Atrophic changes in the brain - what is treatment?

Atrophic processes include a number of endogenous organic diseases, the main manifestation of which is dementia - Alzheimer's disease, Pick's disease, Huntington's chorea, Parkinson's disease and some rarer diseases. In most cases, these diseases begin in adulthood and old age without an obvious external cause. The etiology is largely unclear. For some diseases, the leading role of heredity has been proven. A pathological examination reveals signs of focal or diffuse atrophy without inflammation or severe vascular insufficiency. Features of the clinical picture depend primarily on the localization of atrophy (see section 1.1.3).

General information

Natural aging processes affect the state of the central nervous system. All older people experience memory deterioration and a decreased ability to learn, remember, and process information. In elderly and senile people, brain atrophy occurs (0.1-0.3% of volume is lost per year), associated with age-related physiological processes, but cognitive function does not quickly reach the level of dementia .
Therefore, in patients with a normal level of consciousness, the term “infectious changes” in the brain is often used. Physiological atrophy begins to develop at the age of 40-60 years and reaches severity by 75 years. In psychoneurological diseases ( Alzheimer's disease , Pick's disease , multiple sclerosis , Lewy body disease ), brain atrophy and, accordingly, neurological disorders progress quickly, leading patients to disability. With these diseases, from 0.5 to 1.4% of brain volume is lost per year. Atrophic changes in the brain, what is it? This is a decrease in the volume and density of brain tissue due to the death of neurons, which occurs for various reasons. Typically, atrophy is the outcome of long-term processes in which organic, irreversible changes in the parenchyma occur and nerve connections are destroyed.

In this case, atrophy of the cerebral cortex, subcortical structures (visual thalamus, limbic system, basal ganglia, hypothalamus) and atrophic changes in the cerebellum are observed to varying degrees. Cortical (or external) atrophy is observed in all patients with secondary atrophy. The changes can be generalized (the entire brain is affected) or local (specific areas of the brain are affected).

In some diseases, the white matter of the brain predominantly atrophies, while in others, the gray matter atrophies. Thus, in multiple sclerosis , atrophic changes in the gray matter occur in the early stages; they develop faster than white matter atrophy and are associated with cognitive impairment. As the volume of the cortex decreases, neurological changes progress. Women get sick more often than men and the first signs of pathology appear at 55 years of age. In this regard, it is important to carry out effective treatment that would reduce the rate of atrophic changes. This pathology cannot be cured and sooner or later ends in dementia .
The rate of atrophy determines the speed of onset and severity of disability.

How cerebral neurons die...

Cerebral atrophy affects the frontal areas of the brain (cortex and subcortex). It is this zone that is responsible for intellectual and mnestic functions and emotions. But this disease is classified into several types, which have different locations:

1. Cortical atrophy . Here destruction occurs in the tissues of the cerebral cortex. And most often this appears during the aging process of nerve cells, but other pathological effects on the brain (BM) cannot be ruled out.
2. Multisystem extinction . Characterized by damage to the cerebellum, brainstem trunk, and basal ganglia. Has a build-up effect.
3. Diffuse mortality affects a variety of processes in opposite places. The disease begins its action in the cerebellum area, and then symptoms appear that are characteristic of other areas of the brain.
4. Cerebellar death . Characterized by cerebellar disorders with additional pathological processes in other parts of the brain.
5. Posterior cortical . Causes atrophy of neurons in the occipital and crown areas. Clusters of plaques and tangles of neurofibrillary tangles form, which contribute to death.

Pathogenesis

The development of atrophic processes in most cases is based on deterioration of blood supply. The cerebral cortex is gray matter. The white matter is located under the gray matter. The subcortical substance is formed by the thalamus, caudate and lenticular nuclei, and basal ganglia. It was found that the subcortical substance and the white matter of the hemispheres, located around the ventricles of the brain, are more affected by chronic cerebral ischemia than the gray matter. When cerebral vessels are damaged, the supply to the frontal subcortical areas is disrupted. Large areas of infarction develop in the white matter, in which axons and oligodendrocytes .

Damages to the cerebellum cause a decrease in its function: muscle contractions are discoordinated and it becomes impossible to perform normal movements in the limbs. The coordinated function of the muscles of the speech apparatus is disrupted, resulting in speech becoming slow and intermittent. Ataxia of the respiratory muscles is manifested by jerky breathing. Hypotonia of the tongue muscles causes soft consonants to be pronounced firmly.

