Bell palsy (BP) is an idiopathic, unilateral or ipsilateral, acute weakness of the face in a pattern consistent with peripheral facial nerve dysfunction and paralysis of the seventh cranial nerve with an onset that is rapid and unilateral. Bell’s palsy causes a peripheral lower motor neuron palsy, which manifests as the unilateral impairment of movement in the facial and platysma muscles, drooping of the brow and corner of the mouth, and impaired closure of the eye and mouth. The diagnosis is one of exclusion and most often made on physical exam. The facial nerve has both an intracranial, intratemporal, and extratemporal course as its branches. The facial nerve has a motor and parasympathetic function as well as taste to the anterior two-thirds of the tongue. It also controls salivary and lacrimal glands. The motor function of the peripheral facial nerve controls the upper and lower facial muscles.

Anatomy of the Facial Nerve

The course of the facial nerve can roughly divide into three portions – origin, infratemporal, and extratemporal.

(a) Origin

The motor nucleus of the facial nerve originates within the lower pons and emerges via the cerebellopontine angle (anterior to the anterior inferior cerebellar artery). Here in its intracranial course, it is joined by the nerves intermedius, which consists of the sensory and autonomic fibers of the facial nerve, which originate from the tractus solitaries and superior salivatory nucleus respectively.

The facial nerve then inserts into the internal acoustic meatus (IAM) to begin its meatal segment. The IAM is in the petrous part of the temporal bone between the posterior cranial fossa and the inner ear. Within the intracranial and meatal segments, no branches are given off.

At the IAM, the facial nerve runs in the anterosuperior compartment. Important structures within the IAM are:

  • Superior vestibular nerve
  • Inferior vestibular nerve
  • Facial nerve
  • Cochlear nerve
  • Labyrinthine artery
  • Vestibular ganglion    

(b) Intratemporal

  • Labyrinthine segment – between the IAM+ the geniculate ganglion/first Genu. This area forms the narrowest portion of the facial nerve (and consequently vulnerable to compromise). At the level of the geniculate ganglion, the facial nerve undergoes the first of two sharp bends (first genu).  At this genu, the greater petrosal nerve branches off from the main trunk. The greater petrosal nerve provides preganglionic parasympathetic fibers to the pterygopalatine ganglion (also known as the vidian nerve). The pterygopalatine ganglion provides postganglionic parasympathetic fibers to the lacrimal, nasal, and palatine glands. Proximal lesions are associated with impaired lacrimation, hyperacusis, and loss of taste on the anterior two-thirds of the tongue.
  • Tympanic segment – between the geniculate ganglion and the second genu. The facial nerve traverses the bony fallopian canal on the medial aspect of the tympanic cavity before its second sharp bend (genu). Important relations of the facial nerve at this point include:
  • Anteriorly – Processus cochleariformis (where tensor tympani tendon gets directed to the malleus).
  • Posteriorly – oval window (inferiorly) and the lateral semi-circular canal (superiorly).  The facial nerve runs between the malleus and incus (running medial to the malleus and lateral to the incus).
  • Mastoid segment – from the second genu to the stylomastoid foramen.  After its second genu, the nerve now runs on the posterior aspect of the tympanic cavity. It runs in front and lateral to the ampulla of the posterior semicircular canal and medial to the tympanic annulus.  The chorda tympani runs anteriorly across the tympanic cavity to provide preganglionic parasympathetic fibers to the submandibular ganglion, which then provides parasympathetic innervation to the submandibular and sublingual glands.

