Moderately expressed atrophic changes in the cerebellum, such as: the cerebellum and signs of its damage. Hereditary cerebellar atrophy symptoms and types

The disease was described in 1907 by the English neuropathologist G. Holmes (1876-1965). On CT, the cerebellar hemispheres are reduced. Degenerative processes are also expressed in the cerebellum, in its white matter and nuclear apparatus. Atrophic changes in the structurally immature brain substance lead to aggravation of the problem and development of the disease into the chronic stage.

In a child, cerebellar atrophy may occur due to injury. The changes are concentrated in the parieto-occipital part. Signs of cortical atrophy appear in Everyday life patient.

With a cerebellar tumor, signs of intracranial hypertension appear early. Disorders of cerebellar function can also be congenital, manifesting themselves, in particular, as Zeeman syndrome: ataxia, delayed speech development, and subsequently cerebellar dysarthria.

Fan-coni-Turner syndrome is also a manifestation of congenital cerebellar hypoplasia. 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.

Carrying out a brain examination for the presence of atrophy

Barraquer-Bordas-Ruiz-Lara syndrome manifests itself as cerebellar disorders that occur due to rapidly progressive cerebellar atrophy. Pathological studies reveal pronounced thinning spinal cord, caused by atrophic processes in its posterior and lateral cords.

During the aging process, the human brain decreases in weight and size, and soft tissue atrophy is observed. Natural processes caused by changes in the body occur differently for everyone. MRI for brain atrophy allows you to determine the extent of damage, as well as identify accompanying illnesses: Pick and Alzheimer's disease, senile dementia.

Although the main cause of atrophy is hereditary and age factor, the disease can appear for other reasons. As a result, the pathology is not exclusively a disease of older people. It can be observed in children and at any other age. Signs of atrophy of the cerebral cortex at the second stage can be determined by the patient’s forgetfulness, causeless irritability, and confusion. A diagnosis of first-degree cortical atrophy means that degenerative processes have just begun.

Types of diagnosed atrophies

Moderate cortical cerebral atrophy - occurs in older people, most often in age period from 50 years and older. Atrophy of the cerebral cortex with a decrease in the caliber of the cortical gyri. Violations are related to hereditary factor and may indicate the development of Parkinson's disease, Alzheimer's disease, etc.

Modern treatment methods for brain atrophy include eliminating the factor in the development of degenerative processes. In multiple sclerosis, it is usually possible to identify, in addition to cerebellar pathology, clinical manifestations of damage to other structures of the central nervous system, primarily the visual and pyramidal systems.

The phenotype shows signs of cerebellar syndrome, primarily cerebellar static and locomotor ataxia, scanned speech, and changes in handwriting. It is a consequence of degeneration of the cerebellar nuclei, red nuclei and their connections, as well as cortical-subcortical structures. In an advanced stage of the disease, epileptic seizures and dementia are possible. Usually this disease is accompanied by a pronounced decrease in memory in combination with polyneuropathy.

In sporadic cases of the disease, manifestations are more common akinetic-rigid syndrome and progressive autonomic failure. At this stage of the disease, manifestations of progressive autonomic failure are added, and signs of akinetic-rigid syndrome appear.

Multiple system atrophy is based on selective degeneration of certain areas of predominantly gray matter of the brain with damage to neurons and glial elements. The causes of degenerative manifestations in brain tissue remain unknown today.

And when the cerebellar hemisphere is damaged, it deviates when walking from a given direction towards the pathological focus. Instability is especially noticeable when turning

Determine the development of diffuse atrophy on early stages quite problematic. Posterior cortical - characterized by plaque-shaped deposits that cause cell death. Manias are observed mental disorders, including sexual ones. Although it doesn't exist effective prevention and therapy of the disease, healthy image life can contribute good health patient. Magnetic resonance imaging, using automated analysis of the results, allows us to identify even atrophies with minimal symptoms.

As it develops, cells in the frontotemporal regions on both sides are destroyed, which leads to loss of reason and disturbances in the patient’s behavior. Destruction nerve tissue observed throughout the brain. Subatrophy of the cerebral hemispheres is a symptom of senile dementia. Small lesions do not in any way affect the normal activity of a person and his mental abilities.

Subatrophic changes in the cerebral hemispheres and cerebellum are clearly distinguishable on MRI. Tomography helps to diagnose final diagnosis and exclude other neurological causes.

