Catad_tema Schizophrenia - articles

Schizophrenia: morphological changes in the brain

One area of ​​research in schizophrenia is the analysis morphological changes in the brain, since it is obvious that in this disease, along with the processes of synaptic transmission and receptor activity, the structure of nerve cells, fibers and some parts of the brain also undergoes changes. The search for anatomical changes in the brain is one of the components of etiological research.
The most commonly reported enlargement of the lateral ventricles of the brain; some researchers also point to an increase in the third and fourth ventricles, a decrease in the volume of the temporal lobes and an increase in the size of the pituitary gland. There are several theories about the role of organic changes in the development of the disease. There is an opinion that they take place already by the beginning of the development of the disease and in this case are considered as factors that increase the risk of developing schizophrenia. This theory is supported by recently obtained results of brain ultrasound (increase in the size of the lateral ventricles) of fetuses from the group high risk development of schizophrenia (Gilmore et al., 2000).
According to another theory, anatomical changes play a role in a predominantly exogenous form of schizophrenia or arise for some non-specific reasons (for example, complications in childbirth). It is assumed that the reason for the increase in the size of the pituitary gland (which is observed at the beginning of the disease, at the time of the first psychotic episode) is the increased activity of the hypothalamic-pituitary-adrenal system (HPA). Under the influence of corticoliberin or stress factors, HGS is activated, which leads to an increase in the number and size of corticotropic cells, and hence the size of the pituitary gland (Ryan et al., 2003, 2004; Carmine M Pariante). Other studies show that in patients with schizophrenia, the regulation of myelination of nerve fibers in the frontal lobe is dysregulated. If normally the amount of myelin increases up to a certain age (about 40 years), then in schizophrenia its amount practically does not change with age. It is believed that this leads to a decrease in the ability of the brain to ensure the coordinated activity of neural systems responsible for performing multiple functions. Clinically, these changes are manifested by a variety of symptoms of schizophrenia, including a disorder of cognitive processes. In a number of autopsy studies, a decrease in the number of neuroglial elements in the cortex of the frontal lobes (mainly due to oligodendrocytes) and a decrease in the degree of expression of genes involved in the formation of myelin were noted. It is assumed that a decrease in the number of oligodendrocytes and myelin in the cortical layers leads to neuropil degeneration, resulting in an increase in the density of neurons. The myelin sheath of the nerve fibers of the cortex inhibits the decrease in the volume of the frontal lobes associated with the fixation of certain processes observed in schizophrenia; thus, a decrease in the amount of myelin in the cortical zones may be one of the reasons for the depletion of the neuropil in the frontal cortex. Methods for assessing morphological changes 1. The most sensitive method for detecting myelin is MRI of the brain in several projections using the "inversion-recovery" mode.
2. 1H NMR spectroscopy allows to determine the content of N acetylaspartate (NAA) - a marker of neurons, the level of which can be used to judge the number and density of cells.
3. NMR spectroscopy using the isotope 31 P is used to determine the content of residues of phosphodiesters (lipid metabolism products) and phosphomonoesters (synthesis markers cell membranes). These biochemical markers can be used to indirectly assess the number of neurons and glial cells, their integrity, and the degree of damage. Influence of typical and atypical neuroleptics on the process of myelination Until the age of 30, the content of myelin in patients with schizophrenia is higher than in healthy people, and after 30 years it is significantly lower. This is consistent with observations about high efficiency treatment for early stages disease and an increase in the degree of resistance to therapy and the progression of functional disorders in patients with schizophrenia with age. Many studies have noted a significant effect of antipsychotics on the volume white matter in the brain of patients with schizophrenia, but these data are contradictory. Investigators have reported both increases (Molina et al., 2005) and decreases (McCormick et al., 2005) in cortical white matter volume with long-term use of atypical antipsychotics. Similar results have been observed with long-term therapy with typical antipsychotics (McCormick et al., 2005; Lieberman et al., 2005). Atypical antipsychotics (unlike typical drugs) have been shown to stimulate the formation of new neuroglial elements in the frontal cortex of primates and rodents (Kodama et al., 2004; Selemon et al., 1999; Wang et al., 2004a). It is possible that these drugs can reduce the degree of deficiency of oligodendrocytes and/or myelin in the cerebral cortex. A recent study in a group of men with schizophrenia compared therapy with an atypical antipsychotic (risperidone) and a typical antipsychotic (flufenosine decanoate (PD)). The study showed that in patients with schizophrenia, the structure of the frontal lobes differs from that in healthy people. White matter volume in the risperidone group was significantly higher than in the PD group, with an increase in white matter volume in the risperidone group and a decrease in white matter volume in the PD group compared to the control group. The volume of gray matter in both groups of patients was significantly lower compared with healthy people and less in the risperidone group than in the PD group (George Bartzokis et al., 2007). In at least some cases of increased white matter volume in the risperidone group, a shift in the boundary between gray matter and white matter towards the cortex was also noted (George Bartzokis et al., 2007). In the risperidone group, a decrease in neuronal density was also observed. It is possible that increased myelination during risperidone therapy contributed to a decrease in the rate of fixation-related frontal volume shrinkage. However, these studies do not allow us to determine whether the higher white matter volume in the risperidone group is due to the preservation of myelin, which was initially higher, or is the result of the treatment itself. It is possible that these differences are related to patient demographics (gender, age) and study design (George Bartzokis et al., 2007). Molecular mechanism The observed effect of atypical antipsychotics is not clear. It may be associated with the effect of these drugs on lipid metabolism (Ferno et al., 2005), facilitation of dopaminergic transmission in the prefrontal cortex, since stimulation of dopamine receptors can play the role of a protective factor in relation to oligodendrocytes and promote the formation of new cells. Held in recent times prospective studies have shown that with less effective treatment and a more severe course of the disease, there is a tendency to progression of structural changes in the brain, the main of which are an increase in the size of the ventricles and a decrease in the amount of gray matter. In addition, there is a relationship between anatomical changes and non-compliance with neuroleptic therapy. These data indicate the possibility of antipsychotics to reduce the rate of progression of morphological changes in some patients. Thus, the study of morphological changes in the brain of patients with schizophrenia is one of the promising directions in the study of this disease. The results of these studies will help to better understand the causes of its development, to study the features of the course and the mechanism of action of the drugs used, including antipsychotics.

