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Acute cerebellitis associated with rotavirus infection 
 
Acute cerebellitis associated with rotavirus infection
  Zenichiro Kato, Hideo Sasai, Michinori Funato, Takahiko Asano, Naomi Kondo
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Acute cerebellitis associated with rotavirus infection

Zenichiro Kato, Hideo Sasai, Michinori Funato, Takahiko Asano, Naomi Kondo

Gifu, Japan

Author Affiliations: Department of Pediatrics, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu, Japan (Kato Z, Sasai H, Funato M, Kondo N); Department of Radiology, Gifu University Hospital, 1-1 Yanagido, Gifu 501-1194, Japan (Asano T)

Corresponding Author: Zenichiro Kato, MD, PhD, Department of Pediatrics, Graduate School of Medicine, Gifu University, 1-1 Yanagido, 501-1194 Gifu , Japan (Tel: +81 58 230 6386, Fax: +81 58 230 6387, Email: zen-k@gifu-u.ac.jp)

doi: 10.1007/s12519-011-0298-0

Background: Rotavirus infection is occasionally associated with central nervous system involvement, including cerebellitis. However, the precise clinical sequelae of central nervous system disorders and the usefulness of neuroradiological examination for clinical therapies, such as steroid pulse therapy, have not been clarified.

Methods: We present a case of rotavirus cerebellitis examined by magnetic resonance imaging (MRI), magnetic resonance spectroscopy, and single photon emission computed tomography.

 

Results: MRI demonstrated abnormal intensities in the right cerebellum on fluid attenuated inversion recovery images and, much more obviously, on diffusion-weighted images, but not on T1- or T2-weighted images. Single photon emission computed tomography showed only mild hypoperfusion in the right cerebellum on the 15th day, while 4 weeks later the image showed remarkably low perfusion in the right cerebellum.

Conclusion: The findings of the reported case suggest the importance of performing radiological examinations at early phases of the disease, especially by new modalities such as diffusion weighted imaging, to make timely and appropriate therapeutic decisions.

Key words: cerebellar ataxia; cerebellitis; magnetic resonance imaging; rotavirus; single photon emission computed tomography

World J Pediatr 2013;9(1):87-89


Introduction

Rotavirus infection can occasionally be associated with central nervous system (CNS) involvement including cerebellitis. However, the precise clinical sequelae of CNS disorders and the usefulness of neuroradiological examination for informing clinical guidelines and therapies such as steroid pulse therapy have not been clarified.[1-3] These limitations seem to be due to lack of radiological findings such as magnetic resonance imaging (MRI) abnormalities, which have only been reported in several cases.[1-3]

We present a case of rotavirus cerebellitis examined by MRI, magnetic resonance spectroscopy (MRS) and single photon emission computed tomography (SPECT). The findings suggest the importance of radiological examinations at early phases of the disease, especially using new modalities such as diffusion-weighted imaging (DWI), MRS or SPECT, even after the clinical symptoms have disappeared to uncover the precise CNS manifestation associated with rotavirus infection.

Case report

A 3-year-old girl was admitted to our hospital with a mild fever, accompanied with truncal ataxia and dysmetria predominantly in the right hand, suspected as having acute cerebellar ataxia (ACA). Seven days before admission, she showed a fever of approximately 39°„C, vomiting, and diarrhea. These symptoms persisted for 2 days before her temperature decreased to approximately 37°„C, while neurological abnormalities such as poor response to call and severe truncal ataxia became evident. The next day, she spoke with a slur and showed poor coordination of vocalizations. On admission, she had clear consciousness and response but slurred speech. Both pupils were equal in size and showed a prompt light reflex. Physical examination revealed her hands were clumsy, which resulted in poor feeding and poor picture drawing.

Laboratory data, including ammonia, glucose, serum creatine kinase and amylase levels were normal except for a mildly elevated C-reactive protein of 1.09 mg/dL. Cerebrospinal fluid (CSF) analysis showed 9 leukocytes/mm3 (segmented, 1; mononuclear, 8), a glucose level of 64 mg/dL, and a protein level of 15 mg/dL. Rotavirus antigen was detected in a stool specimen using an immunochromatographic method. MRI demonstrated abnormal intensities in the right cerebellum on fluid attenuated inversion recovery (FLAIR) images and, much more obviously, on DWI, but not on T1- or T2-weighted images (Fig. 1A-E). Immediately after MRI, glycerol (20 g) and prednisolone (5 mg/kg) were administered after a diagnosis of acute cerebellar inflammation (cerebellitis), and the prednisolone therapy (5 mg/kg, twice a day) was continued for 5 days followed by dose tapering. An electroencephalogram taken the next day was normal.

