Pathology of higher nervous activity – Pathophysiology of Nervous System

The pathophysiology of higher nervous activity studies the mechanisms of occurrence and development of deviations from the normal functioning of the higher functions of the human and animal brain. About animals, the term “experimental pathophysiology of higher nervous activity” is used, which implies the simulation of individual symptoms and syndromes of the pathology of the higher functions of the human brain in animals and their study by objective research methods, primarily by the method of conditioned reflexes. The theoretical provisions of the pathophysiology of higher nervous activity are based on the teachings of I.P. Pavlova (Fig. 22-1) on conditioned reflexes.

However, at present, the pathophysiology of the higher nervous activity

Most make extensive use of modern achievements in neurophysiology and neuropathology and is based on experimental data established by combining the method of conditioned reflexes with electrophysiological, morphological, biochemical, and other methods of studying the higher parts of the brain.

An external pathogenic agent reaches the brain in different ways, which significantly determine both the pathogenesis of the disease and its clinical manifestations. Therefore, it is necessary in all cases of violations of higher nervous activity

to identify the main pathway of exposure to a pathogenic agent, starting from the primary link of its application. Given these circumstances, distinguish between functional, post-traumatic, and combined pathology of higher nervous activity.

Under the functional pathology of higher nervous activity to be understood as behavioral disorders, which are caused by exposure to pathogenic stimuli in the external and internal receptors. Under posttraumatic pathologies higher nervous activity refers to behavioral disorders arising from direct exposure to the pathogenic agent to the brain, for example, when it is wound, hemorrhage in brain tissue, brain tumors, and others. By a combination (functionally-traumatic) pathology higher nervous activity refers to disorders arising due to the effect both on the receptor system of the body and directly on the brain, which occurs, for example, with radiation and heat damage to the head, its mechanical damage, etc.

In all three cases, the effect of a pathogenic agent causes primary damage to the brain, its primary disease, therefore, the resulting disturbances of higher nervous activity are primary. Disorders of higher nervous activity caused by other factors or developing as a result of another pathology of the body, for example, an infectious disease, tumors of non-cerebral localization, cardiovascular disease, etc., are secondary. Most often, the secondary pathology of higher nervous activity is the result of asthenization of the nervous system, a decrease in its resistance to psychogenic or other influences.

Functional pathology of higher nervous activity arises for two main reasons: 1) the pathogenic agent directly affects the receptors by the unconditional reflex mechanism; 2) the pathogenic agent has a signal value and acts through the receptors on the brain according to the conditioned reflex mechanism. Also, in humans, due to the presence of the second signaling system, the functional pathology of higher nervous activity can be caused by verbal influence, i.e. the pathogenic agent can affect the higher parts of the brain through the second (speech) signaling system.



All the reasons that can cause the pathology of higher nervous activity are divided into three large groups: 1) arising in the process of interaction of the organism with the environment; 2) genetically determined; 3) due to the combination of the first two. The first group of causes is currently the most studied, it is extremely diverse, and therefore their systematization and the selection of the main etiological factors among them are extremely important.

I.P. Pavlov, using the classical (secretory) method of conditioned reflexes, noted the following factors in the emergence of experimental neuroses: 1) too strong (“superstrong”) conditioned stimuli (meaning their physical properties); 2) too complex conditioned stimuli; 3) extremely accurate differentiation of conditioned stimuli; 4) lengthening the time of action of the differentiating (“inhibitory”) conditioned stimulus; 5) an increase in the number of differentiating stimuli; 6) the simultaneous use of differentiating stimuli; 7) changing the dynamic stereotype.

Later, a student of I.P. Pavlova P.S. Kupalov singled out the following additional “neurogenic” factors: 1) overstrain of the mechanism of regulation of nervous processes; 2) the collision of the process of excitation and inhibition in the cortical center of the unconditioned reflex; 3) collision of different (competing) reflexes; 4) difficult conditioned reflex tasks with a decreased general brain tone; 5) overstrain of synthesizing processes in the cerebral cortex.




The manifestations of the functional pathology of higher nervous activity are varied, but first of all, they relate to mental functions. So, there is a weakening of the analytic-synthetic activity of the brain, a violation of the long- and short-term

memory, regulation of emotions and motivations, regulation of the general functional state of the brain, interhemispheric relations. Usually, these disorders are manifested in eating, sexual, defensive, group behavior, which are most often studied to characterize higher nervous activity. A frequent manifestation of the pathology of higher nervous activity is violations of the sleep-wakefulness cycle, regulation of autonomic and somatic functions: there is a violation of the heart rate, regulation of blood pressure, a trophic supply of the skin (trophic ulcers appear, baldness occurs). Cases of myocardial infarction in animals in a state of experimental neurosis, accompanied by strong emotional arousal, are described.

