What types of garden hearths are there? Residual changes in the lungs after recovery from tuberculosis How often is a solitary lesion in the lung a tumor metastasis?

When performing CT (MR) studies, foci of a dystrophic nature (like gliosis), atrophic nature (like a cerebrospinal fluid cyst), as well as calcification can be detected in the substance of the brain. In chronic tissue ischemia, some other characteristic changes can also be identified, for example, periventricular leukoaraiosis (changes in the structure and density of the substance around the ventricles), often with the presence of small cysts in the basal ganglia, as well as in the outer and inner capsule of the brain. Signs (of a substitutive nature) are also often identified.

Causes and predisposing factors of changes in the brain

Focal changes include pathological processes that occur in a specific area of ​​the brain. Various changes occur in the brain tissue (scars, cysts, necrosis). The most common focal changes of a dystrophic nature are found:

  1. In older people. Thus, the probability of identifying dystrophic foci significantly increases with age. Pathological changes in intra- and extracranial vessels, narrowing of the vascular lumen and cerebral ischemia provoked by these factors play a role here.
  2. In persons suffering from diabetes mellitus. With this pathology, angiopathy often occurs, manifested by changes in the vascular wall, impaired vascular permeability, and impaired vascular patency. Against this background, strokes often occur.
  3. In people with other angiopathy, anomalies in the development of the cerebral vascular bed (for example, an open circle of Willis), thrombosis (disturbances of the lumen of another etiology) of extra- and intracranial arteries.
  4. In persons with exacerbation of cervical osteochondrosis. When the disease occurs, the brain stops receiving sufficient oxygen. As a result of oxygen starvation, areas of ischemia appear.
  5. For those who have suffered a skull or brain injury. Restructuring of the brain substance at the site of contusion after injury can lead to the appearance of a focus of gliosis, cyst or calcification.
  6. In persons exposed to long-term intoxication (exo- or endogenous). Thus, the first group includes people who abuse alcohol, take toxic substances (or are exposed to them at work, for example, workers in paint production workshops). The second category includes people with long-term diseases (infectious, inflammatory).
  7. In patients with oncological processes of the brain, dystrophic foci are detected during examination.

Methods for identifying dystrophic foci in the brain

The main methods for identifying dystrophic (and other) parenchymal lesions in the brain are CT and MRI. The following changes can be identified:

  1. Gliosis type lesions.
  2. Cystic areas due to atrophy (and trauma).
  3. Calcification (as an example, due to impregnation of the hematoma with calcium salts).
  4. Periventricular leukoaraiosis. Although it does not directly relate to focal changes, it is a significant marker of chronic ischemia.

On the CT scan at the level of the third ventricle and the posterior horns of the lateral ventricles, blue arrows indicate areas of a cystic nature (the result of necrosis of the brain substance in the past): small in the area of ​​the right thalamus and larger in size in the occipital lobe on the right. There is also a change in the density of the brain matter around the posterior horn of the right lateral ventricle. The Sylvian fissures are widened, which indicates hydrocephalus (atrophic, replacement).

On the CT scan at the level of the bodies of the lateral ventricles, blue arrows indicate cystic (atrophic) areas in the parietal and occipital lobes on the right (consequences of a stroke). Signs of chronic cerebral ischemia are also visible, more pronounced on the right (periventricular leukoaraiosis).

CT scan of the head at the level of the 4th ventricle, cerebellar peduncles: in the left hemisphere of the cerebellum (at the base, near the left cerebellar peduncle) there is an atrophic area (consequences of a stroke). Notice how the outer cerebrospinal fluid spaces of the brain are expanded.

Blue arrows on the CT scan indicate areas of periventricular leukoaraiosis (around the anterior and posterior horns of both lateral ventricles). The red arrow also indicates “fresh” (on the right in the occipital lobe).

The presence of dystrophic focal changes in the brain in many cases is a consequence of chronic ischemia and is often combined with atrophic (replacement) hydrocephalus, especially in people who drink alcohol for a long time, are exposed to other types of intoxication, or have previously suffered a stroke or head injury.

A CT scan of the head shows signs of replacement hydrocephalus (due to necrosis of the brain parenchyma), with the presence of multiple atrophic foci on the left side - in the occipital lobe (1), in the parietal lobe (2) and on the right side - in the region of the head of the lenticular nucleus , periventricular to the body of the ventricle (3). The diameter of the lateral ventricles is expanded (marked by an arrow). Around the horns of the lateral ventricles there is a hypodense (low density on CT) zone.

Results

Dystrophic focal changes can be detected by CT and MRI in the brain of any person. Their detection may indicate a previous pathology (traumatic, ischemic). If the lesions are small in size and localized in the peripheral parts of the brain or in the white matter, basal ganglia, the prognosis for the patient’s future life is favorable. But focal changes in the brainstem localization, on the cerebral peduncles, and thalamus are more unfavorable and can cause the appearance of neurological symptoms.

Residual changes in the lungs after recovery from tuberculosis

As a result of treatment, complete and traceless disappearance of tuberculosis tubercles may occur, which is accompanied by negative tuberculin reactions. This outcome is possible with a disease of short duration, with so-called fresh processes that occur without extensive caseous necrosis in the center of inflammation. These forms of true healing are quite rare. In the majority of patients (95-96%), cure is associated with the obligatory development of residual changes in the lung tissue.

Residual changes should be understood as various formations in the lung tissue that persist at the time of clinical cure in individuals receiving antibacterial drugs, as well as during spontaneous cure of the tuberculosis process.

It is necessary to distinguish between small residual changes in the lungs and pleura: slight fibrosis, cicatricial changes, single petrifications less than 1 cm in diameter, single, clearly defined foci, pleural layers and large residual changes: severe pneumosclerosis, single or multiple petrifications with a diameter of 1 cm or more, multiple clearly defined foci against the background of pneumosclerosis, large long-existing dense foci, cirrhosis (carnification of the lung with its cirrhotic transformation), the formation of extensive pleural adhesions.

Particular attention is paid to the issue of completing the treatment of cavities (cleaned, sanitized cavities). The cavity can take on a cystic shape, but a “sanitized” cavity, especially with fibrocavernous tuberculosis, does not mean a lasting recovery. After chemotherapy is stopped, the process may progress.

