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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 29  |  Issue : 2  |  Page : 156-158

Herpes zoster infection of maxillary nerve: A case report


1 Department of Oral Medicine and Radiology, A.E.C.S. Maruti College of Dental Sciences and Research Center, Bengaluru, Karnataka, India
2 Department of Oral Medicine and Radiology, Hazaribag College of Dental Sciences, Hazaribag, Jharkhand, India

Date of Submission31-Aug-2016
Date of Acceptance18-Oct-2017
Date of Web Publication9-Nov-2017

Correspondence Address:
Isha Thakur
Department of Oral Medicine and Radiology, A.E.C.S Maruti College of Dental Sciences and Research Center, Bengaluru - 560 076, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiaomr.JIAOMR_105_16

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   Abstract 

Herpes zoster of the trigeminal nerve branches caused by varicella zoster is a clinical entity consisting of erythematous macules, papules, vesicles, bullae, small ulcers and erythematous plaques, with characteristic short acute/pre-eruptive phases and long herpetic periods with pain. It is caused by reactivation of latent varicella infection. Herpes zoster is a less common endemic disease compared to varicella. During the prodromal stage, the only presenting symptom may be odontalgia, which may prove to be a diagnostic challenge for the dentist. Emergency treatment for a misdiagnosis such as trigeminal neuralgia, odontalgia, and acute pulpitis, as well as complications reported in literature such as tooth resorption, periapical lesions, periodontal destructions, and osteomyelitis may cause an irreversible damage to the patient. Hence, the dentist must be familiar with the presenting signs and symptoms in prodrome of herpes zoster infection of trigeminal nerve. The present article focuses on the pathogenesis, clinical picture, difficulties in diagnosis and management of such cases.

Keywords: Neuralgia, odontalgia, teeth, varicella


How to cite this article:
Thakur I, Shilpa B, Satheesha Reddy HB, Koppula SK. Herpes zoster infection of maxillary nerve: A case report. J Indian Acad Oral Med Radiol 2017;29:156-8

How to cite this URL:
Thakur I, Shilpa B, Satheesha Reddy HB, Koppula SK. Herpes zoster infection of maxillary nerve: A case report. J Indian Acad Oral Med Radiol [serial online] 2017 [cited 2019 Aug 21];29:156-8. Available from: http://www.jiaomr.in/text.asp?2017/29/2/156/217905


   Introduction Top


Varicella zoster virus (VZV) belongs to genus varicello – virus, family herpes viridae, subfamily alpha – herpes virnae also known as hhv – 3 (human herpes virus – 3).[1] The virus is widely present in most populations. Primary infection with hzv (α–h virus) leads to varicella (chickenpox), as with all herpes virus, the virus becomes latent, usually in the dorsal ganglia. Whenever there is reactivation, the virus produces herpes zoster infection, commonly called as shingles/herpes zoster.[2] It becomes a challenge to diagnose when herpes zoster affects the oral and maxillofacial region, and should be considered in the differential diagnosis of those presenting with atypical odontalgia.[3] Approximately 13% of the patients present with infections involving any of the three branches of the trigeminal nerve. This case report is regarding herpes zoster infection of the maxillary nerve, which is quite rare, approximately seen in 1.7% of the cases.[4] Immediate management is required to reduce the risk of complications of the infection, especially in immunocompromised individuals, which may be responsible for significant morbidity; within 72 hours the antiviral therapy should be started to prevent post-herpetic neuralgia (PHN).[5],[6]


   Case Report Top


A 24-year-old male patient reported to the department of oral medicine and radiology with acute, severe, and continuous pain in the upper left three teeth since past 1 week. The pain mimicked electric shock like pain. Pain persisted throughout the day and aggravated in the evening and on taking phone calls. Pain was relieved by applying pressure on all the affected teeth with hand. Pain radiated to the left side of face and skull. On questioning further, patient gave a history of herpes zoster infection a week ago, for which he was on medication, which included:

