The precise pathophysiology of Bell palsy remains an area of debate.

The facial nerve courses through a
portion of the temporal bone commonly referred to as the facial canal. A popular theory proposes that
edema and ischemia results in compression of the facial nerve within this bony canal. The cause of the
edema and ischemia has not yet been established. This compression has been seen in magnetic
resonance imaging (MRI) scans with facial nerve enhancement. [5]

The first portion of the facial canal, the labyrinthine segment, is narrowest; the meatal foramen in this
segment has a diameter of only about 0.66 mm. This is the location that is thought to be the most
common site of compression of the facial nerve in Bell palsy. Given the tight confines of the facial canal, it
seems logical that inflammatory, demyelinating, ischemic, or compressive processes may impair neural
conduction at this site.

The location of injury of the facial nerve in Bell palsy is peripheral to the nerve’s nucleus. The injury is
thought to occur near, or at, the geniculate ganglion. If the lesion is proximal to the geniculate ganglion,
the motor paralysis is accompanied by gustatory and autonomic abnormalities. Lesions between the
geniculate ganglion and the origin of the chorda tympani produce the same effect, except that they spare
lacrimation. If the lesion is at the stylomastoid foramen, it may result in facial paralysis only

In the past, situations that produced cold exposure (eg, chilly wind, cold air conditioning, or driving with
the car window down) were considered the only triggers to Bell palsy. Currently, several authors believe
that the herpes simplex virus (HSV) is a common cause of Bell palsy. However, a definitive causal
relationship of HSV to Bell palsy may be difficult to prove because of the ubiquitous nature of HSV.

In 1972, McCormick first suggested that HSV is responsible for idiopathic facial paralysis. [6] This was
based on the analogy that HSV was found in cold sores, and he hypothesized that HSV may remain
latent in the geniculate ganglion. Since then, autopsy studies have shown HSV in the geniculate ganglion
of patients with Bell palsy. Murakami et al, who performed polymerase chain reaction (PCR) testing for
HSV in the endoneural fluid of the facial nerve in 14 patients who underwent surgery for Bell palsy, found
that 11 of the 14 had HSV in the endoneural fluid. [7]

Assuming that HSV is the etiologic agent in Bell palsy is a plausible argument. If this is true, then the virus
is most likely to travel up the axons of the sensory nerves and reside in the ganglion cells. At times of
stress, the virus will reactivate, causing local damage to the myelin.

Additional support for a viral etiology was seen when intranasal inactivated influenza vaccine was strongly
linked to the development of Bell palsy, although whether another component of the vaccine caused the
paresis, which was then accompanied by a reactivation of herpes simplex virus, is not clear. [8, 9]

Besides HSV infection, possible etiologies for Bell palsy include other infections (eg, herpes zoster, Lyme
disease, syphilis, Epstein-Barr viral infection,cytomegalovirus, HIV, and mycoplasma); inflammation
alone; and microvascular disease (diabetes mellitus and hypertension).[10, 11, 12, 13, 14, 15, 16] Bell palsy may be
secondary to viral and/or autoimmune reactions causing the facial nerve to demyelinate, resulting in
unilateral facial paralysis

A family history of Bell palsy has been reported in approximately 4% of cases. Inheritance in such cases
may be autosomal dominant with low penetration; however, which predisposing factors are inherited is

