|Year : 2011 | Volume
| Issue : 2 | Page : 58-62
Etiopathogenesis of lower motor neuron facial palsy: Our experience
M Venugopal, Sheeja Rajan, R Suma, Subin Thomas
Departments of ENT and Plastic Surgery, Government Medical College, Kozhikode, Kerala, India
|Date of Web Publication||20-Dec-2011|
Department of ENT, Government Medical College, Trivandrum, Kerala
Source of Support: None, Conflict of Interest: None
Introduction : Facial nerve is the seventh cranial nerve having important functions, and hence its paralysis can lead to a great deal of mechanical impairment and emotional embarrassment. Etiopathogenisis of lower motor neuron facial palsy is still a diagnostic challenge and the literature has shown varying results pertaining to the same. This study was designed to sketch out the prevalence of disease causation and the profile of peripheral facial palsy patients presenting to the ENT department at Government Medical College, Kozhikode. Materials and Methods : A prospective study involving 60 patients with facial nerve palsy, presented during the period November 2006 to October 2008, was undertaken. Detailed analysis of etiopathogenesis, age and sex distribution, severity of palsy, anatomical levels and follow up for 1 year was done. Results : Trauma, both iatrogenic and non-iatrogenic, was the most widespread etiology in our study, followed by Bell's palsy which is described as the commonest cause in world literature. Majority of the patients belonged to the age group of 31-40 years and there was slight male preponderance Non-iatrogenic facial palsy following road traffic accident was common in young males, while females dominated in infectious palsies. Majority of cases reported with grade III palsy, followed by grade IV. High-resolution computed tomography of temporal bone is exceedingly sensitive in delineating facial canal. Conclusions : Data analysis shows similarity with the existing literature except a novel trend towards amplified incidence of trauma surpassing Bell's palsy. The need for comprehensive history taking, meticulous clinical examination, judicious investigations and appropriate intervention is substantiated by the study.
Keywords: Etiopathogenesis, Facial palsy, Lower motor neuron palsy
|How to cite this article:|
Venugopal M, Rajan S, Suma R, Thomas S. Etiopathogenesis of lower motor neuron facial palsy: Our experience. Indian J Otol 2011;17:58-62
| Introduction|| |
Face is regarded as the interpreter of emotions, mirror of mind, powerhouse of senses and implement for communication. But here is a condition where you cannot express feelings, talk fluently, smile joyfully, control tears, eat properly, sense taste, restrain saliva and have unpleasant hearing. Most of all, you look awesome and asymmetric. Lower motor neuron facial palsy is the severest emotional trauma one can experience.
Facial nerve is the seventh cranial nerve serving vital functions of lacrimation, salivation, taste, hearing and facial expression. Therefore, it needs urgent measures to understand the cause and nature of nerve injury and to undertake immediate steps for restoration and rehabilitation of facial symmetry About 90% of lower motor neuron facial nerve disorders, whether inflammatory, traumatic or neoplastic, happen along its complex intratemporal course.
Over the past two decades, several developments have been made in this arena. Newer technologies like sophisticated radiology, superior electrodiagnostic study and the emergence of intraoperative monitoring are ready to lend a hand. Protracted course within the bony canal, congenital dehiscence, intricate branching, interconnections, segmental blood supply, all these factors show significantly, heading towards causation and final outcome of insult upon the nerve. An array of etiologies commonly Bell's palsy, followed by temporal bone fracture, surgical trauma, herpes zoster, otitis media (OM), cerebellopontine (CP) angle or intratemporal neoplasm (especially facial nerve schwannoma), impart facial nerve paralysis. The nerve testing relies on determination of the scale of distal axonal degeneration (electrodiagnosis), function of accessory branches of the nerve (topodiagnosis) and radiologic imaging in indicated cases. The objective of the present study was to assess the etiopathogenesis and profile of lower motor neuron VII nerve palsy patients who presented to our ENT department.
| Materials and Methods|| |
This study was carried out in patients with lower motor neuron facial nerve palsy, attending ENT OPD of Government Medical College, Kozhikode, during the period November 2006 to October 2008. After obtaining the patient information and filling it systematically, careful history was taken regarding commencement, causation, duration and progression. Functions of facial nerve were evaluated by topodiagnostic level of voluntary movement present in facial musculature during clinical testing. Entire ENT evaluation including neurological examination was completed and further assessment included Schirmer's test, acoustic reflex, routine laboratory investigations, audiological evaluation and electrodiagnostic tests. We undertook comprehensive radiology including high-resolution computed tomography (HRCT) of temporal bone [Figure 1] and magnetic resonance imaging (MRI) [Figure 2].
