Criteria for assessing cognitive impairment after stroke

Deterioration of the neurological condition after stroke is associated with many clinical factors, including hypertension, hyperglycemia, advanced age, hemiplegia, severe stroke, atherothrombotic etiology with damage to large and small vessels, and infarction in the basin of a large vessel. Deterioration of the neurological condition is observed in 35% of patients with stroke and is often accompanied by more unfavorable outcomes (new stroke, stroke progression, hemorrhage, edema, increased intracranial pressure (ICP), epileptic seizure) and is sometimes reversible, except in cases where the causes of deterioration of the neurological condition can be easily established (hypoxemia, hypoglycemia, hypotension).

To define and study the deterioration of the neurological condition, an objective and informative tool is needed, such as the NIHSS scale, the most widely used neurological assessment system in clinical trials. Today, the dynamics of deterioration indicators on the NIHSS scale and the development of process progression are still a subject of debate. For example, the results of a neurological examination often change in the first days after a stroke; therefore, a minor patient reaction to the environment or minor changes in motor functions are most likely not sufficiently indicative as criteria for deterioration of the neurological condition. The advantage of clinical analysis (for example, an increase in the NIHSS score by more than 2 points) is the ability to identify the primary Features of symptoms and manifestations depending on the primary causes of deterioration of the neurological condition neurological damage in the early stages, when intervention is still most effective. Today, an increase in the frequency of fatal outcomes and the development of dysfunction in patients whose NIHSS score has increased by more than 2 points has already been proven. The assessment of clinical features during the development of neurological deficit, presented in the table, can help in the early identification of the primary etiology of the process.

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Stroke symptoms depending on the underlying causes of neurological deterioration

Common symptoms and manifestations of stroke

New stroke

• The emergence of new focal manifestations of neurological deficit
• Loss of consciousness when the lesion is localized on the opposite side or in the trunk

Progression of stroke

• Exacerbation of the existing deficit
• Decreased level of consciousness due to edema

Development of edema

• Depression of the level of consciousness
• Unilateral pupil dilation

Increased intracranial pressure

• Depression of the level of consciousness
• Pathological postures
• Respiratory disorders
• Hemodynamic changes

Epileptic seizure

• Opposite deviation of the eyes
• Focal involuntary movements
• Worsening of the manifestation of neurological deficit
• Sudden deterioration in level of consciousness
• Respiratory disorders
• Hemodynamic changes similar to stroke progression

Hemorrhagic transformation

• In the presence of a volumetric effect - similar to the development of edema
• In the presence of intraventricular stretching - similar to increased intracranial pressure

Neurological deterioration after primary intracerebral hemorrhage occurs in most cases within the first 24 hours and is associated with high mortality (approaching 50%). Hematoma dissemination with space-occupying effect and increased intracranial pressure or hydrocephalus is a common precipitating factor, except in conditions associated with new stroke or signs of herniation, given that secondary deterioration is almost indistinguishable from the primary etiology of the process based on clinical data alone.

There may be an interaction between primary and secondary causes of neurological deterioration, where, for example, hypoxemia or relative hypotension may lead to failure of collateral circulation and subsequent progression of stroke. Monitoring for warning signs preceding deterioration (fever, leukocytosis, hyponatremia, hemodynamic changes, hypo- or hyperglycemia) is mandatory.

Definition of mild cognitive decline syndrome

The definition of mild cognitive impairment syndrome according to the definition of the clinical guidelines on cognitive impairment is a syndrome characterized by "...mild signs of memory impairment (MCI) and/or general cognitive decline in the absence of data on the presence of a dementia syndrome and with the exclusion of a probable relationship between cognitive decline and any cerebral or systemic disease, organ failure, intoxication (including drug-induced), depression or mental retardation."

The diagnostic criteria for MCI syndrome include:

1. patient complaints of mild memory loss, confirmed objectively (usually by family members or colleagues) in combination with signs of mild cognitive decline revealed during examination of the patient in tests of memory or those cognitive areas that are usually clearly impaired in Alzheimer's disease (AD);
2. signs of cognitive deficit correspond to stage 3 on the Global Deterioration Scale (GDS) and a score of 0.5 on the Clinical Dementia Rating (CDR) scale;
3. the diagnosis of dementia cannot be made;
4. The patient's daily activities remain intact, although a slight deterioration in complex and instrumental types of daily or professional activities is possible.

