Physiotherapy treatment of Bell’s Palsy: A case report Case Report
Transcription
Physiotherapy treatment of Bell’s Palsy: A case report Case Report
Case Report Physiotherapy treatment of Bell’s Palsy: A case report James M. Elliott a,b, c Rueckert-Hartman School for Health Professions, Department of Physical Therapy, Regis University, Denver, Colorado, USA b Division of Physiotherapy, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia c Sport and Spine Physical Therapy, Centennial, Colorado, USA a ABSTRACT Facial nerve (Cranial Nerve VII) paralysis can be a disguring disorder with profound physical and social impact upon the patient. A common diagnosis related to facial nerve paralysis is Bell’s palsy. The aetiology of Bell’s palsy is largely unknown, although it may be congenital, iatrogenic, or result from neoplasm, infection, neurovascular insult, trauma, or toxic exposure. Symptoms may include paresis, hyperacusis, decreased production of tears, altered taste, otalgia, aural pressure and facial pain. Although recovery is expected without intervention in most cases, incomplete recovery is not infrequent. This case report describes a physiotherapy treatment based on current best evidence for a patient with left facial nerve paralysis. The patient was a 53-year-old Caucasian male with complete left-facial paralysis with a diagnosis of Bell’s palsy. Signs and symptoms were assessed using a standardized measure of facial disability (Facial Disability Index-FDI). Physiotherapy rehabilitation involved muscle-re-education exercises aimed at restoring normal movement within the affected left facial musculature. In 16 physiotherapy sessions over 4 months, the patient had improved self-reported facial disability (initial FDI score; Physical subscale = 35/100 and Social/Well-being subscale = 55/100. The nal FDI score; Physical subscale = 75/100 and Social/Well-being subscale = 85/100) and signicantly reduced functional impairments. Generally, patients diagnosed with Bell’s palsy may expect complete recovery without medical and/or physiotherapy intervention. However, some cases remain complicated without complete resolution of symptoms. The need to accurately classify these patients exists. In some cases, physiotherapy may provide extreme benet in reducing the physical and social impairments commonly observed in patients suffering from Bell’s palsy. Self-reported outcome measures, such as the FDI, provide an easy method to assess whether patients suffering from various diagnoses are responding to physiotherapy. The use of such outcome measures will also provide objective evidence of efcacy for third-party payers. Elliott JM (2006): Physiotherapy treatment of Bell’s Palsy: A case report. New Zealand Journal of Physiotherapy 34(3): 167-171. Key Words: Bell palsy, Physiotherapy, Rehabilitation INTRODUCTION Bell’s palsy is a complex neuromuscular facial disorder of unknown aetiology commonly affecting the motor neurones of facial muscles receiving their neurological innervations from the seventh cranial nerve (the facial nerve) (VanSwearingen and Brach, 1998). Most patients’ symptoms spontaneously resolve; however some patients continue to suffer in the long-term. Indicators for poor prognosis include complete facial palsy, no recovery of symptoms by three weeks, age over 60 years, severe pain, herpes zoster virus, co-morbid status e.g. hypertension, diabetes, pregnancy and severe degeneration of the facial nerve shown by electrophysiological testing (Holland and Weiner, 2006). Ultimately, the signs and symptoms related to long-term Bell’s palsy may have a negative effect on many aspects of an individual’s lifestyle. From a functional perspective, the ability to drink, eat and express oneself (verbally/non-verbally) can be greatly disturbed. In addition, the psychosocial impact of such a disorder can be life-altering in relation to social functioning. Treatment often NZ Journal of Physiotherapy – November 2006, Vol. 34 (3) consists of a dose trial of antibiotics, antiviral or anti-inammatory agents and in some cases, surgical decompressive procedures at the facial nerve exit zone (stylomastoid foramen) may be considered (Holland and Weiner, 2006). Further to these medical options for the treatment of Bell’s palsy, physiotherapy has been reported to improve the impairments associated with facial paralysis (Brudny et al., 1988; Brudny et al., 1991; Ross et al., 1991; Brach et al., 1997; VanSwearingen and Brach, 1998; Beurskens and Heymans, 2003). The purpose of this case report is to describe current best evidence conservative rehabilitation approach using a facial neuromuscular reeducation scheme for an individual diagnosed with Bell’s palsy CASE DESCRIPTION The patient (“MG”) was a 53-year-old Caucasian male diagnosed with Bell’s palsy of the left facial nerve with severe left facial paralysis. The initial physiotherapy evaluation was conducted 6 weeks following the onset of symptoms of left facial 167 paralysis. At the time of the