Bell’s palsy has remained a subject of continuing interest for many disciplines of medicine. The neurologist, otolaryngologist and the primary care physicians share the knowledge about the controversies associated with the management of this disease. Burning issues revolve around the aetiopathognesis, uncertainty about the disease behaviour and the conflicting approaches towards management strategies. With the advent of magnetic resonance imaging, useful data has been compiled about its precise site of the lesion along the course of the facial nerve. Advancements in the immunocytochemical studies have helped to understand the pathogenesis on some sound reasoning. Bell’s palsy is said to be the commonest cause of facial paralysis. Is it still the diagnosis of exclusion? The present article is meant to examine this issue along with literature update on the management.
Bell’s palsy shows no gender predilection. It is said to effect female teenagers more, but after the fourth decade, males are seen to suffer in a larger number. This distribution looks compatible with some relation to menarche and menopause’ Pregnant women are more at risk to suffer from Bell’s palsy and sometimes it is seen in the postpartum period1. Suggested explanation for this association include fluid retention, hypertension, compromise of vasa nervorum, infections and the autoimmune process2. There is no left or right-sided inclination for Bell’s palsy. Less than 1% of the cases are bilateral. Recurrence rate is about 10% that can present on the same or the contralateral side3 Bell’s palsy runs a familial course in 10% of the patients. Data gathered from South America show about 46% family antecedents to suffer from this condition which is surprisingly high supporting a genetic basis4 Diabetics are more prone to suffer. In recurrent Bell’s palsy abnormal glucose tolerance tests are more frequent5. Evidence regarding the seasonality and epidemicity is lacking6.
The exact cause of Bell’s palsy is still not known. Infections, immunologic and genetic factors have been suggested to play roles in the pathogenesis of the disease. The hypothesis that hypoxia and compression of the facial nerve induced by oedema in the facial canal is widely accepted7. Changes are brought about by the Herpex Simplex virus (HSV) infection8 In the contemporary times, HSV has been demonstrated in the geniculate ganglion by using molecular techniques9. This hypothesis looks more tangible when HSV antibody titres were found to be increased in sufferers of Bell’s palsy, when 2-20% of the patients has demonstrated sudden changes in the antibody titres to Herpes group of viruses (Herpez Zoster, Rubella, Cytomegalo, Adeno, Rhino, Mumps and Ebstien Barr). As the patient recovers from a primary HSV infeciton, the virus subsides in a latency phase in the various cranial and spinal nerve ganglia10 Through some poorly understood mechanism, the virus is reactivated within the ganglion cells. Circulating antibodies guard against the dissemination of the virus. This promotes local ganglionitis which may manifest clinically as hypofunction. The virus may travel up or down the axon to induce a radiculitis of a nerve plexus. It may reach brain stem to excite a local inflammatory response in terms of meningoencephalitis, which may reflect as an increased protein content in the cerebrospinal fluid3.
The virus may infect the Schwaan’s cell in the nerve. It acquires a protein coat from the nerve cell as it escapes through the membrane. This operation excites an autoimmune response to the nerve-cell membrane. To follow this phenomenon is the lymphocytic infiltration in the affected nerve fiber, leading to fragmentation of myelin, demyelination and chromatolysis of the facial nucleus3 The cell function is impaired till such time that the distal disease process resolves. Functional muscle reinnervation revive as remyelination starts.
Until recently there was no agreement on the probable location of the facial nerve segment implicated in the Bell’s palsy. Magnetic resonance imaging studies procured during the course of Bell’s palsy have exhibited enhance in the labyrinthine, geniculate and the proximal tympanic segments of the facial nerve11. Entrapment at the site of meatal foramen as the principle factor has been the subject of debate since long. This happens to be the narrowest point in the fallopian canal. Vulnerable vascular channels, conduction blocakde at this point due to neuropraxic effect, MM enhancement of the segment and above all intra-operative observations favour this hypothesis12. There are counter evidences to suggest that facial nerve is not tightly contained at the meatal foramen as studied in children. This provides a possible explanation for the relative infrequency of Bell’s palsy in the young age13. Data accumulated from the cadaver and animal studies points to the fact that labyrinthine segment of the facial nerve contain fewer and smaller intrinsic blood vessels compared to the mastoid and the tympanic segments. This substantiates the contention that labyrinthine segment is the most likely site of lesion in Bell’s palsy14. Autopsy studies in the temporal bone have shown congestion and infiltration of the nerve in the internal auditory meatus. There was compression of the nerve in the proximal portion while demyelination was observed in the tympanic segment13. Interestingly histopathological analysis showed a sharp line of demarcation between sclerotic nerve proximal to and necrotic nerve distal to the meatal foramen, favouring this to be the ideal location of the lesion15.
