Division of Neuroradiology, Hospital for Sick Children, Toronto, ON, Canada.
Neuroradiology. 2010 Jun;52(6):447-77. doi: 10.1007/s00234-010-0696-3. Epub 2010 Apr 27.
There are three telencephalic commissures which are paleocortical (the anterior commissure), archicortical (the hippocampal commissure), and neocortical. In non-placental mammals, the neocortical commissural fibers cross the midline together with the anterior and possibly the hippocampal commissure, across the lamina reuniens (joining plate) in the upper part of the lamina terminalis. In placental mammals, a phylogenetically new feature emerged, which is the corpus callosum: it results from an interhemispheric fusion line with specialized groups of mildline glial cells channeling the commissural axons through the interhemispheric meninges toward the contralateral hemispheres. This concerns the frontal lobe mainly however: commissural fibers from the temporo-occipital neocortex still use the anterior commissure to cross, and the posterior occipito-parietal fibers use the hippocampal commissure, forming the splenium in the process. The anterior callosum and the splenium fuse secondarily to form the complete commissural plate. Given the complexity of the processes involved, commissural ageneses are many and usually associated with other diverse defects. They may be due to a failure of the white matter to develop or to the commissural neurons to form or to migrate, to a global failure of the midline crossing processes or to a selective failure of commissuration affecting specific commissural sites (anterior or hippocampal commissures, anterior callosum), or specific sets of commissural axons (paleocortical, hippocampal, neocortical commissural axons). Severe hemispheric dysplasia may prevent the axons from reaching the midline on one or both sides. Besides the intrinsically neural defects, midline meningeal factors may prevent the commissuration as well (interhemispheric cysts or lipoma). As a consequence, commissural agenesis is a malformative feature, not a malformation by itself. Good knowledge of the modern embryological data may allow for a good understanding of a specific pattern in a given individual patient, paving the way for better clinical correlation and genetic counseling.
有三种端脑连合,即古皮质连合(前连合)、旧皮质连合(海马连合)和新皮质连合。在非胎盘哺乳动物中,新皮质连合纤维与前连合和可能的海马连合一起穿过中线,穿过终板上部的连合板(连接板)。在胎盘哺乳动物中,出现了一个新的系统发生特征,即胼胝体:它是由半球间融合线形成的,具有特殊的中线胶质细胞群,通过半球间脑膜引导连合轴突到达对侧半球。然而,这主要涉及额叶:来自颞枕新皮质的连合纤维仍然使用前连合进行交叉,而后部枕顶叶纤维使用海马连合,在这个过程中形成胼胝体。前连合和胼胝体随后融合形成完整的连合板。由于涉及的过程复杂,连合发育不全很多,通常与其他多种缺陷相关。它们可能是由于白质发育不良或连合神经元形成或迁移失败、中线穿越过程全局失败或特定的连合部位(前连合或海马连合、前连合)或特定的连合轴突(古皮质、海马、新皮质连合轴突)选择性失败所致。严重的半球发育不良可能阻止轴突在一侧或两侧到达中线。除了内在的神经缺陷外,中线脑膜因素也可能阻止连合(半球间囊肿或脂肪瘤)。因此,连合发育不全是一种畸形特征,本身并不是一种畸形。对现代胚胎学数据的良好了解可能有助于更好地理解特定个体患者的特定模式,为更好的临床相关性和遗传咨询铺平道路。