The information is current as of 17.09.2010

Drama and Mystery: Schizophrenia

The origin of schizophrenia has not yet been established for certain. The onset of this disease has little to do with the age of the patient. On the other hand, some non-obligatory patterns of its course and therapy prognosis are traced, depending on the age at which it first manifests itself.

It should be stated right away that schizophrenia in our time is not treated. However, in most cases, it is possible to slow down its progress or completely remove the symptoms. At the same time, the rejection of drug regulation will certainly entail the resumption of symptoms, regardless of how long they were taken.

The aura of mystery that surrounds schizophrenia is formed and maintained by several features of this disease that make it very different from others. mental disorders. And these features, in turn, purely superficially contain a substantial amount of mystery. Sounds intriguing? Now it will become clear what the essence of the intrigue is ...

Schizophrenics, unlike other “ripe” ones, are one of the last to lose the skill of fascinating communication. They have almost no signs of neuralgia characteristic of many disorders - twitches, antics, tics, unnatural movements. Speech is almost never impaired in terms of syntax. The first and only thing that can often alert when communicating with a patient with schizophrenia is the logic of the judgments themselves, which he communicates in a syntactically completely correct form.

The fact is that the very essence of schizophrenia is the loss of relationships between the individual parts of what is called personality. In such patients, for example, emotions do not depend in any way either on external stimuli, or on mental activity, or on life experience, or on subjective interests.

The situation is exactly the same with their thinking and other components of the brain - cut off from everything else, having no direction vectors, in no way connected with the current situation. That is, while maintaining each function separately, almost intact, their mutual coordination with each other is completely absent.

How is this expressed in practice? Very idiosyncratic. From this moment begins the elusive mystery of the image of a schizophrenic. Let's take speech as an example. When a person talks to someone, how does he build communication?

Firstly, depending on the personality of the interlocutor - his age, status, degree of acquaintance with him, the presence or absence of official or other relationships. Example:

It is clear that in the presence of parents, a teenager will not use profanity, even if he thoroughly owns it and uses the entire main part of the day outside the home ...

Secondly, depending on the topic of conversation and their position on this issue. Example:

The same person, talking in the evening about football with a friend, will certainly be very little similar in his speech characteristics to the one who explained to the boss in the morning the motives for making a decision.

Thirdly, the environment in which the conversation takes place will play a significant role: a telephone dialogue, even with an extremely unpleasant person, if the call caught the subscriber in public place, will certainly turn out to be more neutral than if it happened face to face.

Fourthly, based on all these subtleties, the speaker will additionally try to build his speech in such a way as to be most correctly understood by this particular interlocutor.

And after all, this is far from all that we take into account unconsciously, almost automatically every time we find ourselves in a situation of verbal communication! The milestones from which the schizophrenic repels in his speech behavior are of a completely different kind and type. First of all, due to his illness, he does not perceive the image of the interlocutor as such. He sees his grandmother's advanced age, her faded green coat, the color of her eyes, how many teeth she has, and is even able to understand which political party she has supported since perestroika. But in his head these disparate features cannot form into a general speech picture. Like one to assent that the pensions are not enough, offer to hold her bag or help her read what is written on the store window, etc.

Any healthy person, when talking with a representative of the older generation, would definitely do something of this - albeit for the sake of an elegant “rounding off” of an unnecessary conversation. A schizophrenic cannot do this. Most likely, he will quickly seize the initiative from his grandmother and lead the conversation in such a way that she cannot insert words. The fact is that patients with schizophrenia, along with unity mental manifestations lose the ability to distinguish between the main and secondary details of the object. That is why, in addition to their misfortune, they acquire an almost ingenious inclination. This tendency is to create completely unexpected mental moves by combining objects according to properties that are quite real, really inherent in them ... But usually not those that are considered a reason for comparison.

The embodiment of such a feature sometimes looks very bizarre. For example, a healthy person can hardly offhand name a common property for a sword, an airplane, a computer, and a truck. The most daring assumption would be that they are all made, at least for the most part, of iron. A schizophrenic, on the other hand, can easily determine that all these objects demonstrate the power and greatness of human civilization, symbolize high technology and the superiority of mind over nature, etc., etc.

In fact, after the first two phrases, a whole stream of associative considerations will flow. And he jumps to anything else very quickly. Behind the "greatness of human civilization" one can easily come up with a thought in the spirit of "however, what difference does it make if all these things are just a cluster of atoms that have taken their form."

It is practically impossible to stop the associative series along which the patient's thought jumps. Moreover, if the dialogue does not take place in a clinic where orderlies and a syringe with a powerful sedative are within reach, one should neither argue with such a patient nor interrupt it. Not only his speech, but also his emotions are cut off from reality. Schizophrenics rarely show adequate to the stimulus reactions of this kind.