Bell’s palsy typically presents with an acute unilateral facial weakness, evolving over a period of 24-48 hours. There are certain symptoms, which precede the onset of facial palsy. These include feeling of numbness over face, epiphora, vague feeling of pain, dysgeusia and hyperacusia. The last mentioned symptom is a hallmark of an impending facial palsy3 Incomplete paralysis changes into a complete one over a course of few hours.
The evaluation of Bell’s palsy should start with a thorough history, head and neck examination including a full neurological work out. The practical usefulness of detailed topographic diagnosis in cases of Bell’s palsy is questioned. The site-of-lesion tests that may indicate about the severity or prognosis of the lesion, is doubtful. However, Schirmer’s test for quantification of tearing has practical value to apply eye protection measures effectively, though results are difficult to interpret3.
What is the precise role of electrophysiological studies? They provide useful information about the degree of degeneration in the nerve and carry worth when the paralysis is complete. Testing would be inessential for incomplete cases of Bell’s palsy. Good screening tests could be minimal nerve excitability (MNE) and electroneuronography. Enog is a prognostic indicator of favorable return of function when the degree of degeneration is calculated at 90%. Transcranial Magnetic Stimulation (TMS) is a recent development that is a non-invasive method to excite facial nerve in its intracranial segment close to the internal acoustic meatus. This is the most favored location of the lesion in Bell’s palsy. TMS allows stimulation of the facial nerve above the stylomastoid foramen, facilitating exposure of a greater tract of the nerve. Compared to Enog motor response with TMS predicts good prognosis of the Bell’s palsy at an early stage whereas poor response with Enog predicts less favorable prognosis at a later stage15. Further, TMS is well tolerated and a cheaper tool and does not need to be repeated serially like Enog16. Critics of the TMS have examined the validity of this mode and determined that this mode has failed to provide data which can be correlated to the clinical situation observed at the time of study; further TMS does not furnish prognostic data on the clinical evolution of the lesion17.
One parameter that is worth including in the diagnostic protocol of Bell’s palsy is the presence or absence of acoustic reflex, particularly in children. Shorter duration and higher percentage of recovery have been found in young sufferers of Bell’s palsy with normal acoustic reflex than those with an abnormal or absent reflex18. Absence of acoustic reflex in Bell’s palsy further suggests that this is not a mononeuropathy in the strict sense. It does involve certain of the auditory fibers of the eighth nerve arid is worth considering as a polyneuropathy. Stapedius function is important in speech discrimination at higher level of sound intensity19. However, stapedial reflex findings have demonstrated that this alone is not sufficient to be of prognostic value, but is useful when considered with other clinical parameters and electrical responses20. Central nervous system involvement in Bell’s palsy cases has been postulated. Prolonged brain stem conduction time in a significant number of cases with Bell’s palsy have been picked up as abnormal auditory brain stem responses to support this hypothesis, independent of the site or severity of the paralysis21.
Interfereon is produced in response to viral infection and plays an important part in the defense by their antiviral effects. Elevated serum levels of interferon induced enzyme 2’. -5’ Oligoadenylate synthetase (2’ -5’ AS) could serve as an effective supplementary diagnostic tool in certain cases of Bell’s palsy. Exaggerated levels of 2’ -5’ AS have been found in cases of complete Bell’s palsy22. Elevated serum endothelin levels in cases of Bell’s palsy have been a subject of discussion. Endothelin with its potent vasoconstriction action has been found to be implicated in the aetiology of Bell’s palsy23.
