Vegetative Neuroses
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
This article discusses vegetative neuroses as functional disorders of the autonomic nervous system, tracing historical understanding from the 17th century through early 20th century theories of Eppinger and Hess regarding sympathetic and parasympathetic system imbalances.
Encyclopedia article (1928–1936)
VEGETATIVE NEUROSES, functional diseases of the autonomic nervous system. Even older authors of the 17th century (Fischer, Willis), 18th century (Brachet, Pomme, Whytt, etc.) and early 19th century (Duvernoy, Dubois, von Noorden, etc.) knew of a group of V. n. under the names 'hypochondria,' 'neuroses,' 'emotional constitution,' etc. Vitte, Bichat, Brachet and others attributed the origin of these neuroses to disorders of the sympathetic system. In the early 19th century, Girard described 'acute neurotony' as a result of damage to the vagus nerves, and later Rosenbach, Grasset, etc., described functional disorders of the lungs, heart, and stomach under the name 'vago-neurosis.' Noorden, Gowers emphasized the important role of the vagus nerve in hysteria. Subsequently, the sympathetic nervous system and the vagus nerve were considered as causes of varieties of neuroses (Vulpian, Sude, Huchard, etc.). Grasse recorded the syndrome of so-called 'psychosplanchinic neuropathy,' characterized by disorders of motor, sensory and secretory functions of the intestine, functions of the respiratory and circulatory apparatus, and of the psyche. Finally, in 1910, Eppinger and Hess attempted to reduce the doctrine of V. n. to objective signs and to consider various nervous phenomena in visceral organs in hysteria and neurasthenia as a result of changes in the functions of the autonomic nervous system. On the basis of pharmacological research, Gottlieb and Meyer established that under physiological conditions certain poisons act specifically on the sympathetic and vagus nerves. Thus, pilocarpine, physostigmine, muscarine and choline excite the vagus nerve, atropine paralyzes it; adrenaline acts exclusively on the sympathetic system. In connection with these data, various nerves, even without anatomical connection with the vagus or sympathetic, were classified according to pharmacological reactions either to the first group or to the latter. Thus arose the division into sympathetic and parasympathetic systems. The parallel pharmacological functional difference observed between them later led to the hypothesis of their 'antagonism.' Based on experimental pharmacological research and their clinical observations, Eppinger and Hess concluded that sympathetic and parasympathetic innervations are in a state of prolonged excitation (tonus) and under 'control' and in 'complete dependence' on the endocrine glands. Functionally, both nervous systems are antagonistic. They supply all organs, with the latter being in a certain state of functional equilibrium due to the balancing of each other's appropriate average excitation (tonus) of the sympathetic and parasympathetic apparatus. In case of increased tonus or impulse of one of them, changes develop in favor of one side or the other. Based on the principle of double innervation, Eppinger and Hess concluded that secretory or mechanical effects are closely related to the state of equilibrium of the working organs in connection with the varying degree of prolonged excitation of one system or the other. Under certain conditions even small irritations can cause various more sharp changes, since in such cases only a small additional effect is required for an already excited organ. The parallel functions of antagonists make it impossible for internal organs to pass from one extreme state to another. Too strong or weak tonus of one of these systems can lead to functionally morbid states-'neuroses.' The basis of the latter lies in changes in excitability of the entire autonomic system collectively or of its individual components. Although these changes can be expressed as both strengthening and weakening of tonus, the greatest practical interest is the increase in excitability. Vagotonic state represents a shift of equilibrium in favor of the parasympathetic system, giving adequate irritators the ability to cause symptoms of its increased excitability-so-called 'vagotonia'; sympathicotonic state is a shift of equilibrium toward the sympathetic system with phenomena of its hypertension and creates a picture of 'sympathicotonia.' In contrast to these forms, Guillame proposes a state of decreased excitability of one system with normal tonus of the other-'hypotonia' of the sympathetic or parasympathetic apparatus. In addition, he establishes the syndrome of 'neurotonia' (according to Danielopolu-'amphotonia'), characterized by such a disturbance of the equilibrium of the autonomic nervous system, in