Often, the pathology of higher nervous activity is accompanied by dysregulation of the digestive and excretory functions, the appearance of stomach ulcers, and other parts of the digestive system. With the pathology of higher nervous activity, hyperkinesis of the muscles of the limbs, neck, and other parts of the body may occur. The facts indicate significant neurochemical changes in the blood in experimental pathology, reflecting the dysregulation of the cholinergic and catecholaminergic mediator systems of the body. Different stages of the pathology of higher nervous activity are reflected in changes in the electrical activity of the neocortex and limbic structures of the brain.

Since the pathology of higher nervous activity manifests itself not only in deviations of mental functions but also in disorders of other body functions (regulation of the somatovegetative sphere, etc.), the study of its mechanisms is carried out taking into account changes in the whole organism, including the humoral system. Such a holistic approach to understanding the pathology of higher nervous activity reflects the idea of ​​nervousism and orients the search for mechanisms of disturbance of higher nervous activity at various structural and functional levels (from subcellular to organismic) of its organizations. Somatic disorders arising under the influence of mental factors, at present, especially in the studies of Western scientists, are often denoted by the term “psychosomatic disorders” and are summarized in the concept of psychosomatic medicine.



I.P. Pavlov, as a true physiologist looking for objective criteria for assessing function, immediately after discovering the possibility of the formation of the pathology of higher nervous activity by the method of conditioned reflexes, made many assumptions about the mechanisms of such pathology.

According to the classical ideas of I.P. Pavlov’s mechanism of such a pathology consists of overstrain of excitation, inhibition, or mobility. From whatever external causes the experimental neuroses depended, they were explained by the weakening of the process of internal inhibition, leading to the predominance of the irritable process or disturbances in the normal mobility of excitation and inhibition and, as a consequence, to their pathological lability or inertia.

An imbalance between inhibition and arousal contributes to the irradiation of inhibition along the cortex, and then along with the subcortical structures. In the early stages of development, inhibition has a protective function, it occurs after the nerve cells reach the limit of the possibilities of normal work and therefore is called transcendental inhibition. But after the exhaustion of the protective function of inhibition, the pathology of higher nervous activity begins to form.

These representations of I.P. Pavlova on the mechanisms of occurrence of the pathology of higher nervous activity played an important role in the development of some methods of treatment of such pathology, for example, in the substantiation and development of a method of sleep therapy. Sleep was viewed as a case of inhibition spread over the cortex and subcortex, and therefore, as a factor that protects nerve cells from pathological influences. However, at present, the presented ideas about the mechanisms of pathology have been revised, refined, and developed.

So, neurophysiological studies do not confirm the ability of inhibition to irradiate through the brain in the sense in which it was initially thought. Further, the concept of sleep as a state of diffuse inhibition in the cortex and subcortical structures has been significantly revised based on data indicating that sleep has a complex structure and

consists of several phases, replacing each other in a certain sequence. One of these phases – it is called paradoxical – is characterized by increased brain activity and is accompanied by strong emotional reactions and experiences. Dreams appear most often in this phase.

Modern ideas about the mechanisms of the pathology of higher nervous activity are based on taking into account the role of emotions and memory, as well as humoral factors in the onset of pathology.

The role of negative emotions. They arise under the influence of pathogenic stimuli and can take on a long-term, stagnant character. This is facilitated by long-term suppression of external manifestations of negative emotions (the so-called “unreacted emotions”), accompanied by hormonal and other chemical changes in the blood. These circumstances reduce the resistance of the nervous system to the pathogenic agent, and thus a self-reinforcing pathological system is formed. (“Vicious circle”), disorganizing the activity of other systems. However, such a pathogenic effect of negative emotions arises when they persist for a long time. In the early stages of their emergence, negative emotions often play a biologically positive role, acting as a factor in the emergency mobilization of the whole organism to counteract the pathogenic agent.

The role of memory. Pathological conditioned reflexes can be formed due to the fixation in the long-term memory of those states that arise in the brain under the influence of a pathogenic agent. These states can be reproduced in response to a corresponding conditioned stimulus or an appropriate situation (situational pathological reactions) or be ubiquitous in the form of a stable pathological state. The latter is also formed with the participation of long-term memory.

Another mechanism for the emergence and retention of the pathology of higher nervous activity may be the formation of a pathological temporary connection. Such temporary connections are especially easy to form when the general functional state of the brain is low; they can arise according to a conditioned-reflex or other principles of teaching (imprinting, figurative behavior), be situational or generalized in nature.

The general functional state of the brain changes under the influence of many factors. It decreases as a result

of a long-term limitation of the influx of visual, auditory, tactile, proprioceptive, and other stimuli into the brain, which occurs when changing geographic zones (prolonged stay in polar winter conditions), with prolonged hypodynamia, etc. As a result, the resistance of higher nervous activity to pathogenic factors also decreases, and the pathological reactions that arise are distinguished by a particular severity of the course.

The question of the deep mechanisms of functional pathology of higher nervous activity has received significant development in recent years, which is largely determined by the emergence of new morphological and biochemical approaches to the study of the brain. Thus, it was established by electron microscopy that experimental neuroses are accompanied by destructive changes in the neuronal and glial elements of the neocortex, as well as in its conductive apparatus, while reparative processes occur in parallel with the destructive processes, providing one or another degree of compensation for impaired functions.

