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Bells Palsy

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I have selected Bell’s palsy as a minor health subject for critical analysis for three principal reasons. Firstly, it is the most common disorder affecting the facial nerves (Ardour, 1978). Secondly, research has noted that there appears little consensus in the literature regarding the causes and management of Bell’s palsy. Additionally the diagnosis is one of elimination. Tiemstra and Khatkhate (2007) demonstrate there are many other conditions which can mimic symptoms (See appendix one). I therefore wanted to analyse the available literature in order to be able to competently and safely recognise the condition in the urgent unscheduled care environment.


Petruzelli (1991) states that Bell’s palsy is an acute paralysis of the facial nerve first described by the Scottish surgeon and anatomist, Sir Charles Bell . Niparko (1993) elaborates that it is a generally unilateral paralysis or weakness of facial musculature consistent with facial nerve damage and dysfunction. The anatomy of the facial nerve can be found in appendix two.
Pietersen (2002) states that the cause is unknown, however, whilst the exact aetiology of Bell’s palsy is still debated, viral infections, vascular ischaemia, autoimmune inflammatory disorders and heredity have been postulated as causative. (Adour 1982, Burgess 1984, Lorber 1996). Murakami et al (1996) proposed that reactivation of herpes simplex virus in the geniculate ganglia was causative. A herpes simplex cause is corroborated by Stjernquist-Desatnik, Skoog, and Aurelius (2006). Whilst the exact aetiology is disputed, a greater consensus is reached when considering the pathophysiology.
Tiemstra and Khatkhate (2007) state that Bell’s palsy is thought to be caused by inflammation at the geniculate ganglion. This appears corroborated by Fisch and Esslen (1972) who noted oedematous swelling proximal to the geniculate ganglion in up to 94% of their patients
Fisch and Felix (1983) postulate that swelling in the facial canal results in hypoxia of the facial nerve, stating that inflammation and ischaemia result initially in reversible neuropraxia. Prolonged, severe inflammation results in Wallerian degeneration. Hain (2009) goes on, stating that degeneration occurs over 3-5 days and these patients experience prolonged recovery.
Most sources agree on a range of symptoms, a list of which is found in appendix three.


In the UK, Rowlands et al. (2001) found that Bell’s palsy affected approximately 20.2 per 100,000 people. They continue, saying incidence increases with age but appears equally distributed among the sexes, 49.3% were male and 50.7% female. No seasonal effects were noted. There did not appear to be clustering within households or a hereditary influence. This evidence is partly confirmed by Simon, Everitt and van Dorp (2010) who also state that left and right sides are affected equally often, however, they contest that peak incidence occurs in the 10-40 year age group. Most sources state there is little variation in incidence between races and studies of the racial distribution are limited in number. However, Campbell and Brundage (2001) found a slightly increased incidence in Black and Hispanic subjects in their study of the American military.


