Moderately pronounced atrophic changes in the cerebellum. Congenital atrophy of the cerebellum. Basic functions and disorders of the cerebellum

Brain atrophy is a process gradual death cerebral cells and destruction of interneuronal connections. The pathological process can spread to the cerebral cortex or subcortical structures. Despite the cause of the pathological process and the treatment used, the prognosis for recovery is not entirely favorable. Atrophy can affect any functional area of ​​the gray matter, leading to impaired cognitive abilities, sensory and motor disorders.

ICD-10 code

G31.0 Limited cerebral atrophy

Epidemiology

Most of reported cases are among the elderly, namely women. The onset of the disease can start after 55 years and after a couple of decades lead to complete dementia.

Causes of brain atrophy

Brain atrophy is a serious pathology that occurs as a result of age-related degenerative processes, a genetic mutation, the presence concomitant pathology or exposure to radiation. In some cases, one factor may come to the fore, and the rest are only a background for the development of this pathology.

The basis for the development of atrophy is a decrease in the volume and mass of the brain with age. However, one should not think that the disease concerns only senile age. There is brain atrophy in babies, including newborns.

Almost all scientists unanimously argue that the cause of atrophy lies in heredity, when there are failures in the transmission of genetic information. Surrounding negative factors are considered a background effect that can accelerate the process of this pathology.

Causes of congenital brain atrophy imply the presence of a genetic anomaly of hereditary origin, a mutation in the chromosomes, or an infectious process during pregnancy. Most often this concerns a viral etiology, but bacterial is also often observed.

From the group of acquired predisposing factors, it is necessary to single out chronic intoxication, especially the negative effect of alcohol, infectious processes in the brain, both acute and chronic, traumatic brain damage and exposure to ionizing radiation.

Of course, acquired causes can come to the fore only in 5% of all cases, since in the remaining 95% they are a provoking factor against the background of manifestations of a genetic mutation. Despite the focality of the process at the beginning of the disease, the entire encephalon is gradually affected with the development of dementia and dementia.

At the moment, it is not possible to describe pathogenetically all the processes that take place in the brain during atrophy, since the nervous system itself and its functionality have not been fully studied. However, some information is still known, especially about manifestations of atrophy involving certain structures.

Symptoms of brain atrophy

As a result of age-related changes in the encephalon, as well as other organs, processes of reverse development occur. This is due to the acceleration of destruction and slowing down of cell regeneration. Thus, the symptoms of brain atrophy gradually increase in severity depending on the area of ​​the lesion.

At the beginning of the disease, a person becomes less active, indifference, lethargy appear, and the personality itself changes. Sometimes there is an ignorance of moral behavior and actions.

Then there is a decrease in vocabulary, which ultimately leads to the presence of primitive expressions. Thinking loses its productivity, the ability to criticize behavior and think about actions is lost. In relation to motor activity, motor skills deteriorate, which leads to a change in handwriting and a deterioration in semantic expression.

Symptoms of brain atrophy may affect memory, thinking, and other cognitive functions. Thus, a person may stop recognizing objects and forget how they are used. Such a person needs constant monitoring in order to avoid unforeseen emergencies. Problems with orientation in space occur due to memory impairment.

Such a person cannot adequately assess the attitude of the surrounding people towards him and is often suggestible. In the future, with the progression of the pathological process, there is a complete moral and physical degradation of the personality due to the onset of insanity.

Brain atrophy 1 degree

Degenerative changes in the brain become more active with age, however, under the influence of concomitant additional factors, thinking disorders can develop much faster. Depending on the activity of the process, its severity and the severity of clinical manifestations, it is customary to distinguish several degrees of the disease.

Brain atrophy of the 1st degree is observed at the initial stage of the disease, when there is a minimum level of pathological abnormalities in the functioning of the encephalon. In addition, one should consider where the disease is initially localized - in the cortex or subcortical structures Oh. The first manifestations of atrophy that can be seen from the side depend on this.

At the initial stage, atrophy may have absolutely no clinical symptoms. Perhaps the appearance of human anxiety due to the presence of another comorbidity that directly or indirectly affects the functioning of the encephalon. Then, periodic dizziness and headaches may appear, which gradually become more frequent and intense.

If a person at this stage consult a doctor, then grade 1 brain atrophy under the influence of drugs slows down its progression and there may be no symptoms. Needs to be adjusted with age. medical therapy, choosing other drugs and dosages. With their help, you can slow down the growth and emergence of new clinical manifestations.

Brain atrophy grade 2

The clinical picture and the presence of certain symptoms depend on the degree of brain damage, in particular on damaged structures. The 2nd degree of pathology usually already has some manifestations, due to which the presence of pathological processes can be suspected.

The onset of the disease can be manifested exclusively by dizziness, headache, or even manifestations of another concomitant disease that affects the functioning of the encephalon. However, in the absence of therapeutic measures, this pathology continues to destroy structures and increase clinical manifestations.

So, to periodic dizziness, a deterioration in mental capabilities and the ability to analyze is added. In addition, the level of critical thinking decreases and self-esteem of actions and speech function is lost. In the future, most often, changes in speech, handwriting increase, as well as old habits are lost and new ones appear.

Brain atrophy of the 2nd degree, as it progresses, causes a deterioration in fine motor skills, when the fingers cease to “obey” the person, which leads to the impossibility of performing any work involving the fingers. Coordination of movements also suffers, as a result of which gait and other activities slow down.

Thinking, memory and other cognitive functions gradually worsen. There is a loss of skills in the use of objects familiar to daily use, for example, a TV remote control, a comb or a toothbrush. Sometimes you can notice a person copying the behavior and manners of other people, which is due to the loss of independence in thinking and movements.

Forms

Atrophy of the frontal lobes of the brain

In some diseases, at the first stage, atrophy of the frontal lobes of the brain is observed, followed by progression and spread of the pathological process. This applies to Pick's disease and Alzheimer's.

Pick's disease is characterized by a destructive lesion mainly of neurons in the frontal and temporal regions, which causes the appearance of certain clinical signs. With their help, the doctor can suspect the disease and, using instrumental methods, make the correct diagnosis.

Clinically, damage to these areas of the encephalon is manifested by a change in personality in the form of a deterioration in thinking and the process of memorization. In addition, from the onset of the disease, a decrease in intellectual abilities can be observed. There is a degradation of a person as a person, which is expressed in the angularity of character, secrecy, alienation from the surrounding people.

Motor activity and phrases become pretentious and may be repeated in a pattern. Due to the decrease in vocabulary, there is a frequent repetition of the same information in the course of a conversation or after a while. Speech becomes primitive with the use of monosyllabic phrases.

Atrophy of the frontal lobes of the brain in Alzheimer's disease is slightly different from Pick's pathology, since in this case there is a greater deterioration in the process of remembering and thinking. As for the personal qualities of a person, they suffer a little later.

Atrophy of the cerebellum

Dystrophic lesions can begin with the cerebellum, moreover, without involving pathways in the process. Ataxia and changes in muscle tone come to the fore, despite the fact that the causes of development and the prognosis are more similar to damage to the neurons of the hemispheres.

Atrophy of the cerebellum of the brain can be manifested by the loss of a person's ability to self-service. Damage to the cerebellum is characterized by disorders in the combined functioning of skeletal muscles, coordination of movements and maintenance of balance.

Disorders of motor activity due to pathology of the cerebellum have several features. Thus, a person loses the smoothness of arms and legs when performing movements, intentional trembling appears, which is noted at the end of a motor act, handwriting changes, speech and movements become slower, and chanted speech occurs.

Atrophy of the cerebellum of the brain can be characterized by an increase in dizziness, an increase in headaches, the appearance of nausea, vomiting, drowsiness and impaired auditory function. Intracranial pressure increases, ophthalmoplegia may occur due to paralysis of the cranial nerves, which are responsible for the innervation of the eye, areflexia, enuresis and nystagmus, when the pupil performs involuntary rhythmic oscillations.

Atrophy of the brain substance

The destructive process in neurons can occur during the physiological process due to age-related changes after 60 years or pathological - as a result of any disease. Atrophy of the substance of the brain is characterized by the gradual destruction nervous tissue with a decrease in the volume and mass of gray matter.

Physiological destruction is observed in all people in old age, but the course of which can only be slightly influenced by medicinal effects, slowing down the destructive processes. With regard to pathological atrophy due to the negative effects of harmful factors or another disease, it is necessary to act on the cause of the atrophy in order to stop or slow down the destruction of neurons.

Atrophy of the brain substance, in particular white matter, can develop as a result of various diseases or age-related changes. It is worth highlighting individual clinical manifestations of pathology.

So, with the destruction of the neurons of the knee, hemiplegia appears, which is a paralysis of the muscles of half of the body. The same symptoms are observed when the anterior portion of the posterior leg is damaged.

Destruction of the posterior area is characterized by a change in sensitivity in half of the areas of the body (hemianesthesia, hemianopsia and hemiataxy). The defeat of the substance can also cause a complete loss of sensitivity on one side of the body.

Mental disorders are possible in the form of a lack of recognition of objects, the performance of purposeful actions and the appearance of pseudobulbar signs. The progression of this pathology leads to disorders of speech function, swallowing and the occurrence of pyramidal symptoms.

Cortical atrophy of the brain

Due to age-related changes or as a result of a disease that affects the encephalon, the development of such a pathological process as cortical atrophy of the brain is possible. Most often, the frontal parts are affected, but the spread of destruction to other areas and structures of the gray matter is not excluded.

The disease begins imperceptibly and slowly begins to progress, and the increase in symptoms is noted after a few years. With age and in the absence of treatment, the pathological process actively destroys neurons, which ultimately leads to dementia.

Cortical atrophy of the brain mainly occurs in people after 60 years of age, but in some cases, destructive processes are observed even at an earlier age due to congenital development due to genetic predisposition.

The defeat of the two hemispheres of cortical atrophy occurs in Alzheimer's disease or in other words, senile dementia. The pronounced form of the disease leads to complete dementia, while small destructive foci do not have a significant negative impact on the mental capabilities of a person.

The severity of clinical symptoms depends on the location and severity of damage to the subcortical structures or cortex. In addition, the rate of progression and the prevalence of the destructive process should be taken into account.

Multisystem atrophy of the brain

Degenerative processes underlie the development of Shy-Drager syndrome (multisystem atrophy). As a result of the destruction of neurons in some areas of the gray matter, disturbances in motor activity occur, and control over autonomic functions, such as blood pressure or the process of urination, is lost.

Symptomatically, the disease is so diverse that, for a start, some combinations of manifestations can be distinguished. So, the pathological process is expressed by vegetative dysfunctions, in the form of parkinsonian syndrome with the development of hypertension with trembling and slowing of motor activity, as well as in the form of ataxia - unsteady walking and coordination disorders.

The initial stage of the disease is manifested by an akinetic-rigid syndrome, which is characterized by slow movements and has some symptoms of Parkinson's disease. In addition, there are problems with coordination and genitourinary system. In men, the first manifestation may be erectile dysfunction, when there is no ability to achieve and maintain an erection.

As for the urinary system, it is worth noting urinary incontinence. In some cases, the first sign of pathology may be sudden falls of a person throughout the year.

With further development, multisystem atrophy of the brain acquires new symptoms that can be divided into 3 groups. The first is parkinsonism, which manifests itself in slow awkward movements and changes in handwriting. The second group includes urinary retention, urinary incontinence, impotence, constipation and paralysis. vocal cords. And finally, the third - consists of dysfunction of the cerebellum, which is characterized by difficulty in coordination, loss of a sense of prostration, dizziness and fainting.

In addition to cognitive impairment, other symptoms are possible, such as dry mouth, dry skin, changes in sweating, snoring, shortness of breath during sleep, and double vision.

Diffuse atrophy of the brain

Physiological or pathological processes in the body, in particular, in the encephalon, can trigger the degeneration of neurons. Diffuse atrophy of the brain can occur as a result of age-related changes, genetic predisposition, or under the influence of provoking factors. These include infectious diseases, injuries, intoxications, diseases of other organs, as well as the negative impact of the environment.

Due to the destruction of nerve cells, there is a decrease in brain activity, the ability of critical thinking and control over one's actions is lost. In old age, a person sometimes changes behavior that is not always clear to others.

The onset of the disease can be localized in different areas, which causes certain symptoms. As other structures are involved in the pathological process, new clinical signs appear. Thus, the healthy parts of the gray matter are gradually affected, which ultimately leads to dementia and loss of personality.

Diffuse atrophy of the brain is initially characterized by the appearance of symptoms similar to cortical atrophy of the cerebellum, when gait is disturbed and spatial sensation is lost. In the future, there are more manifestations, as the disease gradually covers new areas of gray matter.

Atrophy of the left hemisphere of the brain

Each section of the encephalon is responsible for a specific function, therefore, when it is damaged, a person loses the ability to perform something, either physically or mentally.

The pathological process in the left hemisphere causes the appearance of speech disorders, such as motor aphasia. With the progression of the disease, speech may consist of separate words. In addition, logical thinking suffers and a depressive state develops, especially if atrophy is localized mostly in the temporal region.

