Development of the child's brain in the prenatal period. Book: C
Dominant of pregnancy- a set of physiological changes in the body during pregnancy.
When exposed to pathogenic factors, a new dominant is often formed in the central nervous system - pathological, and the gestational dominant (normal) is partially or completely inhibited. Suppression of the gestational dominant disrupts: at the beginning of pregnancy - implantation of the embryo (its death is not uncommon); during the period of organogenesis - the formation of the placenta and, accordingly, the development of the embryo (its death is also likely).
The biological system “mother-placenta-fetus” plays a leading role in the development of the fetus. This system is formed under the influence of the mother’s body (neuroendocrine system), the placenta and processes occurring in the fetus’s body.
Critical periods of development are periods of high sensitivity of the fetal body to various influences of internal and external environment, both physiological and pathogenic.
Critical periods coincide with periods of active differentiation, with the transition from one period of development to another (with a change in the conditions of existence of the embryo). In the first period, the pre-implantation stage and the implantation stage are distinguished. The second period is the period of organogenesis and placentation, starting from the moment of vascularization of the villi (3rd week) and ends by the 12-13th week. Damaging factors during these periods can disrupt the formation of the brain, cardiovascular system, and often other organs and systems.
How peculiar critical period, the development period is distinguished at the 18-22nd week of ontogenesis. Disorders manifest themselves in the form of qualitative changes in the bioelectrical activity of the brain, reflex reactions, hematopoiesis, and hormone production.
In the second half of pregnancy, the sensitivity of the fetus to the effects of damaging factors decreases significantly.
PATHOLOGY OF THE PRENATAL PERIOD
1. Gametopathies (disturbances in the period of progenesis or gametogenesis).
2. Blastopathies (disturbances in the period of blastogenesis).
3. Embryopathies (disorders during embryogenesis).
4. Early and late fetopathies (disturbances in the corresponding periods of embryogenesis).
Gametopathies. It's about about disorders associated with the action of damaging factors during the initiation, formation and maturation of germ cells. The causes may be sporadic mutations in the germ cells of parents or more distant ancestors (heritable mutations), as well as many exogenous pathogenic factors. Gametopathies often lead to sexual sterility, spontaneous abortions, congenital malformations or hereditary diseases.
Blastopathy. Disorders of blastogenesis are usually limited to the first 15 days after fertilization. The damaging factors are approximately the same as in gametopathies, but in some cases they are also associated with disorders endocrine system. Blastopathies are based on disturbances in the period of blastocyst implantation. Most of the embryos with disturbances during blastogenesis are eliminated through spontaneous abortions. Average frequency the death rate of embryos during blastogenesis is 35-50%.
Embryopathies. The pathology of embryogenesis is limited to 8 weeks after fertilization. Characteristic high sensitivity to damaging factors (second critical period).
Embryopathies are mainly manifested by focal or diffuse alternative changes and impaired organ formation. The consequences of embryopathies are pronounced congenital malformations, often the death of the embryo. The causes of embryopathies are both hereditary and acquired factors. Exogenous damaging actors include: viral infection, irradiation, hypoxia, intoxication, medications, alcohol and nicotine, nutritional disorders, hyper- and hypovitaminosis, hormonal imbalances, immunological conflict (ABO, Rh factor), etc.
Frequency of embryopathies: in at least 13% of registered pregnancies.
There are early and late fetopathies.
Early fetopathies are divided into:
Infectious (viral, microbial);
Non-infectious (irradiation, intoxication, hypoxia, etc.);
Diabetogenic origin;
Hypoplasia.
As a rule, all damaging factors mediate their influence through the placenta.
Late fetopathy can also be infectious or non-infectious. Among non-infectious ones, intrauterine asphyxia, disorders of the umbilical cord, placenta, and amniotic membranes are of etiological importance. In some cases, late fetopathies are associated with maternal diseases accompanied by hypoxia. Pathogenic factors can act ascendingly through amniotic fluid.
Fetopathies are characterized by persistent morphological changes in individual organs or the organism as a whole, leading to structural disturbances and functional disorders, subdivided into:
1) etiological characteristics: a) hereditary (mutations at the level of genes and chromosomes; gametic, less often during zygotogenesis); b) exogenous; c) multifactorial (associated with the combined action of genetic and exogenous factors).
2) time of exposure to a teratogen - a damaging factor leading to the formation of developmental defects.
