Comparison of Facial Nerve Paralysis in Adults and Children

Facial nerve paralysis is relatively rare, with an annual incidence of approximately 30 per 100,000 individuals in a population. Facial nerve paralysis has various causes, ranging from head injury to idiopathic Bell's palsy, and may occur as a result of injury to the central or peripheral nervous system.1 Since peripherally traveling facial nerves that run along the inside of the facial canal in the intratemporal bones are relatively long, they are at greater risk of injury compared with other cranial nerves. Facial nerve paralysis may induce facial asymmetry, leading to a loss of balanced appearance and function, which may have a deleterious effect on a patient's psychology and social life. Therefore, physicians treating patients with facial nerve paralysis are most frequently asked "what is the probability of improvement?" and "how much improvement will occur?"

Age is a prognostic factor in patients with facial nerve paralysis. For example, age is inversely related to recovery rate2, 3 in adults with Bell's palsy. There have been few comparisons, however, regarding the causality and treatment outcomes in adults and children with facial nerve paralysis. We, therefore, assessed the causes and recovery rates in children and adults with facial nerve paralysis.

The patient cohort consisted of 975 patients with facial nerve paralysis being treated at Kyung Hee Medical Center between January 1986 to December 2005. From their medical records, we retrospectively evaluated their age and sex, the cause of facial nerve paralysis, treatment methods, and recovery rate.

Patients were divided into 6 groups according to their age: 0 - 15 years, 16 - 30 years, 31 - 45 years, 46 - 60 years, 61 - 75 years, and older than 76 years. Patients aged 0 - 15 years were considered children, and those 16 years and older were considered adults. Patients without central nervous system diseases, otologic diseases, and cerebellopontine diseases were determined by medical history as well as by physical examination, and brain or temporal bone MRI. All patients were treated with bed rest, oral corticosteroids, peripheral vasodilators, and physical therapy. Adults were administered 80 mg/day oral prednisolone for the first 4 days, and doseages were tapered to 60 mg/day on days 5 and 6, 40 mg/day on days 7 and 8, 20 mg/day on days 9 and 10, and 10 mg/day on day 11. Children, adolescents, and light-weight adults were administered 1 mg/kg predinosolone for the first 4 days, followed by proportional tapering over the next 7 days.

The degree of facial nerve paralysis was evaluated based on the House-Brackmann classification method. Recovery was evaluated in patients who were followed up for longer than 6 months, with grades I and II recovery defined as satisfactory.

Statistical comparison was performed by the chi-square test, using SPSS for Windows (version 11.5, SPSS Inc., Chicago, IL, USA). A p < 0.05 was considered statistically significant.

Since facial nerves have a long intracranial course and pass through the narrow bony canal within the intratemporal bone, they are more readily injured by middle ear or temporal bone surgery, trauma, infection, and compression caused by tumors in or within the vicinity of nerves. Moreover, facial nerve paralysis may develop secondarily as a result of systemic diseases, or, although rarely, may accompany congenital anomalies. In an analysis of 2,165 patients with facial nerve paralysis, Bell's palsy was the most prevalent cause, followed by incidence of trauma and herpes zoster cephalicus.4 In a second analysis of 161 patients with facial nerve paralysis, the causes were in order of decreasing frequency Bell's palsy, trauma, and chronic otitis media.5 In our overall patient population, the cause of facial paralysis was in the order of Bell's palsy, infection, and trauma. In adults, the order was Bell's palsy, infections, such as herpes zoster oticus, otitis media, otitis media with cholesteatoma, and tuberculosis lymphadenitis, and trauma such as temporal bone fracture, cerebral contusion, facial injury, basal skull fracture, and epidural hemorrhage. The order in children was similar to that in adults: Bell's palsy, infection including herpes zoster cephalicus and acute otitis media, and trauma, including cerebral concussion, temporal bone fracture, and facial injury. The incidence of facial paralysis caused by trauma was significantly higher in children than adults. This may have arisen for various reasons. First, children suffer more severe injuries caused by falls, traffic accidents, and other causes than adults. This is supported by the observation that 10 out of 14 children were H-B grade V, whereas 12 out of 28 adults were H-B grade V. Second, the incidence of facial paralysis due to infection was significantly higher in adults than in children. Finally, there were fewer children in the study than adults.

Numerous studies conducted on factors influencing the prognosis of facial nerve palsy showed younger age,6-8 initial paralysis lower than HB grade III,6-9 and normal responses on nerve excitability tests6, 9 and in stapedial reflex,9, 10 were associated with good prognosis.

As age increases, so does vascular degeneration, which leads to a decrease in peripheral blood supply. These conditions may cause Bell's palsy, with recovery from facial nerve paralysis shown to decrease with increasing age of patients.11 Other studies6-8 found that age is a prognostic factor in patients with facial nerve paralysis. However we found that recovery rate in patients with Bell's palsy was not related to age, with no statistically significant difference between children and adults (p = 0.983).

