Mild to moderate cognitive impairment. Cognitive impairment in vascular diseases of the brain: mnestic and cognitive disorders. Pharmacotherapy of MCI syndrome

V.V. Zakharov
Department of Nervous Diseases MMA named after. THEM. Sechenov, Moscow

One of the most common neurological symptoms is cognitive impairment. Since cognitive functions are associated with the integrated activity of the brain as a whole, cognitive failure naturally develops with a wide variety of focal and diffuse brain lesions. Cognitive disorders occur especially often in old age. According to statistics, from 3 to 20% of people over 65 years of age have severe cognitive impairment in the form of dementia. The incidence of milder cognitive disorders in the elderly is even higher and reaches, according to some data, from 40 to 80% depending on age. The current trend towards an increase in life expectancy and, accordingly, an increase in the number of elderly people in the population makes the problem of cognitive impairment extremely relevant for neurologists and doctors of other specialties.

Determination of cognitive functions
Cognitive functions are usually understood as the most complex functions of the brain, with the help of which the process of rational cognition of the world is carried out. Cognitive functions include memory, gnosis, speech, praxis and intelligence.
Memory is the ability of the brain to assimilate, store and reproduce information necessary for current activity. The memory function is associated with the activity of the entire brain as a whole, but the structures of the hippocampal circle are of particular importance for the process of remembering current events. Severe memory impairment for life events is usually referred to as amnesia.
Gnosis is the function of perceiving information, processing it and synthesizing elementary sensory sensations into holistic images. Primary disorders of gnosis (agnosia) develop with pathology of the posterior parts of the cerebral cortex, namely the temporal, parietal and occipital lobes.
Speech is the ability to exchange information through utterances. Speech disorders (aphasia) most often develop with pathology of the frontal or temporo-parietal parts of the brain. In this case, damage to the temporo-parietal regions leads to various kinds of speech understanding disorders, and with pathology of the frontal lobes, the ability to express one’s thoughts through speech is primarily impaired.
Praxis is the ability to acquire, maintain, and use a variety of motor skills. Praxis disorders (apraxia) most often develop with pathology of the frontal or parietal lobes of the brain. In this case, pathology of the frontal lobes leads to a violation of the ability to construct a motor program, and pathology of the parietal lobes leads to improper use of one’s body in the process of a motor act while the movement program is intact.
Intelligence is the ability to compare information, find commonalities and differences, and make judgments and inferences. Intellectual abilities are provided by the integrated activity of the brain as a whole.
Neuropsychological research methods are used to assess cognitive functions. They represent various tests and tests for memorizing and reproducing words and pictures, recognizing images, solving intellectual problems, studying movements, etc. A complete neuropsychological examination allows us to identify the clinical features of cognitive impairment and make a topical diagnosis. However, in everyday clinical practice, it is not always possible to conduct a complete neuropsychological examination. Therefore, in outpatient practice throughout the world, so-called screening neuropsychological scales are widely used, which make it possible to confirm the presence of cognitive disorders in general and evaluate them quantitatively. An example of such a screening scale is the Brief Mental Status Assessment Scale, which is shown in table.