the patient may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye. The patient may appear to have loss of corneal reflex on the affected side. Ocular examination With weakness/paralysis of the orbicularis oculi muscle (facial nerve innervation) and normal function of the levator muscle (oculomotor nerve innervation) and Mueller muscle (sympathetic innervation). The mouth must be washed after testing with different substances. or granulation tissue. the patient frequently is not able to close the eye completely on the affected side. A careful examination of the head. injection. An otologic cause should be considered if the history or physical examination demonstrates evidence of acute or chronic otitis media. Taste and salivation are affected in many patients with Bell palsy. the upper third of the face is spared while the lower two thirds are paralyzed. or if a history of previous ear surgery is noted. and mouth should raise the suspicion for Ramsay Hunt syndrome (herpes zoster oticus). and corrugator muscles are innervated bilaterally at the level of the brainstem. Concurrent rash or vesicles along the ear canal. or trauma. The orbicularis. Neurologic examination . Focus attention on the voluntary movement of the upper part of the face on the affected side: in supranuclear lesions such as a cortical stroke (upper motor neuron. pinna. which explains the pattern of facial paralysis in these cases. cholesteatoma. vesicles. nose. the side of the forehead with the palsy will remain flat. This is known as Bell phenomenon and is considered a normal response to eye closure. The external auditory canal must be inspected for vesicles. Otologic examination An otologic examination includes pneumatic otoscopy and tuning fork examination. above the facial nucleus in the pons). ears. sugar. The affected side has decreased taste as compared to the normal side. otorrhea. When the patient is asked to raise the eyebrows.Weakness and/or paralysis from involvement of the facial nerve affects the entire face (upper and lower) on the affected side. however. The patient may have decreased sensation to pinprick in the posterior auricular area. For these reasons. The patient who has paralysis of the stapedius muscle will report hyperacusis. The tear reflex may also be absent in many cases of Bell palsy. Tympanic membranes should be normal.[19] Initial inspection Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the side affected with the palsy. eyes. Taste may be assessed by holding the tongue with gauze and testing each side of the tongue independently with salt. the eye rolls upward and inward on the affected side. the contralateral eye blinks when testing the corneal reflex on the affected side. infection. the face becomes distorted and lateralizes to the side opposite the palsy. the presence of inflammation. and vinegar. frontalis. including a tympanic membrane perforation. and throat (HEENT) must be carried out in all patients with facial paralysis. Oral examination A careful oral examination must be performed. When the patient is asked to smile. or other signs of infection raises the possibility of complicated otitis media. On attempted eye closure.

and symptoms tend to peak in less than 48 hours. and cerebellar testing. Because the condition appears so rapidly. The onset of Bell palsy is typically sudden. No evidence of CNS disease is noted in patients with Bell palsy. Neurologic examination includes complete examination of all the cranial nerves. Symptoms of Bell palsy include the following:  Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)  Posterior auricular pain  Decreased tearing . and absence of signs and symptoms of ear or posterior fossa disease. More people first notice paresis in the morning. Bell palsy is a diagnosis of exclusion. History The diagnosis of Bell palsy must be made on the basis of a thorough history and physical examination and use of diagnostic testing when necessary. such as MRI of the brain. who often fear they have had a stroke or have a tumor and that the distortion of their facial appearance will be permanent (see the image below). no evidence of ear or cerebellopontine angle disease is noted. and parotid gland disease. which can invade the facial nerve. lumbar puncture. and electromyography (EMG) where appropriate. most cases of paresis likely begin during sleep. Left-sided Bell palsy. Clinical features of Bell palsy that may help distinguish it from other causes of facial paralysis include sudden onset of unilateral facial paralysis. Because the symptoms require several hours to become evident. patients with Bell palsy frequently present to the emergency department (ED) before seeing any other health care professional. Skin examination Time must also be taken to examine the patient’s skin for signs of squamous cell carcinoma. This sudden onset can be frightening for patients. A neurologic abnormality warrants neurologic referral and further testing. Careful neurologic examination is necessary in patients with facial paralysis. Bell palsy may follow recent upper respiratory infection (URI). sensory and motor testing. In addition. absence of signs and symptoms of central nervous system (CNS) disease.

and ulceration (rare but may occur) Late ocular manifestations include the following: . Progression of the paresis is possible. other causes of facial paralysis must be strongly considered. Lyme disease. whereas other authors argue that this symptom is probably due to lack of mobility of the facial muscles and not lack of sensation. infection. A progression beyond this point suggests a different diagnosis. Some authors believe that this is secondary to involvement of the trigeminal nerve. but it usually does not progress beyond 7-10 days. weakness of the contralateral side. The patient may report inability to close the eye or to smile on the affected side. a central cause should be suspected (ie. Ocular manifestations Early ocular complications include the following:  Lagophthalmos (inability to close the eye completely)  Paralytic ectropion of the lower lid  Corneal exposure  Brow droop  Upper eyelid retraction  Decreased tear output/poor tear distribution  Loss of nasolabial fold  Corneal erosion. He or she also may report increased saliva on the side of the paralysis. If a patient has gradual onset of facial paralysis. Many patients report numbness on the side of the paralysis. Hyperacusis  Taste disturbances  Otalgia Early symptoms include the following:  Weakness of the facial muscles  Poor eyelid closure  Aching of the ear or mastoid (60%)  Alteration of taste (57%)  Hyperacusis (30%)  Tingling or numbness of the cheek/mouth  Epiphora  Ocular pain  Blurred vision Facial paralysis The paralysis must include the forehead and lower aspect of the face. If the patient complains of contralateral weakness or diplopia in conjunction with the supranuclear facial palsy. a stroke or intracerebral lesion should be strongly suspected. Patients who have bilateral facial palsy must be evaluated for Guillain-Barré syndrome (GBS). and meningitis. If the paralysis involves only the lower portion of the face. or history of trauma or infection. supranuclear).

