The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission.
Identifieur interne : 000B20 ( Hal/Corpus ); précédent : 000B19; suivant : 000B21The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission.
Auteurs : Ingmar Blümcke ; Maria Thom ; Eleonora Aronica ; Dawna Armstrong ; Harry Vinters ; Andre Palmini ; Thomas Jacques ; Giuliano Avanzini ; James Barkovich ; Giorgio Battaglia ; Albert Becker ; Carlos Cepeda ; Fernando Cendes ; Nadia Colombo ; Crino Peter ; Helen Cross ; Olivier Delalande ; François Dubeau ; John Duncan ; Renzo Guerrini ; Philippe Kahane ; Gary Mathern ; Imad Najm ; Ci Dem Ozkara ; Charles Raybaud ; Alfonso Represa ; Steven Roper ; Noriko Salamon ; Andreas Schulze-Bonhage ; Laura Tassi ; Annamaria Vezzani ; Roberto SpreaficoSource :
- Epilepsia [ 0013-9580 ] ; 2011-01.
Abstract
PURPOSE: 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. METHODS: Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. KEY FINDINGS: 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). SIGNIFICANCE: 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.
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DOI: 10.1111/j.1528-1167.2010.02777.x
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<author><name sortKey="Spreafico, Roberto" sort="Spreafico, Roberto" uniqKey="Spreafico R" first="Roberto" last="Spreafico">Roberto Spreafico</name>
<affiliation><hal:affiliation type="laboratory" xml:id="struct-155186" status="INCOMING"> <orgName>Department of Epilepsy Clinic and Experimental Neurophysiology</orgName>
<desc> <address> <addrLine>Milan -</addrLine>
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<tutelles><tutelle active="#struct-339110" type="direct"><org type="institution" xml:id="struct-339110" status="INCOMING"> <orgName>IRCCS Foundation Neurological Institute ''Carlo Besta</orgName>
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<idno type="DOI">10.1111/j.1528-1167.2010.02777.x</idno>
<series><title level="j">Epilepsia</title>
<idno type="ISSN">0013-9580</idno>
<imprint><date type="datePub">2011-01</date>
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<front><div type="abstract" xml:lang="en">PURPOSE: 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. METHODS: Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. KEY FINDINGS: 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). SIGNIFICANCE: 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.</div>
</front>
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<author role="aut"> <persName> <forename type="first">Ingmar</forename>
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<author role="aut"> <persName> <forename type="first">Maria</forename>
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<author role="aut"> <persName> <forename type="first">Crino</forename>
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<author role="aut"> <persName> <forename type="first">Helen</forename>
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<surname>Najm</surname>
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<idno type="halauthorid">403884</idno>
<affiliation ref="#struct-155193"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Ciğdem</forename>
<surname>Ozkara</surname>
</persName>
<idno type="halauthorid">606807</idno>
<affiliation ref="#struct-155194"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Charles</forename>
<surname>Raybaud</surname>
</persName>
<idno type="halauthorid">606808</idno>
<affiliation ref="#struct-155195"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Alfonso</forename>
<surname>Represa</surname>
</persName>
<idno type="halauthorid">404213</idno>
<affiliation ref="#struct-46212"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Steven</forename>
<forename type="middle">N.</forename>
<surname>Roper</surname>
</persName>
<idno type="halauthorid">492560</idno>
<affiliation ref="#struct-155196"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Noriko</forename>
<surname>Salamon</surname>
</persName>
<idno type="halauthorid">606809</idno>
<affiliation ref="#struct-156929"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Andreas</forename>
<surname>Schulze-Bonhage</surname>
</persName>
<idno type="halauthorid">606810</idno>
<affiliation ref="#struct-155198"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Laura</forename>
<surname>Tassi</surname>
</persName>
<idno type="halauthorid">407431</idno>
<affiliation ref="#struct-92960"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Annamaria</forename>
<surname>Vezzani</surname>
</persName>
<idno type="halauthorid">606811</idno>
<affiliation ref="#struct-155199"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Roberto</forename>
<surname>Spreafico</surname>
</persName>
<idno type="halauthorid">606812</idno>
<affiliation ref="#struct-155186"></affiliation>
</author>
</analytic>
<monogr> <idno type="halJournalId" status="VALID">12965</idno>
<idno type="issn">0013-9580</idno>
<idno type="eissn">1528-1157</idno>
<title level="j">Epilepsia</title>
<imprint> <publisher>Wiley</publisher>
<biblScope unit="volume">52</biblScope>
<biblScope unit="issue">1</biblScope>
<biblScope unit="pp">158-74</biblScope>
<date type="datePub">2011-01</date>
</imprint>
</monogr>
<idno type="doi">10.1111/j.1528-1167.2010.02777.x</idno>
<idno type="pubmed">21219302</idno>
</biblStruct>
</sourceDesc>
<profileDesc> <langUsage> <language ident="en">English</language>
</langUsage>
<textClass> <classCode scheme="mesh">Cerebral Cortex</classCode>
<classCode scheme="mesh">Humans</classCode>
<classCode scheme="mesh">Malformations of Cortical Development</classCode>
<classCode scheme="mesh">Societies, Medical</classCode>
<classCode scheme="mesh">World Health</classCode>
<classCode scheme="mesh">Advisory Committees</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">PURPOSE: 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. METHODS: Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. KEY FINDINGS: 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). SIGNIFICANCE: 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.</abstract>
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