Coordination motor disorder caused by cerebellar pathology. Its main manifestations include gait disorder, disproportionality and asynergy of movements, dysdiadochokinesis, and changes in handwriting such as sweeping macrography. Typically, cerebellar ataxia is accompanied by scanned speech, intention tremor, postural tremor of the head and torso, and muscle hypotonia. Diagnosis is carried out using MRI, CT, MSCT, MAG of the brain, Dopplerography, cerebrospinal fluid analysis; if necessary, genetic research. Treatment and prognosis depend on the causative disease that caused the development of cerebellar symptoms.

General information

Chronically progressive cerebellar ataxia is often a consequence of alcoholism, etc. chronic intoxications(including substance abuse and polydrug addiction), slowly growing cerebellar tumors, genetically determined cerebral degenerative and atrophic processes with damage to the cerebellar tissue or its pathways, severe form of Chiari malformation. Among the genetically determined progressive ataxias of the cerebellar type, the most famous are Friedreich's ataxia, non-Friedreich's spinocerebellar ataxia, Pierre-Marie's ataxia, Holmes cerebellar atrophy, and olivopontocerebellar degeneration (OPCD).

Cerebellar ataxia with a paroxysmal course can be hereditary or acquired. Among the causes of the latter are TIA, multiple sclerosis, intermittent obstruction of the cerebrospinal fluid pathways, and transient compression in the foramen magnum.

Symptoms of cerebellar ataxia

Cerebellar ataxia is manifested by sweeping, uncertain, asynergic movements and a characteristic unsteady gait, during which the patient places his legs wide apart for greater stability. When trying to walk along one line, there is a significant swaying to the sides. Ataxic disorders increase with a sharp change in the direction of movement or a rapid start of walking after getting up from a chair. Sweeping movements are a consequence of a violation of their proportionality (dysmetria). It is possible to have both an involuntary stop of a motor act before its goal is achieved (hypometry) and an excessive range of movements (hypermetry). Dysdiadochokinesis is observed - the patient’s inability to quickly perform opposite motor acts (for example, supination and pronation). Due to impaired coordination and dysmetria, a change in handwriting that is pathognomonic for cerebellar ataxia occurs: macrography, unevenness and sweep.

Static ataxia is most obvious when the patient tries to get into the Romberg position. For pathology of the cerebellar hemisphere, a deviation, and even a fall, in the direction of the lesion is typical; with changes in its median structures (the vermis), a fall is possible in any direction or backward. Carrying out a finger-nose test reveals not only missingness, but also the intention tremor accompanying ataxia - trembling of the fingertip, which intensifies as it approaches the nose. Testing the patient in the Romberg position with open and eyes closed, shows that visual control does not particularly affect the test results. This feature cerebellar ataxia helps to differentiate it from sensitive and vestibular ataxia, in which the lack of visual control leads to a significant worsening of coordination problems.

As a rule, cerebellar ataxia is accompanied by nystagmus and dysarthria. Speech has a specific “cerebellar” character: it loses its smoothness, slows down and becomes intermittent, stress is placed on each syllable, making speech resemble a chant. Often, cerebellar ataxia is observed against the background of muscle hypotonia and decreased deep reflexes. When tendon reflexes are evoked, pendulum-like movements of the limb are possible. In some cases, titubation occurs - low-frequency postural tremor of the torso and head.

Diagnosis of cerebellar ataxia

Since cerebellar pathology can have a wide variety of etiologies, specialists from various fields are involved in its diagnosis: traumatologists, neurosurgeons, oncologists, geneticists, endocrinologists. A thorough examination of the neurological status by a neurologist makes it possible to determine not only the cerebellar nature of the ataxia, but also the approximate area of ​​the lesion. Thus, pathology in the cerebellar hemisphere is indicated by hemiataxia, the unilateral nature of coordination disorders and decreased muscle tone; about the pathological process in the cerebellar vermis - the predominance of walking and balance disorders, their combination with cerebellar dysarthria and nystagmus.

In order to exclude vestibular disorders, a vestibular analyzer is examined: stabilography, vestibulometry, electronystagmography. If an infectious lesion of the brain is suspected, a blood test is performed for sterility and PCR tests are performed. Lumbar puncture with examination of the obtained cerebrospinal fluid can reveal signs of hemorrhage, intracranial hypertension, inflammatory or tumor processes.

The main methods for diagnosing diseases underlying cerebellar pathology are neuroimaging methods: CT, MSCT and MRI of the brain. They can detect cerebellar tumors, post-traumatic hematomas, congenital anomalies and degenerative changes in the cerebellum, its prolapse into the foramen magnum and compression when adjacent anatomical structures are displaced. In the diagnosis of ataxia of a vascular nature, MRA and Dopplerography of cerebral vessels are used.