and overflow occurs. This condition may occur secondary to compression of the root of the seventh nerve by an aberrant blood vessel. It occurs as tonic contraction of one side of the face. Ask the patient if he or she has experienced trauma. [1] 80% of patients show a reduced sense of taste. It occurs most commonly in the fifth and sixth decades of life. and sometimes the etiology is not found. Mild. Crocodile tears can be observed. which may account for the pain and facial paralysis. Spasms are more likely to occur during times of stress or fatigue and may be present during sleep. Taste disorders While only one third of patients report taste disorders. disfiguring facial paralysis Two thirds of patients complain about tear flow. Fewer tears arrive at the lacrimal sac. The presence of progressive facial hemispasm with other cranial nerve findings indicates a possibility of a brainstem lesion. Cranial neuropathies Some believe that other cranial neuropathies may also be present. generalized mass contracture of the facial muscles. It may be mild and result in slight movement of the mouth or chin when the patient blinks or in eye closure with smiling. contracture of the facial muscles with twitching of the corner of the mouth or dimpling of the chin occurring simultaneously with each blink)  Autonomic synkinesis (ie. which is secondary to weakness of the stapedius muscle. The symptoms in question include the following:  Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves  Dysfunction of the vestibular nerve  Hyperesthesia of the cervical sensory nerves  Vagal or trigeminal motor weakness . The production of tears is not accelerated. Patients may fail to note reduced taste because of normal sensation in the uninvolved side of the tongue. however. [1] The pain frequently occurs simultaneously with the paresis. tumor. Posterior auricular pain Half of the patients affected with Bell palsy may complain of posterior auricular pain. this is not uniformly accepted. rendering the affected palpebral fissure narrower than the opposite one (after several months)  Aberrant regeneration of the facial nerve with motor synkinesis  Reversed jaw winking (ie. crocodile tears-tearing with chewing)  Rare.[1] This is due to the reduced function of the orbicularis oculi in transporting the tears. Facial spasm Facial spasm is a very rare complication of Bell palsy. or demyelination of the nerve root. patients shed tears while they eat. Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. but pain precedes the paresis by 2-3 days in about 25% of patients. One third of patients may experience hyperacusis in the ear ipsilateral to the paralysis. permanent.