Syndromes of cognitive impairment
Focal brain damage leads to impairment of one or more cognitive functions, which are based on a single pathogenetic mechanism. This kind of cognitive impairment is characteristic of the consequences of a stroke, brain contusion, or develops with a brain tumor. However, in the most common neurological diseases, brain damage is not limited to one focus, but is multifocal or diffuse in nature. In such cases, impairment of several or all cognitive functions develops, and several pathogenetic mechanisms for the formation of impairments can be traced.
Cognitive impairment in multifocal or diffuse brain damage is usually classified according to the severity of the impairment. The most severe type of disorder of this kind is dementia. The diagnosis of dementia is based on the presence of memory impairment and other cognitive impairment (at least one of the following: impairment of praxis, gnosis, speech or intelligence) that is so severe that it directly affects daily life. Conditions for diagnosing dementia are also clear consciousness of the patient and the presence of an established organic brain disease, which is the cause of cognitive impairment.
Dementia is most common in older adults, with Alzheimer's disease (AD) being the most common cause of dementia. AD is a degenerative brain disease associated with the progressive death of acetylcholinergic neurons. This disease usually begins after age 65. The first and main symptom of AD is progressive forgetfulness of life events. Subsequently, disturbances in spatial orientation and speech are added to mnestic disorders. In the advanced stages of asthma, patients’ independence is lost and the need for outside help arises.
In AD, those parts of the brain that are directly related to cognitive processes are selectively affected. In contrast, primary motor and sensory cortical fields remain relatively intact, at least during the stages of mild to moderate dementia, so AD is characterized by selective impairment of cognitive functions. Focal neurological symptoms, such as paresis and paralysis, sensitivity disorders, and impaired coordination of movements, are almost always absent. The presence of focal neurological symptoms in combination with mild or moderate dementia argues against the diagnosis of AD or indicates a combination of this disease with another brain pathology, most often vascular.
Cerebrovascular insufficiency is the second cause of dementia in old age after AD. In this case, the direct cause of brain damage is repeated strokes, chronic cerebral ischemia, or, most often, a combination of repeated acute disorders and chronic cerebral circulatory failure. The clinical picture of vascular dementia differs significantly from AD, while memory impairment for life events is relatively unexpressed, and intellectual disorders come to the forefront of the clinical picture. Patients experience difficulty making generalizations, identifying similarities and differences between concepts, and develop significant slowness of thinking and decreased concentration.
Unlike AD, vascular dementia is almost always characterized by a combination of cognitive impairment and focal neurological symptoms, and the syndrome of dyscirculatory encephalopathy (DE) is formed. The most typical manifestations of DE are pseudobulbar syndrome, hypokinesia, increased muscle tone of the plastic type, asymmetric increase in tendon reflexes, gait disturbance, and pelvic disorders. The absence of these focal neurological disorders makes the diagnosis of vascular dementia highly doubtful.
Neuroimaging – computer or magnetic resonance imaging of the brain – is important in the differential diagnosis of AD and vascular dementia. In AD, pathological changes on neuroimaging may be absent or represent cerebral atrophy, most pronounced in the hippocampal region. In contrast, vascular dementia is characterized by significant changes on neuroimaging in the form of cerebral infarctions and diffuse loss of white matter density (so-called leukoaraiosis).