It should be taken into account that the GDS scale is structured by 7 degrees of severity of cognitive and functional impairment: 1st - corresponds to the norm; 2nd - normal aging; 3rd - MCI; 4-7th - mild, moderate, moderately severe and severe stages of Alzheimer's disease. Stage 3 on the GDS corresponding to the MCI syndrome is defined by mild cognitive deficit, clinically manifested by mild deterioration in cognitive functions and associated functional impairment, which disrupts the performance of only complex professional or social activities and may be accompanied by anxiety. The severity scale of dementia - CDR is constructed in the same way. The description of the severity of cognitive and functional impairment corresponding to the CDR assessment - 0.5 is similar to the above description of stage 3 on the GDS scale, but is more clearly structured by 6 parameters of cognitive and functional deficit (from memory disorders to self-care).

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Practical examples of cognitive dysfunction assessment

In the structure of the mild cognitive impairment syndrome, a mild degree of deficit is manifested in more than one of the cognitive areas:

• the patient may become confused or lost when traveling in unfamiliar places;
• employees notice that it has become more difficult for him to cope with the most complex types of professional activities;
• relatives notice difficulties in finding words and remembering names;
• patients have trouble remembering what they read and can sometimes lose or forget where they put valuables;
• testing reveals an attention deficit, whereas actual memory impairment can only be detected with sufficiently intensive testing;
• Patients often deny existing disorders, and when failure to perform tests is detected, they often react with anxiety symptoms.

Patient testing rules:

• During the examination, especially for elderly people with mild cognitive decline syndrome, it is necessary to maintain a calm, relaxing environment, since anxiety and worry can significantly worsen the test results;
• to assess the ability to remember recent events, it is necessary to ask about events that are of interest to the patient, and then clarify their details, the names of the participants in these events, etc., ask about the content of the newspaper read in the morning or about the TV programs watched the day before;
• it is necessary to clarify whether the patient has previously used household appliances or a computer, driven a car, prepared dishes according to complex culinary recipes, and then, with the help of an informant, assess the preservation of the skills and knowledge that the patient previously successfully possessed;
• It is essential to find out whether the patient can plan finances, travel independently, make purchases, pay bills, navigate unfamiliar areas, etc. Patients with mild cognitive decline syndrome are usually able to cope with these types of activities, but sometimes make seemingly random, careless, but serious in their consequences, mistakes or oversights (for example, losing documents);
• In psychometric testing, which should be performed in the absence of a relative, such patients can be fully oriented in all types of orientation. However, they typically have difficulty concentrating (for example, when performing serial counting "100-7"), difficulties in delayed reproduction of learned words. The patient can cope well with copying complex figures, but in the clock drawing test, difficulties may be found in arranging the hands in accordance with the specified time or in the correct arrangement of the numbers on the dial. Patients usually name frequently used objects well, but have difficulty naming their individual parts or rarely encountered objects.

The following neuropsychological (psychometric) tests, for which normative data have been developed, are often used to objectively confirm memory impairment: the Rey test for auditory-verbal memory, the Buschke test for selective memorization, the logical memory subtest of the Wechsler Memory Scale, and the New York University test for semantic memory.

Prototypes of progression of cortical focal disorders - characteristics of preclinical stage of Alzheimer's disease

Analysis of the initial structure of the neuropsychological syndrome of impairment of higher mental functions (HMF) in patients with negative dynamics and in patients whose cognitive status remained stable showed the presence of significant differences between these groups. In individuals with negative dynamics of cognitive status, a regulatory type of impairment of higher mental functions was observed, i.e. the initial syndrome of impairment of higher mental functions was characterized by predominant signs of deficit in the processes of programming and control over activity, indicating pathological stigmatization of the frontal structures. Somewhat less frequently, a combined type of impairment of higher mental functions occurred, determined by a combination of impairments of the deep structures of the brain responsible for the dynamic provision of activity and the involvement of the frontal structures of the brain in the pathological process. In the group of individuals without negative cognitive dynamics, the initial neuropsychological syndrome of impairment of higher mental functions was determined either by neurodynamic-type symptoms or by symptoms from the parietal structures of the subdominant hemisphere in the form of mild spatial impairments.

