Nervous System

NERVOUS SYSTEM. Contents: I. Embryogenesis, histogenesis and phylogeny of the N.s.

54. I. Embryogenesis, histogenesis and phylogeny of the N.s. The nervous system develops together with the most important sense organs from the outer embryonic leaf, the ectoderm. In vertebrates, the rudiment of the greater part of the N.s. is already found at very early stages of development in the form of a thickened ectodermal strip running along the back of the embryo and bounded in front and on the sides by small "nerve" or "brain" ridges. In the anterior part of the embryo, the neural plate forms earlier and is immediately significantly wider; it corresponds to the rudiment of the future brain. Behind, the plate continues to increase for some time as the posterior half of the embryo's body forms. Very early on, on either side at the anterior edge of the medullary plate, small depressions-rudiments* of the future visual organs appear, which in all vertebrates develop as parts of the central N.s. The neural plate deepens, especially along the midline, forming a dorsal or neural groove, while the neural ridges on the sides rise up, so that the entire plate takes the form of a groove. The neural ridges converge over the groove first in the posterior part of the head, and then further, behind and in front, and thus the neural groove is transformed into the "primary neural tube". In front, an opening leading into the neural tube-the neuropore-remains open for some time. Behind, the neural ridges close over the blastopore, capturing its remnants, and thus for some time behind, direct communication is established between the neural and primary intestinal tube (canalis neuroentericus). The neural ridges fuse with each other over the neural tube, the latter becomes isolated from the covering ectoderm, and the cellular material of the neural ridges remains under the ectoderm in connection with the dorsal part of the neural tube in the form of a paired protrusion-the "ganglionic plate". From the neural tube, the Brain with visual organs and the spinal cord develop, while from the ganglionic plate, the greater part of the nerve nodes with their nerves form. Other parts of the ectoderm also participate in the development of the N.s., for the most part, however, closely adjacent to the embryonic neural plate. In front of the neural plate, a paired thickening of the ectoderm, the so-called olfactory placode, gives rise to the olfactory epithelium and the nerves extending from it. On the sides of the neural plate, in the head region, another paired thickening of the ectoderm develops-the dorso-lateral placode, which gives rise to the auditory vesicle, then the inner ear with the auditory ganglion and nerve, and the lateral line organs of fish with their ganglia and nerves. Only the taste organs are formed in the epithelial lining of the anterior part of the intestine, while their ganglia and nerves develop from paired ectodermal thickenings located at the dorsal ends of the visceral clefts (epibranchial placodes). Corresponding to the greater width of the anterior part of the neural plate, the entire anterior part of the neural tube is noticeably swollen from the very beginning. Subsequently* due to the uneven growth of the walls, new swellings appear, separated by constrictions. First, a swelling appears in the anterior part of the brain (archencephalon), separated by a constriction from the posterior part, which gradually transitions into the cylindrical ^: section of the tube, corresponding to the future ^! spinal cord. Soon the anterior swelling divides, by a light constriction, into two, and thus three primary "brain vesicles" form at the anterior end of the neural tube. Further differentiation then leads to the formation of five definitive ^; parts of the brain. From the anterior brain vesicle, a paired protrusion develops forward-the forebrain (telencephalon), which in most vertebrates forms the so-called cerebral hemispheres with the cavities of the lateral ventricles. The remaining \ part of the anterior brain vesicle gives rise to the ¹ diencephalon with the cavity of the III ventricle, and its lateral walls bulge out in the form of optic vesicles. The middle brain vesicle forms the midbrain (mesencephalon); its cavity reduces to the degree of a narrow canal (aquaeductus Syl-i vii, s. iter), connecting the cavities of the III and : IV ventricles. The posterior vesicle gives rise in its anterior part to the hindbrain (metencepha-i lon), the roof of which protrudes in the form of a transverse ^: fold-the cerebellum (cerebellum), and behind it-the medulla oblongata (myelencephalon) ; with the cavity of the IV ventricle, which continues posteriorly into the central canal of the spinal cord. : The brain never retains the form of a straight tube. The rapid growth of its individual parts, especially the dorsal wall, leads to the formation of characteristic : bends. First, the anterior end of the brain bends downward (in the ventral direction), forming a very significant : temporal bend in the region of the midbrain. In : this place, the brain as if folds in half along its ventral wall. Less significant is the posterior (occipital) bend in the posterior part of the medulla oblongata. The third bend is located between the two previous ones in the region of the hindbrain and has the opposite direction (convexity downward); this is the middle bend, or the bend of the pons. The boundaries between the brain parts are partly conventional, but the five parts mentioned are clearly distinguishable and exactly comparable throughout the entire series of vertebrate animals. In different parts of the brain, proliferations and thickenings of various parts of the walls are observed, and these local thickenings actually characterize the parts of the adult animal's brain. The anterior wall of the brain remains thin in the middle and forms the "terminal plate" (lamina terminalis). On either side of it in most vertebrates, paired protrusions develop-cerebral hemispheres. The paired thickenings of the lower part of the anterior wall of these form the olfactory lobes of the brain (lobi olfactorii), while the paired thickenings of their floor-"striated bodies" (corpora striata). In higher vertebrates, the roof of the forebrain (telencephalon) thickens significantly, bearing the name of the mantle (pallium). In the diencephalon, the lateral walls thicken, forming the visual thalamus (thalami optici), while the roof remains very thin, epithelial, and on it the anterior choroid plexus develops. In the posteriorly lying parts, the floor of the brain has considerable thickness. The roof of the midbrain forms paired thickenings-visual lobes (lobi optici) of lower vertebrates, the quadrigeminal bodies (corpora quadrigemi-na) of higher ones. The roof of the hindbrain grows very significantly and gives rise to the cerebellum (cerebellum). In the region of the medulla oblongata, the floor and sides thicken mainly, while the roof remains thin and on it the posterior choroid plexus develops. In the spinal cord, the lateral walls also proliferate, as a result of which the central canal is initially flattened into a vertical slit; later it lags significantly behind in growth, while the lateral walls also grow upward and downward, being separated from each other by more or less deep dorsal and ventral grooves. In addition to the general morphogenetic processes, the processes of microscopic structural development are also of essential importance for understanding the nervous system. The walls of the neural tube initially consist of cylindrical epithelium with homogeneous indifferent cells. Part of these cells for a long time retains the character of epithelial cells, radially arranged around the central canal and connected at their ends with both the inner and outer surfaces of the tube, where they secrete boundary membranes. The nuclei of these cells "ependyma" are located inside, i.e., near the central canal, and their bodies, as the brain walls thicken, stretch into long radial fibers, which have the character of supporting structures. Located between the cylindrical ependymal cells, shorter indifferent cells multiply, migrate into the thickness of the lateral walls, and here differentiate into two kinds of cells: a) branched supporting cells of the neuroglia and b) neuroblasts, which then transform into nerve cells. The transformation of the neuroblast begins with the development of a process, the neurite, which stretches into a long thin thread. Simultaneously with this, neurofibrils (see Nerve cells) are found in the protoplasm of neuroblasts. According to Held's data, the laying of neuroblasts has a syncytial character; neurofibrils pass from one neuroblast to a series of neighboring ones. In further stages of development, nerve cells become isolated from this syncytium. In some cases, this connection between neuroblasts can be detected even in the adult state, either as a developmental anomaly (Bielschowsky) or as a permanent formation (ganglion cells of the retina, nodes of the autonomic N.s.; Dogel). Later, other processes-dendrites-develop, which branch more or less abundantly in the substance of the brain walls (see Nerve cells).

Nerve cells reach varying degrees of differentiation in different parts of the brain; in general, it can be said that in the brain, in its parts most remote from the internal cavity, the most differentiated cells develop. Furthermore, the system of processes and the general form of cells reach the greatest complexity in highly organized vertebrates. In terrestrial vertebrates, in two parts of the brain—in the cerebral hemispheres and in the cerebellum—part of the neuroblasts moves to the outer surface of the organ and forms here a significant layer of gray matter—cortex. Nerve processes extend to the periphery of the brain and continue into the peripheral nerves, forming their axial cylinders, or grow more or less far inside the brain, entering into the composition of its central pathways. The mass of fibers proliferating within the brain forms (together with the elements connecting them, glia) its 'white' matter, whereas nerve cells with their processes constitute (together with glial cells) the 'gray' matter. The peripheral N. s. develops in the closest connection with the central one. Spinal cord nodes, as well as partly cranial nodes, are formed by the isolation of areas of the ganglionic plate, which, as we have seen, develops from the neural ridges fused above the neural tube. In the head area, to this is added cellular material from the mentioned dorso-lateral placode (auditory ganglion), and in fish and amphibians, in addition, the ganglia of the lateral line organs and epibranchial (in fish) participate in the development of nodes of all typical visceral nerves of the head (i.e., facial, glossopharyngeal, and vagus nerves). Ganglia of the autonomic N. s. are formed from cellular material of the same ganglionic plate. The nerve cells of spinal cord nodes develop from 'ganglionic plates.' They take a spindle-shaped form and develop each two processes. One process, the central—corresponding to the neurite—develops somewhat earlier and grows toward the spinal cord, entering into the composition of the dorsal (sensory) roots; the other, peripheral, forms somewhat later and gives terminal branches in the peripheral receptor. Later, the cells of spinal cord nodes, especially in higher vertebrates, change their spindle-shaped form to a bulbous one and become unipolar through the approach and connection of the main parts of both processes. Motor nerves develop somewhat later; their axial cylinders grow from large neuroblasts of the ventral part of the brain outward; they exit as part of the ventral roots and grow toward the somatic musculature. In addition, neuroblasts of the lateral parts of the brain also form motor fibers that, in lower vertebrates, exit through the dorsal roots and nodes, and in higher vertebrates through both roots of the spinal nerves. These 'visceromotor' fibers innervate either directly the striated musculature of the visceral apparatus or through the medium of ganglia of the autonomous system the smooth muscles of internal organs and glands. The processes growing out of the brain and nerve nodes of nerve cells are at first bare axial cylinders. However, they are soon surrounded by myelin and only later connect to form mixed nerves. Only 2 pairs of anterior cranial nerves occupy a special position and are incomparable with other nerves—first, the olfactory nerve, consisting of processes of sensory cells of the olfactory epithelium, which grow from here into the olfactory bulb of the brain, and second, the optic nerve, which is a central tract with neuroglia, developing, like the eye vesicle itself, from the walls of the brain and surrounded, like the latter, by the meninges. Nerves V, VII, IX and X pairs are segmental nerves of the visceral apparatus. The trigeminal nerve corresponds to two nerves—premaxillary (n. ophthalmicus profundus) and mandibular arch; the facial nerve is the nerve of the first visceral cleft (hyoid, tympanic cavity); the glossopharyngeal nerve is the nerve of the first gill cleft, and the vagus nerve is the nerve of all subsequent gill clefts. The auditory nerve is an isolated part of the facial nerve, and the accessory nerve of the XI pair is the posterior visceromotor portion of the vagus nerve, which isolates from the latter only in higher vertebrates, starting with reptiles. The reduction of the lateral line organs and gill apparatus in the transition to terrestrial life is accompanied, of course, by the reduction in higher vertebrates of the corresponding branches of the cranial nerves VII, IX and X. Already in lower vertebrates, part of the visceromotor nerve elements going to the smooth musculature and glands and concentrating in special ganglia lying along the sides of the aorta, as well as on various internal organs, is isolated from the nervous system. In cyclostomes, this autonomous nervous system still consists of separate nodes connected by connecting twigs with the spinal nerves and forming plexuses on various internal organs. Only in higher fish and terrestrial vertebrates do the ganglia of the autonomic N. s. also connect with each other in the body area by a longitudinal marginal trunk. In the head area, the corresponding nerves and ganglia remain in close connection with the cranial nerves and only in places separate from them.