Why does the brain atrophy?

1. Atherosclerotic lesion of cerebral vessels. The death of brain cells begins when atherosclerotic deposits, causing a narrowing of the lumen of blood vessels, cause a decrease in the trophism of neurons, and subsequently, as the disease progresses, their death. The process is disseminated. Brain atrophy caused by atherosclerotic vascular damage is one of the special cases of ischemic atrophy.
2. Chronic intoxication effects. The death of nerve cells in the brain in this form of the disease is caused by the harmful effects of toxic substances on them. Alcohol, drugs, some pharmaceuticals, and nicotine can have a similar effect. The most striking examples of this group of diseases can be considered alcoholic and drug encephalopathy, when atrophic changes in the brain are represented by a smoothing of the relief of the convolutions and a decrease in the thickness of the cerebral cortex, as well as subcortical formations.
3. Residual phenomena of traumatic brain injuries. Hypotrophy and atrophy of the brain as a long-term consequence of head trauma are, as a rule, local in nature. The death of nerve cells occurs in the damaged area of ​​the brain; in their place, cystic formations, glial foci or scars subsequently form. This atrophy is called post-traumatic.
4. Chronic cerebrovascular insufficiency. The most common causes of this condition are the atherosclerotic process, which reduces the patency of cerebral vessels; arterial hypertension and age-related decrease in the elasticity of blood vessels of the cerebral capillary bed.
5. Degenerative diseases of nervous tissue. These include Parkinson's disease, Alzheimer's disease, Pick's disease, cerebral degeneration with Lewy bodies and others. Today there is no clear answer about the reasons for the development of this group of diseases. These diseases have a common feature in the form of gradually developing atrophy of various parts of the brain, are diagnosed in elderly patients and in total account for about 70 percent of cases of senile dementia.
6. Intracranial hypertension. Compression of the brain substance with a long-term increase in intracranial pressure can lead to atrophic changes in the brain substance. A clear example is the cases of secondary hypotrophy and atrophy of the brain in children with a congenital form of hydrocephalus.
7. Genetic predisposition. Today, clinicians know several dozen genetically determined diseases, one of the features of which is atrophic changes in the brain substance. One example is Huntington's chorea.

Classification

Cerebral atrophy occurs:

• Primary. It is rare and is caused by genetic disorders and congenital brain abnormalities. It appears at any age, progresses quickly and cannot be corrected.
• Secondary. It is associated with the impact of adverse factors on the brain, among which are vascular pathology, traumatic brain injury, exposure to radiation, toxic effects, metabolic disorders, and bad habits. With secondary atrophy, eliminating the cause to some extent slows down the development of the disease, and adequate treatment ensures a stable condition for many years and a relatively good quality of life.
• General (the entire volume of the brain parenchyma decreases and the volume of the ventricles and subarachnoid spaces increases).
• Local (the volume of some brain structures decreases).

Depending on the location, there are:

• Cortical atrophy (the main symptom is the involution of the cortex in the temporal and frontal lobes).
• Generalized (changes in all parts of the brain).
• Multisystem (foci develop in several areas).

Depending on the stage:

• Stage I. Organic changes are minimal, but mild neurological disorders are noted. Emotional lability, memory impairment, and decreased concentration are noted.
• Stage II. Severe atrophic manifestations, which are manifested by hearing, speech and vision impairments. Behavior changes, a person commits illogical actions that he cannot explain and quickly forgets about them.
• Stage III. Cortical atrophy is sharply expressed and multiple foci are noted in the hemispheres. The patient cannot care for himself and needs outside help. Personal degradation is expressed to the maximum. This is how a person lives for many years until the destruction of important centers occurs and death occurs.

Cortical cerebral atrophy

This form is manifested by loss of intelligence and behavioral disturbances. The cerebral cortex (gray matter layer) is associated with higher cortical functions: perception, memory, imagination, thinking and speech. It has a complex six-layer structure and the neurons of each layer differ in function. Cortical areas, and accordingly, functions are divided into sensory, associative and motor.

Cortical atrophy occurs with the death of neurons in the frontal lobe cortex. The frontal association area is involved in higher mental functions. It controls behavior, logical thinking, object recognition and speech understanding. After damage to the frontal cortex apathy , there is no critical attitude towards oneself and one’s actions, the patient cannot use past experience, and his behavior becomes inadequate and unpredictable, he commits unmotivated actions. Cognitive (cognitive) abilities are gradually lost: the patient loses the ability to perceive, perceive information, analyze and remember it, and think. In general, cortical atrophy of the brain is characterized by progressive personality degradation, which occurs in stages.

