Facial paresis (FP) is a paralysis of the motor facial nerve, n. Facialis, caused either by a central or peripheral injury of the nerve. Overall, central lesions will only cause paresis in the lower part of the face (since the function of the m. Frontalis and m. Orbicularis oculi is preserved because of bilateral cortical innervation) while a peripheral lesion affects the entire one half of the face according to Eviston et al. (2015).
The incidence of peripheral FP is 15-30 per 100,000 and is most seen in the age group 15-45 years. It is seen a little more frequently in patients with diabetes mellitus and pregnant women. The incidence of central FP has not been determined presented by Eviston et al. (2015).
N. facialis starts at the upper edge of the medulla oblongata between the n. Abducens and n. Vestibulocochlearis. The nerve, which consists of a motor and a combined parasympathetic and sensory component (n. Intermedius) runs through the cerebellopontine angle (CPA) cistern in the posterior cranial fossa and from there into the Internal Acoustic Meatus where it has a close relationship to the inner ear and to the n. Vestibulocochlearis. At the base of the Internal Acoustic Meatus, the two facial components combine and continue into the facial canalis. The nerve leaves the skull through the stylomastoid foramen and then divide on the cheek into the parotid gland according to Eviston et al. (2015).
Nervous facialis innervates motor all mimetic muscles and stirrup, has parasympathetic fibers to the lacrimal and salivary glands, to taste buds from the anterior 2/3 of the tongue and few sensory fibers from the cheek and ear to the trigeminal nucleus, there is attached an anatomical drawing below presented by Eviston et al. (2015).
Symptoms and clinical findings can often be used to determine where during the nerve the lesion is located, but not to determine the aetiology of the paresis.
In the past situations with cold exposure, like cold air conditioning, chilly wind or driving with the car window down could be a trigger for Bell’s palsy. Nowadays the aetiology of Bell’s palsy is still debatable (Taylor, 2021).
However, Reacher’s hypothesis points on herpes simplex virus (HSV) that it is the cause of Bell’s palsy, though it may be difficult to prove that HSV is the cause because of the ubiquitous nature of HSV (Taylor, 2021).
There have been done autopsy that shows HSV in the geniculate ganglion of patients that have Bell’s Palsy. There has also been performed polymerase chain reaction (PCR) testing on the endoneural fluid of the facial nerve in patients who underwent surgery for Bell’s palsy and there were found 11 of 14 cases. HSV can’t be excluded from being the cause of Bell’s Palsy (Taylor, 2021).
There has also been studied other additional causes of Bell’s Palsy, besides HSV, that including infection as Herpes Zoster, Lyme disease, Epstein-Barr, Syphilis, Cytomegalovirus, Human immunodeficiency virus (HIV), inflammation and microvascular disease (hypertension and diabetes mellitus).
Bell’s palsy can also cause the facial nerve to demyelinate, that results in unilateral facial paralysis. Inheritance of family history of Bell’s palsy has been reported with 4% of cases (Taylor, 2021).
Symptoms and signs of peripheral FP is unilaterally reduced force in the facial muscles with reduced ability to smile, frown and close the eye. Symptoms of Bell’s palsy are that approximately 50% of patients believes they have suffered a stroke, 25% fear an intracranial tumor and the remaining 25% are anxious of not knowing what it is (Peitersen, 2002).
Additional symptoms of Bell’s palsy include pain behind or around the ear on the affected side, sometimes extending into the occipital or cervical regions. Loss of the sense of tase on the front two-thirds of the tongue, hypersensitivity to sound in the affected ear (hyperacusis). These associated symptoms are present in 50–60% of the cases of diagnosis of Bell’s palsy according to Lockhart et al. (2009) and Eviston et al. (2015).
When Bell’s palsy is needed to be diagnosed it is made by excluding other causes of unilateral facial paralysis, and 30% to 60% of cases of facial palsy is caused by an underlying disorder that reminds of Bell’s palsy, including central nervous system lesion as a stroke, demyelinating disease, parotid gland tumor, Lyme disease, Ramsay Hunt syndrome, granulomatous disease, otitis media, cholesteatoma, diabetes, trauma, and Guillain-Barré syndrome. If the facial palsy doesn’t improve after 3 weeks, the patient needs to go to a neurologist according to Hohman et al. (2014) and Peitersen (2002).
There have been done randomized placebo-controlled studies, that shows efficacy of steroid therapy, starting within 72 hours of symptom onset. Treatment should be started as soon as possible and no later than 7 days after onset to improve the prognosis. Prednisolone doses and duration of treatment vary. It is proposed Prednisolone 60 mg x 1 for 5 days, tapering with 10 mg daily to 0 mg or 50 mg daily for 10 days without tapering according to Sullivan et al. (2009). Acid pump inhibitors (PPIs) and sleeping pills for side effects are most often added presented by Lockhart et al. (2009).
