Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus
The peculiarities of cognitive dysfunction structure in patients with type 2 diabetes mellitus and stage 2 diabetic encephalopathy characterized by disorders of memory, verbal fluency, attention and orientation, were revealed. Association of cognitive disorders with disease duration, glycosylated he...
Gespeichert in:
| Datum: | 2014 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | English |
| Veröffentlicht: |
Інститут проблем кріобіології і кріомедицини НАН України
2014
|
| Schriftenreihe: | Международный медицинский журнал |
| Schlagworte: | |
| Online Zugang: | http://dspace.nbuv.gov.ua/handle/123456789/68432 |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| Назва журналу: | Digital Library of Periodicals of National Academy of Sciences of Ukraine |
| Zitieren: | Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus / E.L. Tovazhnyanska, I.O. Bezuglova // Международный медицинский журнал. — 2014. — Т. 20, № 1. — С. 13-17. — Бібліогр.: 21 назв. — англ. |
Institution
Digital Library of Periodicals of National Academy of Sciences of Ukraine| id |
irk-123456789-68432 |
|---|---|
| record_format |
dspace |
| spelling |
irk-123456789-684322014-09-24T03:01:49Z Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus Tovazhnyanska, E.L. Bezuglova, I.O. Неврология The peculiarities of cognitive dysfunction structure in patients with type 2 diabetes mellitus and stage 2 diabetic encephalopathy characterized by disorders of memory, verbal fluency, attention and orientation, were revealed. Association of cognitive disorders with disease duration, glycosylated hemoglobin concentration, impaired brain activity, cerebral hemodynamics and cerebrovascular reactivity was established. Выявлены особенности структуры когнитивной дисфункции при сахарном диабете 2−го типа и диабетической энцефалопатии II стадии, которые характеризовались нарушением функции памяти, беглости речи, внимания и ориентации. Установлена связь когнитивных расстройств с длительностью заболевания, концентрацией гликозилированного гемоглобина, нарушением биоэлектрической активности мозга, церебральной гемодинамики и цереброваскулярной реактивности. Визначено особливості структури когнітивної дисфункції при цукровому діабеті 2−го типу і діабетичній енцефалопатії II стадії, що характеризувалися порушенням функції пам’яті, мовлення, уваги та орієнтації. Встановлено зв’язок когнітивних розладів із тривалістю захворювання, концентрацією глікозильованого гемоглобіну, порушенням біоелектричної активності мозку, церебральної гемодинаміки та цереброваскулярної реактивності. 2014 Article Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus / E.L. Tovazhnyanska, I.O. Bezuglova // Международный медицинский журнал. — 2014. — Т. 20, № 1. — С. 13-17. — Бібліогр.: 21 назв. — англ. 2308-5274 http://dspace.nbuv.gov.ua/handle/123456789/68432 616.379–008.64–06:616.831–009.861–073.432.19 en Международный медицинский журнал Інститут проблем кріобіології і кріомедицини НАН України |
| institution |
Digital Library of Periodicals of National Academy of Sciences of Ukraine |
| collection |
DSpace DC |
| language |
English |
| topic |
Неврология Неврология |
| spellingShingle |
Неврология Неврология Tovazhnyanska, E.L. Bezuglova, I.O. Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus Международный медицинский журнал |
| description |
The peculiarities of cognitive dysfunction structure in patients with type 2 diabetes mellitus and stage 2 diabetic encephalopathy characterized by disorders of memory, verbal fluency, attention and orientation, were revealed. Association of cognitive disorders with disease duration, glycosylated hemoglobin concentration, impaired brain activity, cerebral hemodynamics and cerebrovascular reactivity was established. |
| format |
Article |
| author |
Tovazhnyanska, E.L. Bezuglova, I.O. |
| author_facet |
Tovazhnyanska, E.L. Bezuglova, I.O. |
| author_sort |
Tovazhnyanska, E.L. |
| title |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| title_short |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| title_full |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| title_fullStr |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| title_full_unstemmed |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| title_sort |
cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus |
| publisher |
Інститут проблем кріобіології і кріомедицини НАН України |
| publishDate |
2014 |
| topic_facet |
Неврология |
| url |
http://dspace.nbuv.gov.ua/handle/123456789/68432 |
| citation_txt |
Cerebrovascular insufficiency and diabetic encephalopathy in patients with type 2 diabetes mellitus / E.L. Tovazhnyanska, I.O. Bezuglova // Международный медицинский журнал. — 2014. — Т. 20, № 1. — С. 13-17. — Бібліогр.: 21 назв. — англ. |
| series |
Международный медицинский журнал |
| work_keys_str_mv |
AT tovazhnyanskael cerebrovascularinsufficiencyanddiabeticencephalopathyinpatientswithtype2diabetesmellitus AT bezuglovaio cerebrovascularinsufficiencyanddiabeticencephalopathyinpatientswithtype2diabetesmellitus |
| first_indexed |
2025-07-05T18:17:06Z |
| last_indexed |
2025-07-05T18:17:06Z |
| _version_ |
1836831921374494720 |
| fulltext |
13
МЕЖДУНАРОДНЫЙ МЕДИЦИНСКИЙ ЖУРНАЛ, 2014, № 1
© E. L. TOVAZHNYANSKA, I. O. BEZugLOVA, 2014
w
w
w
.im
j.k
h.
