ConditionsLet us help
- Bell’s Palsy
- Moebius Syndrome
- Hemifacial Microsomia
- Ramsay Hunt Syndrome
The Facial Paralysis Center treats virtually all causes of facial nerve disorder. There are many ways to categorize the causes of facial paralysis, but most are based on facial nerve injury, compression, or inflammation. The facial nerve can be injured anywhere along its path from the brainstem all the way into the facial muscles themselves. There can be partial paralysis (facial weakness with some facial movement) or complete paralysis (absolutely no movement). Facial paralysis can affect one side or both sides of the face. It can also be characterized as congenital (existing from birth) or acquired (or, occurring later in life).
Dr. Panossian will perform a thorough evaluation at the time of your consultation and develop a treatment plan based on your unique situation. The team of specialists at the Facial Paralysis Center is then consulted as necessary to implement the treatment plan in order to deliver the greatest efficacy and outcomes. Additional diagnostic studies may be recommended. Treatment plans may include anywhere from simple observation to innovative surgical interventions, depending on the underlying reason for your facial paralysis and its severity.
In addition, Dr. Panossian advocates early monitoring and intervention for newly diagnosed cases of facial paralysis. Early treatment is highly desirable in terms of realizing the greatest improvement with the best aesthetic outcome.
Find out more about the most common causes of facial paralysis by clicking in the column to your left.
What is Bell’s palsy?
Named after an early 19th century Scottish anatomist (Sir Charles Bell), Bell’s palsy describes a dysfunction of the seventh cranial nerve (ie, facial nerve). An inflammatory condition affecting the nerve results in paralysis of the muscles of facial expression. The result is usually a one-sided facial droop that is most often temporary. The term “Bell’s palsy” is misused often to described any instance of facial paralysis.
Why does Bell’s palsy occur?
Bell’s palsy is an acquired condition and occurs in approximately 1 in 5000 people, and its incidence increases with age. It is considered a diagnosis of exclusion, meaning that other known causes of facial nerve dysfunction must be ruled out. It is the result of inflammation within the nerve, a term called mononeuritis. It most notably follows a systemic viral infection such as the common cold, herpes, varicella-zoster virus, Lyme disease, and others. Other theories entertain the possibility of an autoimmune disease process as the source of facial nerve dysfunction. In addition, the condition seems to occur more often in pregnant individuals and diabetics. Most instances of true Bell’s palsy last several days to months, but can sometimes result in permanent paralysis.
What are some problems associated with Bell’s palsy?
Loss of facial nerve function in Bell’s palsy produces similar problems as facial paralysis from other causes. Aside from the obvious facial droop, patients can have problems with eye closure. This can lead to drying of the eyes, tearing, and in the worst case, scarring of the cornea. In addition, inability to move the corner of the mouth can result in speech difficulties and drooling. Smiling is distorted as are other facial expressions. The facial asymmetries are magnified with animation.
Although Bell’s palsy affects motor nerves of the face, unusual tingling sensations have been reported of the overlying skin. In addition, abnormal twitching can develop as the nerve recovers. This is called synkinesis, and it describes a phenomenon whereby the re-innervation of the facial muscles results in “mis-wiring.” This manifests in a variety of abnormal twitching patterns. For example, the eye will blink when smiling or vice versa. In one unusual manifestation of abnormal nerve regeneration, patients can produce tears when eating (gustatolacrimal reflex). The reason for this is that nerve branches supplying these functions are also derived from the facial nerve. Taste itself can be affected.
Can Bell’s palsy be passed on?
In recent years, there have been reports of clusters of families affected with Bell’s palsy. It is difficult to understand why this could occur, but it is believed that an underlying hereditary autoimmune disorder may be the culprit. Otherwise, Bell’s palsy resolves within 3 months in more than 80 percent of patients and does not get passed on.
How is Bell’s palsy treated?
As mentioned previously, most cases of Bell’s palsy resolve spontaneously within 3 months. Others may require antiviral medication and steroids to settle inflammation related to a viral infection. In the case of synkinesis, treatment can prove challenging. Botox injections in specific locations can help interfere with abnormal nerve conduction, while facial therapy can be helpful for strengthening natural nerve pathways.