Atrophy of the left hemisphere of the brain leads to the lack of perception of the full image, the surrounding objects are perceived separately. Parallel to this, a person's ability to read is impaired, handwriting changes. Thus, analytical thinking suffers, the ability to think logically, analyze incoming information and manipulate dates and numbers is lost.

A person cannot correctly perceive and process information consistently, which leads to the inability to remember it. The speech addressed to such a person is perceived separately by sentences and even words, as a result of which there is no adequate reaction to the appeal.

Severe atrophy of the left hemisphere of the brain can cause complete or partial paralysis of the right side with impaired motor activity due to changes in muscle tone and sensory perception.

Mixed brain atrophy

Cerebral disorders can occur as a result of age-related changes, under the influence of genetic factor or associated pathology. Mixed brain atrophy is a process of gradual death of neurons and their connections, in which the cortex and subcortical structures suffer.

Degeneration of the nervous tissue occurs mostly in women over 55 years of age. As a result of atrophy, dementia develops, and that significantly worsens the quality of life. With age, the volume and mass of the brain decrease due to the gradual destruction of neurons.

The pathological process can be observed in childhood when it comes to the genetic pathway of disease transmission. In addition, there are comorbidities and environmental factors, such as radiation.

Mixed brain atrophy covers the functional areas of the encephalon, which are responsible for controlling motor and mental activity, planning, analysis, and also criticizing one's behavior and thoughts.

The initial stage of the disease is characterized by the appearance of lethargy, apathy and a decrease in activity. In some cases, immoral behavior is observed, as a person gradually loses self-criticism and control over actions.

Subsequently, there is a decrease in the quantity and quality composition vocabulary, the ability of productive thinking, self-criticism and understanding of behavior are lost, and motor skills deteriorate, which leads to a change in handwriting. Further, a person ceases to recognize objects familiar to him, and eventually insanity sets in, when there is practically a degradation of the personality.

Atrophy of the parenchyma of the brain

The causes of parenchyma damage are age-related changes, the presence of concomitant pathology that directly or indirectly affects the encephalon, genetic and harmful environmental factors.

Atrophy of the brain parenchyma can be observed due to insufficient nutrition of neurons, since it is the parenchyma that is most sensitive to hypoxia and insufficient intake of nutrients. As a result, cells decrease in size due to compaction of the cytoplasm, nucleus and destruction of cytoplasmic structures.

In addition to a qualitative change in neurons, cells can disappear altogether, reducing the volume of the organ. Thus, atrophy of the brain parenchyma gradually leads to a decrease in the weight of the brain. Clinically, damage to the parenchyma can be manifested by a violation of sensitivity in certain areas of the body, a disorder of cognitive functions, loss of self-criticism and control over behavior and speech function.

The course of atrophy steadily leads to the degradation of the personality and ends lethal outcome. With the help of medicines, you can try to slow down the development of the pathological process and support the functioning of other organs and systems. Symptomatic therapy is also used to alleviate a person's condition.

spinal cord atrophy

Reflexively, the spinal cord can carry out motor and autonomic reflexes. Motor nerve cells innervate the muscular system of the body, including the diaphragm and intercostal muscles.

In addition, there are sympathetic and parasympathetic centers that are responsible for the innervation of the heart, blood vessels, digestive organs and other structures. For example, in the thoracic segment is the center of the expansion of the pupil and the sympathetic centers of innervation of the heart. The sacral region has parasympathetic centers responsible for the functionality of the urinary and reproductive systems.

Atrophy spinal cord depending on the localization of destruction, it can manifest itself as a violation of sensitivity - with the destruction of neurons of the posterior roots, or motor activity - of the anterior roots. As a result of the gradual damage to individual segments of the spinal cord, there are violations of the functionality of the organ that is innervated at this level.

Thus, the disappearance of the knee reflex occurs due to the destruction of neurons at the level of 2-3 lumbar segments, plantar - 5 lumbar, and a violation of the contraction of the abdominal muscles is observed with atrophy of nerve cells of 8-12 thoracic segments. Especially dangerous is the destruction of neurons at the level of the 3-4th cervical segment, where the motor center of innervation of the diaphragm is located, which threatens human life.

Alcoholic brain atrophy

The most sensitive organ to alcohol is the encephalon. Under the influence of alcohol, there is a change in the metabolism in neurons, resulting in the formation of alcohol dependence.

Initially, there is development alcoholic encephalopathy caused by pathological processes in different areas of the brain, membranes, cerebrospinal fluid and vascular systems.

Under the influence of alcohol, the cells of the subcortical structures and the cortex are affected. In the brain stem and spinal cord, fiber destruction is noted. Dead neurons form islands around the affected vessels with accumulations of decay products. In some neurons, the processes of wrinkling, displacement and lysis of the nucleus.

Alcoholic atrophy of the brain causes a gradual increase in symptoms, which begins with alcoholic delirium and encephalopathy, and ends in death.

In addition, there is sclerosis of the vessels with deposition around the brown pigment and hemosiderin, as a result of hemorrhages, and the presence of cysts in the vascular plexuses. Possible hemorrhages in the trunk of the encephalon, ischemic changes and degeneration of neurons.

It is worth highlighting the Makiyafawa-Bignami syndrome, which occurs as a result of frequent drinking in large quantities. Morphologically, central necrosis of the corpus callosum, its swelling, as well as demyelination and hemorrhages are revealed.

Brain atrophy in children

Infrequently, brain atrophy occurs in children, but this absolutely does not mean that it cannot develop in the presence of any neurological pathology. This fact, neurologists must take into account and prevent the development of this pathology in the early stages.

To make a diagnosis, they use a survey of complaints, the stages of the onset of symptoms, their duration, as well as the severity and progression. In children, atrophy can develop at the end of the initial stage of the formation of the nervous system.

Brain atrophy in children at the first stage may not have clinical manifestations, which complicates the diagnosis, because parents from the outside do not notice the deviation, and the destruction process has already started. In this case, magnetic resonance imaging will help, thanks to which the encephalon is examined in layers, and pathological foci are detected.

As the disease progresses, children become nervous, irritable, conflicts with peers occur, which leads to the solitude of the baby. Further, depending on the activity of the pathological process, cognitive and physical impairments can be attached. Treatment is aimed at slowing down the progression of this pathology, maximizing the elimination of its symptoms and maintaining the functioning of other organs and systems.

Brain atrophy in newborns

Most often, brain atrophy in newborns is caused by hydrocephalus or dropsy of the brain. It manifests itself in an increased cerebrospinal fluid, thanks to which the encephalon is protected from damage.

There are many reasons for the development of dropsy. It can form during pregnancy, when the fetus grows and develops, and is diagnosed using ultrasound. In addition, various failures in the laying and development of the nervous system or intrauterine infections in the form of herpes or cytomegaly can become the cause.

Also, dropsy and, accordingly, brain atrophy in newborns can occur due to malformations of the brain or spinal cord, birth injuries, accompanied by hemorrhage and the onset of meningitis.

Such a baby should be located in the intensive care unit, as it needs to be monitored by neuropathologists and resuscitators. There is no effective treatment yet, therefore, gradually this pathology leads to serious violations of the functioning of organs and systems due to their inferior development.

Diagnosis of brain atrophy

When the first symptoms of the disease appear, you should consult a doctor to establish a diagnosis and select an effective treatment. At the first contact with the patient, it is necessary to find out about the complaints that bother, the time of their occurrence and the presence of an already known chronic pathology.

Further, the diagnosis of brain atrophy consists in the use x-ray examination, thanks to which the encephalon is examined in layers to detect additional formations(hematomas, tumors), as well as foci with structural changes. For this purpose, magnetic resonance imaging can be used.

In the case of age-related changes, the treatment of brain atrophy consists in the use of drugs, providing complete care for the person, elimination annoying factors and protection from problems.

A person needs the support of loved ones, and therefore, when the first signs of this pathology appear, you should not immediately send a relative to a nursing home. It is advisable to conduct a drug course to maintain the functioning of the encephalon and eliminate the symptoms of the disease.

For therapeutic purposes, antidepressants, sedatives, including tranquilizers, are widely used, thanks to which a person relaxes and does not react so painfully to what is happening. He should be in a familiar environment, engage in daily activities and preferably sleep during the day.

Effective treatment in our time has not yet been developed, since it is very difficult to deal with the destruction of neurons. The only way to slow down the pathological process is the use of vascular drugs that improve cerebral circulation (Cavinton), nootropics (Ceraxon) and metabolic drugs. As a vitamin therapy, it is recommended to use group B to maintain the structure of nerve fibers.

Of course, with the help of drugs it is possible to slow down the progression of the disease, but not for long.

Treatment of spinal cord atrophy

Destruction of neurons in both the brain and spinal cord has no pathogenetic therapy in view of the fact that it is extremely difficult to deal with genetic, age and other causal factors. When exposed to a negative external factor, you can try to eliminate it, if there is a concomitant pathology that contributed to the destruction of neurons, its activity should be reduced.

The treatment of spinal cord atrophy is mostly based on the attitude of the surrounding close people, since it is impossible to stop the pathological process and, in the end, a person may remain disabled. Good attitude, care and familiar environment are the best that a relative can do.

Concerning drug therapy, then the treatment of spinal cord atrophy consists in the use of B vitamins, neurotropic and vascular drugs. Depending on the cause of this pathology, the first step is to eliminate or reduce the influence of the damaging factor.

Prevention

In view of the fact that the pathological process is almost impossible to prevent or stop, the prevention of brain atrophy can only consist in following some recommendations, with which you can postpone the onset of this pathology in the case of age-related genesis or stop it a little - in other cases.

Preventive methods consist in the timely treatment of chronic concomitant human pathology, since exacerbation of diseases can provoke the development of this pathology. In addition, it is necessary to regularly undergo preventive examinations to identify new diseases and their treatment.

In addition, the prevention of brain atrophy includes maintaining an active lifestyle, proper nutrition and complete rest. With age, atrophic processes can be observed in all organs, in particular in the gray matter. Their frequent cause is atherosclerosis of cerebral vessels.

As a result, it is recommended to adhere to certain recommendations to slow down the process of vascular damage by atherosclerotic deposits. To do this, it is necessary to control body weight, treat diseases of the endocrine system, metabolism, which contribute to obesity.

You should also fight high blood pressure, give up alcohol and smoking, strengthen the immune system and avoid psycho-emotional overstrain.

Forecast

Depending on the part of the brain that has undergone the most destruction, the prognosis and rate of development of the pathological process should be considered. For example, with Pick's disease, destruction of neurons in the frontal and temporal regions is noted, as a result of which personality changes first appear (thinking and memory worsen).

The progression of the disease is observed very quickly, as a result - the degradation of the personality. Speech and physical activity take on a pretentious tone, and the impoverishment of the vocabulary contributes to the use of monosyllabic phrases.

As for Alzheimer's disease, memory impairment is most pronounced here, but personal qualities do not suffer much even with 2 degrees of severity. This is due more to the breaks in interneuronal connections than to the death of neurons.

Despite the presence of the disease, the prognosis of brain atrophy is always unfavorable, as it slowly or quickly leads to the onset of dementia and death of a person. The only difference is the duration of the pathological process, and the outcome is the same in all cases.

It's important to know!

Skin atrophy occurs due to a violation of the structure and function of the connective skin and is clinically characterized by thinning of the epidermis and dermis. The skin becomes dry, transparent, wrinkled, gently folded, hair loss and telangiectasia are often noted.

Brain atrophy is the process of necrosis of its cells, as well as the destruction of connections that connect neurons. This pathology can cover the cortical and subcortical zones, leading to the complete destruction of a person's personality and making it impossible for his subsequent rehabilitation.

There are several of them, depending on localization and other features.

Atrophy of the frontal lobes of the brain

The initial stages of the pathologies described below are accompanied by atrophy of the frontal lobes and a number of specific signs.

Pick's disease

It is characterized by a violation of the integrity of neurons in the temporal and frontal regions of the brain. This creates a recognizable clinical picture, which is fixed by instrumental methods and allows you to make a diagnosis as accurately as possible.

The first negative changes in Pick's disease are a decrease in intelligence and a deterioration in the ability to remember. Further development of the disease leads to personal degradation (the character becomes angular, secretive, aloof).

In movements and verbal expressions, pretentiousness, monosyllabism, constant repetition of patterns are observed.

Alzheimer's disease

For senile dementia of the Alzheimer's type, the appearance of personality disorders is less characteristic, although memory and thinking suffer as much as in Pick's disease.

In the case of both pathologies, the lesion gradually grows, covering the entire brain completely.

It is possible that the focus of degenerative lesions will be localized in the cerebellum. In this case, the conductive paths remain intact. The most obvious symptom is altered muscle tone and the inability to maintain balance and coordinate body position.

Cerebellar atrophy results in the loss of the ability to take care of oneself. Movements lose their smoothness, and their completion is accompanied by intentional (arising from the performance of purposeful actions) trembling.

Speech becomes slow and scrambled, handwriting is jerky. Further atrophy is accompanied by stronger and more frequent attacks of headache and dizziness, nausea and vomiting, drowsiness and deafness.

Intracranial pressure rises noticeably, paralysis of one of the cranial nerves is often detected, which can lead to immobilization of the eye muscles, nystagmus (involuntary rhythmic fluctuations of the pupils), enuresis, and the disappearance of natural reflexes.