ua
УДК 616.379–008.64–06:616.831–009.861–073.432.19
CEREBROVASCULAR INSUFFICIENCY
AND DIABETIC ENCEPHALOPATHY IN PATIENTS
WITH TYPE 2 DIABETES MELLITUS
Prof. E. L. TOVAZHNYANSKA1, I. O. BEZUGLOVA2
1 Kharkiv National Medical University,
2 Municipal Clinical Hospital № 27, Kharkiv
The peculiarities of cognitive dysfunction structure in patients with type 2 diabetes mellitus and
stage 2 diabetic encephalopathy characterized by disorders of memory, verbal fluency, attention and
orientation, were revealed. Association of cognitive disorders with disease duration, glycosylated
hemoglobin concentration, impaired brain activity, cerebral hemodynamics and cerebrovascular
reactivity was established.
Key words: type 2 diabetes mellitus, diabetic encephalopathy, cognitive disorders, cerebrovascular insufficiency,
cerebrovascular reserve.
Type 2 diabetes mellitus (DM) is one of the most
common diseases revealed in 3–15 % of the population
of economically developed countries. Progress in
glycemic control contributed to significant increase
in life expectancy of patients with diabetes, increase
of the number of individuals with long-term history
of the disease and, consequently, increased incidence
of its late complications. Leading complications of
diabetes are disorders of the nervous system revealed
in almost every patient.
Diabetic encephalopathy is resistant cerebral
pathology that occurs in patients with type 2 DM
as a result of chronic hyperglycemia, disturbances
of signaling effects of insulin in the brain as well as
metabolic disorders induced under these conditions.
Chronic cerebrovascular accident plays a role in
the development of encephalopathy in type 2 DM,
the pathogenesis of which is due to formation of
diabetic cerebral micro- and macroangiopathy.
The changes in the small blood vessels (arterioles,
capillaries, venules) are specific to DM nature; those
in the large ones are regarded as early disseminated
atherosclerosis [1–4].
The pathogenesis of microangiopathy in DM
is associated with formation of autoantibodies
against glycosylated proteins of the vascular walls,
increased peroxidation processes with accumulation
of excessive amounts of pro-oxidants, inhibition of
synthesis prostacyclin and nitric oxide, producing
antoaggregate and vasodilator effect. Diabetic
macroangiopathy develops when hyperlipidemia and
disorders of the vascular wall structure are combined
with increase in its permeability, which leads to
formation of atherosclerotic plaques, affecting the
main vessels (macroangiopathy) [4, 5].
An important role in development of the
brain disgemeny at DM is undoubtedly played by
endothelial dysfunction, impaired autoregulation of
cerebral blood flow, increase in blood viscosity and
aggregation properties [1, 3–5]. It is known that
the adequate function of the processes of cerebral
flow autoregulation can compensate hemodynamic
deficiency resulting from various causes owing to
co-operation of anatomical and functional factors of
compensation [6, 7]. Disturbance of autoregulation
in type 2 DM is one of the mechanisms of forming
cerebral dyscirculations, causing tissue hypoxia and
energy metabolism disorders in the nervous tissue.
As a result, neurons develop lactoacidosis and the
energy deficiency promoting structural and functional
abnormalities in the nerve cells and formation of the
clinical picture of diabetic encephalopathy [2, 4, 5, 8].
