Crossed cerebellar diaschisis after status epilepticus in a young child.

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.