Although these data are still preliminary (due to the relatively small number of observations), it can be assumed that a neuropsychological study of the cognitive status of patients with mild cognitive decline syndrome, based on the use of an adapted method by A. R. Luria, can be a valuable tool for assessing the prognosis of this syndrome and, accordingly, for identifying patients with preclinical stage of Alzheimer's disease in this cohort.

In identifying patients with a possible prodromal stage of Alzheimer's disease, the use of a psychopathological approach (and not just a psychometric one) may be effective. This assumption can be supported by data from a retrospective psychopathological analysis of the preclinical course of the disease in patients diagnosed with Alzheimer's disease. Based on the results of studies conducted at the Scientific and Methodological Center for the Study of Alzheimer's Disease and Associated Disorders of the State Scientific Center for Mental Health of the Russian Academy of Medical Sciences, it was possible to establish not only the duration of the preclinical stage of the course in various variants of Alzheimer's disease, but also to describe its psychopathological features in various clinical forms of the disease.

In the preclinical stage of late-onset Alzheimer's disease (senile dementia of the Alzheimer's type), along with mild memory disorders, the following psychopathological disorders are clearly revealed: transindividual senile personality restructuring (or senile-like characterological shift) with the appearance of previously uncharacteristic features of rigidity, egocentrism, stinginess, conflict and suspiciousness, or a sharp, sometimes caricatured sharpening of characterological features. Leveling of personality traits and the appearance of aspontaneity are also possible; often, future patients with the senile type of Alzheimer's disease experience an unusually vivid "revival" of memories from the distant past.

The preclinical stage of the presenile type of Alzheimer's disease is characterized, along with initial mnestic disorders, by mild nominative speech disorders or elements of disorders of the constructive and motor components of praxis, as well as psychopathic personality disorders. At the preclinical stage of Alzheimer's disease, these initial symptoms can be detected only episodically in a situation of stress, anxiety, or against the background of somatogenic asthenia. It has been proven that a qualified psychopathological study of individuals with mild cognitive impairment can reveal early psychopathological symptoms characteristic of Alzheimer's disease, which can be considered as predictors of the progression of cognitive deficit, which in turn increases the likelihood of identifying patients with the prodrome of Alzheimer's disease.

Diagnostic signs that mild cognitive decline syndrome may be the beginning of Alzheimer's disease:

• the presence of the apolipoprotein e4 genotype, which, however, is not detected consistently and in all studies;
• signs of hippocampal atrophy detected by MRI;
• The study of the volume of the hippocampal head allows us to differentiate representatives of the control group from patients with MCI: the degeneration process begins with the head of the hippocampus, then atrophy spreads to the body and tail of the hippocampus, when cognitive functions are affected;
• Functional imaging - when patients with MCI show decreased blood flow to the temporo-parieto-hippocampal region, which is considered a prognostic factor in favor of progression of degeneration leading to dementia.

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Clinical-Neuroimaging Correlations

Modern neuroimaging methods allow us to more accurately represent the MCI substrate and, thus, plan the treatment program more correctly. In addition to specifying the nature, extent, and localization of brain damage associated with the development of stroke, neuroimaging methods reveal additional cerebral changes that increase the risk of developing MCI (silent infarctions, diffuse white matter damage, cerebral microhemorrhages, cerebral atrophy, etc.).

However, the key factor influencing the risk of developing cognitive impairment, according to most studies, is cerebral atrophy. The association with the development of MCI has been shown both for general cerebral atrophy and for atrophy of the medial temporal lobes, especially the hippocampus.