which it is impossible to establish the indisputable predominance of one system over the other. In this state, some phenomena indicate vagotonia, others indicate sympathicotonia. These morbid states, the basis of which lies in changes of physiological tonus, constitute a group of general V. n. According to Eppinger and Hess, vagotonics are people of young or middle age, with easily changing facial coloration, cyanotic, moist, cold extremities, who sweat easily. They show frequent swallowing movements caused by hypersalivation. The pulse is unstable and slowed, but its frequent attacks of acceleration are not uncommon. Deep inspiration causes slowing of the pulse. Symptom of Graefe, strabismus, and eosinophilia are often observed. In relation to sexual function, vagotonics are characterized by easy excitability, erections are sudden, frequent, but not prolonged, ejaculation is rapid and premature. From the digestive organs are noted: variable appetite, heartburn, sour belching, frequent constipation, alternating with periodic diarrhea. After injection of pilocarpine hydrochloride (0.00075-0.01), spasm of accommodation, tendency to bradycardia, arterial hypotension, respiratory arrhythmia, palpitation of the heart and appearance of: extrasystoles, aerophagia, diarrhea, salivation, relative lymphocytosis, belching, gastro-intestinal hypersecretion, profuse sweating, redness of the upper part of the body, nausea, sometimes vomiting, tightness of breathing and unpleasant sensations in the heart region occur. Vagotonia corresponds to functional insufficiency of the chromaffin system (Arvy), and conversely, in it one can note the extraordinary development of the lymphatic system. To subcutaneous injection of 0.001 atropine, the vagotonic subject reacts with tachycardia, dryness of the mouth. Weak reaction corresponds to a pulse of less than 100 beats per minute; increase in beats not exceeding ten per minute is considered a negative reaction. Sympathicotonia is more often found in old people. Eppinger and Hess consider its characteristic signs to be: protrusion of the eyes, absence of Graefe's symptom, Mobius' symptom, Levi's symptom (dilation of the pupil under the influence of adrenaline), dryness of the eyes, rapid pulse, absence of sweating and diarrhea, loss of hair, tendency to increased temperature, absence of eosinophilia, completely free breathing, alimentary glycosuria, polyuria, glycosuria under the influence of adrenaline, absence of reaction to pilocarpine. Injection of adrenaline (0.001) causes tachycardia, lymphocytosis, mydriasis, hypertension, constipation, sharp dermographism, dryness of the skin, absence of sweat, goose skin and sharp pallor, frequent and fine trembling. [Research for sympathicotonia is carried out 5 days after vagotonic. After taking 100.0 of grape sugar on an empty stomach, every hour the urine is tested for sugar. If there is no sugar (alimentary glycosuria) - inject 0.001 adrenaline. The above-mentioned phenomena occur. Then every half hour - testing for sugar, with determination of the time of its appearance and disappearance, as well as its total amount. The degree of sympathicotonia is directly proportional to the intensity of these phenomena.] A number of symptom complexes, based on the observations of Eppinger and Hess (such as, for example, bronchial asthma, pseudo-membranous colitis, Basedow's disease, etc.), can be considered as a result of increased excitability of the vagus nerve. The rich clinical material accumulated since 1910 has provided evidence for the correctness of the basic ideas of Eppinger and Hess. However, analyzing the phenomena caused by disturbance of autonomic reflexes, in many cases one cannot agree with the theoretical explanations of their pathogenesis and their classification. In the process of clinical observations, many paradoxical phenomena were noted. Corrections were made, many provisions proved insufficient to resolve the arising questions. Such circumstances are quite understandable. The theoretical concepts of Eppinger and Hess arose from the knowledge of their time, the focus of which was concentrated in the physiological and pharmacological achievements of Langley and Meyer. In subsequent times, the physiology and pathology of the autonomic nervous system have been enriched with new data, which must be introduced as a necessary correction when discussing the pathogenesis of various morbid symptom complexes of the extensive field of neurology of internal organs. The ideas of Eppinger and Hess have caused fierce criticism and even complete negation; their followers, on the basis of physiological research and clinical observations, have introduced a number of corrections, extremely valuable facts and ingenious hypotheses. The idea of physiological antagonism has caused particularly lively discussion.
