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Hydroencephalodysplasia

An Anatomicoclinical picture

J. A. Picaza, G. Cardelle and R. Martin Jimenez

of Pressure Imbalance in production-absorption of fluid Obstruction of cerebrospinal fluid pathways Genesis Exogenous factor acting late in embryogenesis Genetic factor acting very early in embryogenesis Prognosis and Evolution Tendency to stabilization of pressure Progression of hydrocephalus Treatment Puncture or, in some cases, evacuation Careful surgical management A clinical differentiation may be impossible without radiological assistance in the following two conditions: (i) advanced internal

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Almeida Lima, Lobo Antunes and F. Tomé

certain regions of the gland or even in the infundibulum itself, in a Rhesus monkey and in a cat, respectively. Because of the complex transformations that take place during the embryogenesis of the hypophysis, it is perfectly understandable that immature muscle cells may migrate from the mesoblast, and reach the anlage of the gland. It would be these elements that at a later stage would transform into adult muscle fibers or, alternatively, would pursue an independent development and give rise to neoplasms. On the other hand, although it is a general belief that

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Neurenteric Cysts

Report of a Case of Neurenteric Cyst with Associated Chronic Meningitis and Hydrocephalus

Frederick E. Jackson

pointed out that at an early stage in embryogenesis the notochord lies in juxtaposition to the primitive entoderm. The notochordal plate invaginates and subsequently forms the neural canal. It is quite conceivable that small portions of the surrounding entoderm may retain their apposition to the developing neural ectoderm. Later in the course of embryogenesis, the interposition of the mesoderm forms the covering of the spinal cord, including the bony spinal column. It seems logical, therefore, to explain the mesodermal separation, as manifested by the defects in the

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Harry A. Kaplan, Stanley M. Aronson and E. Jefferson Browder

M uch has been written concerning congenital vascular malformations of the brain, but little has been recorded regarding their anatomical organization. This paper, limited to consideration of lesions within the forebrain, will attempt to define the component design of cerebral arteriovenous malformations on the basis of embryogenesis and adult vascular anatomy. Roentgenograms of vascular malformations in the living patient and dissection of specimens obtained at autopsy bear out the contention that arteriovenous anomalies represent a defect in capillary

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Ove Hassler

do not occur exclusively in the acute angle at the point of bifurcation. However, the complicated embryogenesis and postnatal growing process of the brain probably allow for further speculation concerning a developmental origin of the medial defects. The findings of medial defects in the meningeal arteries, which have another pre- and postnatal development but almost the same histological appearance, may be of interest in this connection. The pathological significance of the medial defects in the cerebral arteries lies to a large extent in the fact that the

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Nicholas J. Manno, Alfred Uihlein and James W. Kernohan

. He furnished the concept and now accepted theory of displacement of ectodermal cells during embryogenesis of the central nervous system. These cells, that is, the cutaneous portion resulting from the differentiation of primitive ectoderm into skin and neural ectoderm, inadvertently participate in closure of the neural groove and become trapped within or near the newly formed neural tube, thereby giving origin to epidermoid and dermoid tumors. Should this phenomenon occur early in life, a dermoid will result, since the tumor will contain completely potential skin

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Epithelial (Epidermoid) Tumors of the Cranium

Their Common Nature and Pathogenesis

Joseph U. Toglia, Martin G. Netsky and Eben Alexander Jr.

their origin by misplacement during embryogenesis (see Case 2). In addition to increasing in size by internal desquamation and accumulation of fluid, epidermoid tumors may acquire neoplastic properties and grow by proliferation of the epithelial cells. The growth capacity of epidermoid tumors usually is not great, but on occasion they may become enormous, as is shown in Case 3. These tumors may even become histologically malignant on rare occasion, 4, 8, 18 as illustrated by Case 4. 3. Tumors derived from oral mucosal and dental epithelium

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Joseph F. Dorsey and Joseph Tabrisky

Congenital cysts, compressing the spinal cord, and extending through the cervical vertebrae into the mediastinum, are rare. The purpose of this communication is to report such a cyst, to describe the operative removal, and to discuss a theory of embryogenesis. 4, 14, 15 Case Report G.B., an 18-year-old man, was first seen on May 20, 1963, complaining of numbness over the outside of the right leg, and stiffness of the right leg. He stated that he was well until December, 1962, when he slipped while carrying a parcel up three steps. On catching his balance

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Olfactory Neuroblastoma

Neurosurgical Implications of an Intranasal Tumor

Franklin Robinson and Gilbert B. Solitare

unlikely origin. 20 Jacobson's vomeronasal organ has been proposed as a possible site of tumor origin. 25 This structure, probably concerned with olfaction in mammals with a keen sense of smell, and most highly developed in the rat, 15 is a vestigial remnant of the olfactory placode in human embryogenesis. Ordinarily it disappears during late fetal development, although it occasionally persists into adult life. 1 However, Herrold 12 found no evidence of cellular atypism of the epithelium of Jacobson's organ in diethylnitrosamine-induced intranasal neuroepithelial

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John C. Van Gilder and Henry G. Schwartz

development from a tiny epidermal implant. Whether this implant is introduced by a needle, or caused by “disordered embryogenesis,” or by implantation through experimental surgery as in this instance, appears to have little influence upon the subsequent development of the tumor. Verbiest, 22 reporting a case history, suggested that liberation of free fatty acids and cholesterin in an epidermoid was responsible for a sterile meningitis following removal. Craig 5 implied that the same mechanism could be responsible for development of a postoperative paraplegia. Although