All patients were followed up biweekly in the first month, then at 2 months, 6 months and 1 year interval. Category of recovery was made along House Brackmann  grade. Notes were also made on remedial procedures instituted in individual cases-physiotherapy, nerve decompression, temporary tarsorrhaphy, gold implant in upper lid, temporalis muscle sling operation, etc.
| Results|| |
A total of 60 cases of lower motor neuron facial palsy, presenting to the ENT Department of Government Medical College, Kozhikode, during the study period from November 2006 to October 2008 were considered. All cases were subjected to thorough clinical examinations and detailed investigations to uncover the causation of facial palsy. Attempt was made to classify them based on etiology to establish the site of lesion and severity of palsy and to expose the pathology.Trauma, both iatrogenic and non-iatrogenic, constituted the major portion of facial palsy [Table 1]. Bell's palsy remained only the second commonest cause. Infections and tumors also contributed a significant portion. Atticoantral disease was the prevalent suppurative middle ear infection causing lower motor neuron facial palsy. Iatrogenic trauma was mostly following radical surgeries like - radical parotidectomy and neck dissection [Table 2]. Fractures of temporal bone constituted majority of traumatic facial palsy [Table 3]. There was a slight male preponderance in the chart. Most of the facial palsies were in the age group 31-40 years [Bar diagram 1]. Infection was predominant in teenage patients [Table 4]. Bell's palsy was common in middle-aged patients and trauma usually occurred in the age group of 21-30 years. Non-iatrogenic trauma (predominantly road traffic accident) was prevalent in young males while iatrogenic trauma occurred more in females [Table 5] Severity was assessed by House Brackmann grading system [Table 6]. Bulk of the cases presented with grade III palsy (30%), followed by grade IV (25%). For the most part, patients with Bell's palsy attending our institution were with grade IV. Non-iatrogenic traumatic facial palsies were found to be with grade III, followed by grade V. Infections on the whole presented with grade V and neoplasms with grade IV palsy. A great number of facial palsies occurred at the geniculate, suprageniculate and infrastepedial regions of the facial nerve [Table 7]. Complete recovery was the end result in more than 50% of cases [Table 8]. The case which died was carcinoma middle ear. We performed gold implant and temporalis muscle transposition for cases which showed no recovery.
|Table 5: Relative sex incidence of facial paralysis relating to etiology|
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| Discussion|| |
Exploration into diverse etiologies of lower motor neuron facial paralysis in 60 patients was performed in our study. The figures draw attention because of the profile of otorhinolaryngology provision in a tertiary referral center. Majority of the cases were unsurprisingly due to causes within the temporal bone, and hence requiring the apprehension of ENT surgeons. Trauma (41.7%) constituted the major proportion of cases. It may be iatrogenic (20%) or non-iatrogenic (21.7%). The nerve is vulnerable to damage in several head and neck surgeries including mastoid and parotid surgeries. Refinement of surgical technique has reduced the incidence of iatrogenic facial palsy in experienced hands (SB Ogale). Our study observed 20% occurrence. This may be due to inevitable palsies which followed radical parotidectomy for malignancy in five cases and radical neck dissection for malignancy infiltrating the parotid in one case. Patel and Poole  in 1998 reported high incidence after superficial parotidectomy for benign parotid tumor. In our center being a teaching institution, few cases of mastoidectomy developed facial palsy which recovered without consequences. Eftekharian A  in 2005 described that while dissecting the cholesteatoma in epitympanum and supratubal recess, the geniculate ganglion and proximal segment of facial nerve are at risk of injury.
Being an institution with wide catchment area and a hospital receiving higher numbers of road traffic accident referrals, 21.7% cases of facial palsy were accounted for trauma, 16.7% cases showed fracture of temporal bone (by and large longitudinal) and 5% showed blunt trauma to temporal region presenting with late onset palsy. Guerrisi  in 1997 reported that 17% of facial palsy was secondary to blunt trauma. Nageris et al. described late onset facial palsy in temporal bone fracture.
The second common cause identified was Bell's palsy (23.3%) which is described as the most frequent reason in world literature (May and Klein 1991). This may be due to the fact that Bell's palsy cases are being mainly treated by general physicians in our institution. Valcyclovir therapy was recently linked with earlier recovery and better long-term facial nerve function, as illustrated by Gilden and Tyler  in 2007.