The difference in residual changes in size and extent, in the nature of the anatomical and histological structures, largely determines the possibility of reactivation of the tuberculosis process. Persons under observation in the VII group of dispensary registration are currently one of the main sources of replenishment of the contingents of patients with active forms of pulmonary tuberculosis. This is due to endogenous reactivation of tuberculosis.

An urgent task of modern tuberculosis therapy is to improve treatment methods to achieve clinical recovery with minimal residual changes. Long-term complex antibacterial therapy leads to the formation of minimal residual changes and more complete types of healing, further reducing the possible risk of relapse of tuberculosis.

The best result is achieved with a fresh and timely identified focal process. Fresh lesions completely disappear, perifocal inflammation is eliminated around older lesions; Fibrous changes and encapsulated lesions are worse or do not undergo reverse development at all.

Residual changes in the form of single foci against the background of cicatricial changes and multiple foci are observed in patients in whom the process was of a certain duration and was very widespread.

In infiltrative-pneumonic pulmonary tuberculosis, the most common residual changes are foci of compaction and fibrosis. More rapid and complete resorption of tuberculous infiltrate is observed in patients with drug-sensitive mycobacterium tuberculosis compared with patients who secrete predominantly resistant strains of mycobacteria. Pulmonary tuberculomas are characterized by a long course of the tuberculosis process, which is determined by the stability of changes in the lung tissue.

In fibrous-cavernous pulmonary tuberculosis, complete resorption of pathomorphological changes is not observed. The formation of single lesions against the background of moderate inductive changes is possible. When fibrous-cavernous pulmonary tuberculosis is cured, residual changes are pronounced with a predominance of the phenomena of pneumosclerosis and fibrosis.

After effective antibacterial therapy has been completed, the involution of residual changes continues for a certain time. The specific changes remaining in the lung tissue continue to decrease, despite the cessation of direct exposure to antibacterial drugs, which is due to favorable immunobiological changes in the body under the influence of the treatment, causing an increase in general and local tissue resistance. In specific foci, the cellular composition changes, the processes of fibrosis and hyalinosis increase, the remaining areas of caseous necrosis continue to partially resolve, become delimited and thicken until calcification occurs. Large foci are reduced, indurated, or transformed into small focal formations. Even the calcification phase in some cases is not final. It is replaced by a phase of dissolution of calcium salts deposited in the lesions. The dynamics of inactive tuberculosis changes become positive over time due to the metabolic processes occurring in them, leading to dehydration and compaction. Antibacterial and restorative treatment accelerates these processes and reduces the potential activity of tuberculous changes. In this regard, repeated anti-relapse courses of antibacterial therapy play a particularly important role, which not only help prevent relapses of the tuberculosis process, but also make it possible to minimize residual changes in the lungs.

Persons in the III group of dispensary registration of patients with inactive tuberculosis of the respiratory system, depending on the size and nature of residual changes, are divided into two subgroups: with large residual changes (subgroup A) and with small residual changes (subgroup B). Persons with large residual changes in this group of dispensary observation are from 3 to 5 years, with small residual changes - up to 1 year. In case of large residual changes with the presence of aggravating factors that weaken the body's resistance, it is necessary to carry out anti-relapse treatment with tuberculostatic drugs in the spring and autumn on an outpatient basis or (if indicated) in a sanatorium. In the grouping of contingents served by anti-tuberculosis institutions, the VII group of dispensary observation was introduced in 1974. This is a group of people with an increased risk of relapse and tuberculosis disease, subgroup A of which includes people with large residual changes transferred from group III of dispensary observation, and with small residual changes in the presence of aggravating factors. They are monitored at the dispensary for life, with a mandatory annual visit to the dispensary and a full clinical and x-ray examination. They should be subject to general health measures aimed at increasing resistance to tuberculosis. In this group, it is possible to conduct courses of chemoprophylaxis when factors appear that weaken the body’s resistance.

They arise due to disruption of cerebral blood flow. This pathological process is manifested by a number of neurological symptoms and is characterized by a progressive course. It is no longer possible to bring lost nerve cells back to life, but you can slow down the course of the disease or completely prevent its development.

Causes and signs of pathology

The doctor should tell you what to do if there is a focal change in the substance of the brain, but the patient himself can suspect the presence of pathology. The disease often has a post-ischemic origin. It is characterized by a violation of blood flow in one of the areas of the hemisphere (hemisphere). It is difficult for some people to understand what this is, so for convenience, the development of changes in brain matter has been divided into 3 stages:

  • First stage. At this stage, signs of focal lesions in the brain matter do not appear. The patient may only feel slight weakness, dizziness and apathy. Occasionally, sleep is disturbed and headaches occur. Foci of vascular origin are just emerging and there are minor disruptions in blood flow;
  • Second phase. As the pathology develops, the course of the disease worsens. This manifests itself in the form of migraines, decreased mental abilities, ringing in the ears, outbursts of emotions and loss of coordination of movements;
  • Third stage. If the disease has reached this stage, then focal changes in the white matter of the brain have irreversible consequences. Most neurons die and the patient's muscle tone rapidly decreases. Over time, symptoms of dementia (dementia) appear, the senses cease to perform their functions and the person completely loses control over his movements.

Subcortical lesions in the white matter, localized under the cerebral cortex, may not appear at all for a long time. Such failures are diagnosed mainly by chance.

Changes in the white matter of the frontal lobes manifest themselves noticeably more actively and mainly in the form of a decrease in mental abilities.

At-risk groups

If there are no signs of the disease, it is advisable to find out what risk groups are for this disease. According to statistics, focal lesions more often occur in the presence of such pathologies:

  • Atherosclerosis;
  • High pressure;
  • VSD (vegetative-vascular dystonia);
  • Diabetes;
  • Pathologies of the heart muscle;
  • Constant stress;
  • Sedentary work;
  • Abuse of bad habits;
  • Overweight.

Damage to the white matter of the brain of vascular origin may occur due to age-related changes. Small single lesions are usually observed in people over 60 years of age.