initial physiotherapy evaluation, the patient did not report any other signicant medical problems with the exception of his status as a non-insulin dependent diabetic (NIDDM). He managed his NIDDM status with diet and exercise. MG reported that his left facial symptoms came on suddenly with mild pain, markedly decreased sensation in the left face, decreased production of tears but without otalgia, altered taste, hyperacusis or aural fullness. He denied ever having suffered any neck pain nor could he recount any previous trauma to his cervical spine. However, he did report insidious long-standing symptoms (~ 20 years) of hearing loss in his left ear accompanied by vague, infrequent bouts of dizziness/unsteadiness of unknown origin. Further questioning aimed at uncovering other precipitating factors or prodromal symptoms related to his dizziness/unsteadiness was unremarkable. He was initially examined by his family physician who prescribed a course of anti-viral (acyclovir) medication, oral steroids (prednisone) and ordered a magnetic resonance imaging study of his head and cervical spine. No imaging abnormalities were discovered. No electrophysiological nerve conduction studies were ordered or performed e.g. blink reex study. He continued to take prednisone at the time of the initial physiotherapy evaluation but the acyclovir medication was discontinued due to lack of response in relation to his facial symptoms. There were no reports of an acute change for his left sided hearing loss accompanying his facial paralysis; however, he did report reduced tear production and sensation loss in the left side of his face. The physiotherapy evaluation further consisted of a qualitative analysis of his resting facial posture and neurological examination of the head and face, which revealed hypo-esthetic response to pinwheel testing in the three terminal branches of the left trigeminal nerve ((V1) ophthalmic, (V2) maxillary and (V3) mandibular). MG’s resting facial posture revealed severe asymmetry with a left sided droop. Voluntary movement of the leftsided facial musculature was barely visible whereas the uninvolved right-sided facial musculature was clearly intact. The physiotherapist (JE) also performed active and passive cervical movements with no significant findings in relation to the patient’s facial symptoms or aberrant movements. To assess self-reported disability at baseline and to monitor treatment progress, the patient completed the Facial Disability Index (FDI), developed by VanSwearingen and Brach (1996). The FDI is a tenitem questionnaire used for assessing the disability of patients with facial nerve disorder. The FDI is designed to provide the clinician with information regarding the disability as well as related social and emotional well-being of the patient. The FDI consists of two subscales; Physical function (items 1-5) and social well-being (items 6-10). The scores range from 0 (complete paralysis) to 100 (normal facial function). The FDI has shown to be reliable and valid as a clinical instrument and has been shown to accurately demonstrate the relationship between impairments, disability, and psychosocial status (VanSwearingen and Brach, 1996). MG’s initial FDI score on initial evaluation was; Physical function subscale = 35/100; Social/Well-being subscale = 55/100. MG was a full-time truck driver for a local moving company. His duties required him to be on the road for 12 hour shifts, twice per week. He lived alone and reported signicant difculty with drinking, eating, speaking and closing his left eye. These functional impairments were consistent with examination ndings of synkinesis (abnormal movement of the face during a desired motion) for his left and right-sided muscles of facial expression e.g. smiling, ‘puckering’ and frowning. MG also remarked on the need to continually use eye drops as well as performing manual closure of his left eyelid in order to relieve the symptoms of a dry, irritated left eye. These symptoms were consistent with the clinical presence of a positive Bell reex on the left side (eye rolling backward during active eye closure) which prevented complete eye closure (Jelks et al., 1979). He appeared motivated to improve his facial function with physiotherapy intervention. It was initially decided that the patient would be seen one time per week for up to 12 weeks, with each session scheduled for 45 minutes. Each session began with a brief re-evaluation of facial motor functioning e.g. active smiling, frowning, ‘puckering’ and eye closure. TREATMENT It was evident that the patient’s goals were to improve his facial functioning as well as decrease his concern for an impaired aesthetic appearance. In order to assist MG achieve his goals, the treating physiotherapist (JE) performed a literature review on current best evidence for Bell’s palsy and physiotherapy treatment. The literature review yielded recommended guidelines described by Brach and VanSwearingen (1999). The authors describe four