Catad_tema Schizophrenia - articles

Schizophrenia: morphological changes in the brain

One of the directions in the study of schizophrenia is the analysis of 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 recent results of cerebral ultrasonography (enlarged lateral ventricles) in high-risk fetuses for 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 31 P isotope is used to determine the content of residues of phosphodiesters (products of lipid metabolism) and phosphomonoesters (markers of cell membrane synthesis). 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 of high treatment efficacy in the early stages of the 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 white matter volume in the brain in 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). The molecular mechanism of the noted 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. Recent 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 was a relationship between anatomical changes and non-compliance with antipsychotic 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

Approximately once a year, and sometimes a little more often, another wrestler with psychiatry appears on the network. In general, they are very stereotypical people with a standard set of claims and a complete reluctance to read any information, let alone look for it, if it does not confirm the fact that psychiatry is a pseudoscience created for the personal enrichment of psychiatrists, pharmaceutical firms and the fight against dissidents. One of the main trump cards of the wrestlers is the fact that people with schizophrenia turn into "vegetables" and only psychiatrists with haloperidol are to blame for this. Repeatedly, my colleagues both at home and in my journal said that the process of turning into a vegetable lies in the disease itself. For the same reason, it is better to treat schizophrenia than to admire the amazing and unique world of a sick person.

The idea that schizophrenia is associated with changes in the brain is not new. It was written about in the 19th century. However, at that time, post-mortem autopsies were the main study tool, and for quite a long time, nothing special and distinctive from all other "brain" diseases was found in the brains of patients. But with the advent of tomography in medical practice, it was nevertheless confirmed that brain changes take place in this disorder.

It has been found that people with schizophrenia lose volume of the cerebral cortex. The process of cortical loss sometimes begins even before the onset of clinical symptoms. It is present even when a person is not receiving treatment for schizophrenia (antipsychotics). For five years of illness, the patient can lose up to 25% of the volume of the cortex in some areas of the brain. The process usually begins in the parietal lobe and spreads further through the brain. The faster the volume of the cortex decreases, the faster the emotional-volitional defect occurs. Everything becomes indifferent to a person and there is no desire for anything - the very thing that is called a "vegetable".

I have some bad news. We are constantly losing nerve cells. This is actually a natural process and it goes quite slowly, but in patients with schizophrenia this process is accelerated. So, for example, normal teenagers lose 1% of the cortex per year, and with schizophrenia 5%, adult men lose 0.9% of the cortex per year, patients 3%. In general, in adolescence, a malignant form of schizophrenia is very common, where in a year you can lose everything you can, and even after the first attack, this process is visible to the naked eye.

For those who are interested, here is a picture showing how the brain loses its cortex during 5 years of illness.

In addition to a decrease in the volume of the cortex, an increase in the lateral ventricles of the brain was also found. They are enlarged not because there is a lot of water, but because the brain structures that lie in the walls are reduced in size. And this is observed from birth.

Here are pictures of twins - the first has schizophrenia (the "hole" in the middle of the brain in the image has dilated lateral ventricles), the second does not have the disease.

People with schizophrenia had cognitive (learning) problems before developing the disease and even before using medications, including impaired information processing and language memory. All of these symptoms worsened as the disease progressed. among other things, they have reduced (also even before the disease) the function of the frontal cortex, which is responsible for criticism (i.e. the correct perception of oneself, one’s actions, comparing them with the norms of society), planning and forecasting activities.

Why this happens to the brain, in fact, no one knows for sure. There are 3 theories that have a fairly good reason.

1. Violation of brain development. It is assumed that already in utero, something goes wrong. For example, patients with schizophrenia have some problems with substances that are very important for brain development - with the same reelin, which should regulate the process of cell movement during brain development. As a result, the cells do not reach the places where they should, form incorrect and rare connections between themselves. There are many more described mechanisms of the same kind, which say that a certain birth defect causes a disease.

