Brain atrophy, grade 1 cortical cerebral atrophy

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.

Parkinson's disease

This is an atrophic disease of the brain in old and senile age, manifested by extrapyramidal and mental disorders, including dementia.

Occurs with a frequency of 0.08 to 0.2%. 11% of patients show symptoms of dementia. Men get sick more often. The disease begins between the ages of 45 and 75 years, more often at 50–65 years. The main symptoms of the disease are tremor, muscle rigidity, hypokinesia, and paralysis. Obligatory disorders also include permanent and paroxysmal autonomic disorders, as well as personality changes in the form of psychopathization. Half of the patients experience depression, including suicidal tendencies. Querulant tendencies, low-grade delirium, and, in later stages of the disease, hallucinosis, visual or tactile, and states of confusion (delirium) may occur. Visceral hallucinosis is very characteristic. In 15–25% of patients, signs of cognitive deficit are detected, and in elderly patients, in addition, defects in memory, praxis and optical-spatial activity are detected. Pictures of dementia resemble those of Alzheimer's disease. Prospective studies have shown that there is a positive correlation between the ilateral presentation of motor disorders and the risk of developing cognitive deficits.

Predisposition to the disease is transmitted in an autosomal dominant manner with 25% penetrance. The main role in the genesis of symptoms is given to dopaminergic dysfunction of the brain, especially neurons of the substantia nigra. Other brain systems, including cortical structures, may also be involved in the disease process.

The leading place in the complex treatment of the disease is occupied by therapy with L-DOPA and drugs containing it (Madopar, Sinemet, Nakom). These drugs are usually combined with the prescription of anticholinergic drugs (midantan, akineton, parkopan, cyclodol, etc.). There is evidence of positive results from the administration of bromocriptine, parlodel, selegiline, Yumex, and cognitive, which increase dopamine levels in the brain. If psychotic disorders occur, it is recommended to prescribe small doses of antipsychotics while simultaneously reducing the doses of antiparkinsonian drugs and detoxification. The prognosis of the disease is determined by the severity of neurological disorders and its progression.

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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.

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.

Alzheimer's disease

This is a progressive disease with increasing impairment of memory, thinking, intelligence, speech, praxis and recognition, ultimately leading to dementia.
Data on the prevalence of the disease are conflicting. According to some reports, it is 4–5% among people over 60 years of age. The main clinical forms of the disease are Alzheimer's disease itself (with onset mainly in presenile age) and senile dementia of the Alzheimer's type (with onset mainly in old age). An atypical form of the disease with a predominance of frontal lobe atrophy and Alzheimer's type dementia within Down syndrome are also distinguished. Here is a description of the main forms of the disease. 1. Alzheimer's disease . In approximately 80% of cases, it begins at the age of 45–65 years, less often - at the age of about 40 or after 65 years. The duration of the disease is on average 8–10 years, possibly protracted (more than 20 years) and catastrophic (from 2 to 4 years). There are three stages of the disease.

Read about diagnosing and treating Alzheimer's disease

The initial stage includes the stage of “doubtful” dementia and the stage of “mild” dementia. The first stage is manifested by mild disturbances in memory, thinking, speech, praxis, and personality, which are noticeable mainly to the patients themselves and which they manage to hide or compensate for for some time. At the stage of mild dementia, impairments become more serious. Memory for current events decreases, chronological and spatial types of memory suffer.

Violations of various thinking operations are revealed. Disorders of speech, praxis, recognition, and psychopathic personality changes are detected. The severity of the disorders is such that patients can no longer cope independently with professional responsibilities and other types of social activities, such as shopping, paying bills, receiving guests, writing texts, etc.

Patients cope with self-care, although they need outside control and encouragement. Affective and delusional disorders are often observed at this stage. These are subdepressions, sometimes chronic and combined with anxiety, hysteriform and hypochondriacal manifestations; episodic or protracted delusional ideas of damage, theft, less often - ideas of relationship, persecution or jealousy. Some patients show increased exhaustion and headaches; the duration of the initial stage ranges from 4–8 to 15–20 years. At the same time, in some patients, memory impairments predominate, while in another, larger group, focal impairments (aphasia, etc.) prevail.