Grade 1 cortical cerebral atrophy is the initial stage of the disease, in which there are no symptoms, but this conclusion can be given with MRI even in young people. At the same time, a person lives a full life and is active in his professional activities, but may periodically experience headaches , irritability and be emotionally unstable. Factors causing cerebral atrophy of the 1st degree may be various intoxications, previous traumatic brain injuries and deterioration of blood supply to the brain with osteochondrosis of the cervical spine .

Generalized atrophy

This is a common atrophy characterized by uniform death of areas of the entire brain. This form is characteristic of extensive ischemic and post-traumatic conditions, as well as neurodegenerative diseases - Alzheimer's disease , Parkinson's disease , Pick's disease and frontotemporal dementia. The progression of neurological symptoms depends on the degree of atrophy of the cortex and subcortical gray matter. Decreased cognitive function is associated with damage to the white matter and parietal cortex.

In this regard, generalized cerebral atrophy of the 2nd degree is characterized by a noticeable decrease in the patient’s ability to think and analyze. The level of critical thinking and evaluation of one's actions is reduced. The patient's habits, speech and handwriting also change. The person loses emotional connection and communication abilities. Neurological disorders - movements and coordination of movements - are more pronounced.

The third degree is characterized by degeneration of gray and white matter. The patient cannot control his behavior, and also needs care and observation, since there is a deterioration in hand motor skills and coordination of movements. The patient cannot use basic household items and is unable to make decisions independently.

Local degeneration is associated with:

• vascular diseases;
• alcohol abuse (atrophy of the cerebellar vermis is noted);
• multiple sclerosis;
• drug use;
• brain injury;
• infection of the central nervous system.

In the early stages of multiple sclerosis, the disease is characterized by degeneration of subcortical gray matter, most pronounced in the thalamus. After this, damage to the cortex develops (the central gyri are more affected), over time, destruction of the white matter is noted, and only then the spinal cord. In multiple sclerosis, not only general atrophy is observed, but also local atrophy - structures that have gray matter are affected: the cerebellum , basal ganglia and thalamus . In multiple sclerosis, gray matter atrophy predominates over changes in white matter, and it determines the degree of disability of patients.

Cerebellar atrophy

The cerebellum is located below the hemispheres and above the brain stem. This formation coordinates movements and their precision, receiving information from the cortex and basal ganglia about the position of the legs. Cerebellar lesions are characteristic of multiple sclerosis , Friedreich's ataxia , olivopontocerebellar degeneration , Pierre-Marie's ataxia . Ataxia (meaning disorder) is a characteristic feature of lesions of this brain formation.

Friedreich's ataxia appears at 10-20 years of age. Patients develop weakness in the legs, falls, staggering and uncertainty when walking, handwriting, speech and hearing are impaired. Muscle atrophy gradually increases (at first it is expressed in the legs, and over time it also covers the arms), deep sensitivity is impaired, cataracts develop, the optic nerve atrophies, and dementia develops. Computed tomography for this disease is ineffective, since a weak degree of atrophy of the hemispheres and cerebellum, expansion of the cisterns, and ventricles is detected in the later stages. Olivopontocerebellar atrophy is considered a form of multiple system atrophy.

Multiple system brain atrophy

This is a variant of a degenerative progressive pathology of the brain, which affects the basal ganglia, cerebellum and centers that are responsible for autonomic reactions. Clinically, multiple system atrophy is manifested by parkinsonism , cerebellar ataxia and autonomic disorders . The disease appears at the age of 50-60, progresses rapidly and leads to death. The muscles become stiff, the patient has difficulty moving, coordination and function of internal organs are impaired.

Depending on the predominant syndrome, the following forms of the disease are distinguished:

• Striatonigral degeneration or parkinsonian form . With it, degenerative changes are most pronounced in the striatum (belongs to the basal ganglia) and the substantia nigra (part of the extrapyramidal system, which plays a role in motor function). The leading symptom is parkinsonism .
• Olivocerebellar atrophy or cerebellar form . The cerebellum, olives and pons are affected. In the clinic, cerebellar syndrome predominates, manifested by impaired coordination and inability to maintain balance.
• Shy-Drage syndrome . In this form, the leading ones are autonomic failure and orthostatic hypotension - in patients, the pressure sharply decreases and a pre-fainting state appears when moving to a vertical position. Patients are also concerned about decreased sweating, darkening of the eyes, urinary disorders, impotence and unsteady gait.