AD and vascular dementia have common risk factors, such as old age, arterial hypertension and atherosclerosis of cerebral vessels, carriage of the APOE4 gene and some others, so very often AD and cerebrovascular insufficiency coexist. Clinical and morphological comparisons indicate that in almost half of the cases of asthma there are cerebral infarctions and leukoaraiosis. On the other hand, 77% of elderly patients with a lifetime diagnosis of AD show morphological signs of a concomitant neurodegenerative process. In such cases, it is customary to talk about a mixed (vascular-degenerative) etiology of dementia. Many authors suggest that the prevalence of mixed dementia exceeds that of “pure” AD or “pure” vascular dementia.
In addition to AD, vascular and mixed dementia, the causes of severe cognitive impairment can be other degenerative brain diseases, traumatic brain injury, brain tumors, impaired absorption of cerebrospinal fluid from the ventricles (the so-called aresorptive hydrocephalus), neuroinfection, dysmetabolic disorders, etc. The literature mentions several dozen nosological forms that can lead to dementia. However, the prevalence of these diseases is not comparable with the prevalence of AD, vascular and mixed dementia. The last three indicated nosological forms are responsible, according to statistics, for 70-80% of dementia in old age.
Dementia is the most severe cognitive impairment. In the vast majority of cases, dementia develops gradually, with severe cognitive impairment hampered by less severe impairments. In 1997, the American neurologist R. Petersen proposed using the term “mild cognitive impairment” (MCI) to refer to cognitive impairment in the predementia stages of organic brain damage. Mild cognitive impairment (MCI) is a deficiency in one or more cognitive functions that is beyond the normal range for age, but does not limit daily activities, i.e. does not cause dementia. MCI is a clinically defined syndrome. With it, cognitive disorders cause concern for the patient himself and attract the attention of others. The diagnosis of MCI is confirmed by data from neuropsychological research methods, which reveal a more pronounced decline in cognitive functions than is acceptable for age. According to epidemiological data, MCI syndrome occurs in 10-15% of elderly people. The risk of developing dementia in this category of the elderly population significantly exceeds the average risk (10-15% per year compared to 1-2%). Long-term follow-up suggests that within five years, 55-70% of patients with MCI develop dementia. The causes of MCI syndrome mirror those of dementia in old age. The most common cause of MCI is a neurodegenerative process, cerebral vascular insufficiency, or a combination of both.
In our experience, along with dementia and MCI syndrome, it is also advisable to distinguish mild cognitive impairment (MCI), while cognitive disorders are minimally expressed and their objectification requires the use of very sensitive neuropsychological techniques. Most often, MCI manifests itself as decreased concentration and short-term memory impairment. Despite their insignificant severity, these cognitive impairments can cause concern for the patient and reduce the quality of life. In the pathogenesis of MCI in elderly people, age-related changes play an important role. It is known that, on average, according to statistics, a person’s cognitive abilities gradually decrease starting from the age of 20-30. In 1994, the World Psychogeriatric League proposed the use of a special diagnostic position - aging associated cognitive decline (AACD) - to designate mild, predominantly age-related impairment of cognitive functions in older people. However, in practice, it is very difficult to distinguish between natural age-related cognitive decline and cognitive disorders associated with the earliest manifestations of vascular and degenerative brain diseases. Therefore, from our point of view, the term “mild cognitive impairment” is more correct.