To summarise the three important branches of the facial nerve given off before the nerve leaving the stylomastoid foramen are (GCS):

Branch/Segment of facial nerve/Target
  • Greater petrosal nerve, Labyrinthine, Pterygopalatine Ganglion (palatine, nasal and lacrimal glands)
  • Chorda Tympani,Mastoid, Submandibular Ganglion (submandibular and sublingual glands)
  • Stapedius, Mastoid, Stapedius

(c) Extratemporal

The nerve travels inferiorly and laterally around the styloid process. Prior to entering the parotid gland, it gives off branches to the three following muscles:

  • Occipitalis
  • Stylohyoid
  • Posterior belly of digastric

Within the parotid gland, the nerve divides the gland into superficial and deep parts. It lies the most superficial structure traversing the parotid gland. Ordered from superficial to deep, the structures within the parotid gland are:

  • The facial nerve (superficial) —> Retromandibular vein —> External Carotid Artery —> Auriculotemporal Nerve (deep)

Within the substance of the parotid gland, it divides into two trunks (cervicofacial and temporofacial) and then five main branches which each are responsible for innervation of the muscles of facial expression. The five branches with their target muscle and action are below :

Branch of the facial nerve, Primary target muscle, Clinical assessment
  • Temporal, Frontalis, Raise eyebrows
  • Zygomatic, Orbicularis oculi, Close eyes
  • Buccal, Puff cheeks out
  • Mandibular, Depressor anguli oris, Show bottom teeth
  • Cervical, Platysma, Clench neck

To summarise, the facial nerve innervates the following muscles

  • Stapedius
  • Stylohyoid
  • Posterior belly of digastric
  • Occipitalis
  • Muscles of facial expression

The most important factor when considering the differential diagnosis of facial nerve palsy is whether the lesion is a lower motor neuron or an upper motor neuron.

Due to bilateral cortical innervation of the muscles of the upper face (in particular orbicularis oculi and frontalis), only lower motor neuron lesions will result in complete facial paralysis, although this is not always the case. Consequently, the most clinically useful assessment of UMN vs. LMN facial nerve palsy is the raising of the eyebrows which assess the frontalis and orbicularis oculi.

Causes of Bell’s Palsy

Idiopathic/Bell Palsy (70%) – Most commonly, the cause for facial nerve palsy remains unknown and has the name ‘Bell palsy. It usually presents as a lower motor neuron lesion with total unilateral palsy.  Damage to the nerve from compression within the bony canal can lead to edema and secondary pressure resulting in ischemia and reduced function. Recovery can take up to 1 year and is incomplete in as much as 13% of patients.

Trauma (10 to 23%) – Fractures involving the petrous part of the temporal bone and facial wounds transecting the branches of the facial nerve can cause facial nerve palsies. It takes an incredibly large force to fracture the temporal bone, and the clinician must look for signs such as hemotympanum, battles sign, and nystagmus. Temporal bone fractures usually occur unilaterally and are classified according to the plane of fracture along the petrous ridge (i.e., longitudinal vs. transverse.  Additionally, iatrogenic injury during otological, parotid and acoustic neuroma surgery can result in traumatic damage to the facial nerve and stretch injury. Clinical history is vital in identifying the likely cause.

Infection

  • Viral (4.5 to 7%) – Herpes Zoster infection resulting in facial paralysis due to geniculate ganglions (also known as Ramsay Hunt syndrome (RHS). The virus remains dormant in the geniculate ganglion. The geniculate ganglion also receives innervation from the glossopharyngeal nerve (CN IX). Consequently, the active virus can produce a prodromal period of otalgia and vesicular eruptions within the external auditory canal as well as the soft palate (distribution of CN IX). Additionally, up to 40% of patients with RHS develop vertigo due to the involvement of cranial nerve VIII (vestibulocochlear nerve).  Outcomes are much worse than with Bell palsy, with just 21% recovering within 12 months.
  • Bacterial – Acute otitis media can cause dehiscence within the facial canal resulting in nerve paralysis. Additionally, cholesteatomas and necrotizing otitis externa can cause facial nerve palsies.  A rare cause of facial nerve palsy is Lyme disease, with symptoms such as a tick bite, fatigue, headache arthralgia, and erythema migrans occurring between 1 to 2 weeks after tick exposure. Cardiac involvement (myopericarditis)  and arthritis can also occur as part of the syndrome. IgM + IgG serology is vital in these patients from an investigative standpoint. Any patient presenting with a history of erythema migrans and foreign travel exposure requires immediate investigation for Lyme disease.

