Criteria for assessing cognitive impairment after a stroke

The deterioration of the neurological state after a stroke is associated with a variety of clinical factors, including hypertension, hyperglycemia, elderly age, hemiplegia, severe stroke, atherothrombotic etiology with large and small vessels, and infarction in the basin of a large vessel. The deterioration of the neurologic 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 sometimes reversible, with the exception of cases when the causes of worsening neurologic states can be easily established (hypoxemia, hypoglycemia, hypotension)

To determine and study the deterioration of the neurological condition, an objective and informative tool is needed, for example, the NIHSS scale is the most widely used neurological evaluation system in clinical trials. Today, the dynamics of NIHSS deterioration indicators and the progression of the process are still disputed. For example, the results of a neurological examination often change in the first days after a stroke; because the patient's insignificant reaction to the environment or small changes in motor functions is most likely not sufficiently indicative of the deterioration of the neurological condition. The advantage of clinical analysis (for example, an increase in the NIHSS score of more than 2 points) is the ability to identify the primary features of the symptoms and manifestations, depending on the primary causes of worsening neurological damage in the early stages, when the intervention is most effective. Today, an increase in the incidence of fatalities and the development of dysfunction in patients whose NIHSS score has increased by more than 2 points has already been demonstrated. Evaluation of clinical features in the development of neurological deficits, presented in the table, can help early detection of the primary etiology of the process.

[1], [2], [3], [4], [5], [6], [7]

Symptoms of stroke depending on the primary causes of worsening of the neurological condition

Frequent symptoms and manifestations of stroke

New stroke

• Emergence of new focal manifestations of neurological deficit
• Loss of consciousness when the focus is located on the opposite side or in the trunk

Progression of a stroke

• Exacerbation of the existing deficit
• Deterioration of the level of consciousness due to swelling

Development of edema

• Depression of the level of consciousness
• Unilateral dilatation of the pupil

Increased intracranial pressure

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

Epileptic fit

• Opposite directional eye deflection
• Focal involuntary movements
• Exacerbation of manifestations of neurological deficit
• Sudden worsening of the level of consciousness
• Breathing disorders
• Changes in hemodynamics are similar to the progression of a stroke

Hemorrhagic transformation

• In the presence of a volume effect - like the development of edema
• If there is an intraventricular stretch - like an increase in intracranial pressure

The deterioration of the neurological state after the primary intracerebral hemorrhage in most cases occurs in the first 24 hours and is accompanied by high mortality (approaching 50%). The spread of a hematoma with a volume effect and an increase in intracranial pressure or hydrocephalus is a frequent provoking factor, except for conditions associated with a new stroke or signs of wedging, given that, based solely on clinical data, the secondary deterioration is almost indistinguishable from the primary etiology of the process.

Interaction between primary and secondary causes of worsening of the neurological condition is possible, for example, when hypoxemia or relative hypotension can lead to failure of the collateral blood supply and subsequent progression of the stroke. It is necessary to monitor the warning signs preceding the deterioration (fever, leukocytosis, hyponatremia, hemodynamic changes, hypo- or hyperglycemia).

Definition of soft cognitive decline syndrome

The definition of soft cognitive decline syndrome according to the definition of the clinical guide to 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 dementia syndrome and with the exclusion of a likely cognitive decline, or cerebral or systemic disease, organ failure, intoxication (including medication), depression or mental retardation. "

The criteria for diagnosing MCI syndrome include:

1. patient complaints of mild memory loss, which are objectively confirmed (usually by family members or colleagues) in combination with signs of mild cognitive decline in memory tests or those cognitive areas that are usually clearly violated in Alzheimer's disease;
2.  signs of cognitive deficiency correspond to Stage 3 on the Global Deterioration Scale (GDS) scale and 0.5 on the Clinical Dementia Rating (CDR) scale;
3. a diagnosis of dementia can not be made;
4. the daily activity of the patient remains safe, although there may be a slight deterioration in complex and instrumental types of daily or professional activity.

