Journal of Manipulative and Physiological Therapeutics
Volume 26, Issue 4 , Page 253, May 2003

Chiropractic care of a patient with vertebral subluxation and Bell’s palsy

  • Joel Alcantara, DC

      Affiliations

    • Research Director, International Chiropractic Pediatric Association, Media, Pa, USA
    • Research Associate, Gonstead Clinical Studies Society, Santa Cruz, Calif, USA
    • ,
  • Gregory Plaugher, DC

      Affiliations

    • Director of Research, Life Chiropractic College West, Hayward, Calif, USA
    • Gonstead Clinical Studies Society, Santa Cruz, Calif, USA
    • Corresponding Author InformationSubmit requests for reprints to: Dr. Gregory Plaugher, Life Chiropractic College West, 25001 Industrial Blvd, Hayward, CA 94545, USA
    • ,
  • Darwin L. Van Wyngarden, DC

      Affiliations

    • Private practice of chiropractic, Ripon, Calif, USA

Received 21 November 2001; received in revised form 5 March 2002

Article Outline

Abstract 

Objective

To describe the chiropractic care of a patient medically diagnosed with Bell’s palsy and discuss issues clinically relevant to this disorder, such as its epidemiology, etiology, diagnosis, care, and prognosis.

Clinical features

A 49-year-old woman with a medical diagnosis of Bell’s palsy sought chiropractic care. Her symptoms included right facial paralysis, extreme phonophobia, pain in the right temporomandibular joint (TMJ), and neck pain. Signs of cervical vertebral and TMJ subluxations included edema, tenderness, asymmetry of motion and posture, and malalignment detected from plain film radiographs.

Intervention and outcome

The patient was cared for with full spine contact-specific, high-velocity, low-amplitude adjustments (Gonstead Technique) to sites of vertebral and occipital subluxations. The patient’s left TMJ was also adjusted. The initial symptomatic response to care was positive, and the patient made continued improvements during the 6 months of care.

Conclusion

There are indications that patients suffering from Bell’s palsy may benefit from a holistic chiropractic approach that not only includes a focus of examination and care of the primary regional areas of complaint (eg, face, TMJ) but also potentially from significant vertebral subluxation concomitants.

Keywords:  Bell’s Palsy, Temporomandibular Joint, Chiropractic

 

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1. Introduction 

Bell’s palsy is considered a benign and common neurological disorder of unknown etiology with an average annual incidence rate of 23 to 25 patients per 100,000 population.1, 2 In 1821, Sir Charles Bell3 (1774-1842) first described this condition in a patient with complete facial paralysis but intact facial sensation after transection of the facial nerve at the stylomastoid foramen. Since then, the condition bears his name, but it was Friedreich4 in 1798 and Powell5 in 1813 that described clinically this neuropathy’s onset, course, and natural history. In chiropractic, many anecdotal claims of successful chiropractic care of Bell’s palsy are often heard, but very few studies (none beyond case reports) have been reported in the Medline indexed literature.6, 7 The possible effects of chiropractic care on this disorder have been theorized by Palmieri.8 This article will report on the chiropractic care of a patient with Bell’s palsy and discuss the epidemiology, pathogenesis, and diagnosis of Bell’s palsy, as well as the possible role/effects of chiropractic intervention.

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2. Case report 

A 49-year-old woman complained of right facial paralysis and the inability to close her right eye, extreme bilateral sensitivity to sound, pain in the right temporomandibular joint (TMJ), and bilateral neck pain.

The patient visited her dentist 6 months prior to chiropractic consultation to have her right posterior molars crowned. Five months later and 1 month prior to consulting for chiropractic care, the patient returned to her dentist to have her left upper first molar prepared for crowning. Ten days after her last visit to the dentist, she related experiencing right-sided neck pain and right mastoid pain. Twenty days after her last dental visit, she began lacrimating profusely in her right eye and began suffering from flaccid facial paralysis ipsilaterally. In addition, she reported experiencing severe hypersensitivity to sound in both ears. The patient consulted a medical doctor for these complaints and was diagnosed with Bell’s palsy.

