Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
CLINICAL AND LABOATORY CHARACTERISTICS OF PSYCHOEMOTIONAL
DISORDERS IN CHILDREN WITH DIABETES MELLITUS
Kodirova Nafisa Nizomiddin kizi,
5
th
year student of Tashkent Pediatric Medical Institute, faculty of II-pediatrics and medical
biology, group № 531-2 pediatrics.
+99893071117
Scientific supervisor:
Alijanova Durdona Abdullajonovna
Tashkent Pediatric Medical Institute. Doctor of Medical Sciences (DSc), Docent of the
Department of Neurology, Child Neurology and Medical Genetics
+998977051909
Abstract:
This review article attempts to analyze and systematize the existing data in
contemporary scientific literature on the etiology, pathogenesis, and clinical manifestations
of cognitive and emotional deficits in children and adolescents with type 1 diabetes mellitus
(T1DM). The publication is aimed at neurologists and pediatricians. Currently, type 1
diabetes in children and adolescents remains one of the most significant medical and social
problems of modern society, requiring comprehensive and thorough study, followed by
maximum optimization of therapeutic and rehabilitation measures. Chronic hyperglycemia
underlies the development of cognitive and psycho-emotional disturbances in T1DM. The
prevalence of neurological disorders in T1DM, according to some authors, varies widely—
from 10% to 74%—and often depends on factors such as age at disease onset, disease
duration, baseline glycemic levels, diagnostic criteria used, and others. Nervous system
pathology in diabetes is observed in approximately 50% of pediatric patients with disease
duration of 3 years or more, while up to 25-30% of children with recently diagnosed
diabetes already exhibit established neurological changes.
Keywords:
diabetes mellitus, children, adolescents, cognitive functions, emotions, glycemia,
insulin.
Objective:
To succinctly present markers of cognitive and emotional disorders in children
with type 1 diabetes mellitus.
Diabetes mellitus (DM) is commonly understood as a group of endocrine disorders
characterized by persistently elevated blood glucose levels.
As of early 2018, according to the International Diabetes Federation (IDF), diabetes was
diagnosed in more than 424.9 million people worldwide, with projections estimating an
increase to 628.6 million by 2045. Many countries report a documented rise in the incidence
of T1DM in the pediatric population. In children and adolescents, type 1 diabetes (T1DM),
characterized by autoimmune destruction of pancreatic β-cells leading to absolute insulin
deficiency, is the most prevalent form. It is noteworthy that, according to many researchers
and recent statistical data, there is a steady increase in other types of diabetes among
children and adolescents, with type 2 diabetes accounting for up to 15-17%, monogenic
diabetes (MODY) for 2-6%, and others [1]. However, these figures should be considered
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
tentative due to varying research capabilities and diagnostic challenges in this patient group
[2].
At the 61st session of the United Nations General Assembly, the global significance of
diabetes, both in adults and children, was emphasized. Delegates also highlighted the
absence of optimal national-level algorithms in some countries for prevention, early
diagnosis, and treatment of diabetes [3].
In 1989, according to the long-term goals of the St. Vincent Declaration, comprehensive
support was decided for the development and implementation of constructive and effective
preventive measures, as well as promotion of research aimed at reducing the number of
severe diabetes complications [4].
In the Republic of Uzbekistan, as in other developed countries, there is a steady increase in
pediatric and adolescent T1DM. According to statistics from the Republican Medical
Scientific Center of Endocrinology of Uzbekistan, over 277,000 patients with diabetes were
registered by 2020, including 3,280 under the age of 18.
As noted earlier, the persistently elevated glycemic levels characteristic of diabetes lead to
functional and structural abnormalities in various organs and systems. Most notably and
severely affected are the eyes, cardiovascular system, kidneys, and especially the nervous
system. The impact of hyperglycemia on the formation, frequency, and severity of diabetes
complications was identified and confirmed by researchers as early as the mid-20th century.
Previous studies involving repeated systematic assessments of glycemic control repeatedly
demonstrated its critical role in reducing the risk of complications at early stages of the
disease. For this reason, many authors recommend close monitoring of patients during the
early disease stages, since early signs of complications due to inadequate glycemic control
tend to progress and do not regress even if glycemic management improves later [5,6].