Biochemical studies of the neocortex in animals in a state of experimental neurosis have revealed both reversible and irreversible disorders of the neurotransmitter system. These morphological and biochemical data are also of great methodological significance: for a long time, the prevailing opinion about neurosis as a functional disease. This meant the absence of structural changes in the brain, which were believed to be characteristic of other forms of pathology of higher nervous activity. The discovery of ultrastructural and neurochemical changes in the brain of animals in a state of experimental neurosis suggests that neuroses also have a structural basis, which confirms the only correct conclusion that any pathology is characterized by structural changes that can be detected by adequate methods of its study.



The pathophysiology of higher nervous activity includes, as one of its most important tasks, the study of the type of higher nervous activity. As observations have shown, the rate of occurrence of pathology, its manifestation, the degree of activation of defense mechanisms is largely determined by the individual characteristics of the nervous system. I.P. Pavlov understood by type the innate properties of the nervous system. The type, he emphasized, is an inborn, constitutional form of manifestation of the nervous system. But since the animal from the day of birth is exposed to the most varied influences of the environment, an alloy of innate traits (type) and traits that are formed in the process of an individual life is ultimately formed.

Since type is the innate property of the nervous system, they are reflected in such innate characteristics of the nervous system as strength, balance, and mobility of nervous processes. Given the various possible and most common combinations of these indicators, I.P. Pavlov identified the following main types of the nervous system: 1) strong, but unbalanced, which is characterized by the predominance of excitation over inhibition; 2) strong, balanced, with great mobility of nervous processes; 3) strong, balanced, with low mobility of nervous processes; 4) weak, characterized by a very weak development of both excitement and inhibition (Fig. 22-2).

Most often, the pathology of the higher nervous system occurs in animals with a weak type of nervous system, therefore such animals are called “suppliers of neuroses.” Nevertheless, the nature of the response of the nervous system to a pathogenic agent is determined not only by the type but also by those features that are acquired in the process of individual life. Therefore, it is now customary to characterize the nervous system in terms of behavioral reactions, in particular, in terms of emotionality, in terms of the regulation of the general functional state of the brain. For example, consider one of the forms of functional pathology of higher nervous activity (behavior), called informational.



Under the information pathology of higher nervous activity

Disorders in the higher functions of the nervous system are understood, as well as the disturbances in the vital activity of other body systems mediated by it, which arise during a prolonged stay of the brain under conditions of an unfavorable combination of the following factors: 1) a certain amount of information to be processed to make an important decision; 2) the factor of the time allotted for such brain work; 3) the level of motivation, which determines the importance of information and the need for its processing.

The combination of these three factors (hereinafter referred to as the information triad) can be unfavorable if, firstly, it is necessary to process a large amount of information (including decision making) with a long deficit of time allotted for such brain work and a high level of behavior motivation. Secondly, there is a lack of information for a long time, and the motivation for behavior (for example, the need to make a decision) is very high.

So, in both cases, a triad of factors influences and unfavorably combines: 1) the amount of information (in the first case, excessive, in the second it is less than necessary); 2) time (in the first case it is not enough, in the second case it is too long) and 3) motivation, which in both cases is very high. If clinical

the picture of the disease corresponds to a neurosis, then they talk about informational neuroses, if it corresponds to other diseases, then it is advisable to talk about the informational pathology of the corresponding nosology.

Within the framework of the concept of informational pathology of higher nervous activity, the mentioned triad of factors is combined into an independent group, which emphasizes its pathogenic significance in modern conditions of human life.

Studies in animals and humans have shown that with this form of pathology, short-term and long-term memory, emotions, signal analysis functions, sexual, eating behavior and other instincts are impaired, the regulation of cardiovascular function, respiration, digestion, and several other systems is impaired. A characteristic of this form of pathology is (in the early stages) certain dynamics, i.e. the sequence of involvement in the pathology of different body systems. In the later stages – persistent dysfunction of many-body systems.

Further, it turned out that the latent period of development of such a pathology, i.e. the time from the onset of the effect on the brain of the above triad of factors to the formation of a stable pathology varies greatly in different people and different animals, both of one and several species. Also, this period is characterized by various changes in behavior, the biological significance of which can in no way be understood as pathological. There are two types of factors that influence the development and formation of information pathology: 1) factors that reduce the stability of the nervous system to the information triad, they can be called risk factors for the emergence of information pathology; 2) protective factors, preventing the development of pathology, raising the resistance of the nervous system to information pathology.

The most frequent and significant risk factors for the occurrence of information pathology of higher nervous activity include prolonged physical inactivity, i.e. decreased motor activity, violation of intraspecific relationships between individuals, for example, a deficiency or perversion of mutual influence between individuals, especially in the early stages of ontogenesis, some genetically predetermined properties of the nervous system that form the type of higher nervous activity, brain trauma, disorders of the nervous system caused by factors that are not appropriate

the definition of the information triad. All of them reduce the resistance of the nervous system to the pathogenic influence of the information triad. When listing the conditions that contribute to the emergence of informational pathology of higher nervous activity, it should be borne in mind that the first place among them in frequency is muscle hypodynamia, which is largely due to the growth of professions predominantly of mental work, which usually require a sedentary lifestyle.