2.1. Chiropractic examination 

On visual inspection, the patient demonstrated obvious right facial paralysis. She could not raise her eyebrow, close her eye, show her upper teeth, smile, frown, or puff her cheeks, all on the right side. Visual spinal inspection was notable for hyperemia at the T1 and T4 spinous areas. Palpation of her paraspinal muscles was notable for tenderness and edema at the C1, T1, T4, and L5 spinal levels. Nervoscope findings9 were positive at C1, C3, T1, T4, T11, L5, and S1 spinal levels. Static and motion palpation findings demonstrated restricted rotation at the C0-1, T1-2, T4-5, T11-12 and L5-S1 motion segments. During palpation of the occiput, gliding of the right mastoid process toward the opposite eye was relatively more restricted when compared to the contralateral side. Based on the examination findings as described, in addition to the radiological studies that will be described shortly, the occiput listing was determined as PSRSRA (+θX, −θZ, +θY).10 The radiologic studies are shown in Fig 1, Fig 2, Fig 3, Fig 4, Fig 5. The decision to obtain radiological studies was based on the patient history and examination findings and, according to the chiropractor, were clinically indicated.11 The anteroposterior open-mouth view is provided in Figure 1. On the anteroposterior cervical views (Fig 2), there is wedging (+θZ) at the C3-4 intervertebral disk (IVD), corroborating restricted left lateral flexion on range of motion analysis of the cervical spine. The C3 spinous process was restricted in motion toward right rotation (−θY), as well as restriction on extension (−θX). The C3 subluxation listing was determined as PLS (−Z, −θY, +θZ).12 The C7 PL (−Z, −θY) was determined similarly with spinous rotation left on radiograph, limited motion on extension, and restricted spinous rotation to the right. Globally, postural assessment reveals the cervical spine is hypolordotic (Fig 3). The 11th thoracic vertebra was listed as to be PRS (−Z, +θY, −θZ). For the described segment (ie, T11), the radiographs demonstrated spinous rotation to the right (+θY) and IVD wedging on the left (−θZ). In addition, there was limited movement of the spinous process on extension, right lateral flexion, and left spinous process rotation. The L5 segment demonstrated on radiographs spinous rotation right and IVD wedging on the left for a subluxation listing of PRI-m inferior (−Z, −θY, +θZ).13 Globally, the lumbar spine is hypolordotic (Fig 4). The left sacroiliac joint was motion restricted in comparison to the right. Gonstead spinographic analysis of the anteroposterior lumbopelvic radiographs (Fig 5) demonstrated a left AS4Ex14 (+θX, +θY) of the left ilium. In addition, the radiographs revealed a left pelvic tilt due, in part, to an 8-mm left leg length deficiency. As a result, the lumbar spine has a left rotatory lumbar curvature and a right upper thoracic curve.

The right TMJ was tender to palpation with jaw restricted on opening and closing. Palpation for joint motion demonstrated that the TMJ deviated on the right upon opening and closing (away from the side of the fixated joint) along with noticeable restriction in mouth opening and closing. Facial sensory testing was unremarkable.

In addition to those mentioned above from the radiographic findings, the full spine radiographs demonstrated osteomalacia with abnormal rib calcification (figure not shown). There was no evidence of other osteopathologies, including fractures and dislocations.

2.2. Chiropractic care 

The patient was seen for a total of 37 visits in a span of 6 months. The left TMJ and the cervical, thoracic, and lumbar spine were adjusted based on subluxation findings following the Gonstead protocol.14 The TMJ was adjusted using the Gonstead unilateral anteroinferior condyle subluxation translational maneuver.15 The patient was seated in the cervical chair with a condyle block to stabilize her cervical spine. Standing behind the patient, the doctor contacts the involved side such that the fingertips are placed on the patient’s chin, the doctor’s pisiform on the ramus of the mandible, and his/her thenar on the lateral pole of the patient’s condyle. The doctor’s stabilization hand is placed on the contralateral side with his/her fingertips on the patient’s chin, the pisiform on the ramus of the mandible, and the thenar on the lateral pole of the condyle. The pattern of thrust is such that the patient is instructed to open her mouth as wide as possible and then to close her mouth slowly. As the patient closes her mouth, the doctor’s stabilization hand pulls in a posterior direction on the contralateral side through the first one third of mandibular movement. The doctor then stabilizes the jaw contralaterally to the involved side by applying a medial force with the stabilization hand. When this stabilization force has been completed, the primary contact hand of the doctor continues to follow the travel of mandibular movement with a sustained force posterior and superior. Just as the mouth is about to close, the primary contact hand will give a light and quick movement posterior, superior, and medial to re-establish the condyle into its fossa.