Hereditary cerebellar ataxia is established based on the results of DNA diagnostics and genetic analysis. The risk of having a child with pathology in a family where cases have been reported can also be calculated. of this disease.

Treatment of cerebellar ataxia

Treatment of the causative disease is fundamental. If cerebellar ataxia has an infectious-inflammatory genesis, it is necessary to prescribe an antibacterial or antiviral therapy. If the cause lies in vascular disorders, then measures are taken to normalize blood circulation or stop cerebral bleeding. For this purpose, angioprotectors, thrombolytics, antiplatelet agents, vasodilators, and anticoagulants are used in accordance with indications. For ataxia of toxic origin, detoxification is performed: intensive infusion therapy in combination with the prescription of diuretics; V severe cases- hemosorption.

Ataxia is not yet hereditary radical treatment. Carried out mainly metabolic therapy: vitamins B12, B6 and B1, ATP, meldonium, ginko biloba preparations, piracetam, etc. To improve metabolism in skeletal muscles, increase its tone and strength, patients are recommended massage.

Tumors of the cerebellum and posterior cranial fossa often require surgical treatment. Removal of the tumor should be as radical as possible. If the malignant nature of the tumor is established, a course of chemotherapy or radiotherapy treatment is additionally prescribed. For cerebellar ataxia caused by occlusion of the cerebrospinal fluid pathways and hydrocephalus, shunt operations are used.

Prognosis and prevention

The prognosis depends entirely on the cause of cerebellar ataxia. Acute and subacute ataxia caused by vascular disorders, intoxication, inflammatory processes, with timely elimination of the causative factor (vascular occlusion, toxic effects, infection) and adequate treatment may completely regress or partially persist as residual effects. Chronically progressive hereditary ataxias are characterized by an increasing aggravation of symptoms, leading to disability of the patient. The most unfavorable prognosis is for ataxia associated with tumor processes.

The prevention of injuries, the development of vascular disorders (atherosclerosis, hypertension) and infection is of a preventive nature; compensation of endocrine and metabolic disorders; genetic counseling when planning pregnancy; timely treatment of pathology of the cerebrospinal fluid system, chronic cerebral ischemia, Chiari syndrome, processes of the posterior cranial fossa.

Cerebellar atrophy is a degenerative disease of the small brain that progresses over time. Develops with vascular disorders, some metabolic disorders, infections, tumors of the nervous system. Atrophic processes lead to speech and paralysis.

Causes of cerebellar atrophy

A decrease in the mass of the cerebellum (cerebellum), its degradation occurs against the background of certain disorders in the body. The reasons for the development of pathology may be failures in circulatory system, metabolism, neuroinfections. To this neurological pathology give the following states:

1. Vascular atherosclerosis.
2. Hemorrhagic or.
3. Meningitis, encephalitis in the brain stem area.
4. Tumor diseases of the trunk.
5. Cysts and scars after hemorrhages.
6. Vitamin E deficiency.
7. Angiopathy in diabetes.
8. Heat stress (shock).
9. Intoxication with alcohol, drugs, toxic substances.

Circulatory disorders

Atrophic changes are often caused by impaired blood flow. At the same time, food nerve cells the cerebellum is limited, they die, which causes various disorders. Leads to circulatory disturbances in the cerebral hemispheres atherosclerotic lesion vessels.

The lumen of the arteries becomes narrow, the wall loses its elasticity. Such vessels are easily clogged with blood clots, since atherosclerosis also causes damage to the internal lining, the endothelium. When the blood circulation of the cerebellum is blocked, its cells undergo death, which leads to a decrease in the functional tissue of the small brain. Often this process occurs in elderly and middle-aged people with metabolic diseases.

Blood flow to the brain stem is also switched off during strokes. Hemorrhagic stroke is usually caused by high pressure, which is not able to withstand the fragile blood vessels of the brain in an elderly person. Ischemic hemorrhage usually occurs due to thrombosis.

Vascular damage in diabetes can also be the cause of atrophic processes in the nervous tissue of the cerebellum. The pathology is called diabetic capillaropathy. Thrombosis and closure of the lumen of blood vessels, which occurs with systemic vasculitis, can cause atrophic processes. This is possible with systemic lupus erythematosus, antiphospholipid syndrome.

