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Table of Contents
Year : 2019  |  Volume : 7  |  Issue : 2  |  Page : 61-64

Postinfectious (Varicella Zoster) myositis and mixed polyneuropathy

Department of Medicine, SBKS MIRC, Sumandeep Vidyapeeth, Vadodara, Gujarat, India

Date of Submission30-May-2019
Date of Decision14-Aug-2019
Date of Acceptance11-Sep-2019
Date of Web Publication02-Jan-2020

Correspondence Address:
Dr. Palak Rajendra Doshi
Room No. 75, Vama Hostel, Sumandeep Vidyapeeth Campus, At and Po. Pipariya, Waghodia, Vadodara - 391 760, Gujarat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JIHS.JIHS_29_19

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We present a case of a 21-year-old male with weakness of all four limbs after primary episode of chicken pox. Nerve conduction studies and magnetic resonance imaging dorsal spine with whole spine and brain screening confirmed polyneuropathy and myositis, respectively. He responded well to intravenous steroids, with complete reversal of symptoms. This case shows that primary varicella zoster infection is a sufficient stimulus to drive antibody generation and precipitate clinical complications.

Keywords: Mixed polyneuropathy, myositis, varicella zoster

How to cite this article:
Muley A, Doshi PR, Kumar S, Kanojiya S, Doshi MV, Patel K. Postinfectious (Varicella Zoster) myositis and mixed polyneuropathy. J Integr Health Sci 2019;7:61-4

How to cite this URL:
Muley A, Doshi PR, Kumar S, Kanojiya S, Doshi MV, Patel K. Postinfectious (Varicella Zoster) myositis and mixed polyneuropathy. J Integr Health Sci [serial online] 2019 [cited 2021 Jan 23];7:61-4. Available from: https://www.jihs.in/text.asp?2019/7/2/61/274529

  Introduction Top

Chicken pox is a viral infection which presents with fever and exanthematous rash which is extremely contagious. It is caused by a neurotropic human herpesvirus, the varicella zoster virus. The virus has the quality of remaining latent after the primary infection in the spinal and cranial ganglia and may be reactivated at a later stage in a state of immunocompromise to present as herpes zoster.

Neurological complications caused by chicken pox include cerebellar ataxia, encephalitis, transverse myelitis, aseptic meningitis, Guillain–Barre syndrome, meningoencephalitis, ventriculitis, optic neuritis, postherpetic neuralgia, herpes zoster ophthalmicus, delayed hemiparesis, peripheral motor neuropathy, myositis, cerebral angiitis, Reye's syndrome, and facial palsies.[1],[2],[3] However, these are rare and are seen in only 0.01%–0.03% cases.[4]

As per our knowledge, there has been no case which reported both polyneuropathy and myositis occurring simultaneously postvaricella. We present a case of 21-year-old male who developed both polyneuropathy and myositis at the same time after an episode of chicken pox.

  Case Report Top

A 21-year-old unmarried male, mechanic by occupation, presented with a complaint of weakness and myalgia of all four limbs for 1 month. He was apparently well 1 month back when he suffered from fever with rash which was diagnosed as varicella zoster. Fever and rash recovered with treatment in a week. However, 7 days after the onset of rash, he developed pain, tenderness, and weakness in his left forearm followed by left hand muscles, so that the patient had difficulty in grasping objects with his left hand. 4–5 days later, he developed similar complaints in his right forearm and hand. 2–3 days after this, the patient developed pain and tenderness in both his thigh and calf muscles along with weakness of both lower limbs such that he had difficulty in walking and standing up from sitting position. At this time, he was investigated outside. His complete blood count (CBC), rheumatoid factor titer, serum uric acid, and serum calcium levels were normal. Urine examination revealed 6–8 pus cells/hpf and calcium oxalate crystals. He was given analgesics, but did not improve. 4–5 days after this, he presented to our hospital with the same complaints which had worsened in intensity. By this time, he had also developed difficulty in dorsiflexion of both feet. There was no bowel and bladder involvement and no history of headache, neck muscle rigidity, nasal regurgitation, altered speech, involuntary movements, diplopia, facial weakness, or asymmetry, but 4–5 days after admission, he developed mild dysphagia which was more for solids than liquids.

The patient gave a history of hepatitis B surface antigen-positive status detected in 2009. He had a family history of his sister having similar fever with rash 1 week after he had developed the same. She was also diagnosed and treated as varicella zoster and had recovered completely with no sequelae.

On examination, his pulse was 108/min and regular and adequate in volume in the right radial artery and blood pressure was 128/90 mmHg in the left arm in supine position. He had nonpitting edema over both forearm muscles and calf muscles with superficial warmth and tenderness [Figure 1].
Figure 1: Swelling over the calf muscles and feet before starting corticosteroids

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Respiratory, cardiovascular, and per abdomen examination were unremarkable. On central nervous system examination, the higher mental function and cranial nerve examination revealed no abnormality. There was no muscle wasting, and tone in all four limbs was also normal. Power in all four limbs was 3+/5. Coordination could not be tested due to weakness. The knee and ankle jerks of both limbs were exaggerated, whereas the deep tendon reflexes of the upper limb, the jaw jerk, and the gag reflex were normal. There was loss of fine touch on dorsal (DL) aspect of both feet, whereas the rest of the sensory system examination was unremarkable. Babinski sign was negative in both the feet. A provisional diagnosis of postinfectious myositis or postinfectious neuropathy was kept in mind and the patient was investigated further on these lines.

