INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE
ISSN: 2692-5206, Impact Factor: 12,23
American Academic publishers, volume 05, issue 04,2025
Journal:
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page 979
COGNITIVE DISORDERS AFTER A STROKE
Atakhonova D.A.
Assistant of the Department of Neurology, ASMI,
Madjidova Ya.N.
Doctor of Medical Sciences, Professor, Head of the Department of Neurology, Pediatric
Neurology and Medical Genetics, Tashkent Pediatric Medical Institute,
Bustanov O.Ya.
Candidate of Medical Sciences, Associate Professor, Head of the Department of Neurology
Andijan State Medical Institute
Introduction.
As medical care for stroke patients improves and mortality decreases, the
proportion of patients with cognitive disorders will increase. An important factor contributing
to the increase in the number of this category of patients is the change in The demographic
situation in the world is an increase in the number of elderly and senile people. In elderly
people, even a small ischemic or hemorrhagic stroke can worsen the existing slight decrease
in cognitive functions associated with age-related changes, chronic cerebral circulatory
insufficiency, hidden by the current neurodegenerative process. At the same time, cognitive
decline worsens the quality of life of patients, leads to impaired social activity and disability.
Key words
: cognitive impairment, ischemic stroke, vascular pathology, memory impairment,
dementia.
Vascular cognitive impairment ranks 3rd in prevalence after dementia in the disease
Alzheimer's disease (AD) and mixed dementia. 6 months after a stroke, moderate cognitive
impairment (MCI) is diagnosed in 45-80% of patients, dementia in 10-15% [2, 3]. After 5
years, dementia develops in 20-25% of patients. The risk of developing dementia after stroke
in patients over 60 years of age in the first 3 months is 9 times higher than in the control
group [4]. The average life expectancy of patients with vascular dementia is about 5 years,
which is less than the life expectancy of patients with asthma [5]. Dementia significantly
increases the risk of recurrent stroke and death from cardiovascular diseases [6].
The development of post-stroke cognitive disorders can be discussed if there is a clear
temporal link between stroke and cognitive decline. functions. Usually, post-stroke cognitive
impairments develop in the first 3 months after a stroke (early post-stroke cognitive decline),
but no later than 12 months (late cognitive decline). A three-month interval is one of the
criteria for vascular dementia NINDS-AIREN [7].
Patients with damage to the dominant hemisphere have a higher risk of cognitive impairment.
Thus, according to A.N. Bogolepova [8], circulatory disorders in the left carotid system were
accompanied by cognitive decline in 46% of cases, circulatory disorders in in the right
carotid artery system – in 15%, in the vertebrobasilar system – in 8% of cases. Additional
INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE
ISSN: 2692-5206, Impact Factor: 12,23
American Academic publishers, volume 05, issue 04,2025
Journal:
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page 980
factors that increase the risk of developing post-stroke dementia are low levels of education,
long-term hypertension, diabetes mellitus, heart disease (atrial fibrillation, heart failure),
additional cerebral pathology (chronic cerebral circulatory insufficiency, atrophic changes in
the brain) [9].
Cognitive decline after a stroke may be based on the following causes.
-A heart attack in the strategic area of the brain that plays the largest role in the regulation of
mental functions (thalamus, striatum, prefrontal frontal cortex, hippocampus, angular gyrus).
The incidence of heart attacks in strategically important areas is approximately 5%. In this
case, cognitive impairments appear suddenly, followed by a stable course or a slight
regression of symptoms. The nature of neuropsychological disorders is diverse and depends
on the location of the lesion. Thus, damage to the thalamus is accompanied by the
development of spontaneity., apathy, adynamia, slowness of mental processes, impaired
memory for current events, decreased concentration, increased drowsiness. The cognitive
defect is explained by secondary frontal dysfunction as a result of impaired thalamocortical
connections. When the thalamus of the dominant hemisphere is affected, thalamic aphasia is
associated with a large number of paraphasias, but with a preserved understanding of spoken
speech and no difficulty in repeating phrases for the doctor. Stroke in the striatum is
characterized by a combination of neurodynamic and regulatory disorders resembling the
subcortical variant of vascular cognitive disorders. Stroke in the prefrontal areas of the frontal
cortex is accompanied by the formation of apaticoabulous syndrome with a decrease in
criticism of one's condition, perseverations, and echolalia. Damage to the angular gyrus
(occipito-parietal-temporal junction) is characterized by the development of visual-spatial
agnosia, constructive apraxia, acalculia, and semantic aphasia.
- Multiinfarction brain damage. This condition is a consequence of large territorial infarcts of
cortical or cortical-subcortical localization. A multiinfarction lesion is caused by thrombosis
or embolism of large cerebral vessels. The loss of more than 50 mm3 of brain matter is
necessary for the development of dementia. Cognitive disorders include operational disorders
associated with damage to the cortical sections of various analyzers, corresponding to the
localization of heart attacks. Along with this, various focal neurological disorders are
observed.
