Paralysis of the facial muscles: ethiology, clinical features, surgical treatment. Face atrophy: ethiology, symptoms, diagnosis, surgical treatment.
Bell’s palsy
Bell’s palsy is a form of facial paralysis resulting from a dysfunction of the cranial nerve VII (the facial nerve) causing an inability to control facial muscles on the affected side. Several conditions can cause facial paralysis, e.g., brain tumor, stroke, myasthenia gravis, and Lyme disease. However, if no specific cause can be identified, the condition is known as Bell’s palsy. Named after Scottish anatomist Charles Bell, who first described it, Bell’s palsy is the most common acute mononeuropathy (disease involving only one nerve) and is the most common cause of acute facial nerve paralysis (>80%).
Bell’s palsy is defined as an idiopathic unilateral facial nerve paralysis, usually self-limiting. The hallmark of this condition is a rapid onset of partial or complete paralysis that often occurs overnight. In rare cases (<1%), it can occur bilaterally resulting in total facial paralysis.[1][2]
It is thought that an inflammatory condition leads to swelling of the facial nerve. The nerve travels through the skull in a narrow bone canal beneath the ear. Nerve swelling and compression in the narrow bone canal are thought to lead to nerve inhibition, damage or death.
Corticosteroids have been found to improve outcomes, when used early, while anti-viral drugs have not.[3] Most people recover spontaneously and achieve near-normal to normal functions. Many show signs of improvement as early as 10 days after the onset, even without treatment.
Often the eye in the affected side cannot be closed. The eye must be protected from drying up, or the cornea may be permanently damaged resulting in impaired vision. In some cases denture wearers experience some discomfort.
Anatomy of the face
Signs and symptoms
Facial nerve: the facial nerve’s nuclei are in the brainstem (they are represented in the diagram as a „θ“). Orange: nerves coming from the left hemisphere of the brain. Yellow: nerves coming from the right hemisphere of the brain. Note that the forehead muscles receive innervation from both hemispheres of the brain (represented in yellow and orange).
Bell’s palsy is characterized by facial drooping on the affected half, due to malfunction of the facial nerve (VII cranial nerve), which controls the muscles of the face. Facial palsy is typified by inability to control movement in the facial muscles. The paralysis is of the infranuclear/lower motor neuron type. The degree of nerve damage can be assessed using the House-Brackmann score.
The facial nerves control a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. They also innervate the stapedial (stapes) muscles of the middle ear and carry taste sensations from the anterior two-thirds of the tongue. Because both the nerve to the stapedius and the chorda tympani nerve (taste) are branches of the facial nerve, patients with Bell’s palsy may present with hyperacusis or loss of taste sensation in the anterior 2/3 of the tongue.
Clinicians should determine whether the forehead muscles are spared. Due to an anatomical peculiarity, forehead muscles receive innervation from both sides of the brain. The forehead can therefore still be wrinkled by a patient whose facial palsy is caused by a problem in one of the hemispheres of the brain (central facial palsy). If the problem resides in the facial nerve itself (peripheral palsy) all nerve signals are lost on the ipsilateral (same side of the lesion) half side of the face, including to the forehead (contralateral forehead still wrinkles).
Although defined as a mononeuritis (involving only one nerve), patients diagnosed with Bell’s palsy may have “myriad neurological symptoms” including “facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness” that are “unexplained by facial nerve dysfunction”.[4] This is yet an enigmatic facet of this condition.
A person attempting to show his teeth and raise his eyebrows with Bell’s palsy on his right side (left side of the image).
Cause
Some viruses are thought to establish a persistent (or latent) infection without symptoms, e.g., the varicella-zoster virus[5] and Epstein-Barr viruses, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggested[6] as a cause behind the acute Bell’s palsy. Studies[7] suggest that this new activation could be preceded by trauma, environmental factors, and metabolic or emotional disorders, thus suggesting that stress—emotional stress, environmental stress (e.g., cold), physical stress (e.g., trauma)—in short, a host of different conditions, may trigger reactivation.
Differential diagnosis
Once the facial paralysis sets in, many people may mistake it as a symptom of a stroke. But there are a few subtle differences. A stroke will usually cause a few additional symptoms, such as numbness or weakness in the arms and legs. And unlike Bell’s palsy, a stroke will usually let patients control the upper part of their faces. A person with a stroke will usually have some wrinkling of their forehead.
One disease that may be difficult to exclude in the differential diagnosis is involvement of the facial nerve in infections with the herpes zoster virus. The major differences in this condition are the presence of small blisters, or vesicles, on the external ear and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existing herpes zoster infection leading to facial paralysis in a Bell’s palsy type pattern is known as Ramsay Hunt syndrome type 2.
Lyme disease may produce the typical palsy, and may be easily diagnosed by looking for Lyme-specific antibodies in the blood or erythema migrans. In endemic areas Lyme disease may be the most common cause of facial palsy.
Pathology
Anatomy of the face.
It is thought that as a result of inflammation of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal, blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bell’s palsy per se. Possible causes include tumor, meningitis, stroke, diabetes mellitus, head trauma and inflammatory diseases of the cranial nerves (sarcoidosis, brucellosis, etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy.[9] In a few cases, bilateral facial palsy has been associated with acute HIV infection.
In some research[10] the herpes simplex virus type 1 (HSV-1) was identified in a majority of cases diagnosed as Bell’s palsy. This has given hope for anti-inflammatory and anti-viral drug therapy (prednisone and acyclovir). Other research[6] however, identifies HSV-1 in only 31 cases (18 percent), herpes zoster (zoster sine herpete) in 45 cases (26 percent) in a total of 176 cases clinically diagnosed as Bell’s Palsy. That infection with herpes simplex virus should play a major role in cases diagnosed as Bell’s palsy therefore remains a hypothesis that requires further research.
In addition, the herpes simplex virus type 1 (HSV-1) infection is associated with demyelination of nerves. This nerve damage mechanism is different from the above mentioned – that edema, swelling and compression of the nerve in the narrow bone canal is responsible for nerve damage. Demyelination may not even be directly caused by the virus, but by an unknown immune system response. The quote below captures this hypothesis and the implication for other types of treatment:
It is also possible that HSV-1 replication itself is not responsible for the damage to the facial nerves and that inhibition of HSV-1 replication by acyclovir does not prevent the progression of nerve dysfunction. Because the demyelination of facial nerves caused by HSV-1 reactivation, via an unknown immune response, is implicated in the pathogenesis of HSV-1-induced facial palsy, a new strategy of treatment to inhibit such an immune reaction may be also effective.[6]
Cranial_nerve
Diagnosis
Bell’s palsy is a diagnosis of exclusion; by elimination of other reasonable possibilities. Therefore, by definition, no specific cause can be ascertained. Bell’s palsy is commonly referred to as idiopathic or cryptogenic, meaning that it is due to unknown causes. Being a residual diagnostic category, the Bell’s Palsy diagnosis likely spans different conditions that our current level of medical knowledge cannot distinguish. This may inject fundamental uncertainty into the discussion below of etiology, treatment options, recovery patterns, etc. See also the section below on Other symptoms. Studies[4] show that a large number of patients (45%) are not referred to a specialist, which suggests that Bell’s palsy is considered by physicians to be a straightforward diagnosis that is easy to manage. A significant number of cases are misdiagnosed (Ibid.). This is unsurprising from a diagnosis of exclusion, which depends on a thorough investigation.
Treatment
Bell’s palsy affects each individual differently. Steroids have been shown to be effective at improving recovery while antivirals have not.
Steroids
Corticosteroid such as prednisone significantly improves recovery at 6 months and are thus recommended.[11] Early treatment (within 3 days after the onset) is necessary for benefit[12] with a 14% greater probability of recovery.[13]
Antivirals
Antivirals (such as acyclovir) are ineffective in improving recovery from Bell’s palsy beyond steroids alone.[14] They were however commonly prescribed due to a theoretical link between Bell’s palsy and the herpes simplex and varicella zoster virus.[3] There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out.[15]
Physiotherapy
Physiotherapy can be beneficial to some individuals with Bell’s palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve.[16] It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles.[16] To reduce pain, heat can be applied to the affected side of the face.[17]
Surgery
Surgery may be able to improve outcomes in facial nerve palsy that has not recovered.[18] A number of different techniques exist.[18] Smile surgery or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. It is unknown if early surgery is beneficial or harmful.[19] Adverse effects include hearing loss which occurs in 3-15% of people.[20] As of 2007 the American Academy of Neurology did not recommend surgical decompression.[20]
Complementary therapy
The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices).[21]
Prognosis
Most people with Bell’s palsy start to regaiormal facial function within 3 weeks—even those who do not receive treatment.[22] In a 1982 study, wheo treatment was available, of 1,011 patients, 85% showed first signs of recovery within 3 weeks after onset. For the other 15%, recovery occurred 3–6 months later. After a follow-up of at least 1 year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. Recovery was judged moderate in 12% and poor in only 4% of patients.[23] Another study found that incomplete palsies disappear entirely, nearly always in the course of one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop sequelae.[24] A third study found a better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis.[7]
Major complications of the condition are chronic loss of taste (ageusia), chronic facial spasm, facial pain and corneal infections. To prevent the latter, the eyes may be protected by covers, or taped shut during sleep and for rest periods, and tear-like eye drops or eye ointments may be recommended, especially for cases with complete paralysis. Where the eye does not close completely, the blink reflex is also affected, and care must be taken to protect the eye from injury.
Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections that branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination – but some nerves may sidetrack leading to a condition known as synkinesis. For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily.
Around 9%[25] of patients have some sort of sequelae after Bell’s palsy, typically the synkinesis already discussed, or spasm, contracture, tinnitus and/or hearing loss during facial movement or crocodile tear syndrome. This is also called gustatolacrimal reflex or Bogorad’s Syndrome and involves the sufferer shedding tears while eating. This is thought to be due to faulty regeneration of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur.
Epidemiology
The annual incidence of Bell’s palsy is about 20 per 100,000 population, and the incidence increases with age.[26] Bell’s palsy affects about 40,000 people in the United States every year. It affects approximately 1 person in 65 during a lifetime. Familial inheritance has been found in 4–14% of cases.[27] Bell’s palsy is three times more likely to strike pregnant women thaon-pregnant women.[28] It is also considered to be four times more likely to occur in diabetics than the general population.[29]
A range of annual incidence rates have been reported in the literature: 15,[27] 24,[30] and 25–53[4] (all rates per 100,000 population per year). Bell’s palsy is not a reportable disease, and there are no established registries for patients with this diagnosis, which complicates precise estimation.
History
This lesion was described by Sir Charles Bell, a Scottish surgeon. In 1829 he presented three cases at the Royal Society of London. Two cases were idiopathic and the third was due to a tumour of the parotid gland.
Although it is named after Sir Charles Bell, the Scottish anatomist who provide the first anatomic basis for trigeminal neuralgia and facial palsy, other European physicians provided earlier clinical descriptions of peripheral cranial nerve 7 palsy. In a recent review article describing history of facial palsy by Greek, Roman, and Persian physicians, [31] and several previous reports [32] indicate that the Persian physician Rhazes (865–925) detailed the first known description of peripheral and central facial palsy in his text book of medicine, al-Hawi. Cornelis Stalpart van der Wiel (1620–1702) in 1683 gave an account of Bell’s palsy and credited Avicenna (980–1037) for describing this condition before him. James Douglas (1675–1742) and Nicolaus Anton Friedreich (1761–1836) also described it.
Bell’s palsy: Treatment guidelines
The most common cause of acute onset unilateral peripheral facial weakness is Bell’s palsy. The incidence of Bell’s palsy is 20-30 cases for 100,000[1] and accounts for 60-70% of all cases of unilateral peripheral facial palsy.[2] Either sex is affected equally and may occur at any age, the median age is 40 years. The incidence is lowest under 10 years of age and highest in people over the age of 70. Left and right sides are affected equally.[3]
Clinical Characteristics
Bell’s palsy is an acute peripheral facial weakness of unknown cause and the diagnosis can be established without difficulty in patients with unexplained unilateral isolated facial weakness. The onset is sudden and symptoms typically peak within a few days. Additional symptoms may include pain in or behind the ear, numbness or tingling in the affected side of the face usually without any objective deficit oeurological examination, hyperacusis and disturbed taste on the ipsilateral anterior part of the tongue.[1] Bilateral idiopathic facial palsy occurs less frequently than unilateral involvement. About 7% of patients with history of Bell’s palsy may experience recurrence. The mean interval to first recurrence is reported at 9.8 years after the first episode.
Diagnosis
The first step in the diagnosis is to determine whether facial weakness is central or peripheral. Peripheral facial palsy involves all the facial muscles ipsilateral to the side of facial nerve involvement where as central weakness involves lower facial muscles contralateral to the lesion in the brain stem above pons and cerebral hemisphere.
Bell’s palsy is differentiated from other causes of facial palsy such as diabetes mellitus, human immunodeficiency virus (HIV) infection, Lyme disease, Ramsay Hunt syndrome (peripheral facial palsy with zoster oticus), sarcoidosis, Sjogren’s syndrome, parotid-nerve tumors, leprosy, polyarteritis nodosa and amyloidosis, by its rapid onset over several hours. Facial palsy secondary to other causes progresses over days to months.
Diagnostic Workup
Diagnosis of Bell’s palsy in a patient with unilateral peripheral facial weakness of unknown cause is purely clinical. However, electrodiagnostic testing done within 14 days of onset may provide prognostic information.
The nerve excitability test determines the excitation threshold by recording the minimum electrical stimulus required to produce visible muscle contraction. A difference greater than 3.5 mA between affected and unaffected sides is considered to be significant in terms of poorer outcome. Measuring the peak-to-peak amplitude of the evoked compound action potential of the involved side compared to the normal side has prognostic importance. If there is a 90% or greater reduction in the amplitude of the affected side, the prognosis is poor.[4]
Currently the trigeminal blink reflex is the only test to measure intracranial pathway of the facial nerve and also useful test to study various postparalysis sequelae such as synkinesis and hemifacial spasms. With recovery of facial function the ipsilateral R1 latency becomes less prolonged and the amount of initial prolongation of this response correlates with greater loss of facial motor function.
Gadolinium contrast magnetic resonance (MRI) study reveals enhancement of internal acoustic meatal segment on the affected side; however, this is a non-specific finding. MRI should not be done routinely and should be the investigation to look for other possible causes for acute facial paralysis especially if there is little or no recovery of function.
Treatment
The aims of treatment in the acute phase of Bell’s palsy include strategies to speed recovery and to prevent corneal complications. Eye care includes eye patching and lubrication, lubricating drops should be applied frequently during the day and a eye ointment should be used at night.[5] Strategies to speed recovery include physical therapy, corticosteroids and antiviral agents.
Bell’s Palsy: Treatment algorithm
Prednisolone
The rationale for the use of corticosteroids in acute phase of Bell’s palsy is that inflammation and edema of the facial nerve are implicated in causing Bell’s palsy and corticosteroids have a potent anti-inflammatory action which should minimise nerve damage and thereby improve the outcome.
Randomized, double-blind, placebo-controlled trials have provided compelling evidence that treatment with prednisolone improves outcome in patients with Bell’s palsy and shortens the time to complete recovery.[6–8] Prednisolone should be used in all patients with facial palsy of less than 72 h duration who do not have contraindications to steroid therapy. The prednisolone dose used was 60 mg per day for 5 days then reduced by 10 mg per day (for a total treatment time of 10 days)[8] and 50 mg per day (in two divided doses) for 10 days.[7] The reported adverse rates were low. Treatment with prednisolone is likely to be cost-effective.[9]
Antiviral Agents
The rationale for the use of antiviral agents is the evidence that the inflammation of the facial nerve in Bell’s palsy might be related to the herpes simplex virus (HSV). In an autopsy study latent HSV type-1 has been isolated from the majority of the geniculate ganglia samples.[10] HSV-1 genome was detected in 79% of facial nerve endoneurial fluid in patients with Bell’s palsy, but not in the controls.[11] However, the benefit of acyclovir or valacyclovir, either as single agents or in combination with prednisolone in Bell’s palsy has not been definitively established.[6–8,12,13] Thus with the available evidence acyclovir or valacyclovir should not be routine and treatment with acyclovir is highly unlikely to be considered cost-effective.[9]
Physical Therapy
In Bell’s palsy various physical therapies, such as exercise, biofeedback, laser, electrotherapy, massage and thermotherapy are used to hasten recovery. However, the evidence for the efficacy any of these therapies, is lacking. Cochrane systemic review of the efficacy of physical therapies, electrostimulation and exercises, on outcome of Bell’s palsy concluded that there was no significant benefit or harm from any of these physical therapies for Bell’s palsy. There was limited evidence that improvement began earlier in the exercise group.[14] Another systematic review examined the effects of facial exercises associated either with mirror or electromyogram biofeedback with respect to complications of delayed recovery in Bell’s palsy and concluded that because of the small number of randomized controlled trials, it was not possible to analyze if the exercises, were effective.[15] However, that the possibility that facial exercise reduces time to recover and sequelae needs confirming with good quality randomised controlled trials.[14]
Prognosis
About 71% of patients with Bell’s palsy have motor function recovery completely within 6 months without treatment.[16,17] By 6 months all patients with Bell’s palsy should show some improvement.[17] Poor prognostic factors include: old age, hypertension, diabetes mellitus, impairment of taste and complete facial weakness.[18] About one-third of patients may have incomplete recovery and residual effect. Among the residual effects include post-paralytic hemifacial spasm, co-contracting muscles, synkinesis, sweating while eating or during physical exertion. The two most common abnormal regeneration patterns are: ‘crocodile tears’ – lacrimation of the ipsilateral eye during chewing and ‘jaw-winking’ – closure of the ipsilateral eyelid when the jaw opens.
Facial Paralysis (Facialisparese)
Definition of Facial paralysis – Facial Palsy
Facial Paralysis is a condition where the facial muscles are paralyzed. This occurs when the nerve controlling the facial muscles (nerve facialis) – or the part of the brain that controls this nerve is not functioning properly. We have two facial nerves and generally only one of the two is affected resulting in paralysis of the muscles on one side of the face only. The most common form of facial paralysis is Bells Palsy where the cause of condition is not known but usually the condition is temporary.Causes of Facial Paralysis or Facial Palsy
Facial Paralysis is most often due to Bell’s Palsy. However, the condition might also arise from:
Infection with herpes simplex or herpes zoster (shingles) virus, chickenpox (varicella zoster) or encephalitis in the form of borrelia often transmitted by the bite of Ticks. In rare cases facial paralysis is a complication arising from middle-ear infection.