I wanted to analyse the efficacy of different treatments that have been postulated for Bell’s palsy. Historically several treatments have been tried, notably oral corticosteroid therapy, oral anti-viral drug therapy, physical therapy, surgical nerve decompression, acupuncture and hyperbaric oxygen therapy. There have been studies of each of these therapies of varying quality.
Tiemstra and Khatkhate (2007) propose that establishing a statistically significant benefit of treatment in trials is difficult because Bell's palsy has a high rate of spontaneous recovery. This seems corroborated by Peitersen (1982) who stated that the prognosis even without treatment is favourable, 85% of patients began to recover within three weeks. Hain (2009) also confirms that 75% of patients experience complete recovery, most within 2 to 3 weeks.
Within the confines of this essay and considering that some proposed treatments have little supporting evidence I have limited my analysis to therapy using corticosteroids and anti-viral medication. An overview of the other therapies is given in appendix five.
Corticosteroids are known to reduce inflammation by inhibiting the synthesis of inflammatory proteins through suppression of their encoding genes (Ismaili & Garabedian, 2004). Therefore, in the treatment of Bell’s palsy it seems reasonable to postulate that steroids would reduce inflammation and subsequent facial nerve ischaemia. Thus they may have an impact on prognosis. Anti-viral medication would also be reasonable given a possible viral aetiology.
Research of the literature reveals seven randomised clinical trials conducted sufficiently well to provide robust evidence. These trials involved a total of 1997 patients and were conducted between 1996 and 2008. The trials analysed are found in appendix four.
The trials conducted by Sullivan (2007) and Engström (2008) have been subdivided into A and B trials as they compare slightly different treatments. Engström (2008B), Sullivan (2007A), Hato (2007) and Adour (1996) compared corticosteroids plus anti-virals versus placebo plus corticosteroids. DiDiego (1998) compared steroids versus anti-virals.
Lagalla (2002), Engström (2008A) and Sullivan (2007B) compared steroids versus placebo and Unuvar (1999) compared steroids against no therapy.
Analysis involved study of the trial data for adverse effects of treatment, rates of recovery and completeness of recovery. Recovery rates between the different drug regimes were studied for comparable effectiveness. Attempts were made to research whether the timing of the start of treatment after symptom onset was significant.
With the exception of Lagalla (2002), all the trials provided data on complete recovery at between 3 and 12 months follow up and reported on incomplete recovery at between 3 months and the end of the trial.
Complete recovery rates amongst those receiving steroids compared to those in the control groups were found to be improved in all trials.
Incomplete recovery rates amongst those who received steroids versus placebo in trials were found to be improved. Unuvar (1999) had no participants with incomplete recovery in the steroid group. In trials comparing steroids plus anti-virals versus anti-virals plus placebo, the groups given steroids together with anti-virals had significantly improved incomplete recovery rates. DiDiego (1998) found improved recovery in the steroid group versus the acyclovir group.
Engström (2008B), Adour (1996) and Hato (2007) discovered a slight improvement in incomplete recovery amongst their patients who were given steroids and anti-virals versus controls.
Sullivan (2007A and 2007B) and Unuvar (1999) reported on those with severe paralysis, or cosmetically disabling sequelae. Unuvar (1999) reported no one with severe effects in the steroid group. Sullivan (2007B) reported 1 person with severe effects in the steroid group versus none in the control group.

Lagalla (2002) and Engström (2008 A and B) reported on apparent synkinesis at follow up. DiDiego (1998) and Lagalla (2002) noted that the incidence of synkinesis in the steroid group was less than the control group. Engström (2008) concurs with this.
Most of the trials noted either the absence of, or included any adverse effects. Unuvar (1999) recorded no adverse effects with their steroid treatment. Lagalla (2002) recorded three individuals in their prednisolone group who complained of temporary sleep disturbances. Both Engström (2008 A and B) and Sullivan (2007 A and B) reported adverse effects. In both trials only 177 minor adverse effects were seen, these appear equally distributed among participants in both control and treatment groups.
Sullivan (2007 A and B) both recorded the amount of cases included in the trials where treatment or placebo therapy was commenced within 48 hours of symptom onset. Sullivan (2007 A and B) reported 112 people in the steroid groups in each trial and 112 in the control groups of each trial that had started in the trial within 48 hours of symptom onset. Of those in the steroid groups, 13 suffered incomplete recovery versus 27 in the control groups. Conclusion:

Analysis of the trial data leads me to conclude that the treatment of Bell’s palsy with corticosteroid therapy leads to significant improvements in complete recovery rates, a significant improvement in numbers of patients left with incomplete recovery and a small reduction in the numbers of those left with cosmetic sequelae after 6 months, this reduction improves at 12 months.
The trials involving corticosteroid therapy within 48 hours of symptom onset also show significant improvement rates.
Anti-virals appear significantly less efficacious than corticosteroids in the treatment of Bell’s palsy. There appears insignificant improvement in recovery rates amongst those treated with steroids and antivirals together. Anti-viral medication alone is not effective.
As the cause is not agreed upon and the benefit implied by anti-virals and steroids together is low, the conclusion is that further trials and research must be completed before recommendation.
The risks of adverse reactions with the short courses of corticosteroids required to treat Bell’s palsy are insignificant and far exceeded by the benefits.

