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If herpes zoster involves the sensory portion of the geniculate ganglion of the facial nerve, it may produce a lower motor neuron facial paralysis.
Shingles is characterized by rash, often very painful, which is due to reactivation of varicella zoster virus.
When appropriate treatment is initiated within hours after onset of symptoms, the disease usually heals within a few weeks without sequelae.
Shingles can be indicative of a weakened immune system and in this context it occurs in patients with AIDS, cancer patients or patients undergoing chemotherapy.
Other factors such as influenza, stress or significant exposure to sunlight may increase the risk of shingles. The first sign of reactivation of the chickenpox virus is the appearance of a burning sensation along the nerve pathways, the appearance of a burn as a belt is very characteristic for Shingles.
The characteristic skin lesions of the disease appear after three days: small vesicles on erythematous cupboards resembling those of chickenpox. The climax is reached after 5 days the blisters break and are gradually replaced by scabs; the scabs fall off after 2 to 3 weeks.
Treatment should be initiated as soon as possible to avoid an unfavorable and the occurrence of complications. Most cases of zoster evolve without complications after initiation of treatment, shingles heals in about a month.
In some patients, there may be a breach of the brain, the meninges or spinal dorsal diaphragmatic paralysis may also occur. An extension of lesions to the entire body surface (generalized herpes zoster) occurs in people with weakened immune systems or under immunosuppression. Copyright © 2012 Rayur, All trademarks are the property of the respective trademark owners. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractThe association of mumps with peripheral facial paralysis has been suggested, but its pathogenesis remains unclear. The varicella-zoster virus remains dormant for many years, to be inactive in the nerve ganglia.
This burning is associated with sensory disorders and severe pain, from the spine and radiating to the sternum. Lesions may occur anywhere in the body (trunk, head, buttocks) but they are limited to a specific nerve territory relatively well defined, and reach only half of the body.
Especially in elderly patients, the pain may persist for months or years after healing of skin lesions.
After the facial nerve, the other cranial nerves most frequently involved in order of decreasing frequency are the eighth, ninth, fifth, tenth, and sixth nerves. Herpes zoster should be distinguished from herpes simplex. An 8-year-old girl simultaneously developed left peripheral facial paralysis, ipsilateral cervical herpes zoster, and bilateral mumps sialadenitis. Herpes simplex most commonly causes an acute viral vesicular eruption of the skin and mucous membranes, caused by herpesvirus hominis.
Elevated anti-mumps and anti-varicella zoster virus IgM antibodies in serological testing indicated recent infection of mumps and reactivation of VZV.

The lesions of herpes simplex originate as erythematous papules which develop into a small localized group of vesicles. The diagnosis of herpes simplex can be confirmed by viral culture, since material aspirated from an early vesicle will ,row readily in tissue culture, usually within one to three days. Molecular studies have provided mounting evidence that the mumps virus dysregulates the host’s immune system and enables the virus to proliferate in the infected host cells. Herpes simplex, unlike herpes zoster, is not associated with cranial nerve involvement, and is consequently not confined to specific dermatomes in the head and neck area. This patient developed a temporary and incomplete left facial nerve paralysis as the result of a herpes zoster infection.
This dysregulation of the immune system by mumps virus may have occurred in our patient, enabling the latent VZV infection to reactivate.1. IntroductionA variety of virus infections have been linked to the development of peripheral facial paralysis. Hilsinger Jr., “Herpes simplex virus in idiopathic facial paralysis (Bell palsy),” The Journal of the American Medical Association, vol. These viruses include herpes simplex virus-1 (HSV-1), varicella zoster virus (VZV), Epstein-Barr virus, cytomegalovirus, and mumps virus.
Increasing evidence suggests that idiopathic peripheral facial paralysis (Bell’s palsy), the most common clinical entity of facial paralysis, is caused by reactivation of HSV-1 [1, 2]. Similarly, it is well recognized that VZV reactivation is responsible for the development of Ramsay Hunt syndrome and zoster sine herpete [3]. However, the association of other viral infections with the pathogenesis of facial paralysis remains largely unclear because of the paucity of reports.We present here a patient who showed the simultaneous development of left peripheral facial paralysis, ipsilateral cervical herpes zoster, and mumps sialadenitis as evidenced by serological studies. Our case, as well as those in previous reports, raises the question whether the so-called mumps-associated facial paralysis is simply caused by mumps virus infection or the additional reactivation of latent VZV.2. Case PresentationAn 8-year-old Japanese girl was referred to our clinic for the evaluation of a left facial nerve paralysis, left cervical zoster, and swelling of the right submandibular area.
She had been vaccinated against mumps at the age of 2 and had no obvious episode of mumps infection previously. Yanagihara, “Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle,” Annals of Internal Medicine, vol.
Although she had also been vaccinated for chickenpox at the age of 2, she developed chickenpox at the age of 4. Electroneurography of the facial nerve revealed nearly complete denervation of the left facial nerve (Figure 1). The patient also had swelling of the parotid glands bilaterally and the right submandibular gland. Computed tomography images of the neck that had been examined in the pediatric department on the eighth day of illness confirmed sialadenitis of the left parotid gland (Figure 2) and right submandibular gland.
We also noted herpes zoster in the left parotid area and posterior cervical area corresponding to the C2-3 area (Figure 3).
Nagashima, “Detection of varicella-zoster virus DNA in patients with acute peripheral facial palsy by the polymerase chain reaction, and its use for early diagnosis of zoster sine herpete,” Journal of Medical Virology, vol. Her left facial movement also gradually improved to be House-Brackmann grade 2 with slight synkinesis 7 months later. Follow-up serological tests 6 weeks after the onset of illness revealed a decrease in both IgM antimumps and anti-VZV antibodies (Table 1).3.

