Lyme disease is caused by the bacteria borrelia burgdorferi. This bacterium is carried by both deer ticks, as well as in the regular tick population. It is endemic to New England, but has spread rather extensively throughout the world, in climates similar to those found in New England. The disease is named after the town in Connecticut where it was first described.

While nobody knows exactly how neural dysfunction occurs in Lyme disease, the clinical picture of Lyme-associated facial paralysis is quite recognizable. People develop symptoms of Lyme disease, either headaches, joint pains, high fevers, a bull’s-eye rash, or any combination of these things. Most often, people experience fatigue and feel quite ill when they have this condition. Then, they can develop unilateral or bilateral facial paralysis, sometimes before starting medical treatment for Lyme disease, and sometimes right after initiating medical therapy with antibiotics.

            Lyme-associated facial paralysis recovers somewhat like Bell’s palsy and other viral reactivation conditions, but sometimes can be more protracted, and not recover as thoroughly or accurately as Bell’s palsy. When it affects both sides of the face, people can develop difficulty with maneuvers like puckering their lips outward.  While it is mandatory to receive antibiotic therapy, it is not clear whether steroids benefit facial nerve outcomes for people who have Lyme-associated facial paralysis.  It is possible that in the future, when we more fully understand the exact mechanism of neural damage in Lyme disease, we will be able to develop better treatment strategies for this condition. In the meantime, it is treated much the same way Bell’s palsy is, and always results in recovery of the facial nerve, though to variable degrees, and sometimes in a very disorganized fashion that can lead to tightness and facial asymmetry. If these develop, they can be effectively treated with a number of medical and surgical therapies.