distinct treatment based categories (initiation, facilitation, movement control and relaxation stages) matched with specic treatment techniques for each category. These categories can provide helpful guidelines for treatment planning and progression (Brach and VanSwearingen, 1999). Based on the findings of his initial clinical assessment, MG tted within the initiation phase “four distinct treatment-based categories … provide helpful guidelines for treatment planning and progression” 168 NZ Journal of Physiotherapy – November 2006, Vol. 34 (3) of treatment according to the system devised by Brach and VanSwearingen (1999). Therefore, the exercises consisted of actively assisting specic facial movements. In particular, MG was instructed on using his ngers to passively move the left corner of his mouth into a ‘smiling’ posture. He was informed to then slowly release his nger pressure, all the while attempting to actively hold the ‘smiling’ posture with the involved musculature. In addition to the ‘smiling’ exercise, MG was instructed to passively raise his left eyebrow with his nger and activate the appropriate musculature upon release of his passive support nger. BIOFEEDBACK Surface EMG (s-EMG) has been advocated as an appropriate form of visual and/or auditory biofeedback for the re-education of muscle activity in facial movement disorders. However, if s-EMG is not available, a hand mirror may be substituted in order provide visual feedback during the performance of exercises (Brach and VanSwearingen, 1999). As sEMG was not available in our clinic, the patient was informed to utilize a hand-held mirror during the performance of his exercises in order to decrease, if not eliminate, unwanted synkinesis. During this initiation phase, MG was instructed to perform these facial exercises with 5-10 repetitions at a frequency of 3-5 times per day. MG was provided explicit instructions to cease performance of the exercises if fatigue set in and/ or the exercises could not be performed without synkinesis. Our primary goal was to initiate the activation of his left-sided musculature and to reduce, if not eliminate, the poor mass synkinesis patterns which were initially present. The patient, intrigued by this approach, began his exercises at somewhat of a ‘feverish’ pace and was informed on treatment number 2 to reduce the effort put forth as he was likely only contributing to a faulty motor control program e.g. over-facilitating the uninvolved right-side. As a result, treatment, at least for the rst ve treatments, consisted of manually ‘walking’ the patient through what was believed to be ‘just enough’ vs. ‘too much’ effort with the initiation exercises. The other issue that the patient had to contend with was the quick onset of muscular fatigue on the left side, likely due to the highload effort put forth initially. When fatigue occurred, the patient was instructed to cease performance of the exercises and then commence later in his day. As previously stated, MG also complained of a dry, irritated left eye and this was accompanied with a positive Bell reex on the left side. The physiotherapist decided to introduce the exercise put forth by VanSwearingen and Brach (1999) in which the patient is instructed to focus both eyes on an object (e.g. the tip of a nger) positioned down and in front of the patient. Once the patient identies the target, he/she should then attempt to close his/her eyes. The patient should ultimately work towards complete eye closure and it is suggested that having the patient focus on a downward target/object may help initiate the closure of the involved upper eyelid. For MG, this approach appeared to counteract the positive Bell reex. Once he was able to actively close his left eye in a consistent manner, the target was moved in a horizontal direction while his eyes were closed. Upon eye-opening, MG was instructed to keep his head still and actively track and locate the object and then repeat the eye-lid closure exercise. This also became part of his home exercise repertoire; 5-10 repetitions of eye closures, 3-5 times per day. Following the 5 th visit, MG’s neurological exam began to change in that he demonstrated symmetrical sensation with pinwheel testing in the (V3) mandibular division of the trigeminal nerve. The return of sensation to the lower third of the face was also accompanied by an increased ability to develop trace activity in the upper left lip corner with active smiling. Sensation remained unchanged in the left (V1) opthalmic and (V2) maxillary divisions of the trigeminal nerve. The loss of sensation to the upper part of the face remained asymmetrical until the 10th visit, whereupon the exam ndings revealed improved, although slightly diminished, sensation throughout the left V1 and V2 distributions. V3 remained symmetrical. Re-evaluation on the 10th treatment session revealed that MG was beginning to demonstrate improved resting facial posture and active initiation of the involved left sided musculature. As