3) localization.
The final results of prenatal pathology are mainly congenital malformations and spontaneous abortions.
HYPOXIA AND ASPHIXIA OF THE FETUS AND NEWBORN
Asphyxia means pathological condition, in which the oxygen content in the blood and tissues decreases and the carbon dioxide content increases.
Hypoxia is a pathological condition in which there is a decrease in oxygen content in tissues.
Depending on the time of occurrence, asphyxia is divided into:
Antenatal (intrauterine);
Perinatal - develops during childbirth (from the 28th week of intrauterine life to the 8th day of the newborn);
Postnatal - arising after childbirth.
According to the classification of L.S. Persianinov, all causes causing hypoxia or asphyxia of the fetus are divided into three groups.
1. Diseases of the maternal body, leading to a decrease in oxygen content and an increase in carbon dioxide in the blood. This includes respiratory and cardiovascular failure, hypertension in pregnancy, blood loss.
2. Disturbances of the uteroplacental circulation. Disorders of hemocirculation in the umbilical cord are caused by its compression or rupture, premature placental abruption, post-term pregnancy, and abnormal course of labor (including “stormy labor”). Impaired blood circulation in the vessels of the umbilical cord itself causes asphyxia, but, in addition, when the umbilical cord is compressed as a result of irritation of its receptors, bradycardia reflexively develops and increases arterial pressure. Death often occurs with increasing slowing of the fetal heart rate. Similar changes can occur when the umbilical cord is stretched.
3. Asphyxia caused by fetal diseases. However, fetal diseases cannot be considered as completely independent, occurring independently of the mother’s body. Fetal diseases include hemolytic disease, congenital heart defects, central nervous system malformations, infectious diseases, and airway disorders.
According to the duration of the course, asphyxia is divided into acute and chronic.
In acute asphyxia, compensation is based on reflex and automatic reactions that increase the cardiac output, accelerate blood flow, and increase the excitability of the respiratory center.
In chronic asphyxia, metabolic processes associated with an increase in the synthesis of enzymes in cells are compensatory activated.
The surface and mass of the placenta, the capacity of its capillary network, and the volume of uteroplacental blood flow also increase compensatoryly.
It is noted that activation compensatory mechanisms accelerated by added hypercapnia.
In chronic asphyxia, the maturation of liver enzyme systems - glucuronyltransferase, as well as enzymes that maintain blood sugar levels - is accelerated.
In the pathogenesis of acute asphyxia, circulatory disorders and acidosis are important. In the fetal body they develop congestion, stasis, the permeability of the vascular wall increases. All this leads to perivascular edema, hemorrhage, vascular rupture and bleeding. Cerebral hemorrhage can cause dysfunction of the central nervous system and even fetal death.
Lack of oxygen is often accompanied by disorders of nucleic acid synthesis, enzyme activity, and tissue metabolism. Chronic asphyxia is one of the causes of vascular tumors brain - angiomas.
Those born in a state of asphyxia often have neurological disorders: their excitation processes prevail over inhibition processes; Often one or another degree of mental underdevelopment is revealed.
On the 20th day, a central longitudinal groove appears in the neural plate, which divides it into right and left half. The edges of these halves thicken, begin to curl and merge, forming the neural tube. The cranial section of this tube expands and is divided into three brain vesicles: anterior, middle and posterior. By the 5th week of development, the anterior and posterior brain vesicles divide again, resulting in the formation of five brain bubbles: telencephalon, diencephalon, midbrain, hindbrain and medulla(myelencephalon). The cavities of the brain vesicles accordingly turn into the ventricular system of the brain.
The telencephalon begins to divide longitudinally on the 30th day, resulting in the formation of two parallel medullary vesicles. Of these, on the 42nd day, the cerebral hemispheres are formed and lateral ventricles ventricular system.
The lateral walls of the diencephalon thicken and form the visual tuberosities. The cavity of the diencephalon forms the 3rd ventricle. The walls of the midbrain bladder also thicken. The cerebral peduncles are formed from its ventral section, and the quadrigeminal plate is formed from the dorsal section. The midbrain cavity narrows to form the aqueduct of Sylvius, connecting the 3rd and 4th ventricles.
The pons is formed from the ventral sections of the metencephalon, and the cerebellum is formed from the dorsal sections. The common cavity of the rhombencephalon forms the 4th ventricle.