Altuntas et al. in 1998, reported 1.7% incidence of facial palsy secondary to CSOM of whom 70% had cholesteatoma. This is analogous to our series (67%). All except one patient in our series improved after mastoid surgery, indicating that the palsy was presumably due to compression effect of cholesteatoma sac. The case which did not improved had eroding cholesteatoma absolutely transecting the facial nerve. The case of facial palsy due to tuberculous OM recovered after antituberculous therapy. Kirsch et al.  in 1996 have reported an increased incidence of tuberculous OM in U.S.A. Malignant otitis externa resulted in facial palsy in two uncontrolled diabetics and the prognosis was unpromising. All the three patients with Ramsay Hunt syndrome responded to acyclovir and steroids. May and Klein listed the incidence of the same as 7% in patients with facial palsy, which is comparable with our study (5%). Yeo SW et al. in 2007 noticed complete revival only in 50% of Ramsay Hunt syndrome.
Tumor was attributed to 8 cases (13.3%) in our study. Schwannoma of 7 th nerve was seen in three cases and acoustic neuroma accounted for two cases. Taken as a whole, the incidence of neoplasm causing facial paralysis showed clear-cut male preponderance of 83%. Rosenberg  in 2000 described that schwannoma of 7 th nerve causes facial palsy only in highly advanced stage.
Majority of patients in our study belonged to the age group 31-40 years. Sex incidence demonstrated trivial male predominance, paralleling a study by Ayala et al. in 2007 which depicted 60% of facial palsy cases as masculine. Non-iatrogenic facial palsy following road traffic accident was common in young males; while infectious palsies were more in females.
Assessment of severity at the time of appearance was done with House Brackmann grading system which showed that the majority reported with grade III palsy (30%), followed by grade IV palsy (25%). Nearly all of the Bell's palsy patient attending our institution had grade IV, which may be because of the referral nature of our center. Yeo and Lee  in 2007 suggested that 96% of Bell's palsy recovered spontaneously.
Topodiagnostic tests showed lion's share of Bell's palsy involving suprageniculate region (44.4%). This is in accordance with the reports of Fish, Esten and Adour regarding bottleneck of facial canal. Bulk of iatrogenic trauma was found to be in the infrastapedial region. Atkins and Osguthorpe have pointed out that second genu of facial nerve is the chosen site of iatrogenic injury. Nearly all cases with fracture of temporal bone had suprageniculate involvement of the 7 th nerve. HRCT of temporal bone is extremely sensitive in delineating facial canal. Electroneuronography is found to be valuable in prognostic evaluation. Literature by Chow et al  in 2002 suggested that electroneuronography helps to make decision after 48 hours of the onset of symptoms.
| Conclusion|| |
The prospective study conducted among 60 patients depicts the vivid etiopathogenesis of lower motor neuron facial palsy cases presenting to otorhinolaryngology department at a tertiary referral center with extensive catchment area. The most common cause of lower motor neuron facial paralysis in this study was trauma accounting for 41.77%, followed by Bell's palsy and infection. Iatrogenic trauma, which is by and large parotidectomy followed by mastoidectomy, slightly superseded non-iatrogenic causes. Non-iatrogenic traumatic facial palsy frequently followed road traffic accidents and was the product of fracture of temporal bone. Cholesteatoma is a chief cause of facial paralysis of infective origin and is frequently due to compressive effect on the nerve. Malignant otitis externa causing facial nerve paralysis had poor prognosis. Neoplasms like schwannoma of 7 th nerve and CP angle tumor accounted for 13.3% of cases of facial paralysis.
The maximum age of incidence was in 31-40 years and the overall sex ratio was 0.9 with a male preponderance. A good number of palsies in this study group belonged to House Brackmann grade III. The most frequent anatomical level of nerve involvement was infrastapedial. In the bulk of Bell's palsy cases, the lesion was suprageniculate. Complete recovery was the result in more than 50% of cases.
Statistical analysis revealed resemblance with the literature reports available, apart from a fresh tendency towards increased occurrence of trauma overtaking Bell's palsy as the most frequent cause. The study enhances the essentiality of all-inclusive history taking, thorough clinical examination, sensible investigations and apt intervention in the analysis of lower motor neuron facial palsy.
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[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]