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. Statistics show that around one in 100 people in Australia will suffer from it at some stage 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 identified: mental activity, perception (hallucinations), attention, will, motor skills are impaired, emotions are weakened, interpersonal relationships are observed, streams of incoherent thoughts are observed, perverted behavior, a deep feeling of apathy and sensation arises. 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 view that this disease occurs more often in rural areas than in cities. Moreover, according to outdated information, schizophrenics from rural areas often move to cities to find privacy. However, scientists refute this myth.

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

But myths aside, the true source of schizophrenia is still a mystery. Previously it was thought that the cause was bad attitude parents towards the child - they usually blamed mothers who were too restrained and cold in their treatment. However, this point of view is now rejected by almost all experts. Parents are much less to blame than is commonly believed.

In 1990, researchers at Johns Hopkins University found a link between shrinkage of 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 a schizophrenic’s head, it is observed increased activity in the part of the brain that is responsible for thinking and speech activity.

In 1992, this hypothesis was supported by a major Harvard study that found a link between schizophrenia and shrinkage of the left temporal lobe of the brain, especially the part responsible for hearing and speech.

Scientists have found a connection between the degree of thought 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 this work does not result in new treatments, the scientists believe their discovery provides an opportunity to “further study this serious disease» .

Nowadays every now and then new Hope. A 1995 study from the University of Iowa suggests that schizophrenia may result from 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 related structures, extending from the top of the spine to the back of the frontal lobe, can create a full range of symptoms observed in schizophrenics."

Perhaps the whole brain is involved in schizophrenia, and certain psychological ideas, 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 a specific time for such brain disorders to occur? Although symptoms of schizophrenia usually begin during adolescence, the damage that causes it can begin in infancy. "The exact nature of this neural disorder is unclear, but [it reflects] disturbances 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 at that. A controversial but very intriguing version of the causes of the disease was 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, patients with schizophrenia decreased by 50%. This coincides with the introduction of polio vaccination in these countries. In the UK, the 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, Connecticut scientists found that patients hospitalized with schizophrenia were “significantly more likely to be born during polio years.”

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

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

Doctors David Silbersweig and Emily Stern of Cornell University believe that schizophrenics are unlikely to have serious problems with a brain, but, nevertheless, they managed to discover 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 treatment-resistant schizophrenics who heard voices. One experienced 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, the superficial areas of the brain involved in processing auditory information were activated. Moreover, all patients had 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 true.

The speech of schizophrenics is often illogical, incoherent and confused. They used to think that such people were possessed by demons. Researchers have discovered a much less fantastic explanation. According to Dr. Patricia Goldman-Rakic, a neurologist, the speech problems of schizophrenics may reflect short-term memory deficits. It has been discovered that the prefrontal cortex of schizophrenics is significantly less active. This area is considered the center of short-term memory. Goldman-Rakic ​​says, “If they are unable to retain the meaning of a sentence before moving on to a verb or object, the phrase becomes devoid of content.”

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

Is it the cause of schizophrenia? immune reaction mothers or malnutrition?

Some scientists believe that schizophrenia is caused by damage to the developing fetal brain. A study from the University of Pennsylvania, which included medical data from the entire Danish population, found that severe malnutrition in the mother early in pregnancy, as well as her body's immune response to the fetus, may influence the onset of schizophrenia.

Thanks to the memories

As the body ages, the enzyme prolyl endopeptidase increasingly destroys neuropeptides associated with learning and memory. In Alzheimer's disease, this process accelerates. It causes memory loss and a reduction in active attention time. Scientists from the city of Suresne in France have discovered medicinal compounds 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. 8 February 1990. R. 12.

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

An interview with M. Merzenich is given by I. Ubell. Secrets of the brain // Parade. 9 February 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 urban 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 Barta and colleagues work at Johns Hopkins University School of Medicine in Baltimore.

Ainger N. Study on schizophrenics – why they hear voices // The New York Times. 22 September 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. Doctors Martin Flaum and Nancy Andresen are psychiatrists at the University of Iowa Clinics.

An interview with P. McGuire is conducted by B. Bauer. Brain scans seek roots of imagined voices // Science News. 9 September 1995. P. 166. Dr. Philip McGuire is a psychiatrist from the Institute of Psychiatry in London.

Bower B. Faulty circuit may trigger schizophrenia // Science News. 14 September 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.

A study by D. Silbersweig and E. Stern is presented by K. Leutweiler. Schizophrenia revisited // Science from American. February 1996. P. 22–23. Doctors David Silbersweig and Emily Stern work at medical center Cornell University.

