Mime Therapy

Introduction

In 1975, the Facial Research Unit of the Wihelmina Gasthuis in Amsterdam made a film called “Peripheral Facial Paralysis”. This film was created for medical professionals to highlight the need for early assessment and effective intervention in patients with facial disorders Paralysis/paresis. In this film, Jan Bronk, director of the Dutch Mime Center, shows how mimic muscles work. Beginning in 1997, Bronk and otolaryngologist Pieter Devriese began considering the potential impact of mime use on patients with facial paralysis. [1]

The following page summarizes the main information found in the article Using mime therapy as a rehabilitation method for patients with facial paralysis – Beurskens and colleagues.

Mime Corporel

Mime is a form of performing art that uses non-verbal expressions to convey a story. Mime is the most famous form of pantomime. [1] Mime corporel A specific type of pantomime created in 1987 by Etienne Decroux. [1] As stated by Beurskens and colleagues, the basic principles of pantomime lower extremity it’s 1]

• Movement is the rhythm of the body in space and time
• Exaggerated movements reveal the essence of the movement

Development of Mime Therapy

[2]

Jan Bronk developed the principles of mime corporel into a specific teaching model, and has also adapted mime for use in other fields, including health and rehabilitation. [1] Through the analysis of the face and facial expressions, he was able to help patients with facial paralysis/paresis.

The following domains are considered in the mime corporel analysis:[1]

• Breathing
  • Facial expression disorder linked to other tense areas of the body
  • Breathing can help relieve this tension
• Articulation
  • Mime teaches students the expressive possibilities of movements that usually occur unconsciously
  • Understanding this can help to correctly interpret the expression
• Alertness and awareness of direction of movement
  • can be used to help communicate different feelings
• Expression
  • Mime can be used to enhance non-verbal communication

Physiotherapy and Mime Therapy

Beginning in 1980, physical therapists who studied under Bronk began using his methods to treat facial patients. Some parts of the method have been modified to create a more comprehensive processing method, including:

• Facial muscle stretching
• Countermovement and coordination exercises help reduce synkinesis

Mime therapy is now used to promote facial symmetry both at rest and in motion, and to control synkinesia. [1]

Mime Therapy Components

As will be discussed in more detail below, the components of mime therapy include:[1]

1. Anamnesis (i.e. medical history)
2. Face and neck self-massage
3. Breathing and relaxation exercises
4. Exercises to enhance coordination and reduce synkinetics on both sides of the face
5. Exercises to help eyes and lips close
6. Letter and word exercises
7. Facial expression exercises

History Patient Information Regarding Treatment and Prognosis [1]

• The first treatment segment of the program focuses on explaining to the patient the cause, treatment and possible prognosis of dysfunction
• Patients were assessed using the Sunnybrook Facial Grading System House-Brackmann Scale and Facial Disability Index
• Patient is photographed and/or videotaped while resting while exhibiting five facial expressions
• Also provide patients with information about
  • Mime therapy
  • The Importance of Participating in Family Planning
  • The need to incorporate exercise into everyday life

Self-Massage[1]

• Patients are taught self-massage
  • The face and neck should be massaged for approximately 10 to 15 minutes daily to relax the facial musculature and improve blood circulation
  • Includes stroking and massaging on both sides of the face
• Teach patients to spot areas of decreased and increased tension
• Stretching is also encouraged
  • The patient should stretch slowly along the course of the muscles on the affected side of the face
  • The stretch should be held for about 15 seconds

Breathing and Relaxation Exercises[1]

• Because the mind and body work together, it is necessary to relax the body in order to relax the face
• Patients should be taught to recognize any tension in the body and compare it to relaxation of the general and facial muscles

Specific exercises for coordinating the two halves of the face and reducing synkinesis [1]

The basic exercise principles are as follows:

• Basic exercises should be done at varying speeds and amplitudes
• Should exercise one side of the face
• The lower jaw should be relaxed
• It is important to exercise the mouth and eyes while inhibiting synkinesis through slow small movements and counteraction

Eye and Lip Closure Exercises[1]

• Patient practices eye and lip closure at varying speeds/forces

Articulations[1]

• These exercises are designed to increase the patient’s awareness of lip movement and mouth position for various sounds
• Vowels and consonants and words for pronunciation

Expression Exercises[1]

• These exercises are designed to develop awareness of the connection between the use of specific muscles and certain facial expressions
• Patients can use specific muscles to regulate emotions, or they can start with emotions to generate movement

Treatment Session[1]

• On average, patients regularly receive 10 45-minute sessions
• Sessions are then held once a week or less frequently depending on symptom severity
• Follow-up treatment is usually 3 to 6 months
• Provide patients with home regimen plans and workbooks/diaries
• Mime therapy should be used when degeneration (i.e. synkinesis) is evident – this may be around 3 months after the onset of facial paralysis
• Mirrors can be used as biofeedback tools