His CBC showed slightly raised total leukocyte counts, but was otherwise normal. His urine examination, serum electrolytes, renal function tests, total protein/albumin, sickling, rheumatoid arthritis factor, and thyroid function tests were all normal. His liver function test showed normal bilirubin, but the serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase levels were raised slightly; C-reactive protein was also slightly raised, whereas serum calcium was reduced. Vitamin D3 levels were significantly low and Vitamin B12 levels were also on the lower side. Vitamin B12 and Vitamin D3 supplementations were given to the patient, but he did not show any significant improvement, rather his symptoms increased in intensity as the time passed. Hence, a cerebrospinal fluid (CSF) examination, nerve conduction study/electromyography (NCS/EMG), and magnetic resonance imaging (MRI) DL spine with whole spine and brain screening were done. The CSF examination was unremarkable, but the NCS/EMG was suggestive of mild demyelinating pure motor neuropathy and the MRI-DL spine with whole spine and brain screening showed the possibility of inflammatory myositis [Table 1]. The patient was given tablet acyclovir and intravenous corticosteroids for 5 days. With this, he showed a significant improvement in symptoms (probably due to myositis responding to steroids) with reduction of pain, tenderness, and swelling over the muscles with reduced difficulty in walking and dorsiflexion of the feet [Figure 2].
Table 1: Laboratory reports of the patient

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Figure 2: Swelling over the calf muscles and feet decreased after 5 days of intravenous corticosteroid therapy

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After 5 days, he was discharged on oral corticosteroids and acyclovir with advice of physiotherapy. There was a gradual improvement after discharge, and on follow-up after 30 days, he was able to walk with support.

  Discussion Top

Myositis is defined as an inflammation of voluntary muscles, which presents with pain, tenderness, swelling, and weakness of voluntary group of muscles. Infectious myositis may be due to wide variety of pathogens including bacteria, viruses, parasites, and fungi. Bacterial myositis presents as focal muscle infection, whereas viruses and parasites tend to cause diffuse disease with generalized myalgias and multifocal myositis.[5] Viruses are reported as the most common etiologies of nonbacterial infectious myositis cases in the U.S. and the rest of the developed world. It may be caused by a variety of viral agents, including influenza (the most common etiology), parainfluenza, enteroviruses (coxsackievirus and echovirus), adenovirus, severe acute respiratory syndrome-coronavirus, HIV, herpes viruses (varicella, herpes simplex, Epstein–Barr, and cytomegalovirus), parvovirus B19, dengue, and West Nile virus.[6],[7] Although it results in spontaneous recovery in most of the cases, complications such as rhabdomyolysis, myoglobinuria, acute renal failure, cardiac arrhythmias, and compartment syndrome which could be potentially dangerous have also been associated with significant morbidity.[8] Many explanations have been suggested as the pathogenic basis for these complications such as direct viral invasion[9] or immune-mediated allergic mechanism. However, allergy-mediated injury has been reported to be the cause in most pathologic studies.[10] However, most of the times, the neurological sequelae are in relation to reactivation of latent disease, whereas those following primary infection are rare.[11]

This case presented with a combination of polyneuropathy and myositis, that too following the primary infection. It progressed to dysphagia also, but responded well to intravenous steroids. Hence, this case brings to notice that neurological complications postvaricella can occur even following primary infection and that one should keep high index of suspicion for detecting these as they are reversible with treatment without any residual involvement.

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 patientsunderstand 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


Conflicts of interest

There are no conflicts of interest.

  References Top

Caheid Y, Husein C. Severe neurological complications of chickenpox: Report of four cases. Eur J Gen Med 2005;2:177-9.  Back to cited text no. 1
Gnann JW Jr. Varicella-zoster virus: Atypical presentations and unusual complications. J Infect Dis 2002;186 Suppl 1:S91-8.  Back to cited text no. 2
LaGuardia JJ, Gilden DH. Varicella-zoster virus: A re-emerging infection. J Investig Dermatol Symp Proc 2001;6:183-7.  Back to cited text no. 3
Wilson RE, Ford FR. The nervous complications of Variola, Vaccinia and Varicella with report of cases. Bull Johns Hopkins Hosp 1927;40:337.  Back to cited text no. 4
Singh H, Talapatra P, Arya S, Gupta V. Viral myositis as a close mimicker of polymyositis. Ann Trop Med Public Health 2013;6:324.  Back to cited text no. 5
  [Full text]  
Singh U, Scheld WM. Infectious etiologies of Rhabdomyolysis: Three case reports and review. Clin Infect Dis 1996;22:642-9.  Back to cited text no. 6
Montgomery SP, Chow CC, Smith SW, Marfin AA, O'Leary DR, Campbell GL, et al. Rhabdomyolysis in patients with west nile encephalitis and meningitis. Vector Borne Zoonotic Dis 2005;5:252-7.  Back to cited text no. 7
Bagley WH, Yang H, Shah KH. Rhabdomyolysis. Intern Emerg Med 2007;2:210-8.  Back to cited text no. 8
Puchhammer-Stöckl E, Popow-Kraupp T, Heinz FX, Mandl CW, Kunz C. Detection of varicella-zoster virus DNA by polymerase chain reaction in the cerebrospinal fluid of patients suffering from neurological complications associated with chicken pox or herpes zoster. J Clin Microbiol 1991;29:1513-6.  Back to cited text no. 9
Steiner I, Kennedy PG, Pachner AR. The neurotropic herpes viruses: Herpes simplex and Varicella-zoster. Lancet Neurol 2007;6:1015-28.  Back to cited text no. 10
Cresswell F, Eadie J, Longley N, Macallan D. Severe guillain-barré syndrome following primary infection with varicella zoster virus in an adult. Int J Infect Dis 2010;14:e161-3.  Back to cited text no. 11


  [Figure 1], [Figure 2]

  [Table 1]


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