Implications for practice

The most significant implication is the ability to recognise the signs and symptoms of Bell’s palsy and differentiate the condition from other significant diseases which mimic it and are not treatable in the primary or pre-hospital setting. The importance of accurate history taking and relevant questioning is noted in the differentiation process.
The knowledge that recovery has a good prognosis even without treatment enables the practitioner to provide reassurance to patients who may feel deeply distressed by the cosmetic aspects of the condition.
Practitioners will now be able to confidently prescribe a course of oral corticosteroids in the knowledge that they will have significant benefits in overall recovery with no significant adverse effects in the majority of patients. They will also be more informed about the other treatment regimes that have been postulated and could consider those treatments for patients for whom steroid therapy is contra-indicated.


Adour, K. Byl, F. Hilsinger, R. Kahn, Z. Sheldon, M. (1978) ‘The true nature of Bell’s palsy: Analysis of 1000 consecutive patients’, Laryngoscope, 88, pp. 787–801
Adour, K. Ruboyianes, J. Von Doersten, P. Byl, F. Trent, C. Quesenberry, C. et al. (1996) ‘Bell’s palsy treatment with acyclovir and prednisone compared with prednisone alone:a double-blind, randomised, controlled trial’, Annals of
Otology, Rhinology and Laryngology, 105 (5), pp.371–8.
Bickley, L and Szilagyi, P. (2009) Bates’ Guide to Physical Examination and History Taking. 10th edn. Philadelphia: Wolters Kluwer Health
Burgess, L. Yim, D. Lepore, M. (1984) ‘Bell’s palsy: the controversy revisited’,Laryngoscope , 94(11 pt 1),pp.1472–6
Campbell, K. and Brundage, J. (2002) ‘Effects of Climate, Latitude, and Season on the Incidence of Bell’s Palsy in the US Armed Forces, October 1997 to September 1999’, American Journal of Epidemiology, 156 (1), pp. 33-39
De Diego, J. Prim, M. De Sarria, M. Madero, R. Gavilan, J. (1998) ‘Idiopathic facial paralysis: A randomised, prospective and controlled study using single-dose prednisone versus acyclovir three times daily’, Laryngoscope, 108 (4 pt 1), pp.573–5.

