Ramsay Hunt syndrome: Report of two cases with identification of the varicella-zoster herpes virus genome in cerebrospinal fluid

Abstract

Like other alpha-herpesviruses, varicella-zoster virus (VZV) establishes latency in neural ganglia following primary Infection (varicella). Reactivation of latent VZV infection from dorsal root ganglia results in herpes zoster (HZ). HZ eruption is characterized by a localized cutaneous lesions accompanied by neuralgic pain that occurs most commonly in older and immunocompromised persons, especially human immunodeficiency virus (HIV) infected patients. Commonly reported complications include VZV pneumonia, meningitis, encephalitis, and hepatitis. Distinct neurologic syndromes have been described associated with HZ as a variety of cranial and peripheral nerve palsies, including Bell's palsy and Ramsay Hunt syndrome. Ramsay Hunt syndrome is the second most common cause of peripheral facial paralysis, with a varied clinical presentation. The facial paralysis in this syndrome occurs in 60-90 % of cases, is peripheral and may precede or appear after of the cutaneous lesions with a worse prognosis than idiopathic Bell paralysis. Here we present 2 cases of HZ of geniculate ganglia with peripheral facial paralysis coinciding with vesicular herpetic otic lesions (multimetameric Ramsay Hunt syndrome). In the two cases amplifiable varicella-zoster viral DNA was found in cerebrospinal fluid by RT-PCR Multiplex.