CT and MR imaging of acute cerebellar ataxia

Shoji, Hiroshi; Hirai, Shunsaku; Ishikawa, Kinya; Aramaki, M.; Satō, Yoshihiro; Abe, Toshi; Kojima, Kazuyuki

doi:10.1007/bf00587826

Cited by 23 publications

(8 citation statements)

References 5 publications

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“…We hypothesise that in most cases, the diagnosis of PCD is carried out at later stages of the disease, when the cerebellar atrophy has been established after an initial inflammatory response. Supporting this idea, we found close similarities between our case and the case of Shoji et al 8 with acute infectious cerebellar ataxia. In that case, the cerebellar oedema disappeared 1 month later, whereas in our case evolved to atrophy.…”

supporting

confidence: 90%

Abscess of the medulla oblongata following endotracheal intubation

Payne¹,

Hickman²,

Howard³

2006

Journal of Neurology, Neurosurgery & Psychiatry

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supporting

confidence: 90%

Abscess of the medulla oblongata following endotracheal intubation

Payne¹,

Hickman²,

Howard³

2006

Journal of Neurology, Neurosurgery & Psychiatry

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“…[25] Inflammation of the cerebellum in childhood may be infectious, postinfectious or due to vaccines. [25][26][27][28][29][30][31][32][33][34][35] Infectious agents may also be varied. Some of the patients may be asymptomatic through infection or may display only mild symptoms.…”

mentioning

confidence: 99%

“…[25][26][27][28][29][30][31][32][33][34][35] Therefore, we aimed to determine the relationships of measles, mumps, rubella, cytomegalovirus (CMV), Ebstein-Barr Virus (EBV), HSV and VZV, which may all be agents of cerebellar inflammation, to ADHD. [25][26][27][28][29][30][31][32][33][34][35] As far as we are aware, no controlled studies on Turkish children and adolescents with ADHD to determine their status of immunity to viral agents have been conducted up to now.…”

mentioning

confidence: 99%

Subclinical immune reactions to viral infections may correlate with child and adolescent diagnosis of attention-deficit/hyperactivity disorder: A preliminary study from Turkey

Bekdaş¹,

Tufan²,

Hakyemez³

et al. 2014

Afr H. Sci.

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“…Some investigators have suggested the pathophysiology of acute cerebellar ataxia involves oedematous cerebellitis based on MRI4 and SPECT5 findings. In our case, no abnormalities were noted, possibly because the cerebellitis was mild as suggested by the clinical course.…”

Section: Discussionmentioning

confidence: 99%

Acute cerebellar ataxia with human parvovirus B19 infection

Shimizu

Ueno

Komatsu

et al. 1999

Archives of Disease in Childhood

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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...

show abstract

CT and MR imaging of acute cerebellar ataxia

Cited by 23 publications

References 5 publications

Abscess of the medulla oblongata following endotracheal intubation

Abscess of the medulla oblongata following endotracheal intubation

Subclinical immune reactions to viral infections may correlate with child and adolescent diagnosis of attention-deficit/hyperactivity disorder: A preliminary study from Turkey

Acute cerebellar ataxia with human parvovirus B19 infection

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