Neuropediatrics 2012; 43(02): 055-058
DOI: 10.1055/s-0032-1309306
Short Communication
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Crossed Cerebellar Diaschisis after Status Epilepticus in a Young Child

Anne Koy
1   Department of General Pediatrics and Neonatology, University Children's Hospital Düsseldorf, Düsseldorf, Germany
,
Dirk Klee
2   Institute of Diagnostic and Interventional Radiology, University Hospital Düsseldorf, Düsseldorf, Germany
,
Artur-Aron Weber
1   Department of General Pediatrics and Neonatology, University Children's Hospital Düsseldorf, Düsseldorf, Germany
,
Michael Karenfort
1   Department of General Pediatrics and Neonatology, University Children's Hospital Düsseldorf, Düsseldorf, Germany
,
Ertan Mayatepek
1   Department of General Pediatrics and Neonatology, University Children's Hospital Düsseldorf, Düsseldorf, Germany
› Author Affiliations
Further Information

Publication History

30 July 2011

13 February 2012

Publication Date:
03 April 2012 (online)

Abstract

We report on a 3.8-year-old girl who was born preterm. Due to a posthemorrhagic hydrocephalus she had a ventriculoperitoneal shunt. Magnetic resonance imaging (MRI) showed mild atrophy of the left cerebellum. She was found unresponsive in a febrile state. After the application of midazolam she regained consciousness. There were no epileptic discharges on electroencephalogram. MRI with diffusion-weighted sequences showed areas of hyperintensity in the right cerebrum. After the patient deteriorated again, MRI showed signs of increased intracranial pressure and high signal intensity throughout the right cerebral and left cerebellar hemispheres, suggesting crossed cerebellar diaschisis (CCD) most likely resulting from a nonconvulsive status epilepticus (SE). A follow-up MRI showed progressive brain atrophy. CCD after SE might be caused by cortical excitatory input through the cortico-pontine-cerebellar pathway. Alternatively, the cerebral edema in SE may decrease neuronal cell activity in the contralateral cerebellar hemisphere. The unilateral cerebellar atrophy before the onset of CCD might be attributed to impaired neuronal connections after peripartal cerebral injury. This case presents a young child with a combination of two CCDs, at first due to perinatal brain injury, and at second to SE. MRI with diffusion-weighted sequences can detect CCD at an early stage.

 
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