Inflammatory processes, intoxication and organic pathologies

Encephalitis in the area close to the cerebellum leads to damage to Purkinje cells, myelin fibers of the small brain. Inflammation occurs against the background of septic conditions and neuroinfections.

Tumor formations, cysts and scars in the cerebellum area can cause atrophy of its cells and the occurrence of cerebellar disorders. The development of atrophic processes is also possible with heavy metal poisoning.

Chronic alcoholism can provoke pathological change nerve cells of the cerebellum. Some medications (Phenytoin, lithium preparations) disrupt the function of the cerebellum, promoting its atrophy.

Symptoms

The main manifestations of atrophy are motor ones, since the cerebellum coordinates motor acts. Symptoms of atrophy include:

1. Nystagmus (involuntary movements of the eyeballs).
2. Tremor at rest or movement.
3. Speech impairment (rhythmic chanting speech).
4. Decreased muscle tone.
5. Gait change ().
6. Dysdiadochokinesis.
7. Dysmetria (problems with determining the distance between an object and oneself).
8. Paralysis - hemiplegia.
9. Ophthalmoplegia.
10. Swallowing disorder.

Dysdiadochokinesis is a coordination disorder in which the patient is unable to perform rapid alternating movements. Dysmetria is a loss of control over the patient's range of motion.

Dysarthria manifests itself in unclear pronunciation of words, incorrect construction of phrases, and chanted speech. Speech is rhythmic, the stress in words is not semantic, but corresponds to the rhythm.

Intention tremor is a trembling of the limbs when approaching a target. Postural tremor is involuntary vibration of body parts when trying to maintain a posture. Decreased muscle tone is associated with atrophy of nerve fibers. Ataxia manifests itself in unsteadiness of gait. Ophthalmoplegia is paralysis of the eyeballs.

Headaches accompanied by nausea and vomiting, decreased reflexes, and involuntary emptying of the bladder and bowels are also possible. Mental disorders that arise against the background of the cause that led to atrophic changes are also often observed.

With atrophic changes in the cerebellum, other brain structures are often affected: the inferior olives, pontine nuclei. The development of infectious processes against the background of impaired blood supply is possible.

Treatment of cerebellar atrophy

For gait disorders, paralysis of the eyeballs or their involuntary movements If you have unsteady gait, you should consult a neurologist. The study of reflexes will reveal the localization of damage to the central nervous system. To detect organic pathologies, magnetic resonance imaging of the head is necessary. Cheaper methods are ultrasound and computed tomography.

With cerebellar atrophy, the consequences are irreversible and cannot be treated. Therapy is aimed only at correcting them and preventing progression. Patients lose the ability to self-care and need help and disability benefits.

If the disease is caused by circulatory or metabolic disorders, then therapy should be aimed at correcting them. The presence of tumors requires treatment with cytostatics and other chemotherapy drugs. In some cases it is shown radiation therapy or surgery.

For cerebellar atrophy, treatment includes rehabilitation of the patient, use psychotropic drugs to correct tremor: Clonazepam and Carbamazepine. To reduce the intensity of tremor, limb weights are used.

Conclusion

With a disease such as cerebellar atrophy, the prognosis is unfavorable, since cell death has already occurred. However, it is necessary to prevent further degradation of the nerve tissue. Disability is provided.

A short overview of what hereditary cerebellar atrophy. Hereditary cerebellar atrophies include various clinical forms, such as congenital atrophy cerebellum, Friedreich's disease, hereditary spastic ataxia, Pierre Marie's disease, late form of cerebellar atrophy of Ma-ri-Foy-Alajouanin, Holmes' cerebro-olivary atrophy, Menzel's olivopontocerebellar atrophy, Magado-Joseph disease, Hunt's myoclonic cerebellar dyssynergia, Marinescu-Segrain syndrome, atactic form of myoclonic epilepsy in adolescents.

What are hereditary cerebellar atrophies?

Hereditary cerebellar atrophy with isolated lesions of the cerebellum or with spinal conduction systems involved is benign. And diseases with damage to afferent and efferent pathways cerebellar hemispheres with concomitant pathology of the brain stem are characterized by a severe clinical picture and a rapidly progressive course.

A molecular genetic study of hereditary cerebellar atrophies revealed a pathological gene that was mapped to chromosome loci 6q, 12q, 14q, 16q, 3p, 6p, 12p.

According to these data, six types of dominant hereditary cerebellar atrophies are distinguished, as well as dento-rubropa-lidolyuns atrophy and Machado-Joseph disease.

