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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 29  |  Issue : 4  |  Page : 350-353

Trigeminal Herpes Zoster: Early Recognition and Treatment –A Case Report


Department of Oral Medicine and Radiology, Dental College and Research Centre, Teerthanker Mahaveer University, Moradabad, Uttar Pradesh, India

Date of Submission26-Oct-2017
Date of Acceptance15-Jan-2018
Date of Web Publication15-Feb-2018

Correspondence Address:
Dr. Upender Malik
Department of Oral Medicine and Radiology, Dental College and Research Centre, Teerthanker Mahaveer University, Moradabad - 244 001, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiaomr.jiaomr_102_17

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   Abstract 


Herpes zoster is a clinical manifestation of the reactivation of latent varicella zoster virus infection. It is a self-limiting viral infection characterized by painful vesicular eruptions with erythema typically presenting as unilateral dermatomal rash of considerable morbidity, especially in elderly patients. It can be fatal in immunosuppressed or critically ill patients. We present a case of a 52-year-old male who presented with herpes zoster infection involving the V3dermatome, focusing upon early intervention in the management of this condition.

Keywords: Antivirals, herpes zoster, neurotrophic, shingles


How to cite this article:
Malik U, Sunil MK, Gupta C, Kumari M. Trigeminal Herpes Zoster: Early Recognition and Treatment –A Case Report. J Indian Acad Oral Med Radiol 2017;29:350-3

How to cite this URL:
Malik U, Sunil MK, Gupta C, Kumari M. Trigeminal Herpes Zoster: Early Recognition and Treatment –A Case Report. J Indian Acad Oral Med Radiol [serial online] 2017 [cited 2019 May 22];29:350-3. Available from: http://www.jiaomr.in/text.asp?2017/29/4/350/225462




   Introduction Top


Herpes zoster, also known as shingles, is a secondary manifestation of varicella zoster virus infection.[1] In the head and neck region, trigeminal ganglion involvement is seen; and on reactivation of virus, manifestations in the form of multiple vesicles along the course of the any one of the three divisions, namely V1, V2, V3, are seen, which are unilateral in presentation and are extremely painful.[2],[3] Owing to the mortality and morbidity associated with herpes zoster infection of trigeminal nerve, early intervention is essential to prevent the chances of superinfections and reduce the mortality and morbidity associated with the condition.


   Case Report Top


A 52-year-old male patient, reported to the OPD of Dental College and Research Centre, Teerthanker Mahaveer University, Moradabad with the chief complaint of partially healed blisters over the left side of the face along with oral ulcerations for the past 3–4 days with intense pain and swelling over the area affected by ulcerations both extraorally and intraorally. On examination, multiple patchy healed ulcerations and few vesiculations extraorally, with inflammation around the ulcerated region was present for 3–4 days. Partly healed areas showed scabbing and crustation of the lesions limited to the mandibular division of trigeminal nerve.

On intraoral examination, there were shallow, small, irregular, multiple ulcerations covered with grayish, yellowish, white pseudomembranous slough with an erythematous marginal halo affecting the left lateral border and dorsal surface of the tongue. The patient was severely debilitated and looked very feeble and weak. Keeping in view the unilateral presentation of the lesion restricted only to the mandibular division of the trigeminal nerve a provisional diagnosis of herpes zoster involving left mandibular division of trigeminal nerve was made [Figure 1] and [Figure 2]. Investigations was advised to the patient including complete hemogram, ELISA for HIV, and varicella zoster virus antibody panel IgG and IgM along with PAP. An orthopantomogram (OPG) to rule out odontogenic causes showed periapical abscess in relation to 37 and generalized periodontitis. Incidental finding of well-defined, heart-shaped radiolucency in relation to 11 and 12 region in between the root apex of 11 and 12 measuring around 1 cm in diameter mediolaterally and 1.5 cm superior-inferiorly suggestive of nasopalatine duct cyst was observed [Figure 3]. Blood investigation reports showed leukocytosis, and varicella zoster virus antibody panel showed IgG >150 U/ml with IgM value >12 U/ml, suggestive of active varicella zoster virus infection. The patient was advised to take famcyclovir 500 mg twice daily for 10 days along with 500 mg paracetamol thrice daily for pain relief. Prednisolone 5 mg once daily was also prescribed along with multivitamins and multiminerals for nutritional support. After 1 week, most intraoral and extraoral lesions healed almost completely with scarring and hypopigmentation [Figure 4]. After 10 days, the patient completely recovered from the condition but a persistent pain was present in the region of V3 dermatome, for which he was prescribed gabapentin 200 mg once a day followed by twice daily; he remains on the treatment for the same.
Figure 1: Vesicular eruption effecting the left mandibular region