The leading clinical syndrome of diabetic
encephalopathy is cognitive dysfunction. Development
of mild to moderate cognitive dysfunction significantly
reduces the quality of life of the patients with
DM, limits theirs ability to carry out effectively
recommendations for the treatment of the disease
and neurological complications, and is associated
with significant risk of subsequent development of
dementia and severe disability [3, 9–11]. Experimental
and clinical data on relationship of diabetic macro-
and microangiopathy with formation of small
(lacunar) cerebral infarctions, which often develop
without clinical stroke and/or leukoaraiosis has
been accumulated. These structural changes in the
brain substance are considered as the morphological
substrate of cognitive dysfunction [12–15]. A certain
role of insulin resistance, frequent hypoglycemic
episodes, emotional disorders, as well as combination
of type 2 DM and hypertension in development of
cognitive disorders in DM has been established [3,
15–17]. However, despite the available literature
data, the pathogenesis of cognitive dysfunction in
type 2 DM is not fully understood.
The purpose of the work was to establish the
association between impaired cerebral hemodynamics
and formation of cognitive disorders in type 2 DM
НЕВРОЛОГИЯ
14
НЕвРОЛОгИя
w
w
w
.im
j.k
h.
ua
The study involved 87 patients (61 females and
26 males) with type 2 DM and stage 2 diabetic
encephalopathy, aged 56,3±5,9 with mean disease
duration of 9,3±4,5 years (main group). Diabetes
severity was defined as medium in 64,4 % of
patients and severe in 35,6 % of cases. Glycosylated
hemoglobin (HbA1c) level in the group of the patients
ranged from 7,2 to 8,8 %. Insulin was administered
as basic hypoglycemic therapy in 54 % of patients,
tablet formulations were administered to 46 %. Among
diabetes complications distal diabetic polyneuropathy
was present in 72,4 % of patients, 91,9 % patients
had diabetic angiopathy in the fundus, 27,6 % signs
of diabetic nephropathy. Stage I or II hypertension
was noted in 89,7 % of patients with DM, 86,2 % of
patients had lipid metabolism disorders demonstrated
by biochemical blood analysis. The patients with the
history of heart attacks and strokes who had severe
or unstable concomitant somatic pathology were
excluded from the study. The controls were 30 age-
matched apparently healthy individuals.
Cognitive function was determined using a brief
mental status evaluation scale Mini-mental State
Examination (MMSE) and the scale of cognitive
abilities Addenbrooke’s Cognitive Examination-R
(ACE-R) [18–20]. The latter is a questionnaire
including 26 tasks, divided into five domains:
attention and orientation, memory, speech fluency,
language, visual and spatial skills. Maximum total
score is 100.
The study of blood flow in the large arteries of
the head and intracranial arteries was performed using
extra- and intracranial Doppler study according to
standard techniques using 2, 4, 8 MHz transducers
with Spectromed-300 unit (Russia). Vasodilatator
reserve and reserves of collateral circulation were
assessed by compression test and evaluation of
Overshoot coefficient [21].
The state of spontaneous bioelectrogenesis was
assessed according to electroencephalography findings
obtained with computer electroencephalograph DX-
NT32; bioelectric activity of the brain was studied
by recording the endogenous evoked potentials (EP)
of the brain with computer myograph Neuro — MEP
(Neurosoft, RF); the structural state of the brain
substance was objectified by brain MRI.
The obtained data were statistically processed
using statistical software application package
Statistiсa-6. Mean values and average error were
calculated. To determine the significance of differences
in the samples parametric and nonparametric
Wilcoxon and Student’s criteria were used. The
differences were considered significant at p < 0,05.
To perform correlation analysis, Spearman rank
correlation coefficient (r) was calculated.
The main complaints of the patients with
type 2 DM and stage 2 diabetic encephalopathy
were impaired memory of current events, decreased
performance, headache (98,2 % of cases), dizziness
(85,5 %), unsteady gait (74,6 %), emotional lability
(63,6 %), asthenia (38,2 %), sleep disorders (69,1 %).
Neurological examination revealed cephalgic
syndrome (96,5 % of cases), cognitive dysfunction
(94,3 %); static-coordination disorders (86,1 %),
psychoemotional disorders ranging from emotional
lability to depressive syndromes (89,5 %); intracranial
hypertension (84,2 %), pyramidal insufficiency of
central type (49,1 %); polyneuropathy syndrome
(96.5 %), sleep disorders (66.7 %), etc.