Her symptoms of truncal ataxia and slurred speech quickly improved, but difficulty walking, predominantly on the right foot, and poor fine motor coordination of the right hand, as observed during picture drawing or toothbrushing, persisted for 1 week. One week after admission (14 days after the first symptoms), MRI showed remarkable improvement with mild abnormal intensities observed only on DWIs (Fig.1F). Simultaneous MRS showed a metabolic abnormality of a low NAA/Cr ratio in the right cerebellum (NAA/Cr: right 0.69; left 0.95), indicating neuronal damage in the right cerebellum (Fig.2A and 2B). Three weeks after admission the patient showed complete improvement clinically and the radiological findings on MRI, including DWI, normalized. SPECT showed only mild hypoperfusion in the right cerebellum on the 15th day, while 4 weeks later the image showed remarkably low perfusion in the right cerebellum (Fig.2C and 2D).

Polymerase chain reaction analysis did not reveal the presence of rotavirus genome in her CSF, but did in her stool and subsequent sequencing identified the strain as group A, serum type 1.

Discussion

To date, four cerebellitis cases during rotavirus infection have been reported (Table).[1,4,5] In one case, only antibiotics were administered, and in the other three cases, the intervals from admission to the start of steroids were 2, 7 and 26 days respectively (Table). Usually when a clinical diagnosis of ACA is made, there would be an observational period without any specific therapy.[6,7] Our case was initially admitted to our hospital with a diagnosis of ACA, but the DWI revealed the lesion clearly (Fig. 1), which led to the decision to use steroid immediately. The initial MRIs on T1 or T2 weighted images were described as normal in three of the four reported cases (Table), but abnormal findings might have been detected on FLAIR or DWI, as observed in our patient.[8,9] There may be an increased risk to have neurological sequele after cerebellitis[1,4,5] if there is a longer lag before therapeutic intervention. Currently, ACA may be defined by acute cerebellar symptoms with the absence of obvious radiological findings, but future radiological techniques should narrow the clinical definition, identifying new categories.[9,10]

Acknowledgements

We thank Seiko Sawatari for performing the rotavirus polymerase chain reaction analysis on the specimen.

Funding: None.

Ethical approval: Not needed.

Competing interest: None declared.

Contributors: Kato Z wrote the first draft of this paper. Kato Z, Sasai H, Funato M and Kondo N treated the patient and obtained the clinical and laboratory data. Kato Z and Asano T analyzed the radiological data. All the authors contributed to the intellectual content and approved the final version.

References

1       Dickey M, Jamison L, Michaud L, Care M, Bernstein DI, Staat MA. Rotavirus meningoencephalitis in a previously healthy child and a review of the literature. Pediatr Infect Dis J 2009;28:318-321.

2       Fukuda S, Kishi K, Yasuda K, Sejima H, Yamaguchi S. Rotavirus-associated encephalopathy with a reversible splenial lesion. Pediatr Neurol 2009;40:131-133.

3       Kato Z, Orii KE, Morimoto M, Sasai H, Funato M, Sawatari S, et al. A transient lesion in the corpus callosum during rotavirus infection. Pediatr Neurol 2009;41:467-469.

4       Nigrovic LE, Lumeng C, Landrigan C, Chiang VW. Rotavirus cerebellitis? Clin Infect Dis 2002;34:130.

5       Shiihara T, Watanabe M, Honma A, Kato M, Morita Y, Ichiyama T, et al. Rotavirus associated acute encephalitis/encephalopathy and concurrent cerebellitis: report of two cases. Brain Dev 2007;29:670-673.

6       Kato Z, Shimozawa N, Kokuzawa J, Iwamura M, Hirata T, Yamagishi A, et al. Magnetic resonance imaging of acute cerebellar ataxia: report of a case with gadolinium enhancement and review of the literature. Acta Paediatr Jap 1998;40:138-142.

7       Sawaishi Y, Takada G. Acute cerebellitis. Cerebellum 2002;1:223-228.

8       Kato Z, Kozawa R, Teramoto T, Hashimoto K, Shinoda S, Kondo N. Acute cerebellitis in primary human herpesvirus-6 infection. Eur J Pediatr 2003;162:801-803.

9       Robertson RL, Glasier CM. Diffusion-weighted imaging of the brain in infants and children. Pediatr Radiol 2007;37:749-768.

10     Takanashi J. Two newly proposed infectious encephalitis/encephalopathy syndromes. Brain Dev 2009;31:521-528.

Received March 11, 2011 Accepted after revision July 1, 2011

 

 
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