Síndrome de Ramsay-Hunt: a propósito de dos casos en que se identificó el genoma del virus de la varicela-zóster en líquido cefalorraquídeo

Like other alpha-herpesviruses, the varicella-zoster virus (VZV) remains latent in the neural ganglia following the primary varicella infection. The reactivation of the VZV in the dorsal root ganglia results in herpes zoster. Herpes zoster eruption is characterized by localized cutaneous lesions and neuralgic pain mostly in older and immunocompromised persons, especially those living with the human immunodeficiency virus (HIV). The most commonly reported complications include VZV pneumonia, meningitis, encephalitis, and hepatitis. Several neurologic syndromes have been described associated with herpes zoster localized in cranial areas including peripheral nerve palsies and the Ramsay-Hunt syndrome, which has a varied clinical presentation and is the second most common cause of peripheral facial paralysis. Facial paralysis in this syndrome occurs in 60 to 90% of cases and it may precede or appear after the cutaneous lesions with a worse prognosis than idiopathic Bell paralysis. Here we present two cases of herpes zoster from the geniculate ganglia with peripheral facial paralysis that appeared simultaneously with vesicular herpetic otic lesions (multimetameric Ramsay-Hunt syndrome). In the two cases, amplifiable varicella-zoster viral DNA was found in the cerebrospinal fluid by RT-PCR Multiplex.