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].