Acute myelitis with multicranial neuritis caused by Varicella zoster virus: a case report

Abstract

Background Varicella zoster virus (VZV) can remain lifelong in the latent state in ganglionic neurons and adrenal glands after the initial infection. However, it can be reactivated anytime and can trigger several severe neurological manifestations such as encephalitis, meningitis, Ramsay-Hunt syndrome, cerebellitis, myelitis, and stroke. In addition, due to the diversity of clinical manifestations, clinical diagnosis of VZV can be difficult, especially in the absence of varicella. Here, we describe the case of a 52-year-old male who presented with symptoms of acute myelitis as well as polycranial neuritis, and was finally diagnosed with VZV infection through metagenomic next-generation sequencing (mNGS). Case presentation A 52-year-old male came to our hospital with complaint of headache, fever, weakness of right lower limb, abdominal distension, and hearing loss. T2-weighted MRI revealed a hyperintense lesion in the spinal cord extending from T8 to T11. In addition, enhanced MRI showed small patches and strips hyperintensities in both the spinal cord and meninges. Plain abdominal radiographs and abdominal computed tomography (CT) scan displayed air-fluid levels and incomplete bowel obstruction. Moreover, electrophysiological evaluation of the peripheral neuropathy in the extremities was found to be normal. Finally, by using metagenomic next-generation sequencing (mNGS) we found that the copy number of VZV DNA in cerebrospinal fluid (CSF) was significantly increased and IgG antibody against VZV in CSF was also noted to be positive. Hence, VZV infection was identified in patient’s central neuron system. Finally, after a few days of low dose steroid treatment, the patient's symptoms were found to be significantly improved. Conclusions The findings indicate that we should pay proper attention to the various symptoms caused by VZV infection due to the clinical heterogeneity, especially in the absence of cutaneous lesions.

Features of Audio-Vestibular Deficit and 3D-FLAIR Temporal Bone MRI in Patients with Herpes Zoster Oticus

“…In RHS, symptoms of audio-vestibular deficits, such as hearing loss and vertigo, are commonly accompanied by FNP [2][3][4][5][6][7][8][9]. In addition, paralysis of other cranial nerves can be associated with RHS [10][11][12][13][14][15]. Regarding pathological causes of audio-vestibular deficit, it is controversial whether or not the lesioned sites are inner ear endorgans or vestibulo-cochlear nerves [16,17].…”

“…Although the contrast-enhanced 3D-T1-weighted image (CE-3D-T1WI) has been used to identify the facial nerve (CN-VII) in patients with FNP [18][19][20], it is difficult to identify abnormal findings in the inner ear endorgans of CE-3D-T1WI in RHS patients. Recently, 3D-fluid-attenuated inversion recovery sequence (3D-FLAIR) MRI has been widely used as a tool to observe changes in inner ear structure or nerves in RHS patients [9][10][11][12].…”