ArticleActa neuropathologica communications2013
Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent: evidence from layer-specific marker expression.
Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 23 citations in OpenAlex.
- Architecture and cellular composition of focal cortical dysplasia type II: qualitative review of histological studies.Frontiers in cellular neuroscience · 2025Review
- Hypometabolic patterns of focal cortical dysplasia in PET-MRI co-registration imaging: a retrospective evaluation in a series of 83 patients.Frontiers in neuroscience · 2023Article
- Synaptic alterations and neuronal firing in human epileptic neocortical excitatory networks.Frontiers in synaptic neuroscience · 2023Article
- Prognostic analysis in children with focal cortical dysplasia II undergoing epilepsy surgery: Clinical and radiological factors.Frontiers in neurology · 2023Article
- Reorganization of Parvalbumin Immunopositive Perisomatic Innervation of Principal Cells in Focal Cortical Dysplasia Type IIB in Human Epileptic Patients.International journal of molecular sciences · 2022Article
- Modeling Herpes Simplex Virus 1 Infections in Human Central Nervous System Neuronal Cells Using Two- and Three-Dimensional Cultures Derived from Induced Pluripotent Stem Cells.Journal of virology · 2019Article
- Effect of early embryonic deletion of huntingtin from pyramidal neurons on the development and long-term survival of neurons in cerebral cortex and striatum.Neurobiology of disease · 2018Article
- Article
- Multimodal MRI profiling of focal cortical dysplasia type II.Neurology · 2017Article
- Specific pattern of maturation and differentiation in the formation of cortical tubers in tuberous sclerosis omplex (TSC): evidence from layer-specific marker expression.Journal of neurodevelopmental disorders · 2016Article
- Basic mechanisms of epileptogenesis in pediatric cortical dysplasia.CNS neuroscience & therapeutics · 2015Review
- Layer-specific gene expression in epileptogenic type II focal cortical dysplasia: normal-looking neurons reveal the presence of a hidden laminar organization.Acta neuropathologica communications · 2014Article
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9 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundFocal cortical dysplasias (FCD) are local disturbances of neocortical architecture and a common cause of pharmaco-resistant focal epilepsy. Little is known about the pathomechanisms leading to architectural abnormalities associated with FCD.
resultsIn the present study we compared 52 FCD cases originating from the frontal or temporal lobe with or without Ammon's horn sclerosis (AHS) with regard to structural and molecular differences. We applied layer-specific (ER81, RORß, SMI32, TLE4) and interneuron (calbindin, parvalbumin) markers by means of immunohistochemistry, in situ hybridization (ISH), and real time RT-PCR and correlated our findings with clinical parameters. We found that: (1) Structural abnormalities were most prominent in layers III-VI including changed morphology of individual neurons or dispersion, blurring and thinning of layers. These alterations were most pronounced in isolated frontal FCD, whereas the most homogeneous group was FCD IIIa. (2) Numbers of calbindin- and parvalbumin-positive interneurons varied considerably within the different FCD groups, but were not generally reduced. A significant decrease was only found for calbindin-positive interneurons in frontal FCD, and for parvalbumin-positive interneurons in FCD IIIa. (3) Interestingly, FCD IIIa presented with significant changes in the numbers of calbindin- or TLE4-positive neurons when compared to isolated FCD or controls. (4) Correlations between clinical and cellular parameters strongly depended on FCD localisation and age of the patients.
conclusionsIn summary, our data suggest that late cortical development is disturbed in FCD, yet most likely by different causes depending on brain region, FCD type and FCD severity.
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