Acute cerebellar ataxia with human parvovirus B19 infection

Abstract

A 2 year old boy developed acute cerebellar ataxia in association with erythema infectiosum. During the disease, genomic DNA and antibodies against human parvovirus B19 were detected in serum but not in cerebrospinal fluid. Parvovirus B19 associated acute cerebellar ataxia might occur due to transient vascular reaction in the cerebellum during infection. (Arch Dis Child 1999;80:72-73) Keywords: acute cerebellar ataxia; erythema infectiosum; human parvovirus B19 Although human parvovirus B19 (PVB19) is well known to cause erythema infectiosum, it also has other pathological manifestations such as aplastic crisis, thrombocytopenia, purpura, myocarditis, and arthritis. In central nervous system (CNS) disease, meningitis and encephalitis have been reported in association with this viral infection, but acute cerebellar ataxia has not previously been documented. We report a case of acute cerebellar ataxia associated with PVB19 infection. Case reportA 2 year old boy presented to his physician because of frequent vomiting. He was diagnosed with cyclic vomiting and received intravenous fluids. Over the next day he developed truncal ataxia and nystagmus, resulting in an inability to walk and to maintain a sitting position. On the fourth day he was seen in our hospital with bright red erythema on both cheeks and a maculopapular lacy erythema on his extremities. The rash subsided two days later although he still had mild ataxic gait and horizontal nystagmus. As the patient was not cooperative, detailed neurological examinations was diYcult except for patellar tendon reflexes, which were normal. He was diagnosed with acute cerebellar ataxia. A toxicology screen was not performed, and there was no recent history of vaccination or drug intoxication.White blood cell count was 8.0 × 10 9 /l, with 42.5% polymorphs, 2% eosinophils, 1.5% basophils, 6% monocytes, and 48% lymphocytes. C reactive protein was 0.1 mg/dl and erythrocyte sedimentation rate was 9 mm in the first hour. Cerebrospinal fluid (CSF) was normal with cell count 9/µl, protein 8 mg/dl, and glucose 65 mg/dl. Oligoclonal bands were not found and myelin basic protein was < 0.5 ng/ml in CSF. Serum electrolytes and urinary analysis by the stick test and microscopy were normal. Serology was negative for antibodies to varicella zoster virus, coxsackie B1, B2, B3, B5 viruses, and Mycoplasma pneumoniae. IgM and IgG antibodies against PVB19 were positive at a standard dilution of 1:200 in serum but negative at four dilution points between 1:50 and 1:400 in CSF. PVB19 DNA investigated by polymerase chain reaction (PCR) 1 was also positive in serum but negative in CSF. Nested PCR using six diVerent primer sets revealed that the strain of PVB19 in our case was not a special variant virus. Magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) performed on days 8 and 10 after presentation respectively showed no abnormal findings. An electroencephalogram on day 10 was also normal. Therefore, this case was thought to be acute cerebellar a...

Neurologic Manifestations Associated with Parvovirus B19 Infection

“…Other neurologic manifestations associated with PVB19 infection occurred only in immunocompetent patients and included acute cerebellar ataxia with nystagmus in a child, which occurred concurrently with a rash and resolved within a week [34]; Guillain-Barré syndrome involving the legs, with onset 5 days after the diagnosis of erythema infectiosum, in a child who experienced gradual improvement [35]; peripheral facial nerve paralysis in a child with a mononucleosis-like syndrome and parotitis who developed a rash 6 days later and improved after 6 weeks [43]; velopalatine hemiparalysis that manifested 1 week after diarrhea and lasted for 10 weeks [44]; and dysesthesias or paresthesias of the hands, legs, and face that lasted up to 8 months [45,46,62].…”

Neurological manifestations of human parvovirus B19 infection

“…On only one occasion has it been associated with B19 infection characterised by the typical EI rash [106]. In this case, B19 DNA and anti-B19 IgM and IgG antibodies were detected in serum but not in CSF.…”

Parvovirus B19 nonstructural (NS1) protein as a transactivator of interleukin‐6 synthesis: Common pathway in inflammatory sequelae of human parvovirus infections?

“…Case reports have linked acute and recurrent B19 infection or viral persistence with neurologic disorders such as neuralgic amyotrophy [Puechal et al, 1998], acute cerebellar ataxia [Shimizu et al, 1999], encephalopathy [Watanabe et al, 1994], meningitis [Okumura and Ichikawa, 1993], paresthesia [Faden et al, 1992], transverse myelitis, vertigo, and seizures [Torok, 1997], whereas Nakashima et al [1999] failed to find associations of B19 infection with multiple sclerosis. Both preand post-natal parvovirus B19 infections have been associated with cardiopulmonary disorders including: fetal myocardial necrosis [Lambot et al, 1999]; neonatal and adult cardiomyopathy [Heegaard et al, 1998;Barton, 1999]; severe interstitial lung disease associated with hepatitis and myositis [Bousvaros et al, 1998]; and pneumonia [Wardeh and Marik, 1998].…”