In case of closed defect of eyelids, to avoid drying out of the cornea, eyeglass bandage, viscous eye drops x 4 daily and eye ointment for the night. In addition to lack of physical coverage, decreased tear production also predisposes to dehydration of the cornea. If the patient’s paresis does not improve after a few days, there should be a subacute referral to an ophthalmologist, there should be consideration of tarsorrhaphy according to Eviston et al. (2015).
Follow-up under the ENT (ear, nose, and throat) specialist, or otolaryngologist is appropriate, as any later examination and treatment is otological presented by Eviston et al. (2015).
The patient can be referred to a practicing otologist or possibly subacute time at the ENT department, by agreement with the otologist on duty. There needs to be reminded of giving the patient their copy of journal, these follow-up takes place privately according to Grogan et al. (2001) and Gantz et al. (1999). Some studies have documented the effect of massage and facial exercises, they may work as psychological treatment for patients (Peitersen, 2002).
There is seen recovery in 85% of patients with Bell’s palsy within 3 weeks. The remaining 15% will improve within 3-5 months. Full recovery is seen in 70% within 6 months of onset, according to Eviston et al. (2015).
Patients over 60 years of age with no improvement after 3 weeks have a poor prognosis. Improving motor skills within 3 weeks is associated with good prognosis. In the absence of function after 3 weeks, function cannot be expected until after 3-4 months, as new outgrowth of axons is awaited. It can take up to 1 year before full or partial recovery (Peitersen, 2002).
Active treatment accelerates recovery and improves the result in those who receive only subtotal recovery. Special training in front of a mirror (biofeedback) has shown an improvement in the prognosis presented by Eviston et al. (2015).
If there is no improvement after a month the patient should be referred. A referral is also indicated if there is only partial recovery after 6–9 months. If progression of the degree of paresis is seen, the patient must be referred for an MRI scan to rule out pathology such as tumor according by Sullivan et al. (2009).
The aetiology of Bell’s palsy is still unclear, but there have been done more studies about what could be causing it and the symptoms of Bell’s palsy seem to vary with each individual, from mild to severe. Studies have shown that symptoms are caused by swelling and inflammation of the facial nerve. To prevent long-term eye complications, eye protection remains very crucial.
Eviston, T. J., Croxson, G. R., Kennedy, P. G., Hadlock, T., & Krishnan, A. V. (2015). Bell’s palsy: aetiology, clinical features and multidisciplinary care. Journal of neurology, neurosurgery, and psychiatry, 86(12), 1356–1361. https://doi.org/10.1136/jnnp-2014-309563
Gagyor, I., Madhok, V. B., Daly, F., & Sullivan, F. (2019). Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). The Cochrane database of systematic reviews, 9(9), CD001869. https://doi.org/10.1002/14651858.CD001869.pub9
Gantz, B. J., Rubinstein, J. T., Gidley, P., & Woodworth, G. G. (1999). Surgical management of Bell’s palsy. The Laryngoscope, 109(8), 1177–1188. https://doi.org/10.1097/00005537-199908000-00001
Grogan, P. M., & Gronseth, G. S. (2001). Practice parameter: Steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 56(7), 830–836. https://doi.org/10.1212/wnl.56.7.830
Gronseth, G. S., Paduga, R., & American Academy of Neurology (2012). Evidence-based guideline update: steroids and antivirals for Bell palsy: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology, 79(22), 2209–2213. https://doi.org/10.1212/WNL.0b013e318275978c
Hohman, M. H., & Hadlock, T. A. (2014). Etiology, diagnosis, and management of facial palsy: 2000 patients at a facial nerve center. The Laryngoscope, 124(7), E283–E293. https://doi.org/10.1002/lary.24542
Peitersen E. (2002). Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies. Acta oto-laryngologica. Supplementum, (549), 4–30.
Sullivan, F. M., Swan, I. R., Donnan, P. T., Morrison, J. M., Smith, B. H., McKinstry, B., Davenport, R. J., Vale, L. D., Clarkson, J. E., Hernández, R., Stewart, K., Hammersley, V., Hayavi, S., McAteer, A., Gray, D., & Daly, F. (2009). A randomised controlled trial of the use of aciclovir and/or prednisolone for the early treatment of Bell’s palsy: the BELLS study. Health technology assessment (Winchester, England), 13(47), iii–130. https://doi.org/10.3310/hta13470
Taylor, D. (2021, May 4). Bell Palsy. Medscape. https://emedicine.medscape.com/article/1146903-overview
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