Examination of patients with cognitive impairment
violations
Complaints of memory loss or decreased mental performance are grounds for a neuropsychological examination. Moreover, such complaints can come from both the patient himself and his relatives or immediate environment. The latter is a more reliable diagnostic sign, since the patient’s self-assessment of the state of his cognitive functions is not always objective.
In routine clinical practice, neuropsychological testing may be limited to simple screening scales such as the Mini-Mental State Examination. Complicating the neuropsychological study protocol is not always advisable. The use of complex tests, while increasing the sensitivity of the method, leads to a decrease in the specificity of the results obtained, since their performance largely depends on the age and level of education of the patient.
However, in approximately half of patients with active complaints of memory loss, the use of simple screening scales does not confirm the presence of cognitive impairment. The most common cause of subjective complaints of memory loss in the absence of objective confirmation is emotional disorders in the form of increased anxiety or decreased mood. Therefore, all patients with complaints of memory loss should carefully evaluate the emotional sphere. The likelihood of depression is especially high with complaints of memory loss in young or middle-aged people. Another reason for the lack of objective confirmation of cognitive impairment in active memory complaints is the insufficient sensitivity of neuropsychological screening scales. Therefore, in addition to assessment and medicinal correction of the emotional state, in such cases it is advisable to dynamically monitor the patient and repeat clinical and psychological studies at intervals of three to six months.
If there is objective confirmation of cognitive impairment, one should try to establish their cause, i.e., a nosological diagnosis. It should be borne in mind that cognitive disorders are not always a manifestation of a primary brain disease. Not so rarely, dementia or less severe disorders arise as a result of systemic dysmetabolic disorders, which, in turn, are a complication of various endocrine or somatic diseases. Most often, cognitive disorders of a dysmetabolic nature are associated with hypothyroidism, liver or kidney diseases, and vitamin B12 or folic acid deficiency. Therefore, identifying dementia or less severe cognitive impairment requires a comprehensive assessment of the patient’s health status and treatment of concomitant somatic and endocrine diseases.
Optimization of drug therapy is also important. It should be remembered that many drugs, especially psychotropic ones, have a negative effect on memory and other cognitive abilities. The most adverse effects on cognitive function are exerted by anticholinergics, tricyclic antidepressants, antipsychotics and benzodiazepines. These drugs should be avoided if possible, especially in the elderly. Alcohol abuse is also unacceptable.
It is important to examine not only the patient’s somatic status, but also his emotional state. It was already mentioned above that emotional disorders of the anxiety-depressive series can cause subjective cognitive disorders. However, severe depression can also cause objective cognitive impairment and even mimic dementia (so-called pseudodementia). If depression is suspected in an elderly person, it is permissible to prescribe antidepressants ex juvantibus, and antidepressants with minimal anticholinergic effect, for example selective serotonin reuptake inhibitors, should be used.
The presence of cognitive impairment certainly requires examination of the neurological status and computer X-ray or magnetic resonance imaging (MRI) of the brain. In general, nosological diagnosis is based on the characteristics of cognitive disorders, the nature of concomitant focal neurological symptoms and neuroimaging data. Thus, the predominance of memory impairment in the clinical picture, the absence of focal neurological symptoms and hippocampal atrophy on MRI are characteristic of AD. Relative preservation of memory for life events, pronounced neurological symptoms and cerebral infarctions on MRI indicate a vascular etiology of cognitive impairment. The combination of the above clinical signs may indicate mixed (vascular-degenerative) cognitive disorders. Rarer causes of cognitive impairment have specific neuropsychological and neurological features, which in most cases allow a correct diagnosis.