Research by P. Goldman-Rakic ​​is presented 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. 15 October 1992. P. 14.

A study by J. Megginson Hollister et al. is 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.

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

Catad_tema Schizophrenia - articles

Schizophrenia: morphological changes in the brain

One of the areas of research in schizophrenia is 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 also undergoes changes nerve cells, fibers and some parts of the brain. The search for anatomical changes in the brain is one of the components of etiological research.
Enlargement of the lateral ventricles of the brain is most commonly reported; 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 already occur at the onset 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 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 exogenously caused form of schizophrenia or arise for some reason nonspecific reasons(for example, complications during childbirth). It is assumed that the reason for the increase in the size of the pituitary gland (which is observed at the onset of the disease, at the time of the first psychotic episode) is increased activity of the hypothalamic-pituitary-adrenal axis (HPA). Under the influence of corticotropic hormones or stress factors, the HPA activation occurs, which leads to an increase in the number and size of corticotropic cells, and consequently 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 brain's ability to coordinate the 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 was noted frontal lobes(mainly due to oligodendrocytes) and a decrease in the expression of genes involved in the formation of myelin. It is assumed that a decrease in the number of oligodendrocytes and myelin in the cortical layers leads to degeneration of the neuropil, 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 discharge of the neuropil in 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. NMR spectroscopy on 1H hydrogen nuclei makes it possible to determine the content of N acetyl aspartate (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 phosphodiester residues (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. The influence of typical and atypical neuroleptics on the process of myelination Before 30 years of age, the myelin content in patients with schizophrenia is higher than in healthy people, and after 30 years of age it is significantly lower. This is consistent with observations of high treatment effectiveness on early stages diseases 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 reported a significant effect of antipsychotic medications on white matter volume in the brain of patients with schizophrenia, but these data are conflicting. Researchers 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 were observed with long-term therapy with typical antipsychotics (McCormick et al., 2005; Lieberman et al., 2005). Atypical antipsychotics (as opposed to 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 oligodendrocyte and/or myelin deficiency in the cerebral cortex. One recent study compared treatment with an atypical antipsychotic (risperidone) and a typical antipsychotic (fluphenosine decanoate (FD)) in a group of men with schizophrenia. The study found that patients with schizophrenia have a different frontal lobe structure than healthy people. White matter volume in the risperidone group was significantly higher than in the PD group, with the risperidone group experiencing an increase in white matter volume and the PD group experiencing a decrease in white matter volume compared with the control group. Gray matter volume was significantly lower in both patient groups compared to healthy controls and lower 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, there was also a cortical shift in the boundary between gray matter and white matter (George Bartzokis et al., 2007). A decrease in neuronal density was also observed in the risperidone group. It is possible that increased myelination with risperidone therapy contributed to the reduction in the rate of fixation-related volume loss in the frontal lobes. However, these studies cannot determine whether the greater volume of white matter in the risperidone group is a consequence of the preservation of myelin, which was initially larger, or a result of the treatment itself. It is possible that such differences are related to demographic characteristics patients (gender, age) and study design (George Bartzokis et al., 2007). The molecular mechanism of the observed effect of atypical antipsychotics is not clear. It may be related to the effect of these drugs on lipid metabolism (Ferno et al., 2005), facilitating dopaminergic transmission in the prefrontal cortex, since stimulation of dopamine receptors may act as a protective factor for 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 for the 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, a relationship was noted between anatomical changes and non-compliance with antipsychotic therapy. These data indicate the potential 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 promising directions in studying of this disease. The results of these studies will help to better understand the reasons for its development, study the features of the course and mechanism of action of the drugs used, including antipsychotics.

Information current as of 09/17/2010

Hallucinogenic psychoactive drugs 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 transient intoxication psychosis, clinical picture which resembles schizophrenia (Bowers, 1987; Tennent and Groesbeck, 1972).
Maybe Also(although this is by no means proven) that substance abuse can trigger the onset of schizophrenia.

Relatives Patients with schizophrenia sometimes see 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 50-60s, LSD was used as an experimental drug in psychiatry, and the percentage of individuals (among voluntary trial participants and among patients) who developed long-term psychosis such as schizophrenia almost did not exceed the corresponding figure for general populations (Cohen, 1960; Malleson, 1971).

True, carried out in Sweden A study found that military recruits who used marijuana frequently and in large quantities were six times more likely to subsequently develop schizophrenia (Andreasson et al., 1987). However, this pattern may be explained by the fact that individuals predisposed to schizophrenia were more likely to resort to marijuana use as a way to cope with premorbid symptoms of the disease.

