Facial nerve Synkinesis Following Bell’s palsy
July 4th, 2011 by Administrator

The author: Professor Yasser Metwally


July 4, 2011 — Facial paralysis is a disfiguring disorder that has a great impact on the patient. Facial nerve paralysis may be congenital, neoplastic, or result from infection, trauma, toxic, or iatrogenic causes. The most common cause of unilateral facial paralysis is Bell palsy, also known as idiopathic facial paralysis. Bell palsy is thought to account for approximately 60-75% of acute unilateral facial paralysis.

In 1550, Fallopius noted the narrow lumen in the temporal bone through which a part of the seventh cranial nerve passes. In 1828, Charles Bell made the distinction between the fifth and seventh cranial nerves, he noted that the seventh nerve was mainly involved in the motor function of the face and the fifth nerve was mainly concerned with the sensory perception of the face.

Even today, controversy still surrounds the etiology and treatment of Bell palsy. Clinical features of Bell palsy that may help distinguish this from other causes of facial paralysis include sudden onset of unilateral facial paralysis (less than 48 hours), absence of signs and symptoms of CNS disease, and absence of signs and symptoms of ear or posterior fossa disease.

The majority of patients who suffer from Bell palsy have neurapraxia or local nerve conduction block. These patients are likely to have a prompt and complete recovery of the nerve. Patients with axonotmesis, with disruption of the axons, have a fairly good recovery but it is usually not complete. The risk factors thought to be associated with a poor outcome in patient’s with Bell palsy include (1) age greater than 60 years, (2) complete paralysis, and (3) decreased taste or salivary flow on the side of paralysis (usually 10-25% compared to the patient’s normal side). Other factors thought to be associated with poor outcome include pain in the posterior auricular area and decreased lacrimation.

Patients generally have a good prognosis; approximately 80-90% of the patients will recover without noticeable disfigurement within one and a half to three months. Patients aged 60 years or older have approximately a 40% chance of complete recovery and have a higher rate of sequelae. Patients younger than 30 years have a 10-15% chance of partial recovery and sequelae. If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the disease, which include synkinesis, crocodile tears, and rarely hemifacial spasm.

  • Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It may be mild and result in slight movement of the chin when the patient blinks, eye closure with smiling, or contracture around the mouth while blinking. Crocodile tears are observed; patients shed tears while they eat.

  • Facial spasm is a very rare complication of Bell palsy. It occurs as tonic contraction of one side of the face. Spasms are more likely to occur during times of stress or fatigue and may occur during sleep. This condition may occur secondary to compression of the root of the seventh nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root. It occurs most commonly in the fifth and sixth decades, and sometimes the etiology is not found. The presence of progressive facial hemispasm with other cranial nerve findings indicates a possibility of a brainstem lesion.

  • Diabetics are 30% more likely to have only partial recovery; recurrence of Bell palsy is also more common among diabetics. Bell palsy accounts for only 23% of bilateral facial paralysis. The majority of patients with bilateral facial palsy have Guillain-Barré syndrome (GBS), sarcoidosis, Lyme disease, meningitis (neoplastic or infectious) or bilateral neurofibromas in patient’s with Neurofibromatosis 2. Recurrent Bell palsy occurs in 10-15% of patients. It may occur on the ipsilateral or contralateral side of the initial palsy. It is usually associated with a family history of recurrent Bell palsy. Approximately 30% of patients with recurrent ipsilateral facial palsy were found to have tumors of the seventh nerve or parotid gland. Patients with recurrent ipsilateral facial palsy should undergo MRI or high-resolution CT to rule out neoplastic or inflammatory (multiple sclerosis or sarcoidosis) cause of recurrence.