I. Shmal'gauzon, cells that migrate along the course of nerves from the ganglionic plate, and later also from the ventral wall of the brain. These cells_u corresponding in origin to cells of the neuroglia, give rise to the Schwann sheath of nerve fibers. (For various theories of the histogenesis of the peripheral nervous system-see Neuronal theory.) The central nervous system of vertebrates is built on a special type, differing significantly from the nervous system of invertebrates. If in the latter it also develops as a rule in the outer embryonic leaf, nevertheless its cellular elements form solid trunks or more often a series of nerve nodes isolated from each other, connected by a system of commissures. Only in vertebrates does a tubular central nervous system form, apparently as a result of further differentiation of a certain part of the sensory plate. The anterior end of the neural tube is connected with the oldest sense organ of vertebrates-the olfactory organ, and in this same area, through the differentiation of the lateral walls of the tube, the visual organs also develop. The development of these two most important sense organs led to the progressive development of the anterior part of the neural tube, which formed the oldest part of the brain, "archencephalon," which later divided into the primary forebrain and midbrain. Further behind, important sensory centers also developed in connection with special lateral line organs, and this, as well as the development of the visceral apparatus, led to the development of the primary hindbrain. In the system of lateral line organs, a special development occurred in a group of lateral head organs-they specialized as an organ of equilibrium, and later also as an organ for perceiving sound vibrations. The ear thus developed in turn had to influence the evolution of the central nervous system, especially the medulla oblongata. Thus, the isolation of the anterior part of the neural tube as the brain from the posterior part, i.e., from the spinal cord, is determined primarily by the location of the sense organs, and then also by the respiratory apparatus and the food-capturing apparatus in the head area. And during further evolution of vertebrates, this inextricable connection between the central nervous apparatus and its peripheral organs can be easily traced. For the brain and cerebellum in vertebrates-see Brain, Cerebellum. In the peripheral nervous system--in the ganglia, nerves and their branches--in lower vertebrates the segmental arrangement is more or less clearly expressed even in the head area. With the exception of the first two pairs of nerves, which occupy a special position, the other cranial nerves correspond in their development and functional composition partly to the ventral, motor roots (nerves of the eye muscles III, IV and VI pairs and the hypoglossal nerve), partly to the sensory roots or mixed spinal nerves (nerves V, VII, VIII, IX, X and XI pairs). In the trunk area, the dorsal and ventral roots are initially separate nerves (lancelet, * If. Anatomy of the Nervous System. The nervous system is divided into cerebro-spinal and autonomic, which in turn are subdivided into the central nervous system and the peripheral. The central nervous system includes the brain and spinal cord, i.e., those parts that are enclosed in bony coverings-in the skull and spine, and the peripheral nervous system includes all cranial and spinal nerves, starting from their roots and up to the endings of the nerves in the skin, muscles, etc., this also includes their plexuses, and in the autonomic nervous system also the trunks. See Varolian bridge, Autonomic nervous system, Brain, Cerebellum, Medulla oblongata, Spinal cord, the corresponding cranial nerves, large spinal nerves, the corresponding plexuses; histological structure and histopathology of the nervous system-see Nerve cells, Nerve fibers, Nerves, Nerve endings, Neuroglia, Neuronal theory, etc. III. Physiology of the Nervous System. Functions of the nervous system as a whole. The structure of the nervous system of humans and higher animals has a dual character. Its more complex cerebrospinal part consists of isolated highly differentiated neurons. The other autonomic part, retaining structural features of the nervous system of lower animals, represents a reticulated nerve syncytium with primitive ganglion cells included in it. Accordingly, the nervous system performs two basic functions. Its cerebrospinal part connects the sense organs with effector organs. Its role is in establishing relationships between the organism and the environment. The organism reacts to the influence of the external world with corresponding movements and thereby adapts to the conditions of existence. This is the biological "behavioral" function of the nervous system. The autonomic system (sympathetic and parasympathetic) performs a more modest, purely physiological role. Innervating smooth muscles, glands and other internal organs, it manages their work, regulates metabolic processes, growth, restitution, etc. (see Autonomic nervous system). The cerebrospinal and autonomic systems are parts of a single whole. They are connected with each other morphologically and functionally. Recently it has been shown that the same organs (skin, skeletal muscles) are supplied with both cerebrospinal and autonomic nerve fibers (the principle of dual innervation). Experiments by Orbeli and his colleagues established that a tired skeletal muscle resumes its work when stimulated by appropriate sympathetic fibers, which have a beneficial trophic effect on it. Moreover, apparently the cerebrospinal system itself is a kind of "executive organ" in relation to the autonomic system, which establishes the functional state of its neurons at one level or another. It follows that the autonomic system participates in the behavioral activity of the organism. But conversely, the cerebrospinal system can interfere with the work of autonomic organs. Thus, observations by hypnotists have shown that verbal suggestion, made under hypnosis, can have a powerful influence on the autonomic functions of the body (phenomena of "imaginary burning" and others). Thus, there is a relationship of interaction between the cerebrospinal and autonomic systems. The basic form of activity of both cerebrospinal and autonomic nerve centers is the reflex. A reflex is understood as the reaction of a nerve cell in response to excitation coming to it from the periphery. The reflex act of highly organized animals and human beings consists of the following moments: irritation is perceived by the corresponding sense organ (receptor); at this moment the physical or chemical energy of the stimulus is transformed into the energy of excitation, which is conducted along the centripetal fiber to a certain part of the brain; here, excitation, passing from neuron to neuron, switches to the centrifugal nerve conductor, which innervates the executive organ (effector)-a gland or muscle. As a result, the organism performs a certain movement, or secretion, more or less beneficial to it in a given situation. A reflex should be distinguished from the direct reaction of a nerve cell in response to the irritating action of some substance contained in the blood. An example is the work of the respiratory center, stimulated by the acidity of the blood. Automatic acts are a special case of interaction between the autonomic nervous system and the third guiding principle of the body-the endocrine system (see Internal secretion). Innervating the endocrine glands, the autonomic nervous system regulates the processes of hormone production. On the other hand, elements of the autonomic nervous system are the main point of action of the hormones themselves. Through the autonomic nervous system, and also apparently by direct action on the brain, muscles and internal organs, the endocrine system influences both the internal organs and the behavioral activity of the organism. Methods for studying nervous activity. The methodological techniques used in the physiology of the nervous system can be divided into two categories: 1) methods of action on nervous tissue, 2) methods of recording and analyzing its reaction to various influences. Both the first and the second, in turn, can be divided into two groups: a) physiological methods, in which special physiological apparatus is used, and b) biophysical, biochemical methods, in which apparatus borrowed from the richest arsenal of physics, as well as physical and organic chemistry is used. Methods of physiological action are various kinds of operations performed on the nervous system in situ-extirpations, cuts, ligatures, etc. These research techniques are used mainly in the private physiology of the nervous system and serve to clarify the functions of individual nervous structures. For the general physiology of the nervous system, the methods of physical or chemical action are of incomparably greater importance. These include various techniques for stimulating and damaging both the entire nervous system as a whole and its various isolated parts, for example methods of applying direct and alternating current, injections, irradiation, heating, cooling, etc. Nerve processes, in contrast to processes occurring in muscles and glands, do not have direct physiological detection.

Therefore, the nervous properties, states, and processes can only be judged indirectly—by the easily observable effects of those organs which are served by a given nervous formation. The accounting and analysis of such physiological indicators or indices of nervous activity are naturally conducted by physiological methods of research (recording muscle curves, counting drops, etc.). In this way, fundamental discoveries were made in the physiology of the N. s. An example can be the works of Vvedensky (indicator-muscle contraction) and Pavlov (indicator-secretion of salivary glands). In the N. s. itself, we can only capture physical, chemical, and physicochemical processes, adapting for this purpose the corresponding physical and chemical research methods. From the intensity and qualitative characteristics of these processes, we can judge the physiological states and changes in nervous tissue. Thus, these processes acquire the significance of physicochemical indicators of nervous activity. But special interest in the study of 'neurophysical' and 'neurochemical' processes is acquired because they are not only indicators but also those components from which physiological nervous processes are synthetically built. Physical processes in the nervous system. The N. s. produces electrical and thermal energy. Bioelectric phenomena have been known since the time of Galvani. If a pair of non-polarizing electrodes connected to a galvanometer are applied to an isolated nerve, so that one electrode touches the undamaged surface of the nerve and the other to an injured or killed part of it, the galvanometer will indicate the presence of a constant electric current. The direction of this current, called the current of rest, shows that the damaged part of the nerve is electronegative in relation to its normal parts. In other words, the tissue reacts to damage by developing a persistent negative charge. Not only a damaging agent, but any agent that causes even a slight and transient change in the excitability and conductivity of the nerve (e.g., a solution of some salt or poison) is already capable of changing its electrical state. A nerve area altered in this way becomes either electronegative or, in other cases, electropositive in relation to the undamaged parts of the same nerve. The alteration current observed in this case differs from the current of rest by its gradual increase and temporary nature: after the removal of the acting agent, the nerve returns to its original electrical and physiological state. Thus, every functional change in the nerve is accompanied by the development of an electrical potential, the intensity of which allows us to judge the nature and depth of the change. The basic fact is as follows: the current of rest undergoes a rapidly decreasing change in time whenever the nerve is brought into a state of excitation. Analysis of this phenomenon, called the current of action, shows that the excited point of the nerve, like the damaged area, is charged negatively. But this focus of electronegativity differs in its fleeting and mobile nature. Arising at the irritated point of the nerve, it does not remain there but, together with the excitation, moves along the nerve conductor in the form of a wave. All these phenomena in nerves were established by the famous founders of electrophysiology (Du Bois-Reymond, Hermann, Bernstein, Biedermann), but the most important of them—the electrical wave of excitation—became the object of direct observation only after Einthoven's string galvanometer (1903) was applied to the tasks of physiology. This instrument allows registering the fleeting waves passing through the nerve in the form of photographic curves. In our time, in many cases, even the string galvanometer is no longer sufficient. The action currents of the nerve are extremely weak; their power does not exceed several tenths of a microwatt. It was necessary to amplify them many times over in order to obtain electrograms suitable for precise study. This was achieved by the application of amplifying radio technology specially adapted for the purposes of electrophysiology, as well as by the use of various types of oscilloscopes. In this way, the exact form of a single electrical wave was established, and from it, the wave of excitation itself. The total duration of the electrical wave of the nerve (p. ischiadici of a frog at 20°) is 1.6 sigma, of which 0.4 sigma is spent on the rise of the curve and the rest of the time on the fall. The maximum voltage developed by the excited nerve reaches 25 mV (Rosenberg, 1927). Knowing the duration of the wave at a given point and its speed of propagation, it is not difficult to calculate its length. For the nerve, this value is 5.4 mm. It is clear that with rhythmic stimulation we have a whole series of such waves following one after another. It should be noted that the curve recorded when connecting the entire nerve as a whole to the galvanometer represents the result of the integration of hundreds and thousands of elementary electrical waves flowing in the individual nerve fibers of which the nerve is composed. Therefore, from such a curve we cannot yet judge the characteristics of the excitation wave in a single nerve element. Americans Gasser, Erlanger, and Bishop attempted to solve this problem by means of variational-statistical analysis of the integral curve of the nerve's action current. But the direct way to solve the question consisted in registering the action current from a single nerve fiber, which was recently achieved by Adrian (1926). Action currents for a long time served as the only direct indicator of the active state of nervous tissue. Therefore, they were studied with great diligence not only on the isolated nerve but also on various parts of the brain (starting with Caton, 1874). All the bioelectric phenomena described above were obtained when connecting to the galvanometer both the spinal and medulla oblongata, as well as the exposed cortex of the hemispheres of animals and humans (in the latter case in patients with skull defects). For example, stimulation of the eye by light or the ear by a sounding tuning fork causes action currents in the corresponding areas of the cortex, however, these have a more complex appearance than in the nerve. Such studies, on the one hand, make possible galvanometric research of cortical localization, on the other—allow us to judge the rhythm of excitations in nerve centers. Subsequently, it turned out that the rhythm of central excitation can also be studied with a simpler experimental setup—by connecting to the galvanometer motor nerves and muscles. In this way, Piper (1912) established that human muscles under conditions of voluntary innervation give 50 electrical excitation waves per second. This means that during a voluntary act, the brain itself works with a rhythm of 50 excitations per second. It is interesting that with physical fatigue this rhythm decreases to 25-35 per second (electrophysiological symptom of fatigue). In recent times, these phenomena have been studied in detail by Wachholder and Altenburger (from 1925). Thermal energy is produced by the nerve in negligible quantities. Therefore, it was possible to conduct fully reliable measurement experiments only recently in the famous laboratory of Hill. By an elaborate thermoelectric technique, it was established that 1 g of a resting nerve in 1 second releases about 0.0002 small calories of heat. With stimulation, heat production increases more than 3 times. At the same time, as in the muscle, heat production occurs in 2 phases: the initial phase coincides with the moment of applying the stimulus, the second, delayed phase lasts 9-10 minutes after the cessation of stimulation (Gerard, 1927). Theoretically important is that thermal and electrical energy develop in the excitable nerve in parallel with each other (Hill, 1927). Attempts to measure heat production in the brain in situ should be treated with special caution. The observed changes in brain temperature can often be reduced to changes in blood temperature or its distribution in the cerebral vessels. More reliable are experiments with the isolated brain (Baglioni, 1917). But from these experiments, according to Winterstein, only two conclusions can be made with certainty—that heat production occurs in nerve centers and that it increases with excitation. Recent research raises the question of the production of radiant energy by nervous tissue. The work of Vasiliev, Frank, and Goldenberg (1930) established that a nerve irritated by sectioning, like a contracting muscle and some other tissues, gives ultraviolet radiation in the form of mitogenetic rays of Gurvich (see Mitogenetic rays). The question of the production of electromagnetic waves by the brain (Lazarev and others) remains open. Chemical dynamics of the nerve process. The systematic study of the chemical dynamics of nervous tissue began only in 1900 with the works of Verworn and Winterstein. At present, we know that the central N. s. is the site of intense metabolic processes. Thus, an isolated frog brain at rest consumes 10% to 25% of the organic material contained in it within 24 hours. The exchange covers all groups of components of nervous tissue—carbohydrates, proteins, lipoids, and salts.