Stopping at the phenomenon of the antagonistic action of both divisions of the autonomic nervous system under pharmacological and electrical irritation, Eppinger and Hess come to the conclusion that both these divisions function under physiological conditions in the normal organism. The mechanism of both systems is similar to two scales. The resultant of these systems is represented by the beam. The usual equilibrium can be disturbed either due to unloading one pan or overloading the other. On the basis of an analysis of blood pressure curves under the action of adrenaline, Dresel established that sympathetic irritation is accompanied by parasympathetic irritation, whereby the disturbance of equilibrium is immediately restored. These data do not justify the comparison with scales. Dresel illustrates the relationship of both systems by comparing them to two parties of people pulling a rope in opposite directions during a game. When one party begins to develop greater force, the other increases its pull to pull the rope toward itself. The latter oscillates in both directions, but if the forces of both parties are equal, it remains in its original balanced position. Both systems can increase their action if prompted by irritation of one of them. True antagonism can be observed only under experimental conditions, with isolated irritation of the antagonist. Under natural conditions, however, irritation of one system leads to excitation of the other, so that true antagonism cannot be spoken of. According to Peritz, there is no isolated excitability of one half of the autonomic nervous system: both parts of this system, closely connected with each other, are subject to the same excitatory factor. Guillaume distinguishes, besides vagotonia and hypersympathicotonia, also neurotonia, in which symptoms of both conditions are observed, with special instability of the tone of visceral organs and with special tendency (seemingly paradoxical) to react strongly to psychic, thermal, mechanical, and especially pharmacological excitants. In addition, he describes the syndrome of complete hypotonia—a state of the organism in which the autonomic system does not react or reacts little to ordinary irritants. This is a state of strong hypotonia of the sympathetic system, with some hypotonia of the parasympathetic. Danielopolu considers both divisions of the autonomic nervous system independent of each other and proposes to introduce the concepts of vegetative hyper- and hypotonia. The evolution of views on tone, reflecting the failures and disappointments that arose in different researchers due to the contradictory nature of the accumulated material and the paradoxical nature of existing methods, has introduced much that is unclear and confused into the doctrine of the autonomic nervous system and has finally led to such poorly understood and vague concepts as 'excitability,' 'irritability,' etc. Meanwhile, if we approach the study of the autonomic nervous system, starting from the positions and laws of the somatic nervous system (and this we must do on the basis of the close connection of the vegetative nervous system with the animal), it becomes obvious how cautiously one must treat such concepts as, for example, 'antagonism.' The experimental data of Ascher, Abelin, Scheinfinkel on the action of the sympathetic nerve on the permeability of vessels and specific cells for inorganic substances (e.g., chlorine in the function of parasympathetic nerves) as an apparatus in charge of the secretion of liquid parts of saliva, and the works of Pavlov's school showed that we often deal not with antagonistic, but with synergistic work of systems. If we add to this the opinion of Levi that the sympathicus converts salivary zymogen into zymase, transferring it to a dissolved state, and the parasympathetic nerve, by forcing the secretion of liquid parts of saliva, washes away this enzyme, we get a complete picture of the phenomenon of cooperative work in the field of the autonomic nervous system. Data on the vegetative innervation of organs indicate that the phenomenon of antagonism is incomprehensible also from an anatomical point of view. Thus, the seminal vesicles, vas deferens, ureters, Fallopian tubes, muscles of the hair and skin, as well as sweat glands, according to modern views, are innervated only by the sympathetic apparatus. Consequently, the various, so-called 'antagonistic,' functions of these organs are controlled only by the sympathetic system. Heterogeneous function is also inherent in the parasympathetic system. Thus, e.g., the small intestines and the cardiac part of the stomach receive from the n. vagus both inhibitory and excitatory fibers. Besides these data, indicating the diversity of functions of the vegetative apparatus associated with anatomical peculiarities, the very concepts of excitation and inhibition will hardly bring clarity to the concept of 'antagonism.' Often weak irritations of the same nerve give relatively strong reactions, inhibit and even paralyze it. Finally, the final phenomena obtained from the difference in excitations of one and the other system certainly cannot be called 'antagonistic,' just as we do not call, e.g., the result of the joint function of the muscles of the arm and forearm 'antagonistic.' The division by Eppinger and Hess of the autonomic nervous system into two antagonistic divisions arose from the belief in the specific action of pharmacological agents. Subsequent numerous investigations have not justified these views. It has been established, e.g., that the specific excitant of the sympathetic nervous system—adrenaline—far from always shows its selective influence, but also excites other divisions of the nervous system. The so-called 'parasympathetic poisons' in most cases are not selective with respect to the entire parasympathetic system. Thus, pilocarpine acts mainly on the glands, muscarine on the heart. The position that subjects reacting to sympathicotropic substances are not sensitive to vagotropic substances and vice versa (Bauer) has not been confirmed. Many researchers have come to the conclusion that, generally speaking, there is no pharmacological