Brain in schizophrenia

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

With the help of such techniques Magnetic resonance imaging (MRI) has revealed changes in the size of various brain structures, especially in the temporal lobes. The fluid-filled cavities (ventricles) in the depths of these lobes are often expanded, and the volume of tissue of the lobes themselves is reduced. The greater these observed changes, the more severe the patient’s thinking and thinking disorders. auditory hallucinations(Suddath et al., 1990).

Some techniques Imaging studies such as positron emission tomography (PET) can assess ongoing brain function and provide a similar picture of abnormalities. PET scans reveal increased activity in the temporal lobes, especially in the hippocampus, a structure located in the temporal lobe responsible for orientation and ultra-short-term memory (Tamminga et al., 1992).

Building a functional Images another kind - through recording of electrophysiological parameters of the brain using an electroencephalograph - shows that most patients with schizophrenia seem to have an excessively increased response to repeated 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 thought to screen out irrelevant stimuli (eg, the frontal lobe) show reduced activity in PET scans (Tamminga et al., 1992).

Due to this difficulty screening sensory stimuli, postmortem studies of brain tissue have revealed disturbances in a certain type of brain cells—inhibitory interneurons. These neurons inhibit the activity of the main nerve cells, preventing them from responding to too many input signals. In this way, they protect the brain from being overloaded with too much sensory information coming from environment.

In the patient's brain schizophrenia the amount of “chemical messengers” or neurotransmitters (primarily gamma-aminobutyric acid (GABA)) released by these interneurons is reduced (Benes et al., 1991; Akbarian et al., 1993), which implies that the inhibitory function 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. Schizophrenia researchers have long been interested in the role of dopamine, since certain psychoactive drugs (such as amphetamines) that enhance the effects of dopamine can cause psychoses resembling schizophrenia, and psychoactive drugs that block or weaken its effects are effective in treating psychosis (Meltzer and Stahl, 1976). .

Dopamine enhances brain cell sensitivity to irritants. Typically, such heightened sensitivity is beneficial, increasing a person's level of awareness during periods of stress or danger, but for a person with schizophrenia, whose brain is already in a state of heightened activity, the additional exposure to dopamine can be a factor that pushes him into psychosis.

Of these research Data suggests 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 insufficient ability to filter out unwanted stimuli. This problem is exacerbated by the reduction in volume of the brain's temporal lobes, where sensory input is typically processed; as a result, it becomes even more difficult for a person to respond adequately to new stimuli.

Schizophrenia is a mental illness associated with the breakdown of emotional reactions and thinking processes. Symptoms of this disease include delusions, hallucinations, disorganized thinking, and, as a result, social dysfunction.

Is schizophrenia visible on MRI?

According to the latest data, the reasons for the development of this pathology are two factors, one of which is predisposition:

1. anomalies vascular bed brain: anterior and posterior trifurcation of the internal carotid artery, anomaly of the communicating artery of the brain
2. abnormalities of gray and white matter of the brain. More often, the pathology consists of local atrophy (of an area of ​​the brain).
3. pathology of the venous sinuses.
4. pathological activity in the frontal and temporal lobes of the brain.

The second factor is important, of course, the triggering factor for the development of schizophrenia, so to speak, is mental trauma, no matter at what age it first occurred, but childhood is more susceptible to mental trauma.

MRI as a method that is sensitive to the development factors of schizophrenia of the first group.

Anomalies of the vascular bed of the brain are perfectly revealed by this MRI technique - angiography. Anomalies of the vascular bed occur in a third of patients with schizophrenia. As a result of a pathology such as trifurcation (tripling of the internal carotid artery, but normally doubling) of the right or left internal carotid artery, ischemia of a certain area of ​​the brain occurs, which is a powerful predisposing factor.

Below are examples of neuroimaging of patients with schizophrenia using MRI technologies.

Patient with schizophrenia. An MRI was performed - angiography revealed trifurcation of cerebral vessels in the patient. One of the common brain abnormalities, a complication, which is schizophrenia.

This fMRI (functional MRI) image compares brain activity in a normal patient and a patient with schizophrenia, who also has arterial trifurcation.

MRI for schizophrenia

Back in 2001, a group of researchers from the University of California reliably determined based on evidence-based medicine MRI features in patients with schizophrenia using only classical T1 and T2 sequences.

Such signs include

1. disturbances in the structure of the white matter of the brain. Pathology was more common in the temporal lobes in patients who were newly diagnosed with schizophrenia, and pathological foci were also detected in the frontal lobes, but this localization is more common in older patients who undergo a repeat MRI study.
2. The volume of the cerebral ventricle is larger in patients with schizophrenia.