a result, it was decided to progress the patient to the next category of treatment; the facilitation stage. It was also decided that the patient would be seen every other week secondary to his demanding job hours and apparent independence with both the activeassisted and eye-closure exercises and reduced signs of synkinesis. In keeping with the guidelines put forth by Brach and VanSwearingen (1999), resistive exercises were introduced and aimed at facilitating the left-sided musculature. Specifically, MG was instructed on how to use his nger to provide resistance to the desired facial movements e.g. smiling, ‘puckering’ and raising his eyebrow on the left side. Once again, careful attention was taken to avoid muscular fatigue of the involved side and overfacilitation of the uninvolved side. MG was instructed to increase the number of repetitions to 20 and to perform the exercises (1-2 times per day) once in the morning and once before going to bed at night. He continued this regime over the next two months. On the 16th and nal visit, MG demonstrated complete independence with his facilitation “avoid muscular fatigue of the involved side and over-facilitation of the uninvolved side” NZ Journal of Physiotherapy – November 2006, Vol. 34 (3) 169 a) b) 170 a) b) Figure 1. Qualitative images of resting facial posture a) October, 2005 and b) February, 2006 Figure 2. Qualitative images of active smile a) October, 2005 and b) February, 2006 exercises. This was consistent with marked improvement in his resting facial posture and active control of specic facial movements e.g. smiling, raising his left eyebrow without synkinesis and complete left eyelid closure. MG was asked to complete the FDI once more. This indicated improvement in both the physical function subscale = 75/100 (from 35/100 at baseline) and the social/ well-being subscale = 85/100 (from 55/100 at baseline). MG’s improved scores were accompanied with self-reports of signicant improvement with drinking, eating, speaking and closing his left eye. Based on these signs and symptoms, improved FDI scores and his reports of satisfaction in relation to his perceived aesthetic appearance (see Figs. 1 and 2), MG was discharged from physiotherapy following 16 total visits spread over 4 months. Despite not progressing to the movement control category, MG demonstrated signicant functional improvement in his left facial Bell’s palsy. He vowed to continue with his exercises as he felt that they may be required to prevent further problems related to symptoms of facial paralysis. DISCUSSION Features of successful outcomes for patients suffering from Bell’s palsy are likely to be reliant on accurate diagnoses and appropriate followup with a team-oriented approach. Delivery of conservative, categorical physiotherapy care has provided evidence for successful outcome in some cases of patients with Bell Palsy (Brach and VanSwearingen, 1999; Beurskens and Heyman, 2003). In some cases, additional pre-testing may be of value in determining the aetiological features leading to the accurate diagnosis. For example electrophysiological nerve conduction study of the blink reex in patients with Bell’s palsy usually demonstrates prolonged latencies and/or absent early and late responses to stimulation (Kimura et al., 1976; Leon-Sarmiento, 2002). Although a blink reex study was not initially performed on NZ Journal of Physiotherapy – November 2006, Vol. 34 (3) this particular patient, the results of such a test would yield objective evidence of the physiological status of the facial nerve. This may then provide some prognostic information and allow for early and appropriate classication of patients with symptoms of facial paralysis. While unknown, it may be that MG’s insidious onset of Bell’s palsy is related to his past medical history, including hearing impairments and vague bouts of dizziness/unsteadiness. The seventh and eighth cranial nerves (facial and vestibulocochlear) consistently course towards the internal auditory canal within the cerebellopontine angle (Haines, 2006). Lesions, such as contact compression of the seventh and eighth cranial nerves with the neurovascular loop formed by the anterior inferior cerebellar artery, in this anatomical region are not uncommon (Maurer et al., 2000). The resultant symptoms may include unilateral sensorineural hearing loss, tinnitus, vestibular disorders and hemifacial symptoms (Gierek et al., (2000). This particular patient does have a long-standing history of otologic impairment (hearing loss in the left ear and vague complaints of dizziness/unsteadiness). The clinical question may then become whether or not his history of hearing impairments and dizziness/ unsteadiness are related to vascular compression of the cranial nerves at the cerebellopontine angle. Therefore, it is reasonable to speculate as to whether or not MG’s insidious onset of Bell’s palsy may have been reective of neurovascular compression of the seventh and eighth cranial nerves