ArticleActa neuropathologica2011
Neuronal migration disorders in microcephalic osteodysplastic primordial dwarfism type I/III.
Article in Acta neuropathologica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Research models of neurodevelopmental disorders: The right model in the right place.Frontiers in neuroscience · 2022Review
- Malformations of Cerebral Cortex Development: Molecules and Mechanisms.Annual review of pathology · 2019Review
- Lissencephaly: Expanded imaging and clinical classification.American journal of medical genetics. Part A · 2017Article
- Effect of methotrexate exposure at late gestation on development of telencephalon in rat fetal brain.The Journal of veterinary medical science · 2016Article
- Posterior fossa in primary microcephaly: relationships between forebrain and mid-hindbrain size in 110 patients.Neuropediatrics · 2014Article
- An unusual association of microcephalic osteodysplastic primordial dwarfism type I with cardiac and brain anomalies.Journal of clinical neonatology · 2014Article
- Cellular and axonal diversity in molecular layer heterotopia of the rat cerebellar vermis.BioMed research international · 2013Article
- Dystroglycan on radial glia end feet is required for pial basement membrane integrity and columnar organization of the developing cerebral cortex.Journal of neuropathology and experimental neurology · 2012Article
- Microcephalic osteodysplastic primordial dwarfism type I with biallelic mutations in the RNU4ATAC gene.Clinical genetics · 2012Article
- A developmental and genetic classification for malformations of cortical development: update 2012.Brain : a journal of neurology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Microcephalic osteodysplastic primordial dwarfism (MOPD) is a rare microlissencephaly syndrome, with at least two distinct phenotypic and genetic types. MOPD type II is caused by pericentrin mutations, while types I and III appear to represent a distinct entity (MOPD I/III) with variably penetrant phenotypes and unknown genetic basis. The neuropathology of MOPD I/III is little understood, especially in comparison to other forms of lissencephaly. Here, we report postmortem brain findings in an 11-month-old female infant with MOPD I/III. The cerebral cortex was diffusely pachygyric, with a right parietal porencephalic lesion. Histologically, the cortex was abnormally thick and disorganized. Distinct malformations were observed in different cerebral lobes, as characterized using layer-specific neuronal markers. Frontal cortex was severely disorganized and coated with extensive leptomeningeal glioneuronal heterotopia. Temporal cortex had a relatively normal 6-layered pattern, despite cortical thickening. Occipital cortex was variably affected. The corpus callosum was extremely hypoplastic. Brainstem and cerebellar malformations were also present, as well as old necrotic foci. Findings in this case suggest that the cortical malformation in MOPD I/III is distinct from other forms of pachygyria-lissencephaly.
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