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Figure 2: Image showing multiple ulceration on the dorsum of the tongue

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Figure 3: Incidental finding of well-defined heart shaped radiolucency in relation to 11 and 21

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Figure 4: Healed lesions on the face after treatment

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   Discussion Top


Infection with varicella zoster virus was first documented in the writings of ancient civilizations as a vesicular rash of unknown causes. A relationship between herpes zoster and chickenpox was suggested in 1888 and was finally proven in the 1950s. Since then, much progress has been made in preventing and treating the disease with the introduction of a live attenuated vaccine in 1974, treatment with acyclovir in the 1980s, and complete DNA sequencing in 1986, all of which may ultimately lead to the eradication of varicella zoster virus infection.[4]

Varicella zoster virus is a neurotrophic virus belonging to alpha herpes viridae and consists of an icosahedral nucleocapsid enclosed in a lipid envelope with double stranded DNA at its centre. Primary infection with varicella zoster virus causes chickenpox which manifests itself in the early childhood as multiple macula vesicular eruptions starting mainly in the trunk region and spreading centrifugally to involve the extremities, including genitals. Oral manifestations are rare manifesting as vesiculo-ulcerative eruptions which ultimately heal within 2–3 weeks. These lesions are always preceded by a prodrome of fever, headache, rash, malaise, and nausea.[5] After resolution of the primary infection, the varicella zoster virus remains latent in the nerve cell bodies, and less frequently, the non-neuronal satellite cells of the dorsal root, cranial nerve, or autonomic ganglia.[6] Herpes zoster infection is the secondary infection which occurs upon reactivation of varicella zoster virus, affecting approximately 1 million patients per year and carries a lifetime risk of 10–30%, affecting approximately 1 million patients per year.[7]

The lesions typically erupt within one or two adjacent dermatomes, with thoracic (50–60%), cervical (10–20%), and trigeminal (10–20%) being more commonly involved, while lumbar (5–10%) and sacral (5%) shows the least involvement. Immunocompromised patients show greater affinity to develop secondary herpes zoster with other biological agents being latent infectious processes, including bacterial and viral. Prodromal symptoms that herald herpes zoster infection include pruritus, dysesthesia, and pain along the distribution of involved dermatome.

Oral involvement is also dermatomal in distribution and often presents as vesicles affecting the palate, uvula, tonsils, tongue, buccal mucosa and floor of the mouth with odontalgia, devitalized teeth, internal resorption, pulpal necrosis, developmental anomalies, sudden exfoliation of teeth, facial scarring, jaw osteonecrosis, and severe periodontitis.[7] Ramsay–Hunt syndrome results from geniculate ganglion involvement, consisting of a triad of unilateral facial paralysis, painful vesicular eruptions of the external ear (zoster oticus), with accompanying tinnitus, vertigo, and deafness.[8] Involvement of nasocilliary branch of ophthalmic nerve is characterized by Hutchinson's sign, which is an early sign of herpes zoster opthalmicus, manifesting in the form of vesicles on tip, side, or root of nose.

Complications of herpes zoster infection although less commonly manifested are chiefly recognized in immunocompromised individuals and includes postherpetic neuralgia, chronic sensory loss at site of rash, limb weakness, and autonomic dysfunction related to the site of the rash. Neurological complications includes Bell's palsy, Ramsay–Hunt syndrome, encephalitis, meningitis, myelitis,[9] transient ischemic attacks and strokes, and ophthalmologic complications such as keratitis, scleritis, uveitis, and acute renal necrosis.[10]

Early zoster and zoster infection presenting in the sacral and cervical area may be difficult to distinguish from herpes simplex. In these cases, diagnosis can be confirmed by sending swabs to the virology laboratory, but treatment should not be delayed while waiting for test results.[8] In a majority of herpes zoster infection patients, the condition is self-limiting and healing is usually complete. The management is indicated in herpes zoster infection to alleviate symptoms of pain and malaise to restrict the spread as well as duration of the skin lesions, to prevent the development of postherpetic neuralgia and ophthalmological complications, and to control mortality and morbidity associated with superinfections.