A 2-year follow-up of elderly patients who did not have dementia 3 months after a stroke showed that the cognitive decline detected in them correlated not with an increase in vascular changes, in particular leukoaraiosis, but with an increase in the severity of atrophy of the medial temporal lobes.

The revealed clinical and neuroimaging indicators correlate with the results of pathomorphological studies, according to which the severity of cognitive deficit in patients with cerebrovascular pathology correlates to a greater extent not with territorial infarctions caused by damage to large cerebral arteries, but with microvascular pathology (microinfarctions, multiple lacunar infarctions, microhemorrhages), as well as with cerebral atrophy, which may be a consequence of vascular damage to the brain and a specific neurodegenerative process, such as Alzheimer's disease.

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Criteria for differential diagnosis of cognitive impairment

Test results do not always provide reliable diagnostic value, so certain criteria are used to differentiate between Age Associated Memory Impairment (AAMI), mild cognitive decline, and Alzheimer's disease.

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Criteria for diagnosing age-related memory decline:

In normal aging, the elderly person himself complains of a worsening of his memory compared to what he had in his youth. However, problems in everyday life associated with "poor" memory are usually absent, and when testing memory, patients are clearly helped by prompts and repetition.

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Diagnostic criteria for mild cognitive impairment:

In mild cognitive decline, not only memory impairment is detected, but also a slight deficit in other cognitive functions. During examination, the patient is helped by repetition and notes, and prompting is of little use. Memory impairment is reported not only by the patient, but also by an accompanying person from his immediate environment (relative, friend, colleague), who notes deterioration in the performance of complex types of daily activities, and sometimes the presence of signs of anxiety or the patient's "denial" of existing cognitive disorders. Memory impairment in patients who have suffered a stroke is represented by an increased slowing down and rapid exhaustion of cognitive processes, a violation of the processes of generalization of concepts, apathy. The leading disorders may be slowness of thinking, difficulty switching attention, decreased criticism, a decrease in mood background and emotional lability. Primary disorders of higher mental functions (apraxia, agnosia, etc.) may also be observed, which occurs when ischemic foci are localized in the corresponding parts of the cerebral cortex.

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Diagnostic criteria for asthma:

Unlike previous patients, patients diagnosed with Alzheimer's disease, even at the stage of initial (mild) dementia, show clearly expressed memory impairment and other cognitive functions that impair the patient's daily behavior, and often also have certain psychopathological and behavioral symptoms.

It should be taken into account that in addition to the presented diagnostic criteria, the neurological status is characterized by:

• central paresis of the limbs or reflex changes (increased deep reflexes, positive Babinski and Rossolimo reflexes);
• ataxic disorders, which can be of sensory, cerebellar and vestibular nature;
• apraxia of gait due to dysfunction of the frontal lobes and disruption of cortical-subcortical connections, often found in dementia;
• slowing of walking, shortening and unevenness of the step, difficulty in starting movements, instability when turning and an increase in the area of support due to a frontal imbalance;
• pseudobulbar syndrome, manifested by reflexes of oral automatism, increased mandibular reflex, episodes of forced crying or laughter, and slowness of mental processes.

Thus, the diagnosis of post-stroke cognitive impairment is based on clinical, neurological and neuropsychological data, the results of magnetic resonance or computed tomography of the brain. In establishing the vascular nature of cognitive impairment, an important role is played by the history of the disease, the presence of risk factors for cerebrovascular pathology, the nature of the disease, the temporal relationship between cognitive disorders and vascular pathology of the brain. Cognitive impairment can also occur as a result of intracerebral hemorrhage, in which the underlying disease is often damage to small arteries, developing against the background of long-term hypertension or amyloid angiopathy. In addition, post-stroke cognitive impairment is most often caused by repeated (lacunar and non-lacunar) infarctions, many of which are detected only by neuroimaging ("silent" cerebral infarctions), and combined damage to the white matter of the brain (leukoaraiosis). Multi-infarct dementia (cortical, cortical-subcortical) is a common variant of post-stroke dementia. In addition, in such patients, with the development of cognitive impairment, Alzheimer's disease subsequently develops.

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Is mild cognitive decline really a prodrome of Alzheimer's disease?

