Cortical laminar necrosis related to prolonged focal status epilepticus

Donaire, A
Carreno, M
Gómez, B
Fossas, P
Bargalló, N
Agudo, R
Falip, M
Setoaín, X
Boget, T
Raspall, T
Obach, V
Rumiá, J

¹Hospital Clínic de Barcelona, Barcelona, Spain
²Hospital General Mataró, Barcelona, Spain

Correspondence to: Dr Mar Carreno Epilepsy Unit, Hospital Clínic de Barcelona, Villarroel 170, 08036, Barcelona, Spain; [email protected]

Received 14 November 2004

Revised 29 April 2005

Accepted 04 May 2005

Competing interests: none declared

The patients detailed in this report gave their informed consent for their details to be published

Journal of Neurology, Neurosurgery, & Psychiatry 77(1):p 104-106, January 2006.

Cortical laminar necrosis (CLN) is radiologically defined as high intensity cortical lesions on T1 weighted MRI images following a gyral distribution. Histopathologically, CLN is characterised by pannecrosis of the cortex involving neurones, glial cells, and blood vessels. It has been reported to be associated with hypoxia, metabolic disturbances, drugs, and infections. We present two patients who developed CLN and permanent neurological deficits after prolonged and repeated focal status epilepticus. The possible mechanisms leading to CLN in these patients are discussed, together with the implications of prompt and aggressive treatment in similar cases.