Recovery rates have been shown to depend on the cause of facial nerve paralysis, with one study showing complete recovery in 64% of patients with Bell's palsy, 55.4% of patients with herpes zoster oticus, 78% of patients with otitis media, and 43% of patients with temporal bone fracture.12 In contrast, others3 have reported that the recovery rate in patients with Bell's palsy was higher than that in patients with herpes zoster oticus. We found, however, that the recovery rate in Bell's palsy patients (91.8%) did not differ significantly from that in patients with herpes zoster oticus (p = 0.171).

Another important prognostic factor is electroneurography, with satisfactory recovery observed in 98% of patients with scores higher than 25% on the healthy side when electroneurography was performed within 10 days of onset.13 Although electroneurography is an objective recording method for facial nerve paralysis as well as being a useful test for assessing the ratio of axons without Wallerian's degeneration, it cannot accurately predict prognosis of patients with facial nerve paralysis caused by herpes zoster oticus.14

Various methods have been used to treat facial nerve paralysis, depending on causality. Spontaneous recovery, however, has been observed in 85% of patients with Bell's palsy, with 71% showing complete recovery (grade I), and another 13% showing satisfactory recovery (grade II).15 Oral steroids are a preferred treatment for patients with Bell's palsy, although it produces mixed results. For example, a retrospective assessment found that prednisone effectively prevented nerve degeneration,16 whereas a prospective, double blind trial found that steroids had no effect when started within 2 days of the disease onset.17 Since the etiology of Bell's palsy is thought to include viral infection,18 the combination of steroids and the antiviral agent acyclovir has been used to treat this condition. Patients treated with steroids and acyclovir had a higher recovery rate than those treated with steroids alone; 92% vs. 76% in one trial,19 and 96.5% vs. 89.7% in another.20 We found that the recovery rate with steroid monotherapy was 85.1%, whereas that with steroid and acyclovir was 92.5%, although the difference was not statistically significant.

Even in studies reporting that more than 80% of Bell's palsy patients achieve complete recovery, approximately 16% of patients do not achieve even satisfactory recovery.21

Surgical methods have, therefore, been utilized to correct incompletely recovered facial nerve paralysis, including methods such as cross-facial nerve grafts with the hypoglossal or spinal accessory nerve, nerve cross-over using the phrenic nerve, or muscle transfer using the temporalis or masseter muscle.22, 23 Recently, the suprascapular nerve has been used for extracranial facial nerve reinnervation.24 In addition, non-invasive methods or Botulinum toxin A may resolve the excessive tension at the opposite side of the paralyzed face, as well as other diverse methods have been attempted.

Another important treatment method is physical therapy. Thus, in addition to drug treatments, all of our patients were referred for physical therapy to the Department of Rehabilitation Medicine. For these patients, physical therapy primarily consisted of neuromuscular retraining of the paralyzed nerve.25 Through electrical stimulation, EMG feedback, and facial expression exercises, this physical therapy regimen enables patients to understand facial exercises and paralysis and to induce natural face movements. These exercises can help prevent the atrophy and contracture of the facial muscles and maintain facial symmetry. The development of synkinesis in patients with facial nerve paralysis can be reduced by neuromuscular retraining.26 In addition, in our department, pamphlets on facial expression exercise were distributed to all facial nerve paralysis patients. Thus, after discharge from the hospital, patients can be trained to move each facial muscle while watching themselves in a mirror.

The facial expression program performed in our department27 consisted of training the expression of each facial muscle, with frowning induced by moving the frontalis muscle, forming waveforms between the eye brows by moving the corrugator supercilii muscle, making wrinkles by moving the procerus muscle, protruding the lips by moving the orbicularis oris muscle, smiling widely by moving the zygomaticus major muscle, protruding the lower lip by moving the mentalis muscle, lowering both ends of the mouth by moving the depressor anguli oris muscle, and filling the mouth with air and exhaling by moving the buccinator muscle. Patients with residual Bell's paralysis who performed such facial muscle exercises showed improvements in their level of paralysis.28

Patients with facial nerve paralysis caused by herpes zoster otitis were treated with acyclovir (800 mg, 5 times daily) and prednisone (60 mg daily for 3 - 5 days). Injections of 100 mg of hydrocortisone and intravenous administration of 5 mg/kg acyclovir every 8 hors for 7 days were shown to induce recovery in 82.6% of patients.29

Due to the disposition of our country, most adults were treated with acupuncture, compared with only 12% of children with Bell's palsy. Acupuncture has been reported to stimulate the central nerve system by secreting chemical substances to the muscles, spinal cord, and the brain. Moreover, acupuncture has been reported to conduct electromagnetic signals and to change involuntary body functions.30

Surgical methods are required for patients in whom paralysis developed immediately after trauma or as the result of chronic otitis media or acute mastoiditis. These surgical methods can include facial nerve decompression, end-to-end anastomosis, nerve graft anastomosis, and nerve cross anastomosis, while several of our patients were treated also with temporalis muscle transfer, mastoidectomy, myringotomy, or tumor resection.

In conclusion, facial nerve paralysis in both adults and children is caused by Bell's palsy, infection, and trauma in decreasing order. In contrast to previous studies, we did not observe a statistically significant difference in recovery rate between adults and children.