Very little evidence is available for treating Bells Palsy with Hyperbaric Oxygen Therapy, however, enough anectdotal evidence has been experienced to continue studying hbot as a possibility and to try to determine the effects it has on Bells Palsy. 

If you have evidence whether anectdotal or otherwise that you feel should be added please notify me at rhartsoe@skybest.com
HBOT for Bells Palsy
CHAPTER  17 OF THE HBOT MANUAL
Hyperbaric oxygen as a therapy of Bell's palsy. Undersea Hyperb Med 1997;24(1):35-38; Racic G, Denoble PJ, Sprem N, Bojic L, Bota B; Department of Otolaryngology, University of Zagreb School of Medicine, Split, Croatia. The purpose of this study was to compare the therapeutic effects of hyperbaric oxygen (HBO2) to the effects of prednisone treatment in 79 subjects with Bell's palsy. Patients were randomly assigned either to the HBO2-treated group (n = 42) or to the prednisone-treated group (n = 37). The HBO2 group was exposed to 2.8 atm abs of 100% oxygen for 60 min, twice a day, 5 days a week and was given a placebo orally. The prednisone group was exposed to 2.8 atm abs of 7% O2 (equivalent to 21% O2 in air at normal pressure) following the same schedule as the HBO2 group; prednisone was given orally (total of 450 mg in 8 days). Subjects from both groups were treated in the hyperbaric chamber for up to 30 sessions or to complete recovery, and were followed up for 9 mo. At the end of the follow-up period, 95.2% of subjects treated with HBO2, and 75.7% of subjects treated with prednisone recovered completely. The average time to complete the recovery in the HBO2 group was 22 days as opposed to 34.4 days in the control group (P < 0.001). In the HBO2-treated group, at the beginning, the altered nerve excitability test (NET) was abnormal in five subjects; three of them had normal NET by the end of the follow-up period. In the prednisone group the NET was abnormal in nine subjects at the beginning and they had not recovered by the end of the follow-up (P < 0.05). Our results suggest that HBO2 is more effective than prednisone in treatment of Bell's palsy.

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Man with facial weakness. (Grand Rounds).
Clinician Reviews; 3/1/2002; Anthony, Michael Vincent

A 30-year-old man presented to the emergency department (ED) with limited mobility on the left side of his face and none at all on the fight. The patient was also experiencing hyperacusis, a change in his sense of taste, and speech impairment.

This was his third visit to the ED. During his first visit two days earlier, he complained of facial weakness on the right side of his face subsequent to recent recovery from a viral upper respiratory infection. When a physical examination revealed no unusual findings, the patient was given a prescription for acyclovir and discharged with a diagnosis of Bell's palsy.

The patient returned to the ED the next day reporting that the facial weakness had progressed to the left side of his face. Again, physical examination was unremarkable. It was determined that his symptoms were caused by fatigue, and the patient was instructed to get some rest.

During the most recent visit, the patient was examined by the attending neurologist. The differential diagnosis included sarcoidosis and Guillain-Barre syndrome. Blood workups performed included complete blood cell count, HIV screening, and type-specific and antinuclear antibody testing; spinal fluid and urine were also tested. Both posteroanterior and lateral chest x-rays were performed, as was magnetic resonance imaging (MRI) of the head. All laboratory test results and chest x-rays were within normal limits. MRI revealed questionable swelling of cranial nerve VII on the left side of the face; cranial nerve VII on the right was unremarkable.

Shortly after the evaluation, the patient received a 30-minute infusion of methylprednisolone and an antacid (to combat potential gastric effects). Artificial tears were administered to prevent dehydration of the eyes. Three hours later, methylprednisolone (in conjunction with an antacid) was again administered.

The patient was sent home after his 10-hour stay in the ED. He received a prescription for prednisone to be taken for five days and then tapered for one week. He was advised to continue with the acyclovir regimen. A follow-up appointment was made with the consulting neurologist for three weeks following discharge. The diagnosis was bilateral facial paralysis of unknown etiology (ie, bilateral Bell's palsy).

DISCUSSION

Known causes of facial paralysis include stroke, trauma (eg, laceration, fractures), neoplasm (metastatic lesions, parotid tumors), and congenital defects. (1,2) Bell's palsy, however, is an acute idiopathic condition involving damage to the seventh cranial facial nerve. It is the most prevalent form of facial paralysis' and usually presents unilaterally. Traditionally thought to be a diagnosis of exclusion, unilateral Bell's palsy can be positively identified based on clinical assessment, without performing expensive tests.(3)

Simultaneous bilateral facial palsies (SBFPs) are extremely uncommon and may indicate a more serious disease. In these cases, it is especially important to immediately rule out other causes.(4) See Table 1 (1,5-7)(page 57) for the common differential diagnosis and diagnostic tools.

Some unusual presentations associated with SBFP include HI[V.sup.8] and intracranial hypertension. (9) In these cases, research has shown that the etiology was an unknown infectious process.