The neural plate and neural tube consist of the same type of cells (neural stem cells), in the nuclei of which increased DNA synthesis occurs. At the neural plate stage, cell nuclei are located closer to the mesoderm, at the neural tube stage - closer to the ventricular surface. Synthesizing DNA, the nuclei move in the cylindrical cytoplasm of the cell towards the ectoderm, after which it follows mitotic division cells. Daughter cells establish contact with both surfaces of the neural tube: outer and inner. However, most cells continue to remain close to the ventricular surface and divide at a logarithmic rate of three generations per day. Each generation of cells is subsequently destined for a specific layer of the cortex cerebral hemispheres. The ventricular zone of cells occupies almost the entire thickness of the wall of the medullary roughness. in which the cells are evenly distributed. Then a marginal zone appears, consisting of intertwining cells and axons. Between the marginal and ventricular zones, an intermediate zone appears, represented by sparsely located cell nuclei after mitotic division. Cells whose nuclei are located in the ventricular zone subsequently turn into macroglial cells. Cells outside this zone can transform into neurons, astrocytes and oligodendrogliocytes.
At the 8th week of development, the formation of the cerebral cortex begins and choroid plexuses, which produce cerebrospinal fluid. The wall of the cerebral hemispheres in this period consists of four main layers: the internal (densely cellular) matrix, the interstitial layer, the cortical anlage and the marginal layer devoid of cellular elements.
The formation of the cerebral cortex goes through five stages:
- initial formation of the cortical plate - 7-10 weeks;
- primary thickening of the cortical plate - 10-11th week;
- formation of a two-layer cortical plate - 11-13th week;
- secondary thickening of the cortical plate - 13-15 weeks;
- long-term differentiation of neurons - 16th week or more.
In the 2nd half of gestation, horizontally oriented Cajal-Retzius neurons appear in the marginal part of the cortical plate, which disappear during the first 6 months of postnatal life. Only in the human embryo does a transient subpial layer of small cells appear in the marginal zone of the cortex, which completely disappears by the time of birth.
Features of the cytoarchitectonics of various fields of the cerebral cortex begin to emerge at the 5th month intrauterine development. By the end of the 6th month, the cortex of all lobes has a six-layer structure. At the 4th-5th month, the layer-by-layer structure of the cortex of area 4 (anterior central gyrus) is already determined, and the delimitation of the cortex into fields begins. Large ones are differentiated first pyramidal neurons 5th layer of bark. By the time of birth, most neurons in the deep layers are differentiated, while neurons are more surface layers are lagging behind in their development.
At the 2nd month of intrauterine development, the surface of the cerebral hemispheres remains smooth. At the 4th month, the formation of the olfactory grooves and corpus callosum begins, and the features of the external configuration of the cerebral hemispheres are revealed. The first to form is the Sylvian fissure, at the 6th month - the Rolandic fissure, the formation of the primary fissures occurs parietal lobes, frontal gyri. By the 8th month, the fetal brain has all the major permanent sulci. Then, during the 9th month, secondary and tertiary gyri appear.
The formation of the hippocampus occurs on the 37th day of development. After 4 days, differentiation of its sections begins. At the beginning of the 4th lunar month, its differentiation into fields appears.
The cerebellum begins to form on the 32nd day of development from paired pterygoid plates. Its nuclei are laid in the 2-3rd lunar month; in the 4th month the crust begins to form, which by the 8th month acquires a typical structure.
The nuclear groups of the medulla oblongata are formed quite early, as they provide the functions of respiration, blood circulation and digestion. The medial accessory olives are the first to develop on the 54th day. After 4 days, the laying of olive nuclei begins, which initially look like compact formations. Their division into ventral and dorsal plates is noted in an 8 cm long embryo, and tortuosity appears only in an 18 cm long embryo. The contours of the olives above the ventral surface of the medulla oblongata appear in the 4th month of development.
Spinal cord and spinal canal until the 3rd lunar month of development coincide in length. Subsequently, the spinal cord lags behind the spine in its development. Its caudal end reaches level 3 by the time the child is born. lumbar vertebra. The spinal cord develops faster than the brain. The first to differentiate motor neurons, And neural organization The spinal cord takes on a relatively formed appearance during 20-28 weeks of development. Maturation of the spinal cord ensures early motor functions in the fetus.