Demyelination associated with Bell’s palsy depicts an increased level of myelin associated enzyme 2’3’ cylic nucleotide 3 phosphohydrolase (CNP) in the cerebrospinal fluid studies. Association has been reported between antibodies against Herpes Simplex Virus and elevated CNP activity. Serum levels of C4 containing circulating immune complexes in patients with Bell’s palsy have been detected using ELISA method24.
The fact that facial nerve in cases of paralysis presents an enhanced picture on magentic resonance imaging (MRI) is now well established. This has been made possible after intravenous administration of Gadolinium diethylenetriamine. Most of the Bell’s palsy cases demonstrate facial nerve enhancement usually in the distal internal auditory canal and labyrinthine/geniculate segments. Gadolinium enhancement occurs regardless of the severity of the paralysis25,26. No difference between the pattern of MRI enhancement in acute or chronic Bell’s palsy cases have been observed. Moreover, radiographic resolution appeared to lag behind the clinical improvement27. Gadolinium enhanced MRI has proved its usefulness as a prognostic indicator. The patients with facial nerve enhancement confined to labyrinthine, geniculate and proximal tympanic segments have shown to regain complete facial function. Whereas contrast enhancement in the mastoid segment of the facial nerve have reported a poor outcome regarding complete return of the facial function28. The mechanism of Gadolinium enhancement with MRI in Bell’s palsy is a non-specific phenomenon, which is also seen in cases of traumatic facial lesions. MRI study is worthless, if ordered in every case of Bell’s palsy. It is recommended in cases of recurrent facial palsy, atypical presentations, failure to elicit any electrical excitability or to exclude a tumour. MRI has its specific application when facial nerve decompression becomes mandatory in intractable cases of Bell’s palsy29.
Bell’s palsy is said to be an idiopathic lesion having no apparent cause. However, an indistinguishable presentation can sometimes be a manifestation of Neuroborreliosis, multiple sclerosis, diabetes, facial nerve neurinoma and HIV infection30. It has been reported as a manifestation of the Burkitt’s lymphoma31. A low-grade deep-seated adenocarcinoma of the partoid may present with a picture, which closely mimics Bell’s palsy, when facial weakness is the only initial symptom32. Infectious mononucleosis atypically may manifest itself with facial weakness similar to the Bell’s palsy33. Peripheral facial palsy resembling recurrent Bell’s palsy has been reported to be precipitated by dental manipulation34.
It has been accepted that Bell’s palsy and a number of inner ear disorders may share a common underlying viral aetiology. This could explain as to why some cases who initially presented with Bell’s palsy, lately develop vestibular dysfunction with a wide-ranging spectrum35. Galvanic body’s way test (GBST) has been accepted as a useful tool in the detection of retrolabyrinthine disorders associated with Bell’s palsy. The higher incidene of positive GBST in cases of Bell’s palsy is suggestive that ‘vestibular neuronitis’ may be caused by a similar pathogenesis36. Peripheral facial palsy may be associated with Lyme disease37. Melkersson Rosenthal syndrome is a rare disorder of unknown aetiology characterized by triad of relapsing facial palsy, or facial swelling and fissuring of tongue. The facial paresis is much alike Bell’s palsy38. Since the triad is not seen typically, the diagnosis becomes difficult.
MRI findings in the maxillary sinus in established cases of Bell’s palsy demonstrate a transient inflammatory picture. This may be taken as an incidental finding, as understanding of the patho-physiology is poorly understood39.
The treatment of Bell’s palsy has remained controversial. The burning issue is the need for starting treatment in incomplete palsy. It is now generally agreed apart from reassurance and expressions of optimism that oral corticosteroids should be started in all the cases of Bell’s palsy as soon as the patient is seen, irrespective of the status of the palsy12. The recommended dosage is Prednisolone 1 mg/kg/day for 5-10 days followed by a gradual reduction over the next 5 days. This can be rationalized on the fact that it is difficult to predict which patient will progress to the severe or complete form. If the treatment is delayed until the severeity is determined, irreversible nerve damage may occur.