This type of disease can be the result of both age-related and other destructive changes. If its cause is physiological destruction, drug therapy almost does not positive results and can only slightly slow down the pathological process.

In other cases, the destruction of brain neurons can be stopped by eliminating an external factor or disease that led to atrophy.

Damage to a substance in the knee of the brain leads to the development of hemiplegia (muscle paralysis on one side of the body). A similar effect is produced by a violation of the structure of the anterior part of the hind leg ( posterior region this department is responsible for maintaining sensitivity).

The patient cannot perform purposeful actions and ceases to recognize objects. If left untreated, speech disorders occur, swallowing function is impaired, a pyramidal clinic is detected (pathological reflexes of oral automatism, carpal, foot, etc.)

Cortical atrophy of the brain

When the process affects the cortex, the frontal lobes are predominantly affected, although tissue necrosis of any other brain area is also not excluded. Clear signs pathological condition are revealed only a few years after the onset of its development.

This type of disease is usually experienced by people who have already reached the age of 60. The lack of therapeutic assistance provokes the occurrence of senile dementia in them (observed when two hemispheres are affected at once).

Alzheimer's disease most often leads to the development of bihemispheric cortical atrophy. However, with minor destruction, one can count on the relative safety of a person's mental abilities.

Cortical atrophy is often observed in dyscirculatory encephalopathy (a slowly progressive disorder cerebral circulation various etiologies).

Destruction of the cortical substance can occur not only in senile, but also in young age with an appropriate genetic predisposition.

Shy-Drager syndrome (multisystem atrophy) leads to the loss of the ability to control the autonomic functions of the body (blood pressure, urination). Other signs of pathology include:

• parkinsonian syndrome;
• hypertension;
• trembling of the limbs;
• unsteadiness when walking, unexpected falls;
• problems with coordination;
• decreased motor activity (akinetic-rigid syndrome).

For men, multisystem atrophic changes can be fraught with erectile dysfunction. Further development of the pathology entails the appearance of three new groups of symptoms:

• parkinsonism(distortion of handwriting, motor awkwardness);
• pathology of the genitourinary and excretory system(incontinence, impotence, constipation, etc.);
• cerebellar dysfunction(dizziness, fainting, impaired muscle coordination).

There is also a feeling of dry mouth, problems with sweating, double vision, shortness of breath and snoring.

Diffuse atrophy of the brain

Often occurs under the influence of infectious diseases, toxins, injuries, pathologies internal organs, negative external influences. Diffuse-atrophic changes reduce brain activity, deprive a person of control over his behavior, making his thinking incapable of criticism.

Symptoms depend on the location of the lesion, but initially resemble those that occur when the cortical structures of the cerebellum are damaged.

It is accompanied by speech pathologies (up to the point that the patient begins to speak in separate words), combined with motor-type aphasia. With predominant damage to the temporal regions, the ability to think logically is lost, depressive moods predominate.

Changes visual perception: a person ceases to see the whole picture as a whole, distinguishes only individual objects. It also deprives him of the ability to read, write, count, navigate dates and analyze information (including speech addressed to him, which causes inadequate behavioral reactions).

All this leads to memory problems. In addition, there may be movement disorders on the right side of the body.

Mixed brain atrophy

In this case, the cerebral cortex and subcortical regions (subcortex) are affected. Most often, this type of pathology is detected in older women over 55 years old, although it can occur even in newborn babies.

The main consequence and main symptom mixed atrophy - progressive dementia, which inevitably affects the quality of life. If the disease was acquired in childhood, then it is most likely that it is genetically determined or arose under the influence of radiation.

The pathological condition is accompanied by almost all the symptoms of atrophy, and on final stages its development, the personality is completely degraded.

It is a consequence of hypoxia (insufficient amount of oxygen) and deficiency of nutrients supplied to neurons. This leads to an increase in the density of the nucleus and cytoplasm of cells, which entails a decrease in their volume and causes the development of destructive processes.

The structure of neurons can not only atrophy, but also be completely destroyed, which means that the cells will simply disappear, leading to a decrease in the weight of the brain as a whole.

There may also be problems with the sensitivity of certain areas of the body. Parenchymal atrophy is fatal, so that a person can live as long as possible, he must be prescribed symptomatic drug therapy.

Alcoholic brain atrophy

This organ is more sensitive than others to the effects of alcohol, which can affect the metabolic processes taking place in neurons, causing addiction in a person.

Alcoholic atrophy is always preceded by the encephalopathy of the same name. The destructive effect of alcohol-containing products applies to:

• cortical-subcortical cells;
• brain stem fibers;
• blood vessels(hemorrhages, cystic formations occur in the plexus area);
• displacement, shrinkage of neuron cells and lysis of their nuclei.

Shortly after the onset of the disease (in the absence of drug treatment and lifestyle changes) atrophy can be fatal.

Separately, the Makiyafawa-Bignami syndrome stands out, which occurs if alcohol is consumed frequently and in large quantities. This leads to swelling of the corpus callosum, the disappearance of myelin sheaths and subsequent necrosis of nerve cells in this area.

Brain atrophy in children

The probability of detecting pathology in a child is small (much less than in adults), but still it exists. However, it is difficult to diagnose the presence of destructive processes during this period, since the symptoms are either completely absent or appear partially and do not cause much concern to parents.

In this case, doctors talk about borderline or subatrophic changes. A disease that progresses latently makes the child conflicted, irritable, withdrawn and nervous. Once mental disturbances become apparent, cognitive and physical helplessness may emerge.

For infants, the danger of the disease is most real in the presence of hydrocephalus (hydrocephalus). You can detect it even during pregnancy with the help of ultrasound.

Also, the causes of atrophy in babies can be:

• failures of the process of intrauterine formation of the central nervous system;
• malformations;
• infectious diseases(herpes and cytomegaly), arising during pregnancy;
• birth trauma.

After the birth of such an infant, he is placed in the intensive care unit, where he is under the constant supervision of a resuscitator and a neuropathologist. Due to the lack of a reliable method of treatment, the course of the further development of the child and the likelihood of complications is difficult to predict.

Degrees of the disease

In accordance with how actively and severely the process proceeds, as well as taking into account the general clinical picture, two levels of pathology development are distinguished.

Brain atrophy 1st degree

The first degree implies minimal impairment of brain function. It is characterized by the presence of focal symptoms, that is, signs, the appearance of which depends on the area of ​​the lesion.

The initial stages of the development of pathology can be completely asymptomatic. At the same time, patients often worry about other diseases that can directly or indirectly affect the brain.

If at the very beginning of this phase you consult a doctor and get the necessary medical care, then the development of pathology will noticeably slow down. However, over time, drug therapy will need to be changed (increase the dose, use other drugs).

Brain atrophy 2nd degree

In the second degree, there are clear signs of the disease, indicating the destruction of brain structures. If left untreated, the clinical picture deteriorates markedly, leading to cognitive impairment, decreased analytical abilities, the development of new habits, and the appearance of other typical symptoms.

Gradually, almost all actions associated with fine motor skills (movements of the fingers) become inaccessible to the patient. The general motor function also decreases: gait and, in general, motor activity slow down. This is exacerbated by poor coordination in space.

There are problems with self-service: a person forgets how to use the remote control, cannot comb his hair or brush his teeth. There is a habit of copying the actions and gestures of others, as the ability to think independently disappears.

Causes of brain atrophy

The disease can be provoked:

• viral or bacterial infections that have arisen during pregnancy;
• chronic anemia;
• genetic mutations (key factor);
• age-related disorders leading to a decrease in the volume and mass of the brain;
• postoperative changes;
• associated pathologies;
• radiation exposure;
• stroke
• infectious diseases of the brain (acute and chronic types);
• excessive alcohol consumption;
• traumatic brain injury (TBI).

In 95% of cases, only the presence of a genetic predisposition is decisive, and all other factors only support the further development of the process.

With age, the cells of the brain (as well as other organs of the body) are restored worse and worse, their destruction takes root. As a result, the symptoms of atrophy become more pronounced.

At the initial stages of the disease in humans, it is noted:

• decline ability to work;
• impaired memory and other cognitive functions(leads to the inability to navigate in space);
• emotional lethargy and indifference;
• personality changes;
• ignoring the degree of morality of their actions;
• vocabulary reduction(oral and written speech becomes primitive);
• unproductive and uncritical thinking process(actions are made thoughtlessly);
• fine motor disorder(handwriting deteriorates);
• susceptibility to suggestion;
• inability to recognize and use objects;
• epileptic seizures(especially typical for local atrophies).

The patient must always be under control so as not to harm himself or other people.

Diagnostics

When examining the brain, MRI (magnetic resonance imaging) is used to quickly identify atrophic foci. The following diagnostic methods can also be used:

• examination of the patient and obtaining anamnestic data(according to the words of the patient or his relatives, a picture of the development of the disease is compiled);
• X-ray examination of brain structures(allows to identify tumor formations, cysts, hematomas and atrophic foci);
• cognitive tests(reveal the level of thinking and the severity of the patient's condition);
• dopplerography study vessels in the area cervical and heads.

The neuropathologist uses the results obtained to make an accurate diagnosis and determine the course of subsequent treatment.

Therapy

If the disease has a genetic origin, then it is impossible to get rid of it. Doctors can only support the functioning of the systems and organs of the human body for a certain period of time. This will be enough for the patient to lead a normal life.

Atrophies caused by age-related changes require mandatory medical treatment that will help to cope with the main symptoms. In addition, the patient needs care and a minimum of stressful or conflict situations.

Doctors often prescribe antidepressants and tranquilizers. It is best if the patient is daily in his usual conditions and engage in usual things. Sleeping during the day can also help keep him healthy.

It is difficult to fight destructive processes. In most cases, modern medicine offers only drugs that stimulate cerebral circulation and metabolism, but they will not help to fully recover. You can only slightly delay the inevitable deterioration of the condition. Some folk remedies give the same effect.

Today, experts are trying to treat atrophy with stem cells that are extracted from the bone marrow. This method is considered quite promising, it is also used for problems with the optic nerve, retinal detachment and other pathologies.

According to some patients, stem cells can even save a person from disability. However, there is no scientific confirmation of this yet.

Prevention

Prevention of brain atrophy will maximize life expectancy, postponing the onset of the pathological process. There are several ways to achieve this:

• timely treatment chronic diseases;
• regular preventive examinations;
• maintaining acceptable level of physical activity;
• rejection use alcohol and smoking;
• adherence to the principles healthy eating;
• normalization of the sleep-wake cycle(lack of sleep in atrophy is extremely dangerous);
• taking actions aimed at preventing atherosclerosis of cerebral vessels ( maintenance of normal body weight, treatment endocrine diseases, activation of metabolic processes).

In addition, you need to control the level of blood pressure, strengthen the immune system and avoid stressful situations.

Forecast

Regardless of the treatment and the cause of the pathology, it is difficult to talk about the favorable prognosis. Atrophy can affect any area of ​​the brain and lead to irreversible impairment of motor, visual and other functions.

Although in the initial stages the disease is local in nature, later it becomes generalized (almost the entire organ atrophies). For 20 years, the pathology develops so much that a person acquires complete dementia.

Outcome

The death of brain cells is a problem that is difficult to solve completely because this process partly is quite natural and inevitable. However, there is a big difference between brain atrophy at 70 and at 40. In the second case, one can judge the untimely onset of the destruction of cortical and subcortical cells, which requires a mandatory referral to specialists and the passage of a supportive therapeutic course.

In this section, we will only touch on those cerebellar ataxias that debut after 40 years and can mimic some clinical forms. CVHM (chronic cerebrovascular disease) , in particular VBN.

These forms of cerebellar ataxia include:

• hereditary spastic ataxia;
• olivopontocerebellar atrophy (hereditary and sporadic forms);
• cerebroolivar atrophy of Holmes;
• paraneoplastic cerebellar degeneration.

Hereditary spastic ataxia- genetically heterogeneous (with different types of inheritance) ataxia. The onset of the disease is at the age of 30-50 years. The main symptoms are (Ivanova-Smolenskaya I. L et al., 1998):

• progressive cerebellar ataxia;
• progressive lower spastic paraparesis (only an increase in tendon reflexes is observed in the hands);
• spastic-atactic gait disorder.

Many patients may experience additional neurological symptoms:

• dysarthria;
• nystagmus;
• oculomotor disorders;
• atrophy optic nerves;
• cognitive impairment (up to the degree of dementia).

An MPT study revealed atrophy of the spinal cord. At morphological study degeneration of the lateral columns of the spinal cord (more in the lumbosacral segment), degeneration of the structures of the middle cerebellar peduncle, medulla oblongata, and pons nuclei are found.

The course of the disease is in most cases slowly progressive.

Olivopontocerebellar atrophy- genetically and clinically heterogeneous forms. In addition to hereditary spinocerebellar atrophy (types I, 2, 3 and 4), sporadic forms are distinguished.

The hereditary origin of the disease(autosomal dominant type of inheritance) can usually be established in patients with the onset of the disease at the age of 30-40 years, sporadic cases - at the age of 50 years and older.

