CASE 2218 Published on 15.09.2003

Varicella-Zoster virus myelitis

Section

Neuroradiology

Case Type

Clinical Cases

Authors

Spero M, Rumboldt Z

Patient

62 years, female

Categories
No Area of Interest ; Imaging Technique MR, MR, MR, MR
Clinical History
The patient presented with left arm weakness and sensory loss, three months after treatment for herpes zoster.
Imaging Findings
The patient presented with sudden left arm weakness and sensory loss. Three months earlier she had been treated for herpes zoster of the left upper arm, occiput and neck. Five days prior to admission she developed a nonspecific left arm skin rash. Deep tendon reflexes were brisk in the left arm; pain, light touch, position and vibration sensations were decreased in the C4-5 dermatomal distribution. CSF contained 9 mononuclear cells and slightly elevated proteins. EMG showed a severe radicular lesion at the C5 and C6 level on the left.

Cervical spine MR imaging revealed a high-signal-intensity spinal cord lesion on T2-weighted images, involving C3 to C5 segments, predominantly in the grey matter on the left. The lesion showed no contrast enhancement.

The patient was started on intravenous acyclovir and dexamethasone, and her neurological deficits started to disappear.
Discussion
Herpes zoster represents a reactivation of latent varicella zoster virus (VZV) infection and is usually manifested as peripheral or cranial neuropathy. Defective cellular immunity may increase the likelihood of VZV reactivation (1), e.g. in patients with lymphoma, leukaemia, the acquired immune deficiency syndrome, metastatic cancer, or systemic lupus erythematosus. Myelitis is a rare neurological complication of herpes zoster, which is diagnosed based on the close temporal relationship between the onset of skin lesions and myelitis. The pathogenesis may be direct viral invasion of the cord, vasculitis with ischaemic necrosis, or an immunological-parainfectious mechanism (2). Direct invasion is often inferred from the eccentric location of the enhancement near the dorsal root entry zone, and the correspondence between the level of the cord lesion and the dermatomal distribution of the skin lesions in a patient with shingles. VZV has been isolated from the brain and spinal cord, thus indicating that direct invasion does occur. Clinical findings after acute VZV infection usually include self-limited paraparesis, with or without sensory loss and sphincter dysfunction. MRI findings in documented cases (4,5) of VZV myelitis include diffuse hyperintensity on T2-weighted images that extends over several levels and probably represents oedema, as well as less extensive focal or multifocal enhancement on post-contrast T1-weighted images, which may represent direct viral invasion or blood-cord barrier breakdown. The clinical course of zoster myelitis is quite variable: acute, subacute, chronic, or remitting exacerbating myelopathy have all been described. The prognosis ranges from benign and self-limiting to progressive and fatal. This variability may in part be ascribed to the possible diverse pathological mechanisms of injury, as mentioned above. Early therapeutic intervention with acyclovir prevents multiplication and spread of the virus in the spinal cord, and, together with absence of serious predisposing disease, contributes to good prognosis (3).

To the best of our knolwedge there have been no previous reports of varicella-zoster myelitis affecting predominantly the grey matter.
Differential Diagnosis List
Varicella-Zoster myelitis
Final Diagnosis
Varicella-Zoster myelitis
Case information
URL: https://www.eurorad.org/case/2218
DOI: 10.1594/EURORAD/CASE.2218
ISSN: 1563-4086