In recent decades, growing attention has been paid, rightly so, to the adverse effects of
diabetes on the central nervous system (CNS). Earlier research highlighted that CNS
pathologies stand apart among diabetes complications due to the complexity of innervation,
resulting in heterogeneous clinical manifestations, diagnostic difficulties, and challenges in
therapeutic and rehabilitative decisions [7].
Diverse nervous system dysfunctions in children and adolescents with T1DM have been
repeatedly confirmed by epidemiological studies, emerging as early as 2 to 8 years after
disease onset, or even sooner in some patients. The reported prevalence of neurological
disorders varies widely from 10% to 74%, often depending on age at diagnosis, disease
duration, baseline glycemia, diagnostic criteria, etc. [8,9]. Nervous system pathology in
diabetes is noted in approximately 50% of pediatric patients with disease duration of 3 years
or more, while up to 25-30% of children with more recent diagnoses already show
established neurological changes. It should be emphasized that these figures mainly relate to
diabetic neuropathy (DN), as for many years DN—specifically diabetic peripheral
neuropathy—was considered the sole and most common nervous system complication in
diabetes [10,11]. However, over recent decades, this view has been challenged by research
demonstrating both direct and indirect effects of diabetes on structural and functional brain
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
changes, primarily manifesting as cognitive impairments (CI). Furthermore, CI have been
identified as the most common nervous system abnormalities in diabetes [12].
In 2002, N.N. Yakhno proposed the following definition of cognitive impairment:
"Cognitive impairments are subjective or objective deviations in higher cortical functions,
which may be organic or functional brain disorders of various origins, affecting optimal
learning processes and the efficiency of professional, social, and daily functioning" [13].
Unfortunately, even with modern advanced medical technology, medicine cannot yet
prevent the development of various diabetes complications. Most researchers attribute this to
the late detection of brain abnormalities, caused primarily by (1) a blurred subjective clinical
picture and (2) the subclinical and hidden nature of the pathology. Compared to peripheral
nervous system damage, brain-related complications in diabetes remain a poorly studied
aspect of neurodiabetology [14]. Moreover, fundamental questions about the mechanisms
underlying cognitive impairments in children and adolescents with T1DM remain
insufficiently explored, despite previous studies demonstrating various pathogenetic
components of CI in this condition [15].
In summary, complications of diabetes, especially those affecting the brain, are highly
prevalent and, moreover, represent an inevitable and predictable phenomenon requiring
special monitoring.
Clinical Components of Cognitive and Emotional Impairments in Type 1 Diabetes
The so-called higher cortical or higher brain functions, or cognitive functions, are considered
the most complex brain processes that play a key role in the meaningful perception and
understanding of the world, as well as in purposeful interaction with it. These complex
functions
include:
–
Gnosis
, whose mission is the perception of information received from the sensory organs
(vision,
hearing,
smell,
touch,
taste,
and
tactile
sense);
–
Thinking
, which involves processing and analyzing incoming information, including the
ability to synthesize, identify similarities and differences, produce logical conclusions, and
form
associative
connections;
–
Memory
, which is responsible for storing and recalling acquired information;
–
Speech
,
which
enables
the
exchange
of
information;
–
Praxis
, meaning purposeful motor activity.
In children, the most important, or basic, cognitive components are formed by the age of 6–7
years, while the more complex ones develop between ages 12 and 15, continuing to improve
throughout life. However, it is essential to take into account individual characteristics and
capabilities of each person. It is also important to remember that the ability for social and
everyday adaptation in today’s rapidly changing world, especially in individuals with
diabetes, directly depends on the state of their cognitive abilities.
Cognitive impairments, along with other neurological disorders, are among the most
significant and, in many cases, the leading or sole manifestations of organic brain pathology
with varying degrees of severity.
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
Another current issue is that a large number of patients with diabetes continue to live
unaware (often due to medical staff’s lack of professionalism) and, consequently, with
untreated cognitive impairments. This persists despite many studies demonstrating the
inevitable presence of cognitive deficits in patients with type 1 diabetes and all related
consequences. This pathology’s formation is even more significant when it occurs in
childhood with type 1 diabetes.
One such study was conducted in 2015 by Duarte J.M.N., showing the consistent presence
of cognitive pathology in diabetes, with manifestations in children and adolescents usually
mild or moderate, but tending to worsen with age, disease duration, and poor glycemic
control.