Classic Presentation

Typically, the onset of facial paralysis in patients with Bell's palsy is sudden. Paralysis may be preceded by pain in front of or behind the ears that can last until after paralysis becomes complete, usually between three and 72 hours. Patients may complain that the face feels stiff or pulled to one side but will have no demonstrable sensory loss. Hyperacusis (ie, abnormal acuteness of hearing due to increased irritability of the sensory neural mechanism) on the affected side, drooling, excessive tearing, and a change in the sense of taste can accompany facial paralysis. (2)

Bell's palsy affects approximately 25 persons per 100,000. Although incidence increases with age, peak incidence occurs from ages 10 to 40 years. (1,3) Men are affected at the same rate as women. At risk are those who have had influenza, a cold, or some other upper respiratory infection; persons with hypertension or diabetes; and pregnant women. (10-14) The right side of the face is affected 63% of the time. (2) Human herpesvirus 1 has been implicated as the likely cause of Bell's palsy. (15)

Between 60% and 80% of patients will experience a complete resolution of symptoms, while the remaining cases will have some residual--or even permanent--effects. (1,14) Indicators of a favorable prognosis include incomplete paralysis, younger age, and electro-diagnostic tests showing normal nerve excitability. (16)

Treatment

Although most Bell's palsy patients do not require specific treatment, a common regimen prescribed for facial paralysis is physical therapy, which can be used alone or in conjunction with surgery. The most serious complication of the cornea. This can be averted by using an artificial tear solution or applying a lubricating ointment. (2)

Antiviral agents (if infectious processes are suspected to be the cause of paralysis) and corticosteroids are usually prescribed to treat Bell's palsy. Research has shown that patients who receive such treatment within three days of symptom onset experience higher recovery rates than those who start therapy after four or more days. (17) Steroid treatment have been shown to be of little benefit when initiated more than four days after the onset of paralysis. While research has shown that patients given methyl-cobalamin with concomitant steroid therapy to treat Bell's palsy experience greater improvement than those treated with steroids alone, (18) use of this combination is not yet widespread.

Other nonsurgical treatments to combat the effects of facial paralysis include mime therapy, in which patients measure progress by the symmetry of their smile and judgment of their smile by others (19), myofeedback (19,20); hyperbaric oxygen treatments, which have been shown to be more effective than treatment with prednisone (21); and the use of high-voltage electrical muscle stimulation and chiropractic manipulation. (22)

Surgical intervention to reanimate the face is typically reserved for those cases in which the lesion in the facial nerve has been located. (23) Surgery types include cross facial nerve grafts, (24) rectus abdominis muscle transfers, (25) and nerve decompression. (26) Once general reanimation has been established, other therapies can be used to regain control of movement.

Psychosocial Implications

To choose the most appropriate treatment options, clinicians must take into account what their patients consider an acceptable level of functionality, as well as patients' values about their own health and social/moral structures. (27)

The psychosocial impact of facial paralysis can trigger depression, social withdrawal, or both. According to Neely and Neufeld, (28) the importance of the face as a symbol of personal identity and a tool for both verbal and nonverbal communication is often overlooked as part of the psychosocial impact of facial disfigurement. Results from their study show that the quality of patients' smiles influenced how they were perceived by others (see "One Patient's Experience With Bilateral Bell's Palsy," page 58).

CONCLUSION

Clinical assessment is sufficient to diagnose cases of unilateral Bell's palsy. However, when a patient presents with a complaint of SBFP, a complete and comprehensive examination must be performed. The distinctions among extracranial, intratemporal, infectious, traumatic, and idiopathic origin will dictate what type of treatment is necessary.

A conservative, all-inclusive approach is best. Treatment, whether with physical therapy, drugs, or surgery, should be aimed at what the patient feels is an appropriate recovery goal. Because the face is such an important component of nonverbal communication, the more fully patients can return to their original physical state, the better.

Table 1 (1,5-7) 
 
DIFFERENTIAL DIAGNOSIS FOR BELL'S PALSY 
 
Disease              Symptoms                     Diagnostic tools 
 
Melkersson-          Congenitally fissured 
Rosenthal            tongue, orofacial edema, 
syndrome             facial palsy (5) 
 
Mobius'              Congenital facial diplegia 
syndrome             ophthalmoplegia (6) 
 
Guillain-Barre       Ascending motor weakness,    Nerve conduction 
syndrome             usually beginning in legs    velocity; 
                    and possibly leading to      electromyography (1) 
                    respiratory muscle 
                    paralysis 
 
Facioscapulohumeral  Progressive weakness in      Serum creatine kinase; 
muscular dystrophy   the face, neck, upper        electromyography (1) 
                    torso, and upper arms 
 
Myasthenia gravis    Weakness and fatigue,        Computed tomography; 
                    particularly of the          electrodiagnostic 
                    extraocular, pharyngeal,     studies (1) 
                    facial, cervical, and 
                    respiratory musculature 
 
Sarcoidosis          Shortness of breath, cough,  Imaging studies; 
                    skin and ocular lesions;     bronchoscopy; lymph 
                    weakness, fatigue, fever,    node biopsy (1) 
                    malaise (7) 

REFERENCES

(1.) Medline Plus Health Information. Medical encyclopedia. Available at: www.nlm.nih.gov/medlineplus/encyclopedia.html. Accessed February 28, 2002.