A special role belongs apparently to glucose, galactose, and cerebrosides containing galactose (cerebrin), as well as phosphatides (lecithin). By administering these substances to the preparation from outside, it is possible for some time to maintain in it a state of dynamic equilibrium of metabolic processes. The metabolic processes in the N. s. either have an oxidative nature in themselves or are at least closely connected in their course with oxidative processes, since with insufficient influx of oxygen, metabolism weakens and ceases altogether. In an oxygen-free environment, just as in the case of muscle, lactic acid is formed and accumulates from glucose, which however is not subjected to reverse synthesis into glucose. Among other metabolic products, carbon dioxide, phosphoric acid, and ammonia have so far been detected. All metabolic processes established for the central N. s. also occur in the peripheral nerve, but with significantly less intensity. The question of the qualitative features of metabolism in the brain compared to metabolism in the peripheral nerve has not yet been sufficiently studied. According to Winterstein's data, changes in the functional properties of nervous tissue are not in any definite relationship with changes in basal metabolism: excitability can increase without an increase in metabolic processes, and conversely, metabolic processes can intensify without a simultaneous increase in excitability. We have a different picture in the case of irritation. When nervous tissue passes into an active state, all chemical processes occurring in a state of rest are intensified and accelerated 2-3 times. For example, the frog's sciatic nerve in a state of rest absorbs 16 cm³ of oxygen per 1 g of its weight in 1 hour; when irritated by alternating current, it already absorbs 34 cm³, i.e., more than twice as much. With excessively prolonged irritation, this difference decreases by V₃ or more, which indicates nerve fatigue (Gerard and Meyerhof, 1927). These experiments show that irritation is closely connected with oxidative processes as a source of energy. But unlike muscle, the excitable nervous tissue, being in an oxygen-free environment, does not increase the content of lactic acid. Apparently, the process of irritation is not conditioned by its formation. A significant increase in ammonia production (by 2-3 times) indicates a connection between irritation and protein metabolism. Very important is the fact that during irritation, the respiratory coefficient of the nerve (i.e., the ratio of the amount of CO₂ released to the amount of O₂ absorbed) increases significantly (from 0.77 to 0.97). This allows us to assume that the chemistry of nervous tissue during irritation differs not only quantitatively but also qualitatively from the chemistry of resting tissue. Numerous attempts to establish the influence of mental work, i.e., excitation of the cerebral cortex centers, on the overall metabolism of the human body have so far remained unproductive and contradictory (Atwater and Benedict, 1917). In these experiments, it is very difficult to eliminate the involuntary movements and muscle tensions that, accompanying mental effort, can themselves increase gas exchange and thus serve as a source of error. Therefore, the most convincing should be considered those experiments in which, one way or another, immobilization of the subject was achieved. Grafe (1920-23), who studied the effect of strong emotions induced in hypnosis, with simultaneous suggestive exclusion of muscle activity, found that the overall gas exchange increases on average by 4-5. Much more striking results were obtained in the study of phosphorus metabolism in humans. Thus, Kestner and Knipping (1922) found that after intense mental work, the content of phosphoric acid in the blood increases on average by 100%. Laws of irritation and conduction. The most technically convenient and least damaging to tissue irritant is electric current. As early as 1859, Pfluger found that when a constant current is closed through a nerve, excitation occurs at the point of application of the cathode, which is replaced by a state of increased excitability; in the area of the anode, on the contrary, a decrease in nerve excitability (depression) is observed. These phenomena are called electrotonic. Dubois-Reymon (1849) made the first attempt to establish quantitative laws of irritation: to obtain a minimal physiological effect, the irritant must reach a certain magnitude (threshold of irritation); however, irritation is achieved not by the absolute strength of the current, but by fluctuations in its strength (more precisely, the density of current in the nerve). Dubois-Reymon gave this proposition a corresponding mathematical formulation. Later, however, it turned out that not only intensity and its fluctuations determine the irritating property of the agent: it can be very strong and yet not give the slightest signs of tissue excitation if it acts on it for too short a time. This observation served as a starting point for clarifying the true law of irritation, which states that there is a functional dependence between the strength of the irritating current and the time of its action, determining the conditions for achieving threshold irritation. Graphically, this dependence is expressed by a hyperbola of the type r = a/t + b, where r is the current strength, t is the time of its action, and a and b are constant quantities. This "hyperbolic law of irritation", established through the efforts of a number of outstanding physiologists (Hoorweg, Nernst, G. Weiss, etc.), allowed Lapicque (starting from 1901) to carry out a radical reform in the concept of excitability and in the methodology of its determination. Usually, the degree of excitability is determined by the magnitude of the irritating induction current, and this magnitude is expressed in conventional units of measurement - centimeters of distance between the primary and secondary coils of the induction coil; no attention is paid to the duration of irritation. By studying the excitability of various tissues in various representatives of the organic world, Lapicque showed that there are sharp differences between them in regard to the necessary duration of the irritant's action. In order to bring a frog's nerve or skeletal muscle into a state of excitation, it is sufficient for the irritant to act for only thousandths or ten-thousandths of a second. For the neuromuscular tissue of mollusks, hundredths of a second are necessary, and for the smooth muscles of different animals, already whole seconds. Thus, the same segment of time has different value for different organic formations. Each of them possesses its own chronaxia (time value). Lapicque's method of measuring excitability is as follows. First, the voltage of the current is found which, regardless of the duration of its action, causes signs of nerve excitation. This magnitude, corresponding to the usual threshold of irritation but expressed in volts, Lapicque calls the rheobase (current base). Then, taking twice the rheobase, with the help of special apparatus, the smallest time is found at which this current causes threshold excitation. This time, expressed in fractions of a second, is the chronaxia. Thus, the threshold of irritation, and with it the degree of excitability, is determined by Lapicque not univocally, as was done before him, but bivalently - by the magnitudes of rheobase (threshold of intensity) and chronaxia (threshold of duration). Chronaxia is a new and extremely characteristic indicator of the functional state of tissues. In 1915, Lapicque proposed a method for determining the chronaxia of human nerves and muscles, and the neurologist Bourguignon widely used it for clinical purposes. It turned out that a nerve and the muscle innervated by it have the same chronaxia (of the order of ten-thousandths of a second). Synergists have the same chronaxia (isochronia). On the contrary, antagonists have different chronaxias (heterochronia), and the nerves serving flexors have a smaller chronaxia than the nerves serving extensors. At present, a wealth of material has been accumulated on the study of normal chronaxia of various human nerves, muscles, and sense organs, as well as deviations from the norm in nerve degeneration, neuroses, mental diseases, physical fatigue, etc. These data have great diagnostic significance and can serve as an example of the fruitful use of the achievements of theoretical physiology for practical purposes. The next cardinal question is what is the connection between the strength of irritation and the magnitude of the physiological response. An elementary experiment on a nerve-muscle preparation shows that with an increase in nerve irritation, the height of muscle contractions increases up to a certain maximum, above which they cannot rise. On this basis, some physiologists have claimed (Vvedensky) and continue to claim that within certain limits there is a gradational dependence between the strength of irritation and the intensity of excitation: excitation in each individual nerve fiber can be greater or lesser in intensity, depending on the strength of irritation. Some authors have tried to find a logarithmic dependence here, identical to the psychophysical Weber-Fechner law (Preyer, Pfeffer).

However, Gotch (1902), and after him the workers of the Cambridge school (Keith, Lucas, Adrian), developed the opposite view, which is now shared by most physiologists: between the strength of stimulation and the magnitude of excitation in a single nerve fiber there is an alternative relationship—either stimulation gives no excitation at all (if it does not reach the threshold) or it immediately gives the maximum effect (if it reaches the threshold). In the occurrence of excitation there is no 'more or less', there is 'all or nothing'. The fact of an increase in physiological effect with stronger stimulation is explained by the unequal excitability of the nerve fibers composing the nerve: with threshold stimulation only a few, the most excitable fibers are excited—hence the barely noticeable effect; with stronger stimulation a larger number of fibers are involved, and the effect becomes greater; finally, with maximum stimulation all fibers are excited, which leads to the maximum possible effect. In recent times this view has received a number of confirmations, the most important of which was given by Adrian (1927); the amplitude of action currents conducted from a single nerve fiber remains unchanged with stimulations of different strength; with increasing stimulation only the rhythm of the elicited action currents increases. However, the dispute between representatives of the two directions is still not concluded. The passage of the excitation wave through a given point of the nerve does not remain without influence on its functional properties: the excitability and conductivity of the excited point fall to zero. This phenomenon is known as the absolute refractory phase. From the state of excitation the tissue automatically passes to the state of rest, and its functional properties first gradually increase to the original level (relative refractory phase), then exceed it (supernormal phase), and finally return to normal. For the nerve (sciatic nerve of the frog at 15°) the duration of these phases has been accurately measured: absolute refractoriness covers the time interval from 0 to 0.003 sec., counting from the moment of application of stimulation, relative refractoriness—from 0.003 to 0.015 sec.; supernormal—from 0.015 to 0.030 seconds (K. Lucas). Thus in the course of the excitation process two periods can be distinguished: the transition from rest to excitation, coinciding with the absolute refractory phase, and the longer restorative (or compensatory) period, including the relative refractory and supernormal phases. According to the latest data of Amberson and Downing (1929) the restorative period ends only after 0.1-0.2 sec., and is accompanied by the development of weak electropositivity (positive after-effect of Hering). The phenomenon of the refractory phase has enormous theoretical significance. It explains the rhythmic character of the excitation process; its duration determines the so-called intrinsic rhythm of excitation of various tissues, as well as the greater or lesser ability to reproduce the rhythm of stimulation, i.e., the elementary functional mobility. The laws of conduction can be expressed in the following propositions. From the stimulated point excitation spreads with equal ease in both directions; in other words, the nerve fiber possesses bidirectional conductivity, despite the fact that under natural conditions excitation waves are conducted in it always in only one direction (from the brain to the periphery or vice versa). Excitation spreading along a given fiber is not transmitted to other fibers of the same nerve (law of isolated conduction). Excitation waves, as well as their electrical component—the action current—are not transmitted through a ligated or killed section of the nerve. As for the speed of propagation of excitation, first measured by Helmholtz (1850), it reaches its maximum value in myelinated nerves of warm-blooded animals and humans (60-75 m/sec.); in the nerves of the frog it is two to three times less (20-30 m/sec.), and in the nerves of invertebrates (Anodonta) does not exceed 3-5 m/sec. It should be added that the nervous phenomena listed in this chapter are regularly related to each other. For example, the greater the conduction speed of the nerve, the higher its excitability and the shorter its chronaxia (Lapicque and Legendre, 1913). Theories of stimulation and conduction. Modern theories of nervous processes can be divided into two groups: physical (more precisely physicochemical) and purely chemical. The former trace their origin from Bernstein, Loeb, and Nernst and are currently being developed by Hober, Lazarev, and many others under the name of ionic theories of excitation. The mechanism of stimulation is depicted by these authors as follows. The nerve fiber represents a colloidal formation impregnated with an electrolyte, which contains various ions carrying positive (cations) and negative (anions) electric charges. The main role belongs to the cations. Some of them act in an exciting manner, others, on the contrary, in an inhibiting manner. Loeb, Lazarev, and others consider the monovalent cations of alkali metals (potassium and sodium) to be exciting, and the divalent cations of alkaline earth metals (calcium and magnesium) to be inhibiting. Bethe attributes the exciting action to hydrogen ions (H+). Any stimulus, e.g., an electric current, causes the movement of ions. On their path the moving ions encounter so-called semipermeable membranes, consisting of compacted colloids. Due to their low permeability, accumulation of the ions carried by the current occurs on them. If at the same time a predominance of more mobile exciting ions (increase in the so-called ionic coefficient of Loeb ~ = K, where C1 is the concentration of exciting ions, C2 is the concentration of inhibiting ions, and K is a constant value) arises, then the tissue is stimulated. If, on the contrary, there is a predominance of inhibiting ions (decrease in coefficient K), which for example occurs at the point of application of the anode, then the tissue enters a state of inhibition. In answer to the question why the accumulation of monovalent and divalent ions on colloidal membranes leads to opposite physiological effects, the following answer is given: exciting ions cause loosening (swelling) of the colloidal membranes, while inhibiting ions act on them in a compacting manner (coagulation). Thus the processes of stimulation and inhibition are reduced to reactions between tissue ions and colloids. What the colloidal membranes are, the change of which constitutes the essence of the nervous process, whether they are located on the surface of the axis cylinders or neurofibrils—opinions differ. Conduction of excitation along the nerve fiber from a physical point of view is accomplished by means of action currents, which, like the excitation itself, arise as a result of changes in ion concentrations (Hermann, Cremer). The supporters of this theory have defended their views since the time of Matteucci (1863) with experiments on artificial nerve models, on which they try to reproduce not only the electrical but also the physiological nerve processes. The greatest fame is enjoyed by the model constructed by Lillie (1919). It consists of a tube filled with strong nitric acid, along the axis of which runs an iron string. In strong nitric acid iron does not dissolve because on its surface a layer of higher oxides forms, protecting the iron from further action of the acid. The string represents a neurofibril, the acid represents the perifibrillar substance, and the oxide layer represents the membrane separating them. If in any way this layer is locally damaged, then in such an 'irritated point' a special electrochemical process arises, which spreads wave-like from it in both directions. This process, which in Lillie's opinion is analogous to excitation, spreads by means of vortex polarization currents, very similar to the action currents of the nerve. The speed of propagation is of the same order as in the nerve. The model has its own threshold of stimulation, its own chronaxia, refractory phase, obeys the 'all or nothing' law. But against the physical theories speak experiments with the measurement of the temperature coefficient of nerve processes. With an increase in temperature by 10° the speed of propagation of excitation and the course of the refractory phase increases almost twofold, which corresponds to the temperature coefficient of chemical reactions and significantly exceeds its value for physical processes: (Snyder). Even Pflüger compared excitation with the decomposition of an explosive substance. At present a similar view has supporters mainly among the followers of the Cambridge school (Adrian, Kato). In its most developed form we find the chemical theory in Beritov (1924). He bases his views on the concept of 'excitable substance', which according to the teaching of Ehrlich he considers a side chain branching off from the main nucleus of the molecule of living substance. The essence of excitation is in the transient, easily reversible decomposition of this molecule, more precisely—in the detachment of the side chain from its nucleus. Under the influence of the stimulus all the excitable substance contained in the nerve decomposes at once and completely (hence the 'all or nothing' law).