Along with the progressive cerebellar ataxia with olivoponto-verbellar atrophy, the following are observed:

• dysarthria, dysphagia;
• estrapyramidal symptoms - in hereditary forms - tremor, torsion-dystonic hyperkinesis, myoclonus; with a sporadic form - parkinsonism;
• oculomotor disorders;
• increase in cognitive impairment (in some cases to the degree of dementia);
• orthostatic hypotension (with sporadic forms);
• MRI study showed atrophy of the cerebellum, pons and medulla oblongata.

Morphological examination reveals a multisystem lesion: nervous system, including:

• degeneration of the inferior olives, the middle peduncle of the brain, the cerebellar cortex;
• degeneration of the subcortical ganglia, cerebral cortex, cerebellar cortex, cells of the anterior horns of the spinal cord, spinal cord conductors, nuclei of cranial nerves.

Cerebellar olivar atrophy of Holmes- a rare form of hereditary and inherited in an autosomal dominant manner) cerebellar ataxia.

The disease debuts in people older than 40 years, then slowly progresses (20 years or more), the only symptom at the debut is unsteadiness when walking. In the future, cerebellar dysarthria, moderate disorders of coordination in the hands join. An MRI study revealed atrophy of the cerebellar vermis. Sick long time save active image life.

Paraneoplastic cerebellar degeneration

Cerebellar degeneration can be observed in some cancer(Grinberg D.A. et al., 2004). Most often, it occurs with difficult-to-diagnose small cell lung cancer, which may not manifest itself either clinically or radiologically for a long time. Neurological symptoms usually develop against the background of the absence of symptoms of an oncological disease, which greatly complicates the establishment of the cause of the disease and "tempts" neurologists to diagnose VBN (vertebrobasilar insufficiency).

Cerebellar degeneration can also occur with ovarian cancer, breast cancer, Hodgkin's lipoma. The basis of the pathogenesis of napaneoplastic cerebellar degeneration is the production of antibodies to tumor antigens, which simultaneously react with cerebellar Purkinje cells (and with other nerve cells).

Clinical symptoms are presented:

• static ataxia;
• dynamic ataxia;
• dysarthria;
• in some cases, with the prevalence of the paraneoplastic process to other formations of the central nervous system, cognitive impairment (up to the stage of dementia), bulbar, pyramidal symptoms, and polyneuropathy can be observed.

In the cerebrospinal fluid in paraneoplastic cerebellar degenerations, lymphocytic pleocytosis and a moderate increase in protein can be observed. Neuroimaging (CT or MRI) is of little help in diagnosis.

Cerebellar symptoms develop over several months, in some cases there is a stabilization of the process and even remission with successful treatment underlying disease.

The main differential diagnostic features of the difference between cerebellar ataxia and VBI are:

• the absence of exacerbations, vascular cerebral episodes, characteristic of VBI, with progressive cerebellar ataxia;
• no dizziness;
• absence of severe cardiovascular pathology.

In cases of hereditary cerebellar ataxia, the establishment correct diagnosis medical genetic counseling helps, and in cases of olivopontocerebellar atrophy - direct DNA diagnostics (Illarioshkin S.N. et al., 1996, 2002).

If a patient shows signs of cerebellar damage, then in most cases, the first thing to think about is the possibility of a cerebellar tumor (astrocytoma, angioblastoma, medulloblastoma, metastatic tumors) or multiple sclerosis. With a tumor of the cerebellum, signs of intracranial hypertension appear early. In multiple sclerosis, it is usually possible to identify, in addition to cerebellar pathology, clinical manifestations of lesions and other structures of the central nervous system, primarily the visual and pyramidal systems. In classical neurology, Charcot's triad characteristic of multiple sclerosis is usually mentioned: nystagmus, intentional trembling and chanted speech, as well as Nonnet's syndrome: coordination disorder, dysmetria, chanted speech and cerebellar asynergies. Cerebellar disorders are the main and with post-traumatic syndrome Mann, which is characterized by ataxia, discoordination, asynergy, nystagmus. Trauma or infectious lesions can cause cerebellar Goldstein-Reichmann syndrome: static and coordination disorders, asynergy, intentional trembling, decreased muscle tone, hypermetry, megalography, impaired perception of the mass (weight) of an object in the hands. Disorders of the cerebellum function can also be congenital, manifesting, in particular, Zeeman's syndrome: ataxia, delayed speech development, and subsequently cerebellar dysarthria. Congenital cerebellar ataxia is manifested by a delay in the development of the child's motor functions (at the age of 6 months, he cannot sit, he starts walking late, while the gait is ataxic), as well as speech delay, prolonged persistence of dysarthria, sometimes mental retardation, often manifestations of microcrania. On CT, the cerebellar hemispheres are reduced. Compensation usually occurs by about 10 years of age. brain function, which, however, can be disturbed under the influence of harmful exogenous influences. Progredient forms of the disease are also possible. A manifestation of congenital hypoplasia of the cerebellum is Fanconi-Turner syndrome. It is characterized by disturbances in statics and coordination of movements, nystagmus, which are usually accompanied by mental retardation. The rare Betten's disease, which is inherited by an autosomal recessive type, also belongs to the congenital ones. It is characterized by congenital cerebellar ataxia, which manifests itself in the first year of life with disturbances in statics and coordination of movements, nystagmus, gaze coordination disorder, and moderate muscle hypotension. Dysplastic signs are possible. A child late, sometimes only at 2-3 years of age, begins to hold his head, even later - to stand, walk, talk. His speech was changed according to the type of cerebellar dysarthria. Possible vegetative-visceral disorders, manifestations of immunosuppression. After a few years, the clinical picture usually stabilizes, the patient to some extent adapts to the existing defects. Spastic ataxia, proposed by A. Bell and E. Carmichel (1939), is the autosomal dominant type of cerebellar ataxia, which is characterized by the onset of the disease at 3-4 years of age and is manifested by a combination of cerebellar ataxia with dysarthria, tendon hyperreflexia, and increased muscle tone according to spastic mud, while possible (but not obligate signs of the disease) atrophy of the optic nerves, retinal degeneration, nystagmus, oculomotor disorders. Feldman's syndrome is inherited according to an autosomal dominant type (described by the German physician N. Feldmann, born in 1919): cerebellar ataxia, intentional trembling and early graying of hair. It manifests itself in the second decade of life and then slowly progresses, leading to disability in 20-30 years. Late cerebellar atrophy, or Tom's syndrome, described in 1906 by the French neurologist A. Thomas (1867-1963), usually manifests itself in people over 50 years of age with progressive atrophy of the cerebellar cortex. The phenotype shows signs cerebellar syndrome, primarily cerebellar static and locomotor ataxia, chanted speech, changes in handwriting. In an advanced stage, manifestations of pyramidal insufficiency are possible. The combination of cerebellar disorders with myoclonus is characterized by Hait's myoclonic cerebellar dyssynergy, or myoclonus ataxia, while the symitomocomplex in the clinical picture manifests intentional tremor, myoclonus that occurs in the hands, and later acquires a generalized character, ataxia and dyssynergy, nystagmus , scrambled speech, decreased muscle tone. It is a consequence of the degeneration of the cerebellar nuclei, red nuclei and their connections, as well as cortical-subcortical structures. In the advanced stage of the disease, epileptic seizures and dementia are possible. The prognosis is bad. Refers to rare forms of progressive hereditary ataxia. It is inherited in an autosomal recessive manner. It usually appears at a young age. The nosological independence of the symptom complex is disputed. The disease was described in 1921 by the American neurologist R. Hunt (1872-1937). Among the degenerative processes, Holmes's cerebellar degeneration, or familial cerebellar-olivar atrophy, or progressive atrophy of the cerebellar system, mainly the dentate nuclei, as well as the red nuclei, occupies a certain place, while manifestations of demyelination are expressed in the upper cerebellar peduncle. Characterized by static and dynamic ataxia, asynergy, nystagmus, dysarthria, decreased muscle tone, muscle dystonia, head tremor, myoclonus. Almost simultaneously, epileptic seizures appear. Intelligence is usually preserved. The EEG shows paroxysmal dysrhythmia. The disease is recognized as hereditary, but the type of its inheritance is not specified. The disease was described in 1907 by the English neurologist G. Holmes (1876-1965). Alcoholic cerebellar degeneration is a consequence of chronic alcohol intoxication. The cerebellar vermis is predominantly affected, with cerebellar ataxia and impaired coordination of leg movements primarily manifested, while hand movements, oculomotor and speech functions are impaired to a much lesser extent. Usually this disease is accompanied by a pronounced decrease in memory in combination with polyneuropathy. Paraneoplastic cerebellar degeneration is manifested by cerebellar ataxia, which can sometimes be the only clinical symptom due to malignant tumor, without local signs indicating the place of its occurrence. Paraneoplastic cerebellar degeneration may be, in particular, a secondary manifestation of breast or ovarian cancer. The Barraquer-Bordas-Ruiz-Lara syndrome is manifested by cerebellar disorders that occur in connection with rapidly progressive cerebellar atrophy. The syndrome in patients with bronchial cancer, accompanied by general intoxication, was described by the modern Spanish physician L. Barraquer-Bordas (born in 1923). Rarely, recessive X-chromosomal ataxia is a hereditary disease that manifests itself almost exclusively in men as a slowly progressive cerebellar insufficiency. It is transmitted in a recessive, sex-linked type. Family paroxysmal ataxia, or periodic ataxia, also deserves attention. It debuts more often in childhood, but it can manifest itself later - up to 60 years. The clinical picture is reduced to paroxysmal manifestations of nystagmus, dysarthria and ataxia, decreased muscle tone, dizziness, nausea, vomiting, headache, lasting from several minutes to 4 weeks. Attacks of familial paroxysmal ataxia can be triggered by emotional stress, physical overwork, fever, alcohol intake, while focal neurological symptoms are not detected between attacks in most cases, but sometimes nystagmus and lungs are possible. cerebellar symptoms. The morphological substrate of the disease is recognized as an atrophic process mainly in the anterior part of the cerebellar vermis. First described the disease in 1946 by M. Parker. It is inherited in an autosomal dominant manner. In 1987, with familial paroxysmal ataxia, a decrease in the activity of pyruvate dehydrogenase of blood leukocytes to 50-60% of normal level. In 1977, R. Lafrance et al. drew attention to the high preventive effect of diacarb, later flunarizine was proposed to treat familial paroxysmal ataxia. Acute cerebellar ataxia, or Leiden-Westphal syndrome, is a well-defined symptom complex, which is a parainfectious complication. Occurs more often in children 1-2 weeks after the transferred common infection(influenza, typhus, salmonellosis, etc.). Rough static and dynamic ataxia, intentional trembling, hyermetria, asynergia, nystagmus, chanted speech, and decreased muscle tone are characteristic. In the cerebrospinal fluid, lymphocytic pleocytosis and a moderate increase in protein are detected. At the beginning of the disease, dizziness, disorders of consciousness, convulsions are possible. CT and MRI showed no pathology. The flow is benign. In most cases, after a few weeks or months - a complete recovery, sometimes - residual disorders in the form of mild cerebellar insufficiency. Marie-Foy-Alajouanina disease is a late symmetrical cortical atrophy of the cerebellum with a predominant lesion of pear-shaped neurons (Purkinje cells) and the granular layer of the cortex, as well as the oral part of the cerebellar vermis and degeneration of the olives. Manifested in persons aged 40-75 years of balance disorder, ataxia, gait disturbance, coordination disorders, and decreased muscle tone, mainly in the legs; the intentional trembling in the hands is expressed insignificantly. Speech disorders are possible, but do not belong to the obligate signs of the disease. The disease was described in 1922 by French neuropathologists P. Marie, Ch. Foix and Th. Alajouanine. The disease is sporadic. The etiology of the disease has not been elucidated. There are opinions about the provocative role of intoxication, primarily alcohol abuse, as well as hypoxia, hereditary burden. The clinical picture is confirmed by head CT data, which reveals a pronounced decrease in the volume of the cerebellum against the background of diffuse atrophic processes in the brain. In addition, it is characteristic high level aminotransferases in the blood plasma (Ponomareva E.N. et al., 1997).