Leading neurological syndrome in patients with
stage 2 diabetic encephalopathy was mild cognitive
disorder (27–26 points), moderate (25–24 points)
severity by MMSE scale. Evaluation of the intellectual
functions using ACE-R scale showed that total score
decreased to 73–79 (lower limit of the normal values
for this age group is 85–86 points [20]), which
corresponded to moderate cognitive dysfunction.
The memory was deteriorated most significantly,
by 36,8 %, p < 0,01 (9–14 points by ACE-R scale
at age norm over 19 points), speech fluency by
25,6 %, p < 0,01 (6–8 points by ACE-R scale at the
age norm over 10 points), attention and orientation
by 11,8 %, p < 0,05 (13–16 points by ACE-R scale
at age over 17 points). Linguistic functions and
visiospatial abilities had a tendency to reduction
(by 5,6 and 8,4 %, respectively, p > 0.05), in the
majority of cases they remained on the lower limit
of age norm. This character of cognitive deficiency
reflects disorders of fronosubcortical regions of the
brain and neurodynamic of brainstem and subcortical
structures [11].
All observed patients had diffuse changes in brain
bioelectrical activity in the form of disorganized basic
rhythms, smoothed zone differences, elevated slow-
wave activity index. The investigation of indicators
of endogenous EP in patients with stage 2 diabetic
encephalopathy at type 2 DM showed increased
latency of peak P 300 to 359±13 ms (p < 0.05) vs. the
controls (314±18 ms). In addition, the resultant wave
of endogenous EP in the group of the investigated
patients was often smoothed and peak P 300
amplitude was decreased. The revealed negativization
of induced brain activity was neurophysiological
correlate of cognitive decline in type 2 DM.
Doppler sonography revealed decrease in linear
blood flow velocity (LBFV) in the internal carotid
artery (ICA) by 33,9 %, in the middle cerebral artery
(MCA) by 34,5 %, in the subclavicular artery (SA) by
44,7 %, in the common carotid artery (CCA) by 32,6 %
in patients with stage 2 diabetic encephalopathy
against a background of type 2 DM with respect
to those of the controls and the signs of increased
vascular tone in all investigated vessels according
to increase of pulsatility index (PL) and circulatory
resistance (RL) on average in 1,8 and 1,75 times
(Table 1).
Disorders of cerebral vascular reactivity
in the examined patients with stage 2 diabetic
encephalopathy were characterized by decreased
capacity of collateral flow (anatomical level of
cerebral vascular reserve), which was confirmed by
depression with respect to benchmarks of residual
15
НЕвРОЛОгИя
w
w
w
.im
j.k
h.
ua
blood flow velocity in the MCA (V2) at the time of
the ipsilateral CCA compression by 28,1 % (Table 2).
This reflected impaired patency of the perforating
and connective arteries, possibly as a result of their
secondary obliteration as a manifestation of diabetic
microangiopathy. Reduction of Overshoot index in
patients with stage 2 encephalopathy and type 2
DM vs. the controls by 26,9 % indicated exertion
of the functional cerebrovascular reactivity, in
particular its myogenic component due to disorders
of in the structure of the vascular wall and its tone
in DM. 2.3-fold increase in the recovery time of
blood flow velocity to the initial values reflected
disturbance in the metabolic circuit of vascular
reactivity as a manifestation of general dismetabolic
processes developing in the organism at DM:
disturbances of the polyol pathway of glucose
oxidation, excessive accumulation of sorbitol and pro-
oxidants, development of hyperlipidemia, deficiency
of depressor factors, irreversible glycosylation of
proteins, including those of vascular walls [1, 4, 5, 8].
Table 2
Hemodynamics of blood flow in intracranial
arteries during compression tests
Hemadynamic values Main group Controls
V1 МCА (cm/s) 40,9±5,7* 63,8±9,7
V2 МCА (cm/s) 22,3±1,6* 31,8±3,4
V3 СМА (cm/s) 46,7±4,9* 86,8±7,1
Overshoot coefficient
(conventional units)
1,13±0,04* 1,36±0,09
Blood flow velocity
recovery time Т (с)
14±3* 6±2
Brain MRI in patients with stage 2 encephalopathy
at type 2 DM demonstrated the signs of cortical
hypotrophy in the area of the frontal and parietal
lobes (78,4 % of cases), lacunar defects (33,4 %),
signs of leukoaraiosis (21,6 %). Thus, in type 2 DM
the most common morphological type of brain lesion
was cortical atrophy indicating more significant effect
of chronic hyperglycemia on the corticoatrophic
changes in the brain.