The biological significance of the second group of factors is to protect the body from the onset of pathology or (if it occurs) in the activation of compensatory mechanisms aimed at limiting and suppressing developing pathological processes.



Self-regulation of behavior is aimed at avoiding the pathogenic influence of factors of the information triad. Below are the observations that made it possible to establish the property of the brain of animals to self-regulate its behavior to eliminate the pathogenic effect on the higher nervous activity and other systems of the body of an unfavorable combination of factors of the information triad. Also, the properties of some limbic structures of the brain were found to increase the resistance of higher nervous activity to its informational pathology.

Let us consider specific behavioral manifestations of self-regulation of higher nervous activity aimed at eliminating external pathogenic causes. In dogs, motor-alimentary conditioned reflexes were developed: in response to conditioned signals, the animals ran up to one of three feeders located on the floor of the experimental room, where they received a piece of meat (Fig. 22-3). Each conditioned stimulus was associated with one of the feeding troughs, and reinforcement was performed only if the animal solved the problem – it ran up to the feeding trough corresponding to the signal value of the stimulus. Usually, after eating meat, the animal immediately returned to the starting point, since the next conditioned stimulus was turned on only when the animal was at the starting point.

A different picture of behavior is observed after pathogenic conditions arise caused by a violation of the ratio

information triad. In the example under consideration, this ratio was violated by decreasing the time due to the shortening of the intervals between individual signals. At the same time, the level of motivation (which was high, since the animal was hungry) did not change and the volume of information load did not change – the animals were presented with the same number of conditioned stimuli. So, the animals carried out the same volume of analytical and synthetic activity, but under conditions of the arisen lack of time. Already after several presentations of signal stimuli under these conditions, the following behavior change was observed: when the conditioned signal was triggered, the animal immediately left the starting place and ran to the corresponding feeder, but the time to return to the starting place increased, and the greater the deficit of time allotted for solving the entire volume of the problem, the slower the animal returned to the starting place. Thus the animal

itself increased the interval between the conditioned signals, and hence the time of the entire experiment, i.e. itself eliminated the lack of time and led to the optimal ratio of the factors of the information triad. This behavior significantly increased the period of formation of pathological reactions, i.e. period of preneurosis, and in some cases prevented the development of neurosis.

Similar behavior is observed if it is not the time of the experiment between conditioned signals that change, but the load on the analytic-synthetic activity of the brain increases.

The understanding of these reactions as having a biologically positive significance is acquiring a fundamental character: until recently, they were considered as early symptoms of pathology and, accordingly, were suppressed (“treated”) instead of taking measures to enhance them. The described reactions reflect the self-regulatory activity of the brain. Hence the great practical importance of these conclusions – it is necessary to find ways to activate and enhance the corresponding self-regulatory forms of behavior. This is important in all periods of the illness, but especially at the stage of pre-illness, when the self-regulatory mechanisms of the brain are well expressed and their purposeful strengthening can play a decisive role in increasing the psychophysiological resistance of the organism.

The central mechanisms of the protective activity of the brain. After the beginning of the impact of a pathogenic agent (for example, an unfavorable combination of the information triad) on higher nervous activity, pathological processes develop in certain structures of the brain, which are detected by electrophysiological, biochemical and ultrastructural studies, which disrupt the normal interaction between individual brain formations (new correlations arise between them) … After fixing all processes in long-term memory, stable pathological states of the brain are formed, which manifests itself externally in various non-adaptive reactions.

At the same time, brain structures are activated that prevent the development of pathological processes. One of the external manifestations of such a protective activity of the brain is the self-regulatory forms of behavior described above. Also, two more types of defense reactions develop in the brain: activation of brain structures, nonspecifically increasing the resistance of the nervous system to external influences, and activation of brain structures, suppressing the formation of pathological processes.

These conclusions are confirmed empirically using the technique of locomotor self-stimulation of the brain. For this, irritating electrodes are implanted in animals in various formations of the brain, through which an electric current is passed. The current is switched on by the animal itself while it moves across the floor, which is divided into sections. Each site is telemetrically connected to a specific irritating electrode, i.e. with a certain brain structure. As soon as the animal stands on one of the floor areas, stimulation of the corresponding brain formation is turned on. Everything described takes place in a room where, according to the previously stated method, informational pathology of higher nervous activity is generated (see Fig. 22-3).

It has been established that if an animal has the ability to choose between structures for their self-stimulation, then at the initial stages of the development of informational pathology of higher nervous activity, it predominantly stimulates the transparent septum (Fig. 22-4), i.e. instead of moving on the floor of the experiment

In the experimental room in various directions, it lingers for a long time (many minutes) in the area associated with irritation of the transparent partition. Such activation of this structure prevents the development of information pathology of the higher nervous activity or significantly increases the period of its occurrence. A similar effect, although less pronounced, is noted with self-stimulation of the lateral hypothalamus or medial tonsil. It is obvious that the transparent septum, the lateral hypothalamus, and the medial part of the amygdala play a protective function and prevent the development of pathology of higher nervous activity.