Dystrophic nature of the damage

In addition to damage caused by vascular origin, there are other types of disease, for example, single focal changes in the brain substance of a dystrophic nature. This type of pathology occurs due to lack of nutrition. The reasons for this phenomenon are as follows:

  • Weakened blood supply;
  • Osteochondrosis of the cervical spine in the acute stage;
  • Oncological diseases;
  • Head injuries.

Damage to the brain substance of a dystrophic nature usually manifests itself due to a lack of nutrition of brain tissue. The patient experiences symptoms:

  • Decreased brain activity;
  • Dementia;
  • Headache;
  • Weakening of muscle tissue (paresis);
  • Paralysis of certain muscle groups;
  • Dizziness.

Diagnostics

Most people with age develop focal changes in the substance that arise due to tissue degeneration or as a result of disruptions in blood flow. You can see them using magnetic resonance imaging (MRI):

  • Changes in the cerebral cortex. Such a lesion occurs mainly due to blockage or compression of the vertebral artery. This is usually associated with congenital anomalies or the development of atherosclerosis. In rare cases, along with the appearance of a lesion in the cerebral cortex, a vertebral hernia occurs;
  • Multiple focal changes. Their presence usually indicates a pre-stroke condition. In some cases, they can prevent dementia, epilepsy and other pathological processes associated with vascular atrophy. If such changes are detected, a course of therapy should be started immediately to prevent irreversible consequences;
  • Microfocal changes. Such damage is found in virtually every person after life. They can be seen with the use of a contrast agent only if they are of a pathological nature. Fine-focal changes are not particularly noticeable, but as they develop they can cause a stroke;
  • Changes in the white matter of the frontal and parietal lobes subcortically and periventricularly. This type of damage occurs due to persistently elevated blood pressure, especially if the person has had a hypertensive crisis. Sometimes small single lesions are congenital. The danger arises from the proliferation of lesions in the white matter of the frontal and parietal lobes subcortically. In such a situation, symptoms gradually progress.

If a person is at risk, then an MRI of the brain (brain) should be performed once a year. Otherwise, it is advisable to do such an examination once every 2-3 years for prevention. If an MRI shows a high echogenicity of a lesion of disculatory origin, this may indicate the presence of an oncological disease in the brain.

Methods of combating pathology

Gradually affecting the human brain tissue, the disease can cause irreversible consequences. To prevent vascular changes in the white matter of the brain, it will be necessary to stop the symptoms that arise and improve blood flow with the help of medications and physical therapy. Treatment must be comprehensive, which means you will have to change your lifestyle. To do this you will have to follow these rules:

  • Active lifestyle. The patient should move more and play sports. After eating, it is advisable to go for a walk, and it doesn’t hurt to do the same before bed. Water procedures, skiing and running have a good effect. Treatment with an active lifestyle improves general condition and also strengthens the cardiovascular system;
  • Properly formulated diet. For successful treatment, you will have to give up alcoholic beverages and reduce your consumption of sweets, preserves, as well as smoked and fried foods. You can replace them with boiled or steamed food. Instead of store-bought sweets, you can make homemade pie or eat fruit;
  • Avoiding stress. Constant mental stress is one of the causes of many diseases, so it is advisable to relax more and not overwork;
  • Healthy sleep. A person should sleep at least 6-8 hours a day. In the presence of pathology, it is advisable to increase sleep time by 1-2 hours;
  • Annual examination. If a change in the white matter of the brain is diagnosed, the patient should undergo an MRI twice a year. It is imperative to follow all the doctor’s recommendations and take the necessary tests on time.

Treatment of focal changes usually involves changing lifestyle and eliminating the cause of their development. It is advisable to detect the problem immediately in order to be able to slow down its progress. To do this, you should undergo a full examination annually.

The information on the site is provided solely for popular informational purposes, does not claim to be reference or medical accuracy, and is not a guide to action. Do not self-medicate. Consult your healthcare provider.

What is cerebral gliosis

Gliosis of the brain is a secondary disease, a consequence of any disorder of the central nervous system. Its treatment is difficult, or rather, impossible, since the replacement of nerve cells with auxiliary cells is irreversible. However, it is quite possible to stop the growth of such a formation or prevent it.

Clinical picture

The central nervous system includes three types of cells:

  • neurons are functional cells that transmit signals;
  • ependyma - cells lining the ventricles of the brain, they also make up the central canal of the spinal cord;
  • neuroglia are auxiliary cells that provide metabolic processes: trophic, supporting, secretory and other functions. Neuroglia are 10–15 times smaller than neurons, their number exceeds the number of nerve cells by 10–50 times, and make up about 40% of the mass.

When functional nervous tissue is damaged, neuroglia take the place of dead neurons—the lesion. This replacement ensures the continuation of metabolic processes even in the event of death of nerve cells. Glia form a kind of scar tissue.

Their appearance is clearly secondary, since cell death has already occurred, the focus of gliosis only indicates the location of the lesion. Treatment is impossible.

The process of filling with glia cannot be called destructive, whatever the reasons. Foci of neuronal damage in the white matter cannot remain unfilled, because then the metabolic process in the brain is disrupted.

Glia, filling the space, ensure the course of normal metabolic processes, but the cells cannot perform neuroregulatory functions.

Types of gliosis

Foci of neuronal damage lead to deterioration in the functionality of the central nervous system. There is no way to treat them, as already mentioned, since it is impossible to restore dead neural tissue. It is also unacceptable to remove the focus of glia accumulation, since it performs replacement functions.

As a rule, the lesion has a specific area of ​​localization - a focus, although not always.

Based on the location of concentration and form of change, cerebral gliosis can be classified into the following groups:

  • Anisomorphic form - the cellular structure of glia predominates over the fibrous one. The growth is chaotic.
  • Fibrous form – the fibrous structure predominates, the signs of dominance are clearly expressed.
  • Diffuse - there are no lesions, tissue changes are observed not only in the brain, but also in the spinal cord. This picture is typical for diffuse pathological diseases, for example, cerebral ischemia. Treatment, obviously, must begin with eliminating the underlying disease.
  • Focal - has a clearly defined area - the focus. Usually, it turns out to be the result of an inflammatory process that leads to the death of neurons. Here treatment is useless.
  • Regional - lesions are located mainly on the surface of the brain, under the membrane
  • Perivascular – glia surround sclerotic blood vessels. Such changes are often observed in systemic vasculitis. To prevent the development of the disease, it is necessary to treat sclerosis first of all.
  • Subependymal - the lesion is localized in the subependymium - the ventricle of the brain.

