TY - JOUR
T1 - The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission
AU - Blümcke, Ingmar
AU - Thom, Maria
AU - Aronica, Eleonora
AU - Armstrong, Dawna D.
AU - Vinters, Harry V.
AU - Palmini, Andre
AU - Jacques, Thomas S.
AU - Avanzini, Giuliano
AU - Barkovich, A. James
AU - Battaglia, Giorgio
AU - Becker, Albert
AU - Cepeda, Carlos
AU - Cendes, Fernando
AU - Colombo, Nadia
AU - Crino, Peter
AU - Cross, J. Helen
AU - Delalande, Olivier
AU - Dubeau, François
AU - Duncan, John
AU - Guerrini, Renzo
AU - Kahane, Philippe
AU - Mathern, Gary
AU - Najm, Imad
AU - Ozkara, Ciğdem
AU - Raybaud, Charles
AU - Represa, Alfonso
AU - Roper, Steven N.
AU - Salamon, Noriko
AU - Schulze-Bonhage, Andreas
AU - Tassi, Laura
AU - Vezzani, Annamaria
AU - Spreafico, Roberto
PY - 2011
Y1 - 2011
N2 - Focal cortical dysplasias (FCD) are localized regions of malformed cerebral cortex and are very frequently associated with epilepsy in both children and adults. A broad spectrum of histopathology has been included in the diagnosis of FCD. An ILAE task force proposes an international consensus classification system to better characterize specific clinicopathological FCD entities. Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. The ILAE Task Force proposes a three-tiered classification system. FCD Type I refers to isolated lesions, which present either as radial (FCD Type Ia) or tangential (FCD Type Ib) dyslamination of the neocortex, microscopically identified in one or multiple lobes. FCD Type II is an isolated lesion characterized by cortical dyslamination and dysmorphic neurons without (Type IIa) or with balloon cells (Type IIb). Hence, the major change since a prior classification represents the introduction of FCD Type III, which occurs in combination with hippocampal sclerosis (FCD Type IIIa), or with epilepsy-associated tumors (FCD Type IIIb). FCD Type IIIc is found adjacent to vascular malformations, whereas FCD Type IIId can be diagnosed in association with epileptogenic lesions acquired in early life (i.e., traumatic injury, ischemic injury or encephalitis). This three-tiered classification system will be an important basis to evaluate imaging, electroclinical features, and postsurgical seizure control as well as to explore underlying molecular pathomechanisms in FCD
AB - Focal cortical dysplasias (FCD) are localized regions of malformed cerebral cortex and are very frequently associated with epilepsy in both children and adults. A broad spectrum of histopathology has been included in the diagnosis of FCD. An ILAE task force proposes an international consensus classification system to better characterize specific clinicopathological FCD entities. Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. The ILAE Task Force proposes a three-tiered classification system. FCD Type I refers to isolated lesions, which present either as radial (FCD Type Ia) or tangential (FCD Type Ib) dyslamination of the neocortex, microscopically identified in one or multiple lobes. FCD Type II is an isolated lesion characterized by cortical dyslamination and dysmorphic neurons without (Type IIa) or with balloon cells (Type IIb). Hence, the major change since a prior classification represents the introduction of FCD Type III, which occurs in combination with hippocampal sclerosis (FCD Type IIIa), or with epilepsy-associated tumors (FCD Type IIIb). FCD Type IIIc is found adjacent to vascular malformations, whereas FCD Type IIId can be diagnosed in association with epileptogenic lesions acquired in early life (i.e., traumatic injury, ischemic injury or encephalitis). This three-tiered classification system will be an important basis to evaluate imaging, electroclinical features, and postsurgical seizure control as well as to explore underlying molecular pathomechanisms in FCD
U2 - https://doi.org/10.1111/j.1528-1167.2010.02777.x
DO - https://doi.org/10.1111/j.1528-1167.2010.02777.x
M3 - Editorial
C2 - 21219302
SN - 0013-9580
VL - 52
SP - 158
EP - 174
JO - Epilepsia
JF - Epilepsia
IS - 1
ER -