Facial weakness is also called facial palsy (complete lack of motion) or facial paresis (a weakness in facial movement). It is either a congenital deformity from birth or an acquired deformity that causes complete or partial paralysis of facial motion. It can originate in the brain, along the facial nerve or in the muscles of the face, usually affecting one side of the face. Facial nerve weakness can be seen as twitching, paralysis, weakness, inability to close an eye and even numbness in part of the face.
The underlying causes of these symptoms include infection, injury, circulatory disturbance or tumors.
- Facial muscle weakness
- Facial sagging
- Inability to close the eyelid – can lead to eye injuries
- Difficulty chewing and drinking
- Drooling, because of weakness around the mouth
- Sensitivity to light, because the eyelids do not close
- Difficulty speaking, because the side of the face is sagging
- Appearance from asymmetry is very striking and can lead to depression
The most serious complication that may develop as the result of total facial nerve paralysis is an ulcer of the cornea of the eye. It is most important that the eye on the involved side be protected from this complication. Glasses should be worn whenever outside. This will help prevent particles of dust from becoming lodged in the eye. If the eye is dry, eye drops are advised. The drops should be used as often as necessary to keep the eye moist. Ointment may be prescribed for use at bedtime. A moisture chamber is also helpful to keep the cornea moist. In some cases of long standing paralysis, it may be necessary to perform some other ophthalmic procedure, such as a tarsorrhaphy, to help the eyelid close.
This depends on the cause of the facial weakness. In most cases the weakness is secondary to Bell’s Palsy and the facial weakness does improve. In 90% of cases, function of the face improves.
Neuropraxia is the most common type and is associated with Bell’s palsy. Paralysis occurs; however, the peripheral nerve does not deteriorate. Testing will demonstrate a normal or reduced response. Although the nerve fibers are intact, they do not respond to movement commands, like smiling or eye blinking.
Axnotmesis occurs when the inner nerve fibers are not working properly, even though the nerve casing is intact. Testing will demonstrate no response.
Neurotmesis is the worst possible outcome from facial nerve injury. Testing will demonstrate essentially no response, as there is a total anatomic separation of the facial nerve. Prognosis is poor.
The facial nerve resembles an electric cable and contains hundreds of individual nerve fibers. Each fiber carries electrical impulses to a specific facial muscle. The facial nerve has several functions; however its main function is to move the muscles of the face, providing facial expression. In addition to carrying nerve impulses to the salivary and tear glands, it sends impulses to a muscle in the middle ear, which is attached to the stapes (the smallest bone in the middle ear). The facial nerve also has special fibers that provide taste to the tip of the tongue and pain fibers arising from the ear canal.
The facial nerve exits the brainstem and travels across the cerebellopontine angle. It enters a bony canal in the temporal bone of the skull, called the internal auditory canal. It then enters the middle ear space and the mastoid bone of the skull. The nerve exits the skull in front of the ear, where it splits into several branches. It is embedded in the parotid gland, the largest salivary gland, in front of the ear. After branching into many smaller divisions, it then exits the parotid gland before finally reaching the facial muscles. Even though the facial nerve makes many turns in its course from the brain to the face, this course is predictable and usually very uniform.
As a result of facial nerve fibers being involved with different structures and different sites, disorders of the facial nerve may result in twitching, weakness or paralysis of the face, dryness of the eye or the mouth, loss of taste, increased sensitivity to loud sound, and pain in the ear.
The brain tells the facial nerve which muscles to move. The signal travels from the brain to the facial nerve. The nerve then splits into numerous branches along the face (eye, lip, cheek, jaw, etc.). The muscles control facial movements and expressions (eye blinking, smiling, frowning, etc.).
The most important step in making a diagnosis of facial nerve disorders is observing the symmetry and movement of the face. The branches of the facial nerve need to be tested and the degree of weakness noted.
Several methods of grading facial function have been developed to describe facial movement. When there is a disorder that involves the main trunk of the nerve, the House-Brackmann grading system is most commonly used. This method has been adopted as the standard reporting scale by the American Academy of Otolaryngology – Head and Neck Surgery.