In the event of permanent paralysis, defined as lasting 18 months or longer, surgical intervention may be necessary. Various areas will be targeted for reanimation, including the mouth, eyes, and forehead. Both dynamic and static options are used to balance the face and restore better symmetry.
It is important to have a doctor skilled in facial paralysis management follow along to make sure that recovery is happening in steady fashion. Depending on the rate of recovery, the decision to proceed to surgery and which surgical procedure to choose is then considered. There are opportunities to re-establish nerve function and prevent irreversible paralysis, if it is determined early enough that facial nerve regeneration is not occurring as expected. However, in the setting of longstanding Bell’s palsy (greater than 12-18 months), the surgical decision becomes more obvious, and the type of surgery necessary will be different.
What is the recovery like from Bell’s palsy or its treatment?
Most cases of Bell’s palsy will require no intervention. With time (3-6 months), the paralysis will resolve on its own in most cases. A short course of steroids and/or antiviral therapy is sometimes given. The key to management is to make sure there is some evidence of steady improvement during the first several months. A doctor with a specialty in facial paralysis will need to follow along to make sure that recovery is proceeding as expected.
Synkinesis (described above) can develop over the intervening weeks during recovery or after surgery. This can be sometimes quite stubborn and will recover additional treatment using Botox or other surgical approach to disrupt the mis-wired muscles.
In the event that surgery is required to re-establish facial movement, the recovery will depend on the option chosen. In general, all available options will require 2-4 weeks of limited activity and avoidance of exercise, heavy lifting, rough play, or contact sports. Several months are required for nerve regeneration, but patients are allowed to gradually increase their activity level back to normal. Dr. Panossian will discuss the expected postoperative recovery from each of the potential surgical options at the time of your consultation.
What are the risks and complications of surgery to correct Bell’s palsy?
The risks associated with medical therapy are relatively minor. However, surgery for longstanding Bell’s palsy carries certain risks. As with any surgery, there is a small chance of bleeding, infection, or anesthesia problems. Usually, the greatest risk is that the surgery simply doesn’t work. There are a host of reasons for why this might happen, including failed nerve regeneration, postoperative trauma or infection, or prolonged time to recovery of movement (a function of slow nerve regeneration and a long distance to the target muscles). Thankfully, this is rare. More commonly, certain asymmetries can persist in the relaxed state or with animation. These can be minor or more substantial. Sometimes, waiting some time will improve facial asymmetry.
Complications of surgery can include hematoma in the first few days, requiring drainage in the operating room. Infection of the cheek can require a brief hospitalization for intravenous antibiotics and/or surgical drainage. Revisions may be required to correct bad scarring (keloids or hypertrophic scars) or significant asymmetries.
Trauma can occur anywhere along the path of the facial nerve, from the brainstem all the way to its connections with facial muscles. Injury to the facial nerve can result in either complete disruption or bruising and inflammation of the nerve. In the event of a complete disruption (also known as “neurotmesis”), the ability for self-repair is absent. In other words, without direct repair or nerve grafting, the facial nerve will fail to regenerate normally. When only a blunt trauma occurs or if there is swelling and inflammation of adjacent damaged tissues (also known as “neurapraxia”), the nerve is left in continuity and has the ability to fully regenerate and re-establish facial nerve function. There is, at times, an intermediate form of nerve injury where the structural framework of the nerve is maintained but individual nerve fibers may be broken (called, “axonotmesis”). In this event, spontaneous regeneration can occur, but this may sometimes be associated with unwanted twitching or cross-innervation of facial nerve branches, known as “synkinesis.”
Depending upon where along the path the nerve is damaged, the picture of facial paralysis can be quite varied. For example, injury closer to the brainstem or main trunk of the facial nerve as it exits the skull behind the ear can result in complete facial paralysis with no functioning muscles, whereas injury at the level of the branches in the face will result in partial paralysis.
Common causes of trauma-related facial nerve injury include the following:
- Sharp laceration
- Dog bite
- Temporal bone fracture
- Birth trauma
- Severe blunt force trauma
- Gun shot
- Jaw fracture
As with all forms of facial paralysis, early intervention is the gold standard of treatment. A thorough exam and immediate surgical repair, if indicated, are the mainstays of management.