At the early stages of the onset of informational pathology of higher nervous activity, protective (including self-regulatory) forms of behavior and central mechanisms that prevent its development were identified, i.e. the property of the brain was found to self-regulate its behavior to protect the body from the pathogenic influence of the factors of the information triad. The main risk factors for the occurrence of informational pathology of higher nervous activity have been established and etiologically and pathogenetically grounded principles and methods of its prevention and treatment have been developed.



This type of pathology is expressed in the violation of certain forms of behavior. The pathogenesis of disturbances in eating, defensive, sexual behavior, as well as the pathogenesis of disturbances in memory, emotions, and the sleep-wake cycle has been studied in most detail. As noted, the creation of models of post-traumatic pathology of higher nervous activity aims to reproduce various injuries to the human brain caused by a cerebral hemorrhage, brain tumor, gunshot, or other traumatic injuries. The creation of such models is achieved by extirpating the brain tissue, cutting the pathways, electrical coagulation of individual parts of the brain, etc.

Violations of certain forms of behavior have some general, as well as particular manifestations, typical for each form. Common to all are violations of the balance of inhibition and excitation.

These changes can result in a deep suppression of the neocortex function with subsequent involvement of subcortical structures in the process. In other cases, increased excitement is observed. General behavior changes are largely determined by the type or individual characteristics of the nervous system.


Eating pathology

It is described as extensive damage to the neocortex and partial damage to the frontal and orbital cortex. When the frontal parts of the neocortex are damaged (removed), animals are not able to distinguish edible objects from others, therefore they eat things unsuitable for food and do not differentiate between different concentrations of saline solutions. These disorders are explained by damage to the mechanism of afferent formation of the eating behavior system. In case of damage to the orbital (orbital) area of ​​the neocortex, the unconditioned reflex secretion to food irritation sharply decreases, which is explained by the presence of the cortical representation of the food center in this area. With extensive removal of the neocortex or as a result of cutting its pathways, a prolonged decrease in unconditioned reflex food secretion and an almost complete loss of conditioned reflexes developed based on food reinforcement occur. The degree of these disorders increases in the ascending evolutionary series of animals and indicates the increasing role of the neocortex in the regulation of feeding behavior from lower to higher animals.

A variety of deviations from normal eating behavior are noted with damage to the limbic structures of the brain. Thus, in dogs, the destruction of the basal-lateral part of the amygdala causes a violation of conditioned food reflexes and a decrease in the unconditioned reflex response to food stimuli. Deep and characteristic eating disorders arise from damage to the hypothalamus; bilateral destruction of the ventromedial nucleus of the hypothalamus in rodents, carnivores, and primates causes hyperphagia, and damage to the lateral hypothalamus causes aphagia up to the death of animals from cachexia.

This gives reason to believe that the pathogenesis of the described changes in eating behavior is due to a violation of the regulation of hunger and satiety. Meanwhile, numerous observations are convincing that different parts of the hypothalamus are related

to the organization and regulation of other components of eating behavior. So, damage to the middle part of the lateral hypothalamus causes a violation of the initial urge to food, and the destruction of a more lateral area – a violation of the regulation of food intake. So, a violation of different links of eating behavior occurs when a whole series of brain structures are damaged, combined into a system of regulation of eating behavior, while neocortical structures are of paramount importance in the formation of individually acquired food reactions, and hypothalamic structures play an extremely important role in the organization and regulation of unconditionally the reflex component of different parts of eating behavior.


Defensive behavior pathology

As a result of extirpation of the anterior sections of the frontal region of the neocortex in rodents, predators, and primates, an active defensive reaction is enhanced, which sometimes turns into aggressive behavior, worsens the course of conditioned reflex defensive reactions. The pathogenesis of these changes is associated with a weakening of the emotion of fear. The disappearance of the fear reaction is also observed due to damage to the cingulate gyrus. Characteristic changes in defensive behavior take place after damage to the amygdala – fear and aggressiveness disappear in animals, they become tame.

These manifestations of traumatic damage to the amygdala are called Kluver-Bucy syndrome. Due to damage to the ventromedial part of the hypothalamus, active defensive behavior and the emergence of aggressiveness occur, while damage to the posterior part of the hypothalamus enhances the passive-defensive reaction – such animals are cowardly, their emotional reactions are sluggish. It is assumed that the pathogenesis of the described changes in the defensive reaction is of a neurochemical nature and is associated with a dysregulation of the serotonergic system of the brain.


