Month Of Fetal Life Research Articles

The habilitation of the congenital cleft palate patient

1. 1. Preparation of congenital cleft palate patients for normal life is a challenge to the efforts of modern medical science. 2. 2. The causative factors leading to cleft lips and palates are recognized as defects in intrauterine development of the embryo during the second month of fetal life. 3. 3. The etiological factors as to how clefts occur are far better understood than the reasons why they occur. One school of thought holds that a gene defect is responsible, thereby indicating inheritance. Valuable experimentation has proved that clefts may be produced by environmental situations, such as lack of oxygen or subjection of the mother to such drugs as cortisone. 4. 4. The occurrence of clefts is recognized as approximately one in 700 live births. In extremely large samples of population it has been found that 70.83 per cent of all clefts occur in males and 29.17 per cent in females. I have found that far more than twice as many clefts occur on the left side as on the right. It has been authoritatively stated that 16 per cent of all cases presented bilateral clefts. In my sampling, 47.3 per cent were bilateral in the palate and 30.5 per cent were bilateral in the lip. 5. 5. The total habilitation of the patient with cleft lip and cleft palate has been found to be best achieved through the combined efforts of pediatrician, surgeon, psychologist, otolaryngologist, restorative dentist, orthodontist, prosthetic dentist, and speech pathologist. 6. 6. In addition to obvious cosmetic improvement, the speech intelligibility of a patient benefiting from integrated habilitation was found to increase as much as 13.2 per cent, with an average increase for the sample of 7.13 per cent.

Congenital atresia of the colon. Report of two cases.

Congenital atresia of the gastrointestinal tract occurs once in about 1,500 births. Congenital atresia of the colon is rarer still and is estimated at 10% to 15% of this group. 1 Twelve successfully surgically treated cases of colonic atresia have been reported as a collected review. 2 There are two forms of atresia. One presents as an internal diaphragm completely blocking the lumen, while the other form ends as a blind sac. There may be complete detachment of the blind proximal distal colon, or a vestigial fibrous remnant may be present. These congenital abnormalities probably occur in the second or third month of fetal life. Colonic atresia is best explained by an imperfection in the embryological development from the solid stage by the processes of vacuolization and coalescence of cystic spaces in the formation of the intestinal lumen. 3 Report of Cases Case 1. —A one-day-old white girl was admitted

Normal pregnancy and delivery in female pseudohermaphroditism.

As early as 1891 Marchand already suspected a causal relation between female pseudohermaphroditism and adreno-cortical hyperfunction. Young (1937) confirmed this assumption. It is now known that a congenital adrenal hyperplasia, active from the third to the fifth month of fetal life, leads to pseudohermaphroditism. A hyperplasia developing in later fetal months or after birth causes adrenal virilism, i. e. the typical adrenogenital syndrome. Zondek & Finkelstein (1954) demonstrated that an increase of 3α,17-20α-pregnanetriol-11-one in urine is an indication of a congenital adrenal hyperplasia. Eberlein & Bongiovanni (1955) have also arrived at similar conclusions. Wilkins et al. (1950, 1951, 1952) obtained remarkable results with cortisone medication, results later confirmed by Bartter et al. (1951), Kelley et al. (1952), Pattee et al. (1954), Tobin (1954) and Smith & de Alvarez (1955). Wilkins' therapy is based on the theory that in patients in whom the production of hydrocortisone is absent the administration of

Atresia of the foramina of Luschka and Magendie; a cause of obstructive internal hydrocephalus.

The commonest causes of noncommunicating hydrocephalus in infancy are developmental obstructions at the aqueduct of Sylvius or in the region of the foramina of Luschka and Magendie. Malformation of the aqueduct is most frequently observed, but atresia of the foramina of Luschka and Magendie or functional blockage secondary to an Arnold-Chiari malformation are not uncommon. Embryologically, the foramen of Magendie is usually formed by the fourth month of fetal life. At this stage of development the cerebellum is dumbbell-shaped with an underdeveloped vermis in the midline connecting two primitive cerebellar hemispheres. Since fluid has already started to form within the cerebral vesicles, the failure of normal formation of the posterior foramina leads to fluid accumulation in the fourth ventricle, inhibiting further development of the cerebellum. As the posterior fossa is thus enlarged because of the cystic dilatation of the fourth ventricle, the developing occipital lobes of the cerebrum cannot push

C19 steroids, 17alpha-hydroxycorticosterone and a sodium retaining factor in human fetal adrenal glands.