Stroke – i.e. blood clot or bleeding in the brain
Nerve inflammation, for example Guillain-Barré syndrome
Fractured skull – the underside of the cranium
Brain Tumor or tumor in the major salivary gland
Surgical damage to the nerve facial nerve – or compression from a tumor Symptoms of facial paralysis
Facial paralysis/palsy usually develops abruptly. The face looks asymmetrical when only one side is paralyzed. The eyelid and the corresponding corner of the mouth drop and there might be ear pain on the same side as well.
Sensory ability is usually normal but the following abilities might be adversely affected or obstructed:
Smiling.
Inflatation of cheeks.
Pointed lips (as if you should kiss).
Squinting.
Frowning.
Wrinkle the brow or close the eye.
Prior to incident there may have been discomfort or pain around the ear and impaired hearing and reduced sense of taste connected with the anterior 2/3 of the tongue.
If none of the above movements can be performed the paralysis stems from damage to the nerve somewhere in the passage from the brain to the muscles and the condition is called peripheral facialisparese. If the cause of facial paralysis is damage to the nerve cells at the nerve root level it is called central facialisparese. It will then be possible to frown and possible to squint at the paralyzed side, since the part of the facial nerve, which runs to the upper facial muscles are controlled from two different neurons in the brain. The other parts of the face will be paralyzed as with peripheral facialisparese.Diagnosis
If half the face is paralyzed medical attention is required. The examination will determine the degree of paralysis and if there is suspicion of a central facialisparese a CT or MRI scan of the brain will be performed. If there is suspicion of infection, for example encephalitis, borrelia or herpes virus a lumbar puncture may be performed and blood samples taken for examination.Treatment of Facial Paralysis
Bells Palsy usually needs no treatment as it recovers spontaneously. It the condition is caused by infection antibiotics targeted at the micro-organism will be prescribed. In case of a tumor surgery might be relevant and sometimes the treatment might be a surgical effort to relieve the affected nerve from suspected compression. In some rarer cases transplant of a healthy nerve particle from the skin might be attempted.
If the eye cannot be closed and there is reduced tear production artificial tear liquid is provided. If this is not enough one option might be to stitch together the outer part of the eyelids (tarsorafi) to keep the eye partially closed.Prevention of facial paralysis
Most forms of facial paralysis cannot be prevented. However, prevention is possible if the facial paralysis is associated with infection with borrelia (Tick bite) by early treatment with antibiotics while there are still only skin symptoms around the Tick bite named erythemamigrans. Vigilance and quick action is advisable in case of Tick bites.Complications and outlook
The progression and outlook for facial paralysis depends on the cause. Four out five cases are Bells Palsy where the patient recovers spontaneously within some week or maybe a couple of months. If the condition stems from blood infection often there is full recovery but in some cases there is permanent nerve damage.
A permanent facial paralysis can cause problems.
The person might involuntarily discharge saliva with the mouth hanging and there might be problems eating. The affected eye might tend to dry up and the tear production diminished which might lead to cornea inflammation or scratches in the cornea.
What is facial palsy?
This is paralysis of part of the face caused by non-functioning of the nerve that controls the muscles of the face, especially the muscles around the eye and to the mouth. This nerve is called the facial nerve.
What is the facial nerve?
The nerve affected in facial palsy, the facial nerve, is one of the cranial nerves. It is also called the seventh cranial nerve. It has a complex course from the brain stem to reach the muscles of facial expression. It supplies and controls the muscles that lift the eyebrows high, the muscles that close the eyelids, the muscles of the cheek and around the mouth.
What are the causes of facial palsy?
Facial palsy can be congenital i.e. present at birth or shortly after, or can be acquired. Acquired causes of facial palsy include most commonly Bell’s palsy. This can have no cause or be secondary to infection, or can be because of lack of the blood supply to the nerve. Sometimes a tumour, such as an acoustic neuroma, or parotid gland, or temporal bone tumour can compress the nerve and damage it. Birth trauma or skull fracture can also cause a facial palsy.
What are the symptoms of facial palsy?
Facial paralysis usually affects one half of the face. There is a flattening of the affected half of the face, with loss of the forehead wrinkles and horizontal lines, a droopy eyebrow, difficulty closing the eye, an inability to whistle and the corner of the mouth pulled down.
Why are the eye changes so important?
The eye findings are particularly important, as the upper eyelid can be a little bit too high and the lower eyelid can sag and have an ectropion (outward turning of the lid margin) resulting in a watering eye, inability to close the eye and exposure or drying of the cornea. The eye can become red, the vision blurred and occasionally the vision can be severely affected by an exposure keratopathy, with an ulcer then scarring of the cornea and loss of useful vision.
How is facial palsy managed?
Most patients can be managed medically, with local eye drops and ointment to lubricate and wet the eye. There are many artificial tear preparations available. Simple horizontal taping of the eyelids at bedtime is very beneficial. Some patients require upper eyelid lowering with Botox (Botulinum Toxin A), which specifically paralyses the eyelid muscle which opens the eye, and allow the eyelid to drop over the surface of the eye and protect it if there is a severe keratopathy present.
When is a surgery required?
Surgery may be advised for facial nerve palsy if there is difficulty in protecting the eye from incomplete closure of the eye causing drying and there is a lot of discomfort and/or effect to the eyesight. Surgery is also done to improve symmetry and regain the normal anatomy, in order to improve not only cosmesis, but help improve the function of the eyelids and reduce watering. Surgery is also done on the forehead, brow, midface and lower face and corner of the mouth to improve symmetry.
Common surgical procedures for facial palsy
Lateral tarsorrhaphy
this is the surgical closure of the outer portion of the eyelids to reduce the ength of the eyelids that is open and decrease the evaporation and improve the coverage of the eye by the eyelids. This is usually done in an emergency. It is not the best rehabilitative procedure and it has a poor cosmetic result, can cause a blinkering effect to the vision towards the side of the surgery, and is therefore reserved for special cases only. The lateral tarsal strip is preferred.
Lateral tarsal strip this is a tightening of the lower eyelid when there is lower eyelid laxity, sagging and ectropion. The lower eyelid is shortened and re-attached a little higher to improve eyelid losure and comfort. An augmented strip – tarsorrhaphy is ofteeeded for facial palsy to help close the yelid fully on blinking.
Lateral tarsal strip tarsorrhaphy
a combined procedure called an augmented lateral tarsal strip tarsorrhaphy can be done when there is a lot of lower eyelid laxity, sagging and ectropion, and in this surgery there is a long lateral tarsal strip performed with a very small lateral tarsorrhaphy combined, which does not shorten the lower eyelid opening so much as to affect vision or appearance, but does help protect the eye well.
Medial canthoplasty
this surgery is done at the medial corner of the eyelids (in a corner) and consists of some specially positioned stitches to pull up the sagging lower eyelid towards the inner corner. It is usually done in conjunction with a lateral tarsal strip, or augmented lateral tarsal strip tarsorrhaphy.
Gold weight upper eyelid
more animated and better closure of the upper eyelid can be obtained by placement of a gold weight in the upper eyelid.
Drooping eyebrow surgery
this is called brow ptosis correction and there are several different procedures to improve the position of the drooping eyebrow. Some of these procedures are done over the eyebrow, whilst others are carried out via the forehead or small scalp incisions. Brow ptosis can be necessary as part of the rehabilitation in a patient with longstanding facial palsy.
Face surgery
The midface or cheek can be lifted to help improve the lower lid position and more extensive facelift type surgery done to improve the symmetry between the two sides of the face and help restore the normal anatomy. Incisions in front of the ear and into the hairline are used. A sling of the patients own leg fascia (fascia lata) or an inert strip of material can be used to help resuspend the mouth.
Non-surgical procedures
Botulinum Toxin A chemodenervation upper eyelid lowering: in certain urgent situations the front of the eye, or cornea, becomes ulcerated and very painful, or the eye red. This is called exposure keratopathy with severe keratitis. Lubricants and other eye drops may not be adequate to improve this and it is necessary to lower the upper eyelid temporarily.
This is done by a small injection underneath the upper eyelid of Botox, or Botulinum Toxin A, to temporarily paralyse the muscle that lifts the eyelid open and allow the eyelid to drop over the eye (protective ptosis) so that the keratitis or ulcer can heal. These injections can last up to three months and be repeated, or definitive surgery done.
Specific eye problems with facial palsy
Neurotrophic keratitis
patients with facial palsy due to the facial nerve, or seventh cranial nerve, loss of function may also have loss of the nerve which controls the sensation of the eye, called the trigeminal or fifth cranial nerve. These patients are usually those who have had surgery for a large acoustic neuroma tumour, where there has been involvement of both the facial nerve to the muscles and the sensory nerve to the front of the eye.
This results in diminished or no sensation on the front surface of the eye, so that the patient cannot feel dryness, or foreign bodies, or trauma to the surface to the eye, and as a result have a much higher risk of corneal ulceration. The options are:
Emergency eyelid closure with tarsorrhaphy to allow for the ulcer on the front of the eye to heal.
