Abstract

Objective: To report a case of postpartum bilateral facial weakness that preceded the diagnosis of preeclampsia. Introduction: Bell’s palsy is a neuromuscular disorder that can cause paralysis or weakness of the face. It is the most common cause of unilateral facial weakness; however, bilateral weakness is rare. Bell’s palsy is one of the most common neuromuscular disorders observed in pregnancy, though the link between the two is not entirely clear. Proposed etiologies include reactivation of human herpes viruses, immune mediated inflammatory demyelination of the facial nerve, and microangiopathy as a result of systemic hypertension. There have been several case reports and studies suggesting a correlation between preeclampsia and Bell’s palsy. We present a rare case of postpartum bilateral Bell’s palsy in the setting of preeclampsia. Design: Case report. Results: Our patient is a 24 year-old G6P4116 Caucasian woman with no significant past medical history who presented with bilateral facial weakness and headache. She was postpartum day four from a spontaneous vaginal delivery of dichorionic diamniotic twins at 35 weeks at an outside hospital. She denied any elevated blood pressures during her pregnancy. Initially, on postpartum day two she had reported a severe headache that initially affected her occipital region bilaterally before migrating to her ears and forehead. At this time the patient was normotensive and was discharged home on analgesics. On postpartum day three, she returned to another emergency department with a worsening, severe headache. She was sent home with a diagnosis of anxiety. On postpartum day four, her symptoms persisted and she came to the emergency department at our facility. During our initial evaluation, her blood pressure was 170/98. She was admitted for severe preeclampsia and given IV magnesium and nifedipine. However, her headache persisted and she developed bilateral facial weakness, neck pain, and swelling. She reported that she was unable to move her face and had difficulty smiling. Her face was expressionless. She denied nausea, vomiting, dysphagia, double vision, gait disturbances, hearing loss, fever, shortness of breath, numbness, or tingling. She denied recent travel, sick contacts, or animal or tick bites. She was evaluated by neurology and her initial physical exam revealed intact cranial nerves, though the patient appeared to have difficulty squeezing her eyes shut and smiling. Periorbital edema was noted. Facial symmetry and sensation were intact bilaterally. She had difficulty saying the letter “P.” Her MRIs of both brain and cervical spine, chest x-ray, and lumbar puncture were all normal. Our working diagnoses included bilateral Bell’s palsy, Guillain-Barré and Miller-Fischer syndromes. The antibody panel drawn for Miller-Fischer syndrome subsequently resulted as negative. Our patient received three days of IVIG and was discharged on a week supply of prednisone 60mg with a taper thereafter. At discharge, she had severe bilateral facial droop. She was unable to puff out her cheeks or raise her eyebrows. Neurology recommended outpatient follow up. One month after discharge she had residual right sided facial droop, but the deficits of the left side of her face had mostly resolved. Discussion: Current literature suggests a correlation between preeclampsia and Bell’s palsy. There is some thought that elevated blood pressure leads to facial nerve compression secondary to edema or microemboli. One report suggested that the onset of Bell’s palsy antepartum or postpartum may be a predictor of preeclampsia. An English language PUBMED search revealed six case reports on bilateral Bell’s palsy in either the pregnant or postpartum state. Cases reported occurred in either the third trimester or within the first week postpartum. This was consistent with the onset of our patient’s symptoms during her first week postpartum. In one case, neurological symptoms preceded preeclampsia. Our patient complained of headaches and neck pain prior to having elevated blood pressures. Three of these cases included twin gestations, as did our case. Outcomes varied, with some patients seeing complete resolution of symptoms within weeks to others having recurring symptoms over a year. Providers should consider the relationship between preeclampsia and Bell’s palsy when treating pregnant or postpartum patients with new onset neurological symptoms. Pregnant and postpartum patients are at greater than three times increased risk for Bell’s palsy and have more severe symptoms and longer recovery times compared to the average population. It is important that obstetricians and gynecologists assess for signs of preeclampsia in pregnant or postpartum patients with concerns for Bell’s palsy, as well as refer patients for a complete neurological workup. Ultimately, more research is needed to further understand the relationship between preeclampsia and Bell’s palsy.

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