Bilateral Facial Palsy Following Trigeminal Zoster with Zoster Oticus

Abstract

To the editor: Bell's palsy commonlyoccurs with an annual incidence of about 25 per 100,000 (1). However, bilateral facial palsy is a rare clinical condition, less than 1%as frequent as unilateral paralysis (2). Varicella zoster virus (VZV) infection to the geniculate ganglion causes ipsilateral facial palsy and auditory nerve deficit called Ramsay Hunt syndrome (3). Wereport here a case of trigeminal zoster with zoster oticus complicating facial diplegia and meningiti s. A 22-year-old man developed clusters of clear vesicles on an erythematous base on the back of the right auricle, right perioral and periorbital areas, and experienced intermittent neuralgic pain in these affected areas and dull pain in the occipital region. A few days later, he developed low grade fever, bilateral difficulty in moving the facial muscles, and nausea. The patient had a past history of chicken pox at the age of 6. On admission, his body temperature was 38.3°C, with regular pulse, and blood pressure of 154/84 mmHg. There were no tick bites or eruptions on the extremities suggesting Lymedisease. He had headache without neck stiffness or Kernig's sign. He also showed facial diplegia that wasmoderate on the left and severe on the right, without taste disturbance, and tinnitus in the right ear without hearing impairment. Bell's phenomenon was present on the right side. There was no abnormality in other cranial nerves, or in motor, sensory, cerebellar and autonomicfunctions. Routine laboratory findings including urinalysis, blood chemistry, serological and immunological tests were normal. WBC count was 3,600/mm3with atypical lymphocytes (2%). Cerebrospinal fluid (CSF) pressure was 140 mmH20, and the total cell number was elevated to 379 cells/mm3 (neutrophils, 5; mononuclear cells, 374). CSF glucose, protein, and chloride levels were 57 mg/dl, 61.9 mg/dl, and 121 mEq//, respectively. At the sixth day from the onset, the complement fixation (CF) IgG titer for VZVwas 1:256 in serum, and 1:4 in CSF. Twoweeks later, those titers had changed to 1:128 in serum and 1:1 in CSF, and 1: 64 in serum after 6 weeks. The CF IgG titer for herpes simplex virus in serum on admission, and 6 weeks later were 1:16 and 1:16, respectively. Cranial CT was normal. VZVgenome analysis in CSF by PCR was not performed. On re-examination of CSF, cell count and protein concentration were 20 cells/mm3, and 37.8 mg/dl, respectively.

Isolated facial diplegia in Guillain–Barré syndrome: Bifacial weakness with paresthesias

“…Bilateral facial weakness in these patients was more often associated with meningoencephalitis and CSF lymphocytic pleocytosis than unilateral disease. Herpesviruses frequently attack the facial nerve, and there are several reports of facial diplegia attributed to acute infection by Epstein–Barr virus, herpes simplex virus type 1 (HSV‐1), and varicella‐zoster virus . Of the 14 cases of Epstein–Barr virus–related facial weakness, 5 were bilateral.…”