Urgent upper eyelid lowering with Botox (Botulinum Toxin A) protective ptosis.
Increased lubrication, punctual plugs to stop the tears draining away and eye padding with taping at night.
Definitive surgery to narrow the eyelid opening so that there is excellent eyelid coverage by the eyelids and protection of the cornea.
NB: It is important to warn patients with a neurotrophic keratitis that they are at risk of severe loss of vision, unless great care is taken, and one or more of the above steps may be required if they develop a corneal ulcer.
Crocodile Tears
This is a rare sequelae facial nerve paralysis, when the facial nerve tries to grow back along its old pathway but misdirects and goes instead to the lacrimal gland and to the muscles of the jaw, so that when the patients chews there is embarrassing tearing. The treatment is Botulinum Toxin mini injections to the lacrimal gland.
Blepharospasm or aberrant regenerataion of the facial nerve to the eyelid closing muscle
Patients with facial nerve palsy may have some regeneration of the nerve and, if this goes along the wrong pathways, can cause the eyelids to close up slightly and to have spasm, as well as the muscles of the side of the face (cheek) and to the mouth. These patients may require Botox, or Botulinum Toxin A, treatment to the muscles which are in spasm.
Causes of Facial Paralysis
1. Congenital
Birth Trauma: several factors during the birth of a child may lead to facial nerve injury and associated paralysis. These include instrumentation (the use of forceps during the delivery), birth weight over 3.5 kg (7.7 lb), and first pregnancy. A contributing factor may be compression molding of the fetus while passing through the birth canal. In this setting, the facial nerve undergoes stretch injury and requires time to regenerate. The overall prognosis is excellent, with up to 90% of children achieving complete recovery of their facial nerve function without surgical or medical intervention 1. In rare instances where transection injury is highly suspected, surgical exploration may be warranted.
Mobius Syndrome: this syndrome was described in the 19th century and is characterized by concomitant facial nerve and abducens nerve palsies 2. Clinically, patients are unable to move their face and have extreme difficulty expressing emotion. This may be accompanied by oral incompetence, drooling, low self-esteem, and social isolation – all of which add to the challenges of those suffering from this condition. In this patient group, free muscle transfer has been successfully utilized for rehabilitation of facial movement 3, 4. Ideally, such intervention would be performed prior to school entry, in an attempt to avoid psychological trauma from peer ridicule during early formative years.
Melkersson-Rosenthal Syndrome: recurrent facial paralysis, facial swelling, and tongue fissures characterize this rare syndrome. While typical care of recurrent flare-ups includes steroid and anti-inflammatory medications, controversy remains over the management and prevention of facial palsy. Isolated case reports describing facial nerve decompression 5 (drilling out its bony confines to prevent nerve pressure during bouts of swelling) suggest that long-term resolution of facial nerve dysfunction is possible with this more aggressive approach.
Hemifacial Microsomia: represents a spectrum of congenital facial anomalies, arising due to lack of development of one side of the face. This syndrome is marked by hemifacial soft tissue deficiency and poor development of the lower jaw, maxilla, and external ear. In cases of accompanying facial weakness or paralysis, reconstructive surgery can be planned together with craniofacial repair, directed at correcting jaw and ear abnormalities. Facial symmetry and smile restoration can be especially effective with free muscle transfer, as it provides a secondary benefit of facial augmentation 6.
2. Infectious
Bell’s Palsy: this condition is also known as idiopathic (cause unknown) facial paralysis and represents its most common cause. Recent evidence suggests that herpes simplex virus is the most likely agent behind Bell’s palsy 7. The incidence of this condition approaches 30 per 100,000 people. Typically, the onset of paralysis occurs over a period of 24 – 72 hours and may be accompanied by other symptoms, such as pain around the ear, decreased taste, and diminished hearing on the affected side.
While the overwhelming majority of patients recover their facial nerve function, a small minority retains a deficit, which is typically complicated by aberrant facial movements (synkinesis). Steroids and anti-viral medicines have been found helpful in improving functional recovery of the facial nerve in the acute stages of the disease 8, 9. In select instances, where electrical activity of the nerve is severely depressed, surgical decompression of the nerve’s bony channel has been shown to be beneficial 10. In those with poor recovery and synkinesis, chemodenervation (paralysis) with Botox and intensive physical therapy offer a promising rehabilitative option.
Ramsey-Hunt Syndrome: is caused by reactivation of Varicella Zoster virus (a herpes family virus) in the facial nerve, leading to facial paralysis on the involved side. This is accompanied by formation of vesicles and pain in the ear (zoster oticus), which clinically distinguishes this condition from Bell’s palsy. Other symptoms, such as hearing loss, tinnitus (noise in the ear), vertigo (imbalance), nausea, and vomiting may be present as well. These are thought to arise from irritation of the hearing and balance nerves, which are situated adjacent to the inflamed facial nerve in the temporal bone.
While no randomized studies exist on the treatment of this infrequent condition, a combination of steroids, antivirals, and pain medications are used to control inflammatory injury of the facial nerve 11, 12, 13. This regimen is based on the experience with Bell’s palsy (steroids) as well as treatment of zoster infections in other parts of the body (with anti-viral medications). Prognosis for facial nerve recovery is poor in Ramsey Hunt syndrome, with chronic neuralgia (pain) commonly persisting following the resolution of infection.
Otitis Media / Mastoiditis: is an acute infection of the middle ear and mastoid (bone behind the ear), which in rare cases (less than 1%) may result in facial nerve paralysis. Swelling around the nerve and toxic substances released by bacteria are thought to be causative factors behind facial nerve involvement.
Successful treatment consists of prompt recognition and eradication of infection. This includes broad- spectrum antibiotics and incision of the tympanic membrane with placement of a ventilation tube, allowing to obtain bacterial specimen for culture. A mastoidectomy (removal of infection in the adjacent mastoid bone) may be performed in select cases of associated mastoiditis. Prognosis for complete facial nerve recovery is excellent with the above interventions 14, 15.
Cholesteatoma: is a slow-growing skin cyst that over time causes destruction in the ear by exerting pressure on surrounding structures and causing flare-ups of chronic infection. The incidence of facial paralysis in a setting of cholesteatoma approaches 3%16. Prompt recognition of this disease process and surgical eradication are critical in successfully releasing pressure from the facial nerve and removing the source of chronic infection and inflammation.
Poor prognostic factors for recovery include extension of cholesteatoma into the petrous apex (deep portion of the temporal bone) and delayed surgical treatment 17. Patients who undergo early intervention are more likely to recover their facial nerve function completely.
Lyme Disease: is caused by Borrelia Burgdorferi – a bacterium transmitted to humans through the bite of infected ticks. Typical symptoms and signs in acute stages of Lyme disease include headache, weakness, fever, and erythema chronicum migrans (a characteristic target-shaped rash that develops at the site of tick bite).
While the incidence of accompanying facial paralysis reaches 11%, it completely resolves in 99.2% 18. A high index of suspicion for Lyme disease should arise in a patient presenting with a recent history of tick bites, during summer months, and in endemic areas (the national risk map is available on the CDC website http://www.cdc.gov/ncidod/dvbid/lyme/riskmap.htm). Lyme titers should be obtained for confirmation and antibiotic therapy instituted, following published guidelines by the infectious disease society of
Other: A number of additional infectious processes can impair facial nerve function and include diseases such as HIV (human immunodeficiency virus), TB (tuberculosis), infectious mononucleosis, and other 20, 21, 22, 23. These conditions typically have other associated symptoms in affected individuals and require a high index of suspicion to make the diagnosis. Previous history and risk factors of exposure influence the decision to pursue these diagnostic possibilities in a setting of facial paralysis.
The mainstay of management is targeted medical therapy, unless associated mastoiditis (infection involving the mastoid bone, through which the facial nerve passes) is identified on work-up. In this instance, mastoidectomy (surgical removal of infected mastoid bone) should be performed to control the infection and swelling around the facial nerve.
3. Systemic & Neurologic
Conditions in this category include autoimmune diseases, diabetes, sarcoidosis, Guillain-Barre syndrome, multiple sclerosis, and other. Infrequently, these can present with isolated facial paralysis 24,25,26,27. Correct diagnosis and prompt medical intervention form the initial treatment strategy, with anticipated recovery of facial movement in most cases.
4. Traumatic
Traumatic injuries to the head and cranium represent one of the most common causes of acquired facial paralysis. In instances of blunt trauma, in which no lacerations or fractures occur, the facial nerve retains its continuity and is expected to recover 28. In a setting of suspected nerve laceration (penetrating trauma through facial skin and soft tissues), immediate surgical exploration with nerve repair is warranted. Ideally, this would take place within 3 days of injury, during which the distal portion of the facial nerve can still be stimulated and, thus, identified during surgery.
When facial trauma results in the temporal bone fracture, accompanying facial nerve injury can occur in 5-10% of cases. Full recovery is expected in those patients who experience delayed onset of facial paralysis. In contrast, approximately 40% of those with immediate onset of paralysis recover poorly 29. In many cases of significant facial trauma, other concomitant acute conditions may delay examination and testing of the facial nerve. However, delayed surgical exploration, even months after the injury, can still be performed 30, 31, 32 with reasonable success rates of functional improvement and recovery.