If the second sign of schizophrenia is just a reliable sign that a radiologist should always keep in mind, then the second sign prompted scientists to put forward a hypothesis about the functioning of the brain in schizophrenia. After the advent of such a method as fMRI (functional MRI), this hypothesis was confirmed. Indeed, diagnostic specialists, when examining a patient with early schizophrenia (figure below), reveal an increase in the signal in the frontal lobe, and with late schizophrenia in the temporal lobe (figure below).

A patient with late-onset schizophrenia has an undulating course. An fMRI was performed, which showed increased activity in the temporal lobe.

Patient with early schizophrenia

MRI - increased activity in the frontal and occipital lobes.

Brain MRI for schizophrenia

This classic MRI shows a patient with schizophrenia and a normal patient on the left at the same level of the head. The difference is obvious: the arrow indicates the expansion of the lateral ventricles typical sign according to MRI in patients with schizophrenia, which we wrote about earlier.

Many psychiatrists do not fully understand the principle of the MRI method, its capabilities in particular fMRI and such a method as DTI, therefore they often neglect it. The last two MRI methods allow us to detect changes that occur in brain cells at the cellular level. Classic MRI protocols are good for imaging such pathological changes for schizophrenia: as a change in the substance of the brain, determining the size of the ventricle, to exclude diseases that can simulate schizophrenia. For example, a person’s consciousness and psyche have changed dramatically; psychiatrists clinically diagnose schizophrenia, and the patient turned out to have Alzheimer’s disease, which was not difficult to identify with an MRI study. In another case that excluded the diagnosis, a person had auditory hallucinations suspected of schizophrenia. After an MRI, a schwannoma of the sound-conducting nerve was revealed, which is a tumor. Therefore, from the point of view of evidence-based medicine additional diagnostics is a necessary aspect of a correct diagnosis.

This image shows a patient with Alzheimer's disease. Initially, schizophrenia was suspected. On MRI: a decrease in brain volume; on T2 sequences a hyperintense area is visualized, indicating to us chronic ischemic changes brain.

MRI shows schizophrenia

Scientists have long proven that MRI is effective in diagnosing schizophrenia. Researchers at Friedrich Alexander University Erlangen (Germany) proved in 2008 that MRI can differentiate (distinguish) diseases with symptoms similar to schizophrenia. Based on this study, also described reliable signs schizophrenia on MRI:

1. Vascular changes - congenital anomalies of arteries, venous sinuses, anerism of cerebral vessels. Due to the redistribution of blood flow in the brain, others are better supplied with blood, so this sign on MRI is also one of the triggering factors in the development of schizophrenia.
2. Signs of hydrocephalus are expansion of the lateral ventricles, an increase in the size of the third ventricle, expansion of the subarachnoid space. Expansion of the horns of the lateral ventricles
3. Damage to the white matter of the brain. Most often this is atrophy of the white matter of the brain.
4. Chronic cerebral ischemia, which often occurs as a consequence of vascular changes in the brain.
5. Brain abnormality (developmental abnormality). The anomaly is localized in the brain stem, cerebellum, and pituitary gland, which leads to functional impairment of these parts of the brain. Rathke's pouch cyst, Verge's cyst.

This information helps the radiologist in his work, so you can say for sure that the radiologist will pay attention to one of these signs and make correct conclusions about the diagnosis.

A patient with schizophrenia was found to have frequent concomitant disease(comorbid disease) Rathke's pouch cyst.

Does MRI show schizophrenia?

In schizophrenia, a redistribution of blood flow in the brain occurs, which is not always noticeable when scanning in classical MRI sequences. If you use fMRI (functional MRI), diagnosing pathological foci in the brain becomes easier. Schizophrenia does not always immediately show signs such as atrophy, vascular abnormalities, and so on on MRI. fMRI allows one to suspect schizophrenia in normal person without pathological symptoms in the form of hallucinations and disorders of consciousness. In schizophrenia, certain areas of the brain are more susceptible to arousal. This has been proven as abnormal areas of the brain release more dopamine. Some scientists suggest that this congenital pathology, which makes itself felt over time after exposure to mental trauma.

This still clinically healthy young man underwent an MRI examination

Came in with headaches. Many noted that he had a twist, but they couldn’t say anything bad about him. Classical MRI revealed no significant changes in the brain in this patient. In fMRI, abnormal activity in the frontal lobe is evidence of early schizophrenia.

