Facial paralysis

Overview

Muscles are moved by the brain transmitting information to them through the nerves. It is a completely automated procedure that most individuals are completely unaware of. When this mechanism is disrupted, it might result in paralysis. When a condition affects the face nerves, facial paralysis can occur.

Face nerve paralysis is a typical issue in which the facial nerve paralyzes whatever structures it innervates. Because the facial nerve's course is extensive and winding, there are a variety of conditions that might induce facial nerve paralysis. Bell's palsy is the most common, a disease with no known cause that can only be diagnosed by ruling out other serious causes.

Facial paralysis definition

Facial nerve palsies are a common and important presentation for ENT surgeons, as well as in general medicine. Because the facial nerve is such an important structure for communication and emotion, its damage can have a substantial impact on one's quality of life.

Differentiating between a lower motor neuron (LMN) and an upper motor neuron (UMN) palsy is critical in the first assessment of a patient with facial paralysis, since the likely causes and, hence, therapy, differ dramatically. A doctor can determine the likely cause of facial nerve palsy by combining anatomy with clinical history and examination, and then directing treatment accordingly.

Epidemiology

While most instances are determined to be idiopathic, any doctor should rule out a cerebrovascular stroke or other significant underlying disease. There is currently no convincing evidence that facial nerve palsies are more common in any gender or ethnicity, and people of all ages may be afflicted. However, it is general knowledge that facial nerve palsies more typically afflict people aged 15 to 45.

The most prevalent cause of facial nerve paralysis is Bell palsy, which accounts for around 70% of all facial nerve paralysis. Trauma is the second most common cause of facial nerve palsies, accounting for 10 to 23 percent of cases. Between 4.5 and 7% of cases are caused by viral infection resulting in facial nerve palsy, while between 2.2 and 5% are caused by neoplasia.

Facial paralysis causes

Idiopathic/Bell Palsy (70%)

Most of the time, the origin of facial nerve palsy is unclear, and it is referred to as 'Bell palsy.' Bell palsy affects 10 to 40 people out of every 100,000. It's an exclusionary diagnosis.

A lower motor neuron lesion with complete unilateral palsy is the most common symptom. A viral prodromal phase is considered to exist, and it can be recurring in up to 10% of patients; nonetheless, the existence of a facial nerve palsy usually manifests fully within the first 24 to 48 hours. Edema and secondary pressure can result in ischemia and impaired function if the nerve is compressed within the bone canal. Recovery can take up to a year, and up to 13% of patients do not finish it.

Trauma (10 to 23%)

Facial nerve palsies can be caused by fractures affecting the petrous section of the temporal bone and facial wounds transecting the branches of the facial nerve. The temporal bone must be fractured with a tremendous amount of power, and the doctor must watch for indications such as hemotympanum, battles sign, and nystagmus.

Temporal bone fractures are characterized according to the plane of fracture along the petrous ridge. Iatrogenic injury during otological, parotid, and acoustic neuroma surgery can also cause facial nerve traumatic damage and stretch injury. The importance of clinical history in determining the likely etiology cannot be overstated.

Infection

Herpes Zoster infection leading in facial paralysis owing to geniculate ganglionitis (also known as Ramsay Hunt syndrome) is a viral illness that affects 4.5 to 7% of people (RHS). In the geniculate ganglion, the virus is latent. The glossopharyngeal nerve also supplies innervation to the geniculate ganglion (CN IX(

As a result, the active virus might cause otalgia and vesicular eruptions in the external auditory canal and soft palate during the prodromal stage (distribution of CN IX). Furthermore, due to the involvement of cranial nerve VIII, up to 40% of individuals with RHS have vertigo (vestibulocochlear nerve). The prognosis is substantially poorer than with Bell palsy, with just 21% of patients recovering after a year.

Bacterial 

Acute otitis media can result in nerve paralysis due to dehiscence inside the facial canal. Face nerve palsies can also be caused by cholesteatomas and necrotizing otitis externa. Lyme disease is an uncommon cause of facial nerve palsy, with symptoms like a tick bite, lethargy, headache arthralgia, and erythema migrans appearing 1 to 2 weeks after tick exposure. The condition might potentially include cardiac involvement (myopericarditis) and arthritis. From an investigative approach, IgM + IgG serology is critical in these cases. Any patient with erythema migrans and a history of foreign travel exposure should be tested for Lyme disease as away.