Evidence for Mime Therapy

• Mime therapy has been found to improve facial symmetry in patients with long-standing facial paralysis:[3]
  • After mime treatment, both asymmetry and linkage of the face at rest were reduced, and the symmetry of the face during voluntary movement was effectively improved.
  • The authors found that mime therapy can be generalized to: [3]
    1. Gender
    2. Age
    3. Duration of paresis
  • Mime Therapy is designed to focus on synkinetic patients. [4] Patients with some movement of only the facial muscles have an advantage over those without any movement in mime therapy because it focuses on movement modification and muscle strengthening. [5]
  • Mime therapy is beneficial as it improves blood circulation and preserves muscle properties. Visual feedback using the mirror helps to perform the exercise correctly, which induces proper facial muscle movement. Since imitation requires great muscularity and body control, it has been shown to be effective in New growth and production of collagen and connective tissue in facial muscles. It in turn helps restore muscle activity and strength. [Sharvani Belle Praveen Kumar (2018)] Thus full facial function can be restored immediately. [6]
  • Mime therapy is very effective in treating facial paralysis. [7]
  • Mime therapy combined with electrical stimulation immediately improves the function and integrity of facial muscles. It also reduces synkinesia in Bell’s palsy. [8]
  • Mime therapy and electromyography biofeedback (EMG BFB) both help to enhance facial muscle integrity and movement. [9]

Limitation

Mime therapy is not helpful in treating patients with chronic flaccid facial paralysis because there are no existing movements to enhance or modify. Because it focuses on the treatment of synkinesis. [5]

It is limited to but not only to:[5]

• Patient’s ability to adhere to a treatment regimen.
• Intellectual Level: Mime therapy is considered a difficult regimen to perform. Therefore, it is believed that only patients with a certain level of intelligence can understand and follow the indicated exercises.