Iatrogenic injury to the facial nerve can occur during facial, bony, or intracranial surgery. The extent of nerve damage largely dictates the type of repair 33. In severe cases, nerve repair may not be possible and other rehabilitative methods must be utilized (diagram – chronic facial paralysis).
5. Neoplastic
Extirpation of cancer situated in the vicinity or invading the facial nerve may require significant nerve manipulation during surgery and possibly partial or complete transection. The most common tumors affecting the facial nerve are acoustic neuroma (vestibular schwannoma), glomus, facial neuroma, and carcinoma (malignancy involving the brain, temporal bone, parotid gland, and soft tissues adjacent to the course of the facial nerve). When the facial nerve continuity is preserved during surgery, post-operative recovery is closely monitored. Stimulation of the nerve at the end of the procedure may provide useful prognostic data. Steroid medications are typically not given in this setting, as several studies have clearly shown lack of benefit 34, 35.
Following surgery, electromyography (EMG) can be utilized to assess re-innervation of facial musculature. Depending on the stage of recovery, as well as individual challenges and concerns, several simple procedures are considered to aid with eye closure, facial symmetry, and oral competence (diagram – intermediate facial paralysis).
How to Cure Bell’s Palsy Facial Nerve Disorders
Bell’s palsy (facial palsy) is characterized by facial drooping on the affected half, due to malfunction of the facial nerve (VII cranial nerve), which controls the muscles of the face. Named after Scottish anatomist Charles Bell, who first described it, Bell’s palsy is the most common acute mononeuropathy (disease involving only one nerve), and is the most common cause of acute facial nerve paralysis. The paralysis is of the infranuclear/lower motor neuron type. Bell’s palsy affects about 40,000 people in the
Here is a treatment for fast relief of symptoms.
Steps
1
Use Lacrilube (found at any drug stores or pharmacy) to help keep eye moisturized.
2
Eat garlic with olive oil (mash the garlic and mix it with the olive oil).
3
Use multivitamin complex with B vitamins (B1,B2,B6,B12).
4
Try to avoid milk.
5
Do a deep massage to the face.
6
Avoid exposure to the wind.
7
Exercise the facial muscles daily (smile, lift your eyebrow,try to whistle, close your eyes etc.).
8
Smile and pull infected side of face up to a normal smile and hold for 10 seconds. Repeat.
9
Put a heating pad on low and put it on infected side of face. Hold for 3 minutes then rest it for 3 min. Repeat.
10
Drink plenty of water.
11
Try acupuncture treatment (start with twice a week).
Masseter To Facial Nerve Transfer
The Facial Paralysis Institute is home to the most cutting edge treatments and surgical procedures available for those suffering from Bell’s palsy and facial paralysis. Various medical issues such as acoustic neuromas, Bell’s palsy, trauma, parotid tumors, and moebius syndrome can cause facial paralysis.
Depending on the severity and longevity of the patient’s facial paralysis, there are multiple options a person has for undergoing surgery to regain facial animation.
Facial paralysis patients travel from across the world to have this procedure performed at the Facial Paralysis Institute in
Understanding The Masseter to Facial Nerve Transfer
The masseter nerve transfer (or trigeminal nerve transfer) has the ability to greatly improve facial reanimation for sufferers of permanent Bell’s palsy or complete facial paralysis. At the Facial Paralysis Institute, this procedure has had tremendous success in helping patients who have been experiencing paralysis for less than three years, though it is not limited to that specific longevity and greatly depends on the etiology and muscle activity.
During the masseter to facial nerve transfer, an experienced facial paralysis surgeon, like Dr. Azizzadeh, makes an incisioear the front of the ear. The facial nerve and masseteric nerve are identified and sewn together under microscopic magnification. The masseteric nerve, which is used to activate chewing muscles, provides neural input into the paralyzed facial nerve, thereby restoring the facial muscle function and smile.
Generally, results can be seen over the course of several months following the masseter nerve transfer procedure.
Post Masseter Nerve Transfer
Following the masseteric-facial nerve transfer surgery (or trigeminal facial nerve transfer), the majority of patients will have a single overnight stay in the hospital. Patients can eat a regular diet beginning the very next day, with a 7-10 day recovery period. During the post-operative period, patients are asked to avoid:
Pressure to the affected cheek
Exercise
Heavy lifting
Vigorous brushing of the teeth
Motion resembling the unaffected side, meanwhile, often develops between the sixth and seventh post-operative months. Older individuals may require longer periods of time to achieve the desired function, but the end result is usually comparable to younger individuals.
The strength and control over the reconstructed smile continues to improve over several years. While biting down will initially be required to produce a smile, the brain has the potential to undergo a re-education process (cerebral adaption), resulting in the production of a naturally occurring and effortless smile over time. In addition to the potential for re-education, the masseter to facial nerve transfer, perfected by Dr. Azizzadeh, has several extra advantages over other nerve donors. The nerve has a high density of motor axons and the ability to produce a strong smile with the proper orientation. The permanent difficulties with speech and swallowing associated with more traditional nerve transfers are also avoided utilizing this technique.
Nerve Transplant facial paralysis treatment, procedures
Patients (under the age of 55) who have had long-term paralysis are able to undergo advanced surgical procedures to re-create dynamic and spontaneous smile mechanism. These nerve transplants give patients the ability to utilize the facial nerve in the normal side of the face to “drive” the facial movement in the paralyzed side. Patients with long-term paralysis (> 2 years) have non-functional muscles; therefore, new vascularized muscle needs to be attached to the cross-facial nerve grafts after the nerve has been “activated”. The nerve grafts need to be activated for 8-12 months before the muscle in transferred. We have also started using these nerve grafts for individuals with partial paralysis who need additional “input” to help better their smile.
Two stage procedures is typically required for cross-facial nerve grafts
Stage 1: Nerve grafts are harvested from the lower leg (sural nerve) and attached to the normal facial nerve (photo of sural nerve)
Stage 2: Gracilis muscle free flap is harvested from the inner thigh and attached to the cross-facial nerve graft and artery/vein in the neck.
Physical therapy is continued for the 18 months. Facial movements are gradually realized about 8 months following the second stage of surgery and continued for 2 years.
House Brackmann Grading System
Grade II: Mild dysfunction
Slight weakness noticeable on close inspection
May have slight synkinesis
Normal symmetry and tone at rest
Grade III: Moderate dysfunction
Obvious but not disfiguring difference between the two sides
Noticeable but not severe synkinesis, contracture, or hemifacial spasm
Normal symmetry and tone at rest
Grade IV: Moderately severe dysfunction
Obvious weakness and/or disfiguring asymmetry
Normal symmetry and tone at rest
Grade V: Severe dysfunction
Only barely perceptible motion
Asymmetry at rest
Grade VI: Total paralysis without any movement
Differential Diagnosis
Bell’s Palsy
Trauma
Temporal bone fracture
Facial laceration
Iatrogenic
Barotrauma
Birth trauma (forceps)
Tumor
Cerebellopontine angle tumor: Schwannoma, meningioma
Parotid
Head & neck tumors
Congenital Toxic Melkersson-Rosenthal Syndrome:
Neurologic
Opercular syndrome: cortical lesion in facial motor area
Millard-Gubler syndrome
Infectious
HSV; Zoster
External & middle ear
Lyme disease
Other: Encephalitis, Poliomyelitis, Mumps, Mononucleosis, Leprosy, Influenza, Coxsackievirus, Malaria, Syphilis, Scleroma, Tuberculosis, Botulism, AIDS
Metabolic
Diabetes mellitus
Hyperthyroidism
Pregnancy
Hypertension
Vitamin A deficiency
Hypoglossal-facial nerve transfer
Before After
In patients with long-term facial paralysis who are older than 55, cross-facial nerve grafts have not produced great results. As a result, Dr. Azizzadeh likes to utilize the hypoglossal nerve or trigeminal nerve as the neural supply for the gracilis muscle transplant (see gracilis muscle section). The nerve of the gracilis muscle is attached to the hypoglossal nerve in the neck. The hypoglossal nerve is responsible for moving the tongue muscle and by attaching a partial portion of the nerve to the transplanted gracilis muscle; the patient has the ability to move the face voluntarily by tongue thrusting. This advanced state of the art procedure creates a natural appearance to the face with the ability for voluntary facial movement. (Source: Dr. B. Azizzadeh, Facial Paralysis Institute)
Uses
The primary use of gracilis free tissue transfer in the head and neck region is in the form of a muscular free flap for the dynamic rehabilitation of long-standing permanent facial paralysis. When combined with cross-facial nerve grafting or used as a single-stage reconstruction, free tissue transfer offers the best prospect for restoring spontaneous emotional facial expression. Benefits of this muscle over other free flaps used for dynamic facial reanimation include consistent anatomy with large caliber vessels, ease of harvest, a 2-team approach, reliability, and acceptable donor site morbidity. Drawbacks include excessive bulk, skin tethering, and a donor site scar that may be minimized with minimally invasive techniques. Secondary procedures to refine the results are ofteecessary to achieve a good final result. Ultimately, the choice of muscle for dynamic facial reanimation depends on the surgeon\’s experience and comfort level. (Source: Jason H Kim, MD, Assistant Professor, Department of Otolaryngology-Head and Neck Surgery,
Summary
For older individuals the Hypoglossal-gracilis free flapwill have less pain and less recovery time for most. Over 95% of individuals will have some pain and minor complications but will also have great results with the surgery. This procedure is used on persons 55 years of age and older to make post operative trauma and recuperation easier. All patients will receive a better looking face regardless. Re-animation of the face will take more therapy and sometimes minor surgeries to get the overall look the patient wants.
