Neurocritical care · 2010
Crossed cerebellar diaschisis in status epilepticus.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Samaniego Edgar A, Stuckert Erika, Fischbein Nancy, Wijman Christine A C
Аннотация
BACKGROUND: Crossed cerebellar diaschisis (CCD) has been reported on positron-emission tomography and single-photon emission computed tomography of stroke patients. Rarely it has been described with brain diffusion-weighted MRI (DWI) of status epilepticus (SE).
METHODS: Case report.
RESULTS: A 53-year-old woman was found unresponsive after cocaine use. A diagnostic electroencephalogram was consistent with ictal SE. A brain DWI showed reduced diffusion in the left temporo-parietal and occipital cortexes, the left thalamus and the right cerebellum. The DWI changes did not correspond to a vascular territory and were attributed to seizure activity and secondary CCD. A 2-week follow-up DWI showed interval near-complete resolution of the diffusion changes. CCD in SE may represent injury caused by excessive neuronal transmission from prolonged excitatory synaptic activity via the cortico-pontine-cerebellar pathway. Alternatively, it may be a result of interruption of the cortico-pontine-cerebellar pathway with loss of cortical inhibitory input.
CONCLUSION: This case documents CCD during SE, providing further evidence of contralateral cerebellar involvement with a supratentorial epileptiform focus.
METHODS: Case report.
RESULTS: A 53-year-old woman was found unresponsive after cocaine use. A diagnostic electroencephalogram was consistent with ictal SE. A brain DWI showed reduced diffusion in the left temporo-parietal and occipital cortexes, the left thalamus and the right cerebellum. The DWI changes did not correspond to a vascular territory and were attributed to seizure activity and secondary CCD. A 2-week follow-up DWI showed interval near-complete resolution of the diffusion changes. CCD in SE may represent injury caused by excessive neuronal transmission from prolonged excitatory synaptic activity via the cortico-pontine-cerebellar pathway. Alternatively, it may be a result of interruption of the cortico-pontine-cerebellar pathway with loss of cortical inhibitory input.
CONCLUSION: This case documents CCD during SE, providing further evidence of contralateral cerebellar involvement with a supratentorial epileptiform focus.