Hearing tests are frequently done to determine if the nerve disorder has involved the hearing mechanism. When the face is totally paralyzed, special hearing tests (auditory brainstem response, audiometry (link) and acoustic reflex tests) may be necessary to localize the problem area.
X-rays may be taken to determine if there is any infection, tumor, or bone fracture. These special X-rays utilize either computerized tomography (a CT scan) or magnetic resonance imaging (a MRI).
There are three electrical tests of the facial nerve function that are used: nerve excitability test, electroneuronography and electromyography. Initial testing should occur between three days and two weeks after onset of the paralysis. Electrical testing is only necessary in patients with a complete paralysis as surgery may be warranted. Patients that do not become completely paralyzed at the maximum of their disease will not need surgical intervention.
Nerve Excitability Testing – The purpose of this testing is to determine the degree of nerve injury and chances for spontaneous recovery. It can also help determine if surgery is warranted. It is only used in patients who on physical examination, have no evidence of facial movement. Facial movement is graded as normal, reduced, barely perceptible or absent. The test may be normal despite the paralysis, indicating a better outlook for return of function. In such cases, the excitability test may be repeated every day or so to detect any change which would indicate progress.
Electroneuronography (link) – This test, also called ENoG, involves the use of a computer to measure the muscle response to electrical stimulation of the facial nerve. Recording electrodes are placed on the face and the facial nerve is stimulated with small electrical currents. The computer records muscle contractions. This test has the ability to quantify the degree of the facial nerve fibers blocked or degenerating.
The most common condition resulting in facial nerve weakness or paralysis is Bell's palsy, named after Sir Charles Bell, who first described the condition. Evidence now points to herpes virus (varicella zoster) reactivation in the facial nerve as the cause of the problem. Human herpes viruses live in nerves even after the initial infection is over. For many reasons, they can be reactivated and cause injury to the nerve in which they live. If the virus lives in the facial nerve, it will cause a facial paralysis. The onset of facial weakness usually progresses and reaches its maximum severity at about two weeks. Patients often complain about having pain behind the ear prior to the onset of the facial weakness. Taste can often be disturbed, and many patients complain that sounds seem unpleasant or too loud.
With Bell’s palsy there is a specific location in the temporal bone where the nerve swells most in its tight bony canal. This swelling results in pressure on the nerve fibers and associated blood vessels. Treatment is directed at decreasing the swelling and restoring the circulation in this location, allowing the nerve fibers to return to normal function. However, normal function may not always be possible. Generally, patients with incomplete weakness at 2 weeks post-onset have a greater than 90% chance of excellent return of function. Patients with complete paralysis, but with good results from electrical testing, can also expect good return of function.
Other facts include:
- It affects 40,000 Americans annually and internationally one out of every 5,000 people
- It is most common between the ages of 30 and 60 years
- It strikes men and women equally
- Bell’s palsy will recur in 10 to 20% of patients
- The time of onset to total unilateral facial paralysis is usually about 24-48 hours
- Spontaneous recovery is common and usually occurs for 85% of all patients in 3-4 months
- 15% of Bell’s palsy patients maintain a life-long residual weakness after resolution of the palsy
- It more often occurs when patients have experienced some prior stressful event, such as surgery
- Diabetes – triples the risk compared to the general public
- Pregnancy – the last trimester increases risk for Bell’s palsy
Bell’s palsy is treated as a viral infection. Steroids are provided to reduce swelling; anti-viral medications are also prescribed. Patients that do become completely paralyzed may benefit from surgical decompression of the facial nerve, if the ENoG deteriorates on the affected side (i.e. less than 90% of the normal side) and if they have not improved with medical therapy.