2. Neurodegeneration - enhanced cell destruction. Here, cases are considered when certain causes, including various metabolic disorders, cause their premature death.

3. Immune theory. The newest and most promising. It is believed that this disease is the result of inflammatory processes in the brain. it’s hard to say why they arise now - maybe the body suits itself (an autoimmune disease) or it’s the result of some kind of infection (for example, there are facts that the flu suffered by the mother during pregnancy increases the risk of developing the disease). However, in patients with schizophrenia, various inflammatory substances are found in the brain, which can be very aggressive to surrounding cells. About similar mechanisms, but with depression
No one claims that neuroleptics are a panacea for schizophrenia. To some extent, the situation with them is now obvious, that we will no longer be able to squeeze more benefit from them than we have now. It is possible to improve the safety profile of the drug, but antipsychotics do not radically solve the issue. We need some new ideas and discoveries in the field of schizophrenia, a new breakthrough in understanding the disease. The latest immune theory sounds very promising. However, for now, antipsychotics are all we have. These medicines allow patients to live in society for a long time, and not stay in the walls of a psychiatric hospital. Let me remind you that just less than 100 years ago, mental illness was a sentence and treatment was reduced only to the maintenance of patients in hospitals. Now only a small proportion of patients are in hospitals, and it is thanks to antipsychotics that this is possible. In fact, in practice, and any psychiatrist will tell you this, it is the lack of treatment that leads to a faster transformation into a vegetable. Destruction of the brain... it is destroyed by disease and without neuroleptics, and in some people it happens quite quickly.

In the brain of schizophrenics, the work of genes responsible for contacts between neurons is weakened. Moreover, this weakening is global - the changes have affected the work of more than fifty genes.

Although schizophrenia is the most common mental illness, it is still a mystery to doctors and scientists. There are several hypotheses about the causes of its occurrence and the mechanism of development, but so far none of them has been fully confirmed. Perhaps the first large-scale molecular genetic study in this area, which was carried out by the team of Jackie de Belleroche, professor of medicine at Imperial College London, will help unravel the mystery. For the first time, they identified 49 genes that work differently in the brain of a schizophrenic and an ordinary person.

brain dead gene map

Scientists worked with the brain after his death. They took 28 brain tissue samples from deceased people who suffered from schizophrenia during their lifetime, and 23 controls were taken from those who were mentally healthy during their lifetime. The brain tissue was provided to them at London's Charing Cross Hospital. For the study purposefully selected areas that are presumably related to the development of the disease are the anterior prefrontal and temporal cortex.

RNA (ribonucleic acid) Unlike DNA, an RNA molecule consists of a single chain of nucleotides. The composition of RNA nucleotides includes a residue of orthophosphoric acid, ribose (instead of deoxyribose in DNA) and a nitrogenous base: adenine, cytosine, guanine, or uracil (instead of thymine in DNA). RNA is formed on the DNA template during transcription. Messenger RNAs (mRNAs) carry information about protein synthesis. Transfer RNAs (tRNAs) carry amino acids to the assembly site of a protein molecule. Ribosomal RNA (rRNA) are part of the ribosomes.

The fact that a genetic study was carried out on a dead brain should not be surprising. If you work with the brain immediately after its death, messenger RNA (mRNA) is stored in the tissue, which is synthesized from the DNA sample during gene expression. To detect all mRNA, molecular biologists use the biological microarray technique. So they get a complete picture of the mRNA in the part of the brain they are interested in, by which they can judge which genes were working in it at that moment.

After examining gene patterns in the schizophrenic and normal brains in this way, scientists at Imperial College London compared their results with independent studies of the same brain regions conducted by US researchers at the Harvard Brain Bank.

Neurons of a schizophrenic contact worse

Synapse Place of contact between neurons. It includes the presynaptic membrane of one neuron, the postsynaptic membrane of another neuron, and the synaptic cleft between them. When a nerve impulse reaches the presynaptic membrane along a long process, the axon, a neurotransmitter is released into the gap in the composition of vesicle vesicles. They pass through the synaptic cleft, reach the postsynaptic membrane on the dendrite, a short process of another neuron, and interact with receptors. So the nerve impulse passes to another neuron.