and malignant primary and metastatic lesions should be considered as well. Lyme disease should be considered as a cause of facial paralysis.  Grade VI .  Grade V . all the other grades are defined as incomplete. grades I and II are considered good outcomes. and fifth cranial nerves simultaneously. Eye closure is incomplete. the diagnosis of Bell palsy is straightforward as long as the patient has undergone a thorough history and physical examination.Moderately severe dysfunction. Ramsay Hunt syndrome must be considered. severe pain.Mild dysfunction. then treatable or preventable nervous system diseases should be sought (eg. infectious. and a slightly weak mouth movement is noted with maximum effort. Normal symmetry and tone is noted at rest. grades III and IV represent moderate dysfunction. or hemifacial spasm is present. Asymmetry is noted at rest. and grades V and VI describe poor results. hemangiomas. No forehead motion is observed.Normal facial function. Gross asymmetry is noted. Forehead movement is slight to moderate. 27] :  Grade I . Grade VI is defined as complete facial paralysis. An obvious but not disfiguring difference is noted between the 2 sides. Approximately 5-10% of untreated Lyme patients may have a peripheral facial nerve palsy. eighth. For example. contracture. complete eye closure is achieved with effort. Symmetry and tone are normal at rest. motor. or vascular lesions leading to seventh cranial nerve (facial nerve) damage may result in further deterioration of the patient’s condition. recurrent palsy. An incomplete facial paralysis denotes an anatomically and. The patients may have a slight synkinesis. Forehead motion is moderate to good. basilar meningitis. to some degree. as follows[26. No movement is noted. If the patient reports sudden onset of hearing loss and severe pain with the onset of facial paralysis. functionally intact nerve.Severe dysfunction. and an asymmetric mouth is noted with maximal effort. Tumors in the temporal bone such as facial nerve neuromas. Normal symmetry and tone is noted at rest. if other cranial nerve. and serologic testing should be performed. No forehead motion is observed.Moderate dysfunction.  Grade IV . and slight mouth asymmetry is noted.  Grade III . Patients with a progressive paralysis of the facial nerve lasting longer than 3 weeks should be evaluated for neoplasm. complete eye closure is achieved with minimal effort. A noticeable but not severe synkinesis. Failure to recognize structural. An obvious weakness and/or disfiguring asymmetry is noted.  Grade II . stroke. If a patient is from the Northeast. Cerebellopontine tumors may affect the seventh. Recurrent ipsilateral facial paralysis must raise the suspicion of a tumor of the facial nerve or parotid gland. Other problems to be considered include the following:  Acoustic neuroma and other cerebellopontine angle lesions  Acute or chronic otitis media  Amyloidosis . In this system. or sensory symptoms were present. The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI. Only a barely perceptible motion is noted. meningiomas. Symptoms associated with seventh nerve neoplasm include slowly progressive paralysis. and mouth movement is only slight. or cerebellar pontine angle tumor). Eye closure is incomplete.Total paralysis. Slight weakness is noted on close inspection. The degree of facial nerve function should be noted in the chart at the initial visit of the patient In most cases. and other cranial nerve involvement. Guillain-Barré syndrome [GBS]. facial hyperkinesis.

including embolic phenomenon  Cholesteatoma of the middle ear  Congenital malformation  Diabetes mellitus  Facial nerve schwannoma  Geniculate ganglion infection  Glomus tumors  Guillain-Barré syndrome  Herpes zoster  HIV  Leukemia/lymphoma  Leukemic meningitis  Lyme disease  Malignant otitis externa  Melkersson-Rosenthal syndrome  Meningitis  Mycoplasma pneumonia  Nasopharyngeal carcinoma  Osteomyelitis of the skull base  Otitis media  Parotid gland disease or tumor  Pontine lesions  Pregnancy (especially third trimester)  Ramsay Hunt syndrome  Sarcoma  Skull base tumor  Teratoma  Tuberculosis  Viral syndromes  Wegener granulomatosis  Wegener vasculitis In the setting of an appropriate history. iatrogenic)  Forceps delivery . basilar artery. Aneurysm of vertebral. additional considerations include the following:  Alcoholic neuropathy  Anesthesia nerve blocks  Basal skull fractures  Barotrauma  Benign intracranial hypertension  Birth trauma  Carbon monoxide exposure  Diphtheria  Facial injuries  Facial trauma (blunt. or carotid arteries  Autoimmune syndromes  Botulism  Carcinomatosis  Carotid disease and stroke. penetrating.