Tumors can affect the facial nerve in a number of ways. Brain tumors in the posterior fossa of the skull, such as medulloblastomas, arise very close to the nucleus, or the origin, of the facial nerve in the brainstem. Compression in this area by such a tumor can cause complete facial paralysis. More commonly, surgery to remove such a brain tumor can result in collateral damage. For many patients, the need to obtain negative tumor margins must outweigh the need to preserve facial nerve activity.
Tumors can also arise anywhere along the path of the facial nerve. An acoustic neuroma is a benign tumor that arises from the lining of nerves, most often the eighth cranial nerve, or the vestibulocochlear nerve. The supportive cells that line all nerves (Schwann cells) are responsible for nourishing the underlying nerve and provide it with the proper chemical balance to transmit signals. When these cells overgrow in a tumor-like fashion, they can compress the adjacent facial nerve and brainstem. Also, in the process of removing the tumor, damage can be sustained to the facial nerve, thereby manifesting as complete facial paralysis.
The parotid gland is the largest salivary gland in the face. It sits in front of the ear as a heart-shaped structure and passes down and around the earlobe region. The facial nerve is intimately associated with the parotid gland. As the nerve exits the skull behind the ear and in front of the mastoid bone, it begins to pass through the parotid gland. It will then arborize within the gland and exit as the main branches of the facial nerve as they move towards their target muscles. The parotid gland can be a source of tumors that can, in turn, have an impact on the facial nerve. Pleomorphic adenoma is the most common parotid tumor and typically presents as a painless swelling near the border of the jaw and in front of the ear. The differential diagnosis can include malignancies such as adenoid cystic carcinoma or adenocarcinoma and inflammation of the gland, called parotitis. Surgical excision is the treatment of choice for all tumors of the parotid gland. This is known as a parotidectomy and is typically performed by an otolaryngologist. However, in a small percentage of cases, removal of the tumor can result in damage to the facial nerve or its branches. This is typically evident immediately at the end of surgery.
Vascular birthmarks or anomalies consist of mostly benign tumors and malformations. Vascular tumors such as infiltrative hemangiomas and Kaposiform hemangioendotheliomas (KHE) can also produce facial nerve problems, most frequently in relation to surgical excision. In many cases, vascular tumors will naturally or with medication go on to involute or disappear with time. Although not technically classified as tumors, vascular malformations can be present at birth and continue to expand over a lifetime. Lymphatic malformations (lymphangioma or cystic hygroma), venous malformations, and arteriovenous malformations (AVM) can cause facial nerve dysfunction through inflammation. Although this can be temporary and frequently resolves with non-steroidal anti-inflammatory medications such as ibuprofen, permanent damage can occur with attempts at surgical excision.
Neurofibromatosis is a unique genetic disorder that can affect any nerve tissue in the body. Tumors form on nerves and can be quite large in some cases. Although the majority of neurofibromas are benign, they can grow large and create significant disfigurement or life-threatening symptoms such as brain compression. Treatment is aimed at controlling the symptoms of growth. Surgical excision is still the preferred option for addressing these tumors. However, when they occur in the face, they can result in significant deformity and a risk of damage to the facial nerve. The Facial Paralysis Center’s neurologists are leaders in the treatment of neurofibromatosis. Contouring procedures are combined with facial nerve exploration. In the event of tumor involvement of the facial nerve, the team is ready to address the resulting facial paralysis in an early fashion.
Dr. Panossian is an expert in the surgical exploration and repair of the facial nerve and is often requested for management of facial nerve injuries resulting from removal of tumors. He is also an expert in vascular anomalies and neurofibromatosis. Contact the Facial Paralysis Center today to discuss your options.
Strokes are often associated with facial paralysis. A stroke is classified as either ischemic (lack of blood flow) or hemorrhagic (blood vessel rupture) and can affect various centers in the brain. When a stroke occurs in the area of the brain that controls movement (primary motor cortex), it can result in loss of function of the muscles it controls. A motor homunculus is a graphic representation depicting what areas are controlled geographically along the frontal lobe cortex. The muscles of facial expression are affected frequently in stroke patients. This can manifest as either facial weakness, partial paralysis, or complete paralysis.
In some cases, stroke patients may qualify for intervention for facial paralysis, if the symptoms of stroke do not resolve. These patients face the same consequences as other facial paralysis patients, including symptoms of drooling, facial drooping, eyebrow droop, incomplete blink and eye closure, watery eye, speech disturbance, and swallowing difficulties.