As noted earlier, cognitive deficit means deterioration compared to individual norms in one
or more brain functions such as memory, attention, thinking, etc. In children, these can be
caused by intellectual disability, brain underdevelopment, or injury around the time of birth
or early postnatal period. In adults, cognitive impairments may develop due to a wide range
of neurological diseases. This is explained by studies showing that approximately 90% of
the brain cortex area belongs to secondary and tertiary cortical centers responsible for
regulating higher brain functions.
According to the literature, impairments of memory functions are among the earliest and
most persistent symptoms of cerebral pathology developed in diabetes; accurate assessment
of their nature and severity allows conclusions about the localization and extent of
pathological processes in the brain.
Currently, classifications of cognitive deficits in diabetes are based on the severity of their
manifestations. According to the most commonly used classifications — DSM-5 and the
classification by N.N. Yakhno — cognitive changes can be divided into severe, moderate,
and mild.
Severe cognitive impairments
are transient or persistent deviations characterized by
high severity, significantly interfering with the patient’s social, professional, and everyday
life. These include intellectual disability, oligophrenia, dementia, as well as pathologies
predominantly caused by genetic factors and brain developmental anomalies.
Moderate cognitive impairments
are acquired deviations in one or several areas of
higher cortical function. Compared to severe impairments, these are less pronounced and do
not cause loss of independence in daily life, although they exceed age norms. Difficulties
arise only during the performance of the most complex and unfamiliar tasks.
Mild cognitive impairments
are neurodynamic manifestations involving impaired
rapid switching between tasks, slower information processing, and working memory.
Patients with mild impairments do not experience difficulties in professional, social, or daily
activities. Such impairments may only be detected through subjective patient reports and
detailed neuropsychological testing.
Many authors believe that cognitive dysfunctions as complications of diabetes mainly occur
in mild and moderate forms, with severe impairments being rare. The most common
manifestations include slowed information processing speed, memory and attention
disorders, and executive dysfunction. Additionally, psychomotor response slows, intellectual
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
flexibility decreases, and visual perception is impaired. It should be noted that
hyperglycemia and hypoglycemia can have different impacts on cognitive deficit
manifestations; for example, elevated glucose levels often affect verbal memory, whereas
lowered glucose impairs visual memory.
Cognitive dysfunction in type 1 diabetes, especially in children and adolescents, can be
detected at early stages of the disease. Opinions on this matter vary among authors, but there
is consensus that cognitive deficit formation in type 1 diabetes is a 100% certainty and that
deficits persist and progressively worsen with patient aging and longer disease duration.
In this study, we concluded that cognitive deficit in children and adolescents with type 1
diabetes begins to develop almost simultaneously with the onset of the main disease. This is
caused by changes in brain metabolism and energy-producing processes, which in turn lead
to impaired oxygen and glucose utilization by brain tissues—both essential for optimal brain
function.
In addition to cognitive deficits, significant changes can also develop in the psycho-
emotional and behavioral spheres of patients with type 1 diabetes. Clinical manifestations of
these disturbances tend to emerge in two phases: the disease debut and the onset of possible
complications. Most children exhibit moderately expressed emotional reactions upon
diagnosis.
In other cases, reactions to the news of the disease are more pronounced, and examinations
reveal initial changes in the psycho-emotional background [31]. Subsequently,
approximately within nine months from the onset of the disease, the level of psychological
activity returns to baseline [27].
There are quite a few publications on this issue in the literature. For example, some
researchers who had the opportunity to observe children with type 1 diabetes almost from
the first days of the disease concluded that the onset of type 1 diabetes itself does not have a
significant impact on the psycho-emotional functioning of patients [32].
In 2019, it was established that a distinctive feature of the initial period of type 1 diabetes is
the activation of pre-morbid personality traits, which are a determining factor in the reaction
to the disease. Such reactions include: anxious suspicion; hyperbolic exaggeration of the
treatment, or conversely, the formation of a frivolous attitude toward the disease. According
to other authors, in individuals suffering from diabetes, the level of personal psycho-
emotional changes at the early stages of the disease is much higher than in those who have
been ill for a long time; this fact is explained by the organism's adaptive capacity to the
disease. This leads to the formation of pathological personality changes — the emergence of
asthenic and obsessive-compulsive disorders, increased irritability, and lack of restraint; in
some cases, manifestations of depression with dysphoria may also appear.