In other words, any carelessly spoken word can be followed by an attack. And people with mental disorders, as you know, are distinguished by physical strength, surpassing even some sports indicators. For that medical staff psychiatric hospitals and armed with rubber truncheons in the order of the norm. This is not a manifestation of sadism or heartlessness, but an objective condition for their work. Patients of such institutions are capable of injuring even armed, specially trained and sports-trained nurses.

We have tried to describe the features of the behavior of a schizophrenic as clearly as possible in order to more clearly emphasize their originality. The speech of such a patient is not incoherent at all. On the contrary, formal logic shines through in all his actions and words. But he cannot focus on one, the most important topic, he continuously moves from one subject to another - including those that are not connected in any way with the previous one ...

The behavior of a schizophrenic does not correspond to his former life experience, neither the current circumstances, nor the norms and rules common to all people. But, no matter how paradoxical this combination may look, there is also a clear meaningfulness in it at the same time. Hence the close affinity of schizophrenia with genius.

Deprived of the opportunity to recognize the integral properties of something and focus on them, the schizophrenic easily finds other, unusual, and nevertheless quite possible interconnections of things. And what a coincidence! - genius is defined precisely as the ability to find a common basis that unites facts that are well known separately, but have not previously been compared!

However, there are a number of reservations here that make it possible to consider schizophrenia as a disease after all - useless both for discoveries and for the patient himself.

Firstly, geniuses, in contrast to "exactly" sick people, invariably retain the basic ideas necessary for successful contact with their own kind. But the ability to distinguish a smart or promising thought from a stupid one is also one of the conditions for discovery. The schizophrenic, having accidentally fallen on a noteworthy paradigm, will not be able to distinguish it from any other. And to develop, refine, prove, test not in practice ... No, none of the other components of genius for this disorder is not just not typical - the disease simply destroys everything else!

Further. Schizophrenia, if left untreated, quickly leads to the degradation of most of the parts into which the personality has broken up. The emotions of a schizophrenic in their basic state are dulled, since there is not enough information from the outside for their active production. Why? We remember that loud music in the neighborhood may not seem loud to him. He can't even hear her! And the reactions under the influence of an irritant that has reached his brain do not initially differ in complexity - perseverance, absolute self-righteousness, aggression ... The only thing that looks the most difficult here is their inadequacy to the circumstances. But, of course, there is nothing for a healthy brain to work on a clue - a person is simply sick and his illness has the property of losing focus on the notorious circumstances. Only and everything.

A person who is unable to develop, maintain and draw on the complexity of the processes of one of his parts in the work of another, quickly degrades. Emotional dullness (in the meaning of the term) is accompanied by a number of defects from other areas. In particular, passivity, lack of will and desire for the simplest actions, exacerbation of susceptibility to insignificant trifles.

The symptom of sensitivity is explained by the fact that in a schizophrenic nothing is small or large. And to form goals in life, you need the ability to prioritize.

The body movements of patients gradually acquire pretentiousness, unnatural and intricate postures are used, but without violating the accuracy of coordination. The latter has to do with the loss of discrimination between how to move naturally and how not. The patient's speech becomes increasingly scarce in terms of the lexical means used. The process ends with characteristic schizophrenic dementia.

In addition, the type of pure, classical schizophrenia is quite rare. Complications in the form of mania, paranoid elements, psychoses are common for her. Moreover, psychosis often takes the form of manic-depressive because schizophrenics are generally prone to a minor mood due to a general lack of information, impressions, sensations, etc. Almost 40% of patients with schizophrenia commit suicide.

There is nothing Freudian or even simply unusual in this. All, except for schizophrenia, mental illness manifests itself as a symptom of the degradation of some part of the personality. In schizophrenia, the scenario is initially different, but it develops in exactly the same way. First, the personality of a schizophrenic breaks up into separate fragments, and any relationship between them disappears. Next, the process of degradation of the formed fragments starts. But already as it grows, individual symptoms of diseases appear that are not associated with schizophrenia and not with former complexes, but with the disintegration of certain fragments of the personality.

Interestingly, schizophrenia can be, in addition to being irreversible, sluggish and, so to speak, fast. The first develops gradually, making itself felt only in the period of exacerbations by individual symptoms. Most often, this is isolation, detachment of the patient, combined with increased resentment and capriciousness. It is also accompanied by neglect of the rules of personal hygiene and appearance, especially noticeable during an exacerbation. During improvements, many of the primary signs disappear altogether. But the light intervals are getting shorter in time, and each subsequent exacerbation is getting harder. And so - until the complete failure of the brakes.

You can live next to a latent schizophrenic for years, believing him to be nothing more than a person with quirks (who doesn’t have them?) or prone to depression. Separate features of schizoid (literally - "similar to schizophrenia") behavior are characteristic of creative and gifted people, owners of a melancholic temperament, as well as people in advanced stages of stress. And, of course, children. Their thinking on the basis of the most unimaginable associations, an actively working imagination, the immediacy of mental reactions - all this is nothing but the attributes of "blooming in all its glory" schizophrenia. Fortunately, they disappear with age. And in schizophrenics, they reappear. Just like in childhood!

Rapidly progressive schizophrenia develops over several months, sometimes years. For her, the transition to hallucinations and delusional ideas is more characteristic, as if immediately - bypassing the symptoms of slovenliness and irritability. The most common hallucination for schizophrenia is the so-called voices in the head. Science has not yet found a full-fledged explanation for this feature, but there are theoretical conclusions on this matter. Schizophrenic "voices" have one significant difference from hallucinations as such. The fact is that the patient himself describes them as if “made”. This turnover means that a person perceives any true hallucination as a completely real image, sound, sensation. Including if it contains absolutely incredible elements.