As long as all the substance remains decomposed, the nerve is unable to respond to a new irritation (refractory phase). The restoration of the decomposed substance does not occur immediately, and the more of it that has been restored, the higher the excitability becomes and the stronger the effects of the irritation (relative refractory phase). The amount of excitable substance depends on the conditions of metabolism: the more favorable they are, the more substance accumulates; and the more there is, the more intense and rapid the nerve process proceeds. All these attempts to reduce nerve phenomena either to physical or to chemical processes cannot be considered correct from a methodological point of view. The nerve process includes both electrical and thermal components, as well as ion-colloidal and purely chemical ones. The task is not to reduce it to one of these, but to show how from all these components a more complex and qualitatively different entity is synthetically formed—the physiological process of excitation. Features of central conduction. The conduction of excitation through nerve centers qualitatively differs from conduction along a nerve fiber. Sherrington (1911) lists the following features of conduction along a reflex arc: 1) The spread of excitation in the centers occurs more slowly than in the nerve. The experiments measuring the latent period of the reflex speak of central delay. The more complex the reflex, and the more nerve cells are included in its arc, the longer the latent period. 2) Centers have the ability to summate excitation: an effect is often not obtained from a single irritation, but a series of successive impulses, accumulating, produces an effect. 3) The intensity of the response to irritation little corresponds to the strength of the irritation: often a strong irritation produces a weaker effect than a weak one, or even remains without any response at all. This indicates the high inhibitory capacity of the centers. 4) The rhythm of the response to irritation often does not correspond to the rhythm of the irritation itself. Centers respond with their own inherent rhythm. 5) The duration of the response of the centers does not coincide with the duration of the irritation: a pronounced aftereffect is usually observed, which sometimes lasts for minutes or more. 6) Unlike the nerve, excitation is conducted along the reflex arc in only one direction (from the centripetal neuron to the centrifugal). This most characteristic property of central conduction is called irreceptivity. 7) The reflex arc exhibits fatigue phenomena, which are little characteristic of the nerve. 8) The activity of the centers depends incomparably more on the conditions of blood circulation (oxygen supply) and is much more sensitive to the action of poisons, hormones, etc. Some features of central conduction are also possessed by nerve endings. Thus, the property of irreceptivity, along with summation and inhibition phenomena, is exhibited by the end plate of a motor fiber, the so-called myoneural connection, which transmits excitation from the nerve to the muscle. Myoneural conduction is something intermediate between central and peripheral conduction. Theories of central conduction. Some physiologists believe that the features of central conduction can be artificially reproduced on a nerve fiber by locally changing its functional properties. This idea was first expressed by Vvedensky (1901) in connection with his theory of parabiosis. According to Vvedensky's data, centers have reduced functional mobility compared to the nerve (see above), and this difference accounts for many of their features. The functional mobility of a nerve, which normally reproduces up to 500 irritations per second, can be artificially altered by prolonged action of a physical or chemical agent. In this case, the nerve section being affected passes through a series of characteristic stages: 1) transforming, in which the nerve loses the ability to reproduce frequent rhythmic irritation, converting it to a lower rhythm (reduction of functional mobility); 2) paradoxical, in which strong and frequent irritations cease to produce a visible effect, while weak and rare ones are still able to cause it; 3) inhibitory, in which waves of excitation entering the altered section further deepen the developing decrease in excitability. With further action of the agent, the section completely loses its functional properties, which, however, can gradually be restored after the agent is removed, with the mentioned stages passing in reverse order. This state of the nerve, in which it temporarily acquires some features of the centers, Vvedensky called parabiosis. The same idea, that experiments with an altered nerve can be the key to understanding central phenomena, was expressed by Verworn. But this viewpoint was developed with particular consistency by the Cambridge school (K. Lucas, Adrian). A normal nerve fiber conducts a wave of excitation without decrement, i.e., its intensity does not decrease as it spreads along the nerve. In an altered section, on the contrary, the wave gradually weakens and dies out. The deeper the state of alteration and the longer the altered section, the more pronounced the decrement. Similar to an altered nerve section, areas of decremental conduction are nerve centers and endings. Using the concepts of decrement, refractory and supernormal phases in combination with the 'all or nothing' principle, Cambridge physiologists gave a theoretical interpretation of both central phenomena (summation and inhibition) and the parabiotic stages of Vvedensky. However, in more recent times, the Japanese scientist Kato (1924-26) subjected the doctrine of decrement to severe criticism: according to his data, an altered nerve section, like a normal one, possesses decrementless conduction. According to Sherrington, the features of central conduction are created not in the nerve cells themselves, but at the points of contact between neurons, in the so-called synapses. In the synapse, the existence of a separating membrane should be assumed, which can modify the process of conduction exactly as it is modified in the reflex arc. For example, the irreceptive conduction of excitation can be explained by the one-way permeability of the membrane with respect to exciting ions. We see here an attempt to construct a physical theory of central conduction. The same character is possessed by Lapic's hypothesis, according to which intercentral transmission of excitation occurs through the irritation of one neuron by the action currents of another. In this case, transmission occurs more easily the less the chronaxia values of neighboring neurons differ from each other (isochronism). If the chronaxia of one of them doubles compared to the chronaxia of another, transmission becomes impossible (heterochronism). With respect to myoneural conduction, Lapic confirmed these propositions with excellent experiments. The chemical theory of central conduction deserves special attention, based on the phenomenon recently discovered by Loewi (O. Loewi, 1921). Its essence consists in that the effects from irritation of an excitatory or inhibitory nerve of one animal are also manifested in another animal if the animals are under conditions of cross-circulation. For example, when the cardiac branch of the vagus nerve of one frog is irritated, an inhibitory effect is obtained on the heart of another. Obviously, when the vagus is irritated, a 'substance' is formed in its endings; this substance is released into the blood, which carries it to the organ of another animal. The same is true for sympathetic cardiac nerve fibers, the endings of which release a substance that stimulates cardiac activity. The existence of such humoral transmitters of excitation and inhibition was then proven, and it turned out that they belong to the category of organic substances. According to the assumption of Sherrington (1925) and I. Samoylov (1921), the same humoral transmission also occurs in synapses. Excitation ceases upon reaching the intercentral endings of the processes of the afferent neuron; but the excited endings release an 'exciting substance,' which, diffusing through the synapse, irritates the endings of the neighboring neuron. Thus, excitation does not spread continuously from neuron to neuron, but as if arises anew in each of them under the influence of intercentral chemical irritations. In the case of reflex inhibition, an 'inhibiting substance' arises in the synapse, which neutralizes the 'exciting' substance and thereby stops intercentral conduction. This theory explains many features of central conduction, in particular the phenomenon of irreceptivity. In the light of the methodology of dialectical materialism, the results obtained in experiments with altered nerves or with peripheral endings cannot be unconditionally used to explain central phenomena. These attempts should be treated with no less caution than the attempts to understand the nature of nerve conduction based on experiments with artificial models. Intercentral relationships. The most essential difference between peripheral and central processes is as follows: in the nerve—waves of excitation spread along its fibers in isolation and independently of each other.

The Central Nervous System, on the other hand, is an area of continuous interaction of nervous processes. The concept of a separate reflex arc is at times a convenient but artificial abstraction. In reality, reflexes and their centers enter into diverse relationships, form coordinating mechanisms, and unite into a harmonious whole called by Sherrington the integrating activity of the Nervous System. This researcher established the principal forms of interaction of spinal reflexes. The foundation of his doctrine is the principle of the common final path, the essence of which can be expressed in a few words. The initial part of any reflex arc is the receptor (afferent) neuron, connected with a specific sense organ. At the end of each arc is located the final (efferent) neuron, conducting excitation to the working organ-muscle or gland. Numerous afferent paths (there are significantly more of them than efferent ones) converge to the same efferent neuron, which thus serves for them not only as the final but also as the common path. If two afferent paths are excited simultaneously, then the motor neuron becomes a 'point of collision' of the excitations meeting in it. The result of such a collision of excitations can be different, obeying the regularities established by Sherrington. Let us note the most important of them: 1) Homogeneous simultaneously elicited reflexes reinforce each other in their action on the common final path. An example can be the following experiment on a dog with the spinal cord severed in the cervical region. Irritation of the skin surface of the shoulder, back, and sides causes a reflex scratching of the hind leg. When this reflex is elicited from any point in the indicated receptor field and at the same time another point of the same field is irritated, then the second irritation reinforces the action of the first. Such mutually reinforcing reflexes are called allied. Here, excitations coming from two points of the body are summed up in the motor neuron, which leads to an enhanced reaction. Reflexes that inhibit muscular activity can enter into the same relationship. In this case, the motor neuron becomes the site of summation of inhibitory impulses. 2) Heterogeneous simultaneously elicited reflexes, converging to their common final path, weaken and inhibit each other. Movement of the left paw, producing a scratching reflex in response to irritation of the left shoulder area _g is interrupted when the right paw is simultaneously irritated, although the irritation that caused the reflex remains in its former strength. Here, excitations converging in the common path inhibit each other. Such mutually incompatible reflexes are called antagonistic. 3) The same motor neuron can serve for the implementation of different antagonistic reflexes, which compete with each other for possession of it. Thanks to such competition, the reflex dominant at a given moment is replaced by another, this by a third, etc., depending on the demands of the moment. But at each given moment the common final path is used for one purpose. This constitutes its coordinating role. However, the most important coordinating mechanism is the so-called reciprocal, i.e., mutual innervation of antagonistic muscles. When the centers of a given muscle group (e.g., flexors) are excited, the centers of antagonists (extensors) are inhibited. Thanks to this, oppositely acting muscles never interfere with each other in their work. Sherrington considers this phenomenon as a special case of the principle of the common final path, however, its intimate mechanism remains to this day unsolved (see Innervation). A special case of intercentral relationships is the phenomenon of dominance. Under dominance Uktomsky (1923) understands a temporarily arising state of nerve cells with increased excitability and the ability to accumulate excitation. Thanks to this, an area of stable excitation is created in the central Nervous System, which exerts a powerful influence on the course of other central processes. This influence is expressed, first, in the tendency of newly arising excitations to be directed to the dominant center, to reinforce its excited state and to switch to the associated efferent path (the rule of reinforcement of dominance); second, in the tendency of the dominance itself to inhibit the centers surrounding it (the rule of associated inhibition). Dominance can be created artificially, by prolonged irritation of the centripetal nerve or by local poisoning of the brain with a substance that raises its excitability. An example of a naturally arising dominance is provided by observations on the male spring frog: any irritation causes in it a weakened local reaction, but instead strengthens the embracing reflex, in the centers of which under the influence of the sex hormone a dominant focus is created. The opposite of the principle of dominance is another principle of intercentral relationships established by Uexkull: arising excitations have a tendency to be directed not to the most active, but to the most resting at a given moment center. Uktomsky points out that one principle does not exclude the other: each of them can have its place at different moments of the organism's existence. Intercentral relationships in the cerebral cortex were studied by the school of Pavlov and then of Bekhterev. The formation of a conditioned reflex occurs due to the closure of a temporary connection between two simultaneously excited centers. New connections give new reactions of the organism to environmental influences. Clarification of the laws of emergence, extinction, and interaction of such individually acquired reactions led to a physiological explanation of many aspects of animal behavior (see Conditioned Reflexes). In intercentral relationships, phenomena of inhibition play no less a role than phenomena of excitation. Pavlov recognizes inhibition as a special physiological process, capable, like excitation, of spreading along nerve paths. In the cortex, with special prominence, stands out the general property of nerve-center work-its contrastiveness: in the same center excitation has a tendency to pass into its opposite-inhibition and vice versa; excitation of some centers causes associated inhibition of other centers and vice versa. These phenomena, discovered by Fursov in the cerebral cortex, were described by Sherrington under the name of spinal induction. It can be said that centers influence each other not only by means of irradiating excitations and inhibitions, but also by means of associated contrast changes in excitability. We cannot here dwell on the highest manifestation of nervous activity-mentality. 'Each new step in physiology of intercentral relationships at its time was used to explain this or that nerve-psychic phenomenon. Thus, Sherrington saw the basis of attention in 'the interference of heterogeneous reflexes and in the cooperation of homogeneous ones.' Uktomsky approached attention and some other psychic acts from the point of view of the principle of dominance. A few years ago, the assertion that in the conditioned reflex the nervous mechanism of psychic phenomena has been found enjoyed wide recognition. According to Bekhterev, thought is an inhibited conditioned reflex. Some followers of Pavlov went even further, trying to reduce even the creative activity of man to the regularities established on the conditioned salivary reflexes of the dog (Savich). This once again expressed the harmful tendency of the mechanistic methodology, already noted by us twice, to reduce the complex to the regularities of the simple. The conditioned reflex apparently represents a relatively simple and not only cortical mechanism. The basic conditioned-reflex regularities were discovered in animals lacking a cortex, e.g., in fish (Frolov). According to the latest data of Zeleny (1930), conditioned reflexes can be formed in a dog completely deprived of cortex. Psychic phenomena are probably connected with more complex, as yet unknown to us types of cortical intercentral relationships. Brucke goes even further, believing that the cortex is the area of implementation not only of special intercentral relationships but also of special elementary processes, different from everything we know from the physiology of the nerve and the lower parts of the central Nervous System. Theories of Inhibition. On the question of the intimate nature of inhibition there exists a number of theories struggling with each other. It is firmly established that inhibition is not fatigue or exhaustion of nervous tissue. Hering (1884), Gaskell (1887) and many others asserted that inhibition is physiologically and physico-chemically opposite to excitation: the basis of the first lies in processes of assimilation, accompanied by the development of a positive electrical charge; the basis of the second-processes of dissimilation, associated with electro-negativity. In recent times, Sherrington has inclined to recognize the opposition between excitation and inhibition (theory of inhibiting and exciting substance, 1925). Followers of the Cambridge school derive inhibition from the phenomenon of the refractory phase (Kato).

