Case Presentation: A 31-year-old man with rheumatoid arthritis (on adalimumab, methotrexate, and prednisone) presented with a 3-day history of fatigue, severe asymmetrical weakness of the lower extremities (left > right), and painful vesicular rash spanning multiple dermatomes in the left > right lower extremities (Image 1). There was no evidence of myelopathy or meningismus on examination. Since clinical presentation was suspicious for varicella zoster virus (VZV) lumbar polyradiculitis, intravenous acyclovir was started. Home immunomodulation was temporarily stopped. He did not receive additional pulsed steroids or VZV immune globulin (VZIG). Whole-spine MRI showed no abnormal cord or root enhancement. Lumbar puncture was not performed.Lower extremity weakness improved within 48 hours. Vesicular rash gradually resolved. The vesicular fluid showed positive RT-PCR for VZV DNA. VZV serology was positive. Adalimumab was slowly restarted 6 weeks after the patient’s initial presentation and he has remained free from other complications. The patient, a physician and avid runner, was again able to run several miles per day 3 months after his initial presentation.

Discussion: VZV radiculitis, particularly when affecting the lower extremities, is a rare manifestation of VZV reactivation that typically occurs in the context of chronic immunosuppression. In this case, VZV reactivation affects the dorsal root ganglia. Given its rarity, several aspects of its diagnosis and management remain incompletely understood. As shown in our patient’s case lumbar puncture may not always be necessary as part of its evaluation, even in an immunocompromised individual, in the context of characteristic VZV skin lesions. In VZV radiculitis MRI may or may not show abnormal root enhancement but can help rule out spinal cord involvement. Based on anecdotal evidence, intravenous acyclovir (typically for 14 days) is a commonly used treatment. Other therapies such as pulsed steroids or VZIG remain controversial. Steroids could aggravate immunosuppression and VZIG use can be associated with aseptic meningitis. Our patient had rapid clinical improvement without the addition of pulsed steroids or VZIG.Another important question is the safety and timing of medication resumption in a patient who needs long-term immunomodulation. Based on a very limited evidence from the transplant literature, our patient’s immunomodulation was restarted once the lesions were healed and he had return of his motor function, approximately 6 weeks later, without further complications. Our case can provide data to help guide this important decision.

Conclusions: Herpes zoster (also known as shingles) is a clinical syndrome caused by reactivation of VZV. While the exact mechanism of reactivation remains unclear, it is well-known that herpes zoster is more severe in immunocompromised individuals. This report illustrates a rare presentation of VZV reactivation in an immunocompromised patient. Our case provides Class IV evidence to better understand the clinical evaluation and treatment of VZV lumbar polyradiculitis.

IMAGE 1: Vesicular rash of varicella zoster virus reactivation spanning multiple dermatomes in the left lower extremity.