At the stage of moderate dementia, impairments in the cognitive sphere and higher cortical functions reach a degree where patients can no longer cope with professional and social responsibilities. They need help even with everyday life and self-care. Neurological disorders appear, such as muscle stiffness, akinesia, hyperkinesis, and seizures. A critical attitude towards the disease nevertheless remains. Along with deficient ones, productive disorders are sometimes observed: episodes of hallucinatory confusion, a state of psychomotor agitation, often not associated with a deterioration in the somatic condition. The aphato-apracto-agnostic syndrome (three A syndrome) characteristic of this stage is finally formed, the weakening of memory takes on the character of progressive amnesia. Confabulation and ecmnesia often do not occur.

The stage of severe dementia is characterized by the breakdown of memory, thinking and intelligence, as well as higher cortical functions. Patients need help even with basic self-care. Basically, only in Alzheimer's disease are such profound disturbances, to the point of insanity, observed, as well as fetal position, contractures, multiple violent motor phenomena, violent laughter and crying, and epileptic seizures. At the same time, there are pronounced somatic changes: weight loss, extreme decrepitness, bulimia, endocrine disorders.

2. Senile dementia of the Alzheimer's type. In approximately 80% of cases, it begins between the ages of 65 and 85 years. The duration of the disease ranges from 4 to 15 years or more. In the initial stage of the disease, significant memory impairment for current events develops, often with a revival of memories of the distant past. Thinking operations suffer, as well as intelligence (creativity, planning, forecasting, etc.). Personality changes are characteristic: egocentrism, narrowing of interests, emotional impoverishment, conflict, opposition and suggestibility. Moral decline and disinhibition of drives are also observed.

The suspicion inherent in patients later develops into a tendency to develop delusions. However, half of the patients experience psychotic episodes with low-level delusions. Subdepressive states are also observed, especially gloomy depression. In the second stage of the disease, memory impairment takes on the character of progressive amnesia. There may be scanty confabulations, as well as states of amnestic disorientation with a “shift of the situation into the past.” At the stage of moderate dementia, disorders of higher cortical functions also become clear. At the stage of severe dementia, a complete breakdown of mnestic-intellectual functions is observed, and serious neurological disorders are also detected.

The etiology of Alzheimer's disease has not been established. The role of genetic factors in the development of familial forms of the disease can apparently be considered proven. However, this role remains unclear in sporadic forms, which account for about 90% of all cases of the disease. Aging is essential.

The leading place in the treatment of patients is occupied by replacement therapy aimed at overcoming neurotransmitter deficiency. To compensate for cholinergic deficiency, tacrine, amiridine, exelon, memantine, Aricept, and reminyl may be recommended. To eliminate the deficiency of other neurotransmitter systems, other drugs are recommended, in particular Yumex and Citalopram. To increase the survival of neurons, nootropics are prescribed, especially Cerebrolysin, as well as vasoactive drugs, in particular sermion or nicergoline. Anti-inflammatory treatment such as indomethacin may be helpful. Therapy for psychotic disorders is carried out with the help of antidepressants, antipsychotics, and tranquilizers. The prognosis of the disease is unfavorable.

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.

The mechanism of brain damage under stress

During stress, cortisol is released from the adrenal glands. Cortisol (also known as hydrocortisone, 17-hydroxycorticosterone, or compound F) is a biologically active hormone produced by the adrenal cortex. These paired endocrine glands, adjacent to the kidneys and projecting at the level of the 6th–7th thoracic vertebrae, produce cortisol with the assistance of adrenocorticotropic hormone (ACTH). In turn, the signal for the production of ACTH comes from the hypothalamus, the control center for neuroendocrine activity located in the brain.

Elevated cortisol levels directly shape pathological processes in the brain.

FRONTAL LOBE

First of all, the frontal lobes, which are responsible for short-term memory, attention, control of emotions, planning, and decision-making, are affected by cortisol.

As a result, under stress, attention is scattered, we cannot make decisions, have difficulty restraining emotions, and are unable to remember where we just put the keys.