If the clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks. Iatrogenic (as in otologic. Serum titers for herpes simplex virus may be obtained. skull base. Lyme  Tuberculous Meningitis In many cases. Antineutrophil cytoplasmic antibody (cANCA) levels are indicated if applicable to exclude Wegener granulomatosis. neurotologic.[2] No specific diagnostic tests are available for Bell palsy. but this is usually not helpful owing to the ubiquitous nature of this virus. imaging may be necessary. though the following may be useful:  Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or fluorescent treponemal antibody absorption (FTA-ABS) test  Human immunodeficiency virus (HIV) screening by means of enzyme-linked immunosorbent assay (ELISA) and/or Western blot  Complete blood cell count  Determination of the erythrocyte sedimentation rate  Thyroid function studies  Serum glucose level  Cerebrospinal fluid analysis If the history and physical examination lead to a diagnosis of Bell palsy. imaging may be useful. the history and physical examination lead to the diagnosis of Bell palsy. Blood glucose or hemoglobin A1c levels may be obtained to determine if the patient has undiagnosed diabetes. Imaging is not required because most patients with Bell palsy improve within 8-10 weeks. then immediate imaging is not necessary. If the patient has a palpable parotid mass. . further investigations should be considered. or parotid surgery)  Infectious mononucleosis  Kawasaki disease  Leprosy  Metastatic disease  Mumps  Polyneuritis  Temporal bone fracture  Tetanus  Thalidomide exposure  Toxic Differential Diagnoses  Anterior Circulation Stroke  Benign Skull Tumors  Brainstem Gliomas  Cerebral Aneurysms  Intracranial Hemorrhage  Meningioma  Meningococcal Meningitis  Neurosyphilis  Sarcoidosis  Tick-Borne Diseases. If the paralysis does not improve or worsens.

and because spontaneous recovery is fairly common. a recent analysis of early MRIs with gadolinium of the intratemporal facial nerve demonstrated the ability to predict the long-term outcome of the facial paralysis. treatment of Bell palsy is still controversial. Imaging is not required because most patients with Bell palsy improve within 8-10 weeks. Antineutrophil cytoplasmic antibody (cANCA) levels are indicated if applicable to exclude Wegener granulomatosis. hemangioma. if the paralysis progresses over weeks. Because persons with true Bell palsy generally have an excellent prognosis. meningioma. these findings (increased signal intensity in the internal auditory canal after administration of gadolinium) correlated favorably with those of electrodiagnostic testing. and sclerosing hemangioma. Serum titers for herpes simplex virus may be obtained. further investigations should be considered. If the clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks. then immediate imaging is not necessary. the geniculate ganglion. imaging may be necessary. but this is usually not helpful owing to the ubiquitous nature of this virus. Perform gadolinium-enhanced MRI when findings are atypical or when the facial nerve paralysis appears central to rule out a tumor or vascular compression. However. The goals of treatment are to improve facial nerve (seventh cranial nerve) function and reduce neuronal damage. Thus. In many cases. [29] Little correlation between the enhancement of the facial nerve and the clinical outcome has been noted. If the paralysis does not improve or worsens. Magnetic resonance imaging (MRI) of patients with Bell palsy may show enhancement of the seventh cranial nerve (facial nerve) at.[2] No specific diagnostic tests are available for Bell palsy. CT scanning demonstrates the architecture of the temporal bone and may be used if some other pathology is suspected. . the possibility is high of a neoplasm compressing the facial nerve. though the following may be useful:  Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or fluorescent treponemal antibody absorption (FTA-ABS) test  Human immunodeficiency virus (HIV) screening by means of enzyme-linked immunosorbent assay (ELISA) and/or Western blot  Complete blood cell count  Determination of the erythrocyte sedimentation rate  Thyroid function studies  Serum glucose level  Cerebrospinal fluid analysis If the history and physical examination lead to a diagnosis of Bell palsy. Radiological evaluation by computed tomographic (CT) scanning and other methods is indicated if there are other associated physical findings or if the paresis is progressive and unremitting. If the patient has a palpable parotid mass. However. imaging may be useful. Tumors that compress or involve the facial nerve include schwannoma (most common). MRI is useful as a means of excluding other pathologies as the cause of paralysis. Blood glucose or hemoglobin A1c levels may be obtained to determine if the patient has undiagnosed diabetes. MRI is preferred for imaging the cerebellopontine angle. the history and physical examination lead to the diagnosis of Bell palsy. or near.