Neoplasia (2.2 to 5%)

A slowly progressing onset of facial palsy should raise the suspicion of malignancy and prompt a full and thorough head and neck examination. Malignancies resulting in facial nerve paralysis include (but are not exclusive to) parotid malignancies, facial and acoustic neuromas, meningioma, and arachnoid cysts. These will all present with varying degrees and manifestations of facial nerve palsy due to the relative location of the tumor.

Facial Nerve Palsy in Children

The causes of facial nerve palsy in children classified as either congenital or acquired. Acquired causes are the same as in adults as described above, and all of the above etiologies can occur in children.

Congenital causes include

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

It is worth noting that surgical decompression of the facial nerve within the labyrinthine segment is not recommended for the pediatric population as research has failed to demonstrate beneficial outcomes, and there is a significant risk of sensorineural hearing loss with the procedure. However, nerve grafts and muscle transfer techniques may still be options for this cohort.

Bilateral Facial Nerve Palsy 

Bilateral facial nerve paresis is an uncommon but essential branch of facial nerve palsy, occurring in between 0.3 to 2% of all facial nerve palsies. Bilateral palsy is important as it is much more likely to represent a systemic manifestation of the disease, with under 20% of cases being idiopathic. Lyme disease represents a significant portion of bilateral facial nerve palsies, accounting for around 35% of cases. Other important differential considerations include Guillain-Barre syndrome, diabetes, and sarcoidosis. Neurological causes of bilateral facial nerve palsy include Parkinson’s disease, multiple sclerosis, and pseudobulbar/bulbar palsy.

Symptoms of Bell’s Palsy

Mild pain in or behind the ear, oropharyngeal or facial numbness, impaired tolerance to ordinary levels of noise, and disturbing taste on the anterior part of the tongue.

  • Weakness or paralysis of the upper and lower facial muscles of the affected side
  • Drooping of ipsilateral eyelids
  • Inability to close the eye completely
  • Dry eye due to inability to close eyes completely
  • Excessive tearing of the eye (epiphora)
  • Drooping of the corner of the mouth
  • Ipsilateral impaired loss of taste sensation
  • Difficulty with eating due to ipsilateral muscle weakness causing food to be trapped on the affected side of the mouth
  • Dribbling of saliva
  • The altered sensation on the affected side of the face
  • Pain in or behind the ear
  • Increased sensitivity to sound (hyperacusis) on the affected side if stapedius muscle is involved
  • Sparing of movement in the upper face (central pattern), or weakness of a specific branch of the facial nerve (segmental pattern), suggest an alternative cause. Bell’s palsy is less commonly the cause of facial palsy in children aged under 10 years (<50%).

Diagnosis of Bell’s Palsy

Physical examination

The key physical examination to find is a partial or complete weakness of the forehead. If forehead strength is preserved, and active a central cause should be investigated. Patients may also complain of a difference in taste, sensitivity to sound, otalgia, and changes to tearing and salivation, and more.

Ocular features include

  • Corneal exposure
  • Lagophthalmos
  • Brow droop
  • Paralytic ectropion of the lower lid
  • Upper eyelid retraction
  • Decreased tear output
  • Loss of nasolabial fold

Testing facial movements – It helps to distinguish between an upper (the forehead will be spared) and lower (entire facial movements are compromised) motor neuronal lesion and sensory lesion. The degree of facial nerve paralysis is evaluated using the House-Brackman grading system.

      Grade          Definition

  • I               Normal symmetrical function throughout are observe
  • II              Slight weakness on close inspection + slight asymmetry of smile problem.
  • III             Obvious non-disfiguring weakness, complete eye closure may be found.
  • IV              Obvious disfiguring weakness, cannot lift the brow, incomplete eye closure, severe synkinesis.
  • V               Barely seen motion, incomplete eye closure, a slight movement of corner of the mouth, absent synkinesis
  • VI              No movement, atonic

Importantly, the difference between grades 3 and 4 is eye closure.