Mac Dougall (1903) considered inhibition to be the result of an "outflow" of excitation as a certain energy from the inhibited centers. In a modified form, this theory was repeated by Beritov (1926) under the name of the "law of conjugate irradiation." The fourth group of authors considers inhibition as the result of interference (i.e., mutual extinction) of meeting excitation waves (Tsion, 1888; in more recent times Verworn, 1914) or as a modification of excitation (Vvedensky, 1901). The latter author brought inhibition closer to parabiosis, under which he understood the state of excessive, prolonged and as if frozen in place excitation, arising as a result of local overstimulation of nervous tissue. The same parabiotic phenomena that arise in a nerve under the action of any physical-chemical agent, in elements with reduced functional mobility (nerve centers and endings) can develop under the influence of a physiological agent—excessively strong and frequent nerve impulses. Thus, according to Vvedensky, the phenomena of central and peripheral inhibition represent a special case of parabiosis, and parabiosis itself is nothing other than modified excitation. In contrast to these "unitary" theories, Vasiliev (1925) raised the question of different types of inhibition (binary theory of inhibition). According to him, along with parabiotic-type inhibition, there exists an anti-parabiotic inhibition opposite to it in its physiological and physical-chemical nature. If the first is caused by an excessive increase in nerve functions, passing into "irritability weakness," then the second consists in a primary suppression of nerve functions, which however has nothing to do with fatigue. These types of inhibition compensate for each other and are opposite in relation to excitation: parabiosis deepens under the influence of incoming nerve impulses, while anti-parabiosis, on the contrary, is removed by them (disinhibition). One can think that various forms of contrast inhibition (including Pavlov's sleep inhibition) have an anti-parabiotic nature. Parabiotic inhibition develops in the central N. s. apparently only in emergency cases—with excessive general or local irritation, with experimental neurosis in animals (experiments of Razenkov and others), perhaps with hysteria, etc. Localization and functional plasticity. The tendency of previous years to see in the N. s. a kind of statistical machine, consisting of countless parts independent of each other, each performing its own, always the same work, is now being overcome. In the study of nervous activity, the moments of dynamism, integrity, and functional plasticity come to the forefront, which by no means excludes a certain localization of functions, especially primitive and phylogenetically old. In opposition to the doctrine of specifically stimulating and specifically inhibitory nerves and centers, Vvedensky developed the position according to which every nerve element can manifest itself both as exciting and as inhibiting, depending on the existing state of functional mobility in it, on the strength and frequency of the impulses coming to it. According to Sherrington, the same final common path can serve for different purposes, depending on which carrying neuron seizes it at a given moment. The principle of dominance by Ukhtomsky is in essence a doctrine of the temporary and mobile functions of the N. s., which arise, perform their work and then are replaced by others. The cerebral cortex according to Pavlov's view is an organ for developing new and new, continuously changing connections. At the same time, the idea of static localization of cortical functions is replaced by the view of mobile relationships between excited and inhibited centers. The concept introduced by Pavlov of a "mosaic" of foci of excitation and inhibition suffers from the usual mechanistic approach.

Experiments by Goltz, Magnus and many other authors have proven that, when certain parts of the nervous system are removed, the remaining parts often take over the functions of the lost parts, and thus functional disturbances are more or less compensated. All this indicates the high dynamism and plasticity of nervous activity. In this regard, the works of Minkowsky (1924) and Goldstein (1925) are of particular interest, in which data is presented in support of the view that every reaction of the organism is not determined by any single part of the brain, but is the resultant of the activity of the entire Nervous System as a whole. Clarifying the relationships between the individual and the whole, the static and the dynamic, the hereditarily fixed and the acquired in the course of experience constitutes one of the most important tasks of the physiology of the nervous system. Evolution of nervous activity. This problem, despite its paramount importance in methodological terms, has been little developed. It is based on the factual material of the comparative physiology of the Nervous System, which is closely related to comparative anatomy. Unfortunately, this discipline does not sufficiently attract the attention of physiologists, which leads to gross errors and distortions in various chapters of the physiology of the Nervous System, in particular in the doctrine of neurodynamics. The question can be divided into three parts: 1) evolution of elementary nervous processes, 2) evolution of features of central conduction, 3) evolution of intercentral relationships. A number of processes inherent in the primitive Nervous System we already find in Protozoa and in the simplest nerveless Metazoa: excitation, conduction of excitation, automatism and even an elementary form of coordination, observed in the movement of cilia of some infusoria. But in that case, what significance could the emergence of the Nervous System have? According to Brücke, the original role of the Nervous System consisted in increasing the excitability of the organism, sensitizing it to external and internal irritations. Experiments by Leba (1899) can serve as proof, showing that the excitability of the protoplasm of lower animals (ascidians) is significantly lower than the excitability of their nervous structures. The same can be said about the speed of conduction of excitations (Verworn). The evolution of nerve fiber proceeded in the direction of further increasing excitability and speed of conduction, which was accompanied by a decrease in chronaxy and duration of the refractory phase. In connection with this, the wave of excitation acquired an increasingly less prolonged character. At the same time, the intensity of metabolic processes also decreased, thanks to which the nerve conductor became less and less fatigable (Meyerhof and Schulz, 1929). These positions can be confirmed by a series of numerical data. The degree of perfection of the nerve conductor is closely related to the degree of its myelination: myelinated nerves possess incomparably better conducting properties than non-myelinated ones. However, it is incorrect to reduce the question exclusively to this factor: non-myelinated nerves of warm-blooded animals have a greater speed of conduction than the same nerves of cold-blooded animals. For example, the average speed of conduction of n. olfactorius in pike is on average 20 m/sec, and of non-myelinated nerves of flounder 50 m/sec. Apparently, the ontogenetic development of the functional properties of the nerve to a certain degree repeats the path traversed in phylogenesis. Thus, the chronaxy of n. radialis in a newborn by the second month of life decreases from 0.8 to 0.65 sigma, and by the twelfth month to 0.55 sigma (Banu et Bourguignon; 1921). The evolution of the functional properties of nerve fiber must have played a significant role in the adaptation of the organism to the environment. The faster and more accurately signals were transmitted from the sense organs to the primary centers and back to the working organs, the more perfect the reaction became. The reticular Nervous System of lower invertebrates contains ganglion cells, not yet separated from each other by synapses. Therefore, the features of central conduction observed in vertebrates are not expressed here at all. In such a nerve network, excitation spreads unimpeded in all directions. But already in sea anemones, the first signs of irreceptivity can be detected: in one direction excitation begins to be conducted faster than in the other. Distinct differences between central and peripheral conduction first appeared in vertebrates in connection with the formation of synapses. However, even in the highest of them, various reflex arcs are at different stages of development. Thus, centers of tendon reflexes are not capable of responding with their own rhythm of excitation to the impulses arriving at them. Such centers, retaining some features of peripheral conduction, Brücke calls passive, in contrast to active ones, in which the features of central conduction are fully expressed. But the main stream of evolution went along the line of complications of intercentral relationships. Ramón y Cajal long ago established that the higher the organization of the animal, the more dendrites its ganglion cells have; the largest number of them is characteristic of humans. One can think that with the improvement of morphological connections between neurons, the richness of intercentral relationships also increased. The high coordination of movements in many invertebrates, for example in insects, shows that even in them intercentral relationships have reached a high degree of perfection. Coordination presupposes the presence of central inhibition processes. Peripheral inhibition is expressed in a distinct form already in crustaceans. In invertebrates, however, the first rudiments of dominant phenomena are observed. The ability to form new intercentral connections depending on the conditions of individual life is a distinctive feature of vertebrates. This ability proved to be a new powerful means of adapting the organism to the environment, while at the same time forming the basis for the development of even more complex, but as yet little studied physiological 'mechanisms'. According to the data of the comparative physiology of conditioned reflexes (Tsitovich, Popov, Frolov), one can trace how gradually this ability was perfected in its evolution from fish to humans. We cannot say at what stage of the animal world psyche arose, since we do not know the forms of intercentral relationships with which it is connected. In the series of vertebrates, there is a progressive improvement in the localization of cortical functions. In birds, localization is barely expressed, in dogs and cats it is already manifested with full distinctness, but it reaches the greatest differentiation in humans and monkeys. A distinctive feature of humans is the ability not only to passively adapt to the conditions of existence, but also to actively adapt the environment to the needs of the individual and the collective in the process of the social labor activity characteristic of humans. In connection with this, we see in humans a striking development of motor functions and their organs—the cerebellum and those additional parts of the brain that received the name 'new brain' (neencephalon). Here, new functions—the most delicate and most diverse movements necessary for the performance of labor acts and various nuances of human speech—led to the accelerated development of the corresponding nerve apparatuses. The study of the ontogenesis of nervous functions is no less important. In the works of Shelovanov and his colleagues (starting from 1925), we find rich empirical material clarifying the features of nervous activity in newborn children and puppies and its further development during the first year of life. Perhaps it is difficult to find another area of biology in which the theory of evolution has played such a modest role to this day as in the physiology of the Nervous System. Evolution is of course recognized by physiologists as a fact, but by no means used as a method of explanation. And yet it is hardly any other organ that has undergone such a rapid and complex evolution as the Nervous System. If the contraction of a muscle of a holothurian, frog, dog is essentially one and the same problem, then the nervous activity in different animal types is each time a new problem. With even greater justification, the same can be said about man, whose nervous activity is formed under the influence of not so much biological as social factors, which play a leading role. Hence follows that methodological rule which is so often violated by physiologists: knowledge of the laws established only on the nervous system of lower animals is not sufficient for judging the activity of the nervous system of higher animals and even more so of man. The further progressive development of neurophysiology is possible only on the condition of the reconstruction of this area of knowledge on the basis of materialistic dialectics. Only under this condition will the factual material accumulated in enormous sizes be correctly used both practically and theoretically, the vitalistic and mechanistic directions in neurophysiology, so characteristic of the critical state of this science in the West and so abundantly nourished by the decaying capitalist system, will be overcome.