Occiput and cervical subluxations as previously described (C0: PSRSRA [+θX, −θZ, +θY]), C3: PLS [−Z, +θY, +θZ], and C7: PL [−Z, +θY], respectively) were adjusted in the seated position. For the occiput subluxation, the adjustment was performed as such. The patient is seated with the clinician standing behind the patient, favoring the patient’s right side. The contact points are the clinician’s thenar pad of the right hand over the patient’s right supramastoid groove. The supporting hand stabilized the C1-2 articulation on the opposite side. The pattern of thrust has vector components posterior to anterior (PA), lateral to medial through the C0-1 joint plane line with the patient’s head prepositioned in right rotation.10 For the C3 PLS (−Z, +θY, +θZ) and C7 PL (−Z, +θY) respectively, the patient was seated with the doctor standing behind the patient. The contact points are the clinician’s left palmar and lateral surface of the distal phalanx of the index finger on the inferior lateral aspect of the C3 spinous process. The stabilization hand is placed on the patient’s right side at the C3-4 level. The thrust is an arcing motion through the vertebral body in a PA direction, inferior to superior with a slight +θY rotation through the plane line of the intervertebral disk. At the end of the thrust, a counterclockwise torque is applied. The C7 PL (−Z, +θY) adjustment is similar to the C3 PLS (−Z, +θY, −θZ) except that at the end of the thrust, the counterclockwise torque is not applied.16 The thoracic subluxation (T11: PRS-t [−Z, −θY, θZ]) was adjusted on the hi-lo table with the patient prone. The adjustment is well described by Tanaka et al.17 The lumbar and pelvic subluxations (L5: PRI-m [−Z, −θY, +θZ] and left ilium AS4Ex14 [+θZ, +θY], respectively) were adjusted on the pelvic bench. These adjustments are well described by Plaugher13 and Walters,18 respectively. We recommend the reader attend a Gonstead Seminar or reference the body of literature provided. On the first 3 visits, the patient reported only minimal improvement in Bell’s palsy-related symptoms. With subsequent visits and adjustments, the patient reported improvement. In particular, the patient reported substantial symptomatic relief in the cervical and facial regions after 1 week of treatment. After 20 visits, the patient began to show substantial improvement, such that her facial pain abated and she could close her right eye lightly, smile, move her eyebrows, and puff her cheeks. Facial sensory testing remained unremarkable. After 6 months of care, the patient elected to not continue with chiropractic care.

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3. Discussion 

There is general agreement that Bell’s palsy is an acute, idiopathic, commonly unilateral, peripheral facial paralysis. Simultaneous bilateral facial paralysis is rare with a frequency of less than 1% as compared to unilateral facial paralysis.19 The syndrome occurs more commonly in those aged 15 to 45 years, with the peak incidence for individuals in their 30s. The right and left sides are affected equally, and there is no gender predominance.20

Etiological considerations place Bell’s palsy with an unknown pathogenesis. However, edema and subsequent nerve entrapment of the facial nerve secondary to infection remains as an accepted theory. Works by Fisch et al21 and Fisch22 support this theory. They propose that the entrapment occurs in the labyrinthine segment of the facial canal, creating interference with nerve transmission. Add to this the lack of protective epineural sheath and poor blood supply at this region of the nerve and there results a greater risk for entrapment. Evidence for viral infection as a cause of Bell’s palsy exists.23, 24, 25 Pregnant women and those suffering from diabetes mellitus have a greater incidence of Bell’s palsy.22, 26 The usual site of injury is between the internal acoustic meatus and the stylomastoid foramen. In this patient, involvement of other branches of cranial nerve (CN) VII is indicated by the increase in lacrimation and hyperacusis. The stapedius muscle dampens sound waves and its dysfunction leads to hypersensitivity to sound (hyperacusis). In addition, taste to the anterior two thirds of the tongue may be affected, as well as the submaxillary and sublingual glands.27

Patients with complaints of facial paralysis should be assessed with a thorough history including onset, course, and duration of the complaint, as well as precipitating factors and other symptoms. Specific questions would be past episodes of said complaint, head trauma, ear infection, diabetes, Lyme disease, and pregnancy. The patient should be given a thorough examination of the head and cervical spine, including cranial nerve testing. Gross assessment of the facial nerve involves eye closure, elevation of the eyebrows, smiling, frowning, and pursing of the lips.