This is a group of chronic progressive hereditary diseases in which dystrophic changes mainly in the cerebellum, inferior olives, in the proper nuclei of the bridge and in the structures of the brain associated with them. With the development of the disease at a young age, about half of the cases are inherited in a dominant or recessive manner, the rest are sporadic. In sporadic cases of the disease, manifestations of akinetic-rigid syndrome and progressive autonomic failure are more common. The average age of the patient with the manifestation of the hereditary form of the disease in the phenotype is 28 years, with the sporadic form of the disease - 49 years, the average life expectancy is 14.9 and 6.3 years, respectively. In the sporadic form, in addition to atrophy of the olives, the pons and the cerebellum, lesions of the lateral funiculi of the spinal cord, the black substance and the striatum, a bluish spot in the rhomboid fossa of the IV ventricle of the brain are more often found. Symptoms of the growing cerebellar syndrome are characteristic. Sensitivity disorders, elements of bulbar and akinetic-rigid syndromes, hyperkinesis, in particular myorhythmias in the uvula and soft palate , ophthalmoparesis, decreased visual acuity, intellectual disorders. The disease was described in 1900 by French neuropathologists J. Dejerine and A. Thomas. The disease often debuts with violations when walking - instability, discoordination, unexpected falls are possible. These disorders may be the only manifestation of the disease for 1-2 years. In the future, coordinating disorders in the hands arise and grow: manipulations with small objects are difficult, handwriting is disturbed, intentional tremor occurs. Speech becomes intermittent, blurred, with a nasal tinge and a breathing rhythm that does not correspond to the construction of speech (the patient speaks as if he was being strangled). At this stage of the disease, manifestations of progressive autonomic failure are added, signs of an akinetic-rigid syndrome appear. Sometimes the dominant symptoms for the patient are dysphagia, attacks of nocturnal suffocation. They develop in connection with mixed paresis of the bulbar muscles and can be life threatening. In 1970, German neuropathologists B.W. Konigsmark and L.P. Weiner identified 5 main types of olivopontocerebellar dystrophy, differing either in clinical and morphological manifestations or in the type of inheritance. Type I (Mentzel type). At the age of 14-70 (usually 30-40) years, it manifests itself with ataxia, dysarthria, dysphonia, muscle hypotension, in the late stage - a rough tremor of the head, trunk, arms, muscles, signs of akinetic-rigid syndrome. Pathological pyramidal signs, gaze paresis, external and internal ophthalmoplegia, sensitivity disorders, dementia are possible. It is inherited in an autosomal dominant manner. As an independent form, it was singled out in 1891 by P. Menzel. // type (Fickler-Winkler type). At the age of 20-80 years, it manifests itself as ataxia, a decrease in muscle tone and tendon reflexes. It is inherited in an autosomal recessive manner. Sporadic cases are possible. Type III with retinal degeneration. Manifested in childhood or young (up to 35 years) age by ataxia, tremor of the head and limbs, dysarthria, signs of pyramidal insufficiency, progressive loss of vision with an outcome in blindness; possible nystagmus, ophthalmoplegia, sometimes dissociated sensitivity disorders. It is inherited in an autosomal dominant manner. IV type (Jester-Hymaker type). At the age of 17-30 years, it debuts with cerebellar ataxia or signs of lower spastic paraparesis, in both cases a combination of these manifestations is formed already at an early stage of the disease, which are subsequently joined by elements of bulbar syndrome, paresis of facial muscles, disorders of deep sensitivity -ti. Inherited by dominant type. Vtype Manifested at the age of 7-45 years with ataxia, dysarthria, signs of akinetic-rigid syndrome and other extrapyramidal disorders, progressive ophthalmoplegia and dementia are possible. Inherited by dominant type. 7.3.3. Olivorubrocerebellar degeneration (Lejeune-Lermitte syndrome, Lermitte disease) The disease is characterized by progressive atrophy of the cerebellum, mainly its cortex, dentate nuclei and upper cerebellar peduncles, inferior olives, red nuclei. It is manifested primarily by static and dynamic ataxia, in the future other signs of cerebellar syndrome and damage to the brain stem are possible. The disease was described by French neuropathologists J. Lermitte (Lhermitte J.J., 1877-1959) and J. Lezhon (Lejonne J., born in 1894). 7.3.4. Multisystem atrophy In recent decades, a sporadic, progressive neurodegenerative disease called multisystem atrophy has been isolated into an independent form. It is characterized by a combined lesion of the basal ganglia, cerebellum, brain stem, spinal cord. The main clinical manifestations: parkinsonism, cerebellar ataxia, signs of pyramidal and autonomic failure (Levin O.S., 2002). Depending on the predominance of certain features of the clinical picture, three types of multisystem atrophy are distinguished. 1) olivopontocerebellar type, characterized by a predominance of signs of a cerebellar attack; 2) strionigral type, in which the signs of parkinsonism dominate; 3) Shay-Drager syndrome, characterized by a predominance in the clinical picture of signs of progressive autonomic failure with symptoms of orthostatic arterial hypotension. The basis of multisystem atrophy is the selective degeneration of certain areas of the predominantly gray matter of the brain with damage to neurons and glial elements. The causes of degenerative manifestations in the brain tissue remain unknown today. Manifestations of multisystem atrophy of the olivopontocerebellar type are associated with damage to Purkinje cells in the cerebellar cortex, as well as neurons of the inferior olives, nuclei of the pontine brain, demyelination and degeneration, mainly of the pontocerebellar pathways. Cerebellar disorders are usually represented by static and dynamic ataxia with impaired locomotor movements. Characterized by instability in the Romberg position, ataxia when walking, dysmetria, adiadochokinesis, intentional tremor, there may be nystagmus (horizontal vertical, beating down), intermittency and slowness of the following gaze movements, impaired eye convergence, scanned speech. Multiple system atrophy usually occurs in adulthood and progresses rapidly. Diagnosis is based on clinical data and is characterized by a combination of signs of parkinsonism, cerebellar insufficiency and autonomic disorders. Treatment of the disease has not been developed. The duration of the disease is within 10 years, ending in death.

This is a chronic progressive hereditary disease that manifests itself at the age of 30-45 years, with slowly increasing cerebellar disorders in combination with signs of pyramidal insufficiency, while static and dynamic cerebellar ataxia, intentional trembling, chanted speech, tendon hyperreflexia are characteristic. Possible clonuses, pathological pyramidal reflexes, strabismus, decreased vision, narrowing of the visual fields due to primary atrophy of the optic nerves and pigmentary degeneration retina. The course of the disease is slowly progressive. There is a decrease in the size of the cerebellum, degeneration of Purkinje cells, inferior olives, spinal tracts. It is inherited in an autosomal dominant manner. The disease was described in 1893 by the French neurologist P. Marie (1853-1940). Currently, there is no unanimity in the understanding of the term "Pierre Marie's disease", and the question of the possibility of separating it into an independent nosological form is debatable. Treatment has not been developed. Usually used metabolically active and tonic, as well as symptomatic agents.

Hereditary disease described in 1861 by the German neurologist N. Friedreich (Friedreich N., 1825-1882). It is inherited in an autosomal recessive manner or (less commonly) in an autosomal dominant pattern with incomplete penetrance and variable gene expression. Sporadic cases of the disease are also possible. The pathogenesis of the disease has not been clarified. In particular, there is no idea of ​​the primary biochemical defect that forms its basis. Pathomorphology. Pathological anatomical studies reveal a pronounced thinning of the spinal cord, due to atrophic processes in its posterior and lateral cords. As a rule, the sphenoid (Burdach) and tender (Goll) pathways and the spinal cerebellar pathways of Gowers and Flexig, as well as the crossed pyramidal pathway, which contains many fibers belonging to the extrapyramidal system, suffer. Degenerative processes are also expressed in the cerebellum, in its white matter and nuclear apparatus. Clinical manifestations. The disease manifests itself in children or young people under the age of 25 years. S.N. Davidenkov (1880-1961) noted that more often clinical signs of the disease occur in children of 6-10 years of age. The first sign of the disease is usually ataxia. Patients experience uncertainty, staggering when walking, gait changes (when walking, they spread their legs wide apart). The gait in Friedreich's disease can be called tabetic-cerebellar, since its changes are due to a combination of sensitive and cerebellar ataxia, as well as a usually pronounced decrease in muscle tone. Disorders of statics, discoordination in the hands, intentional tremor, and dysarthria are also characteristic. Possible nystagmus, hearing loss, elements of speech chanting, signs of pyramidal insufficiency (tendon hyperreflexia, pathological foot reflexes, sometimes some increase in muscle tone), imperative urge to urinate, decreased sexual potency. Sometimes hyperkinesis of an athetoid nature appears. An early disorder of deep sensitivity leads to a progressive decrease in tendon reflexes: first on the legs, and then on the hands. Over time, hypotrophy of the muscles of the dietary parts of the legs is formed. The presence of anomalies in the development of the skeleton is characteristic. First of all, this is manifested by the presence of Friedreich's foot: the foot is shortened, "hollow", with a very high arch. The main phalanges of her fingers are unbent, the rest are bent (Fig. 7.5). Possible spinal deformity chest. Sometimes there are manifestations of cardiopathy. The disease progresses slowly, but steadily leads to disability of patients who eventually become bedridden. Treatment. Pathogenetic treatment has not been developed. Prescribe drugs that improve metabolism in the structures of the nervous system, general strengthening agents. With severe deformity of the feet, orthopedic shoes are indicated. Rice. 7.5. Friedreich's foot.

Spinocerebellar ataxias include progressive hereditary degenerative diseases, in which the structures of the cerebellum, the brainstem and the pathways of the spinal cord, mainly related to the extrapyramidal system, are mainly affected.

Multisystem degenerations are a group of neurodegenerative diseases, the common feature of which is the multifocal nature of the lesion with the involvement of various functional and neurotransmitter systems of the brain in the pathological process and, therefore, the polysystemic nature of clinical manifestations.

With damage to the cerebellum, disorders of statics and coordination of movements are characteristic, muscular hypotension and nystagmus. Damage to the cerebellum, especially its vermis, leads to disturbances in statics - the ability to maintain a stable position of the center of gravity of the human body, balance, and stability. When this function is disturbed, static ataxia occurs (from the Greek ataxia - disorder, instability). The patient's instability is noted. Therefore, in a standing position, he spreads his legs wide, balances with his hands. Especially clearly static ataxia is detected with an artificial decrease in the support area, in particular in the Romberg position. The patient is asked to stand up with his feet firmly together and slightly raising his head. In the presence of cerebellar disorders, the patient is unstable in this position, his body sways, sometimes he is “pulled” in some particular direction, and if the patient is not supported, he may fall. In case of damage to the cerebellar vermis, the patient usually sways from side to side and often falls back. With pathology of the cerebellar hemisphere, there is a tendency to fall mainly towards the pathological focus. If the static disorder is moderately expressed, it is easier to identify it in the so-called complicated or sensitized Romberg position. The patient is asked to put his feet in line so that the toe of one foot rests on the heel of the other. The assessment of stability is the same as in the usual Romberg position. Normally, when a person is standing, the muscles of his legs are tense (support reaction), with the threat of falling to the side, his leg on this side moves in the same direction, and the other leg comes off the floor (jump reaction). When the cerebellum (mainly the worm) is damaged, the support and jump reactions are disturbed in the patient. Violation of the support reaction is manifested by the instability of the patient in a standing position, especially in the Romberg position. Violation of the jump reaction leads to the fact that if the doctor, standing behind the patient and insuring him, pushes the patient in one direction or another, then the patient falls with a slight push (pushing symptom). With damage to the cerebellum, the patient's gait is usually changed due to the development of statolocomotor ataxia. The “cerebellar” gait is in many ways reminiscent of the gait of a drunk person, which is why it is sometimes called the “drunk gait”. The patient, due to instability, walks uncertainly, spreading his legs widely, while he is “thrown” from side to side. And when the hemisphere of the cerebellum is damaged, it deviates when walking from a given direction towards the pathological focus. The instability is especially pronounced when turning. If the ataxia is pronounced, then the patients completely lose the ability to control their body and cannot not only stand and walk, but even sit. The predominant lesion of the cerebellar hemispheres leads to a breakdown of its counter-inertial influences, in particular, to the occurrence of kinetic ataxia. It is manifested by awkwardness of movements and is especially pronounced with movements that require precision. To identify kinetic ataxia, tests are carried out for coordination of movements. The following is a description of some of them. Test for diadochokinesis (from the Greek diadochos - sequence). The patient is invited to close his eyes, stretch his arms forward and quickly, rhythmically supinate and pronate the hands. In the case of damage to the cerebellar hemisphere, the movements of the hand on the side of the pathological process turn out to be more sweeping (a consequence of dysmetria, more precisely, hypermetria), as a result, the hand begins to lag behind. This indicates the presence of adiadochokinesis. Finger test. The patient with his eyes closed should withdraw his hand, and then, slowly, index finger touch the tip of your nose. In the case of cerebellar pathology, the hand on the side of the pathological focus makes an excessive movement in terms of volume (hypermetry), as a result of which the patient misses. A finger-to-nose test reveals a cerebellar (intentional) tremor characteristic of cerebellar pathology, the amplitude of which increases as the finger approaches the target. This test also reveals the so-called bradytelkinesia (a symptom of a bridle): not far from the target, the movement of the finger slows down, sometimes even stops, and then resumes again. Finger-finger test. The patient with his eyes closed is invited to spread his arms wide and then bring the index fingers together, trying to get the finger into the finger, while, as with the finger-nose test, intentional trembling and a symptom of a bridle are revealed. Spot-knee test (Fig. 7.3). The patient, lying on his back with his eyes closed, is offered to raise one leg high and then with his heel to fall into the knee of the other leg. With cerebellar pathology, the patient cannot or it is difficult for him to get his heel into the knee of the other leg, especially when performing a test with the leg homolateral to the affected cerebellar hemisphere. If, nevertheless, the heel reaches the knee, then it is proposed to hold it, slightly touching the anterior surface of the lower leg, down to the ankle joint, while in the case of cerebellar pathology, the heel always slides off the lower leg in one direction or the other. Rice. 7.3. Heel-knee test. Index test. The patient is invited several times with his index finger to hit the rubber tip of the hammer, which is in the examiner's hand. In the case of cerebellar pathology in the patient's hand on the side of the affected hemisphere of the cerebellum, a miss due to dysmetria is noted. Symptom of Tom-Jumenty. If the patient takes an object, such as a glass, he spreads his fingers excessively. Cerebellar nystagmus. twitch eyeballs when looking to the side (horizontal nystagmus) is considered as a consequence of intentional trembling of the eyeballs (see Chapter 30). Speech disorder. Speech loses its smoothness, becomes explosive, fragmented, chanted like cerebellar dysarthria (see chapter 25). Handwriting change. In connection with the disorder of coordination of hand movements, the handwriting becomes uneven, the letters are deformed, excessively large (mega-halography). pronator phenomenon. The patient is asked to hold the arms outstretched forward in the supination position, while spontaneous pronation soon occurs on the side of the affected cerebellar hemisphere. Goff-Schilder's symptom. If the patient holds his arms outstretched forward, then on the side of the affected hemisphere, the arm is soon retracted outward. simulation phenomenon. The patient with his eyes closed should quickly give his hand a position similar to that which the examiner had previously given to his other hand. When the hemisphere of the cerebellum is affected, the arm homolateral to it makes a movement that is excessive in amplitude. The Doinikov phenomenon. finger phenomenon. The seated patient is asked to place supinated hands with spread fingers on their thighs and close their eyes. In the case of damage to the cerebellum on the side of the pathological focus, spontaneous flexion of the fingers and pronation of the hand and forearm soon occur. Stewart-Holmes symptom. The examiner asks the patient sitting on a chair to bend the supinated forearms and at the same time, taking his hands by the wrists, resists him. If, at the same time, the patient's hands are suddenly released, then the hand on the side of the lesion, bending by inertia, will hit him in the chest with force. Muscle hypotension. Damage to the cerebellar vermis usually leads to diffuse muscular hypotension. When the hemisphere of the cerebellum is affected, passive movements reveal a decrease in muscle tone on the side of the pathological process. Muscle hypotension leads to the possibility of overextension of the forearm and lower leg (Olshansky's symptom) during passive movements, to the appearance of symptoms of a “dangling” hand or foot when they are passively shaken. Pathological cerebellar asynergia. Violations of physiological synergy during complex motor acts are detected, in particular, during the following tests (Fig. 7.4). 1. Asynergy according to Babinsky in a standing position. If a patient standing with shifted legs tries to bend back, throwing his head back, then normally in this case there is a flexion of the knee joints. With cerebellar pathology, due to asynergy, this friendly movement is absent, and the patient, losing balance, falls back. Rice. 7.4. Cerebellar asynergy. 1 - gait of a patient with severe cerebellar ataxia; 2 - back tilt of the body is normal; 3 - with damage to the cerebellum, the patient, leaning back, cannot maintain balance; 4 - performance of the test for cerebellar asynergy according to Babinsky by a healthy person; 5 - performing the same test in patients with cerebellar lesions. 2. Asynergy according to Babinsky in the deja position. The patient, lying on a hard plane with outstretched legs, divorced to the width of the shoulder girdle, is invited to cross his arms over his chest and then sit down. In the presence of cerebellar pathology, due to the absence of friendly contraction of the gluteal muscles (manifestation of asynergy), the patient cannot fix the legs and pelvis on the support area, as a result, the legs rise and he fails to sit down. The significance of this symptom in elderly patients, in people with a flabby or obese abdominal wall, should not be overestimated. Summarizing the above, one should emphasize the diversity and importance of the functions performed by the cerebellum. As part of a complex regulatory feedback mechanism, the cerebellum acts as a focal point for balancing the body and maintaining muscle tone. As P. Duus (1995) notes, the cerebellum provides the ability to perform discrete and precise movements, while the author reasonably believes that the cerebellum works like a computer, tracking and coordinating sensory information at the input and modeling motor signals at the output.