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

[8], [9], [10], [11], [12], [13], [14]

Practical examples of assessing cognitive dysfunction

In the structure of the syndrome of mild cognitive decline, a mild degree of deficit manifests itself in more than one of the cognitive spheres:

• the patient may become confused or get lost when traveling in unfamiliar places;
• employees notice that it has become more difficult for him to cope with the most difficult kinds of professional activity;
• relatives notice difficulties in finding words and remembering names;
• patients poorly remember what they read, can sometimes lose or forget where they put valuable things;
• when testing reveals a lack of attention, while actual memory problems can be detected only with sufficiently intensive testing;
• patients often deny the violations, and when they identify insolvency in the performance of tests, they often respond with anxiety symptoms.

Patient testing rules:

• during the examination, especially the elderly with a syndrome of mild cognitive decline, you need to maintain a relaxed relaxing environment, since anxiety and anxiety can significantly worsen test results;
• to assess the possibility of remembering recent events, you need to ask about events that are of interest to the patient, and then clarify their details, the names of participants in these events, etc., ask about the content of the newspaper read in the morning or about the telecasts seen the day before;
• it is necessary to clarify whether the patient previously used household appliances or a computer, whether he controlled the car, cooked meals using complex cooking recipes, and then, with the help of an informant, evaluated the safety of skills and knowledge that the patient had previously successfully mastered;
• be sure to find out whether a patient can plan finances, travel independently, shop, pay bills, orientate in unfamiliar terrain, etc. Patients with soft cognitive decline syndrome are usually able to cope with these activities, but sometimes they do casual careless, but serious in their consequences errors or oversights (for example, lose 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, for them, difficulties in concentrating attention (for example, when performing a serial account "100-7") are typical, difficulties in delaying the reproduction of learned words. The patient manages to coping well with the copying of complex figures, however, in the drawing of the clock, difficulties may arise in arranging the hands in accordance with a given time or in the correct arrangement of the digits on the dial. Patients usually refer well to commonly used objects, but they are difficult in the name of their individual parts or rare objects.

The following neuropsychological (psychometric) tests are often used to objectively confirm memory impairments, for which normative data have been developed: Ray's test for auditory memory, Buschke's test for selective memorization, a subtest for the logical memory of the Wexler memory scale, a test of New York University for semantic memory.

Prototypes of progression of cortical focal disorders - a characteristic of the preclinical stage of Alzheimer's disease

An analysis of the initial structure of the neuropsychological syndrome of impairment of higher mental functions (VFR) in patients with negative dynamics and in patients whose cognitive status remained stable showed significant differences between these groups. In individuals with negative dynamics of cognitive status, a regulatory type of disorders of higher mental functions was observed, ie, the initial syndrome of impairment of higher mental functions was characterized by the predominant signs of a deficit from the programming and control processes that indicated the pathological stigmatization of the frontal structures. Somewhat less often, there was a combined type of disorders of higher mental functions, determined by a combination of violations of deep brain structures responsible for the dynamic provision of activity and involvement in the pathological process of the frontal structures of the brain. In the group of persons without negative cognitive dynamics, the initial neuropsychological syndrome of disorders 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 light spatial disturbances.

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 soft cognitive decline syndrome, based on the use of the adapted Luria technique, can be a valuable tool for estimating prognosis this syndrome and, accordingly, to identify in this cohort of patients with preclinical stage of Alzheimer's disease.

When identifying patients with a possible prodromal stage of Alzheimer's disease, the use of a psychopathological approach (and not just psychometric) can be effective. Evidence of this assumption can serve as evidence of a retrospective psychopathological analysis of preclinical disease in patients with diagnosed Alzheimer's disease. According to the results of the research carried out at the Scientific and Methodological Center for the Study of Alzheimer's Disease and Associated Disorders of the State Scientific Center 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 describe its psychopathological features in various clinical forms of the disease.

In the preclinical stage of Alzheimer's disease with late onset (senile dementia of the Alzheimer's type), along with mild mild disorders, the following psychopathological disorders are clearly revealed: transindividual senile personality rearrangement (or senile-like characterological shift) with the emergence of features of rigidity, egocentrism, stinginess, suspicion or a sharp, sometimes caricature, sharpening of character traits. It is also possible to level out personal characteristics and appearance of aspontaneity; often in future patients with senile type of Alzheimer's disease there is an unusually bright "revival" of memories of the distant past.