Differential diagnosis for patients presenting with facial paralysis include idiopathic, bacterial (ie, pseudomonas species), viral (ie, IV virus, herpes simplex, herpes zoster), and spirochete (ie, syphilis, Lyme disease) infection; neoplasms (ie, neuromas, metastasis, lymphoma); neuropathy (ie, cerebrovascular accident, Guillain-Barré syndrome, multiple sclerosis); and trauma (ie, birth, fractures of the mandible or temporal bone).10 Diagnosis of Bell’s palsy is oftentimes one of exclusion.

Medical management of Bell’s palsy involves the use of corticosteroid for its anti-inflammatory effects and pain management, as well as surgical intervention for nerve decompression and restoration of muscle tone.28, 29 Beyond medical intervention, Jaskoviak et al30 described the use of acupuncture to treat Bell’s palsy. They described 9 patients who were provided an average of 9.3 acupuncture treatments over an average period of 6.7 weeks. At the end of this time, 1 patient was completely symptom free, 4 were greatly improved (80% to 95% recovery), 3 were moderately improved (60% to 65% recovery), and 1 was slightly improved (25% recovery). Ulrich31 describes the successful osteopathic cranial manipulative treatment of a patient with Bell’s palsy. Within the realm of chiropractic intervention, previous reports in this journal involve the following.6, 7 Frach et al6 presented a case series of 2 patients with Bell’s palsy. Chiropractic care was described as consisting of mechanical force, manually-assisted (MFMA) chiropractic adjusting and high voltage therapy as “indicated by palpatory and leg-length equality evaluation.” From the authors’ description, we are unable to determine which, if any, vertebral segments were adjusted or if the TMJ received an adjustment. The finding that our patient had dental care, as well as the patients of Frach et al,6 alludes to a possible etiology of Bell’s palsy and may be underappreciated by dentists. There is documentation that Bell’s palsy can occur following dental care.32, 33 As discussed previously, the precise cause of Bell’s palsy remains unclear; however, a variety of mechanisms have been linked to this palsy, including viral reactivation, demyelination, edema, vasospasm, and trauma,34 in addition to the ones described previously. It is also worth noting that in addition to Bell’s palsy, the patient presented and those of Frach had TMJ problems. Shrode7 also presented 2 cases of pediatric patients with Bell’s palsy cared for through chiropractic means. The care was described as consisting of “high-voltage pulsed galvanic current at 80 peaks/s with a 7-inch handheld prove, with intensity to the patient’s tolerance for 10 minutes” and adjustments to the cervical spine. The outcome for these patients under these care strategies was reported to be positive. Insofar as we can deduce from the 2 previous published papers, this is the first report that describes manual adjustments to sites of spinal (ie, full spine) and extraspinal (TMJ) subluxations using the Gonstead Technique in a patient with Bell’s palsy. Since multiple spinal segments as well as the TMJ was adjusted, it was difficult for the clinician to determine if one particular area or segment that was adjusted was responsible for the patient’s symptom resolution. The case report by Shrode7 supports that adjustments of the cervical spine combined with high-voltage galvanism in patients with Bell’s palsy may be beneficial, but their case report does not describe in whole or in part the detection and removal of spinal subluxations. The case report presented here did not utilize adjunct physical therapy modalities. Kessinger et al35 reported on the chiropractic care of 2 patients with Bell’s palsy utilizing adjustments to the upper cervical spine. Of interest and important to address are the findings that adjustments to the cervical spine in the case presented, as well as those of Shrode7 and Kessinger et al,35 are associated with alleviation of symptoms of Bell’s palsy—a facial paralysis. Is this merely an association or is there causation? We discuss this issue when we address the pathophysiology of Bell’s palsy and the possible effects of chiropractic care, the intimate relationship of the craniocervical-mandibular system and how adjustments to the cervical spine can lead to amelioration of symptoms and dysfunction to the TMJ.36