Regarding the problem of psycho-emotional disorders in type 1 diabetes, it is worth noting
that recently, more and more scientific works have been published devoted to the increasing
risk among pediatric patients (especially adolescents) of developing psycho-
endocrinological syndrome as described by Manfred Bleuler, which in turn is considered the
first stage of the manifestation of psycho-organic syndrome [33].
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
According to several studies on the psychological adaptation processes in children with type
1 diabetes, there is a steady increase in personal (trait) anxiety and situational or reactive
anxiety. Referring to statistical data, it is seen that the overall prevalence of anxiety in
children and adolescents with type 1 diabetes ranges from 15 to 42%. High rates of anxiety
disorders in children and adolescents are primarily associated with the specific
characteristics of diabetes itself, such as the constant need for injections and self-monitoring.
Additionally, a connection is observed with parental overprotection, where parents assume
controlling functions [34].
According to many authors, and in our opinion as well, the neuropsychological status of
pediatric patients with diabetes is of great importance in determining the course and
outcomes of the disease. For this reason, parameters of neuropsychological status can be
considered additional, auxiliary factors influencing the effectiveness of therapy [35].
Thus, in pediatric patients with type 1 diabetes, there is a high frequency of cognitive
impairments, and a direct positive correlation exists between early manifestation and the risk
of brain involvement in the pathological process. Moreover, cognitive dysfunctions against
the background of concomitant anxiety-depressive disorders can not only negatively affect
good and long-term glycemic control but also significantly impact social activity, work
capacity, and patients' quality of life.
Neurospecificity Peptides as Markers of Cognitive and Psychoemotional Disorders
Currently, the pathogenesis of cognitive deficit in type 1 diabetes in children and adolescents
remains not fully understood [36]. Several studies have found correlations between higher
cortical function impairments and the degree of glycemia, leading to the assertion that this
metabolic disturbance is the primary cause of cognitive deficit formation in diabetes [37].
It is well known that neuropsychological testing is primarily used to assess the severity of
cognitive deficit; however, these test results are subjective and therefore cannot provide a
complete picture of the changes occurring in higher cortical brain activity. Because of this,
specialists worldwide are continuously searching for specific markers of cerebral disorders
in diabetes [38].
More than 25 years ago, research began on biochemical markers with diagnostic
significance for various brain changes, but to date, an ideal biomarker has not been found.
Among many studied biomarkers, special attention is given to determining the levels of
neurospecific proteins, which can indicate damage occurring in brain tissues in various
pathologies, including diabetes, both in adults and children [39].
Many scientists believe that the ideal marker of cerebral disorders should have the following
characteristics: high specificity; high sensitivity; should be released during irreversible
neuronal damage and provide information about the nature of the damage; detectable in
blood and cerebrospinal fluid (CSF) shortly after injury; easy to measure in laboratory
conditions; and naturally reflect the dynamics of pathology and treatment effectiveness [40].
In the pathogenesis of diabetic encephalopathy, the authors consider that the main role is
played by pathological permeability of the blood-brain barrier (BBB). This fact, i.e.,
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
disruption of BBB structural integrity and normal function, has been demonstrated in several
clinical and experimental studies. Impaired BBB permeability during cognitive deficit
formation leads to the appearance in blood and CSF of certain neurospecific proteins, in
particular neuron-specific enolase (NSE) and protein S-100 [41].
According to the authors, deviations found in protein concentrations in various neurological
diseases can be detected earlier than any structural changes. The particular interest in
analyzing brain-specific proteins lies in the fact that they are assumed to participate in key
nervous tissue functions: generation and conduction of nerve impulses, synaptic
transmission and cell interactions, and actively participate in learning and memory processes.
Neuron-specific enolase (NSE) is an informative neurospecific protein representing a
glycolytic enzyme — 2-phospho-D-glycerate hydrolase. It belongs to the enolase group and
participates directly in the terminal stage of glycolysis, catalyzing the conversion of 2-
phospho-O-glyceric acid to 2-phosphoenolpyruvate. It was first isolated in the 1970s-1980s.