L. Vasiliev. IV. Pathology of the Nervous System. Corresponding to the main function of the nervous system, i.e., the implementation of motor reactions to external irritation, and corresponding to the main anatomical-physiological mechanism of the nervous system, presented in the form of a combination of receptor (sensory), connector (reflex), and effector (motor) apparatuses, all manifestations of nervous system function disorders can be reduced to sensory, motor, and reflex disorders. The anatomical basis of these disorders consists of destruction of fibers connecting the peripheral motor and sensory apparatuses with connector centers, or damage to these centers themselves; accordingly, the main problem in analyzing disorders of nervous system functions is establishing their dependence on impaired conductivity along nerve conductors (conductor disorders) or impaired function of connector centers (reflex, associative disorders). The physiological structure of the nervous system is characterized by a close functional connection between its various constituent apparatuses. Therefore, damage to an individual apparatus, in addition to the loss of its inherent function, in most cases leads to a number of changes in other nervous mechanisms physiologically related to the one damaged by the given pathological process. The main forms of interaction between different nervous apparatuses, as well as the influence of the nervous system on other organs, are the processes of stimulation and inhibition of functions. Thus, when a particular nervous apparatus is damaged by a pathological process, along with the loss or increase of its inherent function, a number of phenomena are usually observed, consisting of disruption of the normal processes of inhibition and stimulation from the damaged apparatus on other physiologically related ones. Among the factors determining the form of symptoms observed in diseases of the nervous system, the processes of phylogenetic and ontogenetic evolution of the nervous system play a significant role. The evolution of the nervous system is a gradual transition from simpler, automatic, innate forms of reactions to more complex, more conscious, forms acquired during individual life. The anatomical basis of this transformation of functions is the gradual superstructure over the primary, phylogenetically older segmental apparatus (spinal cord) of the mantle layer of the brain. In this superstructure of new cortical elements, phylogenetically older elements do not disappear completely, but only change their functions under the influence of impulses from the cerebral cortex. The essence of this influence of the cortex on the segmental apparatus consists not only in using the latter as an intermediate stage in communication between the cortex and peripheral organs, but also in suppressing the automatic functions inherent to the segmental apparatus: the cerebral cortex exerts an inhibitory influence on automatic, phylogenetically older subcortical mechanisms. This fact has extremely important significance for the symptomatology of nervous system diseases: in diseases of the suprasegmental apparatus, along with the loss of its inherent functions, restoration (of phylogenetically older) subcortical mechanisms is observed, which are in a latent state under normal conditions due to the inhibitory influence from the cerebral cortex. Many of the symptoms observed in diseases of phylogenetically newer parts of the nervous system represent nothing more than the manifestation in rudimentary form of the automatic mechanisms of phylogenetically older functions. In other words, in diseases of the suprasegmental apparatus, there is a regression of functions to a lower degree of evolution. This state of functional regression is denoted by the term 'dissolution,' i.e., the process opposite to evolution. Thus, the symptom complex of many lesions of the central nervous system, along with phenomena of loss and strengthening of functions due to the loss of stimulating and inhibitory impulses, is characterized by the appearance of phenomena not normally observed and representing rudiments of phylogenetically older functions; for example, various pathological reflexes (Babinski's symptom, Rossolimo's symptom, Mendel-Bechterew's symptom) represent rudiments of the grasping function of the foot, inherent to human ancestors, observed in the latter in infancy and then passing into a latent state in adults as the static function of the foot is developed. Among the phenomena of functional loss in diseases of the central nervous system, in addition to the direct loss or weakening of the activity of primarily affected centers or their conductors, attention should be paid to the phenomena of so-called diaschisis. The essence of the diaschisis theory, proposed by Monakow, is that the symptoms observed in focal lesions of any area of the brain depend not only on the impairment of function of this directly affected area, but also on other areas which, although undamaged themselves, have anatomical-physiological connections with the site of lesion. In these anatomically undamaged but connected with the lesion site areas, not only functions that depended on impulses coming from the affected area may be paralyzed, but also those that had a certain independence (see Diaschisis). An example of diaschisis can be the temporary loss of knee reflexes observed despite the complete integrity of the spinal cord in sudden extensive lesions of the brain ('flaccid paralysis' in the initial stages of apoplectic stroke); since the brain exerts a restraining influence on spinal reflexes, the elimination of its function should cause an intensification of knee reflexes, which is observed in later stages of hemiplegia; in its initial period, however, a temporary loss of autonomous reflex functions of the spinal cord is observed: the corresponding mechanisms must adapt to the new conditions that have arisen for them due to the cessation of function of elements that usually acted together with them. In their essence, the phenomena of diaschisis represent 'action at a distance,' but they have pathological-physiological causes as opposed to those forms of 'action at a distance' that depend on circulatory, mechanical, and toxic factors. Regarding the peculiarities of pathological-anatomical processes in the area of the nervous system, the following data deserve attention. In any damage to the nervous system, phagocytic activity of cellular elements is observed, capturing and removing products of nerve substance decomposition ('cleaner cells'). This phagocytic function is carried out, firstly, as in other tissues, by vascular lymphoid (mesodermal) elements, and secondly by specific to the nervous system glial (ectodermal) elements. The end products of nerve tissue decomposition captured by phagocytes are carried away through perivascular spaces into the cerebrospinal fluid. This explains the diagnostic importance of cerebrospinal fluid examination, which is the medium for removing products of nerve tissue decomposition. However, the role of glial elements in pathological processes in the nervous system is not exhausted by the removal of decomposition products. When defects in nerve substance are formed due to tissue decomposition, glial elements carry out the process of scar formation: in the area of nerve tissue decomposition, proliferation of glial cells occurs, which increase significantly in size and give off numerous processes ('astrocytes'). In subsequent stages of the recovery process, most cells reduce, and the proliferated fibers, forming dense bundles, fill the defect in nerve tissue, forming the so-called glial scar. Macroscopically, such areas of glial scarring give the impression of tissue wrinkling (hence the name 'sclerotic process'). The described dense glial scars, completely replacing the defect in nerve substance, are formed only in cases of minor tissue destructions. In more extensive destructions of nerve substance, complete filling of the resulting defect with a glial scar does not occur, and 'scarring' in such cases is limited to the formation of dense glial-scar tissue around the resulting cavity. The described process of 'sclerosing' nerve tissue by the development of glial fibers occurs not only in cases of gross damage to nerve tissue but also in the so-called 'secondary degenerations.' This term denotes the progressive decomposition of nerve fibers in cases of their disconnection from their corresponding cells or upon the death of the latter. Secondary degeneration is a trophic-degenerative process developing due to the deprivation of the nerve fiber of trophic influences from the cell. In secondary degeneration, the myelin substance decomposes first, while the fibrillar substance remains preserved for a long time. Such myelin-deprived nerve fibers are sometimes designated by the term 'bare axis cylinders'—a not entirely correct name, since the decomposing myelin is gradually replaced as it is destroyed by the finest glial fibers; thus.

In these cases, the 'bare' axons are only so in the sense of being deprived of their myelin sheath. The plaques that form the pathological-anatomical basis of multiple sclerosis are nothing more than the development of gliosclerotic hardening in areas where the myelin sheath has been destroyed, which in this disease affects nerve fibers not along their entire length, but in separate segments. In the pathology of the Nervous System, a significant role belongs to the peculiarities of the relationships between the Nervous System and various exogenous and endogenous pathogenic factors. At the earliest stages of phylogenetic and ontogenetic development, the central Nervous System penetrates deep into the organism and is isolated from the external environment; this isolation becomes more and more perfect. In this anatomical isolation of the central Nervous System lies its advantage over other tissues of the organism in terms of protection from pathogenic factors, but this is also the reason for the insufficient development of active protective adaptations by the nervous system against various harmful influences: having been placed by the course of evolution in conditions of isolation from external influences, the central Nervous System has not developed adaptations for the active struggle with these influences. The organs and tissues that isolate the central Nervous System from the external environment are for it not only a mechanical but also a biological barrier, and the fate of some diseases of the Nervous System is determined by the degree of participation of other tissues of the organism in the pathological process. These relationships are manifested with particular clarity in the course of infectious diseases of the Nervous System. The more primary the character of the infection of the Nervous System, i.e., the less pronounced the general symptoms or at least the symptoms from other organs, the greater the chances for this infection to turn into a chronically progressive disease; an example of this can be the antagonism between the skin manifestations of syphilis and parasyphilitic diseases of the central Nervous System, disseminated sclerosis, which is a chronically progressive disease not accompanied by any general phenomena, progressive diseases of the striatal system (parkinsonism) after mild cases of epidemic encephalitis, etc. Among the protective adaptations of the central Nervous System, mention should be made of the phenomenon of the so-called hemato-encephalic barrier (see Barrier function-hemato-encephalic barrier). The essence of this phenomenon is as follows: the permeability of the meninges for various substances is not the same in the direction from the blood into the cerebrospinal fluid and, conversely, from the fluid into the blood. Under normal conditions, the permeability of the meninges in the direction from the blood into the fluid is very limited: various medicinal substances, such as iodine, bromine, salicylate, mercury, arsenic, etc., preparations when taken orally or when injected into a vein, cannot be detected in the cerebrospinal fluid. Only with very large doses of some of these substances (for example, bromine and salicylate preparations) can the 'barrier' be disrupted. On the contrary, substances introduced into the cerebrospinal fluid easily penetrate into the blood. The above-mentioned impermeability of the meninges for the passage of substances dissolved in the blood into the cerebrospinal fluid is observed under normal conditions; in inflammatory processes in the meninges, the hemato-encephalic barrier is disrupted and those substances that under normal conditions do not penetrate from the blood into the cerebrospinal fluid can be found in the fluid after their introduction into the blood in various forms of meningitis. This fact of increased permeability of the meninges in acute meningitis was attempted to be used for therapeutic purposes: to enhance the effect of medicinal substances when administered internally or intravenously, artificial irritation of the meninges ('aseptic meningitis') was caused by the introduction of irritating substances into the subarachnoid space: a solution of salt, horse serum, etc. The hopes placed on this method of treatment have not yet been justified. This failure is probably explained by the fact that firstly, the permeability of the meninges that occurs in meningitis turns out to be insufficient for some substances, and secondly, due to the strong dissolution of medicinal substances in the blood, the amount that reaches the cerebrospinal fluid turns out to be insufficient for a therapeutic effect. Patho-anatomically, the lesions of the Nervous System can be divided into 1) direct destruction of nervous tissue under the influence of mechanical effects (trauma), vascular changes (hemorrhage in ruptured vessels, softening due to thrombosis or embolism); 2) inflammatory processes and 3) degenerative changes. Although transitional forms exist between all these forms of lesions and although in their essence inflammatory and degenerative processes represent only different degrees of reaction of nervous tissue to harmful influences, in their extreme manifestations inflammatory and degenerative diseases of the Nervous System differ in the following features: inflammatory processes affect the Nervous System in the form of more or less diffuse foci, while degenerative processes show selective relationship to certain anatomical-physiological systems. In the etiology of inflammatory diseases, exogenous factors predominate (infection); on the contrary, degenerative processes have as their main etiological factor the congenital inadequacy of certain apparatuses. Inflammatory diseases give the maximum of phenomena at the beginning and then end in recovery or recovery with defect; on the contrary, degenerative processes give a minimum of phenomena at first, but progress more or less sharply in their further course. A typical example of degenerative systemic diseases in the motor area are progressive muscular atrophies (spinal, neural, dystrophia musculorum, progressive bulbar paralysis, amyotrophic lateral sclerosis); in the sensory area-tabes dorsalis; combined (sensory and motor) degenerations: funicular myelitis (degeneration of the motor conductor and posterior columns), Friedreich's disease (degeneration of the central motor conductor, posterior columns and cerebellar centripetal conductors). Inflammatory processes in acute and chronic form are observed in the Nervous System in its infectious diseases. Infectious diseases of the Nervous System are usually divided according to the way pathogenic agents penetrate into it into secondary ones, in which the infection of the Nervous System is a complication of various general infectious diseases (lesions of the peripheral or central Nervous System in typhus, scarlet fever, diphtheria, measles, etc.), and primary ones, in which the infection directly penetrates into the Nervous System without causing diseases of other organs. The paths of penetration of infection in primary infections are the lymphatic and circulatory system and, as this is with certainty proven at least for some infections, the peripheral nerves. Primary infections of the Nervous System are caused mainly by neurotropic virus. Among the primary diseases are acute poliomyelitis (Heine-Medin disease), epidemic encephalitis, herpes zoster, post-vaccinal encephalitis, rabies, tetanus. Of the chronic infections of the Nervous System, tuberculosis and syphilis are of the greatest importance. Tuberculous lesions of the Nervous System constitute about 10% of all non-pulmonary tuberculosis diseases. The possibility of 'primary' tuberculosis of the Nervous System is questionable; as a rule, tuberculosis of the Nervous System is a secondary disease, i.e., a complication of an existing tuberculosis focus in some other part of the body. From a pathological-anatomical point of view, tuberculous lesion of the Nervous System can be diffuse (tuberculous meningitis) or limited (isolated tuberculosis, tuberculous encephalitis); in some cases, the Nervous System is damaged due to compression by the products of tuberculous lesions of neighboring areas without the spread of the tuberculous process to the nervous tissue (compression of the spinal cord in tuberculous spondylitis, see below). The most common form of tuberculous disease of the Nervous System is diffuse tuberculous meningitis (see Meningitis, tuberculous meningitis). Much rarer is limited meningoencephalitis. Isolated tuberculosis is a conglomerate of tuberculous neoplasms of very different sizes (from a pea to a fist); its source is usually the vessel wall. The tuberculoma is well demarcated from the surrounding brain tissue, but softening is usually observed in the latter. Isolated tuberculoma is often multiple. In its center, caseous decay is usually observed. The outcomes of the tuberculoma are suppuration, in rare cases calcification, but most often tuberculous meningitis. Clinically, isolated tuberculoma proceeds as a tumor ('tuberculoma') and is observed quite frequently in childhood. Among 'tumors' of the brain in childhood, tuberculoma occupies the first place in frequency; the most common localization of tuberculoma is the cerebellum and the brainstem. The possibility of surgical removal of a brain tuberculoma is not excluded, but it should be borne in mind that surgical intervention in this case is always associated with a great risk in terms of the development of tuberculous meningitis.

