Оценка эффективности комплексной терапии прогрессирующей глаукомной нейропатии

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Мирбабаева, Ф., & Янгиева, Н. (2020). Оценка эффективности комплексной терапии прогрессирующей глаукомной нейропатии. in Library, 20(2), 78–80. извлечено от https://inlibrary.uz/index.php/archive/article/view/14717
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Аннотация

Оценка терапевтической эффективности глиатилина для стабилизации зрительных функций после комплексного лечения больных прогрессирующей глаукомно оптической нейропатии с «нормализованным» давлением. Глиатилинноотропный  препарат,  холиномиметик  центрального  действия  с  преимущественным  влиянием  на  ЦНС.  Включение глиатилина  в  комплекс  лечебных  мероприятий,  направленных  на  поддержание  зрительных  функций  у  больных нестабилизированной  глаукомой, направленных на  различные  звенья патогенеза  глаукомной  оптической  нейропатии позволяют  добиться  стабилизации  процесса  у  89%  больных  далеко  зашедшей  нестабилизированной  глаукомой  в течение 6 месяцев.

Похожие статьи


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78

1SSN2181-7812

www.tma-journals.uz

УДК 617.7

-007.691

ESTIMATION OF EFFICIENCY OF COMPLEX THERAPY OF PROGRESSING GLAUCOMA
NEUROPATHY

Mirbabaeva F.A., Yangieva N.R.

ОЦЕНКА ЭФФЕКТИВНОСТИ КОМПЛЕКСНОЙ ТЕРАПИИ ПРОГРЕССИРУЮЩЕЙ ГЛАУКОМНОЙ
НЕЙРОПАТИИ

Мирбабаева Ф.А., Янгиева Н.Р.

РИВОЖЛАНУВЧИ ГЛАУКОМАТОЗ НЕЙРОПАТИЯНИ КОМПЕЛЕКС ДАВОЛАШНИНГ
САМАРАДОРЛИГИНИ БАХОЛАШ

Мирбабаева Ф.А., Янгиева Н.Р.

Tashkent State Dental Institute

Оценка терапевтической эффективности глиатилина для стабилизации зрительных функций после комплексного

лечения больных прогрессирующей глаукомно оптической нейропатии с «нормализованным» давлением.

Глиатилин

-

ноотропный препарат, холиномиметик центрального действия с преимущественным влиянием на ЦНС. Включение
глиатилина в комплекс лечебных мероприятий, направленных на поддержание зрительных функций у больных
нестабилизированной глаукомой, направленных на различные звенья патогенеза глаукомной оптической нейропатии
позволяют добиться стабилизации процесса у 89% больных далеко зашедшей нестабилизированной глаукомой в
течение 6 месяцев.

Ключевые слова

-,

первичная глаукома, глаукомно оптическая нейропатия, глиатилин, ноотороп.

«Нормаллаштирилган» босимли, риволанувчи глаукоматоз оптик нейропатияли беморларни комплекс даволашдан

кейин, кўрув фаолиятларини барқарорлаштиришучун, глиатилиннинг терапевтик самарадор- лигини баҳолаш.
Глиатилин ноотроп дори воситаси бўлиб, марказий асабтизимига бирламчи таъсир кўрса- тадиган
марказийхолиномиметик воситадир.

Глиатилиннинг барцарорлашмаган глаукома билан огриган беморларда кўрув фаолиятларини сацлаб туришга

қаратилган, глаукоматоз оптик нейропатия патогенезида, турли хил таъсир этувчи, терапевтик чора-тадбир- лар
мажмуига киритилиши, олти ой давомида узок, муддатли барқарор бўлмаган глаукомали беморларнинг 89 фоизида,
жараённи баркарорлаштиришга имкон беради.

Калит сўзлар

-.

бирламчи глокома, глаукома-оптик нейропатия, глиатилин, ноотроп.

rimary glaucoma, despite advances in ophthalmology
still occupies one of the first places among the causes of

blindness throughout the world. Ophthalmologists are well
aware that even with the achievement of persistent I0P
compensation by medication or surgery, every 5th patient
continues to decompose visual functions [1- 3,5]. In this
regard, the problem of treating glaucoma optic neuropathy
is very relevant.