THE embryological development of the human fetal adrenal cortex, and, perhaps, other primates, is unique. During the second month of fetal life, a distinct adrenal cortex is recognized. It reaches its largest relative size during the third and fourth month when it occupies about 0.5% of the total body volume as compared to 0.01% in the adult (Jackson, 1909). The histological picture of the fetal adrenal cortex differs from that of the adult by the presence of the fetal zone, which comprises about 80% of the whole cortex. The fetal zone degenerates rapidly during the first post-natal months. In addition, only the glomerular and fascicular zones of the cortex are fairly well developed in the fetus (Lanman, 1953). In contrast to the available data on the morphology and anatomy of the human fetal adrenal cortex, its physiology remains largely unknown. An excellent review of the subject has been published by Lanman (1953). Large amounts of ascorbic acid (Bourne, 1933) and lipid material (Lanman, 1953) have bee...

Meconium peritoneum.

Meconium peritoneum is a non-bacterial sterile inflammation of the peritoneum caused by the escape of meconium into the peritoneal cavity. It may occur either in the foetal life, at the time of delivery, or very shortly after delivery. The reaction of the peritoneum is partly due to the presence of a foreign body and partly due to chemical action of the meconium. Meconium itself is sterile and consists of casts of epithelial cells, bile salts, bile pigments, fats, salts, mucin and sebaceous material swallowed from liquor amnii. Pancreatic and gastric secretions with their enzymes are added about the fifth month. To set up meconial peritoneal reaction three things must be present: presence of meconium in the gut, a perforation in the gut and peristalsis in the gut for the escape of the meconium. Until the fifth week of foetal life the intestinal tract from the pylorus to the ileocaecal junction remains patent as a narrow lumen. The lumen then becomes obliterated due to epithelial proliferation and it remains so until the twelfth week of foetal life. After this time vacuoles appear in the epithelial cord. These vacuoles coalesce and make the lumen patent. Disturbance in the formation of the cystic spaces or their coalescence, results in stenosis or atresia of the gut. Meconium appears about the third month of foetal life and it forms in the upper part of the intestine.

Effects of the plane of nutrition on growth and the development of carcass quality in lambs Part I. The effects of High and Low planes of nutrition at different ages

Effects of the plane of nutrition on growth and the development of carcass quality in lambs Part I. The effects of High and Low planes of nutrition at different ages

Effects of the plane of nutrition on growth and the development of carcass quality in lambs Part II. Effects on lambs of 30 lb. carcass weight

Effects of the plane of nutrition on growth and the development of carcass quality in lambs Part II. Effects on lambs of 30 lb. carcass weight

Familial occurrence of tuberous sclerosis.

TUBEROUS sclerosis (epiloia) is generally considered a developmental tissue dysplasia, being an expression of anomalous development beginning in the very early months of fetal life. This disease is usually classified as belonging to the group of neurocutaneous syndromes. It is certainly congenital, and several cases have been reported which indicate that there may be a hereditary or familial component. Ross and I1reported that a study of the hereditary factors in this condition demonstrated these factors to be no more outstanding in patients with tuberous sclerosis than in other types of institutional epileptics. A patient showing the characteristic symptom triad of tuberous sclerosis was admitted to the Caro State Hospital for Epileptics on April 12, 1948. She was brought to the institution by her parents and an older sister. It was immediately noticed that the female members of the family presented an unusual occurrence of this disease. The study

Turner's syndrome associated with lichen planus.

Turner¹first described a curious syndrome, observed in 7 female patients, consisting of webbing of the neck, cubitus valgus and infantilism. Sharpey-Schafer²added a case, also in a female patient, of this triad and described the postmortem observations. Recognition of webbing of the neck dates from 1883, when Kobylinski³described it. Four cases were added by Frawley,⁴all in females. Webbing occurs in the Klippel-Feil syndrome, also, apparently a commoner variety, but it is associated with synostosis of the cervical vertebrae with limitation of motion, and there is no infantilism. By these characteristics the Klippel-Feil syndrome is easily differentiated from Turner's. The cause of webbing is not known, but it has been thought to result from amniotic hands, to be a form of atavism or to be a developmental defect dating from the third month of fetal life, when the shoulders and head are in

PALMAR DERMATOGLYPHICS IN MONGOLISM

It has been demonstrated that characteristic dermatoglyphic changes rank high in frequency among the variable stigmata which go to make up the syndrome of mongolism. Though they are not diagnostic alone, it is believed that these objective, measurable and unchanging evidences of mongolism seen in hand prints should be helpful in establishing an early diagnosis. Positive dermatoglyphics rank high in frequency among stigmata reported in typical examples of mongolism by 82 physicians. The technic for preparing prints is a simple one which requires very little practice for perfection; interpretation based on the empiric but definite criteria defined can be accomplished with relative ease. A series of five prints are reproduced. These findings are in keeping with the suggestion that factors responsible for the occurrence of mongolism are operative prior to the third month of fetal life, and are consistent with known facts concerning embryologic development of epidermal ridges of the palms.