Neoplasia (2.2 to 5%)

A gradual onset of facial palsy should raise suspicions of cancer and require a comprehensive head and neck examination. Parotid malignancies, facial and acoustic neuromas, meningioma, and arachnoid cysts are only a few of the cancers that cause face nerve paralysis. Due to the tumor's relative placement, these will all appear with varied degrees and indications of facial nerve palsy.

Facial Nerve Palsy in Children

Congenital or acquired facial nerve palsy in children can be caused by a variety of factors. All of the above etiologies can occur in children, and acquired causes are the same as outlined above for adults.

Congenital causes include:

• Traumatic such as high birth weight, forceps delivery, prematurity, or birth by cesarean section.
• Syndromic cases include those with craniofacial abnormalities such as Moebius syndrome, Goldenhar syndrome syringobulbia, and Arnold Chiari malformations. 
• Genetic causes such as hereditary myopathies (myasthenia and myotonic dystrophy. The chromosome loci 3q21-22 and 10q21.3-22.1 have been isolated as causes of hereditary forms of facial paralysis. 

It's worth mentioning that surgical decompression of the facial nerve inside the labyrinthine section isn't suggested for children since research hasn't shown that it improves results, and there's a considerable risk of sensorineural hearing loss. Nerve grafts and muscle transfer methods, on the other hand, may still be viable solutions for this group.

Bilateral Facial Nerve Palsy 

Bilateral facial nerve paresis is a rare but important branch of facial nerve palsy that affects 0.3 to 2% of those with facial nerve palsy. With just 20% of cases being idiopathic, bilateral palsy is crucial since it is considerably more likely to indicate a systemic manifestation of the illness. Lyme disease is responsible for a large proportion of bilateral facial nerve palsies, accounting for roughly 35% of cases.

Guillain-Barre syndrome, diabetes, and sarcoidosis are all essential differential concerns. Parkinson's disease, multiple sclerosis, and pseudobulbar/bulbar palsy are all neurological causes of a bilateral facial nerve palsy.

Pathophysiology

The source of facial nerve paralysis determines the manner of paralysis. Because the facial nerve runs via a tiny bone canal inside the intratemporal course, any source of nerve inflammation or development will result in ischemic alterations due to compression. Because the labyrinthine portion of the nerve is the thinnest, compression is most likely to occur here.

Furthermore, any skeletal defect or damage might impair the link between the facial nerve and its bone canal, resulting in facial paralysis. Some iatrogenic causes of facial nerve palsy (such as acoustic neuroma surgery) are caused by the procedure's subsequent stretching pressures.

Facial paralysis symptoms

Bell palsy or RHS may be indicated by a patient's history of a viral prodromal phase and facial nerve palsy. Inquiring about the onset of vesicular eruptions can assist differentiate this even further. A thorough otological history (e.g., otalgia, discharge, hearing loss, ear fullness, tinnitus, dizziness) will aid in the diagnosis of otitis externa/media. It might also help with auditory neuroma or cholesteatoma diagnosis. In the case of an UMN facial nerve palsy, a neurological history may be useful in determining the etiology.

Diagnosis

• Bloods:

For all patients hospitalized owing to an infectious etiology of facial palsy, blood tests such as a full blood count, urea and electrolytes, and C-reactive protein are required.

Antibody titers to the varicella-zoster virus would be higher in RHS. Lyme illness causes IgG and IgM levels to rise.

• Special Tests:

An audiogram should be conducted as soon as possible to assess the type and severity of any related hearing loss. Electrophysiological tests are effective for prognosis, although they are costly, time-consuming, and only useful for a limited period of time:

1. Minimal to maximal stimulation tests - On the injured side, the facial nerve is stimulated with a modest current that is gradually raised until the patient tolerates it. A four-stage grading method is then used to compare this reaction to the unaffected side. If there is a clinically significant difference between the two sides, the test is positive.
2. The most precise method for evaluating the amount of palsy is electroneurography (ENOG), which tries to establish muscular action potential amplitude. It entails stimulating the facial nerve near the stylomastoid foramen and detecting a motor response near the nasolabial fold. The typical side is then contrasted to this answer.
3. Electromyography (EMG) identifies activity in the face muscles by detecting fibrillation potentials, which appear after about three weeks following denervation.
4. Magnetic Stimulation – Transcranial stimulation is used to examine intratemporal and brain stem elements of the facial nerve. The test must be done right away since Wallerian degeneration of the nerve will change the results. Because proximal site stimulation with higher than typical stimulus intensities overcomes the block at the damage site and allows facial nerve activity to occur, magnetic stimulation can be useful for intratemporal facial nerve injury when axonal integrity exists. 