Treatment of cognitive impairment
The choice of therapeutic tactics is determined by the severity of cognitive impairment and its etiology. For mild to moderate dementia associated with AD, cerebrovascular insufficiency, or a mixed vascular-degenerative etiology of dementia, the first choice drugs are acetylcholinesterase inhibitors (galantamine, rivastigmine, donepilzine) and/or memantine. The use of these drugs has an undoubted positive effect on memory and other cognitive functions, promotes normalization of behavior, increases adaptation to everyday life and generally improves the quality of life of patients and their relatives. According to some data, the use of these drugs also helps to reduce the rate of progression of cognitive impairment; however, this issue requires further study.
At the stage of moderate and mild cognitive impairment, the effectiveness of acetylcholinesterase inhibitors and memantine has not been proven to date. Since in MCI and MCI cognitive impairment does not have a significant impact on everyday life, the main goal of treatment for mild cognitive impairment is not so much to improve memory as to prevent the progression of cognitive impairment, i.e., prevention of dementia. Therefore, the first choice drugs are drugs with a neuroprotective effect. This effect is expected in so-called vascular and metabolic drugs.
Vascular drugs can be divided into three main pharmacological groups:
phosphodiesterase inhibitors: aminophylline, pentoxifylline, vinpocetine, ginkgo biloba preparations, etc. The vasodilating effect of these drugs is associated with an increase in the cAMP content in the smooth muscle cells of the vascular wall, which leads to their relaxation and an increase in the lumen of blood vessels. Moreover, these drugs have an effect mainly on the vessels of the microvasculature and do not cause a stealing effect;
calcium channel blockers: cinnarizine, flunarizine, nimodipine, which have a vasodilating effect by reducing the intracellular calcium content in the smooth muscle cells of the vascular wall. According to some data, calcium channel blockers have the most pronounced effect on the vessels of the vertebrobasilar region;
a2-adrenergic receptor blockers: nicergoline. This drug eliminates the vasoconstrictor effect of the mediators of the sympathetic nervous system: adrenaline and norepinephrine.
It is important to note that ischemia and hypoxia are of pathogenetic significance not only in cerebral vascular insufficiency, but also in the neurodegenerative process. Therefore, the use of vascular drugs is justified not only in chronic cerebral ischemia, but also in the initial stages of asthma. Many vascular preparations also have additional metabolic and antioxidant properties (for example, standardized extract of Ginkgo biloba).
GABAergic drugs (piracetam and its derivatives), peptidergic drugs and amino acids (Cerebrolysin, Actovegin, glycine, Semax) and some metabolites (encephabol) have a beneficial effect on neurometabolic processes. Neurometabolic drugs have a nootropic effect, optimizing metabolic processes and increasing the plasticity of brain neurons. Under experimental conditions, it has been repeatedly shown that neurometabolic drugs help increase the survival of neurons under hypoxic conditions or when modeling a neurodegenerative process. Therefore, the use of these drugs at the stage of MCI and MCI is absolutely justified.
A very promising drug with neurometabolic action is Actovegin, which is a highly purified deproteinized hemodialysate, which is obtained by ultrafiltration from the blood of calves. The drug contains low-molecular compounds weighing up to 5000 Daltons, such as biologically active amino acids, peptides, nucleosides and oligosaccharides, as well as a number of valuable microelements, while the biochemical composition of Actovegin is strictly standardized.
Experimental models have shown that the biologically active components of Actovegin have a positive effect on intracellular metabolism. Under the influence of Actovegin, the transmembrane transport of glucose and oxygen increases, which leads to an increase in the survival of cell cultures under various adverse effects. In addition, a very important quality of Actovegin is its ability to activate antioxidant enzymes, primarily superoxide dismutase, and thus protect cells from damage by reactive oxygen species formed under hypoxic conditions.
The positive nootropic effect of the drug was demonstrated in a series of clinical studies using a double-blind method. Thus, according to B. Saletu et al., therapy with Actovegin contributes to a statistically and clinically significant reduction in the severity of mnestic and intellectual disorders in mild cognitive impairment of an age-related nature. The nootropic effect of Actovegin was also confirmed by electrophysiological research methods: during therapy with this drug, optimization of the cognitive evoked potential P300 was recorded. Other researchers also testify to the positive effect of Actovegin in mild and moderate cognitive impairment of vascular and degenerative nature.
According to randomized studies, Actovegin has a beneficial effect on cognitive function not only in patients with mild and moderate impairments, but also in dementia. Thus, in a series of studies it was shown that during therapy with Actovegin there is a positive dynamics of mnestic and other cognitive functions in patients with both AD and vascular dementia.
Actovegin has been successfully used in everyday clinical practice for 35 years. The drug is safe to use and is well tolerated. Side effects are rare and do not pose a threat to life or health. This may include a feeling of heat, dizziness, headache, and gastrointestinal disorders.
Thus, cognitive impairment is one of the most common neurological symptoms, especially in elderly patients. To identify cognitive disorders, it is necessary to use neuropsychological research methods. In everyday clinical practice, these can be simple screening scales, the use and interpretation of which does not require special psychological education or experience. Treatment for cognitive impairment depends on its severity and etiology. The most common causes of cognitive impairment in old age are cerebral vascular insufficiency and neurodegenerative process, while acetylcholinesterase inhibitors and memantine have the greatest effect at the stage of dementia. At the same time, at the stage of mild and moderate cognitive impairment, vascular and metabolic drugs with a neuroprotective effect are more appropriate.