antagonism. Especially many disappointments have been brought by attempts to study patients pharmacologically. The concepts of 'mixed,' 'atypical,' and 'paradoxical' reactions have appeared, completely refuting the pharmacological method and discrediting the law of specificity of hormones and poisons. Each new work shatters the numerous and painstaking research of previous authors; new searches begin, a series of conditional, unconditional, and chemical reflex moments are discovered, and finally, the connection of the autonomic nervous system with physicochemical factors in the organs is established (Kraus, Zondek). Naturally, at the present time, when the vegetative apparatus appears to be the center of control and regulation of life processes in the organism, fluctuations in nervous tone, carried out through the system of reflex arcs, must be considered more broadly and in full agreement with the newly discovered moments of reflexology and molecular pathology. One of the factors maintaining the tone necessary for the interaction of organs and the nervous system are the hormones of the endocrine apparatus. Their action is identified with the action of some pharmacological agents. But how to understand the specificity of the action of pharmacological substances and hormones? Best of all and most simply from the modern molecular-physiological point of view. According to Langley, the selective actions of chemical substances on various tissues can be explained by the difference in the anatomical and physicochemical properties of their cells (often cells and tissues, even of the same species, are not quite identical). When the same tissue is innervated by two systems, the difference in the action of poisons and their specificity can be explained either by the fact that nerves of different divisions of the autonomic system cause different changes in the cells where they end, independently of the properties of the cells themselves, or by the fact that the substance of the cells is built differently, independently of the properties of the innervating division of the nervous system. Long before the formation of the nervous system, mutual correlative influences of cell groups arise. These dependent differentiations can be explained by the action of chemical substances arising from the extremely peculiar changes in the basic chemico-physical environment of the cells. In the process of formation of new physiological properties, the development of the autonomic nervous system occurs, connected with the newly formed cells, while the other cells retain their original properties. In a similar way, in the process of formation of the organism, endocrine glands also appear; the latter, in further development, help to modify cells in another direction. In a fully formed organism, there is no specific nervous action on a particular cell. The latter itself contains an inhibitory or stimulating receptive substance and is only activated by the nervous system. Thus, the work of the cell, with the same nerve impulse, is modified depending on the change in the surrounding chemico-physical properties.
Thus, Langley's theory explains the essence of the disruption of the specificity of pharmacological substances and hormones, and also introduces us to the doctrine of the role of molecular physiology and pathology in visceral neurology. After Zondek's work, it became obvious that the study of the chemical-physical conditions of cell work in normal and pathological conditions opens up new paths to understanding the properties and functions of the autonomic nervous system. Parasympathetic irritation, according to Zondek, is a disruption of electrolyte balance in favor of K and OH-ions, while sympathetic irritation is the opposite shift with a predominance of Ca and H-ions. A predominance of Ca or K, due to the addition of Ca and K-ions, as well as a decrease in one of these cations, leads to a vivid expression of one of the two autonomic components. Thus', vagal inhibition of the heart turns into vagal excitation when the aforementioned predominance of K-ions is established. However, the research of Dresel and Reimer refuted the assumption that parasympathetic excitation corresponds to an increase in K in the blood, and sympathetic excitation to Ca (simple, non-ionized). On the basis of their observations, these authors showed that in the blood during parasympathetic excitation there is much Ca, and during sympathetic excitation-little Ca. Dresel seeks an explanation for this circumstance in the tissue consumption of lime during sympathetic excitation. Ionizing in the blood, it quickly diffuses into the tissue. According to this author, the ionic state during sympathicotonia and vagotonia changes as follows.-S y m p a t i c o t o n i a: 1) tissue is acidic, much Ca-colloid, little K-colloid, 2) blood is acidic, much ionized Ca, little deionized Ca, much K.-V a g o t o n i a: 1) tissue is alkaline, little Ca-colloid, much K-colloid, 2) blood is alkaline, little ionized Ca, much deionized Ca, little K.-Zondek thinks that the relationship of ions to the autonomic apparatus is determined by organs. Ions are connected with organs, which for the performance of functions are served by nerves, and since a shift in ions is equivalent to the action of the latter, the organs themselves can perform the function of parasympathetic and sympathetic apparatuses. Weil considers that nerves-organs give direction to the action of ions in the body. From this point of view, Langley's theory of cellular dualism (Langley thinks that the sympathetic and parasympathetic systems innervate different cells; thus, inhibition and acceleration are the work of two cells) takes on a different color: not a dualism of cells, but a dualism of the dissociation state of K and Ca, OH and H-ions in the same cells determines the so-called parasympathetic and sympathetic states. These considerations give boundless prospects for research in still unexplored areas of biology and pathology (for example, in the field of metabolism). The life of individual cells and organs is carried out on the basis of physico-chemical autonomous processes. However, the complex