Children whose parents yell at them, shame them, intimidate them, ignore them, call them names, and even worse, beat them, grow up in constant stress and this affects the frontal lobes of the brain. Even if children are simply constantly controlled in everything and deprived of independence, their frontal lobes become smaller, stop working actively and may, in principle, not develop to normal sizes. This means that children’s academic performance will be low, they will not be able to make the right decisions, control emotions, motivate themselves to study, and will be lazy, slack and susceptible to the influence of bad companies.

For many authoritarian parents, this becomes a revelation: what they try to develop in children through dominant upbringing, they, on the contrary, destroy, namely, independence, responsibility, discipline, motivation to study, control of emotions.

Adults who have problems with responsibility, planning, and self-control, who are lazy, and who are easily irritable and anxious are more likely to have experienced abuse. In childhood, their frontal lobes were considerably reduced by loving and caring parents, who, of course, wanted only the best for their children.

Hippocampus

With chronic stress, the hippocampus and amygdala, part of the brain's limbic system located in the subcortex, also begin to shrink in volume.

The hippocampus stimulates the growth of new neurons in the brain, new neural networks, and takes part in the formation of long-term memory. When the hippocampus is damaged, amnesia, an inability to remember, can occur, although old memories may still be strong. Adults experiencing stress sometimes cannot remember what they ate for breakfast, but they remember in detail what they took in literature in school and can quote poetry for hours.

Children who experience domestic violence become unable to remember new material in school because their hippocampus has shrunk. That's why they get bad marks for unlearned lessons. They simply have nothing to teach, the hippocampus would have to survive on its own, what kind of neurogenesis is there, what new connections are there! Parents who yell at their children for their inability to learn their lessons, calling them stupid and lazy, shrink their hippocampus even more with each scream.

AMYGDALA (AMYGDALA)

The Amygdala is a repository of emotional memory, here is our happiness and our joy, but here are also all our triggers, buttons that others press with all their might. Triggers are stimuli that evoke unpleasant memories. When a trigger occurs, we react very quickly and sometimes painfully. Look how small the amygdala is - just a tiny ball at the end of the hippocampus, but it causes so many problems. She has enormous power and sometimes she just goes wild.

The amygdala is designed for survival and responds to triggers without involving the cerebral cortex. It's just that when we see something that once scared us in the past, the amygdala believes that it is a threat to our life and triggers the sympathetic nervous system without any reasoning, and we instantly feel fear or anger, "flee or defend." Amygdala, in essence, is not bad, it wants to save us. But her reaction can be so strong that she turns into a terrorist and takes over her entire brain; no smart arguments help. From the point of view of evolution, this is correct; in the Stone Age, we had to run away from predatory animals or fight neighboring enemies without delay, simply automatically, in order to escape death. Now there are no wild animals or enemies, but we react like ancient people.

With chronic stress, the amygdala decreases in size, with the same increased levels of cortisol. And it itself is small, but here it shrinks even more. As a result, what does this lead to? We get irritated very easily and quickly fall into panic or depression. People with a reduced amygdala are often incapable of empathy and compassion, which, combined with aggressiveness, is the basis for antisocial personality development. Sociopaths are, as a rule, people who have experienced violence, that is, their amygdala has shrunk to a minimum. They quickly become aggressive and are not able to sympathize, therefore they are predisposed to criminal acts. No remorse, no regret, no shame, no conscience. Although there are also congenital anomalies of the amygdala.

Since the frontal lobes, which are responsible for controlling emotions, also shrink during stress, emotional regulation becomes even more difficult. There is no one to tame the obstinate amygdala.

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 .

Atrophy of the frontal lobes of the brain

Develops against the background of Alzheimer's and Pick's disease. With Pick's disease, patients begin to think worse, and their intellectual abilities decrease. Patients become secretive and lead an isolated lifestyle.

When talking with patients, it is noticeable that their speech becomes one-word and their vocabulary decreases.

Cerebellar lesion

With the development of atrophy of this area of the brain, there is a lack of coordination and a decrease in muscle tone. Patients cannot care for themselves.