Along with initial mild disorders, pre-clinical stages of presenile type of Alzheimer's disease are characterized by mild nominative speech disorders or elements of violations of the constructive and motor component of praxis, as well as psychopathic personality disorders. At the preclinical stage of Alzheimer's disease, these initial symptoms can only be detected episodically in a situation of stress, anxiety, or 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 that can be considered as predictors of progression of cognitive deficits, which in turn increases the likelihood of identifying patients with the prodrome of Alzheimer's disease.

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

• presence of the genotype of apoliprotein e4, which, however, is not constantly detected in all studies;
• signs of atrophy of the hippocampus, detected by MRI;
• the study of the volume of the head of the hippocampus allows to differentiate the control group from patients with MCI: the degeneration process starts from the head of the hippocampus, then the atrophy spreads to the body and tail of the hippocampus when cognitive functions are affected;
• functional imaging - when patients with MCI have a decreased blood supply to the temporo-parietal-hippocampal region, which is considered a prognostic factor, indicative of the progression of degeneration leading to dementia.

[15], [16], [17], [18]

Clinical and neurological correlation

Modern methods of neuroimaging allow to more accurately represent the substrate MCI and, thus, it is more correct to plan the treatment program. In addition to clarifying the nature, extent and location of brain damage associated with the development of stroke, methods of neuroimaging identify additional cerebral changes that increase the risk of developing MCI (mute infarcts, diffuse white matter lesions, cerebral microhemorrhages, cerebral atrophy, etc.).

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

Observation over 2 years for elderly patients who did not have dementia 3 months after the stroke showed that the cognitive decline revealed in them correlated not with the increase in vascular changes, in particular leukoarosis, but with an increase in the severity of the atrophy of the medial parts of the temporal lobes.

The revealed clinical-neuroimaging indicators correlate with the results of pathomorphological studies, according to which the severity of cognitive deficiency in patients with cerebrovascular pathology correlates more with the microvascular pathology (microinfarctions, multiple lacunar infarctions, microcirculation) rather than with territorial infarctions caused by lesions of large cerebral arteries. As well as with cerebral atrophy, which may be a consequence of cerebral vascular injury and specificity eskogo neurodegeneration, such as Alzheimer's disease.

[19], [20], [21]

Criteria for differential diagnosis of cognitive impairment

The results of the tests do not always represent reliable diagnostic significance, therefore, for the differential diagnosis of age-related memory decline (Age Associated Memory Impairment (AAMI), mild cognitive decline and Alzheimer's disease, certain criteria are used.

[22], [23]

Criteria for diagnosing age-related memory decline:

With normal aging, the elderly person himself complains about memory deterioration in comparison with what he was in his youth. Nevertheless, problems in everyday life associated with "bad" memory are usually absent, and when testing memory, patients are clearly helped by hints and repetition.

[24], [25], [26], [27],

Criteria for diagnosing mild cognitive decline in memory:

With mild cognitive decline, not only memory impairments are detected, but also an easy deficit of other cognitive functions. During the examination, the patient is helped by repetition and recording, and the tip gives little benefit. Not only the patient, but also the accompanying person from his immediate circle (relative, friend, co-worker), who notices deterioration in the performance of complex types of daily activities, and sometimes about the presence of signs of anxiety or about the patient's "denial" of existing cognitive disorders, informs about memory disorders. Memory impairment in stroke patients is represented by an increased delay and rapid exhaustion of cognitive processes, a violation of the generalization of concepts, apathy. Leading violations can be slowness of thinking, difficulty switching attention, reducing criticism, lowering the background mood and emotional lability. Primary disorders of higher mental functions (apraxia, agnosia, etc.) can also be observed, which occurs when ischemic foci are localized in the corresponding sections of the cortex of the cerebral hemispheres.

[28], [29], [30], [31], [32], [33]

Criteria for diagnosis of asthma:

In contrast to previous patients, patients with an established diagnosis of Alzheimer's disease even at the stage of initial (mild) dementia show pronounced impairments of memory and other cognitive functions that worsen the daily behavior of the patient, and often also present certain psychopathological and behavioral symptoms.

