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Varicella‑zoster virus‑associated meningitis followed peripheral facial palsy: A case report

Varicella‑zoster virus‑associated meningitis followed peripheral facial palsy: A case report Although central nervous system infection following varicella zoster virus infection is relatively common, subsequent peripheral nervous system infection is comparatively rare. The present case documents a case of meningitis after varicella‑zoster virus (VZV) infection, which was then followed by peripheral facial palsy. Specifically, a 54‑year‑old female patient was first admitted to Shengli Oilfield Central Hospital (Dongying, China) with headache and fever. Physical examination revealed herpes that formed along the intercostal nerve in the left forebreast, armpit and back. Subsequently, neurological examination found cervical resistance in more than three fingers (neck resistance of less than two transverse fingers is not evidence of meningeal irritation; the neck resistance of this patient was approximately three transverse fingers, so the patient was presumed to be positive for meningeal irritation, highly suggestive of meningitis) and Kernig sign was positive. There were no significant abnormalities according to brain MRI and lumbar puncture pressure was 330 mmH2O. In addition, the leukocyte count was 734x106/l, 50% monocyte count, 50% multinucleated cells, chloride levels of 109.1 mmol/l, protein levels of 235 mg/dl and glucose levels of 4.18 mmol/l in the cerebrospinal fluid. DNA and RNA metagenomic detection of pathogenic microorganisms in the cerebrospinal fluid revealed the presence of VZV. The patient was therefore treated with acyclovir, ceftriaxone, mannitol and methylprednisolone, but then developed right peripheral facial palsy at 10 days after treatment. This complication was not found in the literature, and the occurrence of facial neuritis was unexpected. The active period of VZV virus was 21 days, and the patient had herpes 5 days before admission. The active period of the virus was considered to have subsided and the patient was in the recovery period. Moreover, the results of lumbar puncture showed that the white blood cells, the proportion of neutrophils and the protein in cerebrospinal fluid were all decreasing, which also indicated that the patient had entered the recovery period. The patient was discharged 18 days after admission. In conclusion, observations from the present case suggested that the clinical manifestations of VZV infection can be complex and varied, requiring the clinician to have an accurate understanding of its disease progression and treatment. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental and Therapeutic Medicine Spandidos Publications

Varicella‑zoster virus‑associated meningitis followed peripheral facial palsy: A case report

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Publisher
Spandidos Publications
Copyright
Copyright \xC2\xA9 2024 Spandidos Publications
ISSN
1792-0981

Abstract

Although central nervous system infection following varicella zoster virus infection is relatively common, subsequent peripheral nervous system infection is comparatively rare. The present case documents a case of meningitis after varicella‑zoster virus (VZV) infection, which was then followed by peripheral facial palsy. Specifically, a 54‑year‑old female patient was first admitted to Shengli Oilfield Central Hospital (Dongying, China) with headache and fever. Physical examination revealed herpes that formed along the intercostal nerve in the left forebreast, armpit and back. Subsequently, neurological examination found cervical resistance in more than three fingers (neck resistance of less than two transverse fingers is not evidence of meningeal irritation; the neck resistance of this patient was approximately three transverse fingers, so the patient was presumed to be positive for meningeal irritation, highly suggestive of meningitis) and Kernig sign was positive. There were no significant abnormalities according to brain MRI and lumbar puncture pressure was 330 mmH2O. In addition, the leukocyte count was 734x106/l, 50% monocyte count, 50% multinucleated cells, chloride levels of 109.1 mmol/l, protein levels of 235 mg/dl and glucose levels of 4.18 mmol/l in the cerebrospinal fluid. DNA and RNA metagenomic detection of pathogenic microorganisms in the cerebrospinal fluid revealed the presence of VZV. The patient was therefore treated with acyclovir, ceftriaxone, mannitol and methylprednisolone, but then developed right peripheral facial palsy at 10 days after treatment. This complication was not found in the literature, and the occurrence of facial neuritis was unexpected. The active period of VZV virus was 21 days, and the patient had herpes 5 days before admission. The active period of the virus was considered to have subsided and the patient was in the recovery period. Moreover, the results of lumbar puncture showed that the white blood cells, the proportion of neutrophils and the protein in cerebrospinal fluid were all decreasing, which also indicated that the patient had entered the recovery period. The patient was discharged 18 days after admission. In conclusion, observations from the present case suggested that the clinical manifestations of VZV infection can be complex and varied, requiring the clinician to have an accurate understanding of its disease progression and treatment.

Journal

Experimental and Therapeutic Medicine – Spandidos Publications

Published: Oct 28, 2024

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