Static sling
Static sling, Static Suspension, facial paralysis treament
Static suspension is utilized to create better facial symmetry as well improve some of the most difficult side-effects of facial paralysis including drooling and biting of the inner gum. Dr. Azizzadeh typically uses tensor fascia lata (a tendon like structure from the thighs) to support and create a laugh line. This procedure is able to create symmetry of the lips, corner of the mouth and laugh line. The procedure is usually performed through a small incision in the scalp and the fascia is placed under the skin where it is not visible. Dr. Azizzadeh is one of the leading surgeons who have utilized this technique.
Fascia
Tensor Fascia Lata has been used extensively by Dr. Azizzadeh at the Facial Paralysis Institute in
Alloderm
Alloderm is freeze-dried, acellular human dermis which has also been used extensively by Dr. Azizzadeh for many years with great outcome. The advantage of Allorderm is that a second surgical site is not necessary for harvesting of the material. Alloderm can be customized just like Tensor Fascia Lata and is readily available. Alloderm tends to integrate well with surrounding tissue and has a very limited risk of rejection.
Expanded polytetrafluoroethylene (Gore-Tex)
Expanded polytetrafluoroethylene (e-PTFE), known commercially as Gore-Tex, is a synthetic material that has also been used in a select group of patients by Dr. Azizzadeh at the Facial Paralysis Institute in
In a select group of patients, has been utilizing a minimally invasive suture suspension technique with great outcome as a substitue for more invasive procedure. Suture technique provides the perfect support for patients who have partial paralysis or bell’s palsy while undergoing traditional facelift procedures. It can be done through endoscopic midface approach or classic short-flap facelift life approach with the use of advanced endoscopic equipment. Permanat sutures are utilized to achive the results. This technique was the primary method by which treated Mary Jo Buttafuoco on The Oprah Winfrey Show for her devastating facial paralysis. A multivector approach can be utilized to address different regions of the face and mouth.
Temporalis transfer
The temporalis muscle is one of the muscles for chewing (mastication). The trigeminal nerve (cranial nerve 5) is responsible for its activity. As a result, we can use this muscle to provide voluntary facial movement. The procedure transfers the temporalis muscle from the scalp to the corner of the mouth. The patient then learns to move the face by moving this muscle. This procedure has been very successful in rehabilitating facial movement in patients over the age of 55 who have had a long-standing facial paralysis and are not candidates for more advanced facial reanimation (such as cross facial nerve grafts). The procedure is performed via a facelift technique with very good results.
Muscle Transposition Techniques
Indications:
Long standing FNP (> 2yrs)
Loss of multiple cranial nerves
Loss of distal FN stump or atrophy of facial muscles
Muscle Sources:
Temporalis
Masseter
Digastric
With careful postoperative facial neuromuscular re-training program in physiotherapy, patients are encouraged to obtaiatural facial movement. In the primary stage of exercises, voluntary control of the new function can be achieved with most patients. The second stage in which patients are encouraged to obtain the newly learned movements to a state of automatic function in normal facial expression is less predictable. Therefore we feel that muscle transfers give only minor advantages over static suspension operations. We feel that gracilis muscle transfer to trigeminal nerve can provide a more predictable facial movement than temporalis transfer
Patient satisfaction has been shown to be relatively high in several research papers. In a study published in Archives of Facial Plastic Surgery, a mean score of 8.5 (possible score of 10) in patients who underwent this procedure. Four patients were physician graded as excellent to superb. The other 3 patients were rated as having good postoperative results. Movement was identified in every patient and ranged from 1.6 to 8.5 mm, with mean movement of the oral commissure of 4.2 mm. One patient developed postoperative salivary fluid collection that required drainage.
Before & After Temporalis Tendon Transfer
Muscle Transposition Techniques: Temporalis Transfer
Non-spontaneous dynamic reanimation
Good vector control of smile
Does not interfere with potential native nerve regeneration
Dynamic smile can look artificial
Summary
When the right surgical procedure accomplished by a well trained professional that has done extensive testing on the patient, good to very good results are apparent. Dr. Azizzadeh has spent his life working toward and creating state of the art techniques to accomplish the desired goals. The Facial Paralysis Institute has one of the top surgical teams for comprehensive facial paralysis reanimation.
Facelift
Facelift Surgery and facial paralysis
The safety of the facial nerve is perhaps the most important aspect of facelift surgery.
The facial nerve exits the stylomastoid foramen and enters the core of the parotid gland. Within the parotid gland it bifurcates into an upper and lower division. It further divides into 5 main branches including the frontal, zygomatic, buccal, marginal mandibular and platysmal. Permanent iatrogenic facial paralysis is rare due to the extensive arborization of the facial nerve branches. The frontal branch is a terminal branch with limited arborization. Injury to the frontal branch has the highest risk of causing permanent paralysis.
The overall risk of permanent facial nerve paralysis in standard rhytidectomy is between 0.53% to 2.6%.There have been very few reports in the literature regarding the risk for facial nerve injury associated with more invasive facelifting procedures. The “short-flap SMAS rhytidectomy” significantly limits the risk for facial nerve injury by limiting facial subcutaneous and SMAS dissection.
Endoscopic brow lift for facial paralysis
Brow ptosis, also known as sagging of the eyebrows, can occur for a number of reasons. In the cases of facial paralysis and Bell’s Palsy the cause is a dysfunction of a particular facial nerve and there is often little choice of treatment but plastic surgery.
A standard (or ‘open’) brow lift is a significant and invasive surgical procedure, requiring stitches, bandaging and a few days to recover, as well as causing bruising and swelling. Luckily for patients today, there is a minimally invasive brow lift available, know as the endoscopic brow lift. The results of this procedure are the same as an open brow lift, but often with less scarring.
An endoscopic brow lift is carried out by a qualified plastic surgeon who has been trained in using endoscope equipment. After an incision above the temple has been made, the endoscope can be inserted. The endoscope tool is a very small camera on the end of a wire-like tube, with a magnifier. The image that the camera obtains is sent to a screen that the surgeon and their team can see, so that the surgery can be carried out below the skin with only a small incisioeeded. This type of procedure is most commonly known as ‘minimally invasive surgery’ but is also sometimes called ‘keyhole surgery’. As a patient undergoing endoscopic brow lift, you can expect to be in theater for around one hour. A portion of the procedure time will be used to examine the area and plan exactly what is to be done. Once this assessment is complete, an incision is made below the eyebrow, muscles may be loosened or even removed (to reduce further sagging) and the tissues and skin are pulled upwards and held tightly before being stitched up.
Following endoscopic brow lift, there will be some swelling and bruising. Unfortunately this cannot be avoided, but these after-effects should only last from three to seven days. The benefits, on the other hand, are likely to last up to ten years and for someone with facial paralysis this can make a huge difference to their quality of life.
Gold weight and eyelid springs, Ocular management
Ocular Management
The primary ocular signs of facial paralysis include inability to close the eyes completely, drooping of the lower eyelids, dryness or excessive tearing. Any failure to adequately address these issues can predispose the affected eye to corneal ulceration, keratitis, or irreversible loss of vision.
In all instances of complete facial paralysis or isolated impairment of eyelid closure, lubricating eye drops, artificial tears and other eye-protecting measures such as eyeglasses are imperative to minimize the risk of corneal ulceration. The use of antibiotic eyedrops such as chloramphenicol prior to sleep may also reduce the risk of infection in eyes with incomplete closure. Glasses or protective eyewear are mandatory particularly in the acute phase of the disease in order to prevent the entry of foreign particle into the affected eye until resolution of eyelid impairment. The use of a patch, a silk thread, gold weight implantations, and springs have been used effectively in the past to maintain eye closure in instances of eyelid impairment.
Depending on the extent of involvement and the severity of nerve deterioration, the management of eyelid paralysis in facial nerve disorders can involve medical therapy, surgical intervention, or both. Recent studies have suggested that as many as 94% of patients with incomplete paralysis associated with FNP will often recover spontaneously.
Surgical Management
Depending on the underlying etiology, a number of surgical options exist for correcting ocular impairments and hastening recovery in facial nerve palsy. The following is an overview of those surgical options with a particular emphasis placed upon their impact in addressing various clinical characteristics of paralysis of the face.
Gold weight placement
Given the fact that a number of patients with facial paralysis develop incomplete eye closure due to dysfunction of both the upper and lower eyelids, surgical intervention is ofteeeded in order to improve ocular closure and minimize the risk of corneal damage. Implantation of a gold weight in the eyelid has been associated with long-term efficacy in meeting this objective in patients with Facial palsy. The most commonly used procedure involves incising the upper eyelid crease and cutting through the muscle in order to expose the area where the gold weight is anchored directly with sutures. Although gold weight placement maybe clinically beneficial, this procedure alone may be inadequate in some patients with facial paralysis. Thus, lower eyelid reconstruction is ofteeeded in order to achieve maximal results and reduce long-term complications in patients receiving gold weight placement. The surgeons at the Facial Paralysis Institute have begun to institute the use of Platinum chains which can provide even better outcomes than gold weights.