Facial paralysis reconstruction must be weighed against the risk of surgery in stroke patients. These patients tend to be older and may have other morbidities such as high blood pressure, diabetes, and heart problems. If these problems are addressed and managed effectively, then a surgical plan may be instituted. In any case, the mainstay of management in stroke patients is facial and physical therapy. Aside from reanimation procedures, there are several other options for cosmetic improvement that may be more simple such as facelift, browlift, or fascia lata tendon sling placement.
Contact the Facial Paralysis Center today to discuss your options for treatment, if you or a loved one has sustained a stroke.
What is Moebius syndrome?
Moebius syndrome (or, Mobius syndrome) is a rare neurological disorder affecting muscles involved in facial expression and eye movement. It is a congenital condition, meaning that it is present at birth, and is usually bilateral (or, occurring on both sides of the face). It results from the failure of development of cranial nerves VI and VII in the brainstem. Children with Moebius syndrome have a characteristic mask-like facial appearance with no ability to communicate emotions through facial movements. The eyes are unable to rotate in an outward direction. The exact occurrence of Moebius syndrome is unknown, but is estimated at 1 in 50,000 to 500,000 infants.
Why does Moebius syndrome occur?
It is still largely unknown why Moebius syndrome occurs. As with many craniofacial disorders, Moebius syndrome is possibly the result of a combination of environmental and genetic factors. Several chromosomal relationships are associated, including abnormalities in chromosomes 3, 10, and 13. Maternal use of certain medications and recreational drugs have also been implicated. The result of these effects during pregnancy is the failure of development of cranial nerves VI and VII. New studies are being conducted to elucidate the potential genetic relationship.
What are some associated problems of Moebius syndrome?
In Moebius syndrome, facial and eye movement differences are present in virtually all patients. Rarely, the condition will affect only one side of the face (or, unilateral). Additionally, if other cranial nerves are involved, then there can be issues with chewing, tongue coordination, speech, hearing, or balance. Hand and foot deformities can also occur. Moebius syndrome can include other malformations including club feet, missing fingers and/or pectoralis muscle (similar to Poland syndrome), and hearing loss. Other cranial nerves may also be involved on rare occasions. The majority of patients have normal intelligence, although psychological issues are common due to difficulties integrating with family and friends. The lack of facial expression is often the source of stress. Problems with eye closure can rarely result in drying of eyes and corneal scarring. Failure of mouth closure can result in drooling and dental problems.
Can Moebius syndrome be inherited?
Although various genetic markers seem to be associated with Moebius syndrome, the vast majority of cases occur in people with no history of the disorder in their families. There is no clear pattern of inheritance.
How is Moebius syndrome treated?
Children with Moebius syndrome may have a number of issues requiring intervention based on the severity of the condition and the presence of associated malformations. A multidisciplinary team of specialists is critical in managing issues related to speech, hearing, feeding, orthopedics, and psychosocial development. For correction of craniofacial issues, surgery is currently the only option. Correction of eye movements will need to be addressed by an ophthalmologist.
Facial paralysis in Moebius syndrome is typically complete and bilateral. In other words, facial nerves on both sides of the face are absent; therefore, use of cranial nerve VII is not possible in restoring movement as in one-sided facial paralysis. However, cranial nerve V is usually present. This nerve is usually responsible for activation of biting muscles. Based on this concept, one of two methods for lower facial reanimation (or, smile reanimation) is possible: free gracilis muscle transfer or temporalis muscle transfer. These techniques are discussed at great length in the Facial Paralysis section.
Incomplete eye closure causing symptomatic drying or excessive tear production may need to be corrected surgically. Various options exist for achieving this. Please refer to the Facial Paralysis section for further details.
Club foot deformities will need to be corrected by an orthopedic surgeon. Hand deformities are most often characterized by an underdeveloped hand (or, symbrachydactyly). In this condition, a combination of webbing of fingers and missing fingers occurs. The severity of symbrachydactyly can be quite variable. Please refer to the section on Symbrachydactyly for further details regarding improvement of hand function. Chest wall deformities can be corrected towards the end of skeletal development at approximately 16 years of age. Girls with lack of breast development will proceed with breast reconstruction at that time.