A treatise on harelip and cleft palate

Congenital clefts and Gsures are the result of arrested development. Fusion of the globular and maxillary, and the palatal processes in the embryo is completed about the end of the third month of fetal life, so that interference with development takes place prior to that time and continues. Many causes have been given for arrested development, but none have been found to sufficiently explain its occurrence in all cases. The most important causes are faulty nutrition, heredity, and maternal impression. The influence of faulty nutrition has not been clearly proveId in t,he human race, as women who received the most liberal and nourishing diet during the entire period of gestation have frequently given birth to children with clefts. On the contrary, women who existed on the most meager diet and on one or two varieties of food during the entire period of gestation have given birth to perfectly developed children. In animals, especially the lion, the influence of faulty nutrition has been repeatedly proved in the zoological gardens of London and Dublin. The process of growth and developlment depends upon the formation of loops of blood vessels in the embryonic tissue, which become organized tissue. In defective vascular supply may be found a probable cause of arrested development and this would explain its occurrence in early fetal life and at the terminal distribution of the vascular supply. The vascu1a.r supply to the right half of the head is greater than to the left. This probably accounts for the most frequent occurrence of the clefts of the lips and alveolar process on the left side. The frequent occurrence of clefts in the descendants of those who had clefts and in members of the same family points strongly to heredity. In many cases the occurrence of the affliction does not take place until the second, third, or fourth generation. At present the influence of maternal impressions cannot be absolutely denied, but the mother will state positively, that she had not the maternal impressions during gestation, and in many cases where strong maternal impressions existed, the offspring was perfectly developed. Many eminent obstetricians have admitted the possibility of maternal impression being the cause. Clefts may be the result of syphilis. Such clefts should rarely, i.f ever, be operated upon, as union seldom takes place and the operation frequently results in increased destruction of tissue.

The shape of the human being as a function of time

It is shown that the change of shape of the male human being from the 5th month of foetal life to maturity may be represented by a continuous one-parameter set of transformations. The method of analysis described makes it possible to compute the rate of change of shape of the human being as a function of position and age. A class of graded transformations is defined, and it is shown that the transformations of human development belong to it. The rate of change of shape of the human being falls off progressively in time from the 5th month of foetal life to maturity.

Ocular Hypertelorism with Cleft Palate and Giant-Cell Tumor

OCULAR hypertelorism (νπϵρ, too much; τηλϵ apart; οριδω, to separate) as an entity was first described by Grieg (1), in 1924, who presented a complete clinical and pathologic picture. Our review of the literature regarding this developmental, congenital condition reveals that less than thirty cases have been reported to date. Etiologically little is known of this condition. Abernethy (2) and Braithwaite (3) suggest an endocrine basis. Abernethy also made an interesting observation in regard to the hereditary aspect and states: “The shape of the sphenoid, like the number of digits, may be developmentally one of the ‘weak’ spots which, though normally fixed, are more liable to extra-normal variation, whether advantageous or disadvantageous to their possessors, than the other members of the body.” Grieg (1) in his original article remarked: “In this anomaly about the third month of fetal life the lesser wings increase greatly in width, so much so that they may be equal to, or even greater than, the greater sphenoidal wings. The lesser wings of the sphenoid form the posterior part of the roof of the orbit. Thus, due to the enlargement and premature ossification of the lesser wings, the fetal lateral deviation of the orbit remains fixed.” Ogilvie and Posel (4) also account for the peculiar facies thus: “An enlargement of this wing … pushes the whole frontal and maxillary bones upward, forward, and outward. An internasal bone is thus necessary and a retrousse nose develops. The tilting of the frontal bone … explains the combination of low forehead with slight prominence of the frontal eminences.” Reilly (5) comments on the fact that additional deformities and stigmas may be found, such as high palates, syndactylism, and undescended testes. The clinical characteristics are: A. Comparatively large skull with the vertex flattened and a small face (brachycephalic skull). B. Wide spaced orbits with the horizontal axes of the eyes directed more laterally than normal. C. The bridge of the nose widened and flattened, with a retrousse nose. D. Mental deficiency usually although the individual may have normal intelligence. Although hypertelorism as an entity is largely of academic interest, in view of the paucity of cases reported with coexisting congenital anomalies and no previous mention of associated cleft plate and giant-cell tumor, we feel that the case reported here should be added to the literature. G. M., aged four years, was admitted to the hospital on Jan. 27, 1938, with chief complaint of painful micturition and marked dysuria of one week's duration. There was no gross bloody urine but the color of the urine was dark. There was no frequency, vomiting, chills, or fever.

