Approach

It is believed that, in the absence of treatment, ultimate clinical outcomes are dependent on the degree of initial insult to the facial nerve, comorbidities, and anatomical factors such as the diameter of the fallopian canal. Current treatment algorithms are targeted at minimising the initial degree of neural insult, shortening the time to recovery of function, and avoiding the long-term development of severe facial synkinesis, in addition to corneal protective measures in the acute flaccid phase of Bell's palsy.

Corticosteroids and antivirals

Strong evidence from randomised controlled trials and meta-analyses supports the use of oral corticosteroids within 72 hours of symptom onset to shorten the time to complete recovery in adults and improve long-term outcomes, regardless of the baseline severity of facial palsy.[42]​​[43][44][45][46][47][48][49][50][51] [ Cochrane Clinical Answers logo ] [Evidence A]​​​ They are thought to work by decreasing nerve oedema and minimising nerve insult. One systematic review and meta-analysis comparing standard-dose corticosteroids with higher-dose corticosteroids found that higher-dose corticosteroids reduced incomplete recovery in patients with Bell’s palsy but did not identify a suitable dose.[52]​ Caution should be exercised for the use of high-dose corticosteroids in children (aged <16 years) and in patients with poorly controlled diabetes mellitus, immunodeficiency, poorly controlled hypertension, and prior history of psychosis. Make sure to exclude Lyme disease-associated facial paralysis when working up Bell’s palsy, as steroids may worsen long-term outcomes in these patients.[53]​​

Strong evidence recommends against antiviral monotherapy for Bell's palsy, with antiviral monotherapy demonstrating inferior outcomes compared with corticosteroid monotherapy and no benefit compared with placebo.[45][47][48] [ Cochrane Clinical Answers logo ]

However, antiviral therapy concomitant with corticosteroids in the acute phase of Bell’s palsy may be associated with additional clinical benefit, especially for those with severe to complete paralysis. One network meta-analysis found evidence that combined therapy (i.e., corticosteroid plus antiviral agent) was the most effective intervention to improve recovery rate, both in the short- and intermediate/long-term.[54]​ Meta-analyses have also found moderate-quality evidence that the combination of antivirals and corticosteroids reduces long-term sequelae of Bell's palsy (including synkinesis) compared with corticosteroids alone, especially in patients who initially present with complete or near-complete facial palsy.[47][54]​​[55][56][57]​ Importantly, no increase in adverse events from the addition of antiviral therapy to a corticosteroid regimen has been demonstrated, although the evidence is uncertain because of the lack of high-quality studies.[47] [ Cochrane Clinical Answers logo ] ​ For Ramsay Hunt syndrome and zoster sine herpete, combination therapy is recommended.[58][59]

Surgical decompression

Refer patients presenting with Bell palsy and meeting all of the following criteria to a neuro-otologist to discuss the risks and benefits of surgical decompression:

  • Clinically undetectable unilateral facial movement

  • Facial palsy onset within 14 days

  • Electroneuronography (ENoG) performed between 72 hours and 14 days of facial palsy onset demonstrates >90% reduction in the amplitude of the compound muscle action potential (CMAP) using a suprathreshold neural stimulus, compared with the normal side

  • Needle electromyography (EMG) confirms the absence of voluntary motor unit potentials in facial musculature.

The rationale for surgical decompression of the facial nerve is that the removal of approximately 180 degrees of confining fallopian canal bone, together with incision of the epineurium from the porus acousticus to the stylomastoid foramen, provides space for the nerve to swell, reducing progression of the virally triggered compressive neuropathy and subsequent ischaemic neural insult.

In one study, a 30% or greater improvement in satisfactory outcomes was achieved when decompression of the site of pathological constriction (the meatal foramen in 94% of patients) together with neighbouring segments via a middle cranial fossa approach was completed within 24 hours of the point where serial ENoG demonstrated 90% to 94% degeneration.[32] A second trial confirmed that surgical decompression that included the meatal foramen resulted in a clinically and statistically significant improvement in long-term outcomes for patients with a diagnosis of Bell's palsy presenting with severe or complete flaccid paralysis (i.e., House-Brackmann grade V or VI), an ENoG response demonstrating >90% degeneration compared with the contralateral healthy side, and absence of voluntary motor unit potentials on EMG.[60] In that study, 91% of patients meeting the inclusion criteria who underwent decompression within 2 weeks of symptom onset in addition to medical therapy progressed to a final House-Brackmann grade of I or II, compared with 42% of patients who received medical therapy alone.[60][61]​ Both studies were biased by patient self-selection for surgery. Although it has been advocated that decompression is of no benefit in Bell's palsy, conclusions were based on a transmastoid approach in which the meatal foramen was not decompressed.[62] In one meta-analysis, the rates of complete recovery from complete Bell's palsy were significantly higher in patients who underwent facial nerve decompression than in those who underwent conservative treatment; there were no significant differences between the rates of fair and failed recovery.[63] The lack of high-quality data, together with the technical difficulty and associated risks of decompression surgery (e.g., hearing loss, cerebrospinal leak, iatrogenic facial nerve injury), prevents consensus on its utilisation.[64]

A systematic review found that middle fossa decompression performed within 14 days of symptom onset resulted in better facial nerve outcomes than when performed after 14 days. However, this review found that transmastoid decompression does not offer improved outcomes over medical management when it is offered after 15 days of symptom onset.[65]​​

Eye protection

In the flaccid phase of Bell's palsy, prevention of exposure keratopathy is paramount.

Protect the affected eye with glasses, not a patch, during the day, and use artificial tears as needed to prevent damage to the cornea due to dryness caused by incomplete or inadequate eyelid closure. Overnight, the lid may be taped closed using non-irritant tape after the application of a bland ophthalmological lubricant ointment again, patching should be avoided.[66][67]​​ Eye patches are contraindicated because the eye may easily open under the patch leading to corneal abrasion.

Indications for ophthalmological consultation include: only seeing eye affected, suspicion of exposure keratitis, and decreased or absent corneal sensation. Strong consideration for early upper eyelid weight placement or tarsorrhaphy (both of which are reversible) should be given to patients who lack Bell's phenomenon (protective reflex in which the globe rotates upwards and outwards with attempts at eye closure) or whose prognosis for early rapid return of function is poor (complete flaccid paralysis on presentation, older adult, taste disturbance, and diabetes mellitus).[37]

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