Case Presentation: The patient is a 53-year-old male with type 2 diabetes and hypertension who presented to the hospital with right sided facial pain, facial droop, and concurrent right arm and leg weakness. One month prior to admission, he had been treated for a right sided facial rash with Valacyclovir for 3 days. He then developed postherpetic neuralgia with symptoms of facial pain, initiating Duloxetine and Meloxicam by his primary care doctor. During this interval period, he had resolution to his rash, however, then developed right-sided facial swelling, erythema and pain along with concurrent headaches. Over the following days, he developed right arm and leg weakness. On examination, he had crusted lesions from the nasolabial fold extending to the right ear, along the right ophthalmic (V1) and maxillary (V2) divisions of the trigeminal nerve. Neurological examination showed right facial weakness with inability to close the eye, suggesting CN VII palsy; decreased strength of the right arm and leg, suggesting poly-radiculitis; and right facial swelling, suggesting an association with Varicella zoster virus (VZV). MRI brain and brainstem showed an asymmetric hyperenhancement of the right facial nerve. MRI Lumbar revealed a single focus of contrast enhancement measuring approximately 3 mm, just superficial to the thoracic cord posteriorly on the right at the T12-L1 level.A diagnosis of zoster-associated cranial neuritis (involving CN VII) with right upper and lower poly-radiculitis was made, based on clinical, radiological, and laboratory evidence of VZV reactivation. He was started on IV Acyclovir (10 mg/kg every 8 hours) for 14 days with PO Prednisone to reduce inflammation. Adjunctive therapies to treat symptoms were utilized including analgesics and artificial tears with an eye patch to prevent corneal injury. Physical therapy and speech therapy aided in the functional recovery process. Patient had rapid resolution to his symptoms following the appropriate interventions.
Discussion: Herpes zoster is common in middle-aged and elderly individuals, particularly those with diabetes or immunosuppression. Zoster-associated cranial polyneuritis and radiculitis are rare, usually resulting from direct viral spread and inflammatory demyelination of multiple cranial and spinal nerves. The most commonly affected cranial nerves are VII (facial) and VIII (vestibulocochlear), classically described in Ramsay Hunt syndrome. However, multi-cranial neuropathies and poly-radiculitis may occur with subsequent MRI findings of nerve enhancement and CSF pleocytosis may be supporting the diagnosis. Early recognition and prompt antiviral therapy are crucial for favorable outcomes, especially in immunocompromised hosts. The use of corticosteroids, while debated, may expedite recovery in severe inflammation. Prior literature reveals only a handful of similar cases, most presenting with multifocal neurological deficits and often incomplete recovery. Our case highlights the importance of early initiation of antivirals and a multidisciplinary approach to management given possibility of complications.
Conclusions: Zoster-associated cranial neuritis and poly-radiculitis are rare but serious complications of VZV reactivation. High clinical suspicion, especially in patients with dermatomal rash and neurological deficits, is essential for timely diagnosis. Antiviral therapy, coupled with supportive measures, can lead to significant recovery.