Visible separation nerve tissue brain to gray and white matter is caused by the formation of myelin sheaths, which corresponds to the beginning of the functioning of certain systems of the brain and spinal cord. The first myelin fibers appear in the 5th month of intrauterine development in the brainstem, in the cervical and lumbar enlargements of the spinal cord. Myelin covers first the sensory and then the motor nerve fibers. The first signs of myelination of the pyramidal tracts appear in fetuses at 8-9 months.
By the time of birth, most of the spinal cord, the medulla oblongata, many parts of the pons and midbrain, the striatum, and the fibers surrounding the cerebellar nuclei are myelinated. After birth, myelination processes continue, and by the 2nd year of life, the child’s brain is almost completely myelinated. However, during the 1st decade, the projection and association fibers of the visual thalamus continue to myelinate, and in adults, the fibers of the reticular formation and neuropil of the cortex.
In the area of the future site of myelination, proliferation of immature glial cells occurs, foci of which are often regarded as a manifestation of gliosis. Subsequently, these cells differentiate into oligodendrogliocytes. The process of myelination is quite complex and can be accompanied by various errors. Thus, myelin sheaths may be longer than necessary, and double myelin sheaths may form in individual nerve fibers. Sometimes the entire body of a nerve cell or astrocyte is completely covered with myelin. Such hypermyelination can cause the formation of a “marbled state” of the nervous tissue of the brain.
In parallel with the development of the brain, the formation of the meninges occurs, which are formed from the perimedullary mesenchyme. First, the choroid appears, from which, at the 3-4th week of intrauterine development, blood vessels grow into the thickness of the medullary tube. These vessels draw the leaf along with them deep into the nervous tissue. choroid, as a result of which Virchow - Robin spaces are formed around the vessels, having great importance in the absorption of cerebrospinal fluid. Soft bundle meninges into two leaves (arachnoid and vascular) occurs in the 5th month, due to the formation of the holes of Luschka and Majendie. The subarachnoid space is formed. Moderate expansion the ventricular system before the formation of these holes is called physiological hydrocephalus.
The mass of the brain at the end of intrauterine development is 11-12% of total mass bodies. In an adult it is only 2.5%. The mass of the cerebellum in full-term newborns is 5.8% of the mass of the brain.
Unlike the adult brain, in fetuses and newborns the neurons of the various layers of the cerebral cortex are densely located. In the substantia nigra of the trunk, neurons are devoid of myelin, which first appears in these cells during the 3-4th year of life. In the cerebellar cortex, until 3-5 months of the 1st year of life, the outer granular embryonic layer (Obersteiner's layer) is preserved, the cells of which gradually disappear by the end of this year. In the subependymal zone of the newborn's ventricular system, a large number of immature cellular elements, which in some cases are mistakenly interpreted as a manifestation of local encephalitis. These cells can be located diffusely or in isolated foci, along the vessels they can reach the white matter and gradually disappear within 3-5 months of postnatal life.
The human nervous system develops from the outer germinal lobe - the ectoderm. From this same part of the embryo, in the process of development, sensory organs, skin and sections are formed digestive system. Already on the 17-18th day of intrauterine development (gestation), a layer is distinguished in the structure of the embryo nerve cells- neural plate, from which subsequently, by the 27th day of gestation, the neural tube is formed - the anatomical precursor of the central nervous system. The process of neural tube formation is called “neurulation.” During this period, the edges of the neural plate gradually bend upward, connect and grow together (Figure 1).
Figure 1. Stages of neural tube formation (sectioned).
If you look at this movement from above, you might associate it with zipping up a zipper (Figure 2).
Figure 2. Stages of neural tube formation (top view).
One “zipper” is fastened from the center to the cephalic end of the embryo (rostral wave of neurulation), the other from the center to the caudal end (caudal wave of neurulation). There is also a third “zipper” that ensures fusion of the lower edges of the neural plate, which “zips” towards the head end and meets the first wave there. All these changes happen very quickly, in just 2 weeks. By the time neurulation is completed (days 31-32 of gestation), not all women even know that they are having a baby.
However, by this moment, the brain of the future person begins to form, the rudiment of two hemispheres appears. The hemispheres quickly increase in size, and by the end of the 32nd day they make up ¼ of the entire brain! Then an attentive researcher will be able to discern the rudiment of the cerebellum. During this period, the formation of sensory organs also begins.