The performed correlation analysis revealed
association of cognitive dysfunction (total point
by ACE-R scale) with the duration of type 2 DM
(r = –0,34; p < 0,001), concentration of glycosylated
hemoglobin (r = –0,39; p < 0,001), δ-rhythm index
increase (r = –0,31; p < 0,01), increase of peak P 300
latency (r = –0,47; p < 0,01), Overshoot coefficient
reduction (r = +0,41; p < 0,05). The dependence of
reduction of Overshoot coefficient on DM duration
(r = –0,37; p < 0,05), glycosylated hemoglobin
level (r = –0,41; p < 0,01) was determined. These
figures reflect the associations of the revealed
cognitive sand vascular disorders and carbohydrate
metabolism disorders and DM duration, as well
as indicate the presence of complex disorders
of corticosubcortical connections that underlie
development of cognitive disorders in patients with
type 2 DM and can be a marker and predictor of
their development.
Thus, the leading syndrome of diabetic
encephalopathy in type 2 DM are cognitive disorders
clinically characterized by the presence of symptoms of
frontal dysfunction and participation of temporoparietal
brain regions and pathogenetically associated with
negative effects of disorders of metabolic processes
and those of cerebral hemodynamics on the brain.
An important role in development of cerebral
discirculation in type 2 DM is played by disorders
of cerebral vessels reactivity, and deterioration of
collateral and vasodilator links of the vascular reserve.
For screening and diagnosis of cognitive decline in
type 2 DM Addenbrooke’s Cognitive Examination
demonstrated a good validity. In turn, early detection
of cognitive decline and administration of adequate
therapy considering the state of cerebrovascular
reserve allowed preventing its decline in patients with
diabetic encephalopathy in type 2 DM, to improve
their quality of life and social adaptation.
Table 1
Hemodynamics of blood flow in the major arteries
of the head and intracranial arteries at rest
Vessels
LBFV, cm/s PL, conventional units RL, conventional units
main group controls main group controls main group controls
IСА d 35,4±5,8* 53,2±6,4 1,5±0,13* 0,83±0,21 0,97±0,20* 0,55±0,16
IСА s 34,9±6,1* 51,9±5,9 1,6±0,14* 0,82±0,19 0,99±0,20* 0,53±0,15
MСА d 40,9±5,7* 62,4±11,3 1,11±0,11* 0,56±0,14 0,77±0,15* 0,50±0,10
МCА s 41,8±6,9* 65,2±10,7 1,11±0,12* 0,57±0,14 0,80±0,11* 0,51±0,09
SА d 21,7±5,6* 37,6±7,8 1,12±0,13* 0,78±0,11 0,81±0,09* 0,52±0,08
SА s 209±5,9* 38,6±8,7 1,08±0,16* 0,74±0,10 0,89±0,15* 0,52±0,07
CСА 30,7±5,3* 46,4±5,6 0,99±0,19* 0,54±0,19 1,05±0,16* 0,56±0,09
* p < 0,01 with respect to the controls. The same in Table 2.
16
НЕвРОЛОгИя
w
w
w
.im
j.k
h.
ua
R e f e r e n c e s
1. Маньковский Б. Н. Сахарный диабет и �еребр��ас��-и �еребр��ас��-�еребр��ас��-
лярные заб�ле�ания / Б. Н. Мань���с�ий // Н���сти
меди�ины и фарма�ии.— 2007.— № 216.— С. 21–23.
2. Мищенко Т. С. Сахарный диабет и �еребр��ас��лярные
заб�ле�ания: �згляд не�р�л�га / Т. С. Мищен�� //
Зд�р��’я У�раїни.— 2011.— № 1 (15).— С. 39.
3. Sima A. A. F. Encephalopathies: the emerging diabetic
complications / A. A. F. Sima // Acta Diabetol.—
2010.— № 47.— Р. 279–293.
4. Diabetes and Cardiovascular Disease: Writing Group
I: epidemiology / B. V. Howard, B. L. Rodrigues,
P. H. Bennett [et al.] // Circulation.— 2002.—
Vol. 105.— P. 132–137.