Pathology of sexual behavior

It has been established that extensive damage to the neocortex in higher vertebrates disrupts the ability to mate; this re-

the action disappears completely due to damage to 60% of the entire area of ​​the cerebral cortex. However, such animals retain an erection, and they are excited in the presence of a female in estrus. An increase in sexual activity in different animal species was found due to damage to the amygdala. The weakening of sexual activity is noted when even small areas of the anterior hypothalamus are damaged. Less pronounced violations of sexual behavior are observed with damage to other structures of the diencephalon and midbrain.


Memory pathology

Memory impairment is a common symptom of post-traumatic pathology of higher nervous activity and is observed when the brain is damaged at different locations. At the same time, a selective influence of various brain structures on certain forms of memory (conditioned reflex, figurative, long-term, short-term) and memory phases (signal perception, its fixation, and reproduction) was found.

Deep disturbances of all types of memory are observed in higher vertebrates after extensive destruction of the neocortex. To a large extent, for this reason, conditioned reflexes are developed with great difficulty and easily disappear, are not retained. Damage to the prefrontal cortex leads to significant impairment of delayed reactions (they are realized with the participation of short-term memory). At the same time, conditioned reflexes (they are realized with the participation of long-term memory) change insignificantly and for a short time. The projection zones of the neocortex not only perceive but also keep the trail arising from a short-term (less than 100 ms) acting stimulus. This trail retention is necessary for signal analysis, i.e. assessing its biological significance. A significant violation of figurative memory occurs due to damage to the associative areas of the neocortex.

Impairment of short-term memory (impaired delayed reactions) is observed when other parts of the brain are damaged. Damage to various structures of the limbic brain (cingulate and pyriform gyrus, amygdala) causes depression or complete disappearance of short-term memory, but these disorders are reversible, and the function is fully or partially restored within a few months.

Of particular interest is the pathogenesis of memory impairment caused by damage to the hippocampus as the leading symptom of the Korsakov syndrome, which is well known in the clinic. Damage to the dorsal hippocampus causes deeper damage than the ventral. Damage to the hippocampus has a more pronounced effect on short-term than long-term memory. It is also believed that the hippocampus is important in the function of transferring short-term memory to long-term memory and plays a predominant role in the primary fixation of the track, while the function of long-term retention of the track is not associated with the hippocampus. Finally, and it is more likely that the hippocampus influences memory due to its participation in the organization of emotional reactions; as a result of its damage, the regulation of the emotional reaction is disrupted,

Memory impairment is also observed when other structures are damaged. The pathogenesis of memory impairment due to damage to various structures of the brain can be explained based on the concept of the existence of two closely related systems: the cerebral system of memory organization and the cerebral system of memory regulation. In higher vertebrates, the memory organization system is determined by the activity of the forebrain – the neocortex.

The second brain system related to memory function is the memory regulation system, which has a modeling effect on trace responses. The pathogenesis of the effect of damage to these structures is explained by their influence on memory through a change in the emotional response. The duration of the retention of a trace from any stimulus essentially depends on the strength of the emotional reaction caused by this stimulus.

Pathology of emotions

Refers to the frequent manifestations of post-traumatic pathology of higher nervous activity. Most often they occur when the limbic structures of the brain are damaged, but since the regulation of emotions occurs with the participation of the neocortex, pathological changes in the course of emotional reactions are also observed due to damage to the latter. These changes can be expressed in strengthening or weakening of emotions, perversion of the sign of emotions, when, instead of the normally observed position,

negative or negative emotions, their opposite reaction arises.

With extensive removal of the neocortex, a rage response can be observed, but it cannot be considered as a true emotional (“experienced”). Due to damage to the sensorimotor cortex, positive emotions are suppressed, and after damage to the prefrontal areas in dogs, the emotion of fear is initially suppressed, and then this emotion becomes intensified for a long time. In the latter case, the limbic-hypothalamic mechanisms of emotion are freed from the inhibitory effect on them of the prefrontal cortex.

Damage to the frontal areas in monkeys during lobectomy inhibits emotional reactions, as a result of which mimic and aggressive reactions and communication gestures lose their expressiveness and liveliness. A change like the emotional reaction is observed when the hippocampus is damaged – the intensity of emotions to threatening situations decreases, which is explained by the weakening of fear reactions, at the same time, emotional reactions to positive stimuli increase. Due to the removal of the cingulate gyrus, aggressiveness decreases, the animals become affectionate.

Significant disturbances in the course of emotional reactions occur due to damage to the amygdala; these disorders are so characteristic that they are known as “amygdala syndrome”, which consists of increased hunger and increased sexual activity, in suppressing the fear reaction – wild and aggressive monkeys turn into tame.

The following example can serve as evidence that different emotional reactions have a complex representation in the brain and are regulated by different systems: the destruction of the medial part of the amygdala inhibits the manifestation of fear, and the destruction of the dorsal part increases aggressiveness; destruction of the suture of the midbrain in males causes a manifestation of aggressiveness towards females, but does not affect the nature of the reactions that arise about males. At the same time, there are certain specific differences between animals in the manifestation of influence on emotional reactions, which gives rise to the conclusion about the existence of not only an individual but also a specific feature of the localization of the central mechanisms of emotional reactions.