Exposure to hazards during this period can lead to various malformations of the nervous system. One of the most common vices is spina bifida, formed as a result of incorrect “fastening” of the second “zipper” (impaired passage of the caudal wave of neurulation). Even erased, almost imperceptible versions of such spina bifida sometimes reduce the child’s quality of life, leading to various forms incontinence (incontinence of urine and feces). If a child has a problem such as enuresis (urinary incontinence) or encopresis (fecal incontinence), it is necessary to check whether he has an erased form of spina bifida. This can be found out by giving the child an MRI of the lumbosacral spine. If a spina bifida is detected, it is indicated surgical treatment, which will lead to improvement of pelvic functions.
In my practice, there was a case of a 9-year-old boy who suffered from encopresis. Only on the 6th attempt was it possible to take a high-quality MRI image, which showed the presence of spina bifida. Unfortunately, up to this point the child had already been observed by a psychiatrist and received appropriate treatment, since neurologists had disowned him, believing that he had mental problems. Simple operation let the boy return to normal image life, have complete control over your pelvic functions. Even more revealing was the story of a 16-year-old teenager who suffered from encopresis all his life. Neurologists sent him to gastroenterologists, gastroenterologists to psychiatrists. By the time we met, he had already received psychiatric treatment for ten (!!!) years. No one ever ordered an MRI scan for him. Thanks to the fact that our recommendations for further examination were followed, the guy was diagnosed with serious violations V lumbar region spine, which led to compression of the nerves and loss of sensitivity pelvic organs. Obviously, psychiatric treatment, as well as psychotherapy or other methods psychological impact in all these cases they are completely useless and perhaps even harmful.
To prevent the occurrence of such malformations as spina bifida, pregnant women are already early stages During pregnancy it is recommended to take folic acid. Folic acid plays the role of a protector of nervous system cells (neuroprotector), and when taken regularly, the effects of various harmful factors are significantly weakened.
In order to minimize the risk of developmental defects, the expectant mother must also avoid various adverse effects on the body. Such influences include taking sedatives containing phenobarbital (including Valocordin and Corvalol), hypoxia ( oxygen starvation), overheating of the maternal body. Unfortunately, to adverse consequences also leads to taking some anticonvulsants. Therefore, if a woman forced to take such drugs plans to become pregnant, she should consult with her doctor.
Throughout the first half of pregnancy, new nerve cells (neurons) are very actively born and developed in the child’s future brain. First of all, the processes of the generation of new nerve cells occur in the area surrounding the cerebral ventricles. Another area for the birth of new neurons is the hippocampus - inner part temporal cortex of the right and left hemispheres. New nerve cells continue to appear after birth, but less intensely than in the prenatal period. Even in adults, young neurons have been found in the hippocampus. It is believed that this is one of the mechanisms through which, if necessary, the human brain can be plastically rebuilt and restore damaged functions.
Newly born neurons do not remain in place, but “crawl” to the places of their permanent “dislocation” in the cortex and deep structures of the brain. This process begins towards the end of the second month of pregnancy and actively continues until 26-29 weeks of intrauterine development. By the 35th week, the fetal cerebral cortex already has the structure inherent in the adult cortex.
Each neuron has processes through which it interacts with other cells of the body.
Figure 3. Neuron. The long process is the axon. Short branched processes are dendrites.
Neurons that have taken their place in the brain try to establish new relationships with other nerve cells, as well as with cells in other tissues of the body (for example, muscle cells). The place where one cell connects to another is called a “synapse.” Such connections are very important because it is thanks to them that the brain forms complex systems in which information can quickly be transmitted from one cell to another. Inside the cell, information is transmitted from the body to the end in the form of an electrical impulse. This impulse provokes release in synaptic cleft specific chemical substances(neurotransmitters) that are stored at the end of a neuron and through which information is transmitted from the neuron to the next cell.
Figure 4. Synapse
The first synapses were found in embryos at the age of 5 weeks of intrauterine development. The most active formation of synaptic contacts between neurons occurs starting from 18 weeks of intrauterine development. New connections between nerve cells are formed almost throughout life. During active education a child's brain is susceptible to synapses negative influence narcotic substances and some medications that affect the metabolism of neurotransmitters. These substances include, in particular, antipsychotics, tranquilizers and antidepressants - drugs that are used to treat mental disorders. If future mom forced to accept similar drugs, she needs to consult her doctor. And, of course, a pregnant woman should avoid consuming psychoactive substances if she's worried mental development her child.