Ramsay Hunt syndrome (RHS) is also caused by herpes varicella zoster. As with Bell’s palsy, the herpes virux also causes mouth sores, chicken pox, and the herpes reactivation disease commonly known as “shingles”. The patient’s medical history and physical exam provides sufficient information to make a diagnosis. Patients with RHS often have more severe facial weakness, vertigo and ear pain than patients with Bell’s palsy. Patients with RHS will have blisters in the ear, in the region of the concha, and this finding will distinguish RHS from Bell’s palsy. Patients with RHS have worse return of function than Bell’s palsy patients. Unlike Bell’s palsy, there is not a single focal point where the nerve is swollen (edematous) and “entrapped” within the bony canal, but generally multiple areas of the facial nerve are more severely affected. Steroids are provided to reduce swelling and anti-viral medications are also prescribed. The dosages are often higher and medication is given for a longer period of time for RHS compared to Bell’s palsy.
Otitis Media, Lyme disease, traumatic facial disorders, related to surgery
Otitis Media (link)– Facial paralysis or weakness can occur from acute or chronic ear infections. This is a more significant finding in patients with chronic ear infections caused by a cyst in the middle ear space (cholesteatoma -link). It implies that the bony canal through which the facial nerve traverses is eroded by the disease. When it occurs in an acute ear infection, it is usually because there is a congenital abnormality in the bony canal where the facial nerve is exposed to the purulent (infected) material. It is important to have a CT scan of the temporal bones when this complication occurs. Medical therapy includes antibiotics, often intravenously administered, as well as steroids. Surgical intervention is often warranted to drain the infection. Ear tubes are sometimes sufficient, but it is also sometimes necessary to perform a mastoidectomy to remove infection involving the mastoid or a cholesteatoma.
Lyme Disease – Lyme disease is caused by bacterium carried by a tick. The disease has many symptoms, which occur at different time periods. The bacterium enters the blood stream and can cause problems with many different nerves. The facial nerve is the most commonly affected cranial nerve. Facial weakness can be on one side or both. Diagnosis of Lyme disease as the cause of facial paralysis can be made with a blood test, which looks for antibodies to the bacteria. When there is nerve involvement, the recommended therapy for Lyme disease is an antibiotic for 3-4 weeks and steroids.Traumatic Facial Disorders
The most common traumatic cause of facial nerve injury is a skull fracture. This nerve injury may occur immediately after the incident or may develop some days later due to nerve swelling.Surgical Complications
Delayed weakness or paralysis of the face following reconstructive middle ear surgery (myringoplasty, tympanoplasty, or stapedotomy) is uncommon. Fortunately, this type of facial nerve weakness usually subsides spontaneously in several weeks and rarely requires further surgery. Immediate injury to the facial nerve may also occur in the course of some operations on the ear. This complication, fortunately, is very uncommon. It may occur, however, when the nerve is not in its normal anatomical position (a congenital abnormality) or when the nerve is so distorted by the mastoid or middle ear disease that it is not identifiable. In more complicated ear problems, such as tumors of the hearing and balance nerve, the facial nerve may be injured and at times, the nerve must be severed to allow complete removal of the tumor.
The management after surgical injury is determined by the site and degree of injury. CT or MRI scans are often obtained to help diagnose the site of the injury. When the nerve is completely cut, the best outcome occurs with sewing the two ends together. This isn’t always possible, so sometimes it is necessary to use a nerve graft. The donor nerve can come from several areas including, the ankle or neck. Good return of function is expected with these procedures. If there is not enough nerve left to place a nerve graft, it is possible to redirect the hypoglossal nerve (the nerve that moves the tongue) to the facial nerve. This gives excellent return of facial function, and does not affect swallowing and talking as long as there is a functioning hypoglossal nerve on the other side.
These are the most common tumor of the facial nerve. They are benign neoplasms that arise from the Scwhann cells and can occur anywhere along the course of facial nerve. They sometimes can extend intracranially, making it difficult to differentiate between other tumors. These tumors typically produce a gradually progressive facial nerve paralysis. However, the loss may also occur suddenly and mimic a Bell’s palsy. The only way to distinguish it from Bell’s palsy is to obtain an MRI. Hearing loss is the second most common finding in patients with facial nerve tumors. It can be caused by compression of the cochlear nerve with intracranial extension or if the tumor is present in the middle ear. Some tumors can grow to very large size before they cause any symptoms.