In the spinal cord, isolated tuberculosis is observed much less frequently than in the brain; it usually originates from the gray matter of the spinal cord, clinically leading to a picture of an intramedullary tumor. The most common form of tuberculous disease of the spinal cord is its compression in tuberculous spondylitis (see). Tuberculous lesions of peripheral nerves in the form of toxic or infectious mono- and polyneuritis are a rare phenomenon: out of 2,000 patients in one sanatorium, 2 cases of neuritis of the musculo-cutaneous nerve, 1 of the median nerve, and 6 polyneuritis cases were observed, of which 3 developed after artificial pneumothorax (Levy-Valensi); mononeuritis resulting from the direct spread of the tuberculous process to neighboring tissues are observed somewhat more frequently; to this category of lesions belong root symptoms in tuberculous spondylitis, paralysis of cranial nerves in tuberculous meningitis, and the frequently observed lesions of the cervical plexus in tuberculous lymphadenitis of the neck glands. Syphilis represents the most common form of lesions of the N. s., especially if, in addition to syphilitic lesions in the narrow sense, one has in mind metasyphilitic diseases (see Metasyphilis) and deviations in the development of the N. s. in congenital syphilis. The patho-anatomical changes underlying syphilitic lesions of the central N. s. can be reduced to the following phenomena: 1) specific changes in the walls of blood vessels in the form of endarteriitis syphilitica, leading to thrombosis of cerebral vessels and softening of brain substance; 2) luetic inflammation of the meninges and brain substance, characterized by infiltration and the formation of miliary gummas (meningo-encephalitis and meningo-myelitis syphilitica) [see separate table (pp. 135-136), figure 2]; 3) syphilitic inflammation of the roots of cranial or spinal nerves (radiculitis syphilitica); 4) gumma of the brain or spinal cord. In most cases of syphilis of the central N. s., there is a combination of the aforementioned patho-anatomical changes, and only for practical convenience, depending on the predominance of certain symptoms in the clinical picture, such forms as meningitis basilaris, meningo-encephalitis convexitatis, meningo-radiculitis, etc., are clinically isolated. However, vascular syphilitic changes are often observed without there being inflammatory processes in the brain substance or meninges. Syphilis of the central N. s. usually develops in the first years after infection: 60% of all cases of lues cerebro-spinalis occur in the first five-year period. The percentage of diseases of the N. s. with syphilis in relation to the total number of syphilitic patients does not exceed 2-3%, but due to the widespread prevalence of syphilis, the absolute number of patients with cerebral syphilis is quite significant. Antiluetic agents are effective both preventively and therapeutically in luetic lesions, in contrast to metasyphilitic ones, which cannot be prevented or eliminated by antiluetic treatment. Clinically, syphilis of the central N. s. manifests with various symptoms of irritation and loss of motor and sensory functions. In particular, the clinical picture of various syphilitic diseases of the central N. s. is characterized by the following features: 1. Endarteriitis syphilitica - acute development of cerebral stroke of the thrombosis type with subsequent focal loss of functions (hemiplegia, aphasia, hemianopia, etc.) depending on the localization of the softening caused by the occlusion of the vessel. 2. Meningitis (meningo-encephalo-radiculitis) basilaris - headaches, severe pain on percussion of the skull, Kernig's symptom, tension of the occipital muscles, sometimes changes in the fundus of the eye, paralysis of cranial nerves (oculomotorius, facialis, etc.). 3. Meningo-encephalitis convexitatis - slowly progressive focal symptoms; often Jacksonian seizures, headaches, localized pain on percussion of the skull. 4. Gumma gives a picture of a tumor in fresh cases - rapid improvement under the influence of antiluetic treatment. 5. Meningo-myelitis syphilitica - acutely developing picture of spinal cord lesion, usually with meningeal and root symptoms. The accessibility of syphilitic lesions of the central N. s. to antiluetic treatment depends on their nature and stage of development. Softenings due to thrombosis cannot of course be eliminated by antiluetic treatment; inflammatory changes and gumma respond well to treatment in the initial stages of their development, before irreversible changes in the brain substance have occurred under the influence of prolonged compression and fibrous neoplasms. In contrast to the frequency of lesions of the central N. s., syphilitic lesions of peripheral nerves are a rarity, if one does not count the secondary involvement of the roots of cranial nerves in the pathological process in syphilitic diseases of the brain and spinal cord: Syphilitic polyneuritis is an extremely rare phenomenon; very few cases described in the literature are disputed as to their purely syphilitic nature, and many authors believe that the true cause of polyneuritis in these cases was other factors (mercury poisoning, alcohol, accidental infection, etc.). Mononeuritis resulting from involvement in luetic inflammation of the roots of cranial and spinal nerves in luetic meningitis are observed much more frequently. Most cases of isolated paralysis of cranial nerves (oculomotorius, abducens, facialis), so frequently observed in syphilis, apparently also belong to the category of such root neuritis. Among metasyphilitic lesions of nerves, the greatest importance in terms of frequency and specificity is the Argyll-Robertson symptom, the essence of which is the selective lesion of fibers of the nervus oculomotorius innervating the pupillary sphincter, with preservation of other fibers of this nerve. To the category of metasyphilitic neuritis should also be attributed the paralysis of cranial (oculomotorius, abducens) and spinal (ulnaris, peronaeus) nerves observed in the course of tabes dorsalis. Regarding diseases of the N. s. on the basis of congenital syphilis, two categories of phenomena should be distinguished. One of them consists of specific symptoms of syphilis as a result of direct infection with syphilis in utero; the second consists of blastophorous influences (see Blastophoria), i.e., anomalies in the development of the N. s. of the fetus due to damage, "devitalization" of the parental germ plasma. As for the first group of phenomena, all the lesions of the N. s. mentioned above, characteristic of acquired syphilis, can also be observed in congenital syphilis, and some of them may develop during intrauterine life; this is indisputably proven in relation to syphilitic endarteritis and meningitis. Thrombosis of cerebral vessels due to syphilitic endarteritis is one of the causes of the so-called "cerebral palsy" of childhood. Mild forms of luetic meningitis experienced in utero can be the cause of subsequent hydrocephalus developing later; in many cases, however, hydrocephalus is observed from birth. Sometimes congenital syphilis is an indirect cause of brain diseases: in premature births, the symptom complex of Little's disease can develop as a result of hypogenesis of the cortex, and not specifically luetic lesion of it. Metasyphilitic diseases of the N. s. in childhood (tabes, progressive paralysis) are more often caused by congenital syphilis. In congenital syphilitics, isolated symptoms of pupillary immobility to light are often observed. Among metasyphilitic diseases on the basis of congenital syphilis, one can also mention progressive atrophy of the visual and auditory nerves. Blastophorous anomalies of the N. s. in congenital syphilis are characterized by the absence of specific anatomical changes in them; they are either hypoplastic changes or symptom complexes without definite structural changes. "This includes agenesis of nuclei of cranial nerves, developmental defects of the cerebral cortex. With some justification, manifestations of congenital syphilis can be attributed to some cases of psychopathic constitution, mental retardation, epilepsy. Some authors (Kraepelin, Pilcz, Toporkov) expressed the view on the role of congenital syphilis in the pathogenesis of schizophrenia. Vascular lesions represent a very common form of diseases of the central N. s. (see also Brain). The reason for the frequency of cerebral hemorrhages lies in the peculiarities of the structure of cerebral vessels: for adequate blood supply to brain areas without sharp pulsatory contractions of large-caliber vessels in the depth of the brain, it is supplied with thin vessels branching directly from large-caliber vascular trunks; this peculiarity concerns the arteries supplying the large ganglia of the base and the internal capsule: aa. lenticulo-striatae and lenticulo-opticae; these very thin vessels branch off as almost vertical branches from a large-caliber vessel (a. cerebri media).

Thanks to such a sudden departure from a large vessel of small branches, the latter have a relatively high pressure, which especially contributes to the early change in the walls of these small vessels, and in the presence of even mild sclerotic changes, such vessels, due to the loss of elasticity, are especially prone to rupture. All this explains the fact that cerebral hemorrhages are most often observed in the area of the large ganglia of the base and the internal capsule, and the arteries supplying this area are designated by the term 'cerebral hemorrhage arteries'. The main factors of cerebral hemorrhages are changes in the vascular walls (loss of elasticity, violation of integrity due to atheromatous process) and high blood pressure. Thrombosis of cerebral vessels is based on changes in the vascular walls, increased blood clotting and low blood pressure. The most common form of changes in the vascular walls leading to thrombosis is luetic endarteritis; representing a productive process, luetic endarteritis causes narrowing of the vessel lumen, in which complete occlusion can very easily occur [see separate table (art. 135-136), figure 1]. However, thromboses are not uncommon in sclerotic changes of vessels, especially in those periods when there is low blood pressure. Embolism represents the rarest form of vascular lesions of the brain. Usually the material for embolism is a fragment of fibrin from the surface of endocarditically changed heart valve. Most often embolies are observed in stenosis of the mitral opening, less frequently in diseases of the aorta. The source of the embolus can also be the left auricle in mitral defects; if in such cases there is increased blood clotting (acute articular rheumatism, pregnancy, childbirth period), a thrombus can form with subsequent detachment of fibrin particles. Such is the origin of most hemiplegias occurring in the childbirth period. Finally, the cause of embolism of cerebral vessels can be destructive processes of the lung with particles of lung tissue entering the left heart through the pulmonary veins. In contrast to the frequency of vascular diseases of the brain in the spinal cord, such lesions are rare: hemorrhages into the spinal cord are observed almost exclusively in traumatic injuries, thromboses of spinal cord vessels are a not uncommon concomitant phenomenon in syphilitic lesions of the spinal cord. Cysts of brain tissue in the sense of formation in it cavities filled with fluid represent a fairly common phenomenon. By their nature, these cyst-like fluid accumulations can be very different. First of all, it should be borne in mind that in various destructive processes in the brain, e.g. in hemorrhages and softenings, occurring after the resorption of the destroyed substance, the cavities are not filled with a solid scar, as is observed in other tissues, but are filled with fluid. This phenomenon results in the formation of the so-called 'postapoplectic cyst'. Such 'secondary' cysts are sometimes formed in the substance of brain tumors, mainly gliomas, due to hemorrhages in them or necrotic processes; sometimes such cystic transformations of glioma reach significant sizes: almost the entire tumor turns into a cavity, and only its wall represents a thin layer of gliomatous substance. In gliomas, other types of cystic formations lined with cylindrical epithelium are also observed; they are considered as formations corresponding to the remains of the embryonic brain tube. The presence of such cysts in gliomas gave rise to the assumption about the origin of gliomas from the remains of embryonic nerve cells. Cystic cavities are also characteristic of tumors growing from the anterior part of the pituitary gland due to the remains of cells lining the wall of the embryonic canal connecting the pharyngeal cavity with the cranial cavity (canalis cranio-pharyngealis); such tumors, usually located above the sella turcica, contain cystic cavities. Among the cystic formations of the N. s. should be mentioned the accumulations of fluid in the encapsulated cavities of the subarachnoid space [meningitis serosa chronica cystica circumscripta (see Meningitis, serous meningitis)]; such 'cysts of the membranes' can be observed in both the brain and spinal cord. Finally, in the form of cystic neoplasms, cysticercus and echinococcus of the central nervous system proceed. Tumors (see also Brain) represent one of the fairly common forms of diseases of the central N. s: on the contrary, tumors of peripheral nerves are a relatively rare disease. Brain tumors rank second in frequency only to vascular lesions and syphilis. In the spinal cord, tumors represent the most common cause of the compression symptom complex, not yielding in this respect to tuberculous spondylitis. The overwhelming majority of tumors of the central N. system are primary; metastatic tumors in the brain constitute only 4% (statistics of Cushing, covering 1,398 cases); metastatic brain tumors include cancer, sarcoma, hypernephroma. Among the primary tumors, the first place in frequency belongs to gliomas (42% of all brain tumors); followed by pituitary adenomas, endotheliomas (meningiomas), growing from special connective tissue cells of the arachnoid membrane, in places of its penetration into the dura mater (villi, Pacchionian granulations); a fairly common form are tumors growing from the perineurium and endoneurium of the roots of cranial and spinal nerves; most often such neurinomas are observed in the auditory nerve (so-called neurinoma acustici), but they can also develop in other cranial nerves (trigeminus, opticus), as well as in the roots of spinal nerves (more often in the posterior ones), and also in peripheral nerve trunks. Among the rarer brain tumors are cavernomas, cholesteatomas, teratomas, etc. The etiology of tumors of the N. s., like tumors in general, seems to be little clarified. The once expressed view on the role of trauma in the etiology of brain tumors has not been confirmed by observations of the wounded during the world war. From a clinical point of view, to brain tumors can be attributed the cystic forms of tapeworms Taenia solium (cysticercus) and Echinococcus granulosus (echinococcus); patho-anatomically they can be identified with cystic neoplasms. The clinical picture of brain tumors consists of the so-called general and local phenomena. Under general phenomena are meant symptoms of violation of the vital activity of the brain, caused mainly by an increase in intracranial pressure; in addition to a number of subjective symptoms, the general phenomena include very important for the diagnosis of brain tumor changes from the fundus of the eye (stagnant papillas).- Under local symptoms are meant symptoms depending on the direct irritation or destruction of brain tissue by the growing tumor; these include paralysis, disorders of sensitivity, cortical convulsions, etc.- Spinal cord tumors from a clinical point of view are usually divided into extramedullary and intramedullary. The former are characterized by the onset with root pains followed by gradual compression of the spinal cord. Between the stage of root pains and complete transverse lesion of the spinal cord at a certain level, it is often possible to observe a period characterized by the picture of half-lesion of the spinal cord (Brown-Sequard symptom complex). Intramedullary tumors as a rule do not give root pains. Growing mainly from the gray matter of the spinal cord, they usually initially cause phenomena similar to syringomyelia, with a gradual transition to the picture of complete transverse lesion of the spinal cord at a certain limited level of it. Patho-anatomically, the most common forms of spinal cord tumors are sarcomas, fibromas, neurinomas, gliomas. A fairly common phenomenon in the pathology of the nervous system are atrophic processes. In most cases, however, atrophies within the N. s. are a change accompanying other pathological processes; therefore, both in clinical and patho-anatomical sense, most forms of atrophy of the N. s. have not acquired an independent nosological value. In many cases, atrophy represents only a certain stage in the breakdown of nervous tissue; such is, for example, ischemic atrophy preceding necrosis. In addition, it should be borne in mind that between simple atrophy, i.e. simple reduction of nerve elements, and a degenerative process with a reaction from the supporting tissue (glial scar), there are gradual transitions and borderline states. In general, both anatomically and clinically, the term 'atrophy' in the pathology of the N. s. turned out to be associated with processes and phenomena not always strictly corresponding to the content of this term.