The young man did not believe this diagnosis, 8 years later he came back again, but with more severe symptoms. On MRI in classical protocols there were already changes in the form of atrophy of the white matter of the brain. This patient may serve as a bad example for patients, but early treatment this patient could improve his quality of life.

Schizophrenia on MRI of the brain

MRI should be performed not only on patients with suspected schizophrenia for early diagnosis of changes, but also on patients who have had this disease for a long time for possible treatment adjustments. A common sign on MRI in patients is atrophy of the brain substance. Some researchers believe that this process is not just associated with the spread of pathology, but also with the reception medicines, so the treating psychiatrist should also be interested in this. Brain atrophy is easily imaged in the same way as ventricular enlargement, so it does not require complex MRI protocols that can assess neural interactions (fMRI or DTI MRI). Progressive brain atrophy significantly worsens the patient's quality of life, so MRI monitoring is advisable every 6 months.

Absolute (monozygotic) twins are presented. On the right is a patient with schizophrenia, and on the left is a normal patient. MRI was performed at the same level of the brain. The patient has a pronounced increased signal from the medulla, dilatation of the ventricles, and atrophy of the medulla.

The patient has psychosis - manic schizophrenia. MRI of the brain. Arachnoid cysts of the brain were identified.

Schizophrenia is a chronic progressive mental disorder, which is accompanied by structural changes in the brain in both white and gray matter. It is likely that these changes begin even before the appearance of clinical symptoms in some areas of the cerebral cortex, especially those related to the cognitive sphere. Later, these changes are accompanied by a progressive enlargement of the ventricles of the brain. Modern technology Magnetic resonance imaging (MRI) can be a valuable tool for detecting early changes in cortical atrophy and cognitive changes, allowing one to predict how the pathological process in schizophrenia will develop.

It has long been known that the disorder we now call schizophrenia is characterized by progressive clinical symptoms (positive and negative) and cognitive impairment, as well as structural abnormalities of the brain. In the late 1920s, several fairly large pneumoencephalographic studies were carried out, which showed at the macroscopic level that large cerebral ventricles were characteristic of patients with chronic schizophrenia. At that time, this phenomenon suggested a degenerative process. Some of the early pneumoencephalographic studies repeated estimates of brain size in patients several years later and showed progressive changes that correlated with clinical worsening, but only in some patients. It should be noted that although other treatments were available at the time of these studies, antipsychotics had not yet been introduced into clinical practice. This is important because there has recently been a lot of interest in the hypothesis that antipsychotic drugs may be responsible for certain progressive changes in brain structures. Interestingly, studies of chronic patients consistently show ventricular enlargement over time, especially in more severely ill patients with schizophrenia. However, it appears that ventricular dilatation is secondary to underlying cortical changes that may begin after the first episode of psychosis.

To date, numerous structural differences in the brains of chronic patients with schizophrenia and control groups have been reported ( healthy people) identified using computed tomography (CT) and magnetic resonance imaging (MRI). These changes today include: non-localized changes in gray matter and white matter, a decrease in the volume of the temporal lobe and, in particular, abnormalities of the temporal and frontal lobes of white matter, changes in the gyri of the brain (arcuate, straight and flattened). The areas of the brain most affected in schizophrenia are the cerebral cortex, those involved in cognitive processes. The researchers say that over a 2-year illness period, gray matter volume was significantly reduced in patients treated with haloperidol than in controls or patients treated with olanzapine. Although most, but not all, studies have shown that the caudate enlarges during treatment with typical antipsychotic drugs, changes observed in other cortical regions and ventricular enlargement do not yet show with sufficient certainty that they are caused by the drugs.

Initially, during the prodromal stage of schizophrenia, changes in brain structures appear to take place and are manifested in a decrease in the volume of the temporal lobe. When observing those patients with schizophrenia who have suffered a first psychotic episode, further brain changes can already be seen in the cingulate, temporal lobe and parahypocampal gyrus. The basis for these changes detected on imaging may be related to abnormalities in axonal integrity and neural network organization that begin to be first noted during the normal pubertal crisis, as well as throughout the individual's life and even during aging, especially given the "responses" brain on the effect of stress factors.

In conclusion, it should be said that it is likely that structural changes in the brain are detected in both gray and white matter even before the onset of schizophrenia, that active progression of changes may also begin before the onset of clinical symptoms, and that progressive changes in the brain as the disease progresses must be taken into account, because the structural abnormalities brain problems are observed in chronic schizophrenia, primarily affecting thinking. Note that atrophic changes occur early and can progress over more late stages schizophrenia.