Patients with a suspected facial tumor should undergo a complete examination, including a hearing test. The facial function also needs to be documented. Radiological testing, however, is the most useful. CT scans, to evaluate the bones surrounding the facial nerve, and a MRI, to examine the nerve itself, are used in conjunction to give a complete description of the nerve and tumor.Surgical treatment of facial tumors
The ideal goal of surgery for facial tumors is complete removal of the tumor with preservation or restoration of facial function and conservation of hearing. These goals are often difficult to realize. Facial preservation can sometimes occur with vascular lesions, but is much more difficult to achieve with schwannomas. The timing of surgery is controversial. Young patients with poor facial function should have surgery with some form of facial reanimation. This can be achieved with nerve grafting or hypoglossal to facial nerve grafts.
It is less clear how to manage patients with normal facial function. Some otologists argue for early resection with reanimation, while others suggest watchful waiting. The argument for early resection is that it is easier and less dangerous for the patient to remove a tumor while it is smaller. Another argument is that if the tumor extends into the skull toward the brain (intracranially), it will be more difficult to preserve hearing. Others argue that it is reasonable to wait until the facial tumor causes facial weakness and then perform surgery. These are slow growing tumors, and it may take many years for a weakness to result, if at all. Others suggest that surgery be performed to decompress the tumor and remove all bone around it. This will allow it to grow larger with less likelihood of causing weakness. The best outcome that can be expected from a facial nerve graft is grade III with eye weakness and abnormal movement of the face, although the face looks normal at rest. Some surgeons will wait until there is a grade III function before operating.
Surgical approaches to the facial nerve must be tailored to the individual patient, which are determined by the location of the tumor. The approaches include middle cranial fossa approach, transmastoid approach, translabyrinthine approach, or combinations of these. The technical aspects of the surgeries are quite detailed, and require an extensive knowledge of the temporal bone anatomy.
Removal of the facial nerve neuroma requires severing the facial nerve. Usually it is possible to graft it at the time with a skin sensation nerve from the neck. Total paralysis will be present until the nerve re-grows through the graft, usually a period of 6 to 15 months. There will be some permanent facial weakness. When the portion of the facial nerve nearest the brain is destroyed by the tumor, a surgical connection between two nerves, the tongue and facial nerve (hypoglossal-facial nerve anastomosis), (link to below) procedure is necessary.
Removal of a facial nerve neuroma may also require removal of the inner ear structures, resulting in a total loss of hearing in the operated ear and temporary dizziness. Persistent complaints of dizziness are uncommon.
Other Causes of Facial Nerve Weakness
Hemifacial spasm is a neuromuscular disorder characterized by frequent involuntary contractions of the muscles on one side of the face. The disorder occurs in both men and women, although it more frequently affects middle-aged or elderly women. The first symptom is usually an intermittent twitching of the eyelid muscle that can lead to forced closure of the eye. The spasm may then gradually spread to involve the muscles of the lower face, which may cause the mouth to be pulled to one side. Eventually the spasms involve all of the muscles on one side of the face almost continuously. The condition may be caused by a facial nerve injury or tumor. More commonly, hemifacial spasm is caused by a blood vessel pressing on the facial nerve.
Treatment of hemifacial spasm frequently consists of injecting botulinum toxin (commonly called Botox) into the affected muscles. Surgery may be used for some cases. The surgery is performed to rotate or displace the blood vessel off of the facial nerve and is most commonly performed using the retrosigmoid approach. In this operation, the area between the brain and the inner ear is exposed by removing the mastoid bone behind the inner ear.
Circulatory disturbances of the nervous system may cause facial nerve paralysis. The most common example of this is a stroke. A patient that has had a stroke in areas of the brain, which provide input to the facial nerve, will only have weakness of the face below the eyes. A stroke usually has many other symptoms, which indicate the cause of the problem. Treatment is managed by the internist, neurologist, or neurosurgeon.