Its isoenzyme is γγ-enolase, also called neuron-specific enolase, which is abundantly found
in neurons and importantly in neuroendocrine cells. Normal NSE levels in blood are less
than 15 µg/L [42].
From available literature sources, it follows that nowadays this brain-specific marker is
widely used to diagnose acute conditions such as cerebral ischemia, brain hypoxia, and for
studying the pathogenesis of neurological pathologies. Many authors emphasize its great
importance in various nervous system diseases, such as epilepsy; Parkinson’s disease; senile
dementia; Alzheimer’s disease; intrauterine brain damage; diabetes mellitus; brain tumors;
traumatic brain injury (TBI).
Currently, the most studied biomarker is the neurospecific glial protein S-100. This protein
is found in brain tissue complexed with calcium and consists of two subunits: α (10.4 kDa)
and β (10.5 kDa). Its normal blood concentration is less than 0.2 µg/L. An important feature
is that its content in the white matter is higher than in the gray matter, and in the cerebellum
its concentration is greater than in all other brain structures [43].
Protein S-100 is found in cerebral cells such as astrocytes, oligodendrocytes, as well as
ependymal, choroidal, endothelial, and lymphocytic cells of the brain.
Many authors consider, though presumably, that since this protein is widely present in
various cell types, it serves as a marker of widespread blood-brain barrier damage rather
than isolated glial damage [44]. When S-100 protein concentration is low, it exerts a
neuroprotective effect, acting as a growth factor and differentiating neurons and glia,
blocking NMDA receptors. If its concentration is elevated, it stimulates pro-inflammatory
cytokines and leads to cell self-destruction (apoptosis or autolysis). At optimal
concentrations, S-100 protein in the brain performs trophic functions, serves as a barrier
protecting neurons from oxidative stress, and stimulates the growth of nerve processes. It
also stimulates the NF-kappa B complex. Numerous studies focus on the clinic-pathogenetic
role of S-100 protein and its significance in determining the severity and outcomes of
neurological pathologies. For example, increased S-100 protein levels correlate with
worsening auditory evoked potentials and unfavorable outcomes after aneurysm surgeries
[45]. Also, moderate increases in S-100 concentrations in patients with depression are
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
associated with delayed visual evoked potential peaks, which normalize during treatment,
indicating the neurodegenerative significance of S-100.
In the study by Saleh A. et al. (2007), the clinical diagnostic significance of S-100 protein
was demonstrated as an indicator of the severity of higher cortical dysfunction in patients
with hepatic encephalopathy [46].
In the study by Novoselova M.V. et al. (2014), data were obtained showing statistically
significant increases in the levels of the studied neurospecific proteins. Specifically, a
positive correlation was demonstrated between these protein levels and glycated hemoglobin
as well as fasting hyperglycemia, confirming the impact of carbohydrate metabolism
decompensation in patients with type 1 diabetes mellitus [47].
As a result of all these identified disturbances related to the S-100 protein in various
neurological pathologies, this protein has been included in the group of brain C-reactive
proteins and is used as a neurospecific biomarker of central nervous system damage.
Conclusions.
Thus, the development of complications in type 1 diabetes is inevitable,
expected, and requires monitoring. The conducted analysis of domestic and foreign literature
indicates the existence of various pathogenetic mechanisms underlying cerebral impairments
in diabetes, leading to extensive and diverse neuropsychological, psychopathological, and
neurological symptomatology.
There is no doubt that diabetes mellitus negatively affects cognitive function. However, the
specific pathogenetic mechanisms contributing to the formation and progression of cognitive
deficit in patients with diabetes, both adults and children, are not fully understood; the data
are fragmented, limited, and sometimes contradictory. Most literature sources highlight the
significant contribution of hyperglycemia; at the same time, many authors also point to the
more significant influence of hypoglycemia. However, the role of major pathophysiological
consequences of hyper/hypoglycemia, such as tissue (neuronal, glial) hypoxia, endothelial
dysregulation, and activation of angiogenesis, remains insufficiently studied.
There is a lack of comprehensive studies elucidating the relationship between clinical,
biochemical, and neuroimaging changes of the CNS in diabetes. The clinical and diagnostic
significance of neuropeptides such as NSE and S-100 is not fully understood, despite their
demonstrated informativeness in blood serum in many other CNS diseases. Objective
diagnostic criteria for diabetic encephalopathy in childhood, including its earliest and
preclinical stages, are absent.