The size of gliosis is a physical value and can be calculated. It is equal to the increase in neuroglial cells in relation to the number of normal functioning neurons per unit volume. The larger the lesion and the less localized it is, the more difficult the work of the central nervous system is.

Symptoms of the disease

Cerebral gliosis, not being a separate disease, does not have any characteristic symptoms. All disorders associated with disturbances in the functioning of the central nervous system are inherent in many other ailments.

Moreover, unless gliosis is associated with a neurological disease such as multiple sclerosis, there are no symptoms at all. Diagnosed randomly, along with the underlying disease.

The causes of the disease may be different, but the manifestation, if any, is approximately the same:

  • constant headaches, treatment with standard anti-spasm drugs has no effect;
  • changes in blood pressure are not specific;
  • constant dizziness, general weakness or excessive fatigue. The causes of the condition may be different, but against the background of memory deterioration they should cause concern;
  • deterioration in coordination of movements. The cause of the symptom is associated with the replacement of damaged nerve tissue by glia and, accordingly, poor signal transmission;
  • memory deterioration, noticeable decrease in mnestic functions. The reason is the same - lack of functional nerve tissue. Treatment in this case is useless.

Sometimes the disease provokes seizures. As a rule, the cause is a large lesion.

Otherwise, the disease manifests itself in young children. The reason for the replacement of nervous tissue with glia is associated with any congenital pathologies. That is, first, as a result of the disease, nerve cells die, and then the affected area is filled with glia.

For example, Tay-Sachs disease, which results in the development of gliosis, appears at 4–5 months of a child’s life. Symptoms indicate disturbances in the functioning of the central nervous system: regression of physical and mental development, loss of hearing and vision, difficulty swallowing, convulsions. The prognosis in this case is extremely pessimistic, and treatment does not produce results.

This kind of congenital pathology is associated with disorders of fat metabolism. They can be detected if an amniotic fluid analysis is performed at 18–20 weeks of pregnancy. If such a disorder is detected in the fetus, it is recommended to terminate the pregnancy. Treatment is impossible.

Causes of the disease

The causes of gliosis, or rather, the initial disease that led to changes in the substance of the brain, are as follows:

  • multiple sclerosis;
  • tuberculosis;
  • encephalitis;
  • ischemic diseases of the brain;
  • hereditary disorders of fat metabolism;
  • infectious diseases characterized by the creation of an inflammatory focus;
  • traumatic brain injuries.

It is important to distinguish between treating a disease and preventing it. Of course, it is impossible to restore dead nerve tissue, but it is important to prevent further growth of the formation, and thus treat the disease.

Diagnosis and treatment

Only magnetic resonance imaging can diagnose disorders with sufficient accuracy.

The method allows you to clearly determine the volume of changes and its localization, and, therefore, clarify or establish the real causes of the lesion, since the localization of lesions, unlike symptoms, is specific.

It is necessary to treat the primary ailment. Treatment of gliosis is only to prevent pathological spread.

  • To do this, you need to follow some recommendations.
  • Refusal of fatty foods. The pathological distribution of glia is associated with disorders of fat metabolism. Even if there is no such hereditary disease, but a focus of gliosis has already arisen, excessive fat consumption will contribute to the proliferation of non-functional cells. A complete rejection of fats is unacceptable, but their amount should be minimal.
  • A healthy lifestyle - following simple nutritional rules and a regimen of physical activity allows you to prevent most central nervous system disorders and changes in metabolic processes.
  • Regular examination reduces the risk of diseases that cause gliosis.

Replacing dead nerve cells with glia is a completely natural process, ensuring further brain function in the event of non-fatal damage. However, the very appearance of foci of gliosis indicates other diseases that threaten the state of the central nervous system.

Wow. As far as is clear from the description and from the fact that it is essentially impossible to cure this disease, but it is only possible to stop its progression. The disease is very, very serious. Moreover, his symptoms are not all so “screaming” that this is actually something significant. Headaches, changes in blood pressure, memory impairment - all this can be attributed to anything

Thank you, everything is described very clearly.

An MRI revealed cerebral gliosis. Since childhood, I have been slow, absent-minded, and get tired quickly, so I have difficulties with regular work. Doctors say that the reason for this lies in the fact that I am phlegmatic and melancholic. Constant headaches since age 13. The work is difficult, so there is no ability to work, but disability is not recognized. I also suffer from mild chronic anemia, my hemoglobin level is. But at the same time, I want to work, I’m ready to get a job at half the working rate, even for 4,000 rubles a month.

Something is not very pleasing about the picture. and according to all the symptoms, I’ve had this problem for a long time, but it started bothering me six months ago, as a result I had an MRI done. They discovered sinusitis, the main focus of headaches, and this unfortunate gliosis. You know, it’s not very pleasant to feel that you are terminally ill, but the good news is that it is not fatal, the only thing is that your memory will be like that of a fish and you will constantly stumble!

I have frequent headaches. They did an MRI of the head and found gliosis, unstable blood pressure, changes, and nausea and vomiting. I have been suffering from this for 9 years, but my disability is not recognized. Painkillers don't help. I massage my head with my hands or a massager, this helps relieve symptoms. It's hard to live with this disease.

Today we had an MRI and found focal gliosis. As far as I understand, this disease is not curable, and is a complication of some other disease that I have not been diagnosed with. I am a young, tall athlete, a student, without bad habits. I made plans for my life, I thought there would be children, but now I see that there is no point, although even in this situation there is no way to kill yourself with the “heaviness of your burden.” Life is a wonderful thing and I am grateful for what I have already lived, seen, felt.

