Agénese partielle et hypoplasie du Corps Calleux dans l'autisme idiopathique

Aperçu: G.M.

Pour tester l'hypothèse selon laquelle les anomalies du développement du corps calleux (CC) contribuent à la pathogenèse de l'autisme, l'étude a caractérisé le type, la topographie et la gravité de la pathologie CC correspondant aux zones CC réduites qui sont détectées par imagerie par résonance magnétique dans les cerveaux de 11 personnes avec un diagnostic d'autisme et 11 témoins.  

Le CC sensiblement plus mince, la zone CC réduite et le déficit axonal uniforme chez tous les sujets autistes ont été classés comme hypoplasie CC. Ainsi, le sous-produit de l'agénésie et de l'hypoplasie CC partielle est la réduction des connexions axonales entre les zones corticales connues pour être impliquées dans les altérations comportementales observées chez les personnes avec un diagnostic d'autisme. 

J Neuropathol Exp Neurol. 2017 Mar 1;76(3):225-237. doi: 10.1093/jnen/nlx003.

Partial Agenesis and Hypoplasia of the Corpus Callosum in Idiopathic Autism

Wegiel J¹, Flory M¹, Kaczmarski W¹, Brown WT¹, Chadman K¹, Wisniewski T¹, Nowicki K¹, Kuchna I¹, Ma SY¹, Wegiel J¹.

Author information

1

From the Departments of Developmental Neurobiology (JW, WK, KN, IK, SYM, JW), Research Design and Analysis Services (MF), Human Genetics (WTB), and Behavioral Pharmacology (KC), New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York; and Departments of Neurology, Pathology and Psychiatry, NYU Langone Medical Center, New York, New York (TW).

Abstract

To test the hypothesis that developmental anomalies of the corpus callosum (CC), contribute to the pathogenesis of autism, we characterized the type, topography, and severity of CC pathology corresponding to reduced CC areas that are detected by magnetic resonance imaging in the brains of 11 individuals with autism and 11 controls. In the brains of 3 autistic subjects, partial CC agenesis resulted in complete or partial lack of interhemispheric axonal connections in CC segments III-V. In these cases, a combination of focal agenesis and uniform axonal deficit caused reduction of CC areas by 37%, of axon numbers by 62%, and of the numerical density of axons by 39%. In the CC of 8 autistic subjects without agenesis, there was an 18% deficit of the midsagittal CC area, 48.4% deficit of axon numbers, and 37% reduction of the numerical density of axons. The significantly thinner CC, reduced CC area, and uniform axonal deficit in all autistic subjects were classified as CC hypoplasia. Thus, the byproduct of partial CC agenesis and hypoplasia is reduction of axonal connections between cortical areas known to be involved in behavioral alterations observed in people with autism.

2017 American Association of Neuropathologists, Inc. This work is written by US Government employees and is in the public domain in the US.

PMID: 28395085

DOI: 10.1093/jnen/nlx003