A mutation of the same gene (locus 14) may indicate both Machado-Joseph disease and type 3 spinocerebellar atrophy. In this regard, various authors use in diagnosis both clinical signs and ethnic, pathological and cerebellar signs, and others; the onset of the disease, the course of the disease, and the distribution features of cerebellar disorders are also important.

Possible pathognomonic signs of hereditary cerebellar atrophies: ptosis, ophthalmoparesis, strabismus, exophthalmos, fasciculations of the muscles of the face and tongue, dysarthria, pseudo bulbar syndrome, bulbar syndrome, spasticity, muscle hypotonia, amyotrophy, rigidity, muscular dystonia, pyramidal syndrome, myoclonin, coreoathetosis, epileptic seizures, polymorphic hyperkinesis, loss of deep reflexes, impaired deep sensitivity, decreased vision, polyneuropathy, lens opacification, dementia, pelvic disorders, endocrine disorders, progressive cardiomyopathy, multiple skeletal deformities.

Hereditary cerebellar atrophy symptoms

Machago-Joseph disease was first described by R. Rosenberg using the example of a Portuguese family who had clinical manifestations of strionigral and spinocerebellar degeneration. Later similar cases have been described in the USA, India, Japan, and Scandinavia. The gene for this disease is mapped to locus 14q (the gene for spinocerebellar atrophy is also mapped there). The onset of the disease is from 30 years of age and older. R. Rosenberg and K. Konner identified three clinical types of this disease:

Type I – lateral muscular atrophic sclerosis with parkinsonism and dystonia;

Type II – cerebellar ataxia;

Type III – signs of lateral muscular atrophic sclerosis with ataxia.

Hereditary cerebellar atrophies types

The disease is characterized by fasciculations of facial muscles and tongue without their atrophy (first type); progressive exophthalmic ophthalmoparesis (bulging eyes syndrome); sensorimotor polyneuropathy (types 1 and 3); pyramidal disorders (first and second types); extrapyramidal syndrome; parkinsonism (first type); amyotrophies (first and third types). The disease occurs as a result of damage to the dentate nucleus, superior and middle cerebellar peduncles, nuclei cranial nerves, substantia nigra, Clark's columns, spinocerebellar tracts. Malignant form.

Friedreich's disease- hereditary cerebellar atrophy, begins during puberty. The disease is characterized by early disappearance of deep reflexes, impaired deep sensitivity, multiple skeletal anomalies, and progressive cardiomyopathy.

The form of the disease is benign. It occurs due to damage to the posterior cords of the spinal cord, dorsal roots, cells of Clark's columns, spinocerebellar tracts, and Purkinje cells.

Olivopontocerebellar atrophy begins between the ages of 30 and older. It is characterized by the presence of dystonic syndrome, pelvic disorders, pyramidal and extrapyramidal syndrome, deletion. Magnetic resonance imaging reveals demyelination of the transverse fibers of the pons. With this disease, damage occurs to the nuclei and transverse fibers of the pons, cerebellar pores, dentate nuclei and superior cerebellar peduncle, and conductors of the spinal cord. Malignant form.

Holmes Cerebro-Olivary Atrophy manifested by the isolation of manifestations of the atactic syndrome, dissociation of the ataxic manifestations “along the axis” - a minimum of manifestations in the arms, severe disorders in the legs. We can say that this is a “pure” form of cerebellar ataxia. Damage occurs to the cerebellar cortex, inferior olives, and Purkinje cells. Benign form.

Pierre Marie's disease debuts between the ages of 20 and 40. It is characterized by bilateral partial ptosis, pyramidal disorders, and a benign course. The posterior cords, pyramidal tracts of the spinal cord, spinocerebellar tracts, and dentate nuclei are affected.

Cerebellar atrophy of Marie-Foy-Alajouanine occurs between the ages of 30 and older. It is characterized as late cortical cerebellar atrophy. The cerebellar vermis is predominantly affected. Benign form.

Hunt's myoclonic cerebellar dissipation appears before 10 years of life. Characterized by the presence of myoclonus and a malignant course. It occurs as a result of damage to the dentate nuclei, superior cerebellar peduncle, and red nucleus.

Myoclonus also occurs in Hucukar disease, Lafora body disease, and myoclonic epilepsy of adolescents.

Diseases with isolated damage to the cerebellum and (or) involving spinal conduction systems are characterized by a benign course.

If there is damage to the afferent and efferent systems of the cerebellar hemispheres in combination with damage to the brain stem, then the disease is characterized by a malignant course.

