Neuroinvasive Manifestations of West Nile Virus Infection: Lumbar Polyneuropathy, Chorioretinal Lesions, Sensorineural Hearing Loss
Matthew W. Flounders1, Katharine Dermigny2, Leanna Doherty2
1Philadelphia College of Osteopathic Medicine, 2University of Pittsburgh Medical Center, Department of Neurology
Objective:
West Nile virus (WNV) infection is often asymptomatic however reports of serious neuroinvasive manifestations such as encephalitis, chorioretinitis, and acute flaccid paralysis warrant prompt recognition and interdisciplinary treatment.
Background:
A 71 yo woman presented with several days of lethargy, anorexia, and weight loss had an unremarkable initial infectious and metabolic workup. One week later, she developed L>R bilateral lower extremity weakness, radiating lower back pain, acute bilateral blurry vision, and left sided hearing loss. Physical exam was notable for L>R bilateral hip flexor weakness, left knee flexion weakness, and absent left patella and Achilles reflexes. She had patchy loss of sensation to pinprick throughout the medial lower leg. MRI Brain did not show any abnormal T2 lesions. MRI of the C- and T-spine without contrast were unremarkable. MRI of the L-spine demonstrated severe left L5-S1 foraminal narrowing. A LP yielded an opening pressure of 17 cmH2O, negative basic viral studies (HSV, CMV, VZV), negative Lyme PCR, and a normal IgG index. Spinal fluid revealed only elevated protein of 113 mg/dL. EMG was consistent with bilateral lumbosacral polyradiculopathy with evidence of active denervation in bilateral lumbar paraspinal muscles and left-sided S1-innervated muscles. Ophthalmology identified punched out chorioretinal lesions on fundoscopic exam, which prompted testing for WNV. ENT evaluation was notable for bilateral SNHL on audiogram, which prompted an intra-tympanic steroid treatment. After diagnosis, WNV IgG and IgM in serum and CSF returned positive.
Results:
The patient’s weakness improved significantly during hospitalization with conservative therapies and continued after receiving 2mg/kg IVIg over 5 days. She was followed by neuroophthalmology, otolaryngology, and neurology for management of her recovery.
Conclusions:
WNV may present with neuroinvasive symptoms of polyneuropathy, chorioretinal lesions, and sensorineural hearing loss. Diagnosis is confirmed by serologic and spinal fluid studies. The mainstay of treatment is supportive care, while evidence for IVIg is limited.