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The degree of their expression lies. Cognitive disorders are divided into mild, moderate and severe.

Mild cognitive impairment

Memory decreases for current events, last names, first names, phone numbers. Professional - does not suffer for a long time.
At first, the changes are not noticeable to others.
With neuropsychologists And scientific research reveals
minor difficulties: slower completion of tasks, impaired concentration.
Cognitive failure is not specific in nature and is predominantly mnestic.
What we call “age-related” changes (in old age).
In people of other age categories, similar symptoms can occur with chronic stress, prolonged physical and mental overload, health problems (arterial hypertension, diabetes, etc.).
In most cases, they are reversible and, with timely, adequate therapy, optimization of lifestyle and work activity, decrease or disappear completely.

Moderate cognitive impairment

Variants of mild cognitive impairment syndrome

With the amnestic variant memory impairment for current events predominates. The problem is progressive and, over time, can become the onset of Alzheimer's disease.

At Multiple cognitive impairment
Several cognitive functions are affected - memory, spatial orientation, intelligence, praxis, etc. This type of impairment is characteristic of frontotemporal dementia.

Impaired cognitive functions with intact memory
This variant usually occurs with a predominance of speech or praxis impairment. It is observed in neurodegenerative diseases - primary progressive aphasia, corticobasal degeneration, dementia with Lewy bodies.

The earlier the syndrome of moderate cognitive impairment is recognized, the more successful the treatment results will be, which will allow you to maintain a decent quality of life for as long as possible.

Severe cognitive impairment

Under the term " mild cognitive impairment» understand impairments of one or more cognitive functions that go beyond the age norm, but do not reach the severity of dementia. “If you have reached old age and do not notice any signs of senile dementia in yourself, then the first sign is already evident” (T. Oizerman). The syndrome of moderate cognitive impairment in most cases is a pathological condition, as a result of which changes at this stage are not limited to age-related involutive processes. In most cases, it is associated with an incipient brain disease (repeats the etiology of dementia).

According to a number of researchers, mild cognitive impairment syndrome is observed in 15-20% of people over 65 years of age. Long-term observations indicate that within 5 years dementia develops in 60-80% of patients with this pathology. In 20-40% of cases, mild cognitive impairment is stable or slowly progressive (i.e., does not develop into dementia).

Currently, there are three main clinical variants of the disease

(R. Peterson, 2001):

Main symptoms mild cognitive impairment are:

Below are modified diagnostic criteria syndrome of mild cognitive impairment (S. Guateir et. al., 2004):

cognitive impairment, according to the patient and/or his immediate family;

The term "mild cognitive impairment" is now included in latest revision of the International Classification of Diseases (ICD-10) as an independent diagnosis:

The prognosis for the presence of mild cognitive impairment syndrome is quite serious. Thus, the risk of death is 1.7 times higher and the risk of Alzheimer's disease is 3.1 times higher. Unfavorable prognostic signs for moderate cognitive impairment are:

According to Y. Stern et al. (1992) for the development of dementia in persons with higher education, more significant organic changes are necessary (proverb: “ It's never too late to learn »).

Severe cognitive impairment – mono- or multifunctional disorders of cognitive functions, which lead to a complete or partial loss of the patient’s independence in the professional, social and/or domestic sphere, causing greater or lesser dependence on outside help in everyday life. Severe cognitive disorders include dementia and severe monofunctional cognitive disorders: severe aphasia, agnosia or apraxia, Korsakoff syndrome. The presence of dementia or other types of severe cognitive impairment indicates significant brain damage, which often develops as a result of a long-term pathological process. The prognosis in most cases is unfavorable, since severe cognitive impairment is most often progressive, less often stationary.

Severe cognitive impairment includes dementia (dementia) of various etiologies. Dementia, by definition, is multifunctional cognitive impairment when there is a marked decline in at least two cognitive abilities. According to the recommendations of the International Classification of Diseases, Tenth Revision (ICD-10), the diagnosis of dementia is valid if the following signs are present:

Memory impairments, which manifest themselves in impaired ability to memorize new material, and in more severe cases, also in difficulty in recalling previously learned information. Violations manifest themselves in both verbal and non-verbal modalities. Memory disorders must be confirmed using neuropsychological research methods.

Impairment of other cognitive functions, such as the ability to make judgments, think (plan, organize), and process information. These impairments must be confirmed using appropriate neuropsychological methods. A necessary condition for the diagnosis of dementia is a decrease in cognitive functions compared to a higher initial intellectual level.

Impaired cognitive functions are determined against the background of preserved consciousness.

Impaired emotional control or motivation or change in social behavior - at least one of the following: emotional lability, irritability, apathy, antisocial behavior.

The listed symptoms are observed for at least 6 months; with shorter observation, the diagnosis may be presumptive.

The ICD-10 diagnostic criteria for dementia have increasingly come under criticism in recent years due to their overreliance on the clinical picture of Alzheimer's disease. Indeed, memory disorders, which are required for the diagnosis of dementia according to ICD-10, are one of the main manifestations of Alzheimer's disease, but may be absent or expressed to a minor extent in some forms of vascular dementia, frontotemporal dementia, and other brain diseases. Therefore, it would be more correct to define dementia as severe impairments in various cognitive areas, which often, but not always, affect the area of ​​memory.