The outcome of any health care intervention must be examined with respect to the natural history of the offending disorder. The rate of recovery from Bell’s palsy has been given at 80% to 85%.2, 37 According to Petersen et al38 in a study of 1000 patients with Bell’s palsy, 94% of those with incomplete paralysis totally recovered without any intervention, with an overall complete recovery of 71% of cases, 13% having some residual weakness, and 16% with fair to poor recovery. One must consider to what extent the natural history of Bell’s palsy played a role in the recovery of the patient we presented. Alternatively, one can also consider weighing the positive effects of chiropractic care seen in the patient presented (ie, cervical spinal adjustments), particularly with 1 week of chiropractic care. In a study by Katusic et al,2 of the patients with no identifiable risk factors, 96% experienced complete recovery, regardless of the type of medical treatment. Kenrick et al39 showed that no specific treatment, surgical or corticosteroid, was superior over the other. To delineate the role of chiropractic care on patients with Bell’s palsy, more controlled studies are required. To date, no studies have been performed or published beyond case reports on the effectiveness of chiropractic care on these types of patients. Additionally, if indeed spontaneous remission rates are high for Bell’s palsy (usually within 3 to 6 months),35 then the conservative role (ie, drugless) of chiropractic care in decreasing the discomfort and disability of the disease in patients with Bell’s palsy requires further examination.

One of the etiological mechanisms put forth in the pathogenesis of this disease is compression neuropathy as a result of vascular distension due to vasospasm. According to Gussen,40 this apparently occurs in a retrograde fashion via the chorda tympani or other facial nerve branches, such as the greater petrosal nerve and its blood vessels. This retrograde vascular distension results in edematous compression of the facial nerve outside its neural sheath, resulting in reversible or irreversible ischemic degeneration. The degeneration of nerve elements is dependent on the degree of compression. Accompanying degrees of fibrosis within the epineurium as a result of the compression and degeneration may further affect vascular drainage of all connective tissue compartments, ultimately disturbing metabolic ionic exchange within the epineural, perineural, and endoneural structures.

Since its inception, traditional chiropractic approach to patient care has been the detection and removal of vertebral and extravertebral subluxations to maintain health and prevent disease.41 Such an approach to patient care was illustrated in this case utilizing the Gonstead Technique. An obvious issue to address would be the relationship of this disease (ie, Bell’s palsy) to subluxation findings in the spine, more specifically the cervical spine. Such clinical scenarios are not unusual to the chiropractor wherein addressing patient complaints associated with the spine (and extraspinal) results in resolution of a patient’s “unrelated” complaint(s).42, 43 Reconciliation of this scenario in the paradigm of evidenced-based care remains the challenge to our profession. For the patient presented, we provide the following. Neurologically, it is appreciated that reflex effects may exist involving the craniocervical-mandibular system as described elsewhere.36, 44 When one considers the sharing of neuronal pools from cranial nerves V, VII, IX, and X,35, 45 one may hypothesize that adjustments to the cervical spine may activate such reflex effects with salutary outcomes. Furthermore, in previous cases cited in this article as well as ours, there is the observation that the patient’s symptomatology (ie, cervical-mastoid pain) developed prior to the onset of the facial palsy.35 Additionally, theories of the vertebral subluxation complex account for vascular involvement in addition to the classic nerve compression hypothesis.46, 47 Furthermore, adjustments have been shown to cause relaxation effects of muscles and increase range of motion within articulations in addition to its overall analgesic effects.48, 49 Overall, these effects may aid in increasing regional blood flow to the involved areas, especially in the upper cervical spine, and thus improve vascular drainage and resorption of edema causing compression to the facial nerve as discussed above. Reflex effects affecting vasospasm among vascular structures following the facial nerve and its branches may also occur.46 This may again further prevent the resultant neural degeneration as previously described. Overall, the exact mechanisms of our proposed theories are as yet undefined and remain a research challenge.

There are indications that patients suffering from Bell’s palsy may benefit from a holistic chiropractic approach that not only includes a focus on the primary regional areas of complaint (eg, cranium, neck) but also potentially from significant vertebral subluxation concomitants. The chiropractor is well placed, by virtue of his or her emphasis on examination of the nervous system, as well as articular biomechanics, to care for individuals suffering from afflictions in both areas.