The curious thing here is that the brain is not able to distinguish a true hallucination from the effects of reality. And schizophrenics retain the impression that the voices they hear belong neither to their personality nor to objective reality. A touch of "artificiality" remains with them due to the fact that the "voices" in the patient's brain do not merge with any of its categories. He does not consider them something fantastic (again, he does not have criteria for evaluating this), but he is clearly aware that the source of the "voices" is not in his head.

Such strangeness of "voices" gave rise to the assumption in the scientific world that for schizophrenia, strange as it may sound, hallucinations are not typical at all. Under the phenomena similar to them, there is a modified, highly distorted, but continuing "communication" of those disparate processes that once constituted a single personality. The echoes of such a “dialogue” take the form of visions, voices, sensations that the patient perceives as something alien.

If we talk about proven facts, then in the brain of schizophrenics, scientists have discovered a number of structural abnormalities characteristic of this disease. Primarily, we are talking about changes structural organization so-called. prefrontal cortex. On the hemispheres, this is the most convex visually, the frontal part. If you show on the head “outside”, then the prefrontal region starts right above the eyebrows, makes up the entire forehead and ends a centimeter and a half above the hairline. In humans, it is approximately responsible for extracting the necessary knowledge from memory. And the development of that, according to P. K. Anokhin, a mode of action in which the brain first creates an order of actions and compares it with memory for effectiveness. Yes, and after that - it turns into reality. In addition, the prefrontal cortex generates the emotional part of a person's assessment of the event about which he intends to act.

So, in patients with schizophrenia, an abnormally low number of mitochondria is noted in neurons and processes in this area of ​​the cortex. Recall that mitochondria are intracellular formations in which energy is produced to feed the cell itself. Or, in the case of neurons, to generate electrical impulses. A decrease in the number of mitochondria, in other words, reduces the overall electrical potential of brain cells, which slows down and disrupts the processing of information in this area.

In addition, the brain of schizophrenics is characterized by a decrease in the number of synapses in the hippocampus, which is responsible for the transformation of short-term memory into long-term memory. Moreover, the difficulties with the formation of synaptic connections are explained in them by a violation of the structure of myelin molecules - the protein that makes up the white "sheaths" of axons. In schizophrenics, in other words, the braiding of the wires for transmitting the impulse is damaged.

To put it even more directly, the neurons of the cortex in schizophrenics are formed with birth defects. These defects are somewhere on the verge between incompatibility with life and healthy norm. This leads to the conclusion that the cells of the cortex in schizophrenics are weaker than in healthy people. But weaker not so much as not to work at all. And the patient's brain, finding itself in the position of a person with a weakened immune system, as mental loads increase, begins to take measures to prevent serious disorders. And for this, he “sets to the maximum” all the mechanisms available to him for inhibiting the activity of the cortex. Just as a chronically ill person protects parts of the body that are prone to colds from the cold. It must be understood that he forms schizophrenia out of fear that epilepsy will develop ...

And if without jokes, then from this point of view, schizophrenia is just a means of self-defense for improperly formed brain cells! Indeed, the EEG activity of the cortex of a drug-free schizophrenic is strikingly similar to that of a person under hypnosis. It turns out, relatively speaking, that schizophrenia is a state of chronic hypnotization! Impressive, isn't it?

Indirectly, the fact that the neurons of a schizophrenic have reduced performance is also indicated by a fact recently discovered by a group of American scientists. They conducted experiments with the memory of patients with schizophrenia. And found out one interesting feature the process of this mechanism. It turned out that schizophrenics, when trying to remember something, involve many times more cortical zones than people without deviations. Moreover, they much more often experience the phenomenon of synchronization of the efforts of the right and left hemispheres, where in healthy subjects only one of them is activated, as it should be "traditionally".

This means, in fact, that in schizophrenics, each simple mental effort causes twice as much activity of the brain as usual and creates more synapses. But it also means that their brain, it turns out, is not as strictly differentiated by the functions performed as in others. homo sapiens. Which can equally be a sign of both the immaturity (underdevelopment) of the entire substance of the brain, and a way for the brain to reduce the load on each zone or neuron separately.

The understanding of at least part of the mechanisms of schizophrenia is based on the currently widely used and relatively successful drug therapy. At the end of the last century, antipsychotics and antidepressants gained great popularity. At present, as the knowledge of medicine about the features of schizophrenia advances, this series has been expanded and supplemented with atypical antipsychotics that do not cause drowsiness and suppress only specific reactions of the cortex to the threshold of normal. As well as stimulants for the production of a mediator (a substance that activates synapses) dopamine in the cells of the cortex.

The real solution to the problem has not yet been found, which is eloquently indicated by cases of schizophrenia resistant to any type of therapy and combinations of drugs, against which, accordingly, medicine is powerless.

Attention, mystery!

Not all blind people manage to develop skin-optic vision. However, it is quite possible. modern science cannot find a convincing explanation of how the blind, regardless of the reasons for the loss of vision, age and gender, are able in the vast majority to learn to recognize colors with the skin of their hands. Experiments to develop a methodology for teaching this skill were started in the middle of the 20th century. AT different time the corresponding experiments were carried out by the most prominent Soviet scientists. The interest of domestic neurophysiology in the hidden possibilities of the brain was, of course, explained not only by medical prospects, but now this is no longer important.