Additional tests that may be used to assess the lesion of the facial nerve clinically are as follows

  • Blink test (corneal reflex) – It is a manual test that is performed when tapping on the patient’s glabella, a suspension in blinking will occur on the affected side (the ophthalmic division of trigeminal nerve controls afferent limb, and the efferent limb is the temporal and zygomatic branch of the facial nerve).
  • The trigeminal blink reflex test – THe test is the only test to measure the intracranial pathway of the facial nerve and also a useful test to study various post paralysis sequelae such as synkinesis and hemifacial spasms, and face muscle spasticity. With the recovery of facial function and motor movement, the ipsilateral R1 latency becomes less prolonged and the amount of initial prolongation of this response correlates with greater loss of facial motor function.
  • Schirmer test (assessing lacrimation of the lacrimal gland) – It is lacrimation will be decreased by 75% compared to the normal side of your face using a folded strip of blotting paper in the lower conjunctival fornix portion.  It is important to note that a unilateral lesion or bilateral within the geniculate ganglion can produce bilateral lacrimal deficiencies.
  • Stapedial test – This involuntary reaction in response to high-intensity sound stimuli causes contraction of the stapedius muscle and gets mediated by the facial nerve function. Testing of the stapedius muscle reflex can be performed using tympanometry.
  • Salivary Test – Salivation rate is assessed to confirm virus infection from a submandibular duct following stimulation with a 6% citric acid solution. If positive, there will be a reduction in salivation by 25% at the affected side and it also indicates a lesion at or proximal to the root of the chord tympani.
  • Taste test – It is done manually by using salt sweet, sour, and bitter tastes along with the lateral aspects of the anterior two-thirds portion of the tongue. The positive result will also indicate a lesion at or proximal to the root of the chord tympani.
  • Examine the ear – It is done externally to ensure no evidence of otitis externa, otitis media, chronic otitis media, or cholesteatoma, etc. The presence of vesicles may indicate Ramsay-Hunt syndrome.
  • Examine the parotid gland – It is done for any masses that may reveal a parotid malignancy, trauma, cyst formation.  Examination of the oral cavity for parapharyngeal swellings edema and vesicular eruptions is also considered essential in bell’s palsy.
  • Examine the eye – It is initially to establish closure of the lid. If the eye is unable to fully close, then urgent ophthalmology referral and provision of eye protection equipment is advised.

Lab Tests

  • Bloods – Blood tests such as a full blood count, urea and electrolytes, and a C-reactive protein is necessary for all patients admitted to the hospital due to an infectious cause of facial palsy. Varicella-zoster virus antibody titers would appear elevated in RHS. IgG and IgM would become elevated in Lyme disease.
  • Electrophysiological tests – It is suitable for prognosis; however, they are expensive, time-consuming, and has a short time to be useful (less than three weeks after symptom onset)
  • Minimal to maximal stimulation tests – It is the facial nerve stimulated with a low current on the affected side and gradually increased until maximal response or patient tolerability. This response then gets compared to the unaffected side with a 4-stage grading system. The test is positive if there is a clinically significant difference between the two sides.
  • Electroneurography (ENOG) – It is done to establish muscle action potential amplitude and is the most accurate at determining the level of palsy. It involves facial nerve stimulation around the level of the stylomastoid foramen and the detection of a motor response near the nasolabial fold. This response then gets compared with the normal side.
  • Electromyography (EMG) – It is determined activity within the facial muscles through the detection of fibrillation potentials that only manifest after around three weeks of denervation. The needle electromyography may be employed to confirm any subclinical signs of re-innervation, thus acting as a prognostic indicator for the possibility of recovery [rx].
  • Magnetic Stimulation – It is tested infratemporal and brain stem aspects of facial nerve through transcranial stimulation. The test needs to be performed immediately as Wallerian degeneration of the nerve will alter the result findings. Magnetic stimulation can be beneficial for intertemporal facial nerve injury where axonal integrity remains, as proximal site stimulation with higher than usual stimulus intensities overcome the block at the injury site and allow facial nerve activity to occur.
  • An audiogram – should be performed semi-urgently to determine the type of any associated hearing loss and the degree. If the auditory nerve is paralyzed with bells’ palsy then the test is done.