What is the recovery from surgery for Moebius syndrome?
Recovery from surgical correction of Moebius syndrome depends on the deformity being corrected. Some procedures, such as facial reanimation, will require a brief hospitalization, while others such as correction of hand malformations can be done on an outpatient basis. Also, the duration of each surgery is also highly variable from 2 hours to 8 hours.
Patients requiring hospitalization may return to their usual physical activity between 2 and 4 weeks following surgery. Activity restrictions will need to be tailored to the procedure performed and is directly proportional to the intricacy of the intervention. Facial therapy is started usually at 3 weeks postoperatively for facial reanimation using the temporalis muscle or at 3 months when using the gracilis free muscle transfer.
Correction of hand problems usually requires a 2- to 3-week period of casting to ensure proper take of skin grafts (if used) and optimal healing of bone and soft tissues. Following removal of the cast, patients are allowed to shower once again and resume use of the hand. A nighttime splint is worn for 3 to 4 months following surgery.
What are the risks and complications of surgeries for Moebius syndrome?
All procedures for correcting deformities related to Moebius syndrome will carry a different set of risks and potential complications. Thankfully, all procedures are relatively safe when appropriate preoperative evaluation is performed. Airway complications are the most serious issue encountered. Anesthesia pre-evaluation is necessary to stratify risk and to make provisions at the time of surgery for successful intubation and postoperative management.
Bleeding, infection, and anesthetic complications are risks of any surgical procedure. In addition, poor scarring or wound problems can occur rarely. More frequently, achieving perfect symmetry is an impossibility. Improvements can be substantial, but reversing the deformity to a normal state cannot be realized in the majority of patients. Revisional surgery may be required to improve scars, contour, symmetry, or facial movement.
What is hemifacial microsomia?
Hemifacial microsomia is a subset of craniofacial microsomia. It is a spectrum of undergrowth conditions or malformations related to the craniofacial skeleton. They occur in 1 in 3,000 to 25,000 live births, second only to the incidence of cleft lip and palate. The lower jaw (or, mandibular) deformity is the most common manifestation of the disease process. In fact, the severity is classified on the basis of the lower jaw deformity (Pruzansky classification). The underlying problem is an underdevelopment of the craniofacial skeleton, including the external, middle, and inner ear structures as well as the jaw and overlying soft tissue structures (including the cranial nerves). As its name suggests, it usually occurs only on one side of the face (ie, hemifacial or unilateral). The occurrence of this condition is largely unknown.
Why does hemifacial microsomia occur?
It is still largely unknown why hemifacial microsomia occurs. Many syndromic conditions can include hemifacial microsomia, but the majority of isolated cases have no known cause. It occurs during development when 2 specific precursor tissues for facial development (ie, the first and second branchial arches) fail to form properly. As in the majority of cases of cleft lip and palate, the origin of hemifacial microsomia is felt to be mostly multifactorial in nature. In other words, numerous environmental exposures combined with certain unknown genetic factors come together to create the condition. Recent studies are looking into possible identifiable genetic sources that may be causing hemifacial microsomia.
What are the associated problems with hemifacial microsomia?
In hemifacial microsomia, the degree of visible deformity can be subtle or extreme depending on severity. The most common appearance is that of a small lower jaw with a chin point that is shifted to one side. This frequently contributes to bite irregularities or malocclusion (eg, lateral crossbite, cant, or open bite). Involvement of the external ear is common and can produce microtia or anotia (ie, underdeveloped or absent ear, respectively) with possible lack of the canal for hearing. Skin tags and sinus pits may also be present around the ear. The facial nerve (cranial nerve VII) can be affected, producing a one-sided facial weakness or paralysis. If the muscles used for biting are affected, then it may compound the problem of an asymmetric bite and simultaneously amplify the deficiency of facial volume. The cheekbone may also be deficient, and the outer corner of the eye may be displaced downward. Sometimes, the eye itself may be small or absent (ie, microphthalmia or anophthalmia, respectively), or have defects in the iris (or, colobomas). Eyelashes may be partially absent. Macrostomia (or, enlarged mouth opening) is the result of facial clefting.
In addition to the craniofacial deformities described, a number of other congenital deformities may be present. There can be problems with development of the spine, gastrointestinal, cardiac, renal, and pulmonary organs. Several named syndromes, such as Goldenhar and Treacher Collins, are known to have features of hemifacial microsomia.