Glaucoma optical neuropathy fGONJ is usually con-

sidered from the standpoint of mechanical, vascular and
metabolic theories, including numerous risk factors that
increase the likelihood of progression of glaucoma lesions.
Determining the primacy of a factor is always debatable.
Only one thing is obvious: in the case of achieving an
individual level of intraocular pressure (10P) and at the
same time marked progression of GON, it is necessary to
identify other, most likely factors of influence.

Given the multifactorial progression of GON progression,

ophthalmologists usually recommend complex therapy,
prescribing drugs of various pharmacological groups [6-8].
This is often done when they plan to study the effectiveness
and safety of one of the drugs included in complex therapy.

Considering metabolic disorders, among which the

leading place is occupied by excitotoxic damage to the third
retinal neuron and activation of free radical processes in the
retina and optic nerve [1,4], we considered it expedient to
include drugs and treatment meth- ods that improve, on the
one hand, metabolism, on the other hand, neutralize the
negative influence of a number of factors and, on the third
hand, stimulate the activity of retinal neurons and restore
the conductivity of nerve fibers.

Gliatilin is a nootropic drug, a central cholinomimetic

with a primary effect on the central nervous system. Choline
is released from the active substance in the brain; choline is
involved in the biosynthesis of acetylcholine (one of the main
mediators of nervous excitation). Alfoscerate is

biotransformed to glycerophosphate, which is a precursor of
phospholipids.

Acetylcholine improves transmission of nerve impulses,

and glycerophosphate is involved in the synthesis of
phosphatidylcholine (membrane phospholipid), resulting in
improved membrane elasticity and receptor function.
Gliatilin increases cerebral blood flow, enhances metabolic
processes and activates the structure of the reticular
formation of the brain, restores consciousness in traumatic
brain damage. It has a preventive and corrective effect on
factors of involutional psycho-organic syndrome, such as a
change in the phospholipid composition of neuronal
membranes and a decrease in cholinergic activity. Thus,
pharmacodynamic studies have shown that gliatilin acts on
synaptic, including cholinergic, transmission of a nerve
impulse (neurotransmission), plasticity of a neural
membrane, and receptor function.

Despite the existing difficulties in evaluating the effec-

tiveness of neuroprotective therapy due to the lack of abso

P


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79

lutely reliable

criteria for a

number of structural

and func-

tional

indicators, such an assessment is still possible.

The aim of this work

is to evaluate the therapeutic ef-

ficacy

of gliatilin for stabilizing

visual

functions after the

complex treatment of patients with progressive GON with

“normalized” pressure.

Material and methods

We studied the

effectiveness of

treatment in two groups,

the proposed method

in

52 patients (61 eyes] with primary

open-angle glaucoma in the advanced stage with
compensated intraocular

pressure.

Patients of both groups

were comparable in age, concomitant somatic pathology, the
severity of the glaucoma process, their average age was

71.3±1.6 years.

In all

patients, therapists diagnosed systemic

atherosclerosis

with

a predominant damage to the vessels of

the brain

and

cerebrovascular insufficiency.

The analysis of ophthalmostatus indices showed that in

both groups the majority were patients with advanced stages
of glaucoma: 71.3% and 73.6%, respectively. In the 2nd
group, patients

prevailed

in which IOP normalization was

achieved surgically:

79.3%

versus 51.7% in the 1st group.

Therefore, in the latter there were more patients who
needed local antihypertensive therapy to maintain
ophthalmotonus within the target pressure. Nevertheless,
despite a steady level of IOP in the range of 15-17 mm Hg,
negative dynamics of visual functions was noted in all cases,
which served as the basis for the course of stabilizing
therapy.

When conducting complex treatment of patients, their

general somatic state was also taken into account. The
course of neuroprotective therapy included drugs of various
pharmacological groups acting on different pathogenetic
links. All patients received Mexidol 100 mg intramuscularly
1 time per day for 14 days, and patients of the 1st group, in
addition, were injected with gliatilin 1000 mg/4 ml
intravenously in an amount of 10 injections, then continued
the course of taking this drug by mouth 1 capsule 2 times a
day for 3 months.