Canthoplasty Procedure
Canthoplasty is a procedure to reconstruct and/or reshape the corner of the eye. The procedure is often performed to help facial paralysis patients struggling with proper eye closure.
Tarsorrhaphy
Tarsorrhaphy, which describes the sewing of the eyelids to reduce eyelid aperture, has been used infrequently as a result of poor cosmetic results and the compromised peripheral vision that often accompanies the procedure. Although uncommonly used, the benefits of this procedure lie in the fact that it can be reversed in the event of facial nerve function recovery.
Palpebral Spring
Eyelid springs are the only way to dynamically move the eyelids with a normal movement. The eyelid spring, also known as palpebral spring, places a specialized metal that allows the eye to naturally open and close the eyes despite total paralysis. Patients need to be selected carefully in order to obtain ideal results.
Botox
Botox is one of the most effective treatments for patients with Bell’s palsy, partial facial paralysis and synkinesis.
Please read our report/ pres release on Botox and it’s effects in Bell’s Palsy treatment
Botox is one of the most effective treatments for patients with Bell’s palsy, partial facial paralysis and synkinesis
Botox has been a mainstay treatment for patients with synkinesis, partial facial paralysis and bell’s palsy for the past two decades. Botox is a protein derived from botulinum toxin. It relaxes unwanted muscle movements on the normal side of the face and reduces tension in areas of the face that are hyperactive due to synkinesis.
At the Facial Paralysis Insitute, Botox is utilized to address asymmetric facial movement in a novel manner to create a more symmetrical facial movement and reduce the signs of facial paralysis and synkinesis. Botox is most commonly utilized with neuromuscular retraining that will be performed by an experienced physical therapist.
For more information about the use of Botox, please contact the Facial Paralysis Institute in
Woman with facial movement disorder with synkinesis and treatment using Botox.
Parotidectomy
The parotid gland is a key pathway for the facial nerve and can have a significant role if facial nerve disorders.
What is the parotid gland?
The Parotid Gland is an important salivary gland in the body. This gland pumps saliva through the Stensen’s duct, into the mouth. This helps keep the mouth wet and helps with swallowing. Infections, trauma and tumors can potentially cause facial nerve problems. The longer it takes to correct a problem, the more surgery will be needed.
What causes the problems?
The most common causes of facial nerve disorders as a result of the parotid gland is tumors (pleomorphic adenoma), malignancy (adenoid cystic carcinoma, adenocarcinoma), trauma, and infectious process. Even though the mumps have all been eliminated with routine vaccinations, this viral infection will give you an idea of how serious an infection of the Parotid gland can be.
Parotid tumors are typically benign and can be treated with surgery. The most common parotid tumor is pleomorphic adenoma which usually presents with a pain-less lump at the jaw line in front of the ear. Other tumors are typically more concerning and can be malignant such as adenoid cystic carcinoma, adenocarcinoma, and squamous cell carcinoma.
Staphylococcus (Staph infections) aureus is the most common reason the Parotid gland becomes infected and usually if can be contained with antibiotics and anti-inflammatories. Bacteria that create tuberculosis are another factor that can cause Parotid infections. Another bacteria, which causes “Acute suppurative parotitis” is also a painful and similar infection. These can usually be treated by drugs.
Diabetes, bulimia and alcoholism may cause enlarged parotid glands but usually these are not painful and there is a small group of AIDS victims that have experienced parotitis.
However, any blockage to the parotid duct such as a tumor, mucous plug, salivary stone is usually the cause of painful and deadly parotiditis. Calcium is what forms salivary stones. Usually they can be detected by X-ray about 80% of the time.
Chronic inflammation of the parotid gland may be caused by Sjogren’s syndrome. This is caused by an autoimmune disease and can be a serious problem. There is no known cause for Sjogren’s syndrome at this time. Dryness in the eyes, nose, skin and mouth in the facial area along with swelling is an indication of Sjogren’s syndrome.
facial nerve monitor
Where is it?
The parotid gland sits under the skin, and wraps around the back of the jaw at the mandibular ramus. The gland sits in an area which is anterior to the ear. This gland is palpated bilaterally and there is one on each side of the head behind the ear. The facial nerve, although it does not control the gland, it runs through it.
incisions before and after
Treatment
Surgery remains the gold-standard for treating parotid tumors. Old methods of surgery include taking the gland out completely leave scars around the face and usually a dent in the area on the face, making it a more obvious problem.
Facial Nerve Decompression
Facial paralysis is a complex issue and the specific treatment required depends greatly on the cause of the paralysis. For most patients with Bell’s palsy, the facial paralysis is temporary, but sometimes the facial nerve is permanently damaged and requires surgical intervention. Other facial paralysis patients may also benefit from surgical treatment. Facial Nerve Decompression is a procedure that may help some living with permanent facial paralysis regain facial function and a more symmetrical appearance.
What is Facial Nerve Decompression?
Facial nerve decompression is performed when the facial nerve is being compressed in the bony canal of the temporal bone. In some cases, the facial nerve becomes so inflamed as to be pressed, or cramped, within the confined space of the bony canal. When facial nerve decompression is indicated and performed by an experienced facial paralysis surgeon, releasing the pressure on the nerve can lead to gradual improvement in facial paralysis symptoms.
Generally, facial nerve decompression is performed through a middle fossa craniotomy and/or through the mastoid bone behind the ear. Pieces of the bone are removed so that the inflamed facial nerve can expand and the pressure that may be causing some of the facial paralysis symptoms is relieved. Depending on the individual case, the surgeon may perform the procedure through the middle cranial fossa method or a mastoidectomy, or a combination of the two.
Who is a Candidate for Facial Nerve Decompression?
Facial nerve decompression is typically indicated for patients with permanent facial palsy in which the facial nerve is intact, but is inflamed and compressed within the bones of the face. This can be present in patients with facial paralysis as a result of traumatic injury, infection, or Bell’s palsy. Facial nerve decompression is generally indicated after other less invasive treatments for the symptoms of facial palsy have been attempted.
An optimal result after facial nerve decompression surgery is seen about one year after surgery and the surgery is typically most effective on patients who are operated on less than 30 days following the onset of complete facial palsy. Blood work, imaging (MRI and/or CT scans), and other tests such as EMG and ENoG are often performed to determine if facial nerve decompression is a good treatment option.
Acoustic Neuroma Management
An acoustic neuroma is the most common kind of non-cancerous brain tumor.
Post-Acoustic Neuroma Surgery
Acoustic neuroma develops in close proximity to the facial nerve, making it possible for the facial nerve to be damaged during acoustic neuroma removal surgery, and sometimes it is eveecessary to remove a portion of the facial nerve in order to effectively remove the entire tumor. Dr. Azizzadeh works closely with expert oculoplastic surgeon Dr. Massry and Physical Therapist Teresa England to help patients recover from acoustic neuroma removal surgery. Through specialized treatment plans tailored to the individual, they combine facial paralysis expertise, skilled eye care, and muscular retraining therapy to help restore normal facial movements in the acoustic neuroma patient.
Acoustic Neuroma Facial Paralysis
Facial paralysis associated with acoustic neuroma generally occurs as a result of the facial nerve’s proximity to the tumor. Sometimes a section of the facial nerve may need to be removed or manipulated when removing an acoustic neuroma, and, due to the delicate nature of the facial nerve, the residual swelling and damage of the trauma can cause temporary or permanent facial paralysis and synkinesis.
Synkinesis, meaning “simultaneous movement,” is a common occurrence in people with facial palsy. Synkinesis can occur as a result of the abnormal regeneration of the facial nerve after surgery and when the nerve fibers reconnect to the wrong nerve group, it results in undesired facial movements where muscles other than those intended contract. Synkinesis is often treated with Botox injections to relax the hyperactive muscles, but some patients may benefit from surgery.
If a patient does not regain facial movement and/or suffers from severe synkinesis, they may benefit from a nerve transfer surgery. Dr. Azizzadeh is a nerve transfer expert who is highly regarded around the world for his innovative facial paralysis surgery techniques. Depending on your individual case, you may be a candidate for one of the following nerve transfer procedures:
Hypoglossal-Facial Nerve Transfer
Masseter-Facial Nerve Transfer
Gracilis Muscle Transplant
Temporalis Tendon Transfer
Surgery for Synkinesis
It is critical that anyone living with permanent facial paralysis caused by acoustic neuroma visit a facial paralysis expert for any treatment. Dr. Azizzadeh uses a multidisciplinary approach to ensure the best possible outcome for all of his facial paralysis procedures and he uses minimally invasive techniques whenever possible. Dr. Azizzadeh’s goal is to put a smile back on the face of all his facial paralysis patients.
Acoustic Neuroma Dizziness
A common effect of acoustic neuroma is dizziness, and it is usually one of the first symptoms of the problem. Vertigo occurs at the onset because the acoustic neuroma starts from the vestibular nerve—the nerve that is responsible for balance. It is common for patients to experience vertigo early on in acoustic neuroma development, but usually as the body adjusts and compensates for the pressure on the vestibular nerve, the patient’s vertigo symptoms will diminish.
Imbalance can progress as the tumor increases in size, while true vertigo subsides. Both conditions—vertigo and imbalance—can present with the symptom of dizziness. The treatment for acoustic neuroma dizziness will depend on the treatment path taken for the tumor itself and some dizziness may remain immediately following acoustic neuroma surgery due to the trauma experienced by nerves during surgery.