functions of the visceral organs system are possible only with the existence of coordinating factors, and this factor, as in voluntary actions, is the nervous system. If the latter can cause dissociation of Ca and K-ions and H and OH-ions and thereby change the nature of cell work, then dissociation fluctuations associated with cell activity (metabolism, etc.) can change the result of excitation of one or another nerve. Thus, the usual moments-electricity, mechanical and thermal factors, as well as the specific' alkaloids considered: atropine, muscarine, pilocarpine, physostigmine, adrenaline, etc., both in physiological and pathological conditions, depending on various physico-chemical factors, in given organs can give the most diverse reflexes. If we now also take into account all possible pathological conditions that change, distort or completely stop the reaction of organs to impulses from the autonomic nervous system, it becomes completely clear that pharmacological reactions cannot be considered specific, and, on the other hand, the reason and essence of the so-called 'mixed', 'atypical' and 'paradoxical' reactions can be understood. Pathogenesis and etiology of neuroses. If, on the basis of the above, we turn to the pathogenesis of V. n., it is necessary to state that even those few moments that seemed indisputable at present, thanks to new data from physical chemistry, physiology and pathological anatomy, partially lose their significance. First of all, the explanation of fluctuations in disorders of the functions of the V. nervous system by hyperfunction or hypofunction of the adrenal gland is completely unsatisfactory. Dresel and others think that the regulation of tone is carried out by higher autonomic centers of the pallido-striatal system. Isolated symptom complexes of vagotonia and sympathicotonia arise when this regulation is disrupted in the form of the centers losing the ability to restore the disruption of organ innervation caused by an increase in the tone of its individual elements. General hypo- and hypertensions turn out to be the result of an increase and decrease in the tone of higher autonomic centers. Thus, general functional disorders of the autonomic nervous system are considered as depending on functional changes in the autonomic centers 'central neuroses'. Local functional disorders of innervation of visceral organs are the cause of local neuroses. The study of syndromes of disruption of the balance of the autonomic nervous system indicates the following etiological moments. I. Reflex physical causes, the action of which apparently consists in the irritation produced and maintained by them in some place in the body. These include: injuries, bullet wounds (with remnants of shells and with bone fragments causing irritation), displacement of the uterus, mechanical and chemical irritants acting on mucous membranes, especially in the area of distribution of the trigeminal and glossopharyngeal nerves, intestinal worms, changes in the usual living conditions caused by travel, etc. It is necessary, however, to emphasize that mechanical causes should be treated with great caution, as they may be complicated by other additional moments: humoral, psychogenic, etc. II. Exogenous and endogenous humoral causes, depending on substances circulating in the body with selective action or on the lack of substances maintaining tone. These include substances causing a) complete hypersympathicotonia-adrenaline, cocaine; b) partial hypersympathicotonia-ammonia, tyramine; c) hyposympathicotonia-nitrates, caffeine; d) hypervagotonia-pilocarpine, colchicine, muscarine, eserine; e) partial vagotonia-picrotoxin; f) the phenomenon of vagotonia or vagoneurosis-acute or chronic poisoning: with arsenic, naphthol, bromoform, picric acid, phenol or salicylate salts, copper salts, thymol (in alcoholic or oily solutions), Antimony tartaricum, methyl alcohol, gases remaining from combustion, illuminating gas, spoiled (oxygen-poor) air, bacterial toxins. Among endogenous causes, autointoxications originating from the intestine or caused by physical or mental fatigue (neuroses with predominance of vagotonia) play a significant role, as well as endocrine factors (endocrinopathies). The latter include: 1) the state of variable neurosis with disorders of menstrual functions; 2) the syndrome of vagotonia with myxedema, Addison's disease; 3) the symptom of neurosis with predominance of sympathicotonic or, more rarely, vagotonic in Basedow's disease and 4) little studied humoral states associated with the colloidal equilibrium of the blood. III. Mental (emotional) causes. Despite the lack of specific morphological data on the connection of the cortex with autonomic innervation, there are many clinical observations indicating the role of the psyche in the pathogenesis of some autonomic symptom complexes. These include observed in mental trauma: gastrointestinal disorders, diabetes mellitus, diabetes insipidus, disorders of pigmentation, the so-called 'anxiety', 'hypochondria' or fear of serious diseases. From a clinical point of view, reflex causes give neuroses of vagotonic or vagoneurotic nature. Exogenous and endogenous causes in intoxications cause neuroses of vagotonic or vagoneurotic type; in connection with endocrine phenomena, neuroses of types are observed: 1) neurotic, with predominance of sympathicotonic (in Basedow's disease), 2) vagotonic (deficiency of the thyroid gland), 3) variable-neurotic (disorders of menstrual moments). Hereditary and constitutional factors play a certain role in the origin of V. n., and hereditary, or familial forms are often observed (dermatoses, symptom complexes of anaphylaxis, changes in endocrine glands, disorders from the gastrointestinal tract, etc.). V. n. must be distinguished from physiological changes depending on the time of day, year, age, etc. There are physiological fluctuations of three kinds: 1) daily, associated with fatigue, sleep (vagotonia), food; 2) seasonal, by time of year; 3) age-related (in youth a state approaching 'vagotonia', in old age-'sympathicotonia'). In women, to the latter are added fluctuations during menstruation and pregnancy.