In April of this year, my 15-year-old son was diagnosed with VSD. I gave him an MRI. We discovered a cyst near the cerebellum and other little things. He had severe headaches and dizziness. In July, 2 months later, he was taken by ambulance to an adult hospital with a diagnosis of facial paralysis + numbness of the entire right side. Here in Vologda, the city hospital does not have equipment, and in the morning I took him from intensive care to a paid MRI. 5 outbreaks were identified. She brought me back to the intensive care unit, transferred to “neurology” and began to treat only paralysis. After 2 weeks, the treatment was completed. The numbness on the right side remained. Again, on recommendation, we went for a contrast MRI. Already 7 outbreaks! Within 2 weeks, during treatment, 2 new lesions appeared. Our attending neurologist does not know what to do or how to treat my 15-year-old son. She said that in a week his “main” will be watching. Then they will decide what to do next. We wait. I do not know what to do.

I had an MRI the other day. We found a band of gliosis around the lateral ventricles. I have been having headaches for a long time and have been seeing doctors. These literate people know nothing but VSD and osteochondrosis. Sausage is not childish. I don’t know what to do next. But there was so much I wanted to do. It's a shame.

I was also diagnosed with multiple focal gliosis, in both hemispheres of the brain. But what’s interesting is that they brought me in for examination for tinnitus, short-term hearing loss in one ear and memory loss, of course. But no headaches, no dizziness, no unsteadiness of gait were observed. Somehow all these statements by doctors are not convincing. You really don’t know if you have the same diagnosis. What to do? The neurologist scared me and said that this could lead to Alzheimer's disease if left untreated.

The headaches are very strong on one side. No pills help.

Hello! In 2015 I had an MRI of my head. They found tiny particles in the brain. I repeated it this year. The same thing, but they sleep and do not develop. What could it be?

It all started with a head injury and I underwent long, grueling treatments. You know, in any case, I live as I lived, I try not to think about the disease at all! The only reminders of this are headaches and weakness.

Hello. I have an adult son who served in the army and returned home with plans for his future life. And then, out of nowhere, “single foci of gliosis.” And now, to the health problems (which cannot be treated anyway, since we live in a small town), depression and apathy have been added. Tell me how to help and support, how to instill hope in life?

I was born with trauma. They said that I wouldn’t live, then walk and drink. I went and drank, and graduated from school with a silver medal. Then there was an attack of epilepsy, a diagnosis of mass formation. I still got married and gave birth to a child. Then it turned out that there is no volumetric education, but there is something else, insignificant. She gave birth to a second one, although she had to have an abortion according to medical advice. the testimony was sent. Hard work, constant migraines, weak immunity, dizziness and nausea. I'm treating myself. I have already adapted to the constant pain. I didn’t go to the doctor for three years. I had an MRI done for myself yesterday. Gliosis. I don't want to go anywhere. They will again say that it is impossible to live. On the Internet, every third person has gliosis.

My brother had an MRI. Focal gliosis was discovered, but there was no treatment. The neurologist did not give any recommendations. How to continue to live?

As a result of an MRI, gliosis was diagnosed. The disease is not only incurable, but also very unpleasant. They carried me out of the house to the ambulance on a stretcher. Before this, I had been registered for hypertension since I was 27 years old. Neither the doctors nor I myself took the problem seriously, and this is the result. My head is constantly spinning, even in bed, when I turn from side to side. Maybe one of my “colleagues” in misfortune relieves this dizziness with something? After all, it is impossible to swing constantly.

5 years ago I was in an accident with a head injury, and now I have an MRI. I have gliosis in the right occipital lobe.

My daughter was also diagnosed with glial lesions in the brain and was diagnosed with microadenoma, multiple sclerosis. She has constant headaches, also in the cervical, thoracic and lumbar regions. The pain radiates to the arms and legs. Wobbly, weak legs. There is still pain in the heart. There are hormonal imbalances, weak immunity, allergies. There is no treatment as such, only drugs for VSD for blood vessels. Mexidol, Actovegin, Cortexin. In addition, she has a convulsive syndrome and neurosis. He does not sleep at night because melatonin is not produced, although he takes sibazon and finlepsin, eglonil. We live in Makhachkala, republic. Dagestan. There are no normal qualified doctors here. We are all running around, no results. It just keeps getting worse and worse. I don’t have the money to treat her, I’m retired, and I’m still sick myself. I am already 62 years old. And what should we do, who will help?

Hello, fellow sufferers, someone has arrived in your ranks. I had an MRI this afternoon and before going to bed I read the descriptions. "Probably foci of gliosis of vascular origin." Of course, we are all mortal, but when you learn about incurable diseases, it still becomes sad. Health, love and patience to everyone.

I had headaches since childhood. The doctors diagnosed VSD and let me go in peace. I stopped going to them and got used to living with pain. Nevertheless, he played sports and studied hard. Then my physical activity dried up and was replaced by an eight-hour sedentary lifestyle. By the time I was thirty, I stopped remembering what I ate for breakfast. MRI showed a 1.5 cm lesion of gliosis in the right occipital lobe of the brain. The already imperfect vision sank another couple of diopters. I stopped coping at work. Apparently, we will have to change it to something less intellectual. It’s a real pity for the lost knowledge gained in recent years. But I don’t give up. I do all kinds of gymnastics to train my memory and other such garbage. It seems that it has not progressed for a year, in one pore.

Tell me, is it possible to die from gliosis?

I have gliosis in my left lobe. How to treat? Blood pressure 140/110.

Is there really no way to prevent this disease, and how many people live with this diagnosis?

My husband and I were simultaneously diagnosed with multiple foci of gliosis based on MRI results. Treatment has now begun. I understand that it cannot be cured, but at least it is necessary to maintain health at this stage. I will review the diet for the family, limit fats to a minimum, start a more active lifestyle (an hour to an hour and a half walk will not hurt anyone), and get examined annually. But we definitely won’t just give up. There are still so many interesting things ahead!

Hello. Last year I had an MRI. Result: lesions in the left frontal lobe. Neurologists said that everything is fine, you can’t have this at 34 years old. I have been sick since September 6th. Dizziness, heart troubles, nausea, headaches. A diagnosis of panic attacks is made. Deterioration.

God's help to everyone! I join you with my gliosis! This is a signal for us to reconsider our lives, cleanse ourselves of sins, ask everyone for forgiveness and forgive the offenders ourselves. God is merciful and loves us all, and will not give us grief beyond our strength. Let's love everyone! Health to everyone, spiritual and physical!

