ReviewBrain pathology (Zurich, Switzerland)2002
Neurodevelopmental disorders as a cause of seizures: neuropathologic, genetic, and mechanistic considerations.
Review in Brain pathology (Zurich, Switzerland), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 127 citations in OpenAlex.
- Somatic mosaicism and interneuron involvement in mTORopathies.Trends in neurosciences · 2025Review
- Article
- Haploinsufficiency of X-linked intellectual disability gene CASK induces post-transcriptional changes in synaptic and cellular metabolic pathways.Experimental neurology · 2020Article
- Expression of TRPC6 and BDNF in Cortical Lesions From Patients With Focal Cortical Dysplasia.Journal of neuropathology and experimental neurology · 2016Article
- Potassium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- The role of autophagy in epileptogenesis and in epilepsy-induced neuronal alterations.Journal of neural transmission (Vienna, Austria : 1996) · 2015Review
- Disorganization of neocortical lamination in focal cortical dysplasia is brain-region dependent: evidence from layer-specific marker expression.Acta neuropathologica communications · 2013Article
- Surgical pathology of epilepsy-associated non-neoplastic cerebral lesions: a brief introduction with special reference to hippocampal sclerosis and focal cortical dysplasia.Neuropathology : official journal of the Japanese Society of Neuropathology · 2013Review
- The neuropathology of autism: defects of neurogenesis and neuronal migration, and dysplastic changes.Acta neuropathologica · 2010Article
- Astrocytes: biology and pathology.Acta neuropathologica · 2010Review
- Convulsing toward the pathophysiology of autism.Brain & development · 2009Review
- GABA(A) receptor properties in catastrophic infantile epilepsy.Epilepsy research · 2008Article
- Cellular distribution of vascular endothelial growth factor A (VEGFA) and B (VEGFB) and VEGF receptors 1 and 2 in focal cortical dysplasia type IIB.Acta neuropathologica · 2008Article
- Group I metabotropic glutamate receptors: a role in neurodevelopmental disorders?Molecular neurobiology · 2007Review
- Cortical dysplasia: neuropathological aspects.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2006Review
- The neurobiology of the tuberous sclerosis complex.Neuromolecular medicine · 2006Review
- Targeted gene expression analysis in hemimegalencephaly: activation of beta-catenin signaling.Brain pathology (Zurich, Switzerland) · 2005Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
This review will consider patterns of developmental neuropathologic abnormalities-malformations of cortical development (MCD)--encountered in infants (often with infantile spasms), children, and adults with intractable epilepsy. Treatment of epilepsy associated with some MCD, such as focal cortical dysplasia and tubers of tuberous sclerosis, may include cortical resection performed to remove the "dysplastic" region of cortex. In extreme situations (eg, hemimegalencephaly), hemispherectomy may be carried out on selected patients. Neuropathologic (including immunohistochemical) findings within these lesions will be considered. Other conditions that cause intractable epilepsy and often mental retardation, yet are not necessarily amenable to surgical treatment (eg, lissencephaly, periventricular nodular heterotopia, double cortex syndrome) will be discussed. Over the past 10 years there has been an explosion of information on the genetics of MCD. The genes responsible for many MCD (eg, TSC1, TSC2, LIS-1, DCX, FLN1) have been cloned and permit important mechanistic studies to be carried out with the purpose of understanding how mutations within these genes result in abnormal cortical cytoarchitecture and anomalous neuroglial differentiation. Finally, novel techniques allowing for analysis of patterns of gene expression within single cells, including neurons, is likely to provide answers to the most vexing and important question about these lesions: Why are they epileptogenic?
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.