an active infection. peptic ulcer disease.[36] No adverse effects of these treatments have been reported. However. but further randomized controlled trials are needed to confirm any benefit. followed by a taper. Any recommendation on facial decompression surgery had insufficient evidence. Antiviral agents have also been studied in this setting. for example.  Arrange appropriate medical follow-up care. However. [38] and they have been limited in their size. sepsis. [37] This study and other early studies have shown conflicting results using steroids in treating Bell palsy. 3 recent randomized. In 1972. Reviews suggest that physical therapy may result in faster recovery and reduced sequelae. a double-blind. A variety of nonpharmacologic measures have been used to treat Bell palsy. controlled trials showed significant improvement in outcomes when prednisolone was started within 72 hours of symptom onset. A larger double-blind. demonstrated that early treatment with prednisolone significantly improved the chances of complete recovery at 3 and 9 months. The most widely accepted treatment for Bell palsy is corticosteroids. immunocompromise. Treatment may be considered for patients who have the onset of paralysis within 1-4 days of the initial office visit. controlled trial showed that prednisolone significantly shortened the time to complete recovery. and there was no additional benefit from combining acyclovir and prednisolone compared to prednisolone alone. Patients with Bell palsy frequently present to the ED. controlled clinical trial that found that 89% of patients treated with prednisone had full recovery compared with 64% of patients treated with placebo. facial exercises[34] and neuromuscular retraining[35]) and acupuncture. steroids should be strongly considered to optimize outcomes. [3] In contrast. as have combinations of the 2 types of drugs. 4. or malignant hypertension. diabetes mellitus. including physical therapy (eg. renal or hepatic dysfunction. the use of steroids is still controversial because most patients recover without treatment. . The most important consideration is the onset of symptoms. Adour et al conducted a large. One of these 3 recent studies. Once the decision to use steroids is made. [3.  Protect the eye. The American Academy of Neurology (AAN) published a practice parameter in 2001 stating that steroids are probably effective and acyclovir (with prednisone) is possibly effective for treatment of Bell palsy. randomized trial from Scotland involving 551 patients with Bell palsy recruited within 72 hours of the onset of symptoms. sarcoidosis. [4] The recommended dose of prednisone for the treatment of Bell palsy is 1 mg/kg or 60 mg/d for 6 days. pregnancy. Caution should be used in patients with tuberculosis. The role of the ED clinician consists of the following:  Initiate appropriate treatment. 39] Based on these 3 studies. whereas valacyclovir did not affect facial recovery compared to placebo. for a total of 10 days. Many issues must be addressed in treating patients with Bell palsy. acyclovir given alone did not show any significant difference in the rate of facial recovery compared to placebo. the consensus is to start immediately. Corticosteroids Many trials have been carried out to study the efficacy of prednisone in Bell palsy.

0.High-dose steroids (>120 mg/d of prednisone) have been safely used to treat Bell palsy in patients with diabetes[40. 4. if varicella zoster virus (VZV) is suspected.65- 1. The AAN guidelines suggest that the use of acyclovir for the treatment of Bell palsy is only possibly effective and that this agent alone is not effective in facial recovery. Because of increased cost and increased risk of side effects with higher doses.88. Although it is more expensive. 43] Therefore.[47] Six trials (representing pooled data of 1145 patients) were examined and included . prednisone monotherapy was compared with the combination of prednisone and acyclovir. and not acyclovir. valacyclovir cannot be routinely recommended at this time. however.18). optimal dosing has not been established. is useful for facial recovery in Bell palsy. Valacyclovir (Valtrex). 95% confidence interval [CI]. This improvement was noted in those who had severe to complete facial palsy. 500 mg orally twice a day for 5 days.69).[12] Quant et al conducted a meta-analysis of published studies from 1984 to January 2009 that showed no improved benefit (with respect to degree of facial muscle recovery in patients with Bell palsy) with corticosteroids plus antivirals as compared to corticosteroids alone (odds ratio 1. Caution should be given in these cases due to the risk of hyperglycemia. If VZV is the cause of Bell palsy. 29] with 3 recent randomized controlled trials showing no benefit. 95% confidence interval. antiviral agents may be reasonable in certain situations.[45]In another prospective.[46] A Japanese randomized. higher doses may be needed (800 mg orally 5 times a day). [16. 39] However. Evidence supports herpes simplex virus (HSV) as a major cause of Bell palsy. it may be associated with better compliance.83-2. The Scottish study cited earlier suggested that prednisolone. randomized trial with 99 patients. may be used instead of acyclovir. Antiviral agents Evidence evaluating the efficacy of antiviral medicines in Bell palsy has shown limited benefit. In their review. Corticosteroid-antiviral combinations A prospective randomized trial with 101 patients comparing prednisone and acyclovir demonstrated that the prednisone group had a better clinical recovery. This study demonstrated that combination therapy was more effective in preventing nerve degeneration as measured by electrodiagnostic tests. higher doses may be needed (1000 mg orally 3 times a day).[3] A Cochrane review analyzed 7 studies (1987 patients) from 1966-2008 looking at the efficacy of antivirals in the complete recovery from Bell palsy. 0. [42.[3. prospective study of 221 patients with Bell palsy showed significant improvement in facial function using both prednisone and valacyclovir therapy as compared with those who used prednisone alone. 41] . there is evidence to suggest a large percentage of Bell palsy cases may result from a viral infection. antivirals showed no significant benefit over placebo in the rate of incomplete recovery (relative risk [RR]. 0.[44] Acyclovir (Zovirax) is administered at a dosage of 400 mg orally 5 times a day for 10 days.50.