at the cerebellopontine angle? In addition, the question then arises as to whether this patient is at risk for recurrence of his Bell’s palsy symptoms? Finally, it could be argued that a collection of these symptoms should warrant further medical work-up for abnormalities within the vascular loop before a denitive diagnosis can be made. It should also be stated that there is no assumption being made that this particular patient’s successful outcome was solely related to the neuro-muscular re-education scheme. As with many physiotherapy interventions, it can and must be asked whether or not the patient got better because of our intervention or in spite of it? However, this particular patient had suffered from the related symptoms of Bell’s palsy for up to six weeks prior to commencing physiotherapy treatment. Successful resolution of his symptoms was not achieved over that time with traditional medical intervention (anti-viral and anti-inammatory medications). This exceptional patient was extremely motivated and compliant with his physiotherapy exercise program. Therefore, it is believed that along with improved scores on his FDI, his compliance to the prescribed exercises was a large factor into his successful outcome. CONCLUSION Disorders of the facial nerve, including paralysis, are not rare and have a variety of potential causes. The appropriate diagnosis and treatment are very important to achieving the best possible recovery NZ Journal of Physiotherapy – November 2006, Vol. 34 (3) of facial nerve function. Patients suffering from Bell’s palsy may benet from specic categorical physiotherapy treatments designed to improve physical functioning as well as social well-being. The use of the FDI should be advocated in determining the efficacy and progression of physiotherapy treatment of patients with Bell’s palsy. It also provides objective evidence of functional improvement; evidence that is often required by third party payers. Many clinical presentations have different etiologies despite symptom similarities, and caution should be exercised regarding patients having similar clinical presentations. Further clinical investigation and research with a larger population of patients is necessary before a more specic diagnostic/treatment regimen of this type can be recommended. In this regard, however, because of the paucity of available similar documentation in the professional literature, any comments and experiences that other clinical providers have experienced with this type of patient would be welcomed. REFERENCES Beurskens CHG, Heymans PG. Positive effects of mime therapy on sequelae of facial paralysis: stiffness, lip mobility, and social and physical aspects of facial disability. Otol Neurol 2003; 24:677-681. Brach JS, VanSwearingen JM. Physical therapy for facial paralysis: A tailored treatment approach. Physical Therapy 1999; 79(4): 397-404. Brach JS, VanSwearingen JM, Lennerrt J, Johnson PC. Facial neuromuscular retraining for oral synkinesis. Plast Reconstr Surg 1997; 99: 1922-31. Brudny J. Biofeedback in facial paralysis: electromyographic rehabilitation. In: Rubin L, ed. The Paralyzed Face. St. Louis, MO: Mosby-Year Book; 1991;247-264. Brudny J, Hammerschlag PE, Cohen NL, Ransehoff J. Electromyographic rehabilitation of facial function and introduction of a facial grading scale for hypoglossal-facial nerve anastomosis. Laryngoscope 1988; 98: 405-10. Gierek T, Kluczewska E, Pilch J, Zygan L. Vascular compression syndrome of the vestibulocochlear nerve-otolaryngologic and radiologic diagnosis. Otolaryngol Pol 2000; 54(6): 763-7. Holland NJ, Wiener JM. Recent developments in Bell’s Palsy. BMJ 2006; 329(4): 553-557. Jelks GW, Smith B, Bosniak S. The evaluation and management of the eye in facial palsy. Clin Plast Surg. 1979;6:397-419. Kimura J, Giron LT, Young SM. Electrophysiological study of Bell palsy: electrically elicited blink reex in assessment of prognosis. Arch Otolaryngol 1976; 102 (3):104-143. Leon-Sarmiento FE. Blink reex and discomplete facial nerve palsy. Arch Med Res 2002;33(1):85-7. Haines DE (2006): Fundamental neuroscience for basic and clinical applications (3 rd ed.). Philadelphia: Churchill Livingstone, pg.169. Maurer J, Ecke U, Schmidt CL, Stoeter P, Mann W. Vascular origin of cerebellopontine angle syndrome. HNO 2000; 48(2): 142-6. Ross B, Nedzelski JM, McLean JA. Efcacy of feedback training in long-standing facial nerve parresis. Laryngoscope 1991; 101: 744-750. VanSwearingen JS, Brach JS. The facial disability index: 2. Reliability and validity of a disability assessment instrument for disorders of the facial neuromuscular system. Physical Therapy 1996; 76(12): 1288-1300. VanSwearingen JS, Brach JS. Validation of a treatment-based classication system for individuals with facial neuromotor disorders. Physical Therapy 1998; 78(7): 678-689. ADDRESS FOR CORRESPONDENCE: James M. Elliott, 3333 Regis Blvd G-4, Denver CO, 80221, USA. Phone +1 303-458-4022 Fax +1 303-964-5474. Email: jelltt@ regis.edu 171