-Cognitive impairment due to hypoperfusion of the brain. They develop in pathology of
central hemodynamics, when there is a sharp decrease in perfusion pressure in the brain. In
this case, infarcts of varying volume are formed in the area of adjacent blood circulation, at
the junction of vascular basins. The development of such infarcts is largely determined by the
capabilities of collateral circulation, the preservation of autoregulation of cerebral blood flow,
which is often disrupted by hypertension. The severity and nature of cognitive disorders
depend on the location and degree of brain damage.
- A combination of heart attacks with diffuse damage to the white matter. The development
of cognitive disorders is based on damage to small vessels of the brain – microangiopathy on
the background of hypertension. The penetrating arteries, which supply blood to the
subcortical ganglia area and subcortical white matter, are subject to the greatest changes in
hypertension. These arteries belong to terminal-type vessels, i.e. they have practically no
INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE
ISSN: 2692-5206, Impact Factor: 12,23
American Academic publishers, volume 05, issue 04,2025
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collaterals, and their vascularization zone is most vulnerable in regarding ischemia against
the background of fluctuations in systemic hemodynamics. The lesion of white matter is
characterized by a decrease in its density – leukoareosis, expansion of perivascular spaces,
demyelination, gliosis. First, these changes appear near the anterior horns of the lateral
ventricles, and then spread caudally. Subsequently, subcortical leukoarrhoea joins
periventricular leukoarrhoea. Lacunar infarcts resulting from occlusion of small vessels may
manifest as clinical changes characteristic of stroke, but are most often clinically mute. The
predominant localization of lacunae is the shell, caudate nucleus, thalamus, corona radiata,
and bridge of the brain. The clinical picture of cognitive decline in this case is characterized
by gradual progression with impaired executive functions with slow mental processes,
decreased concentration, and thinking flexibility., the ability to analyze information, identify
similarities and differences. At the same time, memory impairments are moderate in nature
and are associated with difficulty in extracting information while maintaining its storage and
recognition. A feature of cognitive disorders of this localization is their frequent combination
with emotional-affective disorders and gait disorders such as frontal dysbasia.
- A combination of vascular brain damage with neurodegenerative changes. The frequency of
a combination of asthma and vascular dementia increases with age. According to
pathomorphological studies, only in 40% of cases post-stroke dementia develops directly due
to vascular causes. The remaining cases are classified as mixed versions. Local vascular brain
damage can generally increase the total volume of brain damage and contribute to the clinical
manifestation of neurodegenerative disease. In other cases In situations with latent asthma, a
small lacunar stroke in a strategically important area, which by itself cannot cause a decrease
in cognitive functions, provokes an increase in cognitive deficit.
A characteristic feature of post-stroke cognitive disorders is a violation of the regulation of
voluntary activity (decreased motivation, flexibility of thinking, impaired planning, reaction
speed, concentration of attention) associated with dysfunction of the frontal lobes with a non-
severe memory defect. As a rule, cognitive The deficiency is combined with focal
neurological symptoms depending on the location of the lesion, as well as with changes in
mood background and emotional lability. A prerequisite for the diagnosis of vascular
cognitive disorders is the detection of changes in magnetic resonance imaging/computed
tomography (MRI/CT).
The degree of cognitive impairment after a stroke can range from mild cognitive impairment
to severe dementia. In contrast to the steadily progressing process in asthma, post-stroke
cognitive impairments can be reversible. Therefore, timely The detection of mild cognitive
impairment and the correction of treatment can stabilize the process for a long time. The most
important difference between the mild cognitive impairment stage and dementia is the
preservation of the main types of daily activity (social, household independence), as well as
criticism of one's condition.
The improvement of cognitive functions after a stroke is largely explained by the phenomena
of neuroplasticity, i.e. the ability of nervous tissue to rebuild due to the involvement of
previously inactive but functionally close areas, the reorganization of pathways and
interneuronal connections, as well as collateral springing of preserved cells with the
formation of new synapses. The stimulation of neuroplasticity processes is provided by the
INTERNATIONAL JOURNAL OF ARTIFICIAL INTELLIGENCE
ISSN: 2692-5206, Impact Factor: 12,23
American Academic publishers, volume 05, issue 04,2025
Journal:
https://www.academicpublishers.org/journals/index.php/ijai
page 982
activation of neurometabolic processes, the release of neurotrophic factors, as well as by
improving the functioning of neurovascular units due to changes in the reactivity of small
vessels. Therefore, the strategy for the treatment of vascular cognitive disorders should
include several areas: improving brain perfusion, the use of neuroprotective agents, as well as
drugs that stimulate metabolism. neurotransmitters (dopamine, norepinephrine, acetylcholine)
involved in cognitive processes. Neurotransmitter drugs have a symptomatic effect in
vascular cognitive disorders – they improve attention, reaction speed, memory, and speech
functions. In controlled studies in dementia, the effectiveness of acetylcholinesterase
inhibitors (donepezil, rivastigmine, galantamine), as well as the antiglutamatergic drug
memantine, has been proven. Correction of risk factors is of great importance. (primarily
hypertension, hyperlipidemia) and prevention of recurrent vascular episodes (using
antiplatelet agents, anticoaculants).
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