Abstract
A previously healthy immune competent 42-year-old female from Surinam was admitted to our hospital, her past medical history was significant for diabetes mellitus type 2. A week before admission she experienced fever, malaise and lethargy. After 24 h the patient developed a vesicular rash on her torso, which spread to involve the entire skin surface. Within a few days the vesicles developed into crusts, she felt progressively tired and experienced weakness in the legs. On neurological examination she was febrile, sensation to touch and pinprick diminished caudal to the fourth thoracic vertebra; there was weakness of the legs grade 4/5 of the medical research council scale (MRCS) and bilateral Babinski signs. MRI of the spine and head CT scan depicted no abnormalities, laboratory examination showed a mild leukocytosis, serology for infections (EBV, CMV, HSV, HIV, TBC), metabolic or vasculitic syndromes were negative, analysis of cerebrospinal fluid showed a pleiocytosis (45 white blood cells/mm3 with 65 % monocytes predominance), 142 mg/dl glucose, 92 mg/dl protein, IgG index 0, 40 and oligoclonal bands. Aquaporine-4 (AqP4) antibodies in serum were negative, VZV DNA was not detected by PCR, anti-VZV IgG antibody in the cerebral spinal fluid was positive (Goldmann-Witmer coefficient ratio 4.31/ Pos). Furthermore we isolated VZV from vesicles on her torso. The patient was started on intravenous therapy with acyclovir (750 mg tid), followed by 3 days intravenous methylprednisolone (1,000 mg qd) with a dexamethasone taper (16 mg qd). Because of a deteriorating renal function after 8 days her dose was adjusted to acyclovir (750 mg qd), which was given for 5 months. Despite therapy her condition deteriorated within weeks leading to a complete tetraplegia with respiratory failure. Repeat MRI of the spine 10 days after admission showed a diffuse increased signal intensity throughout the spinal cord from C2 to T4 level with cord expansion and swelling (Fig. 1). A MRI brain scan showed signs consistent with encephalitis or infarction due to VZV vasculopathy. Since there was no neurological improvement, the immunosuppressive treatment was followed by five cycles of plasmapheresis with no effect. Unfortunately she remained tetraplegic and was supported with continuous positive airway pressure (CPAP). A few months later the patient died in a center specialized in mechanical ventilatory assistance due to respiratory failure. J. M. Zijdewind (&) P. W. Wirtz Department of Neurology, Haga Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands e-mail: j.zijdewind@hagaziekenhuis.nl
Published Version
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