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Transverse Myelitis Caused by Varicella Zoster: Case Reports

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Transverse Myelitis Caused by Varicella Zoster: Case Reports BJID 2007; 11 (February) 179 Transverse Myelitis Caused by Varicella Zoster: Case Reports Sema Yýlmaz1, Hamide Kart Köseoðlu2 and Eftal Yücel2 1Baskent University Konya Medical and Research Center, Division of Rheumatology, Konya; 2Baskent University Faculty of Medicine, Division of Rheumatology, Ankara; Turkey Transverse myelitis is a group of disorders characterized by focal inflammation of the spinal cord and results in loss of motor and sensory function below the level of injury. Occurrence of this condition during or following varicella infection is uncommon. This report describes two cases of transverse myelitis caused by varicella zoster. Key-Words: Varicella zoster, infection, transverse myelitis. Varicella zoster virus (VZV) infection causes a variety of light touch below the level of T5 dermatome, and marked loss neurologic complications, including post-herpetic neuralgia, of vibratory sensation and proprioception in both legs. Deep polyradiculoneuritis, transverse myelitis, vasculopathy, tendon reflexes were normal in the upper extremities, but aseptic menengitis, leukoencephalopathy, dorsal root or decreased in the lower extremities. There was no nuchal cranial nerve ganglionitis, ventriculitis, necrotising angiitis rigidity. and meningoencephalitis [1,2]. Transverse myelitis has been Laboratory findings for complete blood cell count, liver rarely associated with VZV infection. Onset is acute and occurs enzymes, BUN, creatinine, C-reactive protein, erythrocyte shortly after typical cutaneous rash in a dermatomal sedimentation rate and urinalysis were normal. Serological distribution with the development of paraparesis, sensory loss tests for hepatitis B and C, brucellosis, cytomegalovirus, and sphincter dysfunction [3]. No diagnostic test is completely herpes simplex virus, Epstein-Barr virus, PPD and human accurate, since VZV can not usually be isolated from blood or immunodeficiency virus were all negative. The serum was cerebrospinal fluid (CSF) in VZV myelitis. Treatment involves positive for anti-VZV antibodies. CSF was negative for anti- high doses of both steroids and acyclovir. Recovery is usually VZV antibodies.Tests for anti-nuclear antibodies, anti-double spontaneous, though fatal cases have been reported [4]. stranded DNA, and cytoplasmic and perinuclear types of anti- We describe two cases of transverse myelitis during and neutrophil cytoplasmic antibodies were also negative. Cranial following VZV infection that were proven serologically and MRI examination was normal. Cervical MRI demonstrated neurologically. lesions of high signal intensity at C2 and C5-C6 levels, and the appearance was consistent with areas of focal edema. Case 1 Thoracic MRI showed the laminectomy defects, fluid collection A 48-year-old woman was presented to our clinic in April at T1-T4 and enhancement was seen after administration of 2003 with the complaints of right leg weakness and urinary gadolinium. Lumbosacral MRI revealed edema around the incontinence. Two months before, she had experienced a interspinous ligaments at L4-L5 and L5-S1. painful vesicular eruption on the lateral side of her left breast. The patient was diagnosed with transverse myelitis, and Herpes zoster was diagnosed, and she was treated with a 10- treatment was started with oral methylprednisolone 1 mg/kg/ day course of oral acyclovir (800 mg five times daily). In March day was initiated. This was continued for two weeks and was 2003, she had been admitted to another hospital with then tapered by 4 mg each week until 10 mg/day. Gabapentin paresthesia and weakness in both legs. Magnetic resonance 2,000 mg/day, amitriptyline 25 mg/day and citalopram 20 mg/ imaging (MRI) of the spinal cord demonstrated lesions of day were also prescribed. After 3 months, she was able to high-signal intensity at C1-2 and T2-3 levels. The lesions walk supported by canes, and despite mild leg weakness, had appeared to be masses, therefore subtotal laminectomy was normal sensation in her legs and normal sphincter function. performed at T1-3. Histopathologic examination showed perivascular lymphocyte infiltration and reactive gliosis. Case 2 On admission to our center in April, neurologic examination A 52-year-old woman was presented to our clinic in March revealed normal levels of consciousness, cooperation, 2003 with low back pain, paresthesia in both legs. In June of orientation and showed that all cranial nerves were intact. 