Neurotransmitters - specific chemical compounds, thanks to which information is transmitted in the nervous system. A lot in human behavior depends on their correct exchange. Including his mood, activity, attention, memory. There are factors that can affect their exchange. One of these adversely affecting factors is maternal smoking during pregnancy. Exposure to nicotine produces several effects at once. The brain recognizes nicotine as a trigger and begins to develop systems that are sensitive to it. Simply, the number of elements that perceive nicotine in the brain increases, and the transmission of information carried out through nicotine improves. At the same time, there is a negative impact on the exchange of those neurotransmitters that should be produced by the brain itself. First of all, this applies to those substances that are related to ensuring attention and regulating emotions. Studies have shown that maternal smoking during pregnancy several times increases the risk of having a child with attention deficit hyperactivity disorder (ADHD). The second consequence of intrauterine nicotine consumption after ADHD is oppositional defiant disorder, which is characterized by such manifestations as irritability, anger, constantly changing, often negative, mood, and resentment. Another effect of smoking is the deterioration of blood vessels and disruption of fetal nutrition. Children of smoking mothers are born with low birth weight, and low weight at birth is itself a risk factor for the development of subsequent behavior problems. Due to vasospasm caused by exposure to nicotine, the fetal brain is susceptible to ischemic strokes– disturbances in the blood supply to certain areas of the brain, their hypoxia, which has a very detrimental effect on all subsequent mental development.
One of the most important processes occurring in the developing brain of an unborn child is the coating of the long endings of nerve cells (axons) with myelin (myelination). The myelin-covered axon is shown in one of the previous drawings (drawing of a neuron). Myelin is a substance that is somewhat like the insulation that covers wires. Thanks to it, the electrical signal moves from the neuron body to the axon terminal very quickly. The first signs of myelination are found in the brain of 20-week-old fetuses. This process occurs unevenly. The first to be covered with myelin are the axons that form the visual and motor nerve pathways, which are primarily useful to the newborn baby. A little later (almost before birth), the auditory pathways begin to become covered with myelin.
The cells of one of the brain tissues, neuroglia, which produce myelin, are very sensitive to a lack of oxygen. Also, the myelination of the fetal brain can be affected by exposure to toxins, drugs, deficiency of substances necessary for the brain that come from food (in particular, B vitamins, iron, copper and iodine), wrong exchange certain hormones, such as thyroid hormones.
Alcohol is extremely harmful to the normal course of myelination processes. It interferes with myelination and, as a result, can cause severe violations mental development accompanied mental retardation child. Alcohol exposure can also have a nonspecific effect, leading to a variety of developmental defects.
About how intensively the brain of a child in the womb develops is evidenced by the fact that in the period from 29 to 41 weeks, the brain increases almost 3 times! This is largely due to myelination.
Relatively little is known about the mental development of a child in the prenatal period. At the same time, there are some interesting facts.
Starting from 10 weeks of intrauterine development, children suckle thumb(75% - right). It turns out that future right-handers, for the most part, prefer to suck the right finger, and future left-handers prefer to suck the left.
When exposed to contact sound on the abdomen of pregnant women (37-41 weeks of pregnancy) through headphones, reliable activation was found in temporal areas in four and in the frontal in one fetus - the same areas of the cerebral cortex that will subsequently take part in the processing of speech information. This suggests that the child’s brain is actively preparing to exist in the environment that is intended for it.
Literature:
Nomura Y., Marks D.J., Halperin J.M.
Prenatal Exposure to Maternal and Parental Smoking on Attention Deficit Hyperactivity Symptoms and Diagnosis in Offspring // J Nerv Ment Dis. September 2010; 198(9): 672-678.
Read the original article >>
Tau G.Z., Peterson B.S.
. Normal development of brain circuits // Neuropsychopharmacology reviews (2010) 35, 147-168
Read the original article >>
Savelyev S.V. Embryonic pathology of the nervous system. – M.:VEDI, 2007. – 216 p.