Diagnostics

The disease is diagnosed using instrumental methods:

• Magnetic resonance imaging , which determines damage to brain structures. The procedure allows you to accurately diagnose the disease in the early stages and monitor its progress.
• Computed tomography , which makes it possible to identify cerebral vascular diseases, determine the localization of existing tumors and other pathologies that interfere with normal blood circulation. Multislice tomography is considered the most informative. During this examination, even the initial stage of subatrophy can be detected thanks to the layer-by-layer transformation of the image of the problem area of ​​the brain.

Causes

Cerebral atrophy in most cases is secondary in nature and it is worth noting the reasons that lead to this condition:

• Genetic predisposition.
• Chronic cerebral ischemia , causing diffuse damage to the white matter (cerebral atrophy), against which vascular dementia develops. It should be noted that cerebral atrophy in vascular dementia is not very pronounced when compared with Alzheimer's disease , and hippocampal atrophy in chronic cerebral ischemia is the same as in Alzheimer's disease.
• Arterial hypertension hypertensive encephalopathy develops . With this disease, MRI reveals multiple changes in the subcortical zones around the ventricles (leukoaraiosis), cortical atrophy and dilatation of the ventricles. The same changes are observed during physiological aging.
• Antiphospholipid syndrome.
• Central nervous system infections ( meningitis , polio , leptospirosis ).
• State of decortication in coma .
• Atherosclerosis general and cerebral. The condition worsens when atherosclerosis is combined with arterial hypertension.
• Brain tumors.
• Embolism of the cerebral arteries. The source of embolism is fragments of atherosclerotic plaques and blood clots from the heart.
• Atrial fibrillation . In patients with fibrillation, the brain matter as a whole, as well as individual parts, decreases. The frontal regions of the brain and hippocampus are primarily affected.
• Congenital anomalies of cerebral vessels, causing cerebrovascular disorders.
• Blood rheology disorders (increased viscosity, platelet aggregation, etc.).
• Elevated homocysteine . Homocysteine ​​is a sulfur-containing amino acid, an increase in the level of which is associated with the development of vascular disorders of the brain and heart and neurodegenerative processes in the brain. Hyperhomocysteinemia is a risk factor for recurrent strokes and white matter changes. Patients with elevated homocysteine ​​levels have greater hippocampal atrophy.
• Diabetes . Patients with diabetes mellitus are characterized by mild cerebral atrophy of the cortex, subcortical structures and leukoaraiosis . Even an increase in glucose to the upper limit is associated with atrophic changes in the hippocampus and amygdala complex.
• Multiple sclerosis . Already in the early stages, patients experience degenerative changes - neurons and axons die. Axonal damage is observed in active and chronic lesions of sclerosis. In the latter, axon density decreases to 80%. These processes, plus gliosis and demyelination, lead to a decrease in brain volume. Patients with relapsing-remitting sclerosis (it occurs with exacerbations and remissions) lose 0.5-1.3% of brain volume per year.
• Alzheimer's disease . MRI reveals atrophy of the temporal lobe (reduction in the volume of the gyri and widening of the sulci) and hippocampus, which are markers of this disease. The hippocampus plays an important role in memory formation (categorization of information and long-term memory). Any traumatic brain injury accelerates the development of Alzheimer's disease.
• Any intoxication of the body (drug, alcohol, drugs). With alcoholism, diffuse brain atrophy develops.
• Age-related changes.
• Hydrocephalus in children. This pathology is accompanied by structural changes in the brain: thinning of the cortex, reduction of white matter, vascular atrophy and atrophy of the basal ganglia and cerebellum.
• Traumatic brain injury . 3-4 weeks after the injury, minor hemorrhages resolve, the ventricles and subarachnoid space expand, and generalized brain atrophy develops, which is caused by prolonged intracranial hypertension.
• Long-term corticosteroid therapy can cause cerebral atrophy.
• Acute pain. Acute pain that persists for 3 months causes atrophic changes in the cerebral cortex.
• Physical inactivity . A risk factor for the appearance of atrophic processes and a decrease in cognitive cognitive functions is the limitation of physical activity.