The management of the condition depends upon the initiation of antiviral therapy at an early stage i.e., within the first 48–72 hours of the beginning of lesions. Most commonly substituted antiviral medication is acyclovir 800 mg 5 times in a day for 7–10 days. Other antivirals used in the treatment of this condition include famcyclovir 500 mg thrice daily for 7–10 days. Valacyclovir 1000 mg thrice daily for 7–10 days leads to early healing of the lesion and a reduction in the incidence of postherpetic neuralgia. Foscarnet is used for immunocompromised patient with acyclovir-resistant varicella zoster virus, foscarnet 40 mg/kg I/V, every 8 hours until lesions heal.

Corticosteroids, although contraindicated in viral infections, provide beneficial results and are used in addition to antivirals for resolution of acute pain, speeding up healing of the lesion, and enabling rapid return to daily activities. Most commonly used oral corticosteroid is methylprednisolone which is given in a single oral dosage of up to 60 mg per day and can be used along with antivirals. Analgesics are regularly prescribed to alleviate pain in herpes zoster infection and includes nonsteroidal anti-inflammatory drugs such as acetaminophen and opioids such as oxycodone that are used for severe pain. Topical agents such as lidocaine patch 5% and capsaicin also provide pain relief.[10]

Postherpetic neuralgia is the most common complication of herpes zoster infection in which neuralgic type of pain persists along the course of the involved dermatome, which can be managed with the use of anticonvulsants such as gabapentin, phenytoin, carbamazepine, and tricyclic antidepressants such as nortriptylin or amitriptylin. In the present case, the antivirals drugs substituted during the early course of infections lead to complete resolution of the lesion in 2 weeks and there was no need for substituting the antibiotics to cover super added infections. Currently, the patient has developed postherpetic neuralgia and is on the management for the same.


   Conclusion Top


An oral physician can be the first one to recognize the sign and symptoms of the disease, hence, a thorough knowledge of the condition becomes utmost important for proper management of the patient as the condition may be characterized by life-threatening complications.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Roxas M. Herpes zoster, postherpetic neuralgia. Diagnosis and therapeutic considerations. Altern Med Rev 2006;11:102-13.  Back to cited text no. 1
    
2.
Srikrishna K, Prabhat MPV, Balmuri PK, Sudhakar S, Ramaraju D. Herpes zoster: Report of a treated case with review of literature. J Indian Acad Oral Med Radiol 2012;24:51-5.  Back to cited text no. 2
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3.
Forbes HJ, Thomas SL, Smeeth L, Clayton T, Farmer R, Bhaskaran K, et al. A systematic review and meta-analysis of risk factors for postherpetic neuralgia. Pain 2016;157:30-54.  Back to cited text no. 3
    
4.
Cohen KR, Salbu RL, Frank J, Israel I. Presentation and management of herpes zoster (shingles) in the geriatric population. P T 2013;38:217-27.  Back to cited text no. 4
    
5.
Arvin A. Aging, immunity, and the varicella-zoster virus. N Engl J Med 2005;352:2266-7.  Back to cited text no. 5
    
6.
Wollina U. Variations in herpes zoster manifestation. Indian J Med Res 2017;145:294-8.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Gershon AA, Gershon MD. Pathogenesis and current approaches to control of varicella-zoster virus infections. Clin Microbiol Rev 2013;26:728-43.  Back to cited text no. 7
    
8.
Wareham DW, Breuer J. Herpes zoster. BMJ 2007;334:1211.  Back to cited text no. 8
    
9.
Hales CM, Harpaz R, Ortega-Sanchez I, Bialek SR. Update on recommendations for use of herpes zoster vaccine. MMWR Morb Mortal Wkly Rep 2014;22;63:729-31.  Back to cited text no. 9
    
10.
Cohen JI. Herpes zoster. N Engl J Med 2013;369:255-63.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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