Bell’s palsy, also referred to as idiopathic facial nerve palsy or facial nerve palsy, is the most common cause of acute spontaneous facial paralysis. The exact cause of Bell’s palsy is not known however, herpes simplex virus activation is the likely cause of in most cases.
The annual incidence rate is between 13 and 34 cases per 100,000 people. There is no race, geographic, or gender prediction, but the risk is three times greater during pregnancy, especially in the third trimester or in the first postpartum week. The increased risk of Bell’s palsy associated with pregnancy, which is most marked in the third trimester and the first postpartum week, may be caused by pregnancy-related fluid retention leading to compression of the nerve or perineural edema. Other potential etiologic factors include hypercoagulability causing thrombosis of the vasa nervosum and relative immunosuppression in pregnancy. Several studies have found an association of Bell’s palsy with preeclampsia, again suggesting extracellular edema as the mechanism.
Patients with Bell’s palsy typically present with the sudden onset (usually over hours) of unilateral facial paralysis. Common findings include the eyebrow sagging, inability to close the eye, disappearance of the nasolabial fold, and drooping at the affected corner of the mouth, which is drawn to the unaffected side. Decreased tearing, hyperacusis, and/or loss of taste sensation on the anterior two-thirds of the tongue may help to site the lesion in the fallopian canal, but these findings are of little practical use other than as indicators of severity.
Diagnosis of Bell’s palsy is typically clinical. Blood work and imaging studies often yield little in the diagnosis. However, blood work and imaging studies are often performed to rule out other possible causes of the facial paralysis. Lyme disease testing is strongly recommended for adults with acute-onset facial palsy when there is the possibility of exposure in Lyme-endemic areas.
Upon the initial diagnosis of Bell’s palsy, it is important to treat with glucocorticoids to help improve the likelihood of recovery. Most patients recover completely within several months to a year, however up to one-third have unfavorable functional and cosmetic outcomes due to chronic facial weakness. For such patients, surgical procedures and botulimun toxin injections (Botox, Xeomin, Dysport) are available to help mitigate long-term sequelae.
Synkinesia and contractures of the face develop in approximately 15% of patients as a late complication of Bell’s palsy due to disorganized and misdirected nerve regrowth on the side of injury. Synkinesia refers to involuntary contraction or twitching of part of the facial musculature upon voluntary facial movement. Most synkinesia after Bell’s palsy is mild and may not be noticed by the affected individual. More severe or bothersome synkinesia can be treated with botulinum toxin injections.
Botox can be used to selectively inhibit muscle contractility. Common facial muscles targets include the orbicularis oculi, depressor anguli oris, depressor labii inferioris, mentalis, and platysma. The focus of treatment is to help balance the facial muscles to give the face a more symmetrical appearance. In order to do so, it requires a great deal of understanding of not only the muscle anatomy but the type of neuromodulator used.
During the initial consultation a thorough evaluation of muscle strength and symmetry of the face is performed. I then map out the injection points, type of neuromodulator I use, and amount of neuromodulator I use for each injection point. Often I will end up with several syringes but each will only have 2-6 units in each.
I perform plenty of injections of neuromodulators for cosmetic reasons but nothing compares to the feeling of helping someone regain confidence and restore the balance to their face. If you are have been affected by Bell’s palsy I urge you to please schedule a complimentary consultation and take the first steps to achieving a balanced face.
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