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Manufacturer: "Vedi" The original material describes the normal development and early embryonic disorders of the morphogenesis of the human nervous system. The basic principles of the occurrence of neurulation abnormalities in the development of the nervous system of humans and animals have been identified. Molecular mechanisms for encoding morphogenetic information in the embryonic nervous system have been developed. A positional theory of early control has been created and experimentally confirmed embryonic development vertebrate brain. The mechanisms of pathogenesis of the nervous system have been studied and the reasons for the formation of deviations in normal development have been shown. The book is intended for students studying pathological anatomy, embryology, obstetrics, gynecology, neurology, physiology and anatomy, as well as for teachers of biological and medical disciplines. Publisher: "Vedi" (2017)
ISBN: 978-5-94624-032-1 |
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Embryogenesis of the human nervous system . The nervous system originates from the outer germ layer, or ectoderm. This latter forms longitudinal thickening called medullary plate. The medullary plate soon deepens into the medullary groove, the edges of which (medullary ridges) gradually become higher and then grow together with each other, turning the groove into a tube ( brain tube). The medullary tube is the rudiment of the central part of the nervous system. Rear end of tube forms rudiment of the spinal cord, anterior extended end it by constrictions divided into three primary medullary vesicles, from which the brain in all its complexity originates.
The neural plate initially consists of only one layer epithelial cells. During its closure into the brain tube, the number of cells in the walls of the latter increases, so that three layers appear:
· internal (facing the cavity of the tube), from which the epithelial lining of the brain cavities occurs (ependyma of the central canal of the spinal cord and ventricles of the brain);
middle, from which it develops Gray matter brain (germinal nerve cells - neuroblasts);
· finally, the outer one, almost free of cell nuclei, developing into white matter (nerve cell processes - neurites).
Bundles of neurites of neuroblasts spread either in the thickness of the brain tube, forming white matter brain, or exit into the mesoderm and then connect with young muscle cells (myoblasts). In this way there arise motor nerves.
Sensory nerves arise from the rudiments spinal nodes, which are noticeable already at the edges of the medullary groove at the place of its transition into the cutaneous zctoderm. When the groove closes into the brain tube, the rudiments are displaced to its dorsal side, located along the midline. Then the cells of these rudiments move ventrally and are located again on the sides of the brain tube in the form of so-called neural ridges. Both neural crests are laced in a clear pattern along the segments of the dorsal side of the embryo, resulting in a row of spinal ganglia on each side, gangliaspinalia . In the head part of the brain tube they reach only the area posterior medullary vesicle, where the rudiments of sensory nodes form cranial nerves. Ganglion primordia develop neuroblasts, taking the form bipolar nerve cells, one of whose processes grows into the brain tube, the other goes to the periphery, forming a sensory nerve. Thanks to the fusion at some distance from the beginning of both processes, the so-called bipolar ones are obtained false unipolar cells with one process, dividing in the shape of the letter " T", which are characteristic of the spinal nodes of an adult.
Central processes cells penetrating the spinal cord are dorsal roots spinal nerves, and peripheral processes, growing ventrally, form (together with those emerging from the spinal cord efferent fibers, making up the anterior root) mixed spinal nerve . Also arise from neural crests rudiments autonomic nervous system, for details see “Autonomic (autonomic) nervous system.”
Basic processes of embryogenesis of the nervous system.
· Induction: primary and secondary. Primary induction appears at the end of gastrulation and is caused by the movement of chordomesoderm cells towards the cephalic end. As a result of the movement, ectoderm cells are excited and the formation of the neural plate begins from them. Secondary induction is due to the developing brain itself.
· Regulation by hormones and neurotransmitters(serotonin, dopamine, norepinephrine, acetylcholine, opiates, etc.) begins with the first fragmentation of the egg, early intercellular interactions, morphogenetic transformations and continues throughout the life of the individual.
· Proliferation(formation, reproduction and distribution of cells) as a response to primary induction and as the basis for the morphogenesis of the nervous system, occurring under the control of transmitters and hormones.
· Cell migration V different periods development is typical for many parts of the nervous system, especially the autonomic one.
· Differentiation neurons and glial cells includes structural and functional maturation under the regulating trophic influence of hormones, neurotransmitters and neurotrophins.
· Formation of specific connections between neurons is an indicator of active maturation.
· WITH stabilization or elimination interneuron connections occur at the end of brain maturation. Neurons that do not make connections die.
· Development of integrating, coordinating and subordinating functions, which allows the fetus and newborn to carry out independent life activities.