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4. Conclusion 

The unique approach of chiropractic care in which vertebral and extravertebral disorders are managed in concomitant with nervous system afflictions such as Bell’s palsy is not well described in the literature. This descriptive case report of Gonstead Technique procedures adds to the paucity of knowledge currently available regarding chiropractic in patients with Bell’s palsy.

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References 

  1. Hauser WA, Karnes WE, Annis J, Kurland LT. Incidence and prognosis of Bell’s palsy in the population of Rochester, Minnesota. Mayo Clin Proc. 1971;46:258–264
  2. Katusic SK, Beard CM, Wiederholt WC, Bergstralh EJ, Kurland LT. Incidence, clinical features and prognosis of Bell’s palsy, Rochester, Minnesota, 1968-1982. Ann Neurol. 1986;20:622–627
  3. Bell, C. Communication of the Royal Society, July 2, 1821
  4. Friedreich NA. De paralysis musculorum faciei rheumatica. J Erfindungen (Gotha) Vol 8(25). Quoted by Ann Med (Edinburgh) 1800;5:214–26
  5. Powell R. Medical transaction. R Coll Phys. 1813;86:155–159
  6. Frach JP, Osterbauer PJ, Fuhr AW. Treatment of Bell’s palsy by mechanical force, manually assisted chiropractic adjusting and high voltage electrotherapy. J Manipulative Physiol Ther. 1992;15:596–598
  7. 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
  8. Palmieri NF. Idiopathic facial paralysis: mechanism, diagnosis and conservative management. Chiropr Tech. 1990;2:182–187
  9. Plaugher G, Lopes MA, Melch PE, Cremata EE. The inter- and intraexaminer reliability of a paraspinal skin temperature differential instrument. J Manipulative Physiol Ther. 1991;14:361–367
  10. Araghi HJ. Upper cervical spine. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;p. 303–324
  11. Haldeman S, Chapman-Smith D, Peterson DM. Guidelines for chiropractic quality assurance and practice parameters. Gaithersburg (MD): Aspen Publishers; 1993;
  12. Lopes MA, Cremata EE. Spinal examination. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;p. 52–72
  13. Plaugher G. Lumbar spine. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;
  14. Plaugher G. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;
  15. Bachman TR. Extravertebral disorders: temporomandibular joint, nasal septum, and sinus. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;
  16. Plaugher G. Lower cervical spine. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;p. 279–302
  17. Tanaka ST, Plaugher G. Thoracic spine. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;p. 243–265
  18. Walters PJ. Pelvis. In:  Plaugher G editors. Textbook of clinical chiropractic: a specific biomechanical approach. Baltimore: Williams & Wilkins; 1993;p. 150–189
  19. Adour KK, Byl FM, Hilsinger RL, Kahn ZM, Sheldon MI. The true nature of Bell’s palsy (an analysis of 1,000 consecutive patients). Laryngoscope. 1978;88:787–801
  20. Petruzzelli GJ, Hirsch BE. Bell’s palsy. A diagnosis of exclusion. Postgrad Med. 1991;90:115–118
  21. Fisch U, Esslen E. Total intratemporal exposure of the facial nerve (pathologic findings in Bell’s palsy). Arch Otolaryngol. 1972;95:335–341
  22. Fisch U. Surgery for Bell’s palsy. Arch Otolaryngol. 1981;107:1–11
  23. Bance M, Rutka J. Speculation on the etiologic role of viruses in the development of Bell’s palsy and disorders of the inner ear dysfunction (a case history and review of the literature). J Otolaryngol. 1990;19:46–49
  24. Ghonim MR, Gavilan C, Sarria MJ. Bilateral simultaneous Bell’s palsy (two cases following herpes simplex gingivostomatitis). ORL J Otorhinolaryngol Relat Spec. 1988;50:269–272