Pathology of the cycle “sleep-wakefulness”

It has already been noted that for a long time sleep was considered as a passive state of the brain, opposite to wakefulness; believed that the main function of sleep is to energetically restore the brain after many hours of wakefulness. Another I.P. Pavlov opposed the understanding of sleep as a passive state. It is now known that sleep has a complex structure, consists of several phases, and has a multifaceted function. The most common point of view is that sleep consists of two main phases – slow and rapid (paradoxical) sleep, each of which, in turn, is heterogeneous. For example, in the slow phase of sleep, four successive stages are distinguished.

Post-traumatic sleep pathology is reflected in the violation of these phases and stages, while it is important that they have a different central organization, and therefore, brain damage manifests itself in different phases and stages of sleep in a different manner. Thus, injuries in the anterior sections of the neocortex cause a significant reduction in the duration of the REM sleep phase. Damage to the anterior preoptic region of the hypothalamus causes a decrease in the duration of slow-wave sleep. Damage to the anterior sections of the hypothalamus causes sleep disturbance, and damage to the posterior sections causes disturbance of wakefulness.



From the onset of the action of the pathogenic agent on the higher nervous activity to the formation of its stable pathology, a certain time passes, during which, along with the development of pathological processes, the activation of protective, including self-regulatory, mechanisms of the brain takes place. Both the first and the second have complex dynamics of development in time and space, are characterized by certain external – behavioral, autonomic, humoral, electroencephalography, and other manifestations, as well as structural and neurochemical changes in the central nervous system.

Since both pathological and compensatory mechanisms are activated simultaneously, the doctor is faced with the most important

task of their differentiation, the correct determination of the diagnostic value: often early manifestations of compensatory (self-regulatory) brain activity are mistakenly perceived as early symptoms of pathology and, accordingly, are eliminated for “treatment” instead of being maintained and strengthened. All of the above applies to both functional and post-traumatic pathology of higher nervous activity. This issue becomes especially important in the early stages of pathology – pre-pathology, i.e. before pathological reactions acquire a stable course and maladaptive reactions occur.

There are two sides in the compensatory activity of the brain: 1) when behavior is formed, aimed at eliminating the pathogenic situation by its active behavior, and 2) when processes are formed in the central nervous system that prevent the emergence and development of the pathological system. These protective processes are formed with the participation of certain formations of the brain; they also combine into a system, and their protective function consists, firstly, in increasing the resistance of the nervous system to pathogenic agents and, secondly, inactive suppression (inhibition) of the pathological system.



Definition and classification

The term “stress” (from the English. Stress – stress) has long been used in the artistic, medical, etc. the literature usually refers to a subjectively unpleasant state of stress (see section 4.1).

The term “psychogenic stress” is used to denote a form of stress that occurs primarily under the influence of mental factors, ie. unusual (super-strong) stimuli that primarily affect the higher functions of the brain. The problem of psychogenic stress has become especially relevant in connection with a significant increase in the load on mental functions when in many areas of a person’s labor activity, physical labor began to be replaced by mental labor, and most importantly, such a replacement occurred suddenly, in a short period of time, if you approach

to the fact in the historical sense, and therefore without any special preparation for such a replacement.

Psychogenic stress is often referred to as “emotional stress” or “psycho-emotional stress”. Meanwhile, psychogenic stress is always accompanied by emotions, just as emotions are accompanied by stress caused by non-psychogenic factors (burns, trauma, etc.), however, it is secondary. Consequently, the question is: what form of the organism or what function of it is primarily exposed to stressful effects, i.e. what is the “gateway” for the stressor? Moreover, any stress is significantly different from other phenomena (conditions), which is why its further development depends on the subjective significance of the stress factor, the experience of the individual, the type of his higher nervous activity, etc. There are sufficient grounds for classifying psychogenic stress according to several parameters: 1) causes of stress (taking into account the qualitative and physical characteristics of the stressor); 2) manifestations; 3) biological value.


Causes of psychogenic stress

Any external and internal stimulus that differs sharply from the factors that make up the usual environment, and primarily affects the higher functions of the brain, can cause stress. Taking into account the intensity, time of the increase in intensity, and time of action, psychogenic stimuli can cause: 1) acute; 2) subacute; 3) chronic stress.

Acute stress occurs when an unexpected effect on the body of a psychogenic factor, which is super strong in its significance and physical intensity, in the complete absence of the factor of “expectation” of such an impact. This, as a rule, is extremely unpleasant or dangerous information concerning the life, health, well-being of the person who perceives this information, or his relatives. This is a natural phenomenon (earthquake, flood), an outbreak of ethnic conflicts, etc. – everything that belongs to the group of “emergencies”.

Subacute stress occurs under the influence of similar stimuli but in people prepared for their possible occurrence. For example, this is an astronaut trained for a freelance

situation, but knowing neither the time nor the reason, etc. its occurrence. The same stress occurs in a warrior who is ready for a life-threatening combat situation, etc.