Hello. Focal gliosis of the left frontal lobe was discovered two years ago. Severe headaches. Memory seems to be fine. But I have the strongest tremor in my hands and anxiety, and my pulse is 93 - the smallest. My primary disease was determined to be epilepsy, but there was no normal examination. They said it was generally difficult to determine. I would like someone to tell me where it is better to go for a good examination. You know, it’s difficult to live and think that you will be a plant. But I rarely pay attention to this, because it’s easier to live this way.

Tell me, is this dizziness permanent or does it go away? I have only a week since I started having high blood pressure. Who knows, write.

Friends, everything that is written here, of course, does not bring anything pleasant. But, I’ll tell you all this: you need to get treatment and take care of yourself, this should always be the case for everyone. How to monitor and how to treat is a personal choice. And children need to be taught this - to monitor their health, to monitor it. Don’t sit and whine that something has been bothering you in your side or head for six months or even more, but rather monitor and understand the situation. But putting yourself in a grave and starting to think about the end is impossible. You need to think about life, about yourself, about your children. I’m 39, I found out that I have astrogliosis 3 years ago, but the symptoms have been going on since 5-6 years. My head hurts so bad that my eyes feel like they're going to pop out. And the pills don't help. Do you know how you found gliosis?))) Scheduled examinations after two surgeries and three chemo treatments. Like this! Health, long life and goodness to everyone!

Hello. Based on MRI results, isolated foci of gliosis are detected in the subcortical parts of both hemispheres of the brain. This means that this is the diagnosis of “focus of gliosis”, what to do now, what to do next? What do you advise?

I have multiple foci of gliosis in the frontal and parietal lobes, but I do not despair. I look at life with optimism. I lead a healthy lifestyle, I don’t take medications, I only drink dietary supplements from the most famous companies. And I feel good. I am 55 years old and plan to live actively for another 25 years. I wish you all health and long life!

These are all questions. I wonder where the answers are.

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Causes of cerebral gliosis, likely consequences, treatment

To quickly transmit nerve impulses from the human brain to muscle tissue and back, a huge number of neurons are located in the tissues of the central nervous system. Their function includes generating and transmitting signals. Glial cells located in the brain support and ensure the normal functioning of neurons.

What is cerebral gliosis

Most neurologists agree that gliosis changes in the brain are not a separate disease, but rather a consequence of other pathological changes.

Causes of gliosis

As already noted, gliosis is not an independent diagnosis, but rather a consequence of various disorders and abnormalities associated with brain atrophy or necrotic tissue phenomena. Typically, the proliferation of glial cells is observed in the following diseases:

  1. Tuberous and multiple sclerosis.
  • The influence of alcohol - moderate doses of alcohol lead to improved blood circulation and brain metabolism. But excessive drinking causes critical damage to neural connections.

Almost all patients who take drugs, even for medical purposes, experience an initial degree of gliosis.

Depending on the nature and localization of the process, it is customary to distinguish the following types of glial proliferations:

  • Periventricular gliosis of the brain - growths are localized in the ventricles. Often accompanied by carpal tumors.

Numerous supratentorial lesions are a consequence of disruption of normal circulation and indicate the presence of neurological pathological changes.

What manifestations are characteristic of gliosis?

Foci of gliosis of vascular origin in the brain lead to disturbances in brain activity and tissue atrophy. As it develops, the patient begins to experience manifestations characteristic of other diseases of the central nervous system:

  • Regular headaches of high intensity associated with mental activity, attempts to concentrate, etc. Especially often, post-traumatic gliosis changes appear in this way in the temporal lobe of the brain, which is responsible for the associative perception of a person.

Why is gliosis dangerous for human health?

The consequences of gliosis are primarily associated with the localization of the catalyst that caused the pathological changes. Glial formations are a consequence of encephalitis, pressure surges and hypertension, multiple sclerosis and trauma.

What treatment is needed for gliosis?

There is currently no effective treatment for glial scars. When determining how to treat gliosis, the attending physician will conduct a general diagnosis of the body and prescribe therapy aimed at the source - the catalyst that provokes the disease. Prescribed drugs for treatment are also intended to prevent the appearance of new foci of pathological changes.

Methods for determining brain damage in gliosis

How you feel during gliosis changes is not an absolute indication for diagnosing the disease. For successful therapy, it is extremely important to determine the causes of the development of deviations. Therefore, when disorders appear in the functioning of the central nervous system, instrumental diagnostic methods must be carried out:

  • Tomography – brain examinations using CT and MRI are generally accepted examination standards. Diagnostic methods make it possible to get an idea not only of the presence of existing glial formations, but also of the source that caused the changes.

Computed tomography is performed with contrast enhancement and helps to identify abnormalities associated with vascular origin.

An MRI diagnosis indicates metabolic disorders, the presence of tumor formations, the appearance of scars, etc. Magnetic resonance imaging detects gliosis of the white matter of the frontal lobes of the brain, which cannot be determined using other research methods.

Gliotic transformation of the frontal lobes is often caused by aging of the body and occurs in older people, without the presence of “accompanying” pathologies, which are the primary factor of changes.

Traditional medicine against gliosis

Gliosis is not a separate disease. Therefore, there are no drugs that effectively eliminate glial transformations.

  • Prevention of disease - in the early stages of the disease, the body is able to independently cope with negative changes. The patient is advised to change eating habits, lead a healthy and moderately active lifestyle, and stop drinking alcohol and smoking.

Multifocal multiple foci of gliosis in the brain structure are not subject to surgical treatment. The patient is prescribed lifelong conservative therapy. During surgery, tumors are removed, blood vessels are bypassed, or cerebrospinal fluid accumulated due to glial scars is drained.

Folk remedies for gliosis

A few lesions at an early stage can be removed using traditional methods of therapy. Herbs that improve metabolism and stabilize the blood supply system will help.

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Focal formations in the lungs are tissue compactions, which can be caused by various ailments. Moreover, to establish an accurate diagnosis, a doctor’s examination and radiography are not enough. The final conclusion can be made only on the basis of specific examination methods, including blood tests, sputum tests, and tissue puncture.