  1. Tab. Valcivir 1 g tid for 7 days and
  2. Tab. Tryptomer 10 mg SOS


On eliciting medical history, patient reported an episode of dengue fever 9 years back. On extraoral examination, a healed, crusted, well-defined scar approximately 2 × 2 mm below the nasolabial groove and above the upper lip was seen. In addition, very small healing scars were present on the lateral and outer canthus of eye and on cheek on the same side [Figure 1]. On palpation, all cranial nerve examinations appeared to be normal, except the sensation on light touch and pin prick reflex which were reduced on the same (left) side.
Figure 1: Appearance on first visit

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Intraoral examination revealed no carious lesion in relation to 21, 22, and 23. No vestibular tenderness was present in relation to the same teeth, however, all the three teeth were tender on percussion both laterally and vertically. Vitality tests showed that the teeth were vital. Moreover, 36 was found to be carious without pulpal involvement. A provisional diagnosis of herpes zoster of maxillary branch of trigeminal nerve was made on the basis of history and clinical examination. A differential diagnosis of herpes simplex infection of mid face region was made. An intraoral periapical radiograph for 21, 22, and 23 was obtained, which revealed all teeth and surrounding structures to be normal [Figure 2]. A final diagnosis of nonodontogenic pain of neurotic origin due to herpes zoster virus infection of maxillary nerve was made owing to the characteristic (unilateral and localized) dermatomal presentation.
Figure 2: Intraoral periapical radiograph of 21, 22, 23

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The patient was informed about the viral, self-limiting, and contagious nature of the disease and was advised to maintain oral hygiene and continue with the medicine except the tab. tryptomer 10 g, which was replaced by tab. diclofenac sodium-paracetamol combination twice a day for 3 days. A follow-up review was done in the next 7 days; the pain subsided to some level but was still present [Figure 3]. The patient was advised intentional root canal therapy in 21, 22, and 23 for instant symptomatic relief because he wanted to get rid of the pain as soon as possible due to his job priorities and was kept on follow-up review for 3 months. Pain completely disappeared and lesions healed with scarring. No post-therapeutic complications were reported.
Figure 3: Appearance on follow-up visit

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   Discussion Top


A 2–3 days primary acute or pre-eruptive phase with pain and burning or tingling sensation in the involved dermatome is reported in most of the patients with herpes zoster virus infection. Fatigue, headache, low-grade fever, and myalgia may be present.[2] Erythematous macules and papules appear in the eruptive stage, which then turns into vesicular rash with unilateral dermatomal distribution. Over the next 3–5 days, new lesions tend to rise forming bullae. The vesicles rupture with fluid excretion, crusts, and desiccation leaving small ulcers and erythematous plaques without typical scars.[7] Herpes zoster virus infection affects the ophthalmic branch the most, however, all three divisions of trigeminal nerve can get affected.[8] In our case, maxillary nerve was found to be involved. There are 1.5–3 cases of herpes zoster virus infection per 1000 participants; this increases to 10 per 1000 in those over 75 years.[9],[10] However, in our case, age may not be a factor as his age is 24 years. Patient also reported increased stress as his profession demanded receiving phone calls at a call centre 10 h a day. Hence, this could be taken into account as a predisposing factor.

The disease should be diagnosed once the patient reports to the dentist and the differential diagnoses of irreversible pulpitis, acute periapical periodontitis, or acute sinusitis should be considered for atypical odontalgia.[3] Prompt management is required. Recommended therapy should include:

  1. Isolation of the patient
  2. Local management of skin lesions
  3. Control and elimination of pain
  4. Limitation of the extent, duration and severity of the disease with antiviral agents
  5. Treatment of PHN.[3]


