes Lyme disease. Other risk factors include conditions like sarcoidosis, diabetes mellitus, or hypertension.
So, these risk factors seem to trigger inflammation or damage to the lower motor neurons belonging to the facial nerve. As a result, information from both the contralateral and the ipsilateral motor cortex is lost for the upper face, as well as information from the contralateral motor cortex for the lower face. This results in the paralysis of all the muscles on the ipsilateral side of the affected nerve.
Now, the clinical manifestations of Bell palsy typically begin suddenly, and tend to worsen over 48 hours. These include mild weakness to total facial paralysis on one side; as well as a unilateral drooping of the eyelid and mouth, and disappearance of the nasolabial fold, which is the skin fold that runs from the side of the nose to the corner of the mouth. Clients often experience dryness of the affected eye or side of the mouth, a loss of taste sensation on the anterior ⅔ of the tongue, as well as some difficulty drinking and eating, or difficulty with speech. In addition, clients often experience posterior auricular pain, or pain behind the ear. Lastly, some clients can also develop unilateral hyperacusis, where the ear on the affected side may have increased sensitivity to loud noises.
Now, it’s important to distinguish Bell palsy from other causes of facial paralysis, where the underlying problem is in the motor cortex, before the upper motor neurons cross the midline. This only causes paralysis of the lower half of the face on the contralateral side of the lesion, since the upper half of the face is still receiving some information from the ipsilateral motor cortex.
Regarding treatment for Bell palsy, most cases resolve on their own within 6 months, but some clients may benefit from anti-inflammatory medications, like corticosteroids, which can help reduce the nerve inflammation and speed up the recovery. In some cases, physiotherapy can be used after recovery to promote facial muscle control. Fortunately, only a few clients develop permanent facial weakness or paralysis.