It should be borne in mind that in addition to the diagnostic criteria presented, neurological status is characterized by:

• central paresis of extremities or reflex changes (revitalization of deep reflexes, positive reflexes of Babinsky, Rossolimo);
• Atactic disorders, which can be sensitive, cerebellar and vestibular;
• apraxia walking due to dysfunction of the frontal lobes and rupture of cortical-subcortical connections, often found in dementia;
• retardation of walking, shortening and unevenness of the step, difficulty in the beginning of movements, instability in bends and an increase in the area of support in violation of the equilibrium of the frontal genesis;
• pseudobulbar syndrome, manifested by reflexes of oral automatism, revival of the mandibular reflex, episodes of violent crying or laughter, slowing of mental processes.

Thus, the diagnosis of post-stroke cognitive impairment is based on clinical, neurological and neuropsychological data, the results of magnetic resonance imaging or computed tomography of the brain. In establishing the vascular nature of cognitive impairments, an important role is played by the history of the disease, the presence of risk factors for cerebro-vascular pathology, the nature of the course of the disease, the temporal relationship of cognitive disorders and cerebral vascular pathology. Cognitive impairment can also occur as a result of an intracerebral hemorrhage, in which the main disease is often the destruction of small arteries, formed against a background of prolonged hypertonic disease or amyloid angiopathy. In addition, post-stroke cognitive impairment is most often caused by repeated (lacunar and non-lacunar) infarcts, many of which are detected only in neuroimaging ("silent" cerebral infarctions), and a combined lesion of white matter of the brain (leukoarose). Multi-infarct dementia (cortical, cortical-subcortical) represents a frequent variant of post-stroke dementia. In addition, in such patients with the development of cognitive impairment, Alzheimer's disease subsequently develops.

[34], [35], [36], [37]

Is a mild cognitive decline seen as a continuation of Alzheimer's disease?

According to data, from 3 to 15% of people with mild cognitive decline go to the stage of mild dementia every year, that is, Alzheimer's disease can be diagnosed (in about 6 years - about 80%). According to the data, for 4 years of observation, the annual conversion of mild cognitive decline in Alzheimer's disease was 12% compared to 1-2% for healthy elderly. Of greatest interest are the findings of a study carried out at New York University, which was distinguished by the rigor of methodological approaches. It has been shown that as the duration of the observation increases, the proportion of people without progressive (before dementia) cognitive decline significantly decreases in the cohort of patients with mild cognitive decline compared to the cohort of cognitively normal elderly people. The results of the research show that after 5 years 42% of the cohort of people with mild cognitive decline - 211 people - were put on the diagnosis of dementia, and only 7% of the cohort of the age norm - 351 people. A small number of patients are diagnosed with vascular dementia or another neurodegenerative disease (Pick's disease, Lewy body dementia, Parkinson's disease or dementia due to normotensive hydrocephalus).

Thus, with the undoubted necessity of isolating the syndrome of mild cognitive decline intermediate between normal aging and dementia, the criteria and methods for identifying it today can not be considered satisfactory for the detection of the preclinical stage of Alzheimer's disease. It should be borne in mind that the method of determining among the elderly with mild cognitive decline of future patients with Alzheimer's disease can be improved by neuropsychological analysis based on the method of prof. AR Luria, and also with the help of 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 enrolled reached the level of mild dementia and was diagnosed with Alzheimer's disease.

General approaches to the treatment of cognitive disorders

Unfortunately, to date, there are no data from large-scale controlled trials that would prove the ability of a particular treatment method to prevent, inhibit progression, or at least alleviate cognitive impairment. Nevertheless, there is no doubt that the key is to prevent further brain damage, especially a second stroke. For this, a set of measures is applied, including, first of all, adequate correction of vascular risk factors. For example, in a number of studies it has been shown that an adequate correction of arterial hypertension in patients who have had a stroke or a transient ischemic attack reduces the risk of developing not only a repeated stroke but also dementia. To prevent recurrent ischemic episodes, antiaggregants or anticoagulants may be used (with a high risk of cardiogenic embolism or coagulopathies). However, it should be borne in mind that the appointment of anticoagulants and high doses of antiaggregants in patients with neurovisualizing signs of cerebral microangiopathy, especially with extensive subcortical leukoarreosis and microhemorrhagia (detected in the 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 aimed at exercising or "shunting" a defective function are used. It is important to correct affective and behavioral disorders, especially depression, accompanying cardiovascular and other diseases (especially heart failure). It is important to remember the need to abolish or minimize the doses of funds potentially worsening cognitive functions, primarily possessing anticholinergic or pronounced sedative effect.