In a double-blind study, Bell’s palsy was treated with combinations of Acyclovir-Prednisolone and placeboPrednisolone as a control. The outcome with former was superior to that of the latter40. A better return of the volitional muscle motion was observed. Favourable results have been reported with a protocol comprising of the stat intramuscular Prednisolone 60 mg followed by oral steroids. This regimen has accounted for relief in 95% of the sufferers without sequelae41,42. Hyperbaric oxygen as an additional support has shown to enhance the therapeutic benefit in patients with Bell’s palsy in terms of complete and shortened recovery43.
Based on the pathophysiology of Bell’s palsy that oedema and ischemia leads to compression and hypoxia, Stennert recently introduced parenteral large doses of steroid in the early phase of the Bell’s palsy reporting an extremely high rate of 96%41. This protocol of therapy was not widely accepted because of the hepatic, renal and gastric adverse effects associated with it. Modifications of the Stennert method were employed where hydrocortisone sodium succinate, hydroxymethylated starch and Dmannitol were administered with identical results42.
Methylcobalamine when added to the steroid have improved the symptoms of the Bell’s palsy significantly by curtailing the recovery period44.
Stellate ganglion blockade (SGB) in Bell’s palsy has been advocated to increase the microcirculation of the nutrient artery of the facial nerve45. A published report contradicts the efficacy of SGB. A patient with traumatic cervical sytidrome having SGB subsequently developed Bell’s palsy on the same side challenging the validity of the hypothesis46. The role of physical therapy as a supplement to the treatment of Bell’s palsy has been discussed. It is generally considered invaluable for maintaining confidence of the patient, but is unmanageable and an expense difficult to justify. Experimental research has shown that electrical stimulation of the denervated muscle retard ingrowth of the neurofibrils to the motor endplates47. Contrary to this hypothesis high voltage electrical muscle stimulation has shown benefits in terms of accelerated progress in cases of Bell’s palsy48.
Surgical decompression of the facial nerve in Bell’s palsy is a chronicled controversy. Timings of the decompression, appraoches and sites of the decompression and the imperfect regeneration following decompression have remained the issues of disagreement. The criteria for surgical candidacy include acceptable anaesthetic risk, less than 60 years of age, Enog demonstrating 90% or greater degeneration of nerve fibers within 3 weeks of the onset of paralysis, absence of the evidence of neuropraxia or deblocking on EMG and the informed consent14 Those fulfilling the requirement should be subjected to surgery only when the ear is free of infection and the proviso that the other ear has servicable hearing. Middle cranial fossa decompression is the procedure of the choice offered to the selected patients who meet the criteria on strict merit. Surgical decompression of the tympanic and mastoid segments are seldom helpful12,49.
Among the supportive measures for treatiing, Bell’s palsy care of the eye is of fundamental importance. Corneal abrasions and epithelial defects can lead to dreadful sequel, due to foreign body and drying effect. Dark glasses must be worn during the daytime and application of a bland eye ointment is essential during sleep. An early sign of keratitis calls for packing or tarsorraphy. Temporary closure of the eyelid is especially recommended when re-epithelialisation of the cornea becomes problematic. Tube tarsorraphy using plastic tubes sutured externally to the upper and lower eyelids is a newly devised technique50. Here the eyelid closure is accomplished by tightening a loop of suture passed through the tube.
Predicting prognosis of Bell’s palsy is difficult, particularly in the early phase of the disease. It was found that young patients with incomplete paralysis, unaccompanied by post-auricular pain loss of taste sensation, hyperacusis, dry eye and recovery beginning within the 4 weeks of the onset of palsy are likely to make complete recovery. In comparison, older patients with complete palsy, accompanied by postauricular pain, loss of taste, hyperacusia, dry eye and the onset of recovery after the 4 weeks of the onset of palsy are more likely to have incomplete recovery51.
