DISCUSSION:
Ramsay-Hunt syndrome is perhaps an underdiagnosed form of peripheral facial palsy [5], since the diagnosis is mainly based on clinical findings of facial weakness and a vesicular rash [1]. Regarding the timing of these manifestations, the clinical picture includes three possibilities. When the vesicular rash occurs before or simultaneously with the facial palsy, the diagnosis is usually easy. Sometimes the blisters develop only after the onset of facial weakness and occasionally they are not very noticeable and can be overlooked. A minority of patients, like ours, do not develop them at all. One retrospective study showed that in 6% of patients, only the ear canal or the ear drum were affected, without visible blisters outside. This can make the diagnosis more difficult and indistinguishable from Bell’s palsy [2].
Our patient also complained of ear pain, headache and vertigo. This syndrome may also present with acute herpetic neuralgia that can radiate to the face, ear, head and neck [9]. Approximately 50% of patients are expected to have an injury of the vestibulocochlear nerve. This can cause nausea, vomiting, gait insecurity with a tendency to fall to the affected side, vertigo and nystagmus [10]. Damage of the cochlear component leads to tinnitus and hearing loss [11,12].
Analysis of cerebrospinal fluid and brain magnetic resonance imaging has limited diagnostic and prognostic value. However, polymerase chain reaction assays may be useful to detect herpes zoster virus DNA in exudates from ear scrapings or CSF and MRI can visualize inflammation of the cranial nerves [3].
It is important to differentiate Ramsay-Hunt syndrome from other forms of facial palsy, since the former often has more severe paralysis and has less chances of recovery [13]. Treatment of this condition involves both glucocorticoids and antiviral therapy, while for Bell’s palsy it remains uncertain whether antiviral therapy adds benefit [5,8,10]. Antiviral agents improve acute pain, recovery rate and prevent from the occurrence of postherpetic neuralgia [14]. Glucocorticoids have a strong anti-inflammatory action, reducing edema in the nerves involved, which can lead to a hasten recovery [10]. There does not seem to be a difference between the use of oral versus intravenous antivirals [11]. Starting treatment in the first 48 hours of symptoms, as we did in this case, is crucial as nerve damage and therefore prognosis depends on the timing at which the combination therapy is started [5,8,10].