International journal of clinical practice · 2020
Assessment of anti-HSV antibodies in patients with facial palsy in the course of neuroborreliosis.
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Moniuszko-Malinowska Anna, Guziejko Katarzyna, Czarnowska Agata, Kułakowska Alina, Zajkowska Olga, Pancewicz Sławomir, Świerzbińska Renata, Dunaj Justyna, Czupryna Piotr, Róg-Makal Magdalena, Zajkowska Joanna
Аннотация
AIM: There are many causes of facial nerve palsy. The most common causes are neuroborreliosis (NB), idiopathic paralysis or Herpes simplex virus (HSV) reactivation. The aim of this study was to characterize patients with facial palsy in the course of NB and to determine whether HSV-1 reactivation takes place during the acute phase of NB.
METHODS: A retrospective analysis of 66 patients with facial nerve palsy was performed. In 38 patients, facial palsy was caused by Borrelia burgdorferi sl infection. Immunological tests for HSV-1, tick-borne encephalitis virus and B burgdorferi sl in serum and cerebrospinal fluid (CSF) were performed.
RESULTS: In this analysis, 55.2% of NB patients had right nerve palsy and 21% bilateral palsy; 15.8% of patients had erythema migrans (EM). Lymphocytic meningitis was diagnosed in 92% of patients and Bannwarth's syndrome was diagnosed in 47% of patients. IgM anti-HSV-1 antibodies were detected in four patients with NB and two patients with facial nerve palsy of other origin. IgM anti-HSV-1 antibodies were detected in the CSF of three patients (7.9%) with NB, and one of them had bilateral VII paresis and EM simultaneously. Treatment with ceftriaxone or doxycycline led to complete recovery.
CONCLUSIONS: Neuroborreliosis should always be considered as a cause of peripheral facial nerve palsy. Peripheral facial nerve palsy is a significant symptom in the course of NB, especially in patients accompanied by meningitis. Pathomechanism of facial nerve paresis has not been well explained so far and may depend on two independent mechanisms in NB, including HSV-1 reactivation.
METHODS: A retrospective analysis of 66 patients with facial nerve palsy was performed. In 38 patients, facial palsy was caused by Borrelia burgdorferi sl infection. Immunological tests for HSV-1, tick-borne encephalitis virus and B burgdorferi sl in serum and cerebrospinal fluid (CSF) were performed.
RESULTS: In this analysis, 55.2% of NB patients had right nerve palsy and 21% bilateral palsy; 15.8% of patients had erythema migrans (EM). Lymphocytic meningitis was diagnosed in 92% of patients and Bannwarth's syndrome was diagnosed in 47% of patients. IgM anti-HSV-1 antibodies were detected in four patients with NB and two patients with facial nerve palsy of other origin. IgM anti-HSV-1 antibodies were detected in the CSF of three patients (7.9%) with NB, and one of them had bilateral VII paresis and EM simultaneously. Treatment with ceftriaxone or doxycycline led to complete recovery.
CONCLUSIONS: Neuroborreliosis should always be considered as a cause of peripheral facial nerve palsy. Peripheral facial nerve palsy is a significant symptom in the course of NB, especially in patients accompanied by meningitis. Pathomechanism of facial nerve paresis has not been well explained so far and may depend on two independent mechanisms in NB, including HSV-1 reactivation.