Synkinesis means “simultaneous movement.” Synkinesis occurs secondary to abnormal facial nerve regeneration after Bell’s palsy or instances where the facial nerve has been cut and sewn back together. The facial nerve fibers can implant into the different muscles in cases of bells palsy. Additionally, when the nerve is re-sewn, the facial nerve fibers oftentimes reconnect to the wrong nerve group causing undesired and simultaneous facial movement. Synkinesis, therefore, results in abnormal synchronization of facial movement where muscles, other than those intended contract together during a particular movement pattern.

Synkinesis does have some predictable facial muscle patterns and can have a range of severities. It is important to separate true paralysis and synkinesis. If patients have good facial tone and some visible movement, then they do not have full paralysis and many of their abnormal facial movements are a result of synkinesis. The most common effect of synkinesis is when patients experience eye closure during a smile. The eyes tend to twitch or close while the patient is trying to smile or laugh. Synkinesis can also be a powerful cause of inability of the corner of the mouth to move upwards in patients who have regained their facial tone. Patients usually just think that their face is not moving; however, in many patients their inability to smile is secondary to synkinetic (simultaneous) movement of muscles that droop the corner of mouth (depressor anguli oris, platysma, and mentalis muscles) and muscles that elevate the area (zygomaticus major and minor). Other patterns of synkinesis are dimpling in the chin and narrowing of the eyes. In addition to these abnormal movement patterns, synkinesis also causes increased muscle tone with spasm, contracture and tightness of the neck bands and cheeks.

Prevention of Synkinesis

There are some ways to reduce the risk of developing synkinesis after bells palsy. The Chevalier’s method is one of the more common ways of using a “facial re-education” method to prevent synkinesis and educate your facial muscles. Patients are encouraged to maintain facial symmetry by keeping the normal side of face up when speaking, chew food with eyes open, avoid gum, wear sunglasses to prevent squinting, massage the intraoral buccal area, always align face to block associated movement, Stretch orbicularis oculi (eye muscles). Patients are also encouraged to really work on having slow and symmetric movements. The key aspect of prevention is the first 3-4 months after injury or Bell’s palsy. It is important to note that some studies have shown that electrical stimulation can result in increased likelihood of developing synkinesis.

Management of Synkinesis

Once synkinesis has occurred, treatment relies on three distinct modalities: neuromuscular retraining (physical therapy), Botox (botulinum toxin) and surgery. Treatment of synkinesis can be initiated at any time after its occurrence. This may be even years after a patient has suffered Bell’s palsy or facial paralysis.

Neuromuscular retraining and physical therapy of synkinesis is very different than what is performed for other medical problems such as back pain and orthopedic injuries. Facial neuromuscular retraining is more comparable to a vocal therapist that is treating a singer who has hoarseness or poor mechanics. Facial neuromuscular retraining is primarily focused on coordinating appropriate facial muscle movements. This is achieved by inhibiting the activity of the abnormal movement patterns resulting in “auto-paralysis” of unwanted muscles.

The muscles that are contracting abnormally are first identified. Muscles that are contracting out of sequence are inhibited. Small steps are usually taken in order to gradually retrain the muscles as there needs to be significant changes at the neurologic (brain) level for success. Electrical stimulation is avoided as it tends to increase the overactive muscles. Muscles that are extremely overactive in the cheek and neck are actively massaged and stretched. Patients are discouraged from undergoing strong muscle strengthening exercises as again this is more about re-coordination rather than stimulation. Patients are also taught how to elevate the upper eyelids during eating to reduce the eye synkinesis. Ninety percent of the therapy is done with the patient at home. The therapist at the Facial Paralysis Institute typically teaches the patients the appropriate home exercises. Other treatment modalities will focus on mirror and video exercises.

The second mode of therapy for synkinesis is BOTOX (botulinum toxin-A). Botox is used in conjunction with facial neuromuscular therapy in most cases. Botox works by reducing the activity of the muscles that are overactive or uncoordinated. Most common areas of injection are eye muscles (orbicularis), neck bands (platysma), and chin dimpling (mentalis). We also utilize it occasionally for very tight cheek if therapy has been unsuccessful. Botox can also be used to symmetrize the face by reducing the activity of certain muscles on the normal side of the face such as: forehead, lower lip depressors (depressor anguli oris) and crow’s feet (orbicularis).