and direct brow lift.574 patients who received corticosteroids alone and 571 patients who received corticosteroids and antiviral agents. The weights are attached to the upper lid with an adhesive and are available in different skin tones. surgical repair by using a combination of procedures tailored to the patients’ clinical findings works well for improving symptoms and exposure. de Almeida et al found that antiviral agents. and gold-weight implantation.75. or occasionally ointment day and night) is sufficient to prevent the complications of corneal exposure. Patients without severe exposure have received a single procedure or combinations of procedures. Lower-lid ectropion or droop can temporarily be helped by applying tape below the lid margin in the center of the lower lid. when combined with corticosteroids. . implantable devices placed into the eyelid. Clear plastic wrap. Additionally. may be required.[49] Punctal plugs may be helpful if dryness of the cornea is a persistent problem. 0. [47] Contrary to the Quant et al and Cochrane meta-analyses. Occluding the eyelids by using tape or by applying a patch for 1 or 2 days may help to heal corneal erosions. Surgical options include facial nerve decompression. they should be done so in conjunction with corticosteroids. though the results are not as satisfying in patients with Bell palsy as in patients with idiopathic hemifacial spasm. cut to 8 X 10 cm and applied with generous amounts of ointment as a nighttime occlusive bandage. newer antiviral agents may prove more beneficial than older antiviral agents used in the studies analyzed to date. pull the lid laterally and upward to anchor on the orbital rim.56-1. future studies should improve diagnostic efforts to identify herpes virus as a potential etiology. External eyelid weights are available to improve mechanical blink. subocularis oculi fat (SOOF) lift. If antivirals are to be initiated. transposition of the temporalis muscle.00). 95% CI. however. [48] Their meta-analysis examined 18 trials including 2786 patients. Most patients who have had severe corneal exposure due to lagophthalmos with or without paralytic ectropion received a combination of lateral tarsal strip placement. corneal abrasion. tarsorrhaphy. 0. The patient’s eye is at risk for drying. SOOF lift. were associated with greater risk reduction of borderline significance than were corticosteroids alone (relative risk. Whether to use prednisone alone or combination therapy is left to the discretion of the treating physician It is universally accepted that eye care is imperative in Bell palsy. Botulinum toxin can be injected transcutaneously or subconjunctivally at the upper border of the tarsus and aimed at the levator muscle to produce complete ptosis and to protect the cornea. Quant et al suggest that the routine use of antivirals is not warranted. [26] Botulinum toxin may help in relaxing the facial muscles after they have developed mass contraction. facial nerve grafting. Care must be taken to prevent worsening the abrasion with the tape or a patch by ensuring that the eyelid is securely closed. Future studies will be needed to determine which population will most benefit from antiviral therapy. In most cases. topical ocular lubrication (with artificial tears during the day and lubricating ophthalmic ointment at night. and corneal ulcers. In the author’s experience.