Related Articles Synkinesis – PhysiopediaIntroduction and Definition Synkinesis (AKA aberrant regeneration) occurs after facial nerve injury and is a common sequela of facial paralysis. Cause of injury may be Bell’s palsy Ramsay Hunt syndrome (less common) Surgical injury (eg During surgery to remove an acoustic neuroma) Trauma (skull fracture) or other conditions that cause facial paralysis. Synkinesis = syn means together and kinesis means movement. Synkinetic therefore means moving together or moving collectively. Therefore, synkinesis is an involuntary movement Accompanied by voluntary movement. [1] Types of synkinesis are often described by combining the names of the two related muscle groups, the first part referring to the voluntary muscle group and the second part referring to the involuntary muscle group. Example: eye-mouth linkage Is when voluntary eye retraction (such as blinking or raising the eyebrows) causes involuntary mouth movement Mouth-eye linkage refers to involuntary eye retraction accompanied by voluntary mouth movement (such as smiling and pursing lips) Clinically relevant anatomy Learn[edit | edit source] The facial The nerve is the seventh cranial nerve, which controls the muscles of facial expression. More information on the anatomy of the facial nerve can be found here. Injury Mechanism/Pathological Process[edit | Edit source] Inadvertent or mass movement is thought to be caused by Undifferentiated regeneration following compression or injury of the facial nerve. [2] It is thought that synkinesis may be caused by four possible mechanisms: Abnormal regeneration[3][4][5] – Miswiring Re-growth of axons from the facial nucleus to incorrect peripheral muscles The community generally assumes that the site of miswiring is the lesion site (i.e., where the nerve has been damaged by crushing/inflammation), but a 2004 study found that regenerated axons spread throughout their length as well as at the lesion site[4] 6] – Electrical crosstalk between nerve branches is speculated to be due to reduced myelination of nerve fibers, meaning they are poorly insulated and hyperexcitable [7] The theory proposes that once a postsynaptic cell loses input from a degenerating axon, it develops a additional Neurotransmitter receptors, thus becoming hypersensitive As a result of this hypersensitivity, it responds to neurotransmitters supplied by another nearby nerve Maladaptive cortical plasticity[8][9] A 2018 study using MRI found, cortical reorganization in primary sensorimotor areas As well as supplementary motor areas in the brain, many authors suggest that more than one or even a combination of all of these mechanisms may be involved. Clinical presentation [edit | edit source] After the patient undergoes recovery and reinnervation of the affected side of the face Patients with flaccid facial palsy also experience involuntary motor connections that are typical of synkinesia. The most common effects are:[10][11] Partial (or occasional) movement of the eye on the affected side when the mouth is moved (eg, lip puckering while smiling while eating) full) closed, while the unaffected eye remains open = mouth eye When the eyebrows are raised or the eyes are closed, the corner of the mouth on the affected side of the face lifts = eye opening It is important to realize that synkinesis often begins to occur From the fifth or sixth month After the onset of paralysis, although in some cases it can appear as early as the third month after the onset, and usually increases for up to two years after the onset. [12][13] Emergence of co-motion when faces are stationary [Edit | Edit source] When people are not moving, their face co-motion may still be visible. The most common visible manifestations of synkinesia at rest are: Affected eye is smaller than the other Affected nasolabial fold is deeper than the opposite side and is often in an elevated position Mouth corner may be larger than the unaffected side high appearance Synkinesis with facial movement [edit | edit source] The effects of synkinesis are generally more pronounced on facial movements, and as a general rule, more extreme/wide ranges of motion result in greater asymmetry. Left side synkinesis when smiling eg the affected side when smiling The mouth usually does not move to the unaffected side, but the affected eye becomes smaller, as shown in the illustration of synkinesis on the left: same pattern with decreased range of motion of the mouth/lips and increased eye closure Several facial poses are commonly seen under Include lips puckering upper lip to expose teeth. When a person is chewing food, the synmotor behavior of the ipsilateral eye is. Moving towards closure/getting smaller may cause the person to report that I look like I’m blinking when I eat. Scoring/measurement linkage[edit | edit source] The most commonly used measure of facial range of motion by surgeons and physicians is the House-Brackmann scale. [14] Unfortunately, this scale does not rate the abnormal motor associations that occur in synkinesis. The Sunnybrook Facial Grading System [FGS][15] is a more A comprehensive scoring system for facial range of motion, which has a dedicated section for assessing the presence of synkinesia. [16] A 2015 systematic review of the facial nerve grading system determined that FGS met the most criteria for a global assessment of the facial nerve Functional sequelae and response to treatment. It was also determined to have the highest reliability. [17] FGS is sensitive enough to show gains as facial range of motion increases and human co-motion decreases. Joint Movement Assessment Questionnaire Consisting of nine questions, it has been shown to be valid and reliable as a specialized measure of synkinesis. [18] It has also been shown to correlate well with the synmotor component of FGS. Chuang and colleagues also developed a novel classification system consisting of four Category: [19] Mode I: Good smile (i.e., good range of motion) with mild synkinesis Mode II: Acceptable smile with moderate to severe synkinesis Smile with mild synkinesis method Scored synkinesis has not been evaluated in inter-rater and within-rater reliability studies, but in Chuang’s study it was shown to be a useful tool to aid in decision-making management. [19] Management/Intervention[edit | Edit source] Physical therapy intervention[edit | Edit source] Physiotherapy below Interventions have been shown to be effective in reducing or reducing synkinesis: neuromuscular retraining (NMR) [20][21] EMG biofeedback[22][23] non-physiotherapy interventions [edit | edit source] botulinum toxin Injection[24][25][26] Surgery: Rarely used – usually for severe Surgery used for synkinesis that is not responsive to physical therapy and botulinum toxin includes: selective neurolysis [27] selective myectomy [28] selective neurectomy [29] and transfacial nerve transplantation [30 ] Differential Diagnosis [edit | edit source] Synkinesis is a clinical diagnosis. usually easy Diagnosed patients will show clear facial motor linkages only on the affected side and have a history of facial paralysis. Sometimes it is confused with: Facial dystonia Primary blepharospasm Primary hemifacial spasmEdit Source] Facial Palsy UK has a comprehensive website, this page explains more about synkinesis.Neuromuscular Reeducation in Facial Palsy – PhysiopediaIntroduction Facial palsy day 3 When individuals recover incompletely after a facial disorder such as facial palsy, they may experience Various sequelae affecting its facial function. Common sequelae are: Asymmetry Muscle contractures Facial muscle weakness Synkinesia These sequelae can have an impact on the patient’s psychosocial well-being and quality of life. Therefore, it is important to implement effective Treatment to reduce the effects of persistent dysfunction. Neuromuscular facial re-education (NMR) is a treatment that has been shown to be effective in promoting the restoration of facial symmetric movements and eliminating or reducing functional deficits. [1][2][3] Basic concept edit Source] Facial motor expression and function are the result of a combination of different muscle contractions. Unlike skeletal muscles in other parts of the body, the facial muscles do not have a fascial wrap or tendons directly tethering them to the bone. Therefore their origin and insertion can Move freely. [4] They also lack the internal sensory receptors that normally provide intrinsic proprioceptive feedback. [4] Facial expressions result from any of the following:[4] Brain activity involving the motor cortex (i.e., cortical behavior) These expressions are often voluntary network activity subcortical nuclei and parts of the brainstem (i.e. subcortical behavior) these expressions are usually reactionary – i.e. in response to something happening (e.g. shocked laughter sneezing) edit source] because the facial muscles Provides little intrinsic information about posture and movement Without some feedback (e.g. using a mirror or surface EMG biofeedback), it is difficult for the patient to perform voluntary facial movements. [4] This feedback allows the patient to change muscle activity by increasing or decreasing Muscle contraction. [4] However, activation of facial muscles alone is not sufficient to restore facial expression. It has been suggested that since emotion produces specific facial muscle contractions to achieve reactive expressions (such as smiling through subcortical activity), it is possible Facial muscle activity may actually create or enhance mood. [4] Psychological distress is known to influence the relationship between impairment and disability in patients with facial palsy. [4] Therefore, retraining the muscles responsible for certain movements may be beneficial Expression rather than focusing on the recovery of facial movements. [4] From a practical standpoint, it is useful to consider incorporating facial exercises that focus on emotion and expression into rehabilitation programs. For example, ask the patient to recall that she/he had Have fun while practicing smiling to activate the positive effect markers associated with smiling. [4] Neuromuscular facial reeducation [Edit | Editorial source] Neuromuscular facial reeducation is: the process of relearning facial movements using specific and accurate feedback to facilitate (1) Facial muscle activity in functional patterns of facial movement and expression, and (2) inhibition of abnormal muscle activity that interferes with facial function. [4] It is based on patient education and the use of external feedback to enable re-education or physical learning. [1] As just mentioned Facial muscles lack intrinsic feedback information (i.e. they have no internal sensory receptors) and multiple muscle synergy can be produced by small contractions of individual muscles. Therefore, motor rehabilitation should be fine-tuned through neuroplasticity [1] to reduce Risk of developing abnormal movement patterns (ie synkinesis). [1] Physiotherapists must educate patients to ensure they are aware of their motor dysfunction and are able to identify patterns they want to achieve and patterns they wish to avoid. [1] This may reduce the risk to patients Facial palsy sequelae, especially when combined with extrinsic biofeedback, allows patients to alter muscle activity by: increasing muscle activation of muscles that must move but do not move decreasing muscle activation of muscles that do not have to move but do move Approach to treatment editorial source] Evidence supports the use of assessment tools that guide physical therapists in identifying specific treatment goals for each patient based on signs and symptoms or sequelae. The most commonly used assessment tools are: Facial Grading System (FGS) Facial Disability Index (FDI) House–Brackmann Scale Photoshop Method Therapy Classification [Edit | Edit source] Van Swearingen divided patients with facial nerve movement disorders into four treatment-based categories:[4] Initiation Facilitates Motor Control Relaxation priming (i.e., acute phase) [edit | edit source] Features[4][edit | edit source] Moderate to marked asymmetry at rest (eg, drooping face) Marked asymmetry with voluntary movements or other spontaneous expression and function unlinked Difficulty with motor facial functions, such as Eyes closed/blinking Eating Drinking Talking Little or no contraction of affected side Treatment[1][4][edit | edit source] Active assist exercises instruct patient to initiate movement with the aid of the hand and to perform small ranges of motion to prevent Contraction of the unaffected side Massage and stretching of the affected side to improve blood flow in the soft tissuesEdit source] Characteristics[4][edit | edit source] Moderate to moderate asymmetry at rest Patient can initiate movement, but if movement continues, asymmetry becomes apparent Some problems with eating, drinking and gargling with eyes closed (usually mild) Psychosocial problems