(2.) Facial nerve (VII) paralysis. Neuromuscular. Available at: www.neuro.wustl.edu/neuromuscular/nanatomy/vii.htm#anatomy7. Accessed February 28, 2002.

(3.) Ruckenstein MJ. Evaluating facial paralysis: expensive diagnostic tests are often unnecessary. Postgrad Med. 1998;103:187-188, 191-192.

(4.) Keane JR. Bilateral seventh nerve palsy: analysis of 43 cases and review of the literature. Neurology. 1994;44:1198-1202.

(5.) Balevi B. Melkersson-Rosenthal syndrome; review of the literature and case report of a 10-year misdiagnosis. Quintessence Int. 1997;28:265-269.

(6.) Abramson DL, cohen MM Jr, Mulliken JB. Mobius syndrome: classification and grading system. Plast Reconstr Surg. 1998;102:961-967.

(7.) Belfer MH, Stevens RW. Sarcoidosis: a primary care review. Am Fam Physician. 1998;50:2041-2056.

(8.) Krasner CG, cohen SH. Bilateral Bell's palsy and aseptic meningitis in a patient with acute human immunodeficiency virus seroconversion. West J Med. 1993;159:604-605.

(9.) Capobianco DI, Brazis PW, Cheshire WP. Idiopathic intracranial hypertension and seventh nerve palsy. Headache. 1997;37:286-288.

(10.) Bleicher JN, Hamiel S, Gengler JS, Antimarino J. A survey of facial paralysis: etiology and incidence. Ear Nose Throat J. 1996;75:355-358.

(11.) Marson AC, Salinas R. Bell's palsy. West J Med. 2000;173:266-268.

(12.) Savettieri G, Salemi G, Rocca WA, et al. Incidence and lifetime prevalence of Bell's palsy in two Sicilian municipalities. Acta Neurol Scand. 1996;94:71-75.

(13.) Noone J, Longe S. Bell's palsy in the primary care setting: a case study. Clin Excell Nurse Pract. 1998;2:206.211.

(14.) National Institute of Neurological Disorders and Stroke. Bell's palsy information page. Available at: www.ninds.nih.gov/health_and_medical/disorders/bells_doc.htm. Accessed February 28, 2002.

(15.) Billue JS. Bell's palsy: an update on idiopathic facial paralysis. Nurse Pract 1997;22:88, 97-100, 102-105.

(16.) Jabor MA, Gianoli C. Management of Bell's palsy. J La State Med Soc. 1996;148:279-283.

(17.) Hato N, Honda N, Gyo K, et al. Treatment of Bell's palsy with acyclovir and prednisolone [in Japanese]. Nippon Jibiinkoka Gakkai Kaiho. 2000;103:133-138.

(18.) Jalaludin MA. Methylcobalamin treatment of Bell's palsy. Methods Find Exp Clin Pharmacol. 1995;17:539-544.

(19.) Van Gelder RS, Philippart SM, Bernard BG, et al. Effects of myofeedback and mime-therapy on peripheral facial paralysis. Int J Psychol. 1990;25:191-211.

(20.) Visscher CM, Lobbezoo F, Naeije M. Treatment of bruxism: physiotherapeutic approach [in Dutch]. Ned Tijdschr Tandheelkd. 2000:107;293-296.

(21.) Racic G, Denoble PJ, Sprem N, et al. Hyperbaric oxygen as a therapy ofBell's palsy. Undersea Hyperb Med. 1997;24:35-38.

(22.) Shrode LW. Treatment of facial muscles affected by Bell's palsy with high-voltage electrical muscle stimulation. J Manipulative Physiol Ther. 1993;16:347-352.

(23.) House JW. latrogenic facial paralysis. Ear Nose Throat J. 1996;75:720-723.

(24.) Tos T, Krag C. Surgical treatment of sequelae after facial paralysis [in Danish]. Ugeskr Laeger. 2001;163:5647-5651.

(25.) Koshima I, Tsuda K, Hamanaka T, Moriguchi T. One-stage reconstruction of established facial paralysis using a rectus abdominis muscle transfer. Plast Reconstr Surg. 1997;99:234-238.

(26.) Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG. Surgical management of Bell's palsy. Laryngoscope. 1999;109:1177-1188.

(27.) Erde EL, Eden AR. Ethics and the care of persons with Bell's palsy. Soc Sci Med. 1991;32:559-563.

(28.) Neely JG, Neufeld PS. Defining functional limitation, disability, and societal limitations in patients with facial paresis: initial pilot questionnaire. Am J Otol. 1996;17:340-342.

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