Important: the opinion that only tuberculosis can be the cause of multiple focal lung lesions is erroneous.

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Therefore, diagnosis must be preceded by a thorough examination of the patient. Even if the doctor is sure that a person has focal pneumonia, it is necessary to perform a sputum analysis. This will identify the pathogen that caused the development of the disease.

Now some patients refuse to undergo certain specific tests. The reason for this may be reluctance or inability to visit the clinic due to its distance from the place of residence, or lack of funds. If this is not done, then there is a high probability that focal pneumonia will become chronic.

What are foci and how to identify them?

Now focal formations in the lungs are divided into several categories based on their number:

  1. Singles.
  2. Single – up to 6 pieces.
  3. Multiple – dissemination syndrome.

There is a difference between the internationally accepted definition of what lung lesions are and what is accepted in our country. Abroad, this term refers to the presence of areas of compaction in the lungs of a round shape and a diameter of no more than 3 cm. Domestic practice limits the size to 1 cm, and the remaining formations are classified as infiltrates, tuberculomas.

Important: a computer examination, in particular tomography, will allow you to accurately determine the size and shape of the lesion in the lung tissue. However, it is necessary to understand that this examination method also has its own error threshold.

In fact, a focal formation in the lung is a degenerative change in the lung tissue or the accumulation of fluid (sputum, blood) in it. Correct characterization of single pulmonary lesions (SLP) is one of the most important problems of modern medicine.

The importance of the task lies in the fact that 60-70% of such formations that were cured, but then reappeared, are malignant tumors. Among the total number of AOLs identified during MRI, CT or radiography, their portion is less than 50%.

An important role here is played by how lesions in the lungs are characterized on CT. Using this type of examination, based on characteristic symptoms, the doctor can make assumptions about the presence of serious diseases such as tuberculosis or malignant neoplasms.

However, to clarify the diagnosis, additional tests are necessary. A hardware examination is not enough to issue a medical report. Until now, everyday clinical practice does not have a unified algorithm for differential diagnosis for all possible situations. Therefore, the doctor considers each case separately.

Tuberculosis or pneumonia? What can prevent, with the modern level of medicine, from making an accurate diagnosis using the hardware method? The answer is simple - imperfect equipment.

In fact, when undergoing fluorography or radiography, it is difficult to identify OOL, the size of which is less than 1 cm. Interposition of anatomical structures can make larger lesions practically invisible.

Therefore, most doctors advise patients to give preference to computed tomography, which makes it possible to view tissue in section and from any angle. This completely eliminates the possibility that the lesion will be obscured by the cardiac shadow, ribs, or roots of the lungs. That is, radiography and fluorography simply cannot consider the whole picture as a whole and without the possibility of a fatal error.

It should be taken into account that computed tomography can detect not only AOL, but also other types of pathologies, such as emphysema and pneumonia. However, this examination method also has its weaknesses. Even with a CT scan, focal formations may be missed.

This has the following explanations for the low sensitivity of the device:

  1. The pathology is in the central zone – 61%.
  2. Size up to 0.5 cm – 72%.
  3. Low fabric density - 65%.

It has been established that with a primary screening CT scan, the probability of missing a pathological change in tissue, the size of which does not exceed 5 mm, is about 50%.

If the diameter of the lesion is more than 1 cm, then the sensitivity of the device is more than 95%. To increase the accuracy of the obtained data, additional software is used to obtain 3D images, volumetric rendering and maximum intensity projections.

Anatomical features

In modern domestic medicine, there is a gradation of lesions based on their shape, size, density, structure and condition of the surrounding tissues.

An accurate diagnosis based on CT, MRI, fluorography or radiography is possible only in exceptional cases.

Usually in the conclusion only the probability of the presence of a particular disease is given. In this case, the location of the pathology itself is not given decisive importance.

A striking example is the presence of a lesion in the upper lobes of the lung. It has been established that this localization is characteristic of 70% of cases of detection of a primary malignant tumor of this organ. However, this is also typical for tuberculous infiltrates. With the lower lobe of the lung there is approximately the same picture. Here, cancer that has developed against the background of idiopathic fibrosis and pathological changes caused by tuberculosis are detected.

Great importance is given to the contours of the lesions. In particular, a fuzzy and uneven outline, with a lesion diameter of more than 1 cm, signals a high probability of a malignant process. However, if clear margins are present, this is not sufficient reason to stop diagnosing the patient. This picture is often present in benign neoplasms.

Particular attention is paid to tissue density: based on this parameter, the doctor is able to distinguish pneumonia from scarring of lung tissue, for example, caused by post-tuberculosis changes.

The next nuance is that CT allows you to determine the types of inclusions, that is, determine the structure of the OOL. In fact, after an examination, a specialist can tell with high accuracy what kind of substance accumulates in the lungs. However, only fatty inclusions make it possible to determine the ongoing pathological process, since all the others do not belong to the category of specific symptoms.

Focal changes in the lung tissue can be provoked by both a fairly easily treatable disease - pneumonia, and more serious ailments - malignant and benign neoplasms, tuberculosis. Therefore, it is important to identify them in a timely manner, in which a hardware examination method - computed tomography - will help.

Gon's lesion in the lungs is a manifestation of tuberculosis. Without the presence of a path to the root, tuberous formations extending beyond the contours of the mediastinum (lymph nodes), it is difficult to identify the tuberculous affiliation of focal shadowing syndrome.

When analyzing formations up to 1 cm in diameter, you should pay attention to calcification, density, fibrosis, morphological structure, and intensity of darkening. The prevalence of more than 2 ribs is a sign of dissemination.

Digital image: multiple fibrotic foci of both lungs against the background of chronic bronchitis

Ghon's lesion and calcified lesions in the lungs - what is it?

Ghon's lesion is a formation at the apex or upper segments of the lungs, caused by damage to the lung tissue by mycobacteria. Morphological examination of the material reveals a large number of granulation cells and macrophages. The body constantly fights the causative agent of pulmonary tuberculosis, so the dynamics increase slowly. Only when viewing a series of images of the chest organs over a period of 3-6 months can some changes be identified.