The cerebellum (cerebellum) is located under the duplication of the dura mater, known as the tentorium cerebellum (tentorium cerebelli), which divides the cranial cavity into two unequal spaces - supratentorial and subtentorial. In the subtentorial space, the bottom of which is the posterior cranial fossa, in addition to the cerebellum, there is a brain stem. The volume of the cerebellum averages 162 cm3. Its mass varies within 136-169 g. The cerebellum is located above the bridge and the medulla oblongata. Together with the upper and lower cerebral sails, it makes up the roof of the fourth ventricle of the brain, the bottom of which is the so-called rhomboid fossa (see Chapter 9). Above the cerebellum are the occipital lobes of the cerebrum, separated from it by the indentation of the cerebellum. The cerebellum is divided into two hemispheres (hemispherum cerebelli). Between them in the sagittal plane above the fourth ventricle of the brain is the phylogenetically most ancient part of the cerebellum - its worm (vermis cerebelli). The vermis and hemispheres of the cerebellum are fragmented into lobules by deep transverse grooves. The cerebellum consists of gray and white matter. The gray matter forms the cerebellar cortex and the paired nuclei of nuclei cerebelli located in its depth (Fig. 7.1). The largest of them - jagged nuclei (nucleus dentatus) - are located in the hemispheres. In the central part of the worm there are tent nuclei (nuclei fastigii), between them and the dentate nuclei are spherical and corky nuclei (nuclei, globosus et emboliformis). Due to the fact that the cortex covers the entire surface of the cerebellum and penetrates into the depth of its furrows, on the sagittal section of the cerebellum, its tissue has a leaf pattern, the veins of which are formed by white matter (Fig. 7.2), constituting the so-called tree of life of the cerebellum (arbor vitae cerebelli) . At the base of the tree of life is a wedge-shaped notch, which is the upper part of the cavity of the IV ventricle; the edges of this notch form his tent. The cerebellar worm serves as the roof of the tent, and its front and back walls are made up of thin cerebral plates, known as the anterior and posterior cerebral sails (vella medullare anterior et posterior). Some information about the architectonics of the cerebellum is of interest, giving grounds for judging the function of its components. The cerebellar cortex has two cell layers: the inner one is granular, consisting of small granule cells, and the outer one is molecular. Between them is a number of large pear-shaped cells, bearing the name of the Czech scientist I. Purkinje (Purkinje I., I787-1869), who described them. Impulses enter the cerebellar cortex through the mossy and creeping fibers penetrating into it from the white matter, which make up the afferent pathways of the cerebellum. Through mossy fibers, impulses from the spinal cord, vestibular nuclei and pontine nuclei are transmitted to the cells of the granular layer of the cortex. The axons of these cells, together with the creeping fibers passing through the granular layer in transit and carrying impulses from the lower olives to the cerebellum, reach the superficial, molecular layer of the cerebellum. -nom layer of their branching take the direction, the longitudinal surface of the cerebellum. The impulses that have reached the molecular layer of the cortex, having passed through the synaptic contacts, fall on the branching of the dendrites of the Purkinje cells located here. Then they follow the dendrites of Purkinje cells to their bodies located on the border of the molecular and granular layers. Then, along the axons of the same cells crossing the granular layer, they penetrate into the depths of the white matter. The axons of Purkinje cells terminate in the nuclei of the cerebellum. Mainly in the dentate nucleus. Efferent impulses coming from the cerebellum along the axons of the cells that make up its nuclei and take part in the formation of the cerebellar peduncles leave the cerebellum. The cerebellum has three pairs of peduncles: inferior, middle, and superior. The lower leg connects it with the medulla oblongata, the middle leg with the bridge, the upper leg with the midbrain. The legs of the brain make up pathways that carry impulses to and from the cerebellum. The cerebellar vermis provides stabilization of the center of gravity of the body, its balance, stability, regulation of the tone of reciprocal muscle groups, mainly the neck and trunk, and the emergence of physiological cerebellar synergy that stabilizes the balance of the body. To successfully maintain body balance, the cerebellum constantly receives information passing along the spinocerebellar pathways from proprioceptors various parts body, as well as from the vestibular nuclei, inferior olives, reticular formation and other formations involved in controlling the position of body parts in space. Most of the afferent pathways leading to the cerebellum pass through the inferior cerebellar peduncle, some of them are located in the superior cerebellar peduncle. The impulses of proprioceptive sensitivity going to the cerebellum, like other sensitive impulses, following the dendrites of the first sensitive neurons, reach their bodies located in the spinal nodes. Further, the impulses going to the cerebellum along the axons of the same neurons are directed to the bodies of the second neurons, which are located in the inner parts of the base of the posterior horns, forming the so-called Clark columns. Their axons enter the lateral sections of the lateral funiculi of the spinal cord, where they form the spinocerebellar pathways, while part of the axons enter the lateral column of the same side and form the posterior spinocerebellar tract Flexig (tractus spinocerebellaris posterior). Another part of the axons of the cells of the posterior horns passes to the other side of the spinal cord and enters the opposite lateral funiculus, forming in it the anterior spinocerebellar path of Gowers (tractus spinocerebellaris anterior). The cerebellar pathways, increasing in volume at the level of each spinal segment, rise to the medulla oblongata. In the medulla oblongata, the posterior spinocerebellar path deviates laterally and, having passed through the inferior cerebellar peduncle, penetrates into the cerebellum. The anterior spinal tract passes through the medulla oblongata, the pons of the brain and reaches the midbrain, at the level of which it makes its second decussation in the anterior medullary velum and passes into the cerebellum through the superior cerebellar peduncle. Thus, of the two spinal tracts, one never crosses (the non-crossed Flexig path), and the other passes to the opposite side twice (the double-crossed Gowers path). As a result, both conduct impulses from each half of the body, mainly to the homolateral half of the cerebellum. In addition to the spinocerebellar pathways of Flexig, impulses to the cerebellum pass through the inferior cerebellar peduncle along the vestibulocerebellar path (tractus vestibulocerebellaris), starting mainly in the superior vestibular nucleus of Bechterew, and along the olive-cerebellar path (tractus olivocerebellaris), coming from the lower olive. Part of the axons of the cells of the thin and sphenoid nuclei that do not take part in the formation of the bulbo-thalamic tract, in the form of external arcuate fibers (fibre arcuatae externae), also enters the cerebellum through the inferior cerebellar peduncle. Through its middle legs, the cerebellum receives impulses from the cerebral cortex. These impulses pass through the cortico-pontocerebellar pathways, consisting of two neurons. The bodies of the first neurons are located in the cerebral cortex, mainly in the cortex posterior divisions frontal lobes. Their axons pass as part of the radiant crown, the anterior leg of the internal capsule and end in the nuclei of the bridge. The axons of the cells of the second neurons, whose bodies are located in their own nuclei of the bridge, pass to its opposite side and, after crossing, form the middle cerebellar peduncle, ending in the opposite hemisphere of the cerebellum. Part of the impulses that have arisen in the cerebral cortex of the brain reaches the opposite hemisphere of the cerebellum, bringing information not about what has been produced, but only about what is planned to be performed active movement . Having received such information, the cerebellum immediately sends out impulses that correct voluntary movements, mainly by extinguishing inertia and the most rational regulation of the tone of the reciprocal muscles - agonist and antagonist muscles. As a result, a kind of eimetry is created, making arbitrary movements clear, polished, devoid of inappropriate components. The pathways leaving the cerebellum consist of axons of cells whose bodies form its nuclei. Most efferent pathways, including those from the dentate nuclei, leave the cerebellum via its superior peduncle. At the level of the inferior tubercles of the quadrigemina, the efferent cerebellar tracts are crossed (crossing of the upper cerebellar peduncles of Wernecking). After crossing, each of them reaches the red nuclei of the opposite side of the midbrain. In the red nuclei, cerebellar impulses switch to the next neuron and then move along the axons of cells whose bodies are laid down in the red nuclei. These axons form into red-nuclear-spinal pathways (tracti rubro spinalis), Monakov's pathways, which E * soon after exiting the red nuclei undergo a decussation (tire decussation or Forel decussation), after which they descend into the spinal cord. In the spinal cord, the red nuclear-spinal tracts are located in the lateral cords; their constituent fibers terminate at the cells of the anterior horns of the spinal cord. The entire efferent pathway from the cerebellum to the cells of the anterior horns of the spinal cord can be called the cerebellar-red-nuclear-spinal (tractus cerebello-rubrospinalis). It crosses twice (crossing of the upper cerebellar peduncles and crossing of the tegmentum) and eventually connects each hemisphere of the cerebellum with peripheral motor neurons located in the anterior horns of the homolateral half of the spinal cord. From the nuclei of the cerebellar vermis, the efferent pathways go mainly through the inferior cerebellar peduncle to the reticular formation of the brainstem and the vestibular nuclei. From here, along the reticulospinal and vestibulospinal tracts passing through the anterior cords of the spinal cord, they also reach the cells of the anterior horns. Part of the impulses coming from the cerebellum, passing through the vestibular nuclei, enters the medial longitudinal bundle, reaches the nuclei of the III, IV and VI cranial nerves, which provide the movement of the eyeballs, and affects their function. Summing up, it is necessary to emphasize the following: 1. Each half of the cerebellum receives impulses mainly a) from the homolateral half of the body, b) from the opposite hemisphere of the brain, which has cortico-spinal connections with the same half of the body. 2. From each half of the cerebellum, efferent impulses are sent to the cells of the anterior horns of the homolateral half of the spinal cord and to the nuclei of the cranial nerves that provide eyeball movements. This nature of the cerebellar connections makes it possible to understand why, when one half of the cerebellum is damaged, cerebellar disorders occur predominantly in the same, i.e. homolateral, half of the body. This is especially clearly manifested in the defeat of the cerebellar hemispheres. Rice. 7.1. Cerebellar nuclei. 1 - dentate nucleus; 2 - corky nucleus; 3 - the core of the tent; 4 - spherical nucleus. Rice. 7.2. Sagittal section of the cerebellum and brainstem. 1 - cerebellum; 2 - "tree of life"; 3 - front cerebral sail; 4 - plate of four-colon; 5 - aqueduct of the brain; 6 - leg of the brain; 7 - bridge; 8 - IV ventricle, its choroid plexus and tent; 9 - medulla oblongata.