Chronic stress occurs in people who are constantly waiting or under the influence of constantly realizing unusual stimuli, however, of moderate-intensity and prepared for their occurrence. In our reality, these conditions are typical for many modern professions, other forms of life and often become the norm.

There are several methods for simulating psychogenic stress in animals. The most appropriate is the situation of information overload or information deficit in combination with the conditions of limiting the time factor and a high level of motivation for behavior (see section 22.5). It has already been noted that higher nervous activity under conditions of an unfavorable combination of the information triad can cause persistent disorders of higher functions, pathology of higher nervous activity. But the emergence of such a pathology is preceded by a period of activation of protective, including self-regulatory mechanisms, which serve as a manifestation of biologically positive hyperstress. When certain symptoms of pathology occur,

Acute psychogenic stress occurs when a suprathreshold electric current is applied to the paws of animals (for example, rats), in the absence of information for making the right decision, in this case, such behavior that will prevent the flow of current.

Often, to simulate the state of biologically negative stress, especially when experimenting on higher animals (dogs, monkeys), a method of drastically limiting their motor activity is used.


Types of psychogenic stress

Taking into account the biological significance of psychogenic stress, its role in the vital activity of the organism, nor mistress, hyper stress, and hypostress are distinguished.

State of norm stress ensures long-term work of the brain in a constantly changing or monotonous environment and is the basis for minimizing errors in solving daily or unusual tasks, without requiring the activation of additional protective mechanisms of the brain, as it happens in a state of hyper stress. Psychogenic normostress is formed with the participation of long-term memory, which makes it possible to predict possible changes in the environment, or rather, to develop and keep in working readiness the required level of activity of brain functions. Also, the organization of normostress based on long-term memory does not allow “breaking” of the regulatory mechanisms during temporary hyperstress. The stability of normo-stress is its main feature, contributing to the stable and adequate flow of various brain functions. The border of normostress is a certain corridor,

The state of hyper stress arises under the influence of superstrong stimuli and, in terms of its biological significance, can be biologically positive or biologically negative. These two forms of hyper stress are determined by the level of development of adaptive mechanisms, primarily the mechanism of self-regulation. The state of hyper stress, with a sufficient level of development of defense mechanisms, returns to the normostress corridor, or new boundaries of normostress appear (with the constant action of the factors that caused the state of hyper stress). Otherwise, a state of negative hyper stress develops – the conditions for the onset and formation of pathology.

Both biologically positive and biologically negative hyper stress is a form of manifestation of the transitional state (M.M.Khananashvili) of the body, mental functions of the brain. The state of hyper stress is characterized by many features. Its common feature is inadequate, maladaptive behavior under conditions characteristic of norm stress.

Animals, finding themselves in conditions of hypostress, are, using the expression of I.P. Pavlova concerning animals with a weak type of nervous system, “suppliers of neuroses.” People in a state of hypostress have a low threshold of addiction to alcohol and drugs.

A typical pattern of hypostress was simulated in dogs that developed in isolation from 1 to 12 months of age. They were found to be able to form conditioned reflexes and differentiate into sound and visual stimuli of medium strength. However, reflexes acquired a stereotyped character. These animals were characterized by a low threshold for the onset of a depressive state and fear, and much less often – aggressiveness, which is characteristic of biologically negative hyperstress.

The indicators that allow distinguishing the 3 main forms of stress include the effectiveness of preventive measures. Thus, first-year students during the examination session were divided into groups of normo- and hypostress for several criteria. The latter group, as a rule, did not cope with the influences of the information triad; symptoms were indicating the appropriateness of the termination or interruption of studies. These students had a sharp increase in general motor activity (which was understood as “restlessness”, laziness, lack of interest in studies, etc.). Meanwhile, the totality of observations made it possible to recommend the use of intense muscle loads. In these cases, 70% of the students from the hypostress group had an improvement in their mental and physical well-being, and most importantly, the effectiveness of solving mental problems significantly increased.

Manifestations and pathogenesis of psychogenic stress

It is widely believed that negative psychogenic stress often affects the function of the cardiovascular and digestive systems and other systems. Thus, negative psychogenic stress is manifested in the occurrence of a state of chronic anxiety, impaired memory functions, regulation of emotions, research-oriented activity, sexual behavior, and thyroid function. In recent studies, impaired immunity, changes in the level of catecholamines in the blood, urine, and various structures of the brain have been noted. A decrease in dopaminergic receptors was found in the septum of the brain.

It has been established in animals, and this has been confirmed in human studies, that an early symptom of biologically negative stress is a disruption in the relationship between

functional activity of the cardiovascular, respiratory systems, and the function of body temperature regulation.

The existence of a central (cerebral) mechanism for regulating the body’s resistance to super-strong psychogenic factors, biologically causing both positive and negative hyper stress, has been established. This mechanism has its own structural and functional organization and is manifested by specific reactions of the somatic and humoral systems, the nature of which depends on the causes that cause them. The neocortex, thalamus, limbic structures, specific subcortical nuclei determine the self-regulation of animal behavior.