Types of pathology

There are several types of atrophy:

• Multisystem , characterized by changes in the cerebellum, cerebrospinal fluid, and brain stem. The patient has autonomic disorders, erectile dysfunction, unsteadiness of gait, a sharp increase in blood pressure, and tremors of the limbs. Often the symptoms of the pathology are falsely confused with other diseases, for example, Parkinson's disease.
• Cortical , caused by the destruction of 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 rate, and in the future develops into senile dementia.
• Subatrophy . It is characterized by partial loss of activity in a separate area or an entire lobe of the brain. If the process occurs in the frontotemporal region, the patient has difficulty hearing, communicating with people, and has heart problems.
• Diffuse atrophy . At first it has symptoms characteristic of changes in the cerebellum, but later it manifests itself with more specific signs by 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 metabolic disorders, atherosclerosis, surges in blood pressure and other provoking factors.

Symptoms of brain atrophy

The initial symptoms of the disease reflect changes in the mental state of patients. Early symptoms are anxiety and depression . Patients become apathetic, lethargic, they are not interested or attracted to anything, they prefer to retire and constantly stay at home, their night sleep is disturbed. The mask of depression is irritability, dissatisfaction with everything and grumpiness, which are regarded as characteristics of older people.

If depression is a marker of internal atrophy, then anxiety disorders are characteristic of focal and external cerebral atrophy.

Cognitive disorders (memory, attention, concentration, ability to recognize objects and perform actions purposefully) are detected in all patients in the early stages of brain degeneration. Cognitive symptoms and depression are often regarded as senile forgetfulness and low mood. Impaired memory and attention first occur against the background of maintaining professional and everyday skills. As it progresses, social skills are gradually lost (the patient cannot independently go to the store, pharmacy, or visit the clinic, since he lacks purposefulness of actions) and household skills (he cannot simply take care of himself, eat and take a shower). Over time, sloppiness appears, the vocabulary becomes poor, the patient does not comprehend the speech and requests addressed to him. His movements are sweeping, his handwriting changes and his fine motor skills deteriorate.

In severe cases, the patient does not recognize his relatives and friends, cannot navigate the place and cannot answer questions. The specific behavior is that patients constantly repeat actions and words after others. The final stage of brain degeneration is marasmus - complete regression of mental abilities and destruction of personality. At the same time, infant reflexes are activated: a sucking reflex appears, the patient lies in the fetal position, recovers and urinates under himself. He responds to calls with inarticulate sounds.

Symptoms of cerebellar atrophy

Since the cerebellum regulates movements, if it is damaged, the following will be observed:

• Balance and muscle tone problems.
• Gait disturbances (wide-spaced legs, unsteadiness, difficulty turning).
• Fine motor disorders.
• Uncoordinated movements of arms and legs.
• Unsteadiness and frequent falls.

Patients are also worried about headaches , dizziness , attacks of nausea and vomiting, visual disturbances, pronunciation problems, scanned and slow speech, uncoordinated eye movements, and decreased hearing acuity. As it progresses, urinary incontinence , paresis and paralysis .

Main manifestations

Brain atrophy manifests itself depending on which part of the brain the pathological changes begin in. Gradually, the pathological process ends in dementia.

At the beginning of development, atrophy affects the cerebral cortex. This leads to deviations in behavior, inappropriate and unmotivated actions, and decreased self-criticism. The patient becomes sloppy, emotionally unstable, and depression may develop. The ability to remember and intelligence are impaired, which manifests itself in the early stages.

Gradually the symptoms increase. The patient not only cannot work, but also cannot care for himself. There are significant difficulties with eating and going to the toilet. A person cannot complete these tasks without the help of other people.

The patient stops complaining that his intelligence has deteriorated, since he is unable to evaluate it. If there are no complaints about this problem at all, it means that brain damage has reached the last stage. Loss of orientation in space occurs, amnesia appears, the person cannot say his name or where he lives.

If the disease is hereditary, then brain function deteriorates quite quickly. This takes several years. Damage due to vascular disorders can progress over several decades.