Note! A person’s limbs move chaotically, lose their smooth movement in space, and trembling of the fingers appears. The patient's handwriting, conversation and movement become much slower

Patients complain of attacks of nausea and vomiting, drowsiness, a sharp decrease in hearing levels, and urinary incontinence. Upon examination, the specialist determines the presence of involuntary fluctuations in the eyes and the absence of some physiological reflexes.

Gray matter atrophy

Such a process of atrophy may have physiological or pathological causes of development. The physiological factor is old age and the changes that occur as the body ages.

Pathological causes of the death of white matter cells in the brain are diseases that cause the following symptoms:

paralysis of one half of the body;
loss or sharp decrease in sensitivity in a certain area of the body or half of it;
the patient does not recognize objects or people;
violation of the swallowing process;
the occurrence of pathological reflexes.

Diffuse atrophy

Occurs against the background of the following factors:

hereditary predisposition;
infectious diseases;
mechanical damage;
poisoning, effects of toxic substances;
bad environmental situation.

Important! Brain activity sharply decreases, the patient is unable to think sensibly and evaluate his actions. Progression of the condition leads to a decrease in the activity of thinking processes

Mixed atrophy

It most often develops in females after 60 years of age. The result is the development of dementia, which reduces the patient’s quality of life. Brain volume, size and number of healthy cells decrease sharply over the years. Mixed type atrophy is represented by all possible symptoms of brain damage (depending on the extent of the pathology).

Alcohol-related brain damage

The brain is the most sensitive to the toxic effects of ethanol and its derivatives. Alcoholic drinks cause disruption of connections between neurons, leading to a decrease in healthy cells and tissues. Atrophy of alcoholic origin begins with delirium tremens and encephalopathy and can be fatal. The following pathologies may develop:

vascular sclerosis;
cysts in vascular plexuses;
hemorrhages;
disturbance of blood supply.

How does brain atrophy manifest?

The dysfunction of the brain depends on what disease caused the development of the pathology. Here are the main syndromes and symptoms:

Frontal lobe syndrome:
chronic fatigue, apathy;
psycho-emotional instability;
rudeness, impulsiveness;
the emergence of primitive humor.
Psychoorganic syndrome:
decreased mental abilities;
emotional disturbances;
lack of ability to learn new things;
decrease in vocabulary for communication.
Dementia:
pathology of abstract thinking;
change in personal qualities;
impairment of speech, various types of perception (visual, tactile, auditory), motor coordination

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.

Huntington's chorea

This is a hereditary neurodegenerative disease in the middle and second half of life with a predominant lesion of the striatal system of the brain and less severe damage to other subcortical nuclei and the neocortex. The main manifestations of the disease are decreased intelligence, psychotic phenomena and choreic hyperkinesis.

Due to the fact that the latter sometimes does not develop even in the later stages, the process is also referred to as “Huntington’s disease”.

The prevalence of the disease reaches 4–8 people per 100 thousand population. Among patients in psychiatric hospitals it is 1%. The peak incidence rate occurs between 35 and 50 years of age. The disease lasts from 1 to 25 years.

In approximately half of the cases, the disease develops “due to a nervous defect” (Davidenkov, 1932) in the form of a personality disorder, mental underdevelopment and motor “moronism” (clumsiness, poor handwriting, etc.). The disease does not have a single development pattern. Choreic dementia is characterized by damage to the most complex forms of intellectual activity and uneven mental performance. Intellectual deficits are believed to be based on gross disturbances of attention and spasmodic loss of direction in the movement of thoughts. As intellectual impairments develop, they move closer to dementia.

Psychotic phenomena are recorded in 60% of patients. In Alzheimer's disease they occur in 43.5%, and in Pick's disease - in 11% of patients (Sternberg, 1967). In the early stages of Huntington's disease, predominantly psychogenic disorders are observed, including depression with apathy, hypochondria, or dysphoria. Paranoid psychoses with delusions of jealousy, persecution, and poisoning are relatively common. Later, paraphrenic states with delusions of grandeur, hallucinatory and hallucinatory-paranoid psychoses may develop. The most common hallucinations are tactile, visceral and fragmentary verbal. Choreic hyperkinesis is usually slow, low-amplitude, separated by large intervals; It is also typical that they include torsion and athetoid components and occur against a background of mild muscle hypotonia. Muscle strength decreases, eyelid ptosis and dysarthria occur.