at this stage are usually less treated than in the initial stage as symptoms are less severe[4][edit|edit source] Increased active and the resistance movement began in Aggressive assistive exercises to ensure that the unaffected side does not contract Once this movement improves, the patient can begin resistance exercises Education The patient must understand the importance of performing the exercise accurately rather than focusing on the number of exercises performed They must also be able to identify abnormal movement patterns that may develop motor control [edit | edit source] features[4][edit | edit source] asymmetry – more pronounced during movement than at rest by soft tissue contraction or contraction rather than weakness associated with movement produce Significant involuntary movement of facial areas while performing any movement or facial expression Abnormal movement patterns during facial functions, such as difficulty opening eyes when speaking, yawning or eating, or biting the inside of the cheek Treatment[1][4][edit]Edit source ] Massage and stretching of facial contractions Create non-synergic movements and facial expressions in the short term This can be achieved with small movements or receiving very little synkinetics Long-term instructing patients to relearn isolated muscle contractions so that Reduced activation of abnormal motor patterns As patients relearn appropriate activation patterns, they are reclassified into facilitative groups for the rehabilitation process Relaxation[edit|edit source] Features[1][4][edit|edit source] marked as asymmetrical Facial posture at rest is combined with spontaneous twitches and spasms of the facial muscles. These spasms are more frequent and larger during movement, so patients often limit movement to prevent spasticity. Muscle weakness is usually not a significant problem on the unaffected side. 50 Percentage of voluntary movement, which causes soft tissue contractures or tension on the affected side Psychosocial problems are common, as patients often worry about controlling facial spasms Treatment[1][4][edit]edit source] Relaxation exercises such as Jacobson relaxation method Technique Alternating rhythmic movements Muscle inhibition techniques, including sustained stretching or deep friction massage Examples of specific exercises [edit | edit source] Face centering exercises [edit | edit source] Activation of the upper portion of the orbicularis labii levator muscle The inner part of the mouth (i.e., the zygomatic muscle group) and the orbicularis muscle, the patient is instructed to:[4] Suck on the cheek between the teeth Wrap the lips around the teeth making a sustained “ffff” sound Blow through a straw as these muscles accompany facial features Examples include smiling and speaking sounds and expressions such as disgust or confusion [4], the following exercises may be helpful. [4] Bring eyebrows together while blowing, as if thinking Blow and transition to ffffff” sound Continue to alternate these movements while maintaining air Make the sound fffff” by moving your lips and add a smile.[4]Exercise Restoration of eye closure [edit | edit source] It is important to ensure restoration of the joint downward movement of the eyeball and closure of the upper eyelid. When the eyes are closed, the eyeballs usually rest in a downward position. [4] This happens as follows: [4] The levator muscle allows the upper eyelid to descend (i.e. close) The superior rectus muscle contracts immediately after the upper eyelid relaxes, thereby moving the eye upwards A brief contraction of the orbicularis muscle inhibits the superior rectus to prevent this upward movement Eyeball replaces When the orbicularis oculi muscle is weak when the eyes are closed, the eyeball moves upward. This affects the ability of the upper eyelid to droop. This phenomenon is known as the Bell phenomenon and can persist Post-reinnervation/recovery of facial movement. [4] To help with this, patients can be instructed to: look down and close eyes – continue to look down and squint – look down and close eyes home exercise program [edit | edit source] and one-on-one therapy sessions,it can be It is useful to include a home exercise program to help patients strengthen facial motor patterns for motor learning. These exercises should only be practiced at home if the patient is able to perform them accurately (and recognize any inaccuracies). A typical procedure will:[4] Consists of 3 to 5 exercises 5 to 10 repetitions 2 exercises per day It can be divided into two categories based on type Location of incidental pathology: Central facial nerve palsy due to injury above the nucleus of the facial nerve Peripheral facial nerve palsy due to injury at or below the nucleus of the facial nerve [1] Clinically relevant anatomy [edit | edit source] For more details on facial nerve anatomy, see See the facial nerve page. The nucleus of the facial nerve is located in the pons. It takes a rather winding route before exiting the skull through the stylomastoid foramen. It then splits into 5 branches through the parotid gland: Temporal Zygomatic Buccal Mandibular Cervical muscle. Causes of Peripheral Facial Paralysis [Edit | Edit Source] Upper Motor Neuron Causes: [Edit | Edit Source] Stroke Intracranial Tumor Multiple Sclerosis Syphilis HIV Vasculitis Bleeding [2] Lower Motor Neuron Causes [Edit | Edit Source] Special paroxysmal or Bell’s palsy which is the most Common causes of facial paralysis. Its etiology is unknown [3][4], but is likely related to herpes simplex virus infection. [5] Tumor Compression of the facial nerve by a tumor can cause facial paralysis, but more commonly the facial nerve is damaged during surgical removal of the tumor. most common tumor Acoustic neuromas (also known as vestibular schwannomas) are causing facial nerve palsy during surgical resection. Less common tumors that cause facial paralysis (or surgical removal of them) include cholesteatoma, hemangioma, facial schwannomas, or tumors of the parotid gland. Infected with Ramsay Hunt Syndrome – by Shingles infection. This is a syndrome of facial palsy herpetiform vesicular eruption and vestibulocochlear dysfunction. Patients with Ramsay Hunt syndrome generally have a higher risk of hearing loss than those with Bell’s palsy and the course of the disease Illness is often more painful. Recovery from facial paralysis is also lower in patients with Ramsay Hunt syndrome [6][7] Lyme disease – caused by infection with