Currently, more than 20 million people worldwide suffer from dementia, and due to the aging population, the number of cases of dementia increases every year, leading to significant economic losses associated with the need for treatment and care for sick people.

Dementia, like non-dementia cognitive impairment, is a polyetiological syndrome that develops with organic damage to the brain of various natures. The frequency of the main causes of dementia is shown in Fig. 5.2

The most common cause of cognitive impairment, accounting for more than half of all cases of dementia, is Alzheimer's disease. About 10-15% of cases of dementia are caused by vascular diseases of the brain, and another 10-20% of cases are caused by their combination with Alzheimer's disease. Dementia can also be caused by other degenerative brain diseases: dementia with Lewy bodies, frontotemporal dementia. Dementia develops with traumatic brain injury, brain tumor, parkinsonism, multiple sclerosis, herpetic encephalitis, epilepsy, encephalopathy due to HIV infection, neurosyphilis and others. Cognitive disorders can occur with depression, taking certain medications (antipsychotics, tranquilizers, hypnotics, anticholinergics and anticonvulsants), alcoholism and other intoxications, metabolic disorders (hypoglycemia, hypothyroidism, vitamin B1 and B12 deficiency, hypoparathyroidism, liver disease).

For a long time, dementia was divided into cortical, subcortical and mixed (cortical-subcortical) . Cortical dementia is thought to be characterized by symptoms of primary cortical involvement, such as amnesia, aphasia, apraxia and agnosia. Cortical dementias include dementia due to Alzheimer's disease, frontotemporal degeneration and posterior cortical atrophy.

“Subcortical” dementia was first described by M. Albert et al. in 1974 in patients with progressive supranuclear palsy. Then, similar features of cognitive disorders were also described in other diseases with predominant damage to the subcortical basal ganglia (Parkinson's disease, Huntington's disease, Wilson-Konovalov disease, etc.), as well as with severe damage to the white matter of the brain (multiple sclerosis, severe leukoaraiosis of vascular etiology). The main clinical characteristics of “subcortical” dementia are slowness of cognitive processes, memory impairment such as insufficient reproduction, impairment of frontal control functions, visuospatial dysgnosis and dyspraxia. In most cases, these cognitive impairments are combined with emotional disorders in the form of depression or apathy.

Mixed (subcortical-cortical) dementia combines features of both types of dementia. A mixed type of disorder is observed in dementia with Lewy bodies, a combination of Alzheimer's disease with cerebrovascular pathology, corticobasal degeneration, and Creutzfeldt-Jakob disease.

In practice, it is very important that 10-15% of dementias are fully or partially reversible. These include dementias that develop as a result of drug intoxication, depression, metabolic disorders or due to somatic disorders and sometimes other reasons.

A cognitive disorder in a person is a special change that occurs in his cognitive area of ​​activity. They are manifested by a decrease in memory, a deterioration in thinking abilities compared to the initial personal level.

Thanks to the cognitive abilities of the brain, a person has the opportunity to understand the world around him and interact with it. Receiving and processing information that is recorded and stored for a long time allows you to subsequently use it effectively to achieve your goals.

Causes of Cognitive Disorder

Cognitive impairment is characterized by either a functional or organic nature. If there is no direct damage to the brain, they speak of functional disorders.

The causes of cognitive impairment are usually associated with overwork, periodic stress, physical and mental strain, and repeated manifestations of negative emotions. Such disorders occur at any age. After eliminating the pathological factor, these disorders are practically leveled out and extremely rarely require drug intervention.

Develops due to brain damage after injury or illness. As a rule, people in old age are susceptible to this. The changes are deeper and more difficult. Correctly selected drug correction can soften and slow down negative processes.

Most often, organic disorders are a consequence of cerebral circulatory insufficiency, decreased brain mass, its involution (atrophy), which in turn develops with hypertension, vascular diseases accompanied by chronic cerebral ischemia, after. Timely diagnosis and indicated therapy for these diseases are the prevention of complications that arise.