A comprehensive ophthalmological examination was

carried out before, after treatment, after 3 and 6 months. The
following methods were used to assess visual functions:
visometry, perimetry, determination of the critical-
frequency of flicker fusion, eye rheography. Along with this,
a study was made of the electrosensitivity and electrolability
of the optic nerve and retina, and the registration of visually
evoked cortical potentials (VECP).

The state of the visual fields was evaluated in several

ways. Static perimetry was performed using a Humphrey
Visual Field Analyzer II (HFA II] 750i (Germany]. Depending
on the initial visual acuity and the degree of visual
impairment, a screening or threshold study program was
used. When assessing the central field of view (CTO], all
patients underwent correction of visual acuity near.
Screening was performed using the FF- 120 Screening
program using a three-zone strategy. The threshold program
for the study of the visual field included the application of
tests Central 30-2 in the study of the central lens (within

30

°

from the point of fixation of the gaze] and Peripheral 60-2

in the assessment of the peripheral field of vision - the

primary brain (from 30° to

60°].

At

the same time, we

analyzed the threshold foveo

lar photosensitivity,

the sum of

decibel threshold values

in each quadrant

over the entire

field of view, mean devi

ation (MD]

and standard deviation

(PSD] deviations cal

culated

automatically by the device

taking into account

its own

database.

The criteria for

evaluating

the

effectiveness of neu-

roprotective

therapy are not sufficiently

informative, and

from the

point of view of

practical ophthalmology, the study

of

visual functions

- perimetry - remains the most accessible.

Results and discussion

During the

observation

period in a hospital, during

which patients

received drugs,

in no case were adverse

events recorded.

The IOP level

was also normalized during

the entire

observation

period and was at a level not

exceeding 15 mm Hg

(p>0.05

compared with the initial data].

One of the criteria for evaluating functionality is central

visual acuity. Neuroprotective therapy, as a rule, does not
affect this indicator, however, mention of it is important as
indirect evidence of the dynamics of the process.

In our case, central visual acuity remained stable. Some

improvement in vision was noted in some patients in both

groups. Visual acuity indicators increased from 0.32±0.06 to
0.47±0.07 [p<0.05].

One of the objective criteria for assessing the effec-

tiveness of neuroprotective therapy, to a certain extent, can
be considered a study of the visual field. The indicators taken
into account when assessing changes in visual functions, we
considered CPL, foveolar and total photosensitivity, PPZ,
indicators MD and PSD.

The study was conducted before the start of a course of

drug therapy and 3, 6 months after it. All average indicators
tended to improve, especially for the central and peripheral
fields of vision. Moreover, in the group of patients receiving
gliatilin, this trend was more significant. This is all the more
important since the initial data of both groups were
comparable. The boundaries of peripheral vision (the sum of

degrees along 8 meridians] from 307±31° to 365±44
(p<0.05), CFSM from 23±6.0 to 29±7.0 (p<

0

.05] after

treatment. This amounted to 47%, 19%, 26%

of the

initial

level, respectively.

The

study was

conducted before the start of a course of

drug therapy and

3, 6

months after it. All average indicators

tended

to

improve, especially for the central and peripheral

fields of vision. Moreover, in the group of patients receiving
gliatilin, this trend was more significant. This is all the more
important since the initial data of both groups were
comparable. The boundaries of peripheral vision (the sum of
degrees

along 8

meridians] from 307±31° to 365±44

(p<0.05), CFSM from 23±6.0 to 29±7.0 (p 0.05] after

treatment. This relative to 47%, 19%, 26% of the initial level,
respectively.

Against the background of an increase in visual func-

tions, we noted an improvement in hemodynamic

and

electrophysiological parameters.

The

reographic coefficient

increased from 1.52±0.07 to

2.07±0.14% (p<0.05],

which amounted to

36% of the

initial

indicator.

The decrease

in the threshold of electric


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phosphene was 21.1 pA after treatment and 24.2 pA after 6
months of follow-up.

A significant increase in the index of electrolability of the

optic nerve was established by an average of 2.3 Hz after
treatment After half a year of dynamic observation, the
indicator is 3.5 Hz, which is 13% of the initial level, but this
difference is not statistically significant.

As a result of the treatment, a positive dynamics of the

state of visual functions was revealed according to the VECP
study. The amplitude of the P 100