Acoustic Neuroma Eye Care
It is fairly common for acoustic neuroma patients to struggle with long-term eye troubles. In fact, about 50% of acoustic neuroma patients have eye discomfort and eye problems such as decreased eyelid function and tear production. These eye problems can lead to eye irritation and a dry, scratchy feeling in the eye due to a lack of protection. It is also very common for patients to use artificial tears to aid in lubrication and prevent dryness. Because proper eyelid function is crucial to the lubrication and protection of the eyeball, Dr. Azizzadeh and Dr. Massry have several methods for restoring some of the eyelid function lost in patients with acoustic neuroma, including:
Gold Eyelid Weights
Platinum Chains
Eyelid Springs
Tarsorapphy
These procedures can help restore some or all of the ability to close the eyes, which will help keep the eyes protected and prevent eye damage
Surgery for Synkinesis & Partial Facial Paralysis
In most patients with partial facial paralysis with synkinesis, the best course of treatment is physical therapy and/or Botox injections to better coordinate facial movement, improve facial symmetry, and reduce functional tightness. When a patient has tried these methods, but is not experiencing success, surgery may be an option.
Selective Neurolysis for Synkinesis
Selective neurolysis is the most cutting edge advancement in the treatment of patients who cannot generate an appropriate smile with partial facial paralysis and synkinesis. Selective neurolysis is an intricate operation, but the downtime and risks involved for the patient are minimal, along the same lines as those associated with a facelift. The procedure involves releasing the platysma muscle (which pulls the corner of the mouth down, hence preventing upward smile motion) and selectively decreasing the activity of the nerves that counter the smile mechanism to help get an upward trajectory of the mouth and improve synkinesis. These procedures allow spontaneous reanimation of the face.
Static Suspension for Synkinesis
Static suspension, or static sling, is a procedure used to improve facial symmetry in patients with facial paralysis and synkinesis, particularly in the mouth and laugh line area. Dr. Azizzadeh uses sutures or tensor fascia lata (autologous tendon) from the patient’s outer thigh. If tensor fascia is utilized, strips of the tendon are attached to the corner of the mouth on the through a small facelift incision. Dr. Azizzadeh uses endoscopic technology to minimize the quantity and size of incisions, and he is an expert in performing static suspension surgery using the tensor fascia lata. Because the muscle used to create the sling is from the patient’s own body, there is less chance of rejection.
Another option for static sling surgery is to use freeze-dried, acellular human dermis known as Alloderm. Dr. Azizzadeh has experienced great success with Alloderm over the years and a benefit to this procedure is that there is no need for a second incision to get muscle to harvest, such as in the leg for the tensor fascia lata procedure.
Dr. Azizzadeh can also perform a minimally invasive suture suspension procedure in place of the more invasive surgery, which may be a good option for patients with partial synkinesis. Each patient is unique and the most appropriate treatment method for your particular condition will be decided upon during your consultation.
Blepharoplasty for Synkinesis
One of the most common side effects of synkinesis and partial synkinesis is involuntary eyelid closure when smiling, laughing, or opening the mouth. In some cases, this can be treated with a modified blepharoplasty, or eyelid surgery. Depending on your unique situation, Dr. Azizzadeh can customize a treatment plan to help restore normal eyelid function and address your specific needs.
Facelift for Synkinesis
Dr. Azizzadeh can also perform a modified facelift and/or neck lift to improve facial symmetry and minimize the visible effects of facial paralysis and synkinesis. He tailors the facelift to the individual in order to address specific areas affected by synkinesis and obtain optimal aesthetic results.
Dr. Azizzadeh, known around the world for his facial reanimation expertise, performed a facelift on Mary Jo Buttafuoco in 2005 as part of the specialized treatment plan he created to restore balance and animation to her face after she had been shot in the head years earlier. The facelift, performed in conjunction with static facial suspension and a modified blepharoplasty, produced incredible results.
Cross Facial Nerve Graft & Gracilis Muscle Transplant
Some patients with long-term facial paralysis and synkinesis may be candidates for a cross facial nerve graft and gracilis muscle transplant. These cutting-edge surgical procedures, combined with physical therapy, can help restore dynamic facial animation, such as the ability to smile, in facial paralysis patients.
The procedure is typically done in two parts. First, nerve grafts from the lower leg are harvested and fixed to the functioning facial nerve in what is known as a cross-facial nerve graft. The second stage is the gracilis muscle transplant in which a portion of the gracilis muscle free flap from the inner thigh is harvested and attached to the cross-facial nerve graft. Together, these two procedures and physical therapy typically restore some facial movement within 8 months, and patients continue to see improvement for up to two years.
Mobius (Moebius) syndrome
Professor Paul Julius Möbius
Facial paralysis is the most overt symptom related to Mobius syndrome. Children’s facial expression and function are impaired with an inability to suck and smile. Furthermore, the patients have strabismus and present with significant drooling and mask-like appearance Limb anomalies such as club foot can also occur in up to 25% of the patients. This rare syndrome is typically bilateral but can have asymmetric presentation with one side having some limited movement. Professor Paul Julius Möbius (Pictured above) was the first physician to describe this rare disease in 1884.
The treatment options for creating a normal face should be considered before the children enter school. For duel facial paralysis, The Institute for Facial Paralysis prefers to use microsurgical trigeminal-gracilis muscle transfer. This procedure involves transfer of the gracilis muscle (from the inner thigh) to the face and attachment to the trigeminal nerve which controls the muscles for chewing. This muscle and nerve transfer allows the children to control the movement of the face voluntarily. Each side of the face must be performed in separate stages. Typically the first operation is performed when the child has turned 6. The second stage is performed at age 7. The psychosocial implications for surgical reanimation are very important. A child should not go through life with this deformity when something can be done immediately. (Source: National
Other surgical procedures that can be considered are static suspension with tensor fascia lata, temporalis transfer and eyelid reconstruction, but only when it is warranted. Contact us on behalf of your child for their “Mobius reconstruction” needs. We have what is considered the most advanced techniques in the facial paralysis field along with surgeons who are widely known and respected.
Ramsay Hunt Syndrome
What Is Ramsay Hunt Syndrome?
Ramsay Hunt Syndrome is a condition in which shingles compromises the facial nerve, often time resulting in symptoms including hearing loss on the affected side of the face and even temporary facial paralysis as well as a blister like rash near the ear. Ramsay Hunt is caused by the varicella zoster virus, the same virus that brings chicken pox to children, and it is believed that once an individual is healed from the chicken pox, the virus can lay dormant for years and surface again as Ramsay HuntSyndrome later in life. To combat the virus itself, a patient is usually given very high doses of antiviral medications.
If you believe that you may be suffering from the condition, seeking proper medical attention in a timely manner to lower your risk of complications is of the utmost importance as the facial paralysis induced by Ramsay Hunt Syndrome can be much more severe than in instances of other conditions.
Facial Paralysis Caused By Ramsay Hunt Syndrome
Because facial paralysis is a common symptom of Ramsay Hunt Syndrome, world-renowned facial paralysis surgeon
When Ramsay Hunt Syndrome is treated early, patients have the highest chance of getting full recovery. To aid in a symmetrical and balanced appearance in the meantime, Dr. Azizzadeh may utilize Botox therapy and fillers to help bring symmetry to his patient’s faces. Botox works to actually relax the paralyzed muscles in the face creating less of a pull during a smile or other facial expressions.
If you’re experiencing permanent facial paralysis as a result of Ramsay Hunt Syndrome, there are several surgical options that have brought great success to patients from around the globe, including the masseter-to-facial nerve transfer and cross-facial-nerve-transplant.
Ramsay Hunt Syndrome FAQ
Because individuals who suffer from facial paralysis as a result of Ramsay Hunt Syndrome often have a great deal of questions as their condition arises seemingly out of no where, Dr. Azizzadeh has compiled a list of his most frequently asked questions to help you better understand your condition. If you have additional questions, we encourage you to contact our medical practice today.
Q: Is facial paralysis caused by Ramsay Hunt Syndrome painful?
A: Ramsay Hunt Syndrome itself can bring a very painful blister like rash to the individual suffering from the disorder, which can be painful. Facial paralysis as a result of the condition, however, is most likely not.
Q: Am I a good candidate to undergo Botox for facial paralysis?
A: If you’re experiencing an uneven smile as a result of Ramsay Hunt Syndrome, you might be a great candidate to undergo treatment. To find out, it’s important to schedule a consultation at the Facial Paralysis Institute.
Q: Are treatments to help facial paralysis caused by Ramsay Hunt Syndrome covered by insurance?
A: This depends greatly on your insurance provider. At the Facial Paralysis Institute in
Q: Who should administer Botox treatments for facial paralysis?
A: It is ideal to have an experienced facial plastic surgeon give you Botox injections for your condition, as they have the most experience of both the function and aesthetics of the face.
Q: How long does facial paralysis from Ramsay Hunt Syndrome usually last?
A: This greatly depends on how soon you’re able to seek treatment for your condition. The most important part of curingRamsay Hunt Syndrome is to make sure that you visit a physician as soon as you realize you may be suffering from the disorder, as fighting the virus is key to reduce the length of your disorder and future complications.