5. Ефимов А. Диабетичес�ие анги�патии: эти�л�гия
и пат�генез / А. Ефим��, Н. З�е�а, Н. С�р�б�нс�ая //
Лі�и У�раїни.— 2004.— № 11.— С. 36–38.
6. Верещагин Н. В. К пр�блеме ��ен�и �еребр��ас��-пр�блеме ��ен�и �еребр��ас��-
лярн�г� резер�а при атер�с�лер�тичес��м п�ражении
с�нных артерий / Н. в. верещагин, Д. Ю. Бархат��,
Д. Н. Джибладзе // Ж�рн. не�р�л�гии и психиатрии
им. С. С. К�рса���а.— 1999.— № 2.— С. 57–64.
7. Аssessment of cerebrovascular reserve capacity in
asymptomatic and symptomatic hemodynamically
significant carotid stenosis and occlussions / L. Orosz,
B. Fulesdi, F. Hoksbergen [et al.] // Surg. Neurol.—
2002.— Vol. 57.— P. 333–339.
8. С�часні �я�лення пр� пат�генез діабетичн�ї ен-
�ефал�патії / Н. в. Паш���сь�а, П. в. в�л�шин,
в. П. Піша�, в. М. Паш���сь�ий // У�р. не�р�л.
ж�рн.— 2007.— № 3.— С. 29–36.
9. Паньків В. І. К�гніти�ні п�р�шення � х��рих
на ���р��ий діабет 2 тип� / в. І. Пань�і� //
Зд�р��’я У�раїни.— 2008.— № 19.— С. 55–56.
10. Захаров В. В. в�зм�жн�сти анти��сидант�� � лече-
нии �меренных ��гнити�ных нар�шений � б�льных
сахарным диабет�м / в. в. Захар��, в. Б. С�сина //
Зд�р��’я У�раїни.— 2010.— № 1.— С. 18–19.
11. Умеренные ��гнити�ные нар�шения при сахарн�м
диабете 2-г� типа / Е. Л. Т��ажнянс�ая, И. О. Без- / Е. Л. Т��ажнянс�ая, И. О. Без-/ Е. Л. Т��ажнянс�ая, И. О. Без-Е. Л. Т��ажнянс�ая, И. О. Без-Т��ажнянс�ая, И. О. Без-И. О. Без-Без-
�гл��а, М. Б. На�р�з��, Н. С. Бал���ая // Межд�нар.
мед. ж�рн.— 2012.— № 1.— С. 6–9.
12. Differential peculiarities of brain neuroimaging in
patients with Diabetic encephalopathy in dependence
on the type of basic disease / N. V. Pashkovska,
O. A. Olenovych, A. I. Fedin, V. M. Pashkovsky //
Pharmacologyonline.— 2008.— Vol. 2.— P. 41–47.
13. Момот Н. В. К�мп’ютерна т�м�графія � ��мпле�сній
діагн�сти�і діабетичн�ї ангі�патичн�ї ен�ефал�па-
тії / Н. в. М�м�т, Т. Є. Михайличен�� // Енд��ри-
н�л�гія.— 2002.— № 7.— С. 175–180.
14. Brain magnetic resonance imaging correlates of im-
paired cognition in patients with type 2 diabetes /
S. M. Manschot, A. M. A. Brands, Van der Grond [et
al.] // Diabetes.— 2006.— Vol. 55 (4).— P. 1106–1113.
15. Cognitive impairment and MRI correlates in the el-
derly patients with type 2 diabetes mellitus / B. van
Harten, J. Oosterman, D. Muslimovic [et al.] // Age
Ageing.— 2007.— Vol. 36 (2).— P. 164–170.
16. Sima A. A. Insulin, C-peptide, hyperglycemia, and
central nervous system complications in diabetes /
A. A. Sima, H. Kamiya, Z. G. Li // Eur. J. Pharma-Sima, H. Kamiya, Z. G. Li // Eur. J. Pharma-H. Kamiya, Z. G. Li // Eur. J. Pharma-Kamiya, Z. G. Li // Eur. J. Pharma-Z. G. Li // Eur. J. Pharma-Li // Eur. J. Pharma- // Eur. J. Pharma-// Eur. J. Pharma-J. Pharma-Pharma-
col.— 2004.— Vol. 490.— P. 187–197.