Decompression of the facial nerve - Surgical decompression of the facial nerve is indicated in cases of paralysis when the electrical test shows that the nerve function has significantly deteriorated. This operation is performed under general anesthesia and requires hospitalization for 2 to 5 days. The rigid bone around the swollen nerve is removed, relieving the pressure, and allowing the circulation to the nerve to be restored. The degree and rapidity of recovery of facial nerve function depends upon the amount of damage present in the nerve at the time of surgery. Recovery may take 3 to 12 months and may not be complete. Fortunately, it is unusual to develop a hearing impairment following surgery, but this depends on the extent of surgery needed in the individual case.
Facial nerve graft - A facial nerve graft is necessary at times if the facial nerve damage is extensive. A skin sensation nerve is removed from the neck and is used to replace the diseased or damaged portion of the facial nerve. It is interposed between the two portions of the remaining normal nerve. Total paralysis will be present until the nerve re-grows through the graft. This usually takes 6 to 15 months. Some facial weakness is permanent.
Hypoglossal-Facial Nerve Anastomosis - When it is not possible for a facial nerve re-connection by other means, the nerve controlling the muscles of one side of the tongue is connected to the facial nerve. This hypoglossal-facial nerve anastomosis is usually performed 9 to 12 months after the tumor removal. Surgery is performed under general anesthesia. The previous incision behind the ear is opened and extended into the neck. The nerve to the tongue (hypoglossal nerve) is cut and then connected to the facial nerve. In 6 to 12 months, when the tongue nerve grows into the facial nerve, a variable degree of facial motion returns. Facial appearance may be nearly normal at rest. There will be some persistent weakness of the face after surgery. Upon speaking or moving the face to smile, etc., all of the muscles tend to contract at once, which results in a noticeable visual difference from the other half of the face. Weakness and wasting of one half of the tongue develops following cutting of the hypoglossal nerve. This results in some difficulty in speaking, chewing and swallowing. Although the tongue weakness is permanent, it is rare for a severe disability to persist.
No reanimation operation can achieve “normal” facial movement – the patient can never be made exactly as he/she was before the paralysis. Therefore, the aim of this surgery is to achieve the best possible facial function and improved appearance.Surgical Approaches
Middle Fossa Approach - An incision is made above the ear and the brain with its dense covering is elevated. Bone over the facial nerve can be removed to allow decompression or inspection of the nerve in the internal auditory canal, at the geniculate ganglion and into the middle ear.
Mastoid Approach - Through an incision behind the ear, bone over the facial nerve can be removed as it passes across the middle ear and mastoid.
In some patients, usually those with long-standing facial paralysis, additional techniques are used to achieve facial symmetry and movement. These methods can also be used in combination with a facial nerve graft or hypoglossal-facial anastomosis. These procedures are not considered cosmetic, as the facial paralysis is a functional deficit.
Botlinum Toxin Injection for Treatment of Synkinesis
Patients with synkinesis (i.e. mass motor movement) may lack the ability to independently move different segments of the face. They typically complain of involuntary eyelid closure with common movements of the mouth, such as pursing the lips or smiling. Excessive closure of the eye may, in addition to the obvious cosmetic deformity, result in visual impairment. Mass movement on the affected side of the face is most commonly seen several months after the onset of the severe facial paralysis. This occurs as a result of the misdirected nerve fibers re-innervating the wrong facial muscles. Botulinum toxin (i.e. Botox) can be used to alleviate abnormal muscle movements that occur as a result of facial paralysis. Small doses of botulinum toxin are injected into the affected muscle group. In addition to control uncoordinated facial movement (synkinesis), these injections may also be used for benign essential eye spasms (blepharospasm) and hemifacial spasm. The injection typically lasts three to four months in controlling the synkinesis. Repeat injections are required to sustain benefit over long periods of time.
In some patients with stable partial facial movement, it is possible to improve their function with facial retraining. This is a form of physical therapy that involves mirror exercises. Exercising the muscles by wrinkling the forehead, closing the eyes tightly, and smiling forcefully may be beneficial and allow the patient to make the best use of residual facial function. Generally, these exercises are not recommended until approximately one year after the onset of the paralysis.
We do not usually recommend electrical stimulation of the facial muscles.