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. Received Varicella zoster virus (VZV) infection causes a variety of neurologic complications, including post-herpetic neuralgia, polyradiculoneuritis, transverse myelitis, vasculopathy, aseptic menengitis, leukoencephalopathy, dorsal root or cranial nerve ganglionitis, ventriculitis, necrotising angiitis and meningoencephalitis [1,2]. Transverse myelitis has been rarely associated with VZV infection. Onset is acute and occurs shortly after typical cutaneous rash in a dermatomal distribution with the development of paraparesis, sensory loss and sphincter dysfunction [3]. No diagnostic test is completely accurate, since VZV can not usually be isolated from blood or cerebrospinal fluid (CSF) in VZV myelitis. Treatment involves high doses of both steroids and acyclovir. Recovery is usually spontaneous, though fatal cases have been reported [4].We describe two cases of transverse myelitis during and following VZV infection that were proven serologically and neurologically.
Case 1A 48-year-old woman was presented to our clinic in April 2003 with the complaints of right leg weakness and urinary incontinence. Two months before, she had experienced a painful vesicular eruption on the lateral side of her left breast. Herpes zoster was diagnosed, and she was treated with a 10-day course of oral acyclovir (800 mg five times daily). In March 2003, she had been admitted to another hospital with paresthesia and weakness in both legs. Magnetic resonance imaging (MRI) of the spinal cord demonstrated lesions of high-signal intensity at C1-2 and T2-3 levels. The lesions appeared to be masses, therefore subtotal laminectomy was performed at T1-3. Histopathologic examination showed perivascular lymphocyte infiltration and reactive gliosis.On admission to our center in April, neurologic examination revealed normal levels of consciousness, cooperation, orientation and showed that all cranial nerves were intact. The patient exhibited 1/5 lower extremity weakness on the right and 3/5 on the left, diminished sensation to pain and light touch below the level of T5 dermatome, and marked loss of vibratory sensation and proprioception in both legs. Deep tendon reflexes were normal in the upper extremities, but decreased in the lower extremities. There was no nuchal rigidity.Laboratory findings for complete blood cell count, liver enzymes, BUN, creatinine, C-reactive protein, erythrocyte sedimentation rate and urinalysis were normal. Serological tests for hepatitis B and C, brucellosis, cytomegalovirus, herpes simplex virus, Epstein-Barr virus, PPD and human immunodeficiency virus were all negative. The serum was positive for anti-VZV antibodies....