Can hemifacial microsomia be inherited?
Although various genetic markers have been identified in hemifacial microsomia, the majority are of a single occurrence in a family and without a known cause. However, a multifactorial inheritance pattern (ie, some genetic tendency in combination with environmental factors) is suggested based on several observations. First, there does seem to be an increased recurrence risk in families with an affected relative. The risk of an affected individual having an affected sibling, child, or parent (ie, first-degree relative) is estimated at 2 to 3 percent or more. Second, maternal use of certain medications including aspirin, retinoic acid, pseudoephedrine, ibuprofen, and assistive reproductive medications are known to increase the chance of having a child with hemifacial microsomia. Lastly, the higher incidence in identical twins suggests a genetic link. A consultation with a genetics counselor is vital in accounting for all variables contributing to hemifacial microsomia and for providing a better foundation for family planning.
How is hemifacial microsomia treated?
Children with hemifacial microsomia may have a number of issues requiring intervention based on the severity of the condition and the presence of associated malformations. A multidisciplinary team of specialists is critical in managing issues related to breathing, speech, hearing, feeding, cardiac or kidney problems, orthopedic concerns, and psychological development. For correction of craniofacial issues, surgery is currently the only option. Ear tags can be removed very easily on an outpatient basis, whereas jaw deformities are much more complex and require a more aggressive surgical treatment.
Ear reconstruction using either rib cartilage or a porous polyethylene framework (ie, Medpor® implant) can successfully reproduce the shape of an ear. Recreation of an outer ear canal is possible but is largely dependent on the formation of middle and inner ear structures for successful restoration of hearing. Most children with complete occlusion of the ear canal are candidates for a bone-anchored hearing aid (or, BAHA device).
Facial soft tissue asymmetry can be improved with fat grafting from the abdomen to the area of volume loss in the face. In severe cases, a large area of tissue with its blood supply can be transplanted to the face and sculpted to give more effective filling. This is known as a fasciocutaneous free flap. Whereas fat grafting can be done on an outpatient basis, the free flap option requires a short period of hospitalization to ensure graft survival. In some instances, facial augmentation can be done using artificial implants for cheek bone and chin improvement, or to fill wasting in the temples.
For facial weakness or facial paralysis, various options exist for improving movement. For eye exposure issues due to failure of eyelid closure, an upper eyelid gold or platinum weight can be inserted to assist in closure. Alternatively, a piece of fascia taken from another part of the body can be inserted into the upper eyelid opening mechanism in order to lengthen it, thereby achieving good closure and avoiding the use of a foreign implant. In many instances, a lower eyelid procedure may also be required. Specifically, a fusion of the outer corner of the eyelids can help suspend the lower eyelid and prevent the chance of drying. This is called a tarsorrhaphy. Alternatively, a piece of tendon from the wrist area can be used to re-suspend the lower eyelid from the corners of the eyes. Newer muscle transplantation techniques have been tried with marginal success.
For mouth function, restoration of movement at the corner of the mouth is critical for many reasons. Being able to tighten the lips can help achieve closure and improve speech, drooling, and smiling. Several options exist for smile reanimation from cross-face nerve grafting to gracilis muscle free flaps to temporalis muscle transposition. Please refer to the section on Facial Paralysis for further details.
Macrostomia (large mouth opening due to a sideways cleft) repair is done as early as 6 months of age. This involves closing the layers of the cheek in a specific pattern in order to restore symmetry and maintain proper oral function. The surgery takes less than 2 hours and can be done on an outpatient basis.
Revisional surgery is required in many cases of hemifacial microsomia. These can include additional contouring procedures or scar revisions. As a child grows, changes in the craniofacial skeleton may cause shifting of tissues, uncovering new areas that will need to be addressed. The timing of intervention is very important in getting optimal results and should be custom-tailored for each patient.
What is the recovery from hemifacial microsomia surgery?
Recovery from surgical correction of each component of hemifacial microsomia is highly variable. Whereas ear reconstruction can potentially be performed as an outpatient, other aggressive interventions such as jaw surgery and facial reanimation may require a brief hospitalization. Considerations must be made for airway management when operating on the jaws or inside the mouth.