The pathological process develops as follows:

1. At the initial stage, changes in the brain are small, so the patient leads a normal lifestyle. In this case, the intellect is slightly impaired, and the person cannot solve complex problems. Your gait may change slightly, and you may experience headaches and dizziness. The patient suffers from a tendency to depression, emotional instability, tearfulness, and irritability. These manifestations are usually attributed to age, fatigue, and stress. If you start treatment at this stage, you can slow down the development of pathology.
2. The second stage is accompanied by worsening symptoms. Changes in the psyche and behavior are observed, coordination of movements is impaired. The patient cannot control his actions; his actions lack motive and logic. Moderate development of atrophy reduces working capacity and disrupts social adaptation.
3. A severe degree of the disease leads to damage to the entire nervous system, which is manifested by impaired motor skills and gait, loss of the ability to write and read, and perform simple actions. The deterioration of the mental state is accompanied by increased excitability or a complete absence of any desires. The swallowing reflex is impaired, and urinary incontinence is common.

At the last stage, the ability to work and communication with the outside world are completely lost. The person develops permanent dementia and is unable to perform basic activities. Therefore, his loved ones must constantly monitor him.

Tests and diagnostics

When examining a patient, psychodiagnostic examinations are used - tests, Schulte tables, MMSE mental status assessment scale, memorizing 10 words, etc.

• An MRI scan of the brain is also used. MRI is more effective at detecting local changes. Characteristic signs of atrophy are widening of the grooves (cortical atrophy) and enlargement of the ventricles. Based on this, the cerebroventricular index (the ratio of the size of the ventricles to the transverse diameter of the brain) is calculated. With this pathology, MRI reveals: an increase in CVI; expansion of subarachnoid spaces; white matter degeneration; decreased tissue density; reduction in shares in size. Based on the study, a quantitative assessment of atrophy is made. In generalized cortical atrophy, sulcal and ventricular widening is assessed in 13 different areas. Certain diseases are characterized by certain changes: with Pick's disease, atrophy is expressed in the frontal and temporal regions. In Huttington's disease , changes in the heads of the caudate nuclei. Parkinson's disease is accompanied by generalized atrophy and atrophy of the substantia nigra, and in Alzheimer's disease - atrophy of the hippocampus.
• The Fazekas scale evaluates quantitative white matter damage. The score on this scale has prognostic value. If the total score is 3, then the patient loses the ability to care for himself and live independently within a year: 0 - no leukoaraiosis; 1— multiple point lesions; 2 - moderate leukoaraiosis, with a tendency to merge; 3 - severe leukoaraiosis (“confluent”).
• Doppler ultrasound. Detects vascular patency.
• Electroencephalography (studies the degree of brain activity).
• Rheoencephalography (studies the state of blood circulation in the brain).
• Angiography (radiography of blood vessels with a contrast agent).
• Blood pressure monitoring and ECG monitoring if indicated.
• Ophthalmoscopy.
• Biochemical blood test.

Diagnostics and differential diagnostics

Cerebral arthrosis is a disease for which diagnosis may require a detailed history of the patient.

The medical history is studied and the patient is interviewed about his living conditions and well-being.

But to make an accurate diagnosis, professionals send the patient to undergo the following diagnostic tests:

• CT head;
• diffuse optical tomography;
• MEG (measurement and visualization of magnetic fields);
• two-photon or single-photon emission tomography;
• MRI of the head.

And also in rare cases, differential diagnosis is possible. Having a patient's medical history, using a specially created computer program, a diagnosis can be made by exclusion. Based on the facts and symptoms that appear in the patient, the computer reduces the range of all possible diseases to one.

If it is impossible to carry out a complete diagnosis, a partial differential diagnosis can be made.

Diet

Mediterranean diet

• Efficiency: from 2 kg in 7 days
• Terms: from 7 days
• Cost of products: 4000-6000 rubles for 7 days

Diet for Parkinson's disease

• Efficacy: therapeutic effect after a month
• Timing: constantly
• Cost of food: 1600-1700 rubles per week

In addition to drug maintenance treatment, it is important for patients with beginning signs of degenerative age-related processes to follow a diet. The Mediterranean diet has been proven to have a neuroprotective effect and prevent the development of cognitive impairment. Its features are a large amount of vegetables, fruits, fish (at least 3 times a week), which should replace meat, whole grain products and vegetable oils rich in ω-3 PUFAs (flaxseed, rapeseed) and ω-9 PUFAs (olive).

For problems with the cardiovascular system, the patient should receive 1 g of ω-3 PUFAs daily from fatty fish (salmon, herring, mackerel), nuts and flax oil. Mackerel has the highest omega-3 content (2299 mg per 100 g), followed by salmon (1966 mg) and herring (1571 mg). Depending on the type of fish, 50-80 g of it contain the daily requirement of 1 g of ω-3 PUFAs, and a handful of walnuts - 2.5 g of omega-3.