Electrophysiological tests are complimentary and when used appropriately can accurately describe the completeness of degeneration52. TMS is said to be a better mode of early prediction15. In a significant number of cases a contralateral early blink reflex response could be elicited on stimulation of the normal side. This indicates synaptic reorganization in the facial nucleus during regeneration and can be used as a prognostic indicator53. Enog estimates the prognosis of the Bell’s palsy particularly between the first and the third month of onset by serially testing to determine the end-point of degeneration53. Facial nerve latency test (FNLT) is another useful prognostic marker. When latency is within normal limits the damage to the nerve is slight; if the latency is prolonged the prognosis is usually worse54.
Personal computers have been successfully employed to gauge the progress of Bell’s palsy. Movements of the face were photographed with a video camera and fed continuously into the computer by means of digital image processing technique. Special marks placed on the face were extracted and the movements of these marks were quantitatively analyzed. The rate of improvement process can be evaluated by comparing the ratio of affected to normal side facial movements55. MRI studies depict that patients with enhanced segment of the mastoid segment carries a poor prognosis for the complete return of the facial function.
One important issue in the prognositc consideration is the aberrant regenration of nerve fibers after Bell’s palsy. Complications of facial nerve regneration include contractions, synkinesis (associated facial motion), tics (facial spasm) and gustatory tearing (crocodile tears). These are extremely difficult to treat. Synkinesia can be managed by Botulinum toxin injection into the affected muscle with reasonable results56.
1. Hilsinger RLS, Adour KK, Dote HE. Idiopathic facial paralysis, pregnancy and the menstrual cycle, Annals of otology, rhinology and laryngology, 1975;84:433-42.
2. Walling AD. Bells palsy in pregnancy and the puerperium. J., Fam. Prac., 1983;36(5):559-63.
3. Adour KK. Medical management of idiopathic Bell’s palsy, Otolaryngology clinics of Norht America, 1991,:663-73.
4. Gorodezky C, Carraniza JM, Bustamanti A, et al., The HLA system and the T cell subsets in Bell’s palsy, Acta-otolaryngologica-Stockholm, 1991;111(6):1070-4.
5. Adotir Kkd, Wingerd J, Dote HE. Prevalence of concurrent diabetes mellitus and the idiopathc facal paralyss, Diabetes, 1975;24:449-51.
6. Brandenburg NA, Annegers JF. Incidence and risk factors for Bell’s palsy in Laredo, Texas, Neuroepidemiology, 1993; 12(6):313-25.
7. Saito 0, Electrophysiological study on pathophysiology of Bell’s palsy -Distribution of nerve conduction velocities in facial nerve with collision method, Nippon-Jibiinkoka-Gakkai-Kaiho, 1991 ;94(7):906-14.
8. Sugita, 1. Facial nerve paralysis induced by Herpex Simplex Virus infectiion in mice, Nippon-Jibiinkoka-Gakkai-Kaiho, I 993;94 1 (6):685-92.
9. Burgess, RC, Michaels, Bale JF et at. Polymerase chain recaction amplification of Herpes Simplex viral DNA from the geniculate ganglion of a patient with Bell’s palsy. American Journal of otology, rhinology and laryngology, 1 994;l 03(10):775-9.
10. Wildy P. The progression of Herpex Simplex virus to the central nervous system of the mouse, Journal of Hygiene, 1967(65):173-92.
11. Murphy TP, Teller DC. Magnetic facial nerve imaging of the facial nerve during Bell’s palsy, Otolaryngology Head and Neck Surgery, 1991 ;1 05(5):667-74.
12. Marsh MA, Coker NJ. Surgical decompression of idiopathic facial palsy, Otolaryngology clinics of North America, 1991 ;24(3):675-89.
13. Eicher SA, Coker NJ, Alford BR, et al. A comparative study of the fallopian canal at the meatal foramen and labyrinthine segment in young children and adults, Archives of Otolaryngology, Head and Neck Surgery, 1990;l 16(9):1080-5.
14. Balkani T, Fradis M, Jafek BW, et at. Intrinsic vasculature of the labyrnthne segment of the facal nerve-implication for site of lesion in Bell’s palsy, Otolaryngology, Head & Neck Surgery, 1991;1048(1):20-3.
15. Rimpilianen I, Eskola H, Laippelo P, et al. Prognostication of Bell’s palsy using trascranial magnetic stimulation, Acta Otolayrngologica- SuppStockholm, 1997;529: 111-5.