There are abortive forms of Huntington's disease: a) neurological, with a predominance of akineto-hypertensive syndrome; usually begins early, b) with typical hyperkinesis and minimally expressed mental disorders, c) with minimal hyperkinetic and severe mental disorders, d) stationary forms, in which, despite extensive symptoms, the disease lasts for decades, so that patients die from intercurrent diseases. Most patients die in a state of mental insanity; in the terminal stage of the disease, hyperkinesis usually decreases or stops.

It has been established that predisposition to the disease is inherited in an autosomal dominant manner and usually leads to atrophy of the striatum, and to a lesser extent, the cortex. Men get sick more often. Huntington described the disease in two brothers. In 12 families descended from them, 100 cases of the disease were described.

When treating patients, drugs that block dopamine receptors (phenothiazine derivatives, butyrophenones) or reduce the content of dopamine in tissues (reserpine, methyldopa) are used. Psychotic disorders are an indication for the use of aminazine, tizercin, propazine or teralen, and other antipsychotics. The results of therapy are usually disappointing. The prognosis of the disease is generally unfavorable.

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.

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.

Pick's disease

This is a systemic degenerative disease with onset in presenile age, leading to personality and adaptation disorders, and subsequently to total dementia, most often of the frontal and frontotemporal type.
Pick's disease accounts for 0.4 to 2% of all cases of dementia in old age. The prevalence of the disease in people over 60 years of age is about 0.1%. Women get sick slightly more often than men (in a ratio of 1.7:1). The disease begins between the ages of 50 and 70 years. The average duration of the disease is six years.

The disease usually begins gradually and progresses quite quickly. The initial stage of the disease is manifested primarily by personality changes. If the pole of the frontal lobe suffers, then apathy and spontaneity predominate. When the orbital cortex is damaged, a pseudoparalytic syndrome develops with euphoria, disinhibition and impaired abstract thinking; memory does not change significantly. When the temporal lobes are damaged, stereotypies of speech, behavior and movement come to the fore. Other variants of the onset of the disease are much less common: a) asthenia and asthenodepressive symptoms, b) aphasia phenomena, c) psychotic disorders with delusions of persecution, jealousy, harm, d) memory loss, due to which there is a similarity with Alzheimer's disease.

In the middle stage of the disease, against the background of disturbances in the most complex forms of mental activity (planning, forecasting, understanding the meaning of life situations, flexibility, criticality, creativity), focal cortical disorders are also detected. Speech impairments usually predominate. This is dynamic, amnestic or sensory aphasia. Echolalia and standing speech patterns are characteristic. Agraphia, alexia, acalculia, and apraxia are relatively less pronounced. There are attacks of muscle relaxation without complete loss of consciousness, amyostatic syndrome, extrapyramidal hyperkinesis, and rarely spastic hemiparesis. The appearance of epileptic seizures most likely indicates Alzheimer's disease. The initial state is similar in its manifestations to the symptoms of the terminal stage of Alzheimer's disease.

The etiology and pathogenesis of the disease have not been sufficiently studied. Treatment is similar to that for Alzheimer's disease. Relatively early-onset personality and behavioral disorders usually require hospitalization.

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 .

List of sources

Lokshina A. B., Zakharov V. V. Mild and moderate cognitive impairment in dyscirculatory encephalopathy. //Neurologist. magazine – 2006. – T.11, appendix.1. – P.57 – 64.
Vorobyova O. V. Chronic cerebral ischemia: from pathogenesis to therapy (recommendations for an outpatient neurologist) // RMJ “Medical Review” No. 5, 2021. - P. 26-31.
Golubev V.L., Vein A.M. Neurological syndromes: a guide for doctors. 6th ed. – M.: MEDpress-inform, 2021. – 736 p.
Ekusheva E.V. Clinical portraits of “typical” patients in neurologist practice. Consilium Medicum. 2019; 21(9): 131-135.
Odinak M.M., Voznyuk I.A. Neurometabolic therapy for pathologies of the nervous system. Emergency medicine. 2013; 3(50): 72-77.