[52] Subocularis oculi fat lift with lateral tarsal strip procedure The SOOF lift is designed to lift and suspend the midfacial musculature. lateral canthotomy and cantholysis is performed. Pretarsal gold-weight implantation is most commonly performed. [53] A lateral tarsal strip procedure is performed to correct horizontal lower-lid laxity and to improve apposition of the lid to the globe. a weight-adjustable magnet. This study also demonstrated that best results were obtained if the decompression was attempted within 14 days after the onset of paralysis. These procedures are best for patients with poor Bell phenomenon and decreased corneal sensation. Patients with a poor prognosis. The nonsurgical group had a poor result in 58% of the patients. Then. patients must sleep with their head slightly elevated. or extrusion. Complications include migration of the implant. First.6-1. The surgical group exhibited a House-Brackmann grade I or II in 91% of the cases. Therefore.99% pure gold or platinum. symptomatic lagophthalmos. Tarsorrhaphy . inflammation. then. the surgeon can decide if the maxillary segment should be decompressed externally or if the labyrinthine segment and geniculate ganglion should be decompressed with a middle-fossa craniotomy. Sizes range from 0. The implants are inert and composed of 99. as shown on facial nerve electromyography (EMG) within 3 weeks of the onset of paralysis. studies have been mixed as far as benefit from surgery. [50. The SOOF is deep to the orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim. with a House-Brackmann grade III or IV at 7 months.8 g. or palpebral springs can be inserted into the eyelids. Lifting the SOOF may also elevate the upper lip and the angle of the mouth to improve facial symmetry. and the lateral tarsal strip is shortened and attached to the periosteum at the lateral orbital rim. allergic reaction. However. A SOOF lift is commonly done in conjunction with a lateral tarsal strip procedure to tighten the eyelid.[51] A study compared a cohort of patients with degeneration greater than 90% who underwent middle-fossa decompression with a cohort of similar patients who chose not to pursue surgical decompression. identified by facial nerve testing or persistent paralysis. The weight allows the upper eyelid to close with gravity when the levator palpebrae are relaxed. 19] The problem must be localized with magnetic resonance imaging (MRI). They are easily removed if nerve function returns. the anterior lamella is removed. appear to benefit the most from surgical intervention. Gold or platinum weights.Decompression of facial nerve Surgery to decompress the facial nerve is controversial when performed in patients with complete Bell palsy that has not responded to medical therapy and with greater than 90% axonal degeneration. Implants in eyelid Implantable devices have been used to restore dynamic lid closure in cases of severe.

Signs of infection may also be masked in patients taking prednisone. Sterapred) Prednisone is a glucocorticoid that is absorbed readily from the gastrointestinal tract. The procedure can be done in the office and is particularly suitable for patients who are unable or unwilling to undergo other surgery. centrally. Facial nerve grafting or hypoglossal-facial nerve anastomosis Reinnervation of the facial nerve by means of facial nerve grafting or hypoglossal-facial nerve anastomosis can be used in cases of clinically significant permanent paralysis to help restore relatively normal function to the orbicularis oculi muscle or eyelids. Transposition of temporalis Transposition of the temporalis muscle can be used to reanimate the face and to provide lid closure by using the fifth cranial nerve. Central tarsorrhaphy offers good corneal protection. Medial or paracentral tarsorrhaphy is performed lateral to the lacrimal puncta and can offer good lid closure without substantially affecting the visual field. The lateral procedure is most common. glaucoma. Permanent tarsorrhaphy is done if nerve recovery is not expected. it can restrict the monocular temporal visual field. It can be completed as either a temporary or a permanent measure. hypokalemia. Strips from the muscle and fascia are placed in the upper and lower lids as an encircling sling. myopathy. View full drug information Prednisone (Deltasone. A gold-weight implant can be placed or lower-lid resuspension can be performed simultaneously to prevent this complication. but it occludes vision and can be cosmetically unacceptable. peptic ulcer. or medially. Tarsorrhaphy can be performed laterally. It has anti- inflammatory and immune-modulating effects. Direct brow lift Brow ptosis is repaired with a direct brow lift. headache (pseudotumor). Orasone. especially if lid closure is poor. Prednisone can be used but has many adverse effects. Care should be taken in the presence of corneal decompensation because lifting the brow can cause worsening of lagophthalmos.Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together to improve support of the precorneal lake of tears and to improve coverage of the eye during sleep. menstrual irregularities. as well as profound and varied metabolic effects . cataracts. and manifestation of latent diabetes mellitus. however. including fluid retention. Patients initiate movement by chewing or clenching their teeth. Physicians should use caution when using prednisone in patients with the aforementioned conditions.