The earliest large-scale work in this direction was carried out by A. N. Leontiev, Academician of the USSR Academy of Sciences, a scientist whose main activity was in the field of psychology. Together with one of the most prominent physiologists of his time, Academician L. A. Orbeli (we already mentioned him above), they received the first positive results in their test group. Full description experiment, observations and methods A. N. Leontiev made in his monograph "Problems of the development of the psyche" (M .: MGU, 1981). No, in fact, this work, of course, saw the light much earlier - in 1959, but since then it has been reprinted three more times. Here are the data on the latest edition.

And then the entire Soviet Union repeatedly demonstrated their talents to the amazing women Roza Kuleshova (headed by I.M. Goldberg, neuropathologist) and Ninel Kulagina, who was trained in skin-optical vision by a team of physicists led by academician Yu. V. Gulyaev. The results of the experiments allowed both the organizers themselves and the outside scientists to conclude that the phenomenon of skin-optical sensitivity can be developed to a very high accuracy. That is, up to reading ordinary printed (not embossed, printed in Braille!) texts with your fingers.

However, with the collapse Soviet Union further purely scientific work in this direction has ceased. And this was connected not only with socio-historical changes, but also with an ambivalent attitude to the problem, which has not become unambiguous over the past time. In the US, some of these studies have been criticized in connection with proven cases of violation of the conditions of purity of the experiment. And in the mid-1980s, attempts at a similar critical approach were made in the USSR.

There are several problems in assessing the reality of the existence of skin-optical hypersensitivity. First, it is relatively easy to simulate, simply because of the very methodology of the experiment, which creates more "foul play" options than any other. The second problem: this property has made tricks with imitation of skin-optical vision a popular part of the world circus art. That is, many professional illusionists are able to easily demonstrate similar ones, at least with a purely outside"phenomena". The third problem is that science has not been able to detect any special points of sensitivity or receptors that differ in degree of susceptibility from other skin sensors in the skin of the fingers. Which, however, is quite natural ...

Nevertheless, there are plenty of obvious refutations that skin-optic vision is impossible.

Firstly, above it was already possible to observe a number of cases that could only be objectively recorded, and scientific explanation still not eligible. Most likely, no one will ever find particularly sensitive receptors, since the brain does not really need them. Why does he need them, if the essence of the signal he receives from a simple skin receptor and a complex organ like the eye is the same? That's the same...

Secondly, the goals with which an illusionist studies tricks and an academic studies a blind patient are slightly (literally, slightly!) Different. There is no reason for a world-famous scientist to train a subject for years and record hundreds of the smallest details for the sake of non-scientific purposes. The holders of the degree of an academician do not even need to acquire world fame through tricks - they already have it. Thirdly, it should be noted that when trying to demonstrate skin-optic vision as a scientific fact, a serious methodological error was nevertheless made. It was allowed out of good intentions to emphasize the availability of the development of this skill in almost every person, but still ...

It's about poor selection of subjects. In their purely scientific work, A. N. Leontiev and L. A. Orbeli developed sensory skills in blind patients, that is, in principle, incapable of peeping patients. The fact of medically provable blindness of the patient would nullify at once half of the “methodological features” of the demonstration. However, after Leontiev and Orbeli, scientists became interested in the possibility of developing the same hypersensitivity in people with healthy vision. From the position that the ability or inability of a normally functioning brain to reorganize in the right way can explain a lot in the features of its compensation mechanism. That is, the thought of scientists as in itself is understandable. But purely scientific prerequisites played a cruel joke with them - doubts arose that might not have existed ...

Plus, it is possible that if further experiments were also carried out on the blind, this entire campaign would not exist at all. The Soviet media, being an extremely ideological structure, would hardly have allowed the demonstration on the air of any unique abilities by people, the presence of which was never particularly emphasized in the USSR. Soviet ideology really sought to develop among the countries and citizens of the rest of the world the idea that communist states are not characterized by most of the social and medical problems burdening the budgets of the capitalist countries.

One way or another, mistakes were undoubtedly made in the study of skin-optic vision. And they did their harm - such as they could only manage. However modern rules scientific ethics quite allow us to open this issue from new positions. Indeed, since 2006, Western science has been increasingly expressing the opinion that it is necessary to resume work with this mechanism. For example, one can trace the history of the fluctuation of scientific views on the problem and assess the relevance of its solution in our days by the work of Dr. A. J. Larner.

This author supports the latest version - about the relationship of skin-optic vision with the phenomenon of synesthesia. Synesthesia is not a disease and to a certain extent it is characteristic of any person. This is the perception of stimuli of one type through stimuli of another - color through sound or taste, or in any other combination. A healthy phenomenon of synesthesia is associations. Blue seems cold to us, red - hot, orange - sweet, etc. A disease is when a person does not hear the sound itself at all, but sees a whole palette before his eyes, which changes in accordance with the melody. Separately, this phenomenon practically does not occur, but it can accompany some pathologies of the brain.

There is an opinion that skin-optic vision manifests itself in the blind due to the inclusion of synesthetic associations. And A. J. Larner reflected this concept in his paper. This study uses other, already scientifically proven mechanisms of the brain to substantiate the possibility of the real existence of alternative ways to see. Which indicates the growth of a new wave of interest in one phenomenon of the brain from many others, waiting in the wings ...

It is strange how we manage to explore space and study the bowels of the Earth, if we still know practically nothing about own brain… Don't you find it?..

Hallucinogenic psychoactive drugs, such as LSD, can cause short-term episodes of psychosis, and frequent use or overdose of marijuana and stimulants (cocaine, amphetamines) sometimes leads to a transient toxic psychosis, the clinical picture of which resembles schizophrenia (Bowers, 1987; Tennent and Groesbeck, 1972).
Maybe also(although by no means proven) that substance abuse can trigger the onset of schizophrenia.