Imaging

  • CT scan –  If necrotizing or injury and inflammation of otitis externa or a complication of middle ear infection are suspected, or there is a history of head trauma or suspicion of malignancy, a CT of the temporal bones is necessary.
  • MRI  – It is scanning for use and the detection of infratemporal lesions that may be resulting in compression of the facial nerve and particularly useful for imaging the cerebellopontine angle in your brain. MRI scans may also identify the enhancement of the facial nerve around the geniculate ganglion.
  •  Gadolinium-enhanced MRIs – are useful in ruling out neoplasms. It is suggested that any case of BP without resolution within 4 months or first presenting 4 months after symptom onset undergo contrast-enhanced imaging of the parotid gland, temporal bone, and brain. [rx]
  • The nerve excitability test – determines the excitation threshold by recording the minimum electrical stimulus required to produce visible muscle contraction.

Treatment of Bell’s Palsy

The following treatment plan is available for the treatment of bell’s palsy

Non-Pharmacological treatment

  • Eyecare – Eyecare of patients with Bell’s palsy focuses on protecting the cornea from drying and abrasion due to problems with lid closure to the eye and the tearing mechanism that occurs. Artificial tears, adequate lubricant supply, and taping the eyes closed at night that ensures the prevention of corneal ulceration in bell palsy. Lubricating drops should be applied hourly during the day and a simple eye ointment should be used at night. Ophthalmology referral is a recommendation.
  • Facial massage + exercises – promote active rehabilitation and are essential for patients with facial nerve palsy. Facial massages are treatments you can do with a practitioner or on your own. The technique involves stimulating pressure points on the face, neck, and shoulders. Facial massage helps promote healthy skin while relaxing your facial muscles. It has a relaxing and rejuvenating effect, helping you look and feel better.
  • Hyperbaric oxygen therapy – It may improve the time to recovery and the proportion of people who make a full recovery compared with corticosteroids. However, the evidence for this is weak and comes from one small RCT.
  • Facial re-training –  may improve the recovery of facial motor function scores, including stiffness and lip mobility, and may reduce the risk of motor synkinesis in Bell’s palsy, but the evidence is too weak to draw reliable conclusions.
  • Electrical nerve stimulation – It is a proposed method of accelerating recovery in bell’s palsy patients through invoked muscle stimulation. [rx–rx]. Transcutaneous nerve stimulation is an additional new treatment option for those with unilateral facial nerve palsy problems. The technology uses EMG signals from muscles on the intact side of the face to simultaneously stimulate the corresponding muscles and fiber on the side of the paresis. Early trials have shown positive results in significant improvement of facial expression where the affected side is paretic, with some degree of reinnervation.
  • Physical Therapy – In Bell’s palsy various physical therapies, such as exercise, biofeedback, laser, electrotherapy, massage, and thermotherapy are used to recovery. It is
  • Mime Therapy – Neuromuscular retraining or mime therapy refers to the work facial therapists do with patients where they utilize emotional input to access better movement patterns. For example, as the patient practices their balanced smile, they encourage patients to think of something that makes them happy.
  • Hyperbaric oxygen therapy –  or HBOT, is a type of treatment used to speed up healing of carbon monoxide poisoning, gangrene, stubborn wounds, and infections in which tissues are starved for oxygen. If you undergo this therapy, you will enter a special chamber to breathe in pure oxygen in air pressure levels 1.5 to 3 times higher than average. The goal is to fill the blood with enough oxygen to repair tissues and restore normal body function.
  • Transcutaneous electrical nerve stimulation (TENS) – It is a method of pain relief involving the use of a mild electrical current. A TENS machine is a small, battery-operated device that has leads connected to sticky pads called electrodes.
  • Acupuncture – It is a form of treatment that involves inserting very thin needles through a person’s skin at specific points on the body, to various depths. Research suggests that it can help relieve pain, and it is used for a wide range of other complaints.