Brain atrophy is a process of gradual death of cerebral cells and destruction of interneuron 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 brain atrophy

Epidemiology

Most of the reported cases occur in older people, 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, genetic mutation, availability 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 brain volume and mass with age. However, one should not think that the disease concerns exclusively old age. There is brain atrophy in children, 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. Environmental negative factors are considered background influences that can accelerate the process of this pathology.

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

From the group of acquired predisposing factors, it is necessary to highlight chronic intoxications, especially Negative influence alcohol, infectious processes in the brain, both acute and chronic, traumatic brain injury 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 focal nature of the process at the onset of the disease, the entire encephalon is gradually affected with the development of dementia and dementia.

At the moment, it is not possible to pathogenetically describe 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 the manifestations of atrophy involving certain structures.

Symptoms of brain atrophy

As a result of age-related changes in the brain, like other organs, processes of reverse development occur. This is due to the acceleration of destruction and slowdown of cell regeneration. Thus, the symptoms of brain atrophy gradually increase in severity depending on the affected area.

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

Then there is a decrease vocabulary, which ultimately leads to the presence of primitive expressions. Thinking loses its productivity, the ability to criticize behavior and reflect on actions is lost. In relation to motor activity, motor skills deteriorate, which leads to changes in handwriting and deterioration of 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 to avoid unforeseen emergencies. Problems with orientation in space occur due to memory impairment.

Such a person cannot adequately assess the attitude of the people around him and is often suggestible. Subsequently, with the progression of the pathological process, complete moral and physical degradation of the individual occurs due to the onset of insanity.

Brain atrophy 1st degree

Degenerative changes in the brain become more active with age, but when exposed to concomitant additional factors Thought disorders can develop much faster. Depending on the activity of the process, its severity and severity clinical manifestations It is customary to distinguish several degrees of the disease.

Brain atrophy of the 1st degree is observed on initial stage diseases when there is a minimal level of pathological abnormalities in the functioning of the encephalon. In addition, one should take into account where the disease is initially localized - in the cortex or subcortical structures. The first manifestations of atrophy, which can be seen from the outside, depend on this.

At the initial stage, atrophy may have absolutely no clinical symptoms. A person may experience anxiety due to the presence of other concomitant pathology 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 consults a doctor at this stage, then grade 1 brain atrophy is caused by medicines slows its progression and symptoms may be absent. With age, it is necessary to adjust treatment therapy by selecting other drugs and dosages. With their help, you can slow down the growth and appearance of new clinical manifestations.

Brain atrophy 2nd degree

Clinical picture and presence defined by symptom depends on the degree of brain damage, in particular on damaged structures. Stage 2 pathology usually already has some manifestations, thanks to which one can suspect the presence of pathological processes.

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

Thus, in addition to periodic dizziness, there is a deterioration in thinking abilities and the ability to conduct analysis. In addition, the level of critical thinking decreases and self-esteem of actions and speech function is lost. In the future, changes in speech and handwriting most often 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 stop “obeying” a person, which leads to the inability to perform 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 deteriorate. There is a loss of skills in using 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 a loss of independence in thinking and movements.

Forms

Atrophy of the frontal lobes of the brain

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

Pick's disease is characterized by destructive damage mainly to 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 brain is manifested by personality changes in the form of deterioration in thinking and the process of remembering. In addition, from the onset of the disease, a decrease can be observed intellectual abilities. There is a degradation of a person as an individual, which is expressed in angular character, secrecy, alienation from the people around him.

Motor activity and phrases become pretentious and can be repeated as if in a pattern. Due to a decrease in vocabulary, there is frequent repetition of the same information during a conversation or after some time. Speech becomes primitive using 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 a person’s personal qualities, they suffer a little later.

Cerebellar atrophy

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

Atrophy of the cerebellum of the brain can be manifested by a person’s loss of independent self-care abilities. Damage to the cerebellum is characterized by disorders of combined functioning skeletal muscles, coordination of movements and maintaining balance.

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

Atrophy of the cerebellum of the brain can be characterized by an increase in dizziness, increased frequency of headaches, nausea, vomiting, drowsiness and impaired hearing function. Rising intracranial pressure, ophthalmoplegia may occur due to paralysis of the cranial nerves that are responsible for the innervation of the eye, areflexia, enuresis and nystagmus, when the pupil performs involuntary rhythmic vibrations.