Relatives a patient with schizophrenia is sometimes seen as the cause of the disorder in hallucinogens, but they are mistaken: scientific facts do not support this opinion. It is known that in Great Britain and America in the 1950s and 1960s LSD was used as an experimental drug in psychiatry, and the percentage of individuals (among voluntary participants in trials and among patients) who developed a long-term psychosis of the schizophrenic type almost did not exceed the corresponding figure for the general population. populations (Cohen, 1960; Malleson, 1971).

The truth held in Sweden a study found that military recruits who used marijuana frequently and in large quantities were six times more likely to develop schizophrenia later on (Andreasson et al., 1987). However, this pattern may be explained by the fact that persons predisposed to schizophrenia were more likely to resort to the use of marijuana, using it as a way to cope with the premorbid symptoms of the disease.

The brain in schizophrenia

In some patients schizophrenia found organic changes in the brain. Post-mortem analysis of brain tissue revealed a number of structural abnormalities, and new imaging techniques have documented the presence of intravital changes in both the structure and functioning of the brain.

With the help of such methodologies, as magnetic resonance imaging (MRI), revealed changes in the size of various brain structures, especially in its temporal lobes. The fluid-filled cavities (ventricles) deep within these lobes are often dilated, and the volume of the tissue of the lobes themselves is reduced. The greater these observed changes, the more severe the thought disorders and auditory hallucinations present in the patient (Suddath et al., 1990).

Some methods imaging, such as positron emission tomography (PET), assesses the current functioning of the brain and gives a similar picture of abnormalities. PET scans show increased activity in the temporal lobes, especially in the hippocampus, a structure located in the temporal lobe responsible for orientation and ultra-long-term memory (Tamminga et al., 1992).

Building a functional Images of a different kind - by recording the electrophysiological parameters of the brain using an electroencephalograph - shows that most patients with schizophrenia seem to be characterized by an excessively increased response to repetitive external stimuli and a more limited (compared to other people) ability to eliminate unnecessary information (Freedman et al., 1997).

Along with this, we received data that brain structures that are supposed to weed out irrelevant stimuli (eg, the frontal lobe) show reduced activity on PET scans (Tamminga et al., 1992).

Due to this difficulty screening sensory stimuli, post-mortem studies of brain tissue have revealed abnormalities in brain cells of a particular type—inhibitory interneurons. These neurons inhibit the activity of the main nerve cells, preventing them from responding to excessive a large number of input signals. Thus, they protect the brain from being overloaded with too much sensory information from the environment.

In the patient's brain schizophrenia the number of "chemical messengers", or neurotransmitters (mainly gamma-aminobutyric acid (GABA)), released by these interneurons, is reduced (Benes et al., 1991; Akbarian et al., 1993), which implies that the function of inhibition, aimed at preventing brain overload is performed less effectively.

Deviation in the functioning of these interneurons appears to lead to changes in brain cells that release the neurotransmitter dopamine. The role of dopamine has long been of interest to schizophrenia researchers because certain psychoactive drugs (such as amphetamines) that enhance the effects of dopamine can cause psychoses that resemble schizophrenia, and psychoactive drugs that block or reduce its effects are effective in treating psychoses (Meltzer and Stahl, 1976) .

Dopamine amplifies sensitivity of brain cells to irritants. Usually this heightened sensitivity is useful in raising a person's awareness of the situation during periods of neuropsychic stress or danger, but for a schizophrenic patient whose brain is already in a state of hyperactivity, additional exposure to dopamine can become a factor that plunges him into psychosis.

Of these research It follows from the data that in schizophrenia there is insufficient regulation of brain activity by interneurons, as a result of which the brain overreacts to numerous signals coming from the environment, and has an insufficient ability to weed out unwanted stimuli. This problem is exacerbated by the shrinkage of the temporal lobes, where sensory input is normally processed; as a result, it becomes even more difficult for a person to adequately respond to new stimuli.

There are a great many questions about schizophrenia that scientists still cannot answer. But first, let's talk about the most important thing.

Schizophrenia is very common mental illness. According to statistics, about one in 100 people in Australia suffered from it at some point in their lives. Thus, almost everyone has friends or relatives with schizophrenia.

Schizophrenia is a complex condition that is difficult to diagnose, but the listed symptoms are usually detected: mental activity, perception (hallucinations), attention, will, motor skills are disturbed, emotions are weakened, interpersonal relationships are weakened, streams of incoherent thoughts are observed, perverse behavior, there is a deep sense of apathy and feeling hopelessness.

There are two main types of schizophrenia (acute and chronic) and at least six subtypes (paranoid, hebephrenic, catatonic, simple, nuclear, and affective). Fortunately, schizophrenia is treated with cognitive therapy, but most often with medication.

There are many myths associated with schizophrenia. One of them is the point of view that this disease occurs more often in countryside than in cities. Moreover, according to outdated information, schizophrenics from rural areas often move to cities to find solitude. However, scientists refute this myth.

A study of schizophrenia among Swedes indicates that urban dwellers are more susceptible to this disease and they do not move anywhere. Scientists say that the environment can push people to the disease.

But myths aside, the true source of schizophrenia is still a mystery. Previously, it was believed that the reason was the poor attitude of the parents towards the child - usually too reserved, cold mothers were blamed. However, this point of view is now rejected by almost all experts. The fault of the parents is much less than is commonly believed.

In 1990, researchers at Johns Hopkins University discovered an association between a reduction in the superior temporal gyrus and intense schizophrenic auditory hallucinations. It has been theorized that schizophrenia results from damage to a specific area on the left side of the brain. Thus, when voices appear in the head of a schizophrenic, there is increased activity in that part of the brain that is responsible for mental and speech activity.