Atrophic processes that occur in the brain, and intensify with age, lead to more pronounced impairments of cognitive abilities. This condition is known as Alzheimer's disease and has a progressive course. The degree of deterioration in mental function varies greatly; its decline can occur extremely slowly and patients retain the ability to live independently for quite a long time.

Today it is possible to achieve a stable patient condition thanks to new treatment methods. Such disorders can be caused by abnormalities in the brain, metabolic disorders, internal diseases, excessive alcohol consumption, and poisoning.

Symptoms of cognitive impairment

Symptoms of cognitive impairment are determined by the severity of the process and the location of brain disorders. Most often, several or all functions are affected.

Patients demonstrate poor memory, low mental stamina, cannot clearly express their thoughts, cannot concentrate, have difficulty counting, and are disoriented in unfamiliar areas. There is a loss of criticality towards oneself.

Memory loss is manifested by a progressive impairment of remembering current or nearby events, then memory of ancient events is lost. A decrease in the activity of thinking is expressed in helplessness when it is necessary to analyze information, summarize data, and draw conclusions from them. The inability to concentrate makes it extremely difficult to solve specific problems.

Mild cognitive impairment

Mild cognitive impairment is a disorder of higher brain functions caused by vascular disorders. This is the so-called vascular dementia, which begins with mild changes in the cognitive sphere, especially memory, and can progress to dementia. Clinical symptoms include decreased memory, attention, rapid fatigue, and decreased learning ability.

In this case, there are no atrophic processes in the brain, and such disorders are called cerebrasthenic syndrome, in which patients remain relatively safe. Violations are diagnosed based on the results of clinical and psychological studies. The difference from organic disorders is the absence of emotional, behavioral and productive changes.

Moderate to severe cognitive impairment

If there is deterioration in one or more cognitive processes that is beyond the normal range for a given age, but does not reach the level of dementia, then mild cognitive impairment is said to be present. It occurs in 20% of people over 65 years of age. Over the next 5 years, 60% of them develop dementia. Approximately 20-30% of patients exhibit stable or slowly worsening cognitive decline. If several symptoms occur in a short period of time, the help of a specialist is needed.

Severe forms of cognitive disorders in humans include those in which serious problems arise in professional and social activities, and self-care. To diagnose disorders, a neuropsychological testing method is used, which makes it possible to detect the presence and nature of the severity of cognitive impairment. In the early period of occurrence, such disorders are well corrected with medication and various psychological techniques.

Cognitive impairment in children

Recently, a connection between cognitive impairment in childhood and insufficient intake of vitamins and microelements into the child’s body has been traced. The lack of raw, thermally unprocessed, unrefined foods in the diet of a modern child leads to a deficiency of these substances important for health.

The saturation of the body with vitamin C and B vitamins determines the functions of memory, intensity of thinking, clarity, concentration, learning ability, etc.

These problems occur in almost 20% of children and adolescents. Difficulties in writing and reading, hyperactivity with lack of attention, emotional instability, and behavioral disorders are common.

The causes may also be previous diseases, such as brain hypoxia, birth injuries, intrauterine infections, as well as some metabolic disorders and degenerative mental diseases. Detection of pathology as early as possible contributes to effective prevention of disability in such children.

Treatment of cognitive disorders

Treatment of cognitive disorders is selected individually and is largely determined by the causes that led to cognitive disorders and the degree of their severity. Drugs that inhibit acetylcholinesterase in the brain are widely used.

In addition to drug correction, psychotherapy for such patients is used, aimed at developing the ability to change their behavior and thoughts. The main task is to teach the patient an adaptive response to negative thoughts and self-humiliation.

It is also recommended to train your memory with special exercises, for example, memorizing poems. Gradually increasing the complexity of tasks, constantly assessing ongoing changes in a person’s personality, improving adaptation to stress, and constant support from a psychotherapist give the patient a chance to adapt to the changes taking place.