Atrophy of the brain substance

The destructive process in neurons can occur during physiological process due to age-related changes after 60 years or pathological - as a result of any disease. Atrophy of the brain substance is characterized by the gradual destruction of 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 medicine, slowing down the destructive processes. Regarding pathological atrophy due to negative impact harmful factors or another disease, then it is necessary to influence the cause of atrophy in order to stop or slow down the destruction of neurons.

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

Thus, with the destruction of the neurons of the knee, hemiplegia appears, which is paralysis of the muscles of half 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 body areas (hemianesthesia, hemianopsia and hemiataxia). Damage to the substance can also cause complete loss of sensation on one side of the body.

Mental disorders are possible in the form of lack of recognition of objects, 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 brain atrophy

Due to age-related changes or as a result of a disease that affects the encephalon, a pathological process such as cortical atrophy of the brain may develop. Most often the frontal parts are affected, but it is possible that the destruction may spread to other areas and structures of the gray matter.

The disease begins unnoticed and slowly begins to progress, with an increase in symptoms observed after a few years. With age and untreated, 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 in older early age due to congenital genesis of development due to genetic predisposition.

Damage to both hemispheres by cortical atrophy occurs in Alzheimer's disease or in other words, senile dementia. A severe form of the disease leads to complete dementia, while small destructive lesions do not have a significant negative impact on a person’s mental capabilities.

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 prevalence of the destructive process should be taken into account.

Multiple system brain atrophy

Degenerative processes underlie the development of Shy-Drager syndrome (multiple system atrophy). As a result of the destruction of neurons in certain areas of the gray matter, motor activity disorders occur, and control over vegetative functions, for example, blood pressure or the process of urination.

The symptoms of the disease are so diverse that to begin with, some combinations of manifestations can be identified. Thus, the pathological process is expressed autonomic dysfunctions, in the form of parkinsonian syndrome with the development of hypertension with tremors and slower motor activity, as well as in the form of ataxia - unsteady walking and coordination problems.

The initial stage of the disease is manifested by 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.

At further development Multisystem brain atrophy is acquiring new symptoms that can be divided into 3 groups. The first includes 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 cerebellar dysfunction, which is characterized by difficulty in coordination, loss of the feeling of prostration, dizziness and fainting.

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

Diffuse cerebral atrophy

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

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, which is not always clear to the people around him.

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

Diffuse cerebral atrophy is initially characterized by the appearance of symptoms similar to cerebellar cortical atrophy, when gait is disrupted and spatial awareness is lost. In the future, the manifestations become more numerous, as the disease gradually covers new areas of the gray matter.

Atrophy of the left hemisphere of the brain

Each area of ​​the encephalon is responsible for a specific function, so when it is damaged, a person loses the ability to do anything, either physically or mentally.

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

Atrophy of the left hemisphere of the brain leads to a lack of perception of the complete image; surrounding objects are perceived separately. At the same time, the person’s ability to read is impaired, and his 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 consistently process information, which leads to an inability to remember it. Speech addressed to such a person is perceived separately in sentences and even words, as a result of which there is no adequate reaction to the address.

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

Mixed brain atrophy

Cerebral disorders can occur as a result of age-related changes, under the influence of a genetic factor or concomitant 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 nervous tissue occurs mostly in women over 55 years of age. As a result of atrophy, dementia develops, which significantly worsens the quality of life. With age, the volume and weight of the brain decrease due to the gradual destruction of neurons.

The pathological process can be observed in childhood, When we're talking about about the genetic route of transmission of the disease. In addition, there are concomitant pathologies and environmental factors, such as radiation.

Mixed brain atrophy covers the functional areas of the brain responsible for control of motor and mental activity, planning, analysis, and criticism of one’s behavior and thoughts.

The initial stage of the disease is characterized by the appearance of lethargy, apathy and decreased 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 quantitative and qualitative composition of the vocabulary, the ability of productive thinking, self-criticism and comprehension of behavior are lost, and motor skills deteriorate, which leads to a change in handwriting. Next, the person ceases to recognize objects familiar to him and ultimately insanity sets in, when there is practically degradation of the personality.

Atrophy of the brain parenchyma

The causes of damage to the parenchyma 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 supply nutrients. As a result, cells decrease in size due to compaction of the cytoplasm, nucleus and destruction of cytoplasmic structures.

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

The course of atrophy steadily leads to personality degradation and ends in death. With the help of medications, you can try to slow down the development of the pathological process and support the functioning of other organs and systems. Also used symptomatic therapy to alleviate the human condition.