Flaxseed oil is a source of alpha-linolenic acid , from which eicosapentaenoic and decosahexaenoic acids are formed in the body. It is useful to consume not only flax oil, but also whole flax seeds, which contain fiber and phytoestrogens . Other sources of omega-3 include broccoli, melon, cauliflower, canola oil, beans, spinach, and Chinese cabbage.

In addition, it is better to replace omega-6 fatty acids (sunflower oil and soybean oil) with omega-9 - oleic acid found in olive oil. High doses of antioxidant vitamins (vitamins C and E) have been proven to be beneficial for the restoration of vascular endothelium. Flavonoids in red wine, red grapes and chocolate improve endothelial function in large arteries.

Degrees of atrophy

Depending on the development of the process, several stages are distinguished:

• Initial without pronounced clinical signs, with mild isolated manifestations of the disease, but with rapid progression to the next stage;
• The second, which is characterized by a rapid deterioration of the condition from imaginary well-being. The patient’s emotional sphere and area of ​​communication change for the worse;
• Third, with a gradual loss of control over one’s own behavior;
• The fourth, which is manifested by the disappearance of awareness in ongoing events;
• The fifth is equal to complete dementia. A person can become dangerous to society.

Prevention

There is no specific prevention, but following generally accepted recommendations for a healthy lifestyle can to some extent prevent or reduce the severity of degenerative changes in old age.

• Full sleep.
• Physical activity. Sufficient activity in old age has a positive effect on brain function and slows down age-related changes. Individuals with high activity exhibit less atrophy—less damage to white matter and greater volume of gray matter.
• Sufficient intellectual activity.
• Maintain a diet rich in antioxidants, vitamins and omega PUFAs. The results support the possibility of effective use of fish oil in reducing cognitive ability in the elderly and in Alzheimer's disease. Often cognitive impairment is associated with a deficiency of folic acid and vitamin B12 .
• Quitting the use of alcohol and drugs.
• Elimination of risk factors (high blood pressure and blood sugar levels, lipid metabolism disorders, anxiety, depression, sleep disturbances).
• Timely treatment of initial cerebrovascular disorders.
• Prevention of head injuries and infections of the nervous system.
• Genetic counseling for people with a family history of Alzheimer's disease .
• To prevent hydrocephalus in children, which causes brain atrophy, it is important to promptly identify and treat infections in pregnant women.

In children

Brain atrophy in newborns is often caused by hydrocephalus. The disorder is expressed by an increase in the amount of cerebrospinal fluid, which protects the brain from various damages. There are quite a few reasons for this condition. Often the disease develops in the womb due to:

• Infections.
• Viruses.
• Disrupted pregnancy.

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

Pathology can be detected by ultrasound examination. After the diagnosis is made, the child is hospitalized, as he requires serious treatment, which consists of 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.

Forecast

The prognosis for cerebral atrophy is unfavorable, since this pathology is not treated, progresses and is associated at first with a decrease in the quality of life, and then with disability. Irreversible changes in the brain lead to a decrease in intelligence to the point of mental retardation. Cerebral atrophy does not always reduce life expectancy, but significantly worsens its quality. Life expectancy with cerebral atrophy depends on the degree of damage and the rate of progression. With rapid progression and involvement of vital centers, life processes may stop.

Life expectancy with multiple system atrophy is significantly reduced as bulbar palsy , a swallowing disorder, progresses rapidly. Dysphagia is complicated by aspiration of food and pneumonia , often leading to death. asphyxia occur .

What is cortical atrophy

The disease is long-term and can develop over several years. Symptoms of the disease gradually become more severe and often lead to dementia.

People over 50 years of age are most susceptible to cortical atrophy, but the disorder can also be congenital due to a genetic predisposition.

Examples of a process in which both hemispheres of the brain are affected are Alzheimer's disease and senile dementia. In this case, complete dementia is observed with a pronounced form of atrophy. Foci of destruction that are small in size often do not affect a person’s mental abilities.

Reasons for development

The causes of cortical atrophy are complex. The following factors influence the formation of senile dementia:

- changes in the blood supply to brain tissue due to a decrease in vascular capacity, which is typical for atherosclerosis;

- poor oxygen saturation of the blood, leading to chronic ischemic phenomena in the nervous tissues;

- genetic predisposition to atrophic phenomena;

- deterioration of the body's regenerative abilities;

- reduction of mental load.