• Imaging:

A CT of the temporal bones is required if necrotizing otitis externa or a consequence of middle ear infection is suspected, or if there is a history of head trauma or suspicion of cancer.

MRI scanning is excellent for detecting intratemporal lesions that might cause facial nerve compression, and it's especially good for imaging the cerebellopontine angle. MRI scans may also reveal facial nerve amplification surrounding the geniculate ganglion.

Facial paralysis treatment

Conservative

• Eye care is critical for people who have palsies that cause corneal exposure. Corneal ulcers can be avoided by using artificial tears, using enough lubricant, and taping the eyes shut at night. A referral to an ophthalmologist is a suggestion.
• Patients with facial nerve palsy benefit from face massage and exercises, which encourage active recovery.

Medical

• Bell Palsy – If initiated within 72 hours of symptom onset, the administration of steroids and analgesics will aid in the recovery of motor function. If prednisolone 50 mg once a day is started during this time frame, it should be continued for 10 days. If a lowering regimen is selected, 60 mg of prednisolone should be administered once a day, followed by a daily reduction of 10 mg for a total of ten days of therapy. Antivirals were only of little help for bell palsy, according to one research, and this combination should be reserved for Ramsay Hunt syndrome. Without therapy, nearly 70% of people with Bell palsy will regain full motor function within six months.
• The treatment for Ramsay Hunt syndrome comprises steroid therapy, analgesics, and acyclovir 800 mg 5 times a day for 7 to 10 days to battle the viral infection. Facial nerve function is likely to restore in roughly 75% of patients after a full course of therapy. Although there is no evidence that antiviral medication is useful in Ramsay Hunt syndrome, it is nonetheless extensively used.
• A combination of intravenous antibiotics is required for acute otitis media and mastoiditis-related bacterial infection (type and duration according to local microbiological guidance).
• The treatment of Lyme disease is determined on the patient's age and the severity of the infection. If an individual over the age of eight has localized illness, 200 mg of doxycycline once day for a total of 10 days is indicated. A 14-day regimen of amoxicillin or cefuroxime is recommended for children under the age of eight to avoid tooth discoloration from tetracycline usage. Treatment is typically curative in most early and isolated instances.

Surgical

• In Bell palsy: Because ENoG degeneration of more than 90% is linked to a bad prognosis, surgical decompression of the facial canal should be considered. However, as compared to traditional medical care, this has not shown significantly better results.
• For acute suppurative otitis media + mastoiditis, myringotomy +/- ventilation tube and or cortical mastoidectomy is advised.
• Iatrogenic causes: If a facial nerve palsy develops soon after otological surgery, a wait-and-see approach should be used, as this might be caused by the administration of local anesthetics. A cautious therapy with steroids is a possibility if a local anesthetic cause has been ruled out and the surgeon is satisfied that the facial nerve epineurium is intact. Otherwise, a re-examination, face decompression, and/or nerve grafting is required. Edema and infection (which require steroids and antibiotics) can cause delayed palsies after surgery, as can overtight packing in open mastoid surgery, which necessitates removal.
• Temporal bone fracture – If the facial nerve is completely paralyzed, specialized nerve decompression is necessary as soon as the patient's condition permits (usually within 2 to 3 weeks). Surgical exploration is indicated if the diagnosis is delayed and the ENoG degeneration is more than 90%. As far as detecting the location of nerve injury, a detailed examination of the facial nerve will aid in deciding the strategy.

Transcutaneous Nerve Stimulation 

For people with unilateral facial nerve palsy, transcutaneous nerve stimulation is a novel therapy option. The method leverages EMG signals from muscles on the healthy side of the face to activate muscles on the paresis side at the same time. Therapy's ultimate goal is to establish face symmetry. Early experiments have demonstrated promising outcomes in key areas of facial expression where the damaged side is paretic, with some reinnervation.

How acupuncture can help with Bell’s palsy?