Changes in tone related to sexual life are common to both sexes: chastity, sexual excesses, decline in sexual energy, sexual maturity, and the climacteric period (see Vegetative Nervous System, Physiology). On the border between physiological and pathological states are the phenomena of affect (fear, anger, hunger, etc.), usually observed in normal people, but when of great intensity, frequency, and disproportion to the intensity of the causing cause, they pass into a pathological phenomenon. The pathogenesis of V. n. depends on changes in the functions of centers, central and centrifugal sensory and motor pathways. At present, these disorders cannot be registered morphologically, and this is the reason for the uncertainty of the concept of 'functional'. However, not only oppressive changes serve as a criterion for pathological states. Data from molecular pathology indicate that the latter is often the cause of disturbance of physico-chemical equilibrium (disturbance of the colloidal state-'colloidoclazia', etc.). The presence of these new material moments reduces the number of undefined concepts of so-called 'functional' diseases of the vegetative nervous system. It must be hoped that further improvement in histological technique and molecular pathology will completely eliminate them. Clinical syndromes of V. n.-I. Angio-neuroses (see Angioneuroses, Angiotrophoneuroses). In addition to the syndromes outlined in the respective articles, it is necessary to mention angiospasm localized in organs with terminal arteries (brain, heart, spleen, kidneys). In the brain, these forms proceed as so-called 'abortive forms' of hemipareses and hemiplegias. Without a morphological basis, these angiospasms lead to pathological changes in organs with terminal vessels: infarction of the spleen and kidneys, softening of the brain (Kolisko, Spielmeyer, etc.), etc. Angiospasm of cerebral vessels can give the most diverse anatomical and clinical pictures. Prolonged vasodilation proceeds 1) without morphological changes in vessels and brain (vasomotor disorder, climax, migraine); 2) with degenerative-atrophic processes in the brain without damage to the vessels. * Redlich proposes to leave the diagnosis 'angiospasmus cerebri' only for hemiplegias with other symptoms of angiospasm: temporary blindness, intermittent claudication, acrocyanosis, Raynaud's disease, etc. II. Traumatic neuroses of the vegetative nervous system (without morphological changes) are observed after concussions and injuries. They are expressed by changes in heart rate and respiration, vasomotor phenomena, muscle weakness, paresthesias, hyperhidrosis (cold, hot sweat), constipation, loss of appetite, weakening of libido sexualis, a state of melancholy, fear, anxiety. Weak irritations, noises cause a series of sympathico-vagotonic phenomena (tachycardia, sweat, shortness of breath). III. Shock. Sometimes traumatic injuries, hemorrhages, infections and intoxications are accompanied by reactions indicating a violation of the functions of vegetative nuclei (without visible morphological changes) in the form of general hypotonia of the vegetative nervous system. These reactions are expressed by tachycardia, increased respiration, fall in blood pressure, lowering of temperature, stagnation of blood, absence of the Ashner reflex, dilation or constriction of the pupils. This condition is called shock. Without complete occlusion of the lumen, even in significantly changed vessels, complete ischemia occurs only after the addition of angiospasm. IV. Reflex neuroses. Irritations of sensory conductors (or nerves) usually cause disturbances of the functions of the veget. nervous system of both local and general character. The picture of clinical phenomena, especially with local irritations, depends on which system participates in the disturbance of equilibrium. Strong general irritations, according to Guillot, usually give a hyperparasympathicotonic reaction, weak ones-gympathicotonic. Such forms include: \.( Local reflex neuroses.- a) Reflex contractures and causalgias. With damage to the upper, rarely lower extremities, contractures arise, which cannot be classified under the heading of those arising from damage to the neuro-osseous-ligamentous apparatus, scarring, contractures of antagonists, ischemic, psychogenic, etc. Usually they give the extremities extremely bizarre and diverse forms and are accompanied by secretory, trophic and vasomotor disorders (foul sweat, difference in skin temperature, hypersalivation). Sometimes this disease is associated with causalgias-burning pains, the form and topography of which do not coincide with the branches of peripheral somatic nerves. Removal of the irritating causes (bullets, scars), and sometimes periarterial sympathectomy, according to Leriche, eliminate this syndrome.