2001, she had presented with leg pain and a painful itchy The patient exhibited 1/5 lower extremity weakness on the vesicular eruption in her lumbosacral area. Herpes zoster was right and 3/5 on the left, diminished sensation to pain and diagnosed, and she was treated with 10 days of oral acyclovir 800 mg five times daily. During this treatment period, she Received on 6 September 2006; revised 12 December 2006. developed paresthesia and weakness in both legs, urinary Address for correspondence: Dr. Sema Yýlmaz. Vatan cad. Devrim sitesi and fecal incontinence. She was hospitalized. Spinal cord MRI B/Blok. Kat:2 No:29/4. Zip code: 42040 Selçuklu, Konya/Turkey. Phone: + 90-332-3200484. E-mail: [email protected] at the time showed intramedullary lesions of high signal intensity between the T2-T3 and T10 levels with gadolinium The Brazilian Journal of Infectious Diseases 2007;11(1):179-181. enhancement, findings which are consistent with myelitis. © 2007 by The Brazilian Journal of Infectious Diseases and Contexto Antibodies to VZV were detected in serum but not in CSF. Publishing. All rights reserved. The patient was placed on a treatment regimen for transverse www.bjid.com.br 180 Transverse Myelitis Due to Varicella Zoster BJID 2007; 11 (February) myelitis, and was transferred to the rehabilitation unit in to ascending progression and death [6].Patients with rapid another hospital. By the end of therapy, she had improved progression and flaccidity below the level of the lesion have dramatically. the poorest prognosis. Initial neurologic examination on admission in March 2003 The frequency of transverse myelitis during or after showed normal levels of consciousness, cooperation, varicella infection is 0.3% [7]. The characteristic symptoms orientation, as well as intact cranial nerves and normal are typically bilateral sensory deficit at a given level, cerebellar function. Motor function in the upper and lower paraparesis, quadriparesis, motor weakness and abnormal extremities was normal, but diminished sensation to pain and bladder and rectal function. In most cases, transverse myelitis light touch was noted below the T12 dermatome. Vibratory caused by VZV is diagnosed based on detection of typical sensation and proprioception were diminished in the patients’ vesicular lesions in dermatomal distribution that are associated left lower leg. Deep tendon reflexes were normal in the upper with signs and symptoms suggestive of transverse myelitis. extremities, but decreased in the lower extremities. There was However, transverse myelitis associated with herpes zoster have no nuchal rigidity. Ophtalmoscopic examination revealed been described in the absence of typical skin lesions [8]. nothing remarkable. The pathogenesis of neurological complications Laboratory results for complete blood cell count, liver associated with VZV infection is unclear. An allergic and enzymes, BUN, creatinine, C-reactive protein, erythrocyte vascular mechanisms have been suggested for some of these sedimentation rate and urinalysis were normal. Serological neurological complications that occur after both primary tests for brucellosis, hepatitis B and C, herpes simplex virus, varicella infection and herpes zoster [9]. In idiopathic acute cytomegalovirus, Epstein-Barr virus, PPD and human transverse myelitis, there is an intraparenchymal or immunodeficiency virus were negative. Serum was positive perivascular cellular influx into the spinal cord, resulting in for antibodies to VZV. CSF was negative for anti-VZV the breakdown of the blood-brain barrier and variable antibodies. Testing for antinuclear antibodies, anticardiolipin demyelination and neuronal injury. However, the antibodies immunoglobulin G and immunoglobulin M, pathogenesis of VZV myelitis has been thought as a direct cytoplasmic and perinuclear types of anti-neutrophil viral invasion, because VZV particles were found in glial cytoplasmic antibodies, cryoglobulin and complement 3 and cells, and the virus was isolated from the spinal cord of 4 showed nothing abnormal. Cranial and thoracic MRI patients with zoster myelitis. In a detailed report that included examinations were normal; however, lumbosacral MRI showed post mortem examination of the spinal cord, Hogan et al. [10] stenosis of the neural foramen at L4-L5. Electromyography presented evidence of direct invasion of VZV in a patient showed mild loss of motor unit action potentials. with transverse myelitis associated with herpes zoster. The patient was treated with oral methylprednisolone 20 Demonstration of the VZV antigen in CSF cells by mg/day for 3 weeks and was then tapered by 4 mg every week immunofluorescence or isolation of VZV from the CSF is a until 4 mg/day. She was also prescribed amitriptyline 50 mg/ confirmative evidence for viral central nervous system day and gabapentin 600 mg/day. After 10 weeks, she had infection but it is rarely successful [11]. normal sensation in the legs and mild low back pain. In both of our cases, transverse myelitis related to varicella infection was diagnosed on the basis of MRI findings, and on Discussion the development
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