Medication

  • Analgesia – Non-steroidal anti-inflammatory drug is used to erase nerve inflammation, pain, that help to reduce the inflammatory activator from the injured and paralyzed facial nerve. Aceclofenac is the best choice 100mg tablet 2 times daily with antiulcerant such as omeprazole, pantoprazole, dexlansoprazole etc.
  • Prednisolone – It will increase recovery of motor function of facial nerve if it is started within 72 hours of symptom onset or started.  If, within this period, prednisolone 50 mg once a day or divided dosage should be recommended for 10 days. If a reducing regime is preferred, 60mg of prednisolone once a day should be given, followed by a daily reduction of 10mg for a total treatment duration of 10 days gradually. Prednisolone has been used at a dose of 1 mg/kg/day up to a maximum of 80 mg in some studies. Doses of more than 120 mg/day have been used safely in patients with diabetes.[rx]
  • Antiviral drugs – The introduction of antivirals only showed a minimal benefit for bell palsy. It includes steroid therapy that is described above, analgesia + acyclovir 800 mg 5 times a day for between 7 to 10 days to combat the viral infection is identified in the diagnosis.   The antiviral drugs used in trials were aciclovir (400 mg five times daily for five days) or valaciclovir (1000 mg/day for five days).[rx]
  • Combination therapy – A randomized controlled trial found that at nine months of diagnosis, the facial function had recovered in 94.4% of patients who took prednisolone alone, 85.4% of those who took aciclovir alone, and 92.7% of those who received both. The combined treatment is more effective for the treatment of bell’s palsy.
  • Antibiotic – If the localized disease in an individual over the age of eight, 200 mg once daily doxycycline for a total of 10 days is recommended. If under the age of eight, a 14-day course of amoxicillin or cefuroxime to avoid potential tooth staining with tetracycline use. For most early and localized cases, treatment usually is curative. Bacterial infections require a complement of intravenous antibiotic therapy (type and duration according to local microbiological guidance).
  • Methylcobalamin – It is an active form of vitamin B-12. It is very helpful for the treatment of facial palsy or bell’s palsy treatment. The drug is used to demyelinating nerve injury repair and management of neuropathy abnormality.
  • Vitamin B complex – It is an essential supplement for the treatment of b vitamin deficiency. Lake of vitamin b complex the nervous system disease, myalgia, arthralgia, tingling sensation, numbness, paresthesia has occurred. In the treatment of bell’s palsy, it works excellently to healing the facial nerve injury.
  • Vitamin E – It is a group of eight fat-soluble compounds that include four tocopherols and four tocotrienols. Vitamin E deficiency, which is rare and usually due to an underlying problem with digesting dietary fat rather than from a diet low in vitamin E, can cause nerve problems. Vitamin E is a vitamin that dissolves in fat. It is found in many foods including vegetable oils, cereals, meat, poultry, eggs, fruits, vegetables, and wheat germ oil. It is also available as a supplement.
  • Botulinum toxin injection – and facial reanimation through cosmetic surgery are among the proposed methods of treating such long-term sequelae [rx,rx–rx]. Long-term patient satisfaction and quality of life may be monitored using the Facial Clinimetric Evaluation Scale (FaCE) in conjunction with the House-Brackmann scale in these instances [rx].
  • Neurotrophic growth factors –  neuroprotective agents, for example, nimodipine, glial cell-derived+3 neurotrophic factor are work in healing the bell’s palsy. Nimodipine is used to decrease problems due to a certain type of bleeding in the brain (subarachnoid hemorrhage-SAH). Nimodipine is called a calcium channel blocker. The body naturally responds to bleeding by narrowing the blood vessel to slow blood flow.