BENIGN CYSTS AND ADAMANTINOMAS OF THE JAWS

Cysts and cystlike lesions of the jaws are encountered frequently. Adamantinomas are relatively rare. Many of the so-called dentigerous and radicular cysts are small, but these and certain other cysts may become large. This paper deals mainly with larger cysts and with adamantinomas. It is based on a study of a series of 198 cases of benign cyst and of 58 cases of adamantinoma, approximately a third of the cases in each group having come more or less closely under my observation. In the second month of fetal life¹infolding of the gingival epithelium takes place to form the dental ridge. At intervals along the dental ridge epithelial buds push into the mesoderm; these become pedunculated and bulbous and are then known as "enamel organs." In the fourth month the mesoderm pushes into the deeper surface of the bulbous enamel organ, invaginating it and converting it into a bell-shaped stracture

MULTIPLE HEREDITARY HEMANGIOBLASTOMAS OF THE NERVOUS SYSTEM

Angiomatosis of the nervous system has been recognized as a peculiar type of developmental defect since the original and important contribution of Lindau.1He called attention to the association of Hippel's disease (angiomatosis retinae) with angiomatous tumors of the cerebellum and other parts of the central nervous system and with a variety of systemic abnormalities, particularly pancreatic and renal cysts and hypernephroid tumors of the kidney. He considered these lesions to be the result of a perverted development of the mesodermal germinal layer, beginning probably in the third month of fetal life. The clinicopathologic contribution has been amply confirmed by many observers. As further evidence of the anomalous developmental nature of Lindau's disease cases have been described in which the condition is hereditary and in which multiple hemangioblastomas have been found in the central nervous system. The case reported here is such a one. There was a family history

THE CILIARY MARGIN OF THE DILATOR MUSCLE OF THE PUPIL

Not many years ago the nature and origin of the dilator muscle of the pupil were the subject of much speculation. Improvement of the methods of depigmentation and systematic investigation of embryonic development gradually brought to light its epithelial origin and its fine histologic structure. As a basis for the further exposition of this subject I shall briefly review the established details of the embryology of the iris. The most anterior portion of the inner layer of the secondary optic vesicle becomes the pigment epithelium of the iris, the cells at the point of reflection being differentiated into the muscle cells of the sphincter iridis and the most anterior portion of the outer epithelial layer being transformed into the cells of the dilator muscle during the seventh month of fetal life. Some of the outer epithelial cells become separated from the continuous layer and preserve their epithelial character throughout life.

Developmental Changes in the Vertebral Articular Facets

GROWTH and differentiation in any part of the human organism usually progress in a definitely predictable manner. Such governed alteration in size and shape is well exemplified in the development of the vertebræ. Clinical experience has taught us that serious mechanical or metabolic disturbances are required to alter this pattern of growth. Bending is seen, more commonly, in the long bones, but in all diseases leading to osseous deformity there is a constant attempt on the part of the reparative forces of the body, probably through mechanical stimuli, to approach the normal contour of the bone. Abnormalities in the vertebral articular facets may be found at birth, as Putti (1) and Wierszejewski (2) have shown. There may be complete absence of the pedicles and articular facets, or there may be wide lateral separation of the laminæ, e.g., spina bifida, causing the facets to be useless as joints. A more common change, especially in the lumbar region of the spine (3), is a variation in the shape and directional slant of one or both articular facets of a vertebra. One articular facet may be of the normal, crescentic type, while the other may be flat with a varying axis of the articular surface (4). Abnormalities of this sort lead to a difference in the relative stability of the two sides of the vertebral column, with changes in contour appearing in adult life. Strain of the back (5) and scoliosis (6) have accompanied such irregularities of structure (Fig. 1). Changes in the vertebral articular facets occur from many causes during growth. This study was suggested by the changes observed in the articular facets in roentgenograms of children with scoliosis. An attempt was made to determine what structural alterations occurred in the articular facets of the spinal column before maturity was attained. Five hundred roentgenograms of the spinal column in children were studied to determine the presence and frequency of abnormalities in the vertebral articular facets. In the Warren Museum of the Harvard Medical School, an examination was made of the skeletons of children, as well as those of adults, with deformity. Portions of the dorsal spine were removed routinely at 50 autopsies upon children, and the articular facets of these specimens were studied macroscopically and microscopically. The vertebral articular facets attain functional maturity as spinal joints at the seventh to the eighth month of fetal life. They are recognized in the cartilaginous extensions of the vertebral anlage in 14-millimeter embryos, and are found as separated, overlapping articular surfaces in 50-millimeter embryos (7). Their appearance in roentgenograms during infancy varies widely; they are usually first seen between six months and two years of age.