Engström, M. Berg, T. Stjemquist-Desatnik, A. Axelsson, S. Pitkäranta, A. Hultcrantz, M. et al. (2008) ‘Prednisolone and valacyclovir in Bell’s palsy: a randomised double-blind, placebo controlled, multicentre trial’, Lancet Neurology, 7(11), pp. 993–1000.
Fisch, U. and Esslen, E. (1972) ‘Total intratemporal exposure of the facial nerve: Pathologic findings in Bell’s palsy’, Archives of Otolaryngology - Head and Neck Surgery, 95 (4) pp.335–41
Fisch, U. and Felix, H. (1983) ‘On the pathogenesis of Bell’s palsy’, Acta Oto-Laryngologica, 95 (5-6), pp.532–8.
Hain, C. (2009) Dizziness and Balance. Available at: (Accessed: 28th August 2012) Hato, N. Yamada, H. Kohno, H. Matsumoto, S. Honda, N. Gyo, K. Fukuda, S. et al. (2207) ‘Valaciclovir and Prednisolone Treatment for Bell’s Palsy: A Multicentre, Randomized, Placebo-Controlled Study’, Otology and Neurology, 28, pp.408–13.
Ismaili, N. and Garabedian, M. (2004) ‘Modulation of glucocorticoid receptor function via phosphorylation’, Annals of the New York Academy of Science, 1024, pp.86–101
Lagalla, G. Logullo, F. Di Bella, P. Provinciali, F. and Ceravolo, M. (2002) ‘Influence of early high-dose steroid treatment on Bell’s palsy evolution’, Neurological Sciences 23 (3), pp.107–12.
Lorber, B. (1996) ‘Are all diseases infectious?’, Annals of Internal Medicine, 125 (10), pp.844–51.
Murakami, S. Mizobuchi, M. Nakashiro, Y. Doi, T. Hato, N. and Yanagihara, N. (1996) ‘Bell’s palsy and herpes simplex virus: identifcation of viral DNA in endoneurial fluid and muscle’, Annals of International Medicine,124, pp. 27-30.
Niparko, J. Mattox, D. (1993) ‘Bell’s palsy and herpes zoster oticus’, in Johnson, R. and Griffin, J. (ed.) Current therapy in neurologic disease. 4th Edn. St. Louis:Decker
Peitersen, E. (1982) ‘The natural history of Bell’s palsy’, American Journal of Otology, 4 (2), pp.107–11.
Peitersen, E. (2002) ,Bell’s Palsy: the spontaneous course of 2500 peripheral facial nerve palsies of different etiologies’, Acta Oto-Laryngologica, 549 (4)
Pentland, B. Davenport, R and Cowie, R. (2009) ‘The nervous system’, in Douglas, G. Nicol, F and Robertson, C (ed.) Macleod’s Clinical Examination. 12th edn. Edinburgh: Churchill Livingstone Elsevier. Petruzelli, G. and Hirsch, B. (1991) ‘Bell’s Palsy’, Postgraduate Medicine, 90, pp.115–127.
Rowlands ,S. Hooper, R. Hughes, R. and Burney, P. (2002) ‘The epidemiology and treatment of Bell's palsy in the UK’, European Journal of Neurology, 9, pp. 63-67
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Stjernquist-Desatnik, A. Skoog, E. and Aurelius, E. (2006) ‘Detection of herpes simplex and varicellla-zoster viruses in patients with Bell’s palsy by the polymerase chain reaction technique’, Annals of Otology, Rhinology and Laryngology, 115, pp. 306–311
Sullivan, F. Swan, I. Donnan, P. Morrison, J. Smith, B. McKinstry, B. et al. (2007) ‘Early treatment with prednisolone or acyclovir in Bell´ s Palsy’, New England Journal of Medicine, 357 (16), pp.1598–607.
Tiemstra, J. and Khatkhate, N (2007) ‘Bell's palsy: diagnosis and management.’, American Family Physician, 76 (7), pp. 997-1002.
Unuvar, E. Oguz, F. Sidal, M. and Kilic, A. ‘Corticosteroid treatment of childhood Bell’s palsy’, Pediatric Neurology, 21 (5), pp. 814–6. (Accessed: 20th July 2012) (Accessed: 8th September 2012)

Appendix 1

Common Bell’s palsy Mimics

Disease | Cause | Features that distinguish disease from Bell’s palsy | Lyme disease | SpirocheteBorrelia burgdorferi | History of tick exposure, rash, or arthralgias; exposure to areas where Lyme disease is endemic | Otitis media | Bacterial pathogens | Gradual onset; ear pain, fever, and conductive hearing loss | Ramsay Hunt syndrome | Herpes zoster virus | Pronounced prodrome of pain; vesicular eruption in ear canal or pharynx | Sarcoidosis or Guillain-Barré syndrome | Autoimmune response | More often bilateral | Tumour | Cholesteatoma, parotid gland | Gradual onset | The above diseases are peripheral in origin | The diseases below affect the central nerves and do display the characteristic forehead involvement of Bell’s palsy | Multiple sclerosis | Demyelination | Additional neurologic symptoms | Stroke | Ischemia, haemorrhage | Extremities on affected side often involved | Tumour | Metastases, primary brain | Gradual onset; mental status changes; history of cancer |

Information from Tiemstra and Khatkhate (2007)

Appendix 2

Anatomy of the facial nerve

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The facial nerve originates in the Pons within brain stem (Pentland, Davenport and Cowie, 2009 p280), it enters the temporal bone via internal auditory meatus where it forms the geniculate ganglion. It passes through the facial canal and exits the skull via Stylomastoid foramen. It then enters the Parotid Gland and divides into 5 main branches. It goes on to subdivide into 7000 fibres reaching the face, neck, salivary glands and outer ear.
The facial nerve controls muscles of the neck, forehead and facial expression.
It stimulates secretions of the lower jaw, the tear glands and frontal salivary glands and controls perceived sound volume. It also transmits taste from the anterior two thirds of the tongue (Tiemstra and Khatkhate, 2007).