In 4-week-old embryos, the head of the neural tube consists of brain vesicles : anterior - prosencephalon, middle - mesencephalon, posterior - metencephalon, separated from each other by small narrowings. At the end of the 4th week, the first signs of division of the anterior bladder into two appear, from which the final and diencephalon. At the beginning of the 5th week, the posterior vesicle divides to form the hindbrain and medulla oblongata. From the unpaired middle bladder is formed midbrain.
Due to uneven growth developing brain sagittal bends appear in the blisters, oriented with convexity towards the dorsal side (the first two) and ventral - the third :
· parietal flexure - the earliest, arises in the area of the mesencephalic vesicle, separating the midbrain from the intermediate and terminal brain;
· the occipital flexure in the posterior bladder separates the spinal cord from the brain;
· the third bend - the pavement - is located between the first two and divides the posterior vesicle into the medulla oblongata and hindbrain.
The posterior bladder grows more intensively in the ventral direction. Its cavity turns into the IV ventricle with a thin upper wall of ependymal cells and a thick bottom in the form of a diamond-shaped fossa. The pons, cerebellum, and medulla oblongata develop from the posterior bladder. common cavity in the form of the fourth ventricle.
The walls of the mesencephalic vesicle grow laterally more evenly, forming the cerebral peduncles from the ventral sections and the roof plate of the midbrain from the dorsal ones. The cavity of the bubble narrows, turning into a water pipe.
The most complex changes occur with the anterior bladder. From him posterior section the diencephalon is formed. Initially, due to the proliferation of the mantle layer, the dorsolateral walls of the bladder thicken and visual bumps appear, turning the cavity of the future third ventricle into a slit-like space. From the ventrolateral walls appear the optic vesicles, from which the retina eyes. A blind outgrowth of the ependyma appears in the dorsal wall - the future epiphysis. In the lower wall, the protrusion turns into a gray tubercle and a funnel, which connects with the pituitary gland, which forms from the ectoderm of the oral bay (Rathke's pouch).
In the unpaired, anterior part of the prosencephalon, in the early stages, right and left bubbles appear, separated by a septum. The cavities of the bubbles turn into lateral ventricles: the left one into the first ventricle, the right one into the second. Subsequently, they connect to the third ventricle through the interventricular foramina. Very intensive growth of the walls of the right and left bubbles turns them into hemispheres telencephalon, which cover the diencephalon and midbrain. On inner surface thickening of the lower walls of the right and left terminal bladders for development basal ganglia. The corpus callosum and commissures arise from the anterior wall.
The outer surface of the bubbles is smooth at first, but it also grows unevenly. From the 16th week, deep furrows (lateral, etc.) appear that separate the lobes. Later, small grooves and low convolutions form in the lobes. Before birth, only the main sulci and convolutions are formed in the telencephalon. After birth, the depth of the grooves and the convexity of the convolutions increases, many small, unstable grooves and convolutions appear, which determines the individual diversity of options and the complexity of the brain relief in each person.
The greatest intensity of reproduction and settlement of neuroblasts occurs at 10-18 weeks fetal period. By birth, 25% of neurons complete differentiation, by 6 months - 66%, by the end of 1 year of life - 90-95%.
In newborns, the weight of the brain is 340-430 g in boys, 330-370 g in girls, 12-13% of body weight or in a ratio of 1:8.
In the first year of life, the mass of the brain doubles, and at 3-4 years it triples. Then, until the age of 20-29 years, a slow, gradual and uniform increase in mass occurs on average up to 1355 g for men and up to 1220 g for women with individual fluctuations within 150-500 g. Brain mass in adults is 2.5-3% of the mass body or is in a ratio of 1:40. The adult brain contains stem cells, from which, throughout life, the precursors of various neurons and neuroglial cells are formed, which are distributed throughout the brain. different zones and after proliferation and differentiation, they are integrated into working systems.
Brain stem newborns have 10-10.5 g, which is 2.7% of body weight, in adults - 2%. Initial cerebellar weight 20 g (5.4% of body weight), by 5 months infancy doubles, and by the 1st year quadruples, mainly due to the growth of the hemispheres.
In the hemispheres of the telencephalon of newborns, only the main sulci and convolutions are present. Their projection onto the skull differs significantly from that in adults. By the age of 8, the structure of the cortex becomes the same as in adults. In the process of further development, the depth of the grooves and the height of the convolutions increase; Numerous additional grooves and convolutions appear.