Hypertrophic Pyloric Stenosis in the Adult

Hypertrophic pyloric stenosis in the adult as a cause of gastric obstruction has only recently obtained noticeable clinical recognition. Maier (7) noted the condition at autopsy; Maylard (8) directed attention to the importance of congenital stenosis of the pylorus in adults; more recent writers (2, 4, 10) have called attention to the surgical treatment, and Archer (1) and McClure (9) have lately contributed to knowledge of the roentgen aspects of the condition. The small number of cases described by various authors indicates the relative infrequency with which the condition is recognized. Pathology The essential pathology is a thickening of the musculature forming the pyloric sphincter, with resultant narrowing of the lumen. McClure (9) presents excellent illustrations of the gross and microscopic pathology. Etiology The etiology has not been definitely determined. Among the theories advanced are the following: 1. The persistence, through adult life, of a congenital hypertrophy of the pyloric muscle, insufficient to cause severe obstruction in infancy, but becoming aggravated in later years. Horton's (6) observation of the relative thickness of the pyloric muscle in the fifth and sixth months of fetal life is of interest. 2. Pirie's (11) theory is hyperadrenal ism, resultant deficiency in pancreatic secretion, with insufficient neutralization of gastric juices, consequent prolonged pyloric closure, and an eventual occurrence of pyloric hypertrophy and stenosis. Elman and Rowlette (5) suggest that gastric acidity is regulated by the pylorus, rather than that acidity regulates pyloric function. 3. Hypertrophy due to persistent pylorospasm from nervousness or reflex causes (1, 9). Symptomatology and Diagnosis The presence of a pyloric obstruction is to be suspected in all patients who give a history of epigastric pain relieved by vomiting long retained gastric contents. Among the conditions arising for differential consideration are: large esophageal diverticulum; malignancy or ulcer of the pylorus, with spasm; gastric syphilis or neurosyphilis with gastric crises; pylorospasm, without organic lesion; gastric or duodenal polypi; diverticulosis of the duodenum; duodenal ileus; chronic cholecystitis, with or without stones; pressure obstruction from pancreatic or other extrinsic tumors, and psychic vomiting. Roentgenologic examination of the gastro-intestinal tract and gall bladder obviously offers the best means of differentiating these various conditions. The chief roentgenologic findings (1) are essentially: 1. A persistent and unchanging increase in the width of the pyloroduodenal interval, “due to an increase in extent of the pyloric ring.” 2. The presence, in some cases, of associated spastic incisuræ several centimeters distant from the pylorus. 3. Failure of antispasmodics and fluoroscopic manipulation to alter the pyloric picture. 4. A narrow barium stream through the pylorus.

THE PHARYNGEAL TONSIL

This communication summarizes the observations of a research on the embryology, bacteriology and pathology of the pharyngeal tonsil. EMBRYOLOGY Behind the oral plate in the middle line of the roof of the pharynx, anterior to the basioccipital, there is a depression called Sessel's pocket. Its embryologic significance is not understood, but it may be the remains of the pharyngeal opening of the notochord. In and around this recess, the pharyngeal or Luschka's tonsil develops. About the fourth month of fetal life, faint striae appear on this part of the posterior pharyngeal wall, and microscopic examination shows the tissue to consist of reticular tissue enclosing in its meshwork a few scattered lymphocytes. Development of this diffuse lymphoid tissue continues in the superficial fibers of the tunica propria of the pharyngeal mucosa until at 5½ months the pharyngeal tonsil appears as a definite organ. Mucous glands are developed at the base and