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

1. drugs affecting certain neurotransmitter systems,
2. drugs with neurotrophic action,
3. drugs with neurometabolic action,
4. drugs with vasoactive effect.

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

Ginkgo biloba preparations in the treatment of cognitive disorders

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

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

Vabilon is a plant-derived preparation containing ginkgo biloba extract, which improves cerebral and peripheral blood circulation. Biologically active substances of the extract (flavone glycosides, terpenic lactones) contribute to strengthening and increasing the elasticity of the vascular wall, improve the rheological properties of the blood. The use of the drug leads to improved microcirculation, increases the supply of the brain and peripheral tissues with oxygen and glucose. Normalizes metabolism in cells, prevents aggregation of erythrocytes, inhibits platelet aggregation. It enlarges the small arteries, raises the tone of the veins, regulates blood vessels. Vabilon is taken orally during meals or after eating 1 capsule (80 mg) 3 times a day. With violations of peripheral circulation and microcirculation: 1-2 capsules 3 times a day. At a dizziness, noise in ears, disturbances of a dream: on 1 capsule 2 times a day (in the morning and in the evening). In other cases - 1 capsule 2 times a day. The course of treatment is at least 3 months. It has been proved that vobylon normalizes brain metabolism, has antihypoxic effect on tissues, prevents formation of free radicals and lipid peroxidation of cell membrane lipids, promotes normalization of mediator processes in the central nervous system. The effect on the acetylcholinergic system determines the nootropic, and the catecholaminergic system - antidepressant effect.

In addition, in 2011, the work of Professor Yermekkaliev S.B. (Regional Center for Healthy Lifestyle Development, Kazakhstan) on the application of vobylon in the complex therapy of macro- and microcirculation of blood in the ear was performed in the case of blood supply disorders in the brain, which may affect on hearing.

A three-month study, in which vobylon was used to treat tinnitus and hearing disorders of various types, received results from "good" to "very good" in 23 of 28 subjects, half of whom had noises in their ears. The applied dose of the drug vobilon: 180-300 mg / day. In addition, that noise was lost, hearing improved, including with acute hearing loss, decreased dizziness. It has been proven that the prognosis is favorable if deafness is the result of damage to the head, hearing organs or the result of vascular diseases of recent origin. In the event that deafness or partial loss of hearing arose long ago, the prognosis is not so good, but about half of the patients who received the vobylon noted certain improvements. Such patients, as well as elderly patients suffering from dizziness and constant ringing in the ears, were prescribed vobylon. Hearing improvement was observed in 40% of presbyiac patients, and in those patients for whom treatment was ineffective, irreversible disorders of sensory structures of the inner ear were found. The majority of patients showed significant improvement 10-20 days after the start of ginkgo-therapy. The action of vobylon on cerebral circulation was expressed in the rapid and almost total disappearance of vertigo. The researchers conclude that the vobylon can be used not only for treatment, but also for the prevention of otorhinolaryngological problems.

As a result of the studies, it was found that more than half of stroke patients develop cognitive impairment, which can be associated not only with stroke itself, but also with concomitant vascular or degenerative brain damage. Neuropsychological disorders slow the process of functional recovery after a stroke and can serve as an unfavorable prognostic sign. Early recognition and adequate correction of neuropsychological disorders can improve the efficiency of the rehabilitation process and slow the progression of cognitive impairment.

Prof. NK Murashko, Yu. D. Zalessnaya, VG Lipko. Criteria for assessing cognitive impairment after a stroke // International Medical Journal - №3 - 2012