Borrelia burgdorferi from tick bites. About 10% of people with Lyme disease develop facial paralysis – 25 Bifacial palsy occurs in % of these patients[8] Iatrogenic facial nerve injury is most common in temporomandibular joint replacement mastoidectomy and parotidectomy[9] Trauma especially temporal bone and mastoid fractures[1] Congenital very few baby is born Congenital facial nerve dysfunction. Rare causes include: Neurosarcomatosis Otitis media Multiple sclerosis Moebius syndrome Melkersson-Rosenthal syndrome Guillain-Barre syndrome Millard-Gubler syndrome (also known as ventral pontine syndrome) Hemiplegia with ipsilateral corticospinal tract and lateral rectus paralysis due to involvement of abducens nerve Foville syndrome (aka medial inferior pontine syndrome) Eight-thirty syndrome facial palsy with internuclear ophthalmoplegia and horizontal gaze palsy risk factors [Edit | Edit source] Diabetes [10] Pregnancy may lead to elevated blood pressure and increased fluid load due to hypercoagulable state Viral infection and immunosuppression [11 ] ear infection on Respiratory Infection Obesity[1][12][13] Clinical Manifestations[edit | edit source] Paralysis of muscles innervated by the facial nerve occurs on the affected side of the face as follows: Appearance and range of motion [edit | edit source] Inability to close eyes unable to move Lips (for example, puckered up when smiling) When at rest, the affected side of the face may droop. However, if the person is in synkinetic state, the affected side of the mouth may be higher than the unaffected side. Facial synkinesis is defined as “abnormal facial movements that occur in a voluntary or voluntary process Movement, such as voluntary movement of the mouth may cause the eyes to close”[14] Ectropion—that is, the lower eyelid may droop and turn outward Functional impact [edit | edit source] Difficulty eating and drinking as the lack of a lip seal makes it difficult to retain fluids and food In the oral cavity Speech intelligibility is reduced as labial consonants (i.e. b p m v f) all require lip seals Affected eyes are dry – see here for more on this] The facial nerve is the lacrimal, salivary and The muscle that goes to the stapes (stapes) in the middle ear. It also conveys taste sensations from the first two-thirds of the tongue. Facial palsy usually involves: Lack of tear production in the affected eye leading to risk of dry eye and corneal ulcers Two factors lead to Dry eye due to facial nerve palsy: The greater petrosal nerve from the facial nerve is affected – it supplies the parasympathetic autonomic component of the lacrimal gland, which controls eye moisture/tear production The zygomatic branch of the facial nerve supplies the orbicularis muscle Ocular and resulting paralysis resulting in inability (or reduced ability) to close or blink. As a result, tears (or artificial lubricant in the form of drops of gel or ointment) do not distribute properly over the cornea Hyperacusis – that is, sensitivity to sudden loud noises Changes in taste Manifestations of flaccid facial paralysis at rest [edit | edit source] In the early stages of peripheral facial paralysis, whatever the cause, the following differences are usually evident between the two sides of the face: No horizontal line across the forehead on the affected side affected eyes Larger/more open than unaffected Affected eyes do not blink Change in position on affected side or no nasolabial folds Affected corner of mouth is lower than the other The inset here shows left-sided flaccid facial paralysis: Bell Shi Phenomenon [edit | edit source] Differential diagnosis [edit | edit source] Upper motor neurons vs lower motor neurons [edit | edit source] If the forehead is not affected (ie, the patient is able to fully lift the eyebrow on the affected side), then the facial paralysis is likely to be due to the movement Neuronal (UMN) damage. [4] Paralysis including the forehead that prevents the patient from raising the affected eyebrow is a lower motor neuron (LMN) lesion. However, caution is advised in using preserved forehead function to diagnose central lesions. Patient may retain forehead Damage to the pontofacial nucleus with selective damage to the temporal bone or damage to the nerves that distribute the face. It is worth remembering that cortical lesions leading to lower facial paralysis/paresis are usually movement related Ipsilateral tongue defect and thumb finger or hand weakness. [15] [16] Bell’s palsy and Ramsay Hunt syndrome [edit | edit source] Diagnostic procedures [edit | edit source] Laboratory investigations including audiogram nerve conduction studies (ENoG) calculations Computed tomography (CT) or magnetic resonance imaging (MRI) electromyography (EMG) [17][18] According to clinical guidelines from Baugh and colleagues 2013, clinicians should not perform routine laboratory and imaging in patients with new-onset Bell’s palsy Scientific inspection[13] Outcome measures[19][edit | edit Source] Sunnybrook Facial Grading System [20] is often favored by physiotherapists due to its sensitivity and synmotor components Results are expressed as a percentage (using the unaffected side of the face for comparison) and thus intuitively easy to understand facial areas Each of the five standard expressions was assessed using: Eyebrow Raised Eyes Closed Open Mouth Smile Lips Puckered Growling/Bracketing House-Brackmann Facial Rating Scale Linkage Assessment Questionnaire Linear Measure Index Facial Disability Index Lip Length (LL) and Nose (S ) indices Five-point scale of management/intervention [edit | edit source] Medical and surgical treatment depends on the etiology of the facial paralysis. Medical Management Editorial Source] Medical management of these conditions is discussed more in the linked pages, but Bell’s palsy and Ramsay Hunt The syndrome was treated with corticosteroids (prednisone) within 72 hours of onset. [21][4] This can be accompanied by antiviral drugs. [22][23][24] Surgical management [edit | edit source] As discussed in the linked page, tumors such as acoustic neuromas and facial schwannomas occur frequently Surgery. Patients at high risk for corneal ulcers may be offered oculoplastic surgery to protect the eyes. For patients with severe facial paralysis and no nerve function, a variety of surgical procedures are available. These fall into the following categories:[25] Facial rejuvenation surgery Facial restorative surgery involving nerve grafting or