Sometimes atrophic phenomena develop at a more mature age. The causes of such changes may be injuries accompanied by cerebral edema, systematic exposure to toxic substances (alcoholism), tumors or cysts, or previous neurosurgery.

The symptoms of the disease that appear depend on the stage of damage to the cerebral cortex and the extent of the pathological process. There are several stages in the development of brain atrophy:

— asymptomatic stage, during which existing neurology is associated with other diseases (stage 1);

— the appearance of periodic headaches and dizziness (stage 2);

- impairment of thinking and analytical abilities, changes in speech, habits and sometimes handwriting (stage 3);

- at stage 4, there is a violation of fine motor skills of the hands and coordination of movements - the sick person may forget basic skills (using a toothbrush, the purpose of the television remote control);

- inappropriate behavior and inability to adapt to social life (final stage).

Drug treatment of brain pathology associated with atrophy consists of the use of medications, which include:

- drugs that improve blood circulation and brain metabolism (for example, Piracetam, Cerepro, Ceraxon, Cerebrolysin). Taking drugs from this group leads to a significant improvement in a person’s thinking abilities;

- antioxidants that have a stimulating effect on regenerative processes that slow down brain atrophy and stimulate metabolic rate, counteracting oxygen free radicals;

- medications that improve blood microcirculation. The drug Trental is often prescribed, which has a vasodilating effect and increases the lumen of the capillaries.

Sometimes the disease requires symptomatic therapy. For example, if a patient has headaches, non-steroidal anti-inflammatory drugs are prescribed.

Also during the treatment process, you need to monitor the patient’s neuropsychic state. Moderate physical activity and systematic walking in the fresh air are necessary. If the patient's condition can be classified as neurasthenic, the doctor recommends taking mild sedatives.

List of sources

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• Vorobyova O. V. Chronic cerebral ischemia: from pathogenesis to therapy (recommendations for an outpatient neurologist) // RMJ “Medical Review” No. 5, 2021. - P. 26-31.
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Symptoms

Atrophic manifestations will be of a different nature depending on what form of the disease affected the patient, where the focus is localized and how widespread it is. Common clinical signs are:

• Reduced ability to think and analyze;
• Violation in the pace and tone of speech;
• Memory disorder;
• Changes in finger motor skills;
• The appearance of pathological reflexes with convulsions;
• Difficulty in learning new information;
• Reduced vocabulary;
• Emotional imbalance in the form of depression, aggressiveness, resentment, euphoria for no reason;
• Headache with increased fatigue.

All these symptoms eventually lead to the patient’s loss of ability to work.

Treatment

There is no specific therapy aimed at complete recovery. This is due to the fact that the dead part of the brain cannot be restored. The brain will not grow back; it is also impossible for science to transplant it. Modern methods of therapy can only improve the patient’s quality of life and try to prolong it. For this purpose, symptomatic medications are prescribed. The main medications used include:

• Nootropics – “Cerebrolysin”, “Cerepro”, “Ceraxon”, “Actovegin” or “Piracetam”. These medications help normalize blood circulation in the brain and stabilize metabolic processes. This leads to an improvement in the mental activity of patients and a slowdown in the development of other clinical manifestations of the disease;
• Antioxidants - Mexidol, Vitamin C, which reduce hypoxic phenomena in the brain;
• Antiplatelet agents like Aspirin, the purpose of which is to bring blood circulation into balance by improving rheological properties and preventing thrombus formation;
• Sedatives and analgesics to eliminate psychomotor agitation, anxiety, and also to relieve headaches. They use Analgin, Valocordin;
• Antidepressants - Amitriptyline.

In addition to drug therapy, a major role in treatment is played by the daily routine, reasonable dosage of work and rest, physical activity, and food intake. For such patients, a calm psycho-emotional background in a familiar environment, without unnecessary stress, and regular walks in the fresh air are important. They need constant contact with loved ones. Patients should not be abandoned.

Dropping out of society will only accelerate the development of pathology. Communication and, if possible, reading books or newspapers will help people fight atrophy. It is necessary to motivate the patient to achieve an optimistic result. Support his belief in the effectiveness of therapy. This will help in the fight against the disease and also improve the patient’s quality of life.

If brain atrophy has reached its terminal stage, and the disease has invaded deep structures, the patient must be taken to the intensive care unit to support life with the help of special equipment, since dead neurons will not be able to perform their functions.