16. Laranne J, Rimpilianen 1, Karma P, et at. A comparison of transcranial magnetic stimulation with Electronystagmography as a predictive test in patients with Bell’s palsy, European Archives of Otolaryngology, 1995;252(6):344-7.
17. Cocito D, De-Mattei M. Inadequacy of transcranial magnetic stimulation in the neurophysiologic assessment of Bell’s palsy. Electromyography and clinical Neurophysiology, 1992 ;32( 10-11 ):52 1-30.
18. Qiu WW, Yin SS, Stucker FJ, et al. Neurophysiological evaluation of acute facial paralysis in children, Internationt Journal of Pediatric Otolaryngology, 1997;3 :226-36.
19. Wormald PJ, Rogers C, Gatehouse S. Speech discrimination in patients with Bell’s palsy and paralyzed stapedius msucle, Clinical otolaryngology,
20. Portmann M, Daumaan R, Negrovergue M, et al. The prognostic value of stapedial reflex in peripheral facial palsy, Ear, Nose and Throat Journal, 1990;69(1 0):696-7.
21. Kavium M, Jafarey AH. Auditory brain stein response audiometry in patients with Bell’s palsy, Clinical Otolaryngology, 1995;20(2): 135-8.
22. Nakazato H, lkeda M, 2’ -5’ Oligoadenylate synthetase activity in peripheral facial palsy, Nippon-Jiibinkoka-Gakkai-Kaiho, 1995;98(3):457-64.
23. Tojima M, Ikeda M. Evaluation of plasma endothelin levels n facial nerve paralysis, Nippon-Jiibinkoka Jakkai-Kaiho, 1995;98(1 ):2-8.
24. Larsson A, Jonsson L, Sjoquist J. Bell’s palsy, an immune complex disease, Journal of Otology and Latyngology, 1990;52(3):164-7.
25. Schwaber MK, Larson TC, Zealear UL, et al. Gadolinium enhanced magnetic resonance imaging in Bell’s palsy, Laryngoscope, 1990;100(12): 1264-9.
26. Lien R, Dillon WP, Jackler RK. Contrast enhanced MR imaging of the facial nerve in 11 patients with Bell’s palsy. American Journal of Neuro-radiology, 1990;11(4):735-41.
27. Murphy TP, Teller DC. Magnetic resonance imaging of the facial nerve during Bell’s palsy, Otolaryngology, Head and Neck Surgery, 1991 ;1 05(5):667-74.
28. Murphy IP. MRI of the facial nerve during paralysis, Otolaryngology Head and Neck Surgery, 1991;104(1):47-51.
29. Doringer E, Albergger K, Sinzinger G, et al. Idiopathic facial paralysis and MR tomography, Head and Neck Oncology, 1991 ;39(9):362-6.
30. Noya M, Pardo J. Diagnosis and treatment of facial palsy, Neurologica, 1997;1 2(1):23-30.
31. Katz 3, Polliack A, Harushouski T, et al. Bell’s paly as a sign of Burkitt’s lymphoma in children (letter), Blood, 1995;86(5):2052.
32. Chilla R. Paralysis of the facial nerve caused by low-grade adenocarcinoma of the parotid gland-a contribution to the diagnosis of the Bell’s palsy, Laryngo-rhino-otolögica, 1995;74(4):242-4.
33. Wijnia JW, Niekus HI, Hart W, et al. Neurological complications of infectious mononucleosis, Tijdschr Geneeskd, 1994;138(17):884.
34. Shuaib A, Lee MA. Recurrent facial nerve palsy after dental procedures, Oral Surgery, Oral Medicine and Oral Pathology, 1990;70(6):738-40.
35. Bance M, Rutka J, Speculations into the aetiology, role of viruses in the development of Bell’s palsy and disorders of inner ear dysfunction, Journal of Otology and Laryngology, 1990; 19(1 ):46-9.
36. Watanabe, Yaso S, Yasumura S, et al. Retrolabyrinthine disorders in cases with peripheral facial palsy, Acta-Otolaryngologica-Stockholm, 1993;503:202-4.