In China and across the world, acupuncture therapy is frequently utilized to treat Bell's palsy. It is caused by inflammation of the 7th cranial nerve, which affects the stylomastoid foramen and the facial canal. This is known in traditional Chinese medicine (TCM) as Yang Ming and Shao Yang channel blockage.

The primary treatment objective is to clear the meridians of Wind. Acupuncture can restore facial muscle mobility by energizing Qi and boosting blood circulation to the face by stimulating a localized region of facial muscles. Acupuncture treatments once or twice a week are indicated to speed up the recovery of nerve function and paralysis.

Three stages of acupuncture treatments

Treatment for Bell's palsy varies depending on the disease's stage. The most crucial thing is to begin treatment as soon as possible, as acupuncture works best in the acute period.

1. Acute stage

Within ten days of the commencement Wind-cold or Wind-heat affects the Shao Yang meridian, which runs down the sides of the face and relates to the San Jiao and Gallbladder meridians. As a result, acupoints on the Shao Yang meridians will be chosen appropriately.

2. Resting stage

Within three months of the onset. Because Qi grows at this period, stronger Qi can combat pathogenic causes, and most people will recover successfully. The pathogenic element now enters Yang Ming meridian at a deeper level, hence acupoint choices will be concentrated on Yang Ming meridian.

3. Recovery stage

It's been more than 3 months from the beginning. Because the pathogenic element has been there for such a long time, it has penetrated deeper into the meridians, depleting Qi and blood in the body and depriving the face muscles of nutrients. The symptoms are frequently complex, and they might result in facial muscle spasms and connective tissue adhesion, resulting in permanent changes in facial expressions. To address the core cause, local acupoints on the face as well as Zang organ acupoints are chosen.

Prognosis

Factors suggestive of a poor prognosis when associated with a facial nerve palsy include: 

• Complete palsy
• Loss of the stapedial reflex
• No signs of recovery within three weeks
• Age over 50 years
• Ramsay Hunt syndrome
• Poor response to electrophysiological testing

Complications

The consequences of facial nerve palsy are diverse and serious. Conservative eye treatment tries to limit the risk of ophthalmic problems from a facial nerve palsy, such as exposure keratitis and corneal dryness, which can lead to ulceration. Hemifacial spasm, facial asymmetry, and synkinesis are some of the hyperkinetic consequences associated with facial nerve palsy.

• Hemifacial spasm is caused by axonal degeneration of the facial nerve, which causes involuntary muscular spasms on one side of the face.
• Facial asymmetry is a major source of worry for patients, and it can result in severe suffering due to deformity.
• Synkinesis is the combination of deliberate and involuntary facial movements. The most prevalent symptom of synkinesis is ocular-oral synkinesis, which is the involuntary movement of the mouth when the eyes are closed. Gustatory lacrimation, often known as crocodile tear syndrome, is another significant indication of facial nerve synkinesis. 

Facial muscle therapy and botulinum toxin treatment are used to treat these hyperkinetic consequences of facial nerve palsy. To compensate for synkinesis, face muscle treatment aims to strengthen the weaker portion of the facial musculature. Botulinum toxin, on the other hand, is used to treat both synkinesis and hemifacial spasms by paralyzing facial muscles.

Conclusion 

Facial paralysis can be caused by a variety of illnesses and etiologies, including congenital, traumatic, viral, neoplastic, and metabolic conditions. As a result, facial palsy can manifest in a variety of ways, ranging from temporary unilateral paresis to lifelong bilateral paralysis.

Although rarely life-threatening, facial paralysis is a common occurrence that can have profound repercussions on one's quality of life, with significant psychological and physiological consequences. The etiology of the weakness, as well as the treatment given to the patient, have a significant impact on the patient's prognosis and results.

Facial plastic surgeons are frequently called upon to treat the effects of long-term facial paralysis. Any practitioner who works with this population, however, must have a thorough awareness of the numerous etiologies and treatment options for facial paralysis.

Patients who suffer from facial nerve palsy have a unique set of obstacles. To lessen the risk of problems from self-management regimens, patients must be educated. Dealing with dry eyes and mouth, how to tape an eye shut to avoid corneal abrasion/ulceration, eating and drinking, a new development of facial expression, speaking, and linguistic modifications (and development in youngsters) are just a few examples. Providing patients with helpful tips and instructional materials on how to deal with these challenges may have a significant impact on their overall health and result.