Early treatment of herpes zoster virus infection with antivirals within 72 h of disease onset may decrease the risk of PHN. These include acyclovir, famicyclovir, and valacyclovir.[11] The treatment is based on symptomatic relief and antiviral therapy. The drug of choice for the treatment of varicella zoster virus infection is acyclovir 800 mg 5 times a day.[12] Other antiviral agents such as valacyclovir 1000 mg and famicyclovir 500 mg both three times a day have been considered now. These newer drugs overcome the low oral bioavailability of acyclovir and its limited effect in preventing the development of PHN.[13] Corticosteroids have an anti-inflammatory effect used mainly in acute pain. Analgesics (acetaminophen and NSAIDS) and tricyclic antidepressants (TCAs) can be used [Table 1].[2] Viral reactivation and development of herpes zoster infection can be avoided by vaccination with an attenuated form of varicells zoster virus that activates specific t-cell production. It has been demonstrated to reduce the occurrence by 50–70% approximately, the duration of pain of herpes zoster, and the frequency of subsequent PHN in individuals aged more than or equal to 50 years in clinical studies of short term. In contrast, varicella vaccination may increase the incidence of herpes zoster infection due to reactivation of varicella zoster virus.[14]
Table 1: Recommended drugs with dosages and side effects for treatment of herpes zoster virus infection

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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.
Cohen JI. Genomic structure and organisation of VZV. Curr Top Microbiol Immunol 2010;342:1-14.  Back to cited text no. 1
[PUBMED]    
2.
Schmader KE, Dworkin RH. Natural history and treatment of herpes zoster. J Pain 2008;9:S3-9.  Back to cited text no. 2
[PUBMED]    
3.
Tidwell E, Hutson B, Burkhart N, Gutmann JL, Ellis CD. Herpes zoster of the trigeminal nerve third branch: A case report and review of the literature. Int Endod J 1999;32:61-6.  Back to cited text no. 3
[PUBMED]    
4.
Patil S, Srinivas K, Reddy SBH, Gupta M. Prodromal herpes zoster mimicking odontalgia- A diagnostic challenge. Ethiop J Health Sci 2013;23:73-7.  Back to cited text no. 4
    
5.
Mustafa MB, Ardvino PG, Porter SR. Varicella zoster virus: Review of its management. J Oral Pathol Med 2009;38:673-88.  Back to cited text no. 5
    
6.
Jamie SM, John K. Practical considerations in pharmacological treatment of post herpetic neuralgia for primary care provider. J Pain Res 2014;7:125-32.  Back to cited text no. 6
    
7.
Zaal MJ, Volker-Dieben HJ, D'amaro J. Prognostic value of Hutchinson's sign in acute herpes ophthalmicus. Graefes Arch Clin Exp Ophthalmol 2003;241:187-91.  Back to cited text no. 7
    
8.
Ragazziuo MW, Melton LJ, Kurland LT, Chu CP, Perry HO. Population based study of herpes zoster and its sequelae. Medicine 1982;61:310-6.  Back to cited text no. 8
    
9.
Verbin RS, Heineman HS, Stiff RH. Localized odontalgia occurring during herpes zoster of the maxillary division of the fifth cranial nerve: Report of a case. Oral Surg Oral Med Oral Pathol 1968;26:441-5.  Back to cited text no. 9
[PUBMED]    
10.
Donahue JG, Choo PW, Manson JE, Platt R. The incidence of herpes zoster. Arch Intern Med 1995;155:1605-9.  Back to cited text no. 10
[PUBMED]    
11.
Wood MJ, Shukla S, Fiddian AP, Crooks RJ. Treatment of acute HZ: Effect of early (<48hrs) versus late (48-72hrs) therapy with acyclovir and valcivir on prolonged pain. J Infect Dis 1998;178:81-4.  Back to cited text no. 11
    
12.
Dunkle LM, Arvin AM, Whitley RJ, Rotbart HA, Feder HM Jr, Feldman S, et al. A controlled trial of acyclovir for chicken pox in normal children. N Eng J Med 1991;325:1539-44.  Back to cited text no. 12
    
13.
Tyring S, Barbarash RA, Nahlik JE, Cunningham A, Marley J, Heng M et al. Famicyclovir for the treatment of acute HZI: Effects on acute disease and post herpetic neuralgia. Ann Intern Med 1995;123:89-96.  Back to cited text no. 13
    
14.
Kyung HK. Herpes zoster vaccination. Korean J Pain 2013;26:242-8.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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