In 1992, this hypothesis was reinforced by a serious Harvard study, which found an association between schizophrenia and a decrease in the left temporal lobe brain, especially that part of it that is responsible for hearing and speech.

Scientists have found a link between the degree of thinking disorder and the size of the superior temporal gyrus. This part of the brain is formed by a fold of the cortex. The study was based on a comparison of magnetic resonance imaging of the brains of 15 patients with schizophrenia and 15 healthy people. It was found that in patients with schizophrenia, this gyrus is almost 20% smaller than in normal people.

Although no new treatments have been proposed as a result of this work, the scientists believe that their discovery provides an opportunity to "further study this serious disease."

Every now and then, new hope emerges. A 1995 study conducted at the University of Iowa suggests that schizophrenia may be due to pathology of the thalamus and areas of the brain anatomically associated with this structure. Previous evidence indicated that the thalamus, located deep in the brain, helps focus attention, filter sensations, and process information from the senses. Indeed, "problems in the thalamus and its associated structures, extending from the top of the spine to the back of the frontal lobe, can create the full range of symptoms seen in schizophrenics."

It is possible that the whole brain is involved in schizophrenia, and some psychological representations, for example, about oneself, may have a certain connection with it. Dr. Philip McGuire says: "The predisposition [to hearing voices] may depend on abnormal activity in areas of the brain associated with the perception of internal speech and the assessment of whether it is one's own or someone else's."

Is there any specific time for the occurrence of such disorders in the brain? Although the symptoms of schizophrenia usually appear during adolescence, the damage that causes it can occur in infancy. "The exact nature of this nerve disorder is unclear, but [it reflects] abnormalities in brain development that appear before or shortly after birth."

There are experts who believe that schizophrenia can be caused by a virus, and a well-known one. A controversial but very intriguing version of the causes of the disease is put forward by Dr. John Eagles of the Royal Cornhill Hospital in Aberdeen. Eagles believes that the virus that causes polio can also influence the onset of schizophrenia. Moreover, he believes that schizophrenia may be part of the post-polio syndrome.

Eagles bases his belief on the fact that since the mid-1960s. in England, Wales, Scotland and New Zealand, schizophrenia patients decreased by 50%. This coincides with the introduction of polio vaccination in these countries. In the UK, an oral vaccine was introduced in 1962. That is, when polio was stopped, the number of cases of schizophrenia decreased - no one imagined that this could happen.

According to Eagles, the Connecticut researchers found that patients admitted to the hospital with schizophrenia were "significantly more likely to be born during years of high polio prevalence."

Eagles also points out that among the unvaccinated Jamaicans who came to the UK, "the rate of schizophrenia is significantly higher compared to the local [English] population".

Eagles notes that in recent years, the existence of post-polio syndrome has been established. In this syndrome, about 30 years after the onset of paralysis, people begin to suffer from severe fatigue, neurological problems, joint and muscle pain, and increased sensitivity (especially to cold temperature). Post-polio syndrome occurs in approximately 50% of patients with polio. According to Eagles, "The average age of onset of schizophrenia is approaching thirty years, and this is consistent with the concept of schizophrenia as a post-polio syndrome that develops after suffering a perinatal poliovirus infection."

Doctors David Silbersweig and Emily Stern of Cornell University believe that schizophrenics are unlikely to have serious brain problems, but, nevertheless, they managed to find something very interesting. Using PET, they developed a method for detecting blood flow during schizophrenic hallucinations. They conducted a study of six either untreated or untreated schizophrenics who heard voices. One had visual hallucinations. During the scan, each patient was asked to press a button with their right finger if they heard sounds. It was found that during hallucinations surface areas of the brain involved in the processing of sound information. Moreover, in all patients there was a rush of blood to several deep areas of the brain: the hippocampus, hippocampal gyrus, cingulate gyrus, thalamus and striatum. Do schizophrenics really hear voices? Their brain data shows that this is the case.

The speech of schizophrenics is often illogical, incoherent and confused. It used to be thought that such people were possessed by demons. The researchers found a far less fantastical explanation. According to Dr. Patricia Goldman-Rakick, a neurologist, the speech problems of schizophrenics may reflect short-term memory failure. It was discovered that the prefrontal cortex of the brain of schizophrenics is significantly less active. This area is considered the center of short-term memory. Goldman-Rakick says, "If they can't hold on to the meaning of the sentence before they get to the verb or object, the phrase is devoid of content."

In addition to all of the above, there are many questions about schizophrenia that are still unanswered.

Is schizophrenia caused by maternal immune response or malnutrition?

Some scientists believe that schizophrenia is caused by damage to the developing fetal brain. A study conducted at the University of Pennsylvania, which involved medical data from the entire population of Denmark, showed that the occurrence of schizophrenia can be influenced by severe maternal malnutrition. early stages pregnancy, as well as the immune response of her body to the fetus.

Thanks for the memories

As the body ages, the enzyme prolyl endopeptidase increasingly destroys neuropeptides associated with learning and memory. In Alzheimer's disease, this process is accelerated. It causes memory loss and reduced active attention time. Scientists from the city of Suresnes in France discovered medicinal formulations that prevent the destruction of neuropeptides by prolyl endopeptidase. In laboratory tests with rats that had amnesia, these compounds almost completely restored the animals' memory.

Notes:

Juan S. Einstein's brain was doing the washing // The Sydney Morning Herald. February 8, 1990. P. 12.

