2009
DOI: 10.1007/s12028-009-9312-y
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Crossed Cerebellar Diaschisis in Status Epilepticus

Abstract: This case documents CCD during SE, providing further evidence of contralateral cerebellar involvement with a supratentorial epileptiform focus.

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Cited by 37 publications
(29 citation statements)
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References 8 publications
(8 reference statements)
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“…In the specific subset of CCD cases associated with seizure activity, the underlying pathophysiology is thought to involve a prolonged ictal event that hyperactivates the first order cerebral neurons, causing excitotoxicity and disabling the circuit in a form of transneuronal depression [12].…”
Section: Discussionmentioning
confidence: 99%
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“…In the specific subset of CCD cases associated with seizure activity, the underlying pathophysiology is thought to involve a prolonged ictal event that hyperactivates the first order cerebral neurons, causing excitotoxicity and disabling the circuit in a form of transneuronal depression [12].…”
Section: Discussionmentioning
confidence: 99%
“…The first radiographic description was published in 1980, using positron emission tomography (PET) in acute infarct patients [2]. Subsequent reports have described CCD using magnetic resonance imaging (MRI) and characterized the finding in neoplasms, arteriovenous malformations, hemorrhages, and-in conjunction with continuous electroencephalography (cEEG)-have correlated CCD with seizures [9,10,12,13].…”
Section: Introductionmentioning
confidence: 99%
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“…Conventionally, CCD refers to the depression of blood flow and metabolism affecting the cerebellar hemisphere due to a contralateral focal, supratentorial lesion, such as a cerebral infarction or tumor (1, 2). Prolonged seizure activity in SE can uncouple the metabolism and the cerebral blood flow, resulting in tissue hypoxia, anaerobic glycolysis, sodium/potassium pump failure, and cytotoxic edema (3). CCD following SE is caused by excessive neuronal transmission from the prolongation of excitatory synaptic activity via the CPC pathway (3)(4)(5).…”
Section: Discussionmentioning
confidence: 99%
“…Prolonged seizure activity in SE can uncouple the metabolism and the cerebral blood flow, resulting in tissue hypoxia, anaerobic glycolysis, sodium/potassium pump failure, and cytotoxic edema (3). CCD following SE is caused by excessive neuronal transmission from the prolongation of excitatory synaptic activity via the CPC pathway (3)(4)(5). A few cases of CCA after CCD have been reported.…”
Section: Discussionmentioning
confidence: 99%