If tuberculous lesions persist for a long time, the formation of a calcified lesion can be observed. Calcium salts are deposited in places of caseous destruction. This is how the pathogen mummifies, which prevents re-infection of the lung tissue.

Calcified lesions in the lungs are not only manifestations of tuberculosis infection. Occurs in chronic pneumonia, helminthic infestations, fibrosing alveolitis (Hammen-Richie).

Digital radiograph: miliary tuberculosis, lesions on both sides

Gon's outbreak is a rare form of infection in the current period of time. Due to the uncontrolled use of antibiotics, microorganisms have become resistant to antibiotics. When treating other diseases with these drugs, a certain activity of the chemical compound on Mycobacterium tuberculosis is ensured. The bacteria are not completely killed. If microorganisms do not have multidrug resistance, under the influence of antibiotic therapy for pneumonia, bronchitis, and other diseases, a person stops the active progression of tuberculosis without knowing it.

Only when performing the next fluorography is a specific focus at the apex revealed (calcified, dense, fibrous, intense, calcified).

Dense lesions in the lungs with focal opacification syndrome

The syndrome of limited focal darkening includes single (up to 5), multiple shadows (more than 6), the size of which does not exceed 1 cm. With a limited location (up to 2 intercostal spaces), a diagnosis of focal tuberculosis and pneumonia is made.

If the area extends beyond the two intercostal spaces, they speak of a disseminated process. Focal darkening is differentiated into primary and secondary. In diseases with damage to lung tissue, the pathogenesis of the syndrome is accompanied by the following pathogenetic mechanisms:

Displacement of air by exudate, transudate;
Resorption of alveolar air with lobular atelectasis;
Expulsion of air by the substrate outside the alveoli;
Hematogenous metastases due to edema, infarction, tuberculosis;
Lymphogenic metastases (primary tuberculosis, blood diseases);
Contact damage to lung tissue (peripheral cancer, aneurysm).

Ghon's lesion syndrome, polymorphic, fibrous, intense, calcified, can be observed in tumors, inflammation of the lung tissue, and vascular anomalies.

Determining a focal shadow in an image does not always allow one to verify the morphology or etiological factor.

In different diseases, focal opacification syndrome has radiological similarities. The specific gravity of the tumor, fibrous, necrotic, inflammatory focus differs slightly. To differentiate gradations, computed tomography is used to study the density of the shadow. The study allows you to clearly verify calcified, calcified, intense and weak darkening.

In the classic condition, a Gon's lesion in the lungs is clearly visualized on an x-ray. Other nosological forms are not accompanied by accompanying signs that allow verification of the nosology.

Dense lesions in the lungs - what are they?

Dense foci on an x-ray of the lungs indicate either a chronic infection or a healed inflammatory, traumatic process. At the site of prolonged inflammation, scar tissue accumulates, pneumosclerosis forms, and carnification occurs in pneumonia. In all these nosologies, the x-ray shows dense (intense) shadows.

If these changes are present in the image, the clinical picture is not accompanied by pronounced changes. The syndrome of calcification, calcification, scarring can be a manifestation of the following nosological forms:

Tumor;
Aneurysm;
Retention cyst;
Primary cancer;
Focal tuberculosis.

Only with dissemination do signs of severe intoxication appear:

1. Temperature over 39 degrees;
2. General weakness;
3. Cough with sputum;
4. Chest pain.

During the inflammatory process, laboratory changes can be observed: leukocytosis, acceleration of the erythrocyte sedimentation rate. Focal tuberculosis is characterized by specific clinical symptoms:

Pain in the chest;
Cough;
Irritability;
Loss of appetite;
Weakness.

With tuberculosis infection, a blood test is not accompanied by inflammatory changes. To diagnose the disease, the determination of Mycobacterium tuberculosis in the washing waters of the bronchial tract is required. With small peripheral cancer and solitary metastases, changes in blood tests can be observed.

In case of pulmonary infarction, focal darkening syndrome is observed, which occurs with thrombophlebitis of the lower extremities. Clinic – hemoptysis, complaints of pain in the side.

Dense lesions in the lungs in most cases do not require treatment, but before stopping treatment of the patient, a full diagnosis is required to confirm the true focal shadow syndrome. Make sure that the image shows a really large formation that occupies the acini. A similar picture is formed by the interweaving of blood vessels and interstitial cords. A polypositional (multi-axial) examination provides a lot of information. Even traditional radiography of the chest organs in frontal and lateral projections reveals the round nature of the darkening. On a lateral image, it is possible to identify calcified foci of the pleura. With a multiprojection study, it is possible to distinguish between intrapulmonary and pleural calcifications.

If a focal syndrome is detected on an x-ray, a differential diagnosis should be made between tumors, tuberculosis, and pneumonia.

Fibrous lesions in the lungs - what are they?

With inflammatory changes, the focal shadow has medium intensity, uneven, blurred boundaries. In chronic inflammation and fibrous tuberculosis, the darkening is intense with jagged, sharp edges.

Fibrous deposits impair the ventilation of the bronchial tract. The degree of respiratory failure is determined by the extent of the lesion.

If fibrosis is provoked by a tumor, a “belt” can be seen around the rounded shadow, an accumulation of small foci due to the enhanced pulmonary pattern.

In tuberculosis, a vascular “path” departs from the fibrous focus, directed towards the root of the lung. Several convoluted thin strips of vessels directed towards the root are often found in chronic tuberculosis.

Enlarged lymph nodes, a track, a round shadow in the pulmonary parenchyma are most often radiological signs of cancer.

Fibrous polymorphic foci can be observed in focal pneumonia with a long course. With the constant destruction of cells, the sites of destruction are scarred by connective tissue, which persists throughout the rest of a person’s life.

In conclusion, I would like to remind you that polymorphic lesions in the lungs are not always a manifestation of pulmonary pathology. If the syndrome is detected on direct radiographs, there is a possibility of pleural involvement. Pleurisy can be not only exudative, but also dry. After healing, calcifications and fibrous foci remain.

Focal opacification syndrome in the lungs is an x-ray manifestation of many nosological forms. Several methods are used for differential diagnosis.

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