Both studies identified 51 genes whose expression differed from normal in the schizophrenic brain. Of these, 49 genes changed their work in the same direction, that is, either strengthened it or weakened it in both British and American work.

In the schizophrenic brain, the work of genes associated with the packaging of neurotransmitters into vesicle vesicles in synapses has changed. And also responsible for the release of signal enhancers (neurotransmitters) into the synaptic cleft and associated with the cellular cytoskeleton. The difference suggests that in schizophrenia, contact between brain neurons is disrupted.

In search of objective diagnosis and effective treatment

Schizophrenia affects one in a hundred people in the world. Currently, doctors make a diagnosis solely on the basis of a person's behavior. The symptoms of schizophrenia can vary greatly, but typically include disruption of social relationships, decreased motivation, and sometimes hallucinations.

“Most patients are diagnosed with schizophrenia around the age of 20, but if the disease had been diagnosed earlier, patients would have received treatment earlier. Which would have a significant impact on their quality of life,” emphasizes Prof. de Belleroche. It is clear that an accurate knowledge of the physiological and biochemical changes in the body in schizophrenia can lead to the creation of more objective diagnostic methods.

According to some scientists, schizophrenia is caused by too much of the neurotransmitter dopamine in the brain. This is indirectly confirmed by drugs that block dopamine - they improve the condition in schizophrenic patients. Another theory puts the blame on glial cells, the cells of the nervous tissue that form an insulating sheath of myelin material around the nerve fiber. It has been shown that in patients with schizophrenia, the myelin sheath is damaged, which reduces the speed of passage of the nerve impulse.

But for a more accurate understanding of what physiological and biochemical mechanisms cause disease, you need to get to the genes. Moreover, it is desirable directly to the genes working in the brain. "The first step to better treating schizophrenia is to be clear about what's going on in the brain and which genes are involved," says Jacquis de Belleroche. "The new study brings us closer to a potential drug therapy target."

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 individuals predisposed to schizophrenia were more likely to resort to the use of marijuana 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 electrophysiological parameters of the brain using an electroencephalograph - shows that most patients with schizophrenia seem to have 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 an excessively 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 (predominantly gamma-aminobutyric acid (GABA)) released by these interneurons is reduced (Benes et al., 1991; Akbarian et al., 1993), which implies that the 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 increase the effects of dopamine can cause psychoses resembling 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.

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 other 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 a 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 the unity of mental manifestations, lose the ability to distinguish between the main and secondary details of an 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 responses of this kind adequate to the stimulus.

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. That is why the medical staff of psychiatric hospitals is 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 either to his previous life experience, or to current circumstances, or to 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 finally reached his brain are not initially complex - perseverance, absolute certainty that he is right, 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 to be something fantastic (again, he does not have criteria for evaluating this), however, 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. First of all, we are talking about changes in the structural organization of the 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 a 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 we found out one interesting feature of 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 various times, the most prominent Soviet scientists carried out corresponding experiments. 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 their time, Academician L. A. Orbeli (we have already mentioned him above), they obtained the first positive results in their group of subjects. A. N. Leontiev made a complete description of the experiment, observations and methods 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 under the guidance of 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.

Nevertheless, with the collapse of the Soviet Union, further purely scientific work in this direction 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 variants of "cheating" 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 “phenomena” at least from a purely external side. The third problem is that science has not been able to detect any special points of sensitivity or receptors that differ in the 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 more cases that could only be objectively recorded, and are still not subject to scientific explanation. 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 standpoint of the fact 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 the communist states are not characterized by most of the social and medical problems that burden 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. Nevertheless, the modern rules of scientific ethics make it possible 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 to us cold, 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 of seeing. Which indicates the growth of a new wave of interest in one phenomenon of the brain from many others, waiting in the wings ...

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