The final modality for synkinesis is surgery. Surgery is utilized only when physical therapy and botox have been unsuccessful in obtaining the desired results. Static suspension of the corners of the mouth, surgical manipulation of the neck bands and blepharoplasty (eyelid surgery) are commonly utilized to address these concerns. During your consultation, all options are discussed at length if you are an appropriate candidate.


  1. Adour KK, Byl FM, Hilsinger RL Jr: The true nature of Bell’s palsy: analysis of 1,000 consecutive patients. Laryngoscope 1978 May; 88(5): 787-801.
  2. Adour KK, Ruboyianes JM, Von Doersten PG: Bell’s palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial. Ann Otol Rhinol Laryngol 1996 May; 105(5): 371-8.
  3. Adour KK, Bell DN, Hilsinger RL Jr: Herpes simplex virus in idiopathic facial paralysis (Bell palsy). JAMA 1975 Aug 11; 233(6): 527-30.
  4. Adour KK, Wingerd J, Bell DN: Prednisone treatment for idiopathic facial paralysis (Bell’s palsy). N Engl J Med 1972 Dec 21; 287(25): 1268-72.
  5. Aldrich MS, Beck RW, Albers JW: Familial recurrent Bell’s palsy with ocular motor palsies. Neurology 1987 Aug; 37(8): 1369-71.
  6. Atlas S: Magnetic Resonance Imaging of the Brain and Spine. 1996; 988-1001.
  7. Austin JR, Peskind SP, Austin SG: Idiopathic facial nerve paralysis: a randomized double blind controlled study of placebo versus prednisone. Laryngoscope 1993 Dec; 103(12): 1326-33.
  8. Baker RS, Sun WS, Hasan SA: Maladaptive neural compensatory mechanisms in Bell’s palsy-induced blepharospasm. Neurology 1997 Jul; 49(1): 223-9.
  9. Baringer JR: Herpes simplex virus and Bell palsy [editorial; comment]. Ann Intern Med 1996 Jan 1; 124(1 Pt 1): 63-5.
  10. Blunt M: The possible role of vascular changes in the aetiology of Bell’s palsy. J Laryngology Otology 1956; 70: 701.
  11. Boddie HG: Recurrent Bell’s palsy. J Laryngol Otol 1972 Nov; 86(11): 117-20.
  12. Conley J, Selfe RW: Occult neoplasms in facial paralysis. Laryngoscope 1981 Feb; 91(2): 205-10.
  13. De Diego JI, Prim MP, Madero R: Seasonal patterns of idiopathic facial paralysis: a 16-year study. Otolaryngol Head Neck Surg 1999 Feb; 120(2): 269-71.
  14. De Diego JI, Prim MP, De Sarria MJ: Idiopathic facial paralysis: a randomized, prospective, and controlled study using single-dose prednisone versus acyclovir three times daily. Laryngoscope 1998 Apr; 108(4 Pt 1): 573-5.
  15. English JB, Stommel EW, Bernat JL: Recurrent Bell’s palsy. Neurology 1996 Aug; 47(2): 604-5.
  16. Hammerschlag PE, Cohen NL, Palu R: Management of facial paralysis with jump interposition graft hypoglossal-facial anastomosis with gold lid weight. Eur Arch Otorhinolaryngol Suppl 1994; S137-9.
  17. Hauser WA, Karnes WE, Annis J: Incidence and prognosis of Bell’s palsy in the population of Rochester, Minnesota. Mayo Clin Proc 1971 Apr; 46(4): 258-64.
  18. Hendrix RA, Melnick W: Auditory brain stem response and audiologic tests in idiopathic facial nerve paralysis. Otolaryngol Head Neck Surg 1983 Dec; 91(6): 686-90.
