Ramsay Hunt syndrome /Herpes zoster oticus

DEFINITION

 Viral polyneuropathy primarly affecting facial nerve and vestibulocochlear nerve

herpetic vesicular rash + facial nerve palsy = Ramsay hunt syndrome
Palsy: lower motor neuron palsy of the ipsilateral facial nerve.

Epidemylogy:

 2nd commonest cause of lower facial nerve palsy after bell's palsy 9%

PATHOLOGY

 The disease is a reactivated varicella zoster infection (chicken pox) from dormant viral
particles resident in the geniculate ganglion of the facial nerve and the spiral and
vestibular ganglia of VIII

Symptoms:

Auricular pain:

 the 1st symptom to appear

Vesicular Rash:

1. location:
a. concha
b. posteriomedial surface of the auricle (postauricular)
c. EUC
d. mucosa of the palate
e. anterior 2/3 of the tongue

2. Onset:
  In 14 % of patients, the rash is not present initially but develops several days
after the onset of pain and facial palsy.
 25% of cases, the eruption precedes the paralysis; these patients have a higher
likelihood of recovery
 Facial nerve palsy without rash still may be due to Ramsay hunt syndrome

Involvement of other nerves:

 Spread from the facial nerve to the VIIlth and/or other cranial nerves is thought to
occur via the vasa nervorum/ although there are also numerous neurological
anastomoses between the lower cranial nerves within the skull base which allow for
easy viral
 VIII may be involved in Ramsay Hunt syndrome to variable degree in the form of
hearing loss,vertigo and or tinnitus
 The VIII is almost always involved although may not always result in subjective
symptoms (It almost always affects the VIlith nerve,either within the cochlea or at
any site up to the brainstem, albeit the involvement may be asymptomatic)
 Mainly V

Risk factors: decrease immunity

DIAGNOSIS:

 The diagnosis is clinical

Ramsay Hunt syndrome Vs Bell’s palsy:

 More sever symptoms

 Worse prognosis
 Higher rate of seroconvesion to varicella virus

OUTCOMES

 The palsy severity and the prognosis is worse than bell’s palsy
 50% satisfactory return; 50% left with weakness, synkinesis, contractures, and spasm
 Overall full recovery is 20%
 If the palsy is complete, only 10 % will get a full return of normal function
 Even those that recover are likely to have residual synkinesis.
 If the palsy is incomplete, 66 % will recover completely.
 In untreated patients, over 60 % develop a complete facial paralysis within a wk
 This figure is even higher in individuals over the age of 50.
 Overall, approximately 50 % of adults and 80 % of children will achieve full recovery to
House-Brackmann grade 1.
 Complete facial palsies have a poor prognosis if not treated early.
 The elderly have a poor prognosis for return of facial nerve function

Treatment:
Oral acyclovir (800 mg x 5/day) and Prednisolone (1 mg/kg/day) for 10 days.

1. Acyclovir + prednisolone are better than acyclovir alone:

 treatment of acyclovir plus steroids produced a 90 % recovery to grade 1,compared
to 64 % if only steroid was given
2. Better results if Acyclovir + prednisolone were given early in the 1 st 3 days:
 75 % had a complete recovery with early treatment Vs 30% when treatment started
after 8 days
 The early treatment with antiviral agents is also known to significantly reduce the
prevalence of post-herpetic neuralgia
3. There was no difference between the group treated with intravenous antivirals when
compared to the group given oral therapy.
4. Acyclovir does not eradicates the herps infection but shorten the symptomatic period

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