Thus, 'atrophy of the optic nerves,' especially that form which develops after optic neuritis and stagnant papilla, does not represent atrophy in the strict sense of the word; likewise, the so-called senile atrophy of the brain is not a simple atrophy, but a result of vascular arteriosclerotic changes, or, if an independent process from arteriosclerosis, then in any case a complex phenomenon accompanied by specific changes (drusen), not entirely corresponding to the concept of simple atrophy. The so-called 'atrophy sclerosis' (microgyria), which forms the basis of many forms of cerebral palsy in children, also does not represent atrophy in the strict sense of the word; in this case, the matter is either a congenital developmental defect or a consequence of an inflammatory (encephalitic) disease; some forms of atrophic sclerosis have vascular changes at their basis. The forms closest to the concept of atrophy are various forms of primary degeneration; these include progressive nuclear degenerations, progressive ophthalmoplegia, progressive bulbar paralysis, and some cases of spinal muscular atrophy. These forms of disease have the character of primary changes, which are apparently based on conditions of congenital inadequacy of certain parts of the N. s. (abiotrophy).-True hypertrophies in the sense of uniform increase of various tissue elements in the N. s. are not observed. The term 'hypertrophy of the brain' existing in the pathology of the N. s. does not actually denote an increase of all elements, but rather the growth of neuroglia, leading to an increase in the volume and weight of the brain; clinically, this condition is expressed by various degrees of intellectual retardation, epileptoid seizures, and various focal symptoms. Injuries to the N. s., besides the direct destruction of nervous tissue, usually lead to a series of secondary anatomical changes; in the acute period, these changes consist of circulatory disorders (hemorrhages), edema, and inflammatory phenomena; in the subsequent period, along with the destruction of a certain part of the nervous tissue, in many cases, changes related to the regression of the consequences of injury acquire significance: scar processes, cyst formation, activation of dormant infection (abscesses), etc. In many cases, with injuries to the N. s., the destruction of a certain part of it is complicated by the introduction of foreign bodies into its substance. The possibility of these anatomical complications in injuries to the N. s. is the reason that the clinical symptoms observed in them are not exhausted by the phenomena of loss of functions corresponding directly to the area of the brain destroyed by the injury; sometimes the main significance in the clinical picture of injuries to the N. s. is acquired by symptoms that depend not on the direct destruction by the injury, but on the above-mentioned secondary anatomical changes that develop as complications in the acute period (encephalitis, meningitis, abscess) or as regression phenomena in subsequent stages (pressure and irritation from scars, foreign bodies, etc.). The most typical manifestations of such irritation in the area of the brain are cortical epilepsy seizures, and in the area of peripheral nerves—a specific symptom complex consisting of severe pains, vasomotor, and trophic changes. Professional diseases of the N. s. can be divided into two groups: one of them includes lesions of the central and peripheral N. s., associated with poisonings from toxic substances used or obtained in various professions (lead, carbon monoxide, manganese, mercury, benzene, etc.). The second group consists of the so-called professional neuroses, in the pathogenesis of which the main role belongs to the exhaustion of the neuromuscular apparatus due to its intensified functional use in the movements required for a given profession. Clinically, professional neuroses are expressed by convulsions, tremors, neuralgic pains, pareses; in some cases, there are combinations of these disorders, e.g., convulsions accompanied by pains, paretic weakness combined with tremors, etc. Professional neuroses are observed almost exclusively in individuals with a neuropathic constitution; they are characterized by the absence of organic symptoms (atrophy, loss of reflexes, etc.), as well as by the fact that the disorder itself is found, at least at the beginning of the disease, only in movements related to the given profession (act of writing, playing a musical instrument, etc.). In conclusion, it should be mentioned that certain clinical phenomena from the N. s. in the pre-death period and in the first moments after death should be mentioned. As physiology shows, the peripheral neuromuscular apparatus retains its excitability for a considerable time after being extracted from the body, i.e., after being deprived of its blood supply and the influence of the central nervous system. This fact is also manifested in the human body in the form of preservation of the mechanical excitability of muscles during the first hours after death. In the pre-death period, there is a gradual extinction of all associative (associative and reflex) functions, with reflexes disappearing in the reverse order of their ontogenetic development; thus, abdominal reflexes disappear very early, which in humans are developed only in the 6-7th month of extrauterine life; plantar reflexes also disappear early; supraorbital reflexes disappear quite late—closing of the eyelids when tapping over the medial edge of the eyebrows; the disappearance of these reflexes is almost a certain sign of approaching death. The moment of death is characterized by the complete disappearance of all reflexes. Meanwhile, the mechanical excitability of muscles, i.e., their contraction upon direct mechanical irritation (tapping with a hammer), in the first minutes after death turns out to be even somewhat increased, and then, gradually decreasing, persists in some muscles until the onset of RIGOR MORTIS. M. Astvatsaturov. Parasites of the N. s. The brain (in particular the brain) can be a place of normal or accidental habitation of animal parasites. A special parasite of the brain is the brain tapeworm (Taenia multiceps), the bladder stage of which—the coenurus—lives in the sheep's brain, causing a disease called gid. A case of coenurus parasitism in the human brain is known, specifically in the lateral ventricle and in the thickness of the brain tissue; the disease began with aphasia, loss of the ability to write and count. Then there were Jacksonian epilepsy seizures, dizziness, comatose states, unbearable headache, acute frenzy; the last Jacksonian epilepsy seizure ended in death; the disease lasted eight months; individual cases of gid were observed in a calf, a horse, and an antelope. Along with other organs, the human brain can be affected by pork tapeworms (Taenia solium); the localization of pork tapeworms in the brain is very diverse: they can be in any part of the brain, affecting the cortex, located in the meninges or in the brain ventricles. Out of 807 cases of human cysticercosis, the brain was affected in 40.90%. With more careful examination of the brain at autopsies, brain cysticercosis has been detected more and more frequently in the USSR in recent years. Localizing in the subarachnoid tissue of the brain, the cysticercus takes on an irregular, highly branched form, described under the name Cysticercus racemosus, the size of which, in contrast to the usual form of cysticercus, is very significant, reaching 15-25 cm in diameter. Being in the brain, the cysticercus causes meningitis, hydrocephalus, ependymitis, etc. The clinical symptoms of brain cysticercosis are very diverse: epilepsy, convulsions, headaches, vomiting, excitement, disorders of consciousness, vision, speech, etc. The echinococcus, in turn, can affect the brain, developing in the white or gray matter, in the ventricular cavities or in the meninges. In addition, the growing echinococcus cyst can press on the brain from the outside. The symptoms of brain echinococcosis are generally similar to the symptoms of an intracerebral tumor. The usual outcome is the death of the patient.-; From the trematodes, cases of encapsulation in the brain of the lung fluke—Paragonimus westermani—are known, which was accompanied by symptoms of Jacksonian epilepsy and led to death; the eggs of this trematode can accumulate in brain tissue. Cases of encapsulation of ascarids in the brain of dogs, which broke through in the form of migrating larvae from the small to the large circulatory system, have been noted. From the protozoa, trypanosomes of sleeping sickness (Trypanosoma gambiense) can penetrate into the human brain tissue; malaria parasites sometimes accumulate in huge masses completely blocking the brain vessels (coma form of malaria); in amoebic dysentery, cases of amoebic brain abscess (Entamoeba histolytica) have been noted; in neuroglia, the causative agent of Chagas disease—Trypanosoma cruzi—has been found, which in such cases gave phenomena of pareses and paraplegias. A doubtful parasite is Encephalitozoon cuniculi—the supposed causative agent of rabies, described in the brain of a rabbit (Manouelian, Viola). In some animals, the presence of parasites in the brain is not accompanied by any pathological symptoms.

The brain can be irritated as a result of pressure on the meninges by the larvae of certain two-winged insects, for example, the larvae of the sheep botfly. This occurs in sheep when the larvae of Oestrus ovis destroy the ethmoid bone from the nasal cavity side; the result of such irritation is "false vertigo." In humans, the larvae of various flies (for example, those of Wohlfahrt) can penetrate from the nasal cavity into the frontal sinus and destroy its internal bony wall. Similarly, in ear myiasis, larvae can reach the meninges. The symptoms of brain irritation by fly larvae are diverse: convulsions, visual disturbances, loss of speech, signs of meningeal inflammation, etc. The condition can end in death. The brain can be affected by products produced by intestinal parasites; these substances are absorbed and reach the brain by the hematogenous route; for example, ascaridotoxin causes varying degrees of chromatolysis in nerve cells and the appearance of numerous fine canals in their protoplasm, while the cells themselves take on an amoeboid character (Rakhmanov et al.). In chronic helminthic intoxication, changes in the white matter of the brain are observed. The various nervous symptoms observed in human infection with intestinal helminths must be explained by the influence of their products on the nervous system.

E. Pavlovsky. Gonorrheal diseases of the N. s. are usually a complication of primary gonorrhea of the genitourinary organs. Experimental research and autopsies have shown that the gonococcal toxin causes quite clear and definite patho-anatomical changes in the N. s. (parenchymatous neuritis, degenerative changes in the anterior horns, posterior roots, and posterior columns of the spinal cord), which, however, are not specific in any way and resemble the picture of changes observed in similar diseases of the N. s. (neuritis, meningomyelitis, etc.) caused by any other infection or intoxication. Gonorrheal diseases of various organs, including the N. s., depend on the penetration into them from the primary focus of infection not only of the toxin but, as shown by the latest observations, of the gonococci themselves (some authors found gonococci in pus from the spinal cord membranes and in the exudate on the pia mater). Theoretically, it must be assumed that gonorrheal infection can cause all the numerous and diverse diseases of the N. s. that are observed as a result of the action of other infections and intoxications, but in practice one has to deal with only a few conditions. This is explained mainly by the peculiar biological properties of the gonococcus itself (see). The peripheral N. s., having the weakest protective apparatus, most often reacts to gonorrheal infection, and it is often necessary to observe various neuralgias, neuritis, and even polyneuritis. Neuritis is most often localized in the lower extremities, preferably affecting the sciatic nerve. As for the central N. system, with the exception of individual cases where gonorrheal encephalitis, meningitis, etc., were diagnosed, only meningomyelitis remain, which are undoubtedly observed, although by no means frequently. Furthermore, gonorrhea often serves as that exogenous etiological factor which reveals some constitutional disease of the N. s. (neurasthenia, hysteria) that was previously in a latent state. Finally, it should be mentioned that gonorrheal infection causes gonorrheal arthritis, polyarthritis, tendovaginitis, and bursitis, as a result of which the nervous system is secondarily affected, reacting with a variety of symptoms (neuralgias, muscular atrophy, etc.) or even symptom complexes (spondylosis rhizomelica, gonorrheal spondylitis). The diagnosis of gonorrheal diseases of the peripheral N. s. is often very difficult, since there is no single symptom characteristic specifically of gonorrheal infection, and only the totality of all phenomena can help. Here the following are important: 1) the intermittent nature of the temperature, 2) the rapid and stormy development and course of the disease, 3) the localization of the condition (see above), 4) the patient's history and the presence of gonorrhea in other organs. The recognition of gonorrheal meningomyelitis is even more uncertain, and undoubtedly this condition occurs more frequently than it is diagnosed. A benign course and rapid and complete recovery sometimes speak in favor of this form, but on the other hand, severe cases with gonococcal septicemia and septicopyemia ending in death are observed. The diffuse nature of meningomyelitis and its localization in the lumbar-thoracic region are helpful for diagnosis. Ultimately, in the presence of gonorrhea in other organs, the diagnosis can only be made by excluding all other etiological factors, but even in these cases the question of whether there is a purely gonorrheal infection or a combined one is often considered unresolved, all the more so because under the influence of gonotoxin some microorganisms, not possessing pyogenic properties themselves, acquire the ability to cause suppuration. Prevention of gonorrheal diseases of the N. s. reduces to combating primary gonorrheal infection. As for the treatment of gonorrheal diseases of the N. s., one should first of all carry out both local and general therapy for gonorrhea, but in addition to the general specific anti-gonorrheal treatment for all gonorrheal diseases of the N. s., one must simultaneously also carry out the therapy that is usually applied for similar conditions with a different etiology (see Myelitis, Neuralgia, Neurasthenia, Neuritis, etc.).