anastomosis involving muscle displacement Static surgery (i.e. plastic surgery) used to improve symmetry at rest but not in motionEdit source] Most important in the early stages of facial paralysis What to do is to check that the patient is caring for the affected eye in a proper manner. Because the facial nerve is responsible for providing lubrication to the cornea, patients are at high risk of developing dry eye during the first weeks and months of facial nerve palsy. This puts them at risk of Corneal ulcers can cause impaired vision in the affected eye. Therapists should educate patients on dry eye management if other healthcare providers have not done so. Urgent referral if the eye appears red or the patient reports frequent redness Need ophthalmology. Alternatively, they should be referred to the emergency department of an eye hospital. For more information on dry eye, including the risk of manifestations and management of corneal ulcers (e.g. taping/use of artificial lubrication), click here. other physical therapy Includes: Neuromuscular Retraining (NMR) [26][27] For more information on this concept, see the page on Neuromuscular Retraining in Facial Paralysis Electromyography (EMG) and mirror biofeedback [1][28] Stimulation (TES) [29] Proprioceptive neuromuscular facilitation (PNF) Techniques[12] Kabat Techniques[30] Mime Therapy[31] Includes the following treatments:[32] Self-massage Breathing and relaxation exercises to enhance coordination on both sides of the face and reduce synkinetic exercises to help the eyes and lips Practice closed letters Words and facial expression Evidence for practicing physical therapy [edit | edit source] Physical therapy for Bell’s palsy is recommended (weak recommendation) according to clinical practice guidelines [13][33] and neuromuscular re-education techniques were found to be effective in increasing facial extent Movement and symmetry and reduction/minimization of synkinesis[26][34][35][36] Mime therapy improves function in patients with facial paralysis It was found to improve synkinesis and facial asymmetry at rest and Facial symmetry during voluntary movements [19][31] Electrical stimulation is controversial[1][37][38] One study found PNF technique to be more effective than regular exercise[12] One study found PNF and Kabat technique to be more effective than no exercise[30] Complications and sequelae[edit| Edit Source] Synkinesis (aka Anomaly regeneration) occurs after facial nerve injury. Synkinesia occurs in the setting of axonal disruption (i.e. facial nerve injury) and is therefore a normal sequelae of facial nerve injury. Physiotherapy can be very helpful in controlling synkinesis especially neuromuscular retraining Technique and mirror feedback exercises. Effects on quality of life [edit | edit source] A large retrospective study of 920 patients in 2018 investigated the association between the severity of facial paralysis and quality of life. [39] concluded that the severity of facial paralysis Quality of life was found in a large number of patients including various etiologies. In addition, new factors predicting quality of life in patients with facial paralysis were revealed. [39] A 2011 study presented a set of photographs of 40 people with and without facial paralysis Facial paralysis asked viewers to rate photos based on the emotions of the people in them [40]. The results of this survey were interesting: patients with facial paralysis were consistently rated as having negatively affecting performance (i.e., Negative emotions, such as sadness) most of the time. In fact, facial palsy patients are often very aware that even when I am happy, I now look miserable. Resources [edit | edit source] Facial Palsy UK Bell’s Palsy Association NHS Information about Bell’s Palsy Facial Nerve Palsy UK Group This link leads to an introductory video on the effects of facial nerve palsy Facial Nerve Introduction – Physiopedia Introduction to the facial nerve and its process functions and weaknesses are essential to the optimal management of any facial nerve palsy. this The facial nerve (cranial nerve VII) is one of the most important and continuously used nerves in the body, connecting at least 21 muscles to the brain and providing motor innervation to the facial expression muscles that are also involved in chewing speech and our facial expressions Emotional [1][2] The anatomy of the facial nerve is very complex and is often described as an intracranial temporal bone and an extracranial nerve based on its relationship to the skull or temporal bone. [1][2][3] Exploring the course of the facial nerve also highlights its possible weaknesses This in turn may lead to the development of facial paralysis. A very simple explanation of the course of the facial nerve is discussed in the next section to enhance the understanding of its potential site of injury and its effects. Intracranial course of the facial nerve[edit | edit Source] Proximity of facial and vestibulocochlear nerves The facial nerve exits the pons as two separate roots, a motor root called the facial nerve intrinsic and a combined sensory and autonomic root called the intermediary nerve, which crosses the cerebellar pons before it enters brain angle The inner auditory canal/canal of the temporal bone. [1][4] At the inner auditory canal, the facial nerve is next to the vestibulocochlear nerve (also known as the auditory/auditory/8th cranial nerve pair), with intervening intervening nerves. [1] It is near The auditory nerve (8th cranial nerve) at this point may injure the facial nerve. Benign slow-growing tumors called acoustic neuromas (vestibular schwannomas) occasionally grow on the auditory nerve that require surgical removal. [5] Due to the proximity to the auditory nerve During the surgical removal of an acoustic neuroma, the facial nerve can easily be damaged, resulting in facial nerve palsy. [5] In rare cases, growing tumors can also put pressure on the facial nerve, causing facial paralysis. Intratemporal course of facial acoustic neuroma (vestibular schwannoma) Nerves [edit | edit source] At the floor of the nasal passages, the motor root (proper facial nerve) and the intermediary nerve enter the facial canal (fallopian tube), where it merges to form the facial nerve. The facial nerve then forms the geniculate ganglion and 3 small nerve branches originate:[1][4] Petrous Nerve – This supplies parasympathetic nerve fibers to the lacrimal glands of the eyes and the mucous