At the initial stage, the disease is difficult to recognize, since the symptoms are insignificant, and the main causes are poorly understood, but developing rapidly, it eventually leads to dementia and complete incapacity.

What is brain atrophy

The main human organ - the brain, consists of a huge number of nerve cells interconnected. Atrophic change in the cerebral cortex, causes the gradual death of nerve cells, while mental capacity fade over time, but how long a person lives depends on the age at which brain atrophy began.

Behavioral changes in old age are characteristic of almost all people, but due to the slow development, these signs of extinction are not a pathological process. Of course, older people become more irritable and grouchy, they can no longer react to changes in the world around them as they did in their youth, their intelligence decreases, but such changes do not lead to neurology, psychopathy and dementia.

The death of brain cells and the death of nerve endings is a pathological process leading to changes in the structure of the hemispheres, while there is a smoothing of the convolutions, a decrease in the volume and weight of this organ. Most prone to destruction frontal lobes, which leads to a decrease in intelligence and deviations in behavior.

Causes of the disease

At this stage, medicine is unable to answer the question of why the destruction of neurons begins, however, it has been found that the predisposition to the disease is inherited, and birth trauma and intrauterine diseases also contribute to its formation. Experts share congenital and acquired causes of the development of this disease.

• genetic predisposition;
• intrauterine infectious diseases;
• genetic mutations.

One of the genetic diseases that affect the cerebral cortex is Pick's disease. Most often it develops in middle-aged people, it is expressed in the gradual damage to the neurons of the frontal and temporal lobes. The disease develops rapidly and after 5-6 years leads to death.

Infection of the fetus during pregnancy also leads to the destruction of various organs, including the brain. For example, infection with toxoplasmosis, on early dates pregnancy, leads to damage to the nervous system of the fetus, which often does not survive or is born with congenital abnormalities and mental retardation.

1. drinking large amounts of alcohol and smoking lead to spasm of cerebral vessels and, as a result, oxygen starvation, which leads to insufficient supply of white matter cells with nutrients, and then their death;
2. infectious diseases that affect nerve cells (eg, meningitis, rabies, poliomyelitis);
3. trauma, concussion and mechanical damage;
4. severe form kidney failure leads to general intoxication of the body, as a result of which all metabolic processes are disturbed;
5. external hydrocephalus, expressed in an increase in the subarachnoid space and ventricles, leads to atrophic processes;
6. chronic ischemia causes vascular damage and leads to insufficient supply of neuronal connections with nutrients;
7. atherosclerosis, is expressed in the narrowing of the lumen of the veins and arteries, and as a result, an increase in intracranial pressure and the risk of stroke.

Atrophy of the cerebral cortex can be caused by insufficient intellectual and physical activity, lack of a balanced diet and in the wrong way life.

Why does the disease appear

The main factor in the development of the disease is a genetic predisposition to the disease, but various injuries and other provoking factors can accelerate and provoke the death of brain neurons. Atrophic changes affect different parts of the cortex and subcortical substance, however, with all manifestations of the disease, the same clinical picture is noted. Minor changes can be stopped and improved with the help of medications and lifestyle changes, but, unfortunately, it is impossible to completely cure the disease.

Atrophy of the frontal lobes of the brain can develop during fetal maturation or prolonged labor due to prolonged oxygen starvation, which causes necrotic processes in the cerebral cortex. Such children most often die in the womb or are born with obvious abnormalities.

The death of brain cells can also be triggered by mutations at the gene level as a result of exposure to certain harmful substances on the body of a pregnant woman and prolonged intoxication of the fetus, and sometimes it's just a chromosomal failure.

Signs of the disease

At the initial stage, the signs of brain atrophy are barely noticeable; only close people who know the sick person well can catch them. Changes are manifested in the apathetic state of the patient, the absence of any desires and aspirations, lethargy and indifference appear. Sometimes there is a lack of moral principles, excessive sexual activity.

Progressive death of brain cells symptoms:

• a decrease in vocabulary to describe something, the patient selects words for a long time;
• decrease in intellectual abilities in a short period;
• lack of self-criticism;
• loss of control over actions, body motility worsens.

Further atrophy of the brain is accompanied by a deterioration in well-being, a decrease in thought processes. The patient ceases to recognize familiar things, forgets how to use them. The disappearance of one's own behavioral characteristics leads to the “mirror” syndrome, in which the patient begins to involuntarily copy other people. Further, senile insanity and complete degradation of the personality develop.

The changes in behavior that have appeared do not make it possible to make an accurate diagnosis, therefore, to determine the causes of changes in the patient's character, it is necessary to conduct a series of studies.

However, under the strict guidance of the attending physician, it is possible to determine with more likely what part of the brain has undergone destructuring. So, if destruction occurs in the cortex, the following changes are distinguished:

1. decrease in thought processes;
2. distortion in the tone of speech and timbre of the voice;
3. change in the ability to remember, up to complete disappearance;
4. deterioration of fine motor skills of the fingers.

The symptomatology of changes in the subcortical substance depends on the functions that the affected department performs, so limited brain atrophy has characteristic features.

Necrosis of the tissues of the medulla oblongata is characterized by respiratory failure, digestive failure, cardiovascular and immune system person.

With damage to the cerebellum, there is a disorder of muscle tone, discoordination of movements.

With the destruction of the midbrain, a person stops responding to external stimuli.

Cell death intermediate department leads to a violation of the thermoregulation of the body and a metabolic failure.

The defeat of the anterior part of the brain is characterized by the loss of all reflexes.

The death of neurons leads to the loss of the ability to independently support life and often leads to death.

Sometimes necrotic changes are the result of trauma or long-term poisoning. toxic substances, resulting in restructuring of neurons and damage to large blood vessels.

Classification

According to the international classification atrophic lesions divided according to the severity of the disease and the location of pathological changes.

Each stage of the course of the disease has its own specific symptoms.

Atrophic diseases of the brain of the 1st degree or subatrophy of the brain, is characterized by minor changes in the behavior of the patient and quickly progresses to the next stage. At this stage, early diagnosis is extremely important, since the disease can be temporarily stopped and how long the patient lives will depend on the effectiveness of the treatment.

Stage 2 of the development of atrophic changes is manifested in the deterioration of the patient's sociability, he becomes irritable and unrestrained, the tone of speech changes.

Patients with 3 degrees of atrophy become uncontrollable, psychoses appear, the morality of the sick person is lost.

The last, 4th stage of the disease, is characterized by a complete lack of understanding of reality by the patient, he stops responding to external stimuli.

Further development leads to complete destruction, vital systems begin to fail. At this stage, hospitalization of the patient in a psychiatric hospital is highly desirable, as it becomes difficult to control him.

Classification according to the location of the affected cells:

Depending on the age at which brain atrophy begins, I distinguish between congenital and acquired forms of the disease. The acquired form of the disease develops in children after 1 year of life.

The death of nerve cells in children can develop for various reasons, for example, as a result of genetic disorders, different Rh factor in mother and child, intrauterine infection with neuroinfections, prolonged fetal hypoxia.

As a result of the death of neurons, cystic tumors and atrophic hydrocephalus appear. In accordance with where the cerebrospinal fluid accumulates, dropsy of the brain can be internal, external and mixed.

A rapidly developing disease is most often found in newborns, in which case we are talking about serious disorders in the brain tissues due to prolonged hypoxia, since children's body at this stage of life, it is in dire need of an intensive blood supply, and the lack of nutrients leads to serious consequences.

What kind of atrophy does the brain undergo?

Subatrophic changes in the brain precede the global death of neurons. At this stage, it is important to diagnose the brain disease in time and prevent rapid development atrophic processes.

For example, with hydrocephalus of the brain in adults, the free voids released as a result of destruction begin to be intensively filled with the released cerebrospinal fluid. This type of disease is difficult to diagnose, but proper therapy can delay the further development of the disease.

Changes in the cortex and subcortical substance can be caused by thrombophilia and atherosclerosis, which, if not properly treated, first cause hypoxia and insufficient blood supply, and then the death of neurons in the occipital and parietal zone, so the treatment will be to improve blood circulation.

Alcoholic brain atrophy

Brain neurons are sensitive to the effects of alcohol, so the intake of alcohol-containing drinks initially disrupts metabolic processes, and addiction occurs.

The breakdown products of alcohol poison neurons and destroy neural connections, then there is a gradual death of cells and, as a result, brain atrophy develops.

As a result of the destructive effect, not only cortical-subcortical cells suffer, but also the fibers of the brain stem, blood vessels are damaged, neurons shrink and their nuclei are displaced.

The consequences of cell death are obvious: in alcoholics, self-esteem disappears over time, memory decreases. Further use entails even greater intoxication of the body, and even if a person changes his mind, then he still develops Alzheimer's disease and dementia, since the damage done is too great.

multisystem atrophy

Multisystem atrophy of the brain is a progressive disease. The manifestation of the disease consists of 3 different disorders, which are combined with each other in various ways, and the main clinical picture will be determined primary signs atrophy:

At the moment, the causes of this disease are unknown. Diagnosed by MRI and clinical examination. Treatment usually consists of supportive care and reducing the impact of the symptoms of the disease on the patient's body.

cortical atrophy

Most often, cortical atrophy of the brain occurs in elderly people and develops due to senile changes. It mainly affects the frontal lobes, but spread to other parts is not excluded. Signs of the disease do not appear immediately, but eventually leads to a decrease in intelligence and the ability to remember, dementia, a vivid example of the impact of this disease on human life is Alzheimer's disease. Most often diagnosed with a comprehensive study using MRI.

Diffuse spread of atrophy often accompanies a violation of blood flow, deterioration of tissue repair and a decrease in mental performance, a disorder of fine motor skills of the hands and coordination of movements, the development of the disease radically changes the patient's lifestyle and leads to complete incapacity. In this way, senile dementia is a consequence of brain atrophy.

The best known bihemispheric cortical atrophy is called Alzheimer's disease.

Cerebellar atrophy

The disease consists in the defeat and death of small brain cells. The first signs of the disease: discoordination of movements, paralysis and speech disorders.

Changes in the cerebellar cortex mainly provoke such ailments as vascular atherosclerosis and neoplastic diseases brainstem, infectious diseases (meningitis), beriberi and metabolic disorders.

Cerebellar atrophy is accompanied by symptoms:

• impaired speech and fine motor skills;
• headache;
• nausea and vomiting;
• hearing loss;
• visual disturbances;
• at instrumental examination there is a decrease in the mass and volume of the cerebellum.

Treatment consists in blocking the signs of the disease with antipsychotics, restoring metabolic processes, cytostatics are used for tumors, and surgical removal of the formations is possible.

Types of diagnostics

Brain atrophy is diagnosed using instrumental methods of analysis.

Magnetic resonance imaging (MRI) allows you to examine in detail the changes in the cortical and subcortical substance. With the help of the images obtained, it is possible to accurately diagnose the disease already in the early stages of the disease.

Computed tomography allows you to examine vascular lesions after a stroke and identify the causes of hemorrhage, determine the localization of cystic formations that interfere with the normal blood supply to tissues.

The latest research method - multispiral tomography allows diagnosing the disease at an early stage (subatrophy).

Prevention and treatment

Adhering to simple rules, you can significantly alleviate and prolong the life of the sick. After the diagnosis is made, it is best for the patient to remain in their usual environment, as stressful situations can aggravate the condition. It is important to provide the patient with feasible mental and physical stress.

Nutrition for brain atrophy should be balanced, a clear daily routine should be established. Mandatory abandonment of bad habits. Control of physical indicators. Mental exercises. The diet for brain atrophy consists in the rejection of heavy and unhealthy foods, the exclusion of fast food and alcoholic beverages. It is advisable to add nuts, seafood and greens to the diet.

Treatment consists of the use of neurostimulants, tranquilizers, antidepressants and sedatives. Unfortunately, this ailment cannot be completely cured, and therapy for brain atrophy consists in alleviating the symptoms of the disease. Which drug will be chosen as maintenance therapy depends on the type of atrophy and what functions are impaired.

So, in case of disorders in the cerebellar cortex, the treatment is aimed at restoring motor functions, and the use of drugs that correct tremor. In some cases, surgery is indicated to remove the neoplasms.

Sometimes drugs are used that improve metabolism and cerebral circulation, provided good circulation blood and access to fresh air to prevent oxygen starvation. Often, the lesion affects other human organs, therefore, a complete examination at the brain institute is necessary.

Treatment of atrophic changes in the brain

With the slow death of neurons (processing, storing, transmitting information to electrically excitable cells), atrophic changes in the brain develop - cerebral atrophy. In this case, the cortex or subcortex of the brain is damaged. This disorder usually occurs in older people, with the majority of patients being women.