Spinal cord atrophy

Reflexively, the spinal cord can carry out motor and autonomic reflexes. Motor nerve cells innervate the body's muscular system, 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 there is a center for pupil dilation and sympathetic centers for innervation of the heart. Sacral section has parasympathetic centers responsible for the functionality of the urinary and reproductive systems.

Atrophy of the spinal cord, depending on the location of the destruction, can manifest itself as a violation of sensitivity - with the destruction of neurons in the dorsal roots, or motor activity - in the anterior roots. As a result of gradual damage to individual segments of the spinal cord, disturbances in the functionality of the organ that is innervated at this level occur.

Thus, the disappearance of the knee reflex occurs due to the destruction of neurons at the level of the 2-3 lumbar segment, plantar - 5 lumbar, and a violation of contraction abdominal muscles observed with atrophy of nerve cells of 8-12 thoracic segments. The destruction of neurons at level 3-4 is especially dangerous 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 brain. Under the influence of alcohol, a change in metabolism occurs in neurons, resulting in the formation of alcohol dependence.

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

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

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

In addition, vascular sclerosis is noted with deposition around brown pigment and hemosiderin, as a consequence of hemorrhages, and the presence of cysts in the choroid plexuses. Possible hemorrhages in the encephalon trunk, ischemic changes and neuronal degeneration.

It is worth highlighting the Makiyafawa-Binyami syndrome, which occurs as a result frequent use alcohol in large quantities. Morphologically, central necrosis is revealed corpus callosum, its swelling, as well as demyelination and hemorrhage.

Brain atrophy in children

Brain atrophy is not common in children, but this does not mean that it cannot develop in the presence of any neurological pathology. Neurologists must take this fact into account and prevent the development of this pathology in the early stages.

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

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

As the disease progresses, children become nervous, irritable, and conflicts with peers occur, which leads to the child’s seclusion. Further, depending on the activity of the pathological process, cognitive and physical impairments may be added. Treatment is aimed at slowing 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 amount cerebrospinal fluid, thanks to which the encephalon is protected from damage.

There are quite a few reasons for the development of dropsy. It can form during pregnancy, when the growth and development of the fetus occurs, and is diagnosed using ultrasound. In addition, the cause may be various disruptions in the formation and development of the nervous system or intrauterine infections in the form of herpes or cytomegaly.

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 occurrence of meningitis.

Such a baby should be placed in the intensive care unit, as it needs the supervision of neurologists and resuscitators. There is no effective treatment yet, so gradually this pathology leads to serious violations functioning of organs and systems due to their defective development.

Diagnosis of brain atrophy

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

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

In case of age-related changes, the treatment of brain atrophy consists of using medicines, providing full care behind a person, eliminating irritating factors and protecting 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 carry out a course of medication to maintain the functioning of the encephalon and eliminate the symptoms of the disease.

WITH therapeutic purpose Antidepressants and 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 has not yet been developed in our time, since it is very difficult to combat the destruction of neurons. The only way slow down the pathological process - this is the application vascular drugs that improve cerebral circulation (Cavinton), nootropics (Ceraxon) and metabolic drugs. It is recommended to use group B as vitamin therapy to maintain the structure of nerve fibers.

Of course, with the help of medications you can 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 does not have pathogenetic therapy due to the fact that it is extremely difficult to combat genetic, age-related and other causative factors. When exposed to 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.

Treatment of spinal cord atrophy is mostly based on the attitude of the people around them, since it is impossible to stop the pathological process and ultimately the person may remain disabled. A good attitude, care and a familiar environment are the best things a relative can do.

As for drug therapy, the treatment of spinal cord atrophy involves 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, prevention of brain atrophy can only consist of following some recommendations, with the help of which you can delay the onset of this pathology in the case of age-related genesis or slightly suspend it in other cases.

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

In addition, prevention of brain atrophy includes compliance with active image life, proper nutrition And good rest. With age, atrophic processes can be observed in all organs, in particular in the gray matter. A common 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 endocrine system, metabolism that contribute to obesity.

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

Forecast

Depending on the area of ​​the brain that is most affected by destruction, the prognosis and speed of development of the pathological process should be considered. For example, with Pick's disease, there is destruction of neurons in the frontal and temporal regions, as a result of which personality changes first appear (thinking and memory deteriorate).

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

As for Alzheimer's disease, memory impairment is most pronounced here, but personal qualities They do not suffer much even at 2nd degree of severity. This is due mostly to breaks in interneuron connections rather 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 is important to know!

Skin atrophy occurs due to disruption 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, delicately folded, hair loss and telangiectasia are often observed.