DiscussionTo our knowledge, the present report is the first to show simultaneous development of mumps sialadenitis and reactivation of VZV, both of which were evidenced by serological assays, in a case of peripheral facial paralysis. In the present case, cervical zoster and facial paralysis developed six and seven days earlier than the development of sialadenitis, respectively.
The electroneurography of the facial nerve revealed nearly complete denervation on the tenth day of illness.Based on the clinical and laboratory findings, this case may be clinically diagnosed as mumps-associated facial paralysis. In fact, a small number of previous reports have suggested the possible association of mumps viral infection with peripheral facial paralysis [4–6].
However, stapedial reflex in the present case was absent in the left ear, suggesting that the lesion responsible for facial paralysis was not located in the parotid gland but proximal to the root of the stapedius branch, which is commonly observed in cases of Bell’s palsy or Ramsay Hunt syndrome. Although the patient did not show hearing loss, or vesicular eruptions in external ear canal, concha, or pimma, which is a dermatome of the geniculate ganglion, a combination of facial paralysis and upper cervical zoster has been recognized as a subgroup of Ramsay Hunt syndrome [7, 8] and speculated to be caused by the simultaneous reactivation of latent VZV in multiple sensory ganglia or the spread of infection through meningeal inflammation to adjacent ganglia [8].Although it is not clear if the mumps virus infection and VZV reactivation were merely coincidental or were associated in the present case, the time lapse between the two indicates the likelihood of their relation. Harada, “Facial palsy associated with mumps parotitis,” Pediatric Infectious Disease Journal, vol. Assuming that they were actually associated, it is reasonable to speculate that the mumps infection enabled the subsequent reactivation of VZV, since the herpes zoster is a result of reactivation, not the initial infection, of the VZV virus.
The latency period of the mumps virus is usually 2-3 weeks, suggesting that mumps infection in our case may have occurred 1-2 weeks before the development of cervical zoster and facial paralysis.
Recent molecular studies have provided mounting evidence that the mumps virus may dysregulate the immune system of the host so that the virus can proliferate in the infected host cells [9]. Such a dysregulation of immune system may have occurred in our patient, enabling the latent VZV infection to reactivate.
A similar causative association has been suggested in EB virus infection and VZV reactivation [10].Interestingly, besides the small number of case reports describing the development of peripheral facial paralysis in patients with mumps sialadenitis, the association of trigeminal herpes zoster and mumps parotitis has also been reported [11], as well as an increasing titer of mumps IgM in clinically diagnosed cases of Ramsay Hunt syndrome (without clinical sialadenitis) [12]. With the addition of our case, further speculation may be possible that these cases may represent the incomplete clinical presentation of mumps virus infection and subsequent VZV reactivation.4.
Bergström, “Varicella-zoster virus reactivation is an important cause of acute peripheral facial paralysis in children,” The Pediatric Infectious Disease Journal, vol. Hunt, “A further contribution to the herpetic inflammations of the geniculate ganglion,” The American Journal of the Medical Sciences, vol. Samtleben, “Contralateral facial palsy in a case of cervical zoster,” Journal of Neurology, vol. Kato, “Mumps virus V protein antagonizes interferon without the complete degradation of STAT1,” Journal of Virology, vol. Asanuma, “Reactivation of varicella-zoster virus in facial palsy associated with infectious mononucleosis,” The Pediatric Infectious Disease Journal, vol.
With ipsilateral parotitis; coincidence or association?” The Journal of the Medical Society of New Jersey, vol. Devriese, “Serology in facial paralysis caused by clinically presumed herpes zoster infection,” Archives of Oto-Rhino-Laryngology, vol.

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