Therefore, in addressing these problems, the issue of studying cerebral disorders in children
and adolescents with type 1 diabetes using modern neuroimaging, psychometric, and
biochemical methods that cover the main possible links in the pathogenesis of these
disorders remains highly relevant. The obtained data could provide a basis for developing a
set of measures for prevention, treatment, and rehabilitation of CNS disorders, which would
contribute to optimizing current approaches to diabetes management and improving the
quality of life for diabetic patients in the long term.
REFERENCES.
Vo
lu
m
e
5,
Ju
ne
,2
02
5
,
M
ED
IC
AL
SC
IE
N
CE
S.
IM
PA
CT
FA
CT
OR
:7
,8
9
1.
Diabetes Atlas / International Diabetes Federation. – 8 th ed. – [S.l.], 2017. – 147 p.
2.
Decreased Spontaneous Brain Activity and Functional Connectivity in Type 1
Diabetic Patients Without Microvascular Complications / W. Xia, Y. Chen, Y. Luo et al. //
Cell Physiol. Biochem. – 2018. – Vol. 51. – P. 2694– 2703.
3.
Резолюция, принятая Генеральной Ассамблеей 61/225. Всемирный день борьбы
с диабетом.
4.
Майкл Холл, Энн-Мари, Фелтон Сент-Винсентская Декларация 20 лет спустя –
борьбы с диабетом в ХХ веке // Диабет в обществе. – 2009. – 54 (2). - С. 42-43.
5.
Дедов И. И. Эндокринология: национальное руководство / И. И. Дедова, Г. А.
Мельниченко. - 2-е изд., перераб. и доп. - Москва: ГЭОТАР-Медиа, 2021. - 1112 с.
6.
Intensive glucose control versus conventional glucose control for type 1 diabetes
mellitus / B. Fullerton, K. Jeitler, M. Seitz et al. //Cochrane Database of Systematic Reviews.
- 2014. - Issue 2. - Art. No.: CD009122.
7.
Cognitive Dysfunction in Type 1 Diabetes Mellitus / A. Shalimova, B. Graff, D.
Gąsecki [et al.] // J. Clin. Endocrinol. Metab. –2019. – Vol. 104, № 6. – Р.2239–2249.
8.
Дедов И.И., Кураева Т.Л., Петеркова В.А. Сахарный диабет у детей и
подростков: руководство. 2-е изд., перераб и доп. М.: ГЭОТАР – Медиа. 2013. С. 159-
160.
9.
Садикова Г.К., Абдувалиева М.A. Особенности неврологических осложнений у
детей с сахарным диабетом 1-го типа. Молодой ученый 2017;16(150);13–5.
10.
Котов А.С., Елисеев Ю.В. Диабетическая полиневропатия и синдром
диабетической стопы. Эффективная фармакотерапия 2013; 48:32–9.
11.
Мотовилин О.Г., Саверская Е.Н., Хаиров Р.Р. Дети с сахарным диабетом
и социальный мир: проблемы и возможности (социальная оздоровительно-
образовательная программа «Диабет. Танцы. Дети»). Медицинский совет.
2022;16(12):71–84.
12.
Алиджанова Д.А., Маджидова Я.Н. \\ Факторы риска развития СД2 и наиболее
часто встречающиеся неврологические осложнения у детей и подростков \\
«NEVROLOGIYA»—2(86), 2021.
13.
Яхно Н.Н. Когнитивные и эмоционально-аффективные нарушения при
дисциркуляторной энцефалопатии / Н.Н. Яхно, В.В. Захаров // Русский медицинский
журнал. – 2002. – № 10. – С. 539-542.
14.
Башнина Е.Б., Берсенева О.С., Ворохобина Н.В. и др. Эндокринные
заболевания у детей и подростков: руководство для врачей. М.: ГЭОТАР-Медиа, 2017.
416 с.
15.
He J., Ryder A.G., Li S., Liu W., Zhu X. Glycemic extremes are related to cognitive
dysfunction in children with type 1 diabetes: A meta-analysis. J. Diabetes Investig.
2018(а);9(6):1342–1353.
