International Journal of Clinical Case Reports 2017, Vol.7, No.3, 9-14
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re-activated, often after years or, decades of the primary infection and then, causes shingles resulting in
inflammation in the dorsal root ganglia and/or, extra-medullary cranial nerve ganglia (Wadhawan et al., 2015).
The prevalence of herpes zoster increases with advancing age and there is observed a marked increase in its
incidence with aging (Schmader et al., 2011). The reason behind this is attributed to age-related diminished
virus-specific and cell-mediated immunity (Thomas and
987; Johnson and Dworkin, 2003). Under certain
circumstances (predisposing factors) including emotional stress, immuno-suppression, cancer therapy
(chemotherapy and radiotherapy), HIV infection, underlying malignancy, immunosuppressant drugs and dental
manipulations, the virus gets re-activated and causes shingles. The disease is more common in adult life and
affects males and females in equal frequency. The disease process can be grouped into three phases as 1)
Prodrome, 2) Acute, and 3) Chronic phases. Herpes zoster infection (HZI) usually starts with a deep aching or,
burning pain (Neville et al., 2009). The prodrome begins 2-4 days before the appearance of the muco-cutaneous
rashes or, vesicles. The presentation of prodromal pain is dermatomic in nature and may be associated with fever,
malaise and headache (Neville et al., 2009; Wadhawan et al., 2015). Thoraco/lumbar dermatomes are the most
commonly affected sites in herpes zoster infections (HZIs) and account for 50% to 70% of the cases reported;
followed by followed by cervical and trigeminal and sacral dermatomes (Schmader et al., 2011; Cohrs et al.,
2004). The prodromal pain might show variations, such as, cases without painful prodromes typically show
occurrence of pain at the first onset of rashes or, shortly afterwards (Schmader et al., 2011). The acute phase
begins as the involved area develops clustered vesicles in a dermatomal pattern which are unilateral and usually
follow a linear fashion alongside the affected nerve. This acute herpes zoster pain gradually resolves before or,
shortly after the rashes heal. Within a period of 3-4 days, the vesicles become pustular and ulcerate followed by
formation of scab usually in 7-10 days, although, it might take around 2-3 weeks for the lesions to go for complete
resolution in otherwise healthy patients (Neville et al., 2009). The disease is not infectious in the chronic phase,
especially, after the development of scab. After complete healing ensues, scarring with areas of hypo-pigmentation
or, hyper-pigmentation can be seen. Occasionally, dermatomal pain of herpes zoster infections (HZIs) might occur
without appearance of rashes being referred to as zoster sine herpete. It is difficult to identify this condition due to
absent obvious clinical signs (Kasahara et al., 2011). Oral lesions occur with trigeminal nerve involvement.
Ophthalmic division (V1) of the trigeminal nerve is most often affected being called as herpes zoster
ophthalmicus with the common signs being lesions on upper eyelid, forehead and scalp. The common attending
symptoms may comprise conjunctivitis, keratitis, uveitis and optic nerve palsies causing chronic ocular
inflammation, loss of vision and debilitating pain. The maxillary division (V2) of trigeminal nerve leads to
formation of vesicles on hard palate and/or, buccal gingiva on one side which is preceded by prodrome.
Involvement of the mandibular division (V3) results in formation of vesicles and ulcers on mandibular gingivae
and tongue. Ulcers are 1-5mm in size and often, coalesce to form larger ulcers with scalloped borders (Greenberg
et al., 2003). The most common and debilitating complication of herpes zoster infections (HZIs) is post-herpetic
neuralgia (PHN) which is characterized by pain that persists for almost 3 months after the initial presentation of
the rash. Pain is severe, burning, throbbing, aching, itching and often, elicits on light touch. Most of the
post-herpetic neuralgias (PHNs) resolve within 1 year with half of the patients experiencing resolution in the first
2 months after resolution of the lesions. Incidence of post-herpetic neuralgias (PHNs) is upto 50% in patients
above 60 years of age (Neville et al., 2009). There are 4 independent predictors for post-herpetic neuralgias
(PHNs): old age, severe acute pain, severe rash and a shorter duration of rash before consultation indicating more
severity of the lesions (Johnson and Dworkin, 2003). An uncommon complication called James Ramsay Hunt
syndrome results due to the virus spreading from the facial nerve to the vestibulo-cochlear nerve. It is, also,
known as Herpes zoster oticus. The syndrome clinically manifests as facial paralysis, pain in external acoustic
meatus (EAM), pinna and vesicles of external ear attended with loss of taste sensation in the anterior 2/3
rd
of the
tongue, tinnitus, vertigo (Jan et al., 2006). Diagnosis of herpes zoster infections (HZIs) can often be made from
clinical presentation because of its unique unilateral distribution of the lesions (Wareham et al., 2007; Wadhawan
et al., 2015). Other procedures may be necessary in atypical cases such as zoster sine herpete characterized by
severe pain without any evidence of vesicular eruptions (Wadhawan et al., 2015). Identification of the virus in the