37. Ruel M. How many peripheral facial paralysis are manifestation of Lyme disease? A French multicentric study, Annuls Otolaryngologie Chirugie Cervicofacial, 1990;107(4):270-2.
38. Rogers RS, Melkersson-Rosenthal syndrome and orofacial granulomatosis, Dermatology Clinic, 1996;14(2):371-9.
39. Strengquist M, Engstrom M, Thuomous, KA, et al. Inflammatory paranasal sinus disease in Bell’s palsy: Demonstration by MRI imaging, American Journal of Otolaryngology, 1993;14(3):295-300.
40. Adour KK, Ruboyianes JM, Von Doersten PG,et al. Bell’s palsy treatment with Acyclovir and Prednisotone compared with prednisolone alone, a double-blind, randomized, controlled trial, Annuls of Otology, rhinology and laryngology, 1996; 105(5):37 1-8.
41. Inamura H. Tojima A, Saito 0, et al. Conservative treatment of idiopathic facial palsy: Effect of the administration of high dosage steroids in Bell’s palsy: Nippon-Jibinkoka-Gakkaai-Kaiho, 1992;95(2): 172-7.
42. Watanabe S, Kenmochi M, Kinoshita H, et at. Effect of the administration of high dosage hydrocortisonc in Bell’s palsy, Acta-Otolaryngologica-SuppStockholm, 1966;522:108-10.
43. Boju L, Bola B, Hyberbaric oxgen as a therapy of Bell’s palsy. Undersea hyperbaric medium, 1997;24(1):35-8.
44. Jalatuddin MA. Methylcobalamine treatment of Bell’s palsy, Clinical pharmacology, 19951 (8):539-44.
45. Murakawa K, Ishimoto E, Noma K, et at. Circulatory effect of Stelllate ganglion block in idiopathic facial palsy, Masui, 1994;43(3):356-60.
46. Mikawa K, Hiyash M, Goto R, et at. Development of Bell’s palsy despite treatment of post-traumatic headache by Steltate ganglion block, Journal of Internal Medicine, 1991; 19(1):67-9.
47. Mosforth J, Taverner D. Physiology foe Bell’s palsy, British Medical Journal, 1958;675--7.
48. Shrode LW. Treatment of facial muscles affected by Bell’s palsy with high voltage electrical stimulation, Journal ot Manipulative physiological therapy, 1993; 16(5):347-52.
49. Hughes GB. Practical management of Bell’s palsy, Otolaryngotogy, Head and Neck Surgery, 1996;(6):658-63.
50. Rapoza PA, Harrison DA, Bussa Ji, et at. Temporary sutured tube tarsorraphy, a reversible eyelid closure technique, Ophthalmic surgery, 1993;24(5):328-30.
51. Kar N, Banerjee SK. Prediction of recovery of Bell’s palsy from clinical manifestations. Journal of Indian Medical Association, 1992;90(10):267-9.
52. Coker NJ. Acute paralysis of the facial nerve in Otolaryngology, Head and Neck Surgery, (Byron J. Bailey Ed.). J.B Lippincott Co. Philadelphia, 1993, pp. 1717.
53. Nacirniento W, Podolt K, Gracber MD, et at. Contralateral early blink relfex in patients with facial nerve patsy: Indication for synaptic reorganization in the facial nucleus during regeneration, Journal of Neurological Sciences, 1992;109(2):148-55,
54. Danietides V, Skevas A, Kastanioudakis I. Comparative study of evoked electromyography and facial nerve latency test iii the prognosis of idiopathic facial nerve paralysis in childhood, Child Nervous system, 1994;10(2):122
55. Sono M, Murata K, Taneka H, el at. An objective evaluation mehtod for facial mimic motions, Otolaryngotogy, Head and Neck Surgery, 1996;114(1):27-37.
56. Roggenkamper P, Laskawi R, Darnaz W, et at. Involuntary lid closure raised by defective healing of facial paralysis and its treatment with Botulinum toxin, Klinic Monatsbi, 1991;198(4):268-70.