# The Diagnostic Difficulty of Acute, Disabling Neurology: Varicella-Zoster Virus Polyradiculopathy Presenting as Acute Flaccid Paraparesis in an Elderly Male Patient With a History of Poliomyelitis

## TL;DR

An elderly man with a history of polio developed severe leg weakness and was diagnosed with a rare VZV infection affecting the spinal nerves, highlighting the challenges in diagnosing and treating such conditions.

## Contribution

This case highlights the diagnostic complexity and treatment challenges of VZV polyradiculopathy in patients with pre-existing neurological conditions.

## Key findings

- VZV infection was confirmed in the CSF through PCR, leading to a diagnosis of polyradiculopathy.
- Despite antiviral therapy and steroids, the patient showed minimal motor recovery but had some pain relief.
- The case emphasizes the need for better treatment guidelines for VZV-related neurological conditions.

## Abstract

We present the case of a 74-year-old man who presented with acute flaccid bilateral lower limb weakness, urinary retention, and neuropathic pain in a patient with longstanding significant leg weakness secondary to poliomyelitis. This required a clear and detailed history and examination, alongside rationalised urgent investigation, to rule out time-critical, reversible, and preventable causes of ongoing damage before deciding on a treatment plan.

Initial clinical assessment prompted evaluation for spinal stroke and compressive myelopathy, which was ruled out with urgent magnetic resonance imaging (MRI) of the whole spine. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis and elevated protein. This, in conjunction with significant weight loss, raised concern for the possibility of metastatic malignancy. Subsequent viral polymerase chain reaction (PCR) studies confirmed varicella-zoster virus (VZV) infection in the CSF, for which there exists no current consensus treatment. Contrast MRI findings showed leptomeningeal enhancement around the conus medullaris and cauda equina roots. This, coupled with abnormal nerve conduction studies and electromyography (NCS/EMG), led to a diagnosis of VZV-associated polyradiculopathy. Despite 28 days of intravenous aciclovir and a course of high-dose oral steroids, the patient showed minimal to no motor recovery and remained paralysed, dependent on hoists for transfers. The patient did, however, have improvement in neuropathic pain as a result of oral neuropathic pain agents. VZV infection in the central nervous system can have a disastrous outcome and is increasingly detected. Despite this, there is no consensus on evidence-based treatment; therefore, the duration of therapy still requires defining, and other options beyond aciclovir should be explored. This case underscores the diagnostic complexity of acute lower limb weakness, particularly in the context of pre-existing neurological deficit, how a diagnosis of VZV polyradiculopathy can be reached, and the challenges in differentiating this from other neuroinflammatory or malignant causes, as well as the uncertain prognosis even with prompt antiviral therapy.