Generally, avoidance of aggressive play and close supervision is required for the first 2 to 4 weeks following surgery. This restriction will need to be tailored to the procedure performed and is directly proportional to the aggressiveness of the intervention.
Jaw or oral procedures will usually have dietary restrictions (soft diet only) for 6 weeks following surgery. All procedures require some level of scar management. The plastic surgeon should guide patients at every step.
What are the risks and complications of hemifacial microsomia surgery?
All procedures for correcting individual deformities related to hemifacial microsomia will carry a different set of risks and potential complications. Thankfully, all procedures are relatively safe when appropriate preoperative evaluation is performed. Airway complications are the most serious issue encountered. Anesthesia pre-evaluation is necessary to stratify risk and to make provisions at the time of surgery for successful intubation and postoperative management. Many of the risks encountered during surgery for hemifacial microsomia are directly proportional to the severity of the condition. For example, airway obstruction carries a higher likelihood of occurring when the lower jaw is extremely small (ie, Pruzansky III classification) and shifted than when it is only slightly small (ie, Pruzansky I classification).
Bleeding, infection, and anesthetic complications are risks of any surgical procedure. In addition, poor scarring or wound problems can occur rarely. More frequently, achieving perfect symmetry is an impossibility. Improvements can be substantial, but reversing the deformity to a normal state cannot be realized in the majority of patients. Overcorrection or undercorrection may occur. Injected fat may resorb and incompletely correct a contour deficit. Many times, revisional surgery will be required to improve scars, contour, or symmetry, as mentioned above.
Synkinesis in the face is the result of involuntary movements during voluntary contractions. For example, when closing the eye or blinking, the corner of the mouth may twitch. Similarly, smiling may cause blinking. Synkinesis can be quite disconcerting for patients and is a source of social embarrassment for many. The phenomenon occurs usually after a bout of Bell’s palsy or other nerve injury and manifests in the recovery phase.
There are several theories as to why synkinesis occurs. When facial nerve function is altered or destroyed, a regenerative process begins whereby the intact portion of the nerve seeks its target in an effort to re-establish stimulatory pathways. It is during this process that the nerve finds its way to different branches, especially in the central portion of the cheek where it arborizes extensively. Through redundant looped pathways, the branches can intertwine and become miswired. Similarly, target muscle cells may be neurotized unintentionally, contributing further to synkinesis.
Treatment is centered on destruction of these abnormal pathways or by denervation of the unwanted muscles creating the twitch. This can be done with botulinum toxin (Botox®) injections or by selective surgical muscle excision and/or targeted nerve destruction. Again, facial retraining through physical therapy is a key factor in the management of synkinesis.
Ramsay Hunt Syndrome
Ramsay Hunt syndrome, also known as herpes zoster oticus, is a virally-induced condition that can result in facial paralysis. As its scientific name implies, the syndrome results from infection with the herpes zoster virus which causes shingles. This is caused by the same virus that is responsible for chicken pox. After a chicken pox infection, the virus can lay dormant in the body for years until later in life when it can resurface as shingles. Shingles occurs most commonly in elderly individuals and those with some form of immunosuppression. Although rare in children, anyone who has had chicken pox is at risk for developing Ramsay Hunt syndrome.
The diagnosis is usually based on history and physical exam. A painful rash with blistering is characteristic of shingles. In Ramsay Hunt syndrome, the rash occurs over the ear and can affect hearing. Early treatment is required in the first week to avoid progression to hearing loss and facial paralysis. Pain medications in combination with antiviral medications (eg, acyclovir) are initiated at the first sign of symptoms. Steroids may also be used to reduce inflammation. All other measures are directed at controlling the symptoms related to facial paralysis. Eye lubrication must be used aggressively to avoid damage to the eye. Physical therapy is also begun to encourage rapid reinnervation of the facial nerve.
Dr. Andre Panossian is an expert in the field of facial paralysis and has treated countless individuals with Ramsay Hunt syndrome. In conjunction with the Facial Paralysis Center, treatment is initiated in a multidisciplinary fashion to ensure rapid return to normal without having long-term complications. Early intervention also ensures that recovery from facial paralysis is monitored and constantly improving. Treatment options are available from botox injections to help settle spasticity in paralyzed muscles to facial reanimation procedures.