17. Рeripheral and central neurologic complications in
type 2 diabetes mellitus: No association in individual
patients / S. M. Manschot, G. J. Biessels, G. E. Rutten
[et al.] // J. of the Neurol. Sci.— 2008.— Vol. 264.—
P. 157–162.
18. Folstein M. F. «Mini-mental state». A practical method
for grading the cognitive state of patients for the clini-
can / M. F. Folstein, S. E. Folstein, P. R. McHugh //
J. Psychiatr. Res.— 1975.— Vol. 12.— P. 189–198.
19. Трещинская М. А. О�ен�а п�зна�ательных ф�н��ий
«� п�стели б�льн�г�» / М. А. Трещинс�ая // Ней-� п�стели б�льн�г�» / М. А. Трещинс�ая // Ней-п�стели б�льн�г�» / М. А. Трещинс�ая // Ней- / М. А. Трещинс�ая // Ней-/ М. А. Трещинс�ая // Ней-М. А. Трещинс�ая // Ней-Трещинс�ая // Ней- // Ней-// Ней-
р�н-ре�ю.— 2009.— № 5.— С. 25–29.
20. The Addenbrooke’s Cognitive Examination Revised
(ACE-R): a brief cognitive test battery for demen-a brief cognitive test battery for demen-brief cognitive test battery for demen-
tia screening / E. Mioshi, K. Dawson, J. Mitchell
[et al.] // Int. J. Geriatr. Psychiatry.— 2006.— Vol. 21.—
P. 1078–1085.
21. Гайдар Б. В. П�л���личест�енная ��ен�а а�т�рег�-
ля�ии �р���снабжения г�л��н�г� м�зга � н�рме /
Б. в. гайдар, Д. в. С�ист��, К. Н. Храп�� // Ж�рн.
не�р�л�гии и психиатрии им. С. С. К�рса���а.—
2000.— № 6.— С. 38–41.
ЦЕРЕБРОВАСКУЛЯРНАЯ НЕДОСТАТОЧНОСТЬ И ДИАБЕТИЧЕСКАЯ ЭНЦЕФАЛОПАТИЯ
У БОЛЬНЫХ САХАРНЫМ ДИАБЕТОМ 2-го ТИПА
Пр�ф. Е. Л. ТОвАЖНяНСКАя, И. О.БЕЗУгЛОвА
Выявлены особенности структуры когнитивной дисфункции при сахарном диабете 2-го типа и ди-
абетической энцефалопатии II стадии, которые характеризовались нарушением функции памяти,
беглости речи, внимания и ориентации. Установлена связь когнитивных расстройств с длительнос-
тью заболевания, концентрацией гликозилированного гемоглобина, нарушением биоэлектрической
активности мозга, церебральной гемодинамики и цереброваскулярной реактивности.
Ключевые слова: сахарный диабет 2-го типа, диабетическая энцефалопатия, когнитивные наруше-
ния, цереброваскулярная недостаточность, цереброваскулярный резерв.
17© I. O. BEZugLOVA, 2014
МЕЖДУНАРОДНЫЙ МЕДИЦИНСКИЙ ЖУРНАЛ, 2014, № 1
w
w
w
.im
j.k
h.
ua
НЕВРОЛОГИЯ
ЦЕРЕБРОВАСКУЛЯРНА НЕДОСТАТНІСТЬ І ДІАБЕТИЧНА ЕНЦЕФАЛОПАТІЯ
У ХВОРИХ НА ЦУКРОВИЙ ДІАБЕТ 2-го ТИПУ
О. Л. ТОвАЖНяНСЬКА, І. О. БЕЗУгЛОвА
Визначено особливості структури когнітивної дисфункції при цукровому діабеті 2-го типу і діа-
бетичній енцефалопатії II стадії, що характеризувалися порушенням функції пам’яті, мовлен-
ня, уваги та орієнтації. Встановлено зв’язок когнітивних розладів із тривалістю захворювання,
концентрацією глікозильованого гемоглобіну, порушенням біоелектричної активності мозку, це-
ребральної гемодинаміки та цереброваскулярної реактивності.
Ключові слова: цукровий діабет 2-го типу, діабетична енцефалопатія, когнітивні порушення, цере-
броваскулярна недостатність, цереброваскулярний резерв.
П�ст�пила 16.12.2013
|