  19. Jackson CG, von Doersten PG: The facial nerve. Current trends in diagnosis, treatment, and rehabilitation. Med Clin North Am 1999 Jan; 83(1): 179-95, x.
  20. Jackson CG: Facial nerve paralysis: Diagnosis of lower motor neuron facial nerve lesions and facial paralysis. American Academy of Otolaryngology, Head and Neck Surgery 1996.
  21. Keane JR: Bilateral seventh nerve palsy: analysis of 43 cases and review of the literature. Neurology 1994 Jul; 44(7): 1198-202.
  22. Lambert R: Medical Management of Facial Paralysis. Otolaryngology Index 1998; 42: 1-14.
  23. Massey EW: Familial Bell’s palsy. Ear Nose Throat J 1981 Nov; 60(11): 500-2.
  24. Matsumoto Y, Pulec JL, Patterson MJ: Facial nerve biopsy for etiologic clarification of Bell’s palsy. Ann Otol Rhinol Laryngol Suppl 1988 Nov-Dec; 137: 22-7.
  25. May M, Blumenthal F, Klein SR: Acute Bell’s palsy: prognostic value of evoked electromyography, maximal stimulation, and other electrical tests. Am J Otol 1983 Jul; 5(1): 1-7.
  26. May M, Hardin WB: Facial palsy: interpretation of neurologic findings. Laryngoscope 1978 Aug; 88(8 Pt 1): 1352-62.
  27. McCormick DP: Herpes-simplex virus as a cause of Bell’s palsy. Lancet 1972 Apr 29; 1(7757): 937-9.
  28. Morgenlander JC, Massey EW: Bell’s palsy. Ensuring the best possible outcome. Postgrad Med 1990 Oct; 88(5): 157-61, 164.
  29. Murakami S, Mizobuchi M, Nakashiro Y: Bell palsy and herpes simplex virus: identification of viral DNA in endoneural fluid and muscle. Ann Intern Med 1996 Jan 1; 124(1 Pt 1): 27-30.
  30. Olsen KD: Facial nerve paralysis. 2. ‘All that palsies is not Bell’s’. Postgrad Med 1984 Jul; 76(1): 95-7, 100-2, 105.
  31. Petersen B, LaRouere M, Kartush J: Disorders of the Facial Nerve . Otolaryngology Index 1998; 40: 1-19.
  32. Robillard RB, Hilsinger RL Jr, Adour KK: Ramsay Hunt facial paralysis: clinical analyses of 185 patients. Otolaryngol Head Neck Surg 1986 Oct; 95(3 Pt 1): 292-7.
  33. Ruckenstein MJ: Evaluating facial paralysis. Expensive diagnostic tests are often unnecessary. Postgrad Med 1998 Jun; 103(6): 187-8, 191-2.
  34. Shanon E, Himelfarb MZ, Zikk D: Measurement of auditory brain stem potentials in Bell’s palsy. Laryngoscope 1985 Feb; 95(2): 206-9.
  35. Stankiewicz JA: Steroids and idiopathic facial paralysis. Otolaryngol Head Neck Surg 1983 Dec; 91(6): 672-7.
  36. Stankiewicz JA: A review of the published data on steroids and idiopathic facial paralysis. Otolaryngol Head Neck Surg 1987 Nov; 97(5): 481-6.
  37. Wolf SM, Wagner JH, Davidson S: Treatment of Bell palsy with prednisone: a prospective, randomized study. Neurology 1978 Feb; 28(2): 158-61.
  38. Yanagihara N: Incidence of Bell’s palsy. Ann Otol Rhinol Laryngol Suppl 1988 Nov-Dec; 137: 3-4.
  39. Zavlan C, Hou J, Selesnick S: Bell’s Palsy: An Update on Causes, Recognition, Therapy. The Consultant 1999; 39-48.

Leave a Reply must be logged in to post a comment.

»  Substance:WordPress   »  Style:Ahren Ahimsa
© Copyright Yasser Metwally, All rights reserved