Ng production of acid mucin (c)urinary continence recovered after one month, and proprioceptive deficits were the only remaining neurologic deficit after six months. A follow-up MRI study performed 111 days after the surgery revealed no recurrence of the lesion and no spinal cord compression. No recurrence of clinical signs has been observed 18 months after surgery.Discussion Intradural extra-axial "cystic or tumor-like lesions" of the thoraco-lumbar spinal cord are uncommon in young dogs. Histopathological features of epidermoid or dermoid cysts, nephroblastomas or Tarlov cysts are well described [3, 4]. In the present case, the cyst was lined by different types of epithelia that suggested a respiratory, digestive, cutaneous or urinary origin. Structures similar to cilia or a brush border at the apical pole of cuboidal cells and mucus secretion suggested a respiratory or digestive epithelium. The stratified squamous epithelium was similar to a cutaneous epithelium but with no sign of keratinization, in contrast to an epidermoid cyst. Moreover the endodermal origin was supported by theFig. 8 Photomicrograph showing positive staining for carcinoembryonic antigenpresence of mucus and microvilli at the apical pole of some cells and immunhistochemistry. In humans, a neurenteric cyst, also called an enterogenous cyst or endodermic cyst, is a congenital lesion characterized by a mucus-secreting epithelium mimicking the epithelium of the gastrointestinal tract [5]. Neurenteric cysts result from inappropriate partitioning of the embryonic notochordal plate and presumptive endoderm [6]. A failure during embryogenic development could be responsible for the persistence of an abnormal communication between the endoderm and neuroectoderm at 3 weeks of development in the human embryo [5]. Several theories have been proposed to explain the occurrence of neurenteric cysts [7]. For example Mac Donald et al. [8] proposed different mechanisms in which neurenteric cysts may develop: a primary adhesion of endoderm anterior to the notochord, incomplete excalation of the notochord, persistence of the neurenteric canal or formation of an accessory neurenteric canal with a split notochord, and displacement of endodermal cells. Bentley and Smith [9] postulated that the splitting of the notochord is the primary event in this pathology. The subsequent deficiency in the overlying neural plate could allow for an endodermal diverticulum to herniate through the spinal column and make contact with the surface ectoderm. In such a situation, the persistenceCapivasertibCapivasertib Abstract(s)">PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16989806 or complete. In the canine fetus, closure of the neural tube occurs at about 20 days, so that we can expect that the neurenteric cyst formation occurs at this period of development in dogs [10]. A heterotopic epithelium reminiscent of gastrointestinal and respiratory tissue lead to a compressive cystic lesion in the pediatric and adult spine. Histopathological analysis of neurenteric tissue reveals a highly characteristic structure of columnar or cuboidal epithelium withFerrand et al. Irish Veterinary Journal (2015) 68:Page 5 ofor without cilia and mucus globules, as in the present case. Wilkins and Odum described 3 types of neurenteric cysts [11]: type A cysts contain either columnar or cuboidal cells, with ciliated and nonciliated components atop a basal membrane composed of type IV collagen. Type B cysts include all of the features of type A as we.