Atrophy can occur in flight and end with complete dementia. This is associated with the shrinkage of brain mass due to the aging process. But sometimes pathology is observed in childhood. There are many reasons for its appearance. Treatment is usually symptomatic as it is a progressive and incurable disease.

Types of pathology

There are several types of atrophy:

• Multisystem, characterized by changes in the cerebellum, cerebrospinal fluid, brain stem. The patient has autonomic disorders, erectile dysfunction, unsteady gait, a sharp increase in pressure, tremor of the limbs. Often the symptoms of pathology are falsely confused with other diseases, for example, with Parkinson's disease.
• Cortical, caused by the destruction of the tissue of the cerebral cortex due to age-related changes occurring in neurons. The frontal lobes are often affected. The disorder is expressed at an increasing pace, and in the future develops into senile dementia.
• Subatrophy. It is characterized by a partial loss of activity of a particular area or the entire lobe of the brain. If the process occurred in the frontotemporal region, the patient has difficulty hearing, communicating with people, and heart problems appear.
• diffuse atrophy. At first, it has symptoms characteristic of changes in the cerebellum, but later it manifests itself with more specific signs, according to which pathology is diagnosed. The disorder is aggravated by impaired cerebral circulation, and is considered the most unfavorable type of atrophic transformation.
• Cortical or subcortical transformation is caused by thrombosis and the presence of atherosclerotic plaques, leading to oxygen starvation and destruction of neurons in the parietal and occipital regions of the brain. The impetus for the development of pathology is often a violation of metabolic processes, atherosclerosis, jumps in blood pressure and other provoking factors.

Symptoms

The manifestations of the disease are highly dependent on which part of the brain is affected. Cerebellar atrophy of the subcortical zones has the following symptoms:

• During transformation in the medulla oblongata, breathing is disturbed, the cardiovascular and digestive systems suffer, and protective reflexes are inhibited.
• Destructive changes in the cerebellum are characterized by impaired muscle tone and coordination of movements.
• Reactions to stimuli disappear due to the death of midbrain cells.
• Damage diencephalon are manifested by impaired thermoregulation and metabolic metabolic imbalance.
• It is difficult not to notice atrophy of the forebrain - all types of reflex reactions to stimuli are lost.

Complicated damage to the subcortical cells of the brain tissue and structures threatens to lose the ability to live and die in the future. A similar degree of atrophic changes is rarely observed, mainly after serious injury or damage to large vessels.

Atrophy of the cerebral cortex is characterized by the following features:

• Difficulties with the selection of the right words to express thoughts, feelings.
• Decreased ability to self-criticism and to comprehend current events.
• Difficulty in speech.
• Marked memory loss.
• Emotional breakdowns, nervousness.
• Lack of desire to take care of others.
• Impaired motor skills of the hands, change in handwriting for the worse.
• Mental disorder.

The patient gradually loses the ability to recognize objects and to understand what to do with them. He does not orient himself in space due to memory impairments. An atypical manner of imitation of other people is manifested, as a person becomes easily suggestible. In the future, insanity develops, characterized by the complete disintegration of the personality.

Stages of the course of the disease

At first, the patient easily performs the previous functions, if they do not require mental stress. The most common symptoms are:

• Head spinning.
• Headache attacks.
• Absent-mindedness.
• Carelessness.
• Depressive state.

Such signs are often attributed to vascular disorders. If at this stage the disease is diagnosed and competent treatment, then this will help to significantly slow down the necrotic process.

Gradually, the patient's self-control is weakened, his behavior becomes strange, he acts thoughtlessly, sometimes aggression occurs. Coordination disorders are noticed, fine motor skills suffer. Decreased ability to social adaptation. Transformation in the brain affects the awareness of speech. Complaints about their condition cease, as the perception and analysis of real events changes.

The last stage is characterized by the most serious destruction of the brain. Cerebral atrophy leads to dementia. The patient can no longer serve himself, speak, read and write. Psychiatric disorders are noted.

The reasons

It has not yet been possible to establish a complete picture of the development of brain atrophy. But numerous studies of experts say that the main causes of the disease lie in genetic pathologies. Much less often, the symptoms of transformations develop against the background of secondary deformations of the nervous tissue provoked by external stimuli.

Congenital causes include:

• Heredity.
• Viruses and infections that hit the baby in the womb.
• Chromosomal mutations.

One of the genetic diseases that affect the cerebral cortex is Pick's disease, which develops in adults. This is a rare, progressive disorder that affects the frontal and temporal lobes. The average life expectancy after the onset of the disease is 5-6 years. Partial tissue atrophy occurs in the following diseases:

• Alzheimer's disease.
• parkinsonism syndrome.
• Huntington's disease.

Acquired causes include:

• Alcohol abuse and drug addiction, causing chronic poisoning of the body.
• Chronic and acute neuroinfections.
• Trauma, concussions, brain surgery.
• Hydrocephalus.
• Renal failure.
• Ischemia.
• Atherosclerosis.
• Ionizing radiation.

Acquired causes of cerebral atrophy are considered conditional. In patients, they are observed no more than 1 in 20 cases. And with congenital anomalies, they rarely provoke a disease.

Diagnostics

The disease is diagnosed by instrumental methods:

• Magnetic resonance imaging, which determines damage to brain structures. The procedure allows you to accurately diagnose the disease at an early stage and monitor its course.
• Computed tomography, which allows to identify diseases of the cerebral vessels, to determine the localization of existing neoplasms and other pathologies that interfere with normal blood circulation. Multispiral tomography is considered the most informative. During this survey it is possible to detect even the initial stage of subatrophy due to the layer-by-layer transformation of the image of the problem area of ​​the brain.

In children

Brain atrophy in newborns is often caused by hydrocephalus. The disorder is expressed by an increase in the amount of cerebrospinal fluid that protects the brain from various damages. There are many reasons for this state of affairs. Often the disease develops in the womb due to:

Sometimes provocateurs are birth trauma followed by cerebral hemorrhage. Also, atrophy with serious brain changes is associated with hypoxia, Rhesus conflict, and genetic disorders.

Pathology can be detected ultrasound examination. After the diagnosis is made, the child is hospitalized, as he needs serious treatment, which consists in eliminating the symptoms. A lot of effort and time will be required for rehabilitation, but even in the best case, the consequences affect the mental and physical development of the baby. Complicated destruction of brain tissue leads to death.

Therapy

Patients with atrophy require constant care and attention from relatives. Treatment of the disease consists in taking:

• Antidepressants.
• Sedative drugs.
• Light tranquilizers.

• With ischemia, nootropics are prescribed.
• Statins are used for atherosclerosis.
• With increased thrombosis - antiplatelet agents.
• Hydrocephalus is treated with diuretics.
• Vitamin therapy is prescribed to improve metabolic processes.

Medicines that improve blood circulation are also used. They stimulate the process of hematopoiesis, normalize blood circulation, stop tissue necrosis, providing them with oxygen. In the absence of contraindications, a massage is prescribed that improves blood circulation and the patient's psycho-emotional mood.

Since atrophy often develops in older people due to atherosclerosis and jumps in blood pressure, pressure and lipid metabolism must be normalized. Of the antihypertensive drugs, ACE inhibitors and angiotensin antagonists are used.

When pronounced signs of the disease appear, the patient should be in the usual conditions of life, surrounded by a calm, favorable atmosphere. Any stressful situation can aggravate the condition. It is important to provide a person with the opportunity to do ordinary things, to feel needed in the family, not to change habits and the established way of life. He needs healthy balanced diet, physical activity, alternating with rest, observing the regime of the day.

Prevention and diet

The right attitude, active participation in family life, household chores positively affect the patient's condition and inhibit the development of the disease. This is what most experienced professionals tend to do. Contribute to the prevention of disease:

• A categorical rejection of bad habits.
• Sports.
• Proper nutrition.
• Daily monitoring of blood pressure (for this, a tonometer is used, and the indicators are recorded in a notebook).
• Mandatory mental stress(reading, solving crossword puzzles).

Diet plays an important role in maintaining the brain at the proper level. Help improve brain function:

• Nuts (walnuts, peanuts, almonds).
• Fruits (preferably fresh).
• Seafood and fish.
• Cereals, bran.
• Dairy products.
• Greens.

It is desirable to exclude from the menu:

A person who has atrophic changes in the brain should not give up, knowing that this is a disease that is not treated with medicines. Sooner or later it will get worse. The main thing is to slow down the course of the disease, load the mind and body, try to enjoy life and participate in it as actively as possible.

My child, 5 years and 7 months old, is diagnosed by CT scan: signs of moderate atrophic changes in the brain tissue of the frontal and parietal lobes. Rotational subluxation of the atlas.

The child does not speak, two words are only mom and dad, he understands the speech addressed.

All information on the site is provided for informational purposes only and cannot replace the advice of your doctor.

congenital atrophy of the cerebellum

Hereditary congenital atrophy of the cerebellum is a collection of syndromes that are relatively rare. It is difficult to estimate the true prevalence of these diseases, since most cases of congenital cerebellar atrophy are sporadic, and children are usually diagnosed with the cerebellar form of cerebral palsy.

Another subject of discussion is the question of the essence of the pathological process and, consequently, of the adequate designation of this group of diseases: atrophy or aplasia of the cerebellum? Aplasia (or dysgenesis) of the cerebellum implies a violation of the normal ontogenetic development and differentiation of both various parts of the cerebellum and individual cell layers of the cortex. Bearing in mind that these changes can occur under the influence of a variety of exogenous factors(for example, intrauterine cytomegalovirus infection, the use of X-ray therapy in the mother during pregnancy), it is logical to assume that certain hereditary metabolic defects can also lead to the development of congenital aplasia of the cerebellum. On the other hand, the assessment of cerebellar functions in infants is extremely difficult; degenerative changes and death of cellular structures normally formed in early ontogenesis. An additional difficulty lies in the fact that morphological criteria alone are not enough to differentiate congenital developmental defects and an atrophic process at an early onset of the disease, especially since a combination of both conditions can occur. Like most authors, we retained the use of the term "congenital cerebellar atrophy", since even in the presence of true cerebellar hypo- and aplasia, it may be accompanied by the development of secondary atrophic changes.

genetic data. Congenital cerebellar atrophy can be inherited in an autosomal dominant, autosomal recessive, and X-linked recessive manner.

Clinical characteristic. The initial symptoms of cerebellar dysfunction in the first year of a child's life are easy to overlook, as they are not specific enough and are usually masked by a picture of a general delay in motor development. Disturbances in motor development are manifested in the delay in the main stages of the formation of normal motor functions, primarily sitting and walking. Already at the age of several months, intentional tremors can be noted, quite early there is also a tremor of the head and oscillations of the body in the sitting position. When a child tries to fix his gaze, nystagmus can sometimes be noted. Having learned to walk with support, the child may immediately fall if the support is lost. Self-maintenance skills

6 88 balance of the body are given with great difficulty.

Additional symptoms in congenital atrophy of the cerebellum are extremely variable. The most common are mental retardation, dysarthria, nystagmus, oculomotor and pupillary disorders, optic nerve atrophy, deafness, muscle hypotension, pyramidal symptoms, hydrocephalus, growth retardation.

Data from laboratory and functional studies. CT and MRI in patients show signs of atrophy of the cerebellar vermis, expansion of the superior cerebellar cistern. To a lesser extent, signs of atrophy of the cerebellar hemispheres can be expressed, the IV ventricle is usually of normal size. In some patients, these changes are combined with the expansion of the stem cisternal spaces, atrophic changes in the supratentorial parts of the brain, sometimes aplasia of the corpus callosum can be detected.

pathological changes. The morphological picture in various forms of congenital atrophy of the cerebellum is very diverse. Most often, complete or partial agenesis of the cerebellar vermis is described. In addition, hypoplasia of the granular layer of the cerebellar cortex, heterotopia of the cerebellar cortex, gliosis of the pyramidal tracts, dentate nuclei, death of neurons of the inferior olives and nuclei of the brainstem, meningomyelocele and other changes can be detected [Vgiup K., 1991].

Criteria for diagnosis. The main criteria for the diagnosis of congenital cerebellar atrophy are:

The initial symptoms of cerebellar dysfunction are detected in the first year of life;

Cerebellar ataxia, intentional tremor, head tremor, body oscillations;

Signs of atrophy of the cerebellar vermis, expansion of the superior cerebellar cistern (CT, MRI); less pronounced atrophy of the cerebellar hemispheres; IV ventricle is not changed;

The course is mildly progressive up to 10-12 years with further stabilization of the process.

differential diagnosis. Congenital atrophy of the cerebellum should be differentiated from childhood cerebral

paralysis (cerebral palsy). Against cerebral palsy, the presence in the family of several cases of the disease with a similar clinical picture, the absence of a history of factors contributing to the development of cerebral palsy (birth trauma, intrauterine infection, Rh conflict, etc.), the absence of cysts and other changes in CT and MRI studies, often found in cerebral palsy. It should be noted that if hereditary congenital atrophy of the cerebellum is suspected, it is desirable to examine healthy relatives of the patient (including CT and MRI), since there are cases when, even in the presence of total cerebellar agenesis, clinical symptoms of cerebellar dysfunction did not develop.