Types of surgery for facial paralysis

  • Facial nerve decompression – It is an option in cases of virally induced facial nerve palsy and also Bell palsy. A trans-mastoid approach would be best for cases of tympanic or mastoid segment damage to the facial nerve. If the damage extends to the labyrinthine segment, then a middle fossae approach allows appropriate decompression. The trans-labyrinthine method is reserved for cases of infratemporal decompression, where the cochleovestibular function is absent.
  • Facial nerve repair techniques – can subclassify into primary repair and cable grafting. The primary repair offers the highest chance of return of facial nerve function. The aim is to provide a tension-free epineural repair, to avoid traction around the anastomosis and axonal injury. If tension-free repair is not possible, then a cable graft approach is used. Commonly utilized nerves include the medial and lateral antebrachial cutaneous nerves as well as the sural nerve and great auricular nerve.
  • Nerve grafting options – It is done tend to be utilized in intermediate durations of facial paralysis (3 weeks to 2 years) with some studies suggesting the best outcomes if performed within six months of insult. This two-stage procedure involves an initial incision on the functional side of the face, nerve selection for sacrifice depending on desired functional outcome, and coaptation of the sural nerve graft to the donor facial nerve branches with tunneling to the contralateral side of the face. Following a 9 to 12 month waiting period, selected facial nerve branches and the cross nerve grafts undergo secondary neurotrophins.
  • Muscle transfer techniques – It is suitable for those patients with chronic facial nerve palsy (older than two years). Regional muscle transfer most commonly utilizes the temporalis muscle in rare cases; however, the digastric (marginal mandibular nerve injury if occurs) and masseter muscle(smile reanimation) are also options. If using temporalis muscle, it is essential to ensure adequate trigeminal nerve function before proceeding with this procedure. A 1.5 to 2 cm strip of the temporalis is raised and rotated inferiorly beyond the zygoma muscle to the oral commissure to align with the smile vector.

Surgical Indications

In a scientific study, over 90% of degeneration on ENoG is associated with poor prognosis in the case of bell’s palsy, and therefore, surgical decompression of the facial canal should merit consideration. However, this has not shown significantly positive outcomes compared to conventional medical treatment.
  • For acute suppurative otitis media + mastoiditis, myringotomy +/– ventilation tube and or cortical mastoidectomy is advised. But it is done in severe condition or life-threatening conditions of bell’s palsy.
  • Iatrogenic causes –  if a facial nerve palsy is apparent immediately after otological surgery, then a watch and wait for policy should be adopted as this can be due to local anesthetic use. After the exclusion of a local anesthetic cause and assuming the surgeon is confident that the facial nerve epineurium is intact, a conservative approach with steroids is an option. Otherwise, an urgent re-exploration, facial decompression +/- nerve grafting must take place. Delayed palsies post-operatively can be due to edema and infection (requiring steroids and antibiotics) but also from over-tight packing in open mastoid surgery, which requires removal.
  • Temporal bone fracture – if immediate and complete facial nerve paralysis occurs, then specialist nerve decompression is required as immediately as the patient’s condition allows (usually within 2 to 3 weeks). If there are a delayed diagnosis and ENoG degeneration of more than 90%, then surgical exploration is required. Specific assessment of the facial nerve will help to dictate the approach as determining the site of nerve damage.

Complications

In addition to ocular problems, complications of Bell’s palsy include

  • Motor synkinesis (involuntary movement of muscles occurring at the same time as deliberate movement, e.g. involuntary mouth movement during voluntary eye closure)
  • Crocodile tears (tears when eating due to misdirection of regenerating gustatory fibers destined for the salivary glands, so that they become secretory fibers to the lacrimal gland and cause ipsilateral tearing while the patient is eating)
  • Hemifacial spasm is secondary to axonal degeneration of the facial nerve from paralysis and results in involuntary muscle contractions on one half of the face.
  • Facial asymmetry is a significant cause of patient concern and can cause considerable distress through disfigurement.
  • Synkinesis is voluntary facial movements that are accompanied by involuntary movements. The most common manifestation of synkinesis is the involuntary movement of the mouth upon eye closure and is known as ocular-oral synkinesis. Another notable manifestation of facial nerve synkinesis is that of gustatory lacrimation, otherwise known as crocodile tear syndrome.
  • Incomplete recovery
  • Contracture of facial muscles
  • Reduction or loss of taste sensation
  • Problems with dysarthria due to facial muscle weakness.

    References

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