McEwen B., Schmeck H. The Hostage Brain. N. Y.: Rockefeller University Press, 1994, pp. 6–7. Dr. Bruce McEwan is head of the Hatch Neuroendocrinology Laboratory at Rockefeller University in New York. Harold Schmeck is a former national science columnist for The New York Times.

Interview with M. Merzenikh leads I. Yubell. Secrets of the brain // Parade. February 9, 1997. P. 20–22. Dr. Michael Merzenich is a neurologist at the University of California, San Francisco.

Lewis G., David A., Andreasson S., Allebeck P. Schizophrenia and city life // The Lancet. 1992 Vol. 340. P. 137–140. Dr Glyn Lewis and colleagues are psychiatrists at the Institute of Psychiatry in London.

Barta P., Pearlson G., Powers R., Richards S., Tune L. Auditory hallucinations and smaller superior gyral volume in schizophrenia // American Journal of Psychiatry. 1990 Vol. 147. P. 1457-1462. Dr. Patrick Bartha and colleagues work at the Johns Hopkins University School of Medicine in Baltimore.

Ainger N. Study on schizophrenics – why they hear voices // The New York Times. September 22, 1993. P. 1.

Shenton M., Kikins R., Jolesz F., Pollak S., LeMay M., Wible C., Hokama H., Martin J., Metcalf D., Coleman M., McCarley R. Abnormalities of the left temporal lobe and thought disorder in schizophrenia // The New England Journal of Medicine. 1992 Vol. 327. P. 604–612. Dr. Martha Shenton and colleagues work at Harvard Medical School.

Flaum M., Andreasen N. The reliability of distinguishing primary versus secondary negative symptoms // Comparative Psychiatry. 1995 Vol. 36. No. 6. P. 421–427. Dr. Martin Flaum and Nancy Andresen are psychiatrists at the University of Iowa Clinics.

Interview with P. McGuire leads B. Bauer. Brain scans seek roots of imagined voices // Science News. 9 September 1995. P. 166. Dr. Philip McGuire is a psychiatrist at the Institute of Psychiatry in London.

Bower B. Faulty circuit may trigger schizophrenia // Science News. September 14, 1996. P. 164.

Eagles J. Are polioviruses a cause of schizophrenia? // British Journal of Psychiatry. 1992 Vol. 160. P. 598–600. Dr John Eagles is a psychiatrist at the Royal Cornhill Hospital in Aberdeen.

The study by D. Silbersweig and E. Stern is cited by K. Leitweiler. Schizophrenia revisited // Scientifi c American. February 1996. P. 22–23. Drs David Silbersweig and Emily Stern work at medical center Cornell University.

The study by P. Goldman-Rakik is cited by K. Conway. A matter of memory // Psychology Today. January – February 1995. P. 11. Dr. Patricia Goldman-Rakic ​​is a neurologist at Yale University.

Juan S. Schizophrenia – an abundance of theories // The Sydney Morning Herald. October 15, 1992. P. 14.

Research by J. Megginson Hollister et al. cited by B. Bauer. New culprit cited for schizophrenia // Science News. 3 February, 1996. P. 68. Dr. J. Megginson Hollister and colleagues are psychologists from the University of Pennsylvania.

Scientifi c American. Making memories // Scientific American. August 1996. P. 20.

A PHOTO Getty Images

“By studying the anatomy of the brain, we found that patients with schizophrenia are divided into several groups (according to the nature of the disorders), each group has its own symptoms. This allowed us to take a fresh look at this disease. We knew that different patients, suffering from schizophrenia, are often very different symptoms, and now we understand why,” says Robert C. Cloninger, MD, psychoanalyst and geneticist, professor at the University of Washington in St. Louis.

Using the latest brain-scanning technology, scientists examined 36 healthy volunteers and 47 patients with schizophrenia. In schizophrenics, various disorders were found in the corpus callosum - a plexus of nerve fibers that connects the left and right hemispheres and plays essential role in signaling in the brain.

By studying these disorders, the researchers found that certain features revealed by brain scans corresponded to the specific symptoms of the disease. For example, in patients with certain changes with one of the areas of the corpus callosum, strange and disorganized behavior was usually observed. Disorganized thinking and speech, as well as unemotionality, were more often manifested in violations in another area. “Their own” disorders were associated with hallucinations and delusions.

The same group of researchers in 2014 already managed to establish that schizophrenia is not one disease, but a whole group of eight genetically different disorders, each with its own specific symptoms. Then Robert Cloninger and Igor Zwir, Associate Professor at the Department of Information Technology and Artificial Intelligence at the University of Granada (Spain), found a pronounced relationship between certain sets of genes and specific clinical symptoms of the disease.

The current study is further confirmation that schizophrenia is actually a whole heterogeneous group of disorders. Scientists believe that in the future it will be important to establish the relationship of specific groups of genes with the structural features of the brain and specific symptoms in order to be able to prescribe individually tailored therapy to each patient. At the moment, all patients diagnosed with schizophrenia are usually prescribed approximately the same treatment, regardless of the characteristics of the symptoms.

The researchers have developed a special analysis system for processing genetic data and tomography results. This system is similar to the one by which sites like Netflix (online movie theaters) try to predict which films will be popular with viewers.

“We did not at all try to find patients with certain symptoms first, in order to then look for pathological changes in their brain. We just analyzed the data and found certain patterns. Someday, doctors will be able to prescribe precisely tailored treatment to patients with the help of such examinations and accurate knowledge of the genetics of schizophrenia,” says Igor Tsvir.

See J. Arnedo et al. for details. "Decomposition of brain diffusion imaging data uncovers latent schizophrenias with distinct patterns of white matter anisotropy", Neuroimage, vol. 120, October 2015.