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Congenital Anomalies
Published in Swati Goyal, Neuroradiology, 2020
The spinal cord is developed in three main stages − gastrulation, primary neurulation, and secondary neurulation during early embryogenesis. Gastrulation (second or third week) − conversion of the embryonic bilaminar disk to a trilaminar disk, composed of the ectoderm, the mesoderm, and the endoderm. The notochord is formed from the midline mesoderm interacting with the overlying ectoderm.Primary neurulation (third or fourth week) − formation of the neural plate and eventually the closure of the neural tube in a zip-like manner.Secondary neurulation (fifth or sixth week) − formation of the central canal (canalization), with the caudal cell mass undergoing retrogressive differentiation to form the conus medullaris, filum terminale, ventriculus terminalis, and most of the sacrum and coccyx.
Tethered Cord Syndrome
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Nishant Garg, Yahir Santiago-Lastra
The central nervous system is formed through three major processes over the first 2 months postconception, with the most critical portion for TCS occurring during the first 2–4 weeks and then during weeks 9–11.7 These stages are broken down into the following: neurulation (neural tube formation), canalization of the tail bud, and regression.8 Neurulation results in folding of the neural plate on itself to form the neural tube. Any errors during this process are likely to result in disorders associated with TCS such as LMMCs, MMCs, and other spinal dysraphisms. The second major process, canalization of the tail bud, occurs when the caudal cell mass is stimulated through an unknown mechanism to undergo canalization and eventual regression.9 This process continues until the only remaining components are the medulla spinalis below T12 and a distal filum terminale, and any anomalies in this process are thought to result in the increased risk and eventual development of TCS.
Spina bifida and encephalocele
Published in Prem Puri, Newborn Surgery, 2017
Jothy Kandasamy, Mark A. Hughes, Conor L. Mallucci
NTDs result from an abnormality in the process of neurulation. The primitive streak and Hensen’s nodes are present in the embryo at 2 weeks’ gestation. The notochord starts extending rostrally from Hensen’s node, and this induces the process of neural tube formation. Thickening of the ectoderm cephalic to Hensen’s node occurs and forms the neural plate. Folding and later fusion forms the neural tube. This process continues caudally up to the somites, which start to appear from week 3. Other ectodermal tissue closes over this and buries the tube. The unfused rostral and caudal neural folds are called the anterior and posterior neuropores. These close at about 25 days and 30 days respectively, at which point the process of neurulation is complete. At this stage, there are 21–29 somites. Four somites are incorporated into the occipital bone and 20 in the cervical and thoracic vertebrae. Caudal to this, the remainder of the tube forms the caudal cell mass. During the next 4–5 weeks, canalization of this cell mass occurs, followed by regression of the most caudal part, which forms the filum terminale. The notochord separates from the neural tube dorsally and the gut ventrally, forming subchordal and epichordal spaces.
Spine duplication or split notochord syndrome – case report and literature review
Published in The Journal of Spinal Cord Medicine, 2020
Barbara Jasiewicz, Magdalena Stachura, Tomasz Potaczek, Slawomir Duda, Piotr Michno, Stanislaw Kwiatkowski
Spine duplication is a rare condition, with various extents of duplication and various additional anomalies. Two parallel names coexist in the literature: “split notochord syndrome” and “spinal duplication syndrome.”1–3 At the end of the nineteenth-century, Rembe described dorsal enteric fistula for the first time.1 Since then, literature on a combination of congenital defects, including some intestinal (enteric cysts, fistulas), vertebral (duplication), and central nervous anomalies (myelomeningocele), has been published, usually as case reports of single patients.4–37 The name “split notochord syndrome” was proposed by Bentley and Smith6 for lesions caused by partial duplication or separation of the notochord. Dominguez et al.20 proposed the name “caudal duplication syndrome,” which resulted from the deformation of the caudal cell mass and hindgut.20 In some cases, the problems with spinal duplication overshadowed those associated with the gastrointestinal tract, and for these cases, the name “spine duplication syndrome” was used. According to Dias and Pang,38 it was thought to be an extreme form of split cord malformation.
Cystic dilation of a ventriculus terminalis. Case report and review of the literature
Published in British Journal of Neurosurgery, 2019
Masoud Zeinali, Hosein Safari, Saleh Rasras, Reza Bahrami, Mahdi Arjipour, Nima Ostadrahimi
The VT space is formed around the 6th week of pregnancy and reaches its maximum size at the age of 2.5 years. The spinal cord is formed during 3 stages, neurulation, canalization and regression. During the initial phase of neurulation, the proximal spinal cord develops. The distal spinal cord, conus medullaris and filum terminal develop during the canalization and retrogressive distinction stages. During the second stage, the caudal end of neural tube and notochord are incorporated to produce the Caudal Cell Mass. Small vacuoles appear in the caudal cell mass and lead to the formation of an ependymal cell-lined cavity which is connected rostrally to the central canal and finally produces a cavity named “Ventriculus Terminalis”.4–6,8–12
The cystic dilation of ventriculus terminalis with neurological symptoms: Three case reports and a literature review
Published in The Journal of Spinal Cord Medicine, 2018
Syringomyelia should be clearly differentiated from a dilated ventriculus terminalis. The later occurs immediately cephalad to a normally located conus medullaris, is not associated with other dysraphic anomalies and is not related to history of trauma and surgical intervention and is non-progressive on follow-up MRI.4 According to Coleman et al.5 Stilling described a VT in 1859, and in 1875 Krause identified it as a true ventricle lined by ciliated ependymal cells. Krause named it the “fifth ventricle.” The development of the VT, or the fifth ventricle, can be considered a normal process of embryonal development.7 The origin of the VT can be traced to the embryonic development of the spinal cord, which can be subdivided into two stages: neurulation and canalization or retrogressive differentiation.8 Neurulation starts when the embryo is three-weeks old, and it is responsible for the formation of the neural tube through the progressive closure of the neural plate and its separation from the overlying ectoderm. The distal cord develops from a caudal cell mass that forms from the neuralepithelium and a notochord caudal to the primary neural tube. The caudal cell mass develops microcysts that coalesce to form an ependyma-lined tube that fuses with the central canal of the neural tube. With differentiation, the caudal end of the cell mass involutes, leaving a focal prominence in the ependyma-lined canal in the conus medullaris with a fibrous tail, which is the filum terminale.7 The VT appears after approximately 45 days (between the 43rd and the 48th day) after conception.8