According to the data, from 3 to 15% of people with mild cognitive decline annually move to the stage of mild dementia, i.e. they can be diagnosed with Alzheimer's disease (in 6 years - about 80%). According to the data, over 4 years of observation, the annual conversion of mild cognitive decline to Alzheimer's disease was 12% compared to 1-2% for healthy elderly people. Of greatest interest are the data of a study conducted at New York University, which was distinguished by the rigor of its methodological approaches. It has been proven that as the duration of observation increases, the proportion of people without progressive (to dementia) cognitive decline decreases significantly faster in the cohort of patients with mild cognitive decline compared to the cohort of cognitively normal elderly people. The research results show that after 5 years, 42% of the cohort of people with mild cognitive decline - 211 people, and only 7% of the age-normal cohort - 351 people were diagnosed with dementia. A small number of patients are diagnosed with vascular dementia or another neurodegenerative disease (Pick's disease, dementia with Lewy bodies, Parkinson's disease, or dementia due to normal pressure hydrocephalus).

Thus, with the undoubted need to identify a syndrome of mild cognitive decline, intermediate between normal aging and dementia, the criteria and methods for its identification proposed today cannot be considered satisfactory for identifying the preclinical stage of Alzheimer's disease. It should be taken into account that the method for identifying future patients with Alzheimer's disease among elderly people with mild cognitive decline can be improved by neuropsychological analysis based on the method of prof. A. R. Luria, as well as by psychopathological research. The results of a 4-year prospective neuropsychological study of a cohort of 40 elderly people showed that after 4 years, 25% of the total number of patients included in the study reached the level of mild dementia and were diagnosed with Alzheimer's disease.

General approaches to the treatment of cognitive impairment

Unfortunately, there are no data from large-scale controlled studies to date that would prove the ability of a particular treatment method to prevent, slow down progression, or at least alleviate cognitive impairment. However, there is no doubt that prevention of further brain damage, especially recurrent stroke, is of key importance. To do this, a set of measures is used, including, first of all, adequate correction of vascular risk factors. For example, a number of studies have shown that adequate correction of arterial hypertension in patients who have had a stroke or transient ischemic attack reduces the risk of not only recurrent stroke, but also dementia. Antiplatelet agents or anticoagulants (with a high risk of cardiogenic embolism or coagulopathy) can be used to prevent recurrent ischemic episodes. At the same time, it should be taken into account that the administration of anticoagulants and high doses of antiplatelet agents to patients with neuroimaging signs of cerebral microangiopathy, especially with extensive subcortical leukoaraiosis and microhemorrhages (detected in a special MRI mode - on gradient-echo-T2-weighted images), is associated with a higher risk of developing intracerebral hemorrhages. Active physical rehabilitation of patients can be of great importance.

For the purpose of neuropsychological rehabilitation, techniques are used aimed at exercising or "bypassing" the defective function. Of great importance is the correction of affective and behavioral disorders, especially depression, associated with cardiovascular and other diseases (primarily heart failure). It is important to remember the need to cancel or minimize the doses of drugs that potentially worsen cognitive functions, primarily those with cholinolytic or pronounced sedative effects.

To improve cognitive functions, a wide range of nootropic drugs are used, which can be divided into 4 main groups:

1. drugs that affect certain neurotransmitter systems,
2. drugs with neurotrophic action,
3. drugs with neurometabolic action,
4. drugs with vasoactive action.

A significant problem is that for most drugs used in domestic clinical practice, there are no placebo-controlled trial data that would convincingly confirm their effectiveness. Meanwhile, as the results of controlled trials show, a clinically significant placebo effect can be observed in 30-50% of patients with cognitive impairment, even in patients with severe dementia. Moreover, the positive effect of a drug is more difficult to prove after a stroke, given the tendency for spontaneous improvement of cognitive deficit after a stroke in the early recovery period. In patients with vascular dementia, controlled trials have shown the effectiveness of drugs belonging to the first group and mainly affecting the cholinergic system (cholinesterase inhibitors, such as galantamine or rivastigmine), as well as the glutamatergic system (NMDA-glutamate receptor inhibitor memantine). Placebo-controlled studies have shown the efficacy of cholinesterase inhibitors and memantine in postinsular aphasia.