  25. Shaw FE, Graham DJ, Guess HA, Milstien JB, Johnson JM, Schatz GC, et al.  Postmarking surveillance for neurologic adverse events reported after hepatitis B vaccination. Experience of the first three years. Am J Epidemiol. 1988;127:337–352
  26. Torsiglieri AJ, Tom LW, Keane WM, Atkins JP. Otolaryngologic manifestations of pregnancy. Otolaryngol Head Neck Surg. 1990;102:293–297
  27. deGroots J, Chusid JG. Correlative neuroanatomy. 20th ed. East Norwalk (CT): Appleton & Lange; 1988;
  28. Adour KK, Hetzler DG. Current medical treatment for facial palsy. Am J Otol. 1984;5:499–502
  29. May M, Klein SR, Taylor FH. Indications for surgery for Bell’s palsy. Am J Otol. 1984;5:503–512
  30. Jaskoviak P, Frigerio N, Stowe R. Acupuncture treatment of bell’s palsy. J Manipulative Physiol Ther. 1978;1:91–94
  31. Ulrich RG. Osteopathic manipulative treatment of bell’s palsy. AAOJ. 1997;7:28–29
  32. Miles PG. Facial palsy in the dental surgery. Case report and review. Aust Dent J. 1992;37:262–265
  33. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol. 1990;70:738–740
  34. Cousin GC. Facial nerve palsy following intra-oral surgery performed with local anaesthesia. J R Coll Surg Edinb. 2000;45:330–333
  35. Kessinger R, Boneva D. Bell’s palsy and the upper cervical spine. Chiropr Res J. 1999;6:47–55
  36. Alcantara J, Plaugher G, Klemp DD, Salem C. Chiropractic care of a patient with temporomandibular disorder and atlas subluxation. J Manipulative Physiol Ther. 2002;25:63–70
  37. Dalton GE. Bell’s palsy (some problems of prognosis and treatment). BMJ. 1960;1:1765–1770
  38. Peitersen E. The natural history of Bell’s palsy. Am J Otol. 1982;4:107–111
  39. Kenrick MM, Long JA, Corn GB. Facial palsies (follow-up study). Md State Med J. 1977;46:258–264
  40. Gussen R. Pathogenesis of Bell’s palsy. Retrograde epineural edema and postedematous fibrous compression neuropathy of the facial nerve. Ann Otol Rhinol Laryngol. 1977;86:549–558
  41. Gatterman M. Foundations of chiropractic: subluxation. St. Louis: Mosby; 1995;
  42. Elster EL. Upper cervical chiropractic management of a patient with Parkinson’s disease (a case report). J Manipulative Physiol Ther. 2000;23:573–577
  43. Leboeuf-Yde C, Axen I, Ahlefeldt G, Lidefelt P, Rosenbaum A, Thurnherr T. The types and frequencies of improved nonmusculoskeletal symptoms reported after chiropractic spinal manipulative therapy. J Manipulative Physiol Ther. 1999;22:559–564
  44. Knutson GA, Jacob M. Possible manifestation of temporomandibular joint dysfunction on chiropractic cervical x-ray studies. J Manipulative Physiol Ther. 1999;22:32–37
  45. Beckstead RM, Norgren R. An autoradiographic examination of the central distribution of the trigeminal, facial, glossopharyngeal, and vagal nerves in the monkey. J Comp Neurol. 1979;184:455–472
  46. Alcantara J, Plaugher G, Lopes MA, Cichy DL. Spinal subluxation. In:  Anrig C,  Plaugher G editor. Pediatric chiropractic. Baltimore: Williams & Wilkins; 1997;p. 466–478
  47. Wyke BD. The neurology of the cervical spinal joints. Physiotherapy. 1979;65:72–76
  48. Nilsson N, Christensen HW, Hartvigsen J. Lasting changes in passive range of motion after spinal manipulation (a randomized, blind, controlled trial). J Manipulative Physiol Ther. 1996;19:165–168
  49. Vernon H. Qualitative review of studies of manipulation-induced hypoalgesia. J Manipulative Physiol Ther. 2000;23:134–138

 This study was funded by Life Chiropractic College West, Hayward, Calif, and the Gonstead Clinical Studies Society, Santa Cruz, Calif.

PII: S0161-4754(02)54112-9

doi:10.1016/S0161-4754(02)54112-9

Journal of Manipulative and Physiological Therapeutics
Volume 26, Issue 4 , Page 253, May 2003

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