membranes and palate of the nasal cavity Sensory fibers that provide taste sensation to the anterior 2/3 of the tongue and parasympathetic fibers to the submandibular and sublingual salivary glands. The facial nerve then exits the oviduct/facial canal and exits the skull through the stylomastoid foramen of the temporal bone. Due to the nerve’s proximity to the temporal bone, any temporal bone fracture can result in damage to the facial nerve. It is also useful to consider the bony fallopian/facial canals with their long Z-shaped course (3 cm). Bone canals considered as possible entrapment sites Swelling of the nerve, especially when there is insufficient space for the nerve and loss of nerve conduction at the same time. Extracranial course of the facial nerve[edit | edit source] Outside the skull, the facial nerve turns forward and enters The posteromedial surface of the parotid gland, which divides into the temporofacial and cervicofacial divisions, contains five sets of terminal branches that provide the motor supply for the muscles of facial expression. [1] There is a high degree of variability between these terminal branches due to Various peripheral branches and intercommunication between different terminal branches. [6] The complex anatomical relationship of the facial nerve and parotid gland is another vulnerable site for facial paralysis, especially in cases of parotid swelling (as in parotitis) or Parotid gland surgery (parotidectomy). [4][7][8] Facial nerve terminal branches and their proximity to the parotid facial nerve in the facial canal Discussion of anatomical sites where the facial nerve may be damaged Bell’s palsy is the most common Common causes of facial paralysis. The cause of Bell’s palsy is unknown, but reactivation of the herpes simplex virus (cold sore virus) in the geniculate ganglion is suspected to be the most likely cause. [9][10] Post-mortem studies identified underlying pathophysiology for vascular Expanding inflammation and swelling that subsequently compresses the nerves in the narrowed fallopian tubes. The ensuing hypoperfusion (strangulation) and ischemia of the facial nerve leads to damage to axons and myelin, resulting in neurological dysfunction. [9] Diagnosis of [10] Bell’s palsy is still mostly clinical and there are several other conditions to consider in the differential diagnosis, among them stroke (upper motor neuron lesion – patient is still able to wrinkle forehead) and herpes zoster (Ramsay Hunter syndrome) most relevant. [9][10] Recovery After facial nerve injury [edit | edit source] After facial nerve injury, there is an initial period of flaccid paralysis, after which many patients return to movement. [11] The recovery of the facial nerve depends on the degree of damage it receives and the distance it needs to regenerate. anatomical The site of nerve injury can also have a profound effect on the timescale over which damaged nerve fibers regenerate. Considering the rate of axon regeneration at 1 mm/day (1 cm/month), the farther degenerated axons have to regenerate, the longer it will take them to reach the target muscle. Therefore, when setting recovery expectations, one should keep in mind the distance required to regenerate, whether it is a shorter distance such as from the parotid gland (3-4 months) or a shorter terminal branch of the facial nerve (zygomatic bone to eye or cheek to cheek) (5-7 months) injured Longer axons or longer nerve branches from the ear canal, such as the forehead, following Bell’s palsy or Ramsay Hunt syndrome (herpes zoster virus similar lesion site and timescale) or acoustic neuroma surgery The temporal branch of the chin or the mandibular branch of the jaw. It is also useful to keep tertiary nerve damage in mind as it also directly affects the recovery time frame of the nerve: Neuropraxia – temporary loss of function No permanent damage Movement returns to normal within 6-8 weeks Axon rupture – outer sheath intact, But the axon Injury leads to neurodegeneration. Nerve regeneration/regrowth is known to occur at a rate of 1 mm/day (1 cm/month). Nerve rupture – complete severed nerve, requiring surgical repair. Therefore, immediate treatment of Bell’s palsy is primarily aimed at reducing Nerves are swollen to prevent axonal damage, and 10 days of steroids are started within 72 hours of the onset of paralysis. [9][10] Approximately 71% of patients with Bell’s palsy are expected to recover normally, while approximately 30% will suffer an axotomy injury with delayed recovery Recovery of muscle function (5-6 months). [9] Initially, these patients will be able to close their eyes and begin to move their mouths to smile, but have not yet raised their eyebrows, because the temporal branch of the nerve is much longer than that of the buccal or zygomatic branches, and thus requires It takes longer to regrow. A small number of patients may experience delayed recovery following facial nerve injury followed by synkinesia. [10][11] It occurs in the vast majority of people with axotomy injuries to the facial nerve. Facial linkage is defined as “abnormal Facial movements that occur during voluntary or spontaneous movements, such as voluntary movement of the mouth that may cause the eyes to close. [11] Although the exact mechanism of synkinesia is unknown, it has been suggested that it develops as a result of abnormal regeneration of the face Nerves during recovery lead to “miswiring” of the nerves. [11] Synkinesis occurs when more axons reach the muscle, so it only becomes apparent later in the recovery phase around the 3rd month of parotid surgery, 5-6 months in Bell’s palsy, and even later hearing loss Neuroma surgery (6-9 months) due to axonal length. Facial Nerve and All Its Branches Resource[edit | Editorial source] Facial Nerve Facial Paralysis Raslan A Volk GF Möller M Stark V Eckhardt N Guntinas-Lichius O. High variability in innervation of the facial muscles by branches of the facial nerve: a Prospective electrical stimulation study. laryngoscope. 2016 Jun;127(6):1288-95. DOI: 10.1002/lary.26349 Takezawa K Townsend G Ghabriel M. The facial nerve: anatomy and related disorders for oral hygiene professionals. dentistry. 2018 Apr;106(2):103-16. DOI: 10.1007/s10266-017-0330-5 platysma muscle – PhysiopediaSearch Search Search Toggle navigation pPhysiopedia pPhysiopedia About News Contribute Course Resources Categories loading… When citing evidence in academic writing, you should always try to cite the main (original)