Ginkgo Biloba Preparations in the Treatment of Cognitive Impairments

One of the promising approaches to the treatment of post-stroke cognitive impairment is the use of the neuroprotective drug ginkgo biloba.

Biological action of ginkgo biloba: antioxidant, improves microcirculation in the brain and other organs, inhibits platelet aggregation factor, etc. This expands not only the range of possibilities of the drug, but also the range of diseases of various etiologies and genesis: strengthening of the nervous system, depression, attention disorders and/or hyperactivity, migraine, asthma, multiple sclerosis, strengthening of the cardiovascular system, atherosclerosis, asthma, diabetes mellitus, improvement of visual functions, macular degeneration of the retina.

Vobilon is a herbal preparation containing ginkgo biloba extract improving cerebral and peripheral circulation. Biologically active substances of the extract (flavonoid glycosides, terpene lactones) help to strengthen and increase the elasticity of the vascular wall, improve the rheological properties of the blood. The use of the preparation improves microcirculation, increases the supply of oxygen and glucose to the brain and peripheral tissues. Normalizes metabolism in cells, prevents erythrocyte aggregation, inhibits platelet aggregation. Dilates small arteries, increases venous tone, regulates blood filling of blood vessels. Vobilon is taken orally during or after meals, 1 capsule (80 mg) 3 times a day. For peripheral circulation and microcirculation disorders: 1-2 capsules 3 times a day. For dizziness, tinnitus, sleep disorders: 1 capsule 2 times a day (morning and evening). In other cases - 1 capsule 2 times a day. The course of treatment is at least 3 months. It has been proven that Vobilon normalizes brain metabolism, has an antihypoxic effect on tissues, prevents the formation of free radicals and lipid peroxidation of cell membranes, and helps normalize mediator processes in the central nervous system. The effect on the acetylcholinergic system causes a nootropic effect, and on the catecholaminergic system - an antidepressant effect.

In addition, in 2011, work was carried out by Professor Ermekkaliyev S. B. (Regional Center for Problems of Forming a Healthy Lifestyle, Kazakhstan) on the use of vobilon in complex therapy of macro- and microcirculation of blood in the ear in case of impaired blood supply to the brain, which can affect hearing.

A three-month study using Vobilon to treat tinnitus and various types of hearing loss showed results ranging from “good” to “very good” in 23 of 28 subjects, half of whom experienced complete tinnitus relief. The dose of Vobilon used was 180-300 mg/day. In addition to eliminating tinnitus, hearing improved, including acute hearing loss, and dizziness decreased. The prognosis was shown to be favorable if deafness is the result of damage to the head, hearing organs, or recent vascular disease. If deafness or partial hearing loss has been present for a long time, the prognosis is not as good, but about half of the patients receiving Vobilon experienced certain improvements. Vobilon was prescribed to such patients, as well as to elderly patients suffering from dizziness and constant ringing in the ears. Improved hearing was observed in 40% of patients with presbycusis, and in those patients for whom the treatment was ineffective, irreversible damage to the sensory structures of the inner ear was found. Most patients showed significant improvement 10-20 days after the start of ginkgotherapy. The effect of Vobilon on cerebral circulation was expressed in the rapid and almost complete disappearance of dizziness. Researchers conclude that Vobilon can be used not only for treatment, but also for the prevention of otolaryngological problems.

The studies showed that more than half of patients who have suffered a stroke develop cognitive impairments, which may be associated not only with the stroke itself, but also with concomitant vascular or degenerative brain damage. Neuropsychological impairments slow down the process of functional recovery after a stroke and may serve as an unfavorable prognostic sign. Early recognition and adequate correction of neuropsychological impairments can increase the effectiveness of the rehabilitation process and slow the progression of cognitive impairments.

Prof. N. K. Murashko, Yu. D. Zalesnaya, V. G. Lipko. Criteria for assessing cognitive impairment after stroke // International Medical Journal - No. 3 - 2012