Appendix 3

Symptoms of Bell’s palsy

Unilateral Partial or complete Muscle weakness or paralysis
Forehead wrinkles disappear
Overall droopy appearance to face
Nose runs or Nose is constantly stuffed
Difficulty speaking
Difficulty eating and drinking,
Sensitivity to sound (hyperacusis)
Excess or reduced salivation and drooling
Facial swelling
Diminished or distorted taste
Brow droop
Moderate discomfort or pain in or near the ear especially below the ear on the affected side.
Eye closure difficult or impossible
Lack of tears or Excessive tearing (may have Crocodile tears on recovery)
Inability to whistle
Painful teeth.
Lower eyelid droop
Psychological effects
Sensitivity to light

Information taken from Hain (2009) and Bickley & Szilagyi (2009).

Appendix 4

Trials analysed Trial | Participants | Treatment | Adour 1996 | 99 people, paralysis commenced <= 3 days before treatment; all participants over 18 no contraindication forsteroid or acyclovir treatment. | Acyclovir (2000 mg per day for 10 days) and prednisone (1 mg/kg for 5 days tapered to 10 mg/day for remaining 5 days) or placebo and prednisone (1 mg/kg for 5 days tapered to 10 mg/day forremaining 5 days) | De Diego 1998 | 101 included in published analysis. Evaluation within first 96 hours.No contraindications for corticosteroid or acyclovir treatment. | Acyclovir (2400 mg per day for 10 days) or prednisone (1 mg/kg for 10 days then tapered to zeroover next 6 days) | Unuvar 1999 | 42 children (21 males and 21 females) within three days of onset of Bell’s palsy. Age ranged from 24 to 74 months. 21 given steroids, 21 in control group. | Methylprednisolone 1 mg/kg/daily, for ten days, and then withdrawn in three to five days, versus no specific treatment. No placebo was used. | Lagalla 2002 | 62 participants (34 males and 28 females) within three days of onset of onset of Bell’s palsy. Ages ranged from 15 to 84 years | Prednisone 1 g daily intravenously in saline solution for three days and then 0.5 g for the other three days. Saline solution was used as placebo. All participants received intramuscular vitamins for 15 days. | Hato 2007 | 296 participants 152 in VP (valacyclovir+predisolone) group. 144 in PP (predinisolone +placebo) group. All commenced treatment within 7 days of symptom onset. Participants over 15 years. No contraindications to either therapy. 221 patients were included in the final analysis | Randomized to receive prednisolone 60 mg for 5 days, 30 mg for 3 days and 10 mg for 2 days +/-valacyclovir 1000 mg/ day for 5 days. All participants received mecobalamin 1500 micrograms perday following corticosteroids for 6 months or until complete recovery | Sullivan 2007 A | 279 participants within three days of onset of Bell’s palsy.138 given steroids, 141 in control group. | Prednisolone at a dose of 25 mg twice daily, plus acyclovir 400 mg five times daily, versus similar-looking placebo (lactose) plus acyclovir at the same dose, as part of a larger trial | Sullivan 2007 B | 279 participants within three days of onset of Bell’s palsy.134 given steroids, 138 in control group | Prednisolone at a dose of 25 mg twice daily, versus similar-looking placebo (lactose), as part of a larger trial | Engström 2008 A | 422 participants within three days of onset of Bell’s palsy, aged 18 to 75 years.213 given steroids, 209 in control group | Prednisolone at a single dose of 60 mg daily for five days, followed by a dose reduced by 10 mg, per day, with a total treatment of ten days, versus placebo | Engström 2008 B | 417 participants within three days of onset of Bell’s palsy, aged 18 to 75 years.210 given steroids, 207 in control group. | Prednisolone at a single dose of 60 mg daily for five days, followed by a dose reduced by 10 mg, per day, with a total treatment of ten days, versus placebo. Part of a l larger trial. All participants received valacyclovir as two 500 mg tablets three times per day for 7 days |

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