- b) Angina pectoris. The anginal syndrome (see Angioneuroses, Vegetative Nervous System-pathology) can be caused not only by damage to the coronary vessels and ganglioneuritis of the cardiac plexus, but also by irritation of the latter, sudden displacement of the heart or aorta, nicotine (acute poisoning). In addition to the vascular effect, irritation of the vagus nerve is accompanied by spasm of the pharynx, esophagus, vomiting and increased peristalsis.-c) Bronchial asthma is observed either in the form of an obvious reflex syndrome, with tracheobronchial adenopathies and aortitis, or in the form of primary V. n., associated with the phenomenon of anaphylaxis. Both forms depend on irritation of the mixed vagosympathetic bronchial plexuses. Until recently, the sympathetic nerve was considered to inhibit bronchial constriction, while the vagus, on the contrary, was considered to stimulate it. On the basis of experimental data and phenomena during operations of vago- and sympathicotony, it has been established that 1) the muscle and mucous membrane of the bronchi are innervated by the vagus and sympathetic nerves together (wherein the vagus and sympathetic are 'mixed nerves', i.e. they contain both sympathetic and parasympathetic nerves), 2) the sympathetic nerve is the stimulating nerve for bronchoconstrictors. Based on these data, Brtihning and Kiimmel proposed resection of the cervical part of the sympathetic nerve, its three ganglia-an operation in which the branches of the vagus nerve are also severed. The latter, in the opinion of these authors, causes cessation of asthmatic attacks. However, further observations have not given encouraging results, and a priori one can think that disturbance of innervation of an extensive area (meninges, thyroid gland, hypophysis, glands, vessels, etc.) cannot pass without a trace for the organism. g) Tabetic visceral crises,- reaction of the vegetative nervous system to damage of sensory roots. The disturbance of sensitivity in gastric crises: analgesia, tactile hyperesthesia of the lower part of the chest, anesthesia of the mammary area corresponding to IV-VII and VIII-XI D/segments, coincide with the reaction to irritation of the branches of the greater splanchnic nerve leaving here (V-XI D), expressed in the corresponding phenomena of the 'crisis' motor, secretory and vascular moments: constipation, spasm of visceral vessels, partly pains. Irritation of the vagus nerve in gastric crises gives a picture of pupil constriction, laryngospasm, paroxysmal pains in the abdomen accompanied by salivation and gastrorrhea; in intestinal crises-bloody and mucous-membranous diarrhea. Irritation of the parasympathetic nerve is accompanied by rectal, ovarian and testicular crises.-2. General reflex neuroses.-a) Seasickness. It is considered as an expression of disturbed equilibrium of vegetative visceral innervation (Moverick, Pribram and Pinkussen). Irritation (swaying) of the heart in a rolling motion causes sensory-sensory excitations of the vagus nerve (nausea, vomiting) and sympathetic (dilation of pupils, increase in blood pressure, tachycardia and inversion of the cardio-ocular reflex). Sympathicotonic persons are especially prone to seasickness, to a lesser extent-vagotonics. Therefore, probably, children-constant vagotonics-are less susceptible to seasickness. According to Cazamiami, a good therapeutic result in this disease sometimes gives atropin.-b) Anaphylaxis. The so-called anaphylactic shock symptom-complex must also be classified among reflex V. n. The mechanism of cardiac-respiratory phenomena in the latter is closely connected with the state of disturbance of the functions of the vegetative apparatus (existing previously or appearing as a result of injection). This disturbance some authors connect with the constitution, others-with the change in the chemico-physical equilibrium of the intermediate substance and cells (see Anaphylaxis). In the clinical analysis of anaphylactic shock, one can ascertain the symptom-complex of excitation of the parasympathetic system. V. Neuroses in diseases of individual visceral organs.-1. Gastric and intestinal neuroses. Gastric-intestinal neuroses are described under various names: cerebro-gastric neuropathy, vagus neurosis, gastro-neurosis, psychosplanchnic neurosis, etc. Gastric-intestinal neuroses are the result of pathological changes or irritations of the vagosympathetic innervation (plexus Solaris and plexus sp'lanchnicus) in acute and chronic infections and intoxications.
The etiological factor is damage to the autonomic nervous system. Sometimes neuropathic conditions are considered as a factor added to purely organic, minimal and further undefined damage. Usually a picture of secretory and vasomotor nature is observed. In such patients, nausea and a feeling of pressure under the xiphoid process appear after meals, achylia or increased acidity, increased appetite or its absence with a normal-sized stomach, fatigue, drowsiness, very slow digestion, aerophagia, spastic constipation. To these factors are added vasomotor-cardiac, respiratory and secretory phenomena: tachycardia or bradycardia, feeling of pulsation, dizziness, symptoms of fear, extrasystolic arrhythmia, dermographism, hyperemia or spasm of blood vessels, cyanosis, anemia of the fingers, hypersalivation and sweating. These symptoms can be attributed to both sympathicotonic and vagotonic states. In addition to these disorders, spastic condition of the stomach is observed, giving an hourglass shape, hyperplasia and hypertrophy of the stomach muscles. Increased sensitivity and pain are explained by spasm of the pylorus and cardia. In the same patients, depending on different conditions, phenomena of achylia or increased acidity may occur. Often the etiological factor of gastrointestinal neuroses are acute and chronic infections and intoxications.-2. Membranous colitis (colitis membranacea, colitis mucosa), a disease closely related to gastrointestinal neuroses, characterized by catarrh of the large intestine, accompanied by attacks of colicky pains and excretion of mucus in the form of membranes and imprints of the intestinal tube, containing eosinophils and Charcot-Leyden crystals. This disease represents a combination of sensory and secretory neuroses, occurring in neurasthenics, hysterics and other neurotics. In this disease, treatment with atropine and adrenaline is successfully applied.-3. Gallstones. Attacks of biliary colic accompany irritation of the sphincter of the ductus choledochus (Aschoff). Etiological factor: menstruation, pregnancy, dietary errors, body position, physical movements, psychological influences. According to Eppinger and Hess, these attacks can be caused by irritation of the n. vagi and injection of pilocarpine.-4. Paroxysmal tachycardia and bradycardia. The pathogenesis of paroxysmal tachycardia should be sought in irritation of the sympathetic cardiac accelerating nerves and a decrease in the tone of the n. vagi. The vascular system also participates in this symptom complex. Paroxysmal bradycardia accompanying some forms of neurasthenia can be explained by temporary irritation of the n. vagi or paresis of the sympathetic nerve. Post-infectious organic damage to the cardiac plexuses is also the cause of this symptom complex. The known experiment of Goltz can be the basis for explaining paroxysmal bradycardia, in which when tapping the abdomen of a frog, dilation and arrest of the heart in diastole occurs. When the n. vagi is cut, these phenomena disappear. Clinically, this symptom complex is observed in catarrhs of the stomach. Arising after ordinary acute dyspepsia, it often becomes stationary.-5. Enuresis nocturna (nocturnal enuresis) 5S8 is observed in children with a tendency to vagotonia and passes with the onset of sexual maturity. It is often accompanied by irritation of the genital organs and abnormal urination in quantity or quality. Most often, involuntary urination occurs during periods of fatigue or deep sleep. It can be eliminated: a) with atropine (Doxiades and Hamburger), b) by eliminating reflex irritations coming from the anus and genital organs, c) with psychotherapy (Guillaume).-6. Vegetative neuroses in lesions of the nose, ears and eyes. Many conditions - dizziness, noise and abnormal sensations in the ears without anatomical damage - result from a disturbance in the balance of the autonomic nervous system (often in connection with disorders of ovarian functions and with the climacteric period). Disturbance of innervation of the blood vessels of the nasal mucosa often leads to blockage of the nasal passages. Some juvenile forms of glaucoma are considered by Lyrangl and Guillaume as vegetative sympathicotonic neuroses.-7. Nervous dermatoses. Functional nervous dystrophies of the skin: urticaria, pemphigus, purpura, skin gangrene, graying or loss of hair can be the result of acquired irritability of the autonomic nervous system (L. Mueller).-8. Neuroses related to the sexual sphere. A number of functional disorders of the sexual organs: ejaculatio praecox, insufficient erection, increased libido or its absence, impotence depend on irritation or paresis of the autonomic nervous system. Some forms of leucorrhea, poly- and dysmenorrhea are associated with excitation of the parasympathetic system.-9. Neuroses in diseases of the endocrine glands. Pathohistological examination of the autonomic nervous system in endocrine diseases often reveals pictures of various changes in its nerves and ganglia (see Autonomic nervous system, pathology). Treatment of V. n. In addition to the preventive and physical therapeutic measures indicated in the articles Angioneuroses and Angiotrophoneuroses, calcium therapy is recommended. To achieve an acute effect (Drezeel), injections of a 5-10% solution of CaCl2 in the amount of 2-3-5-10 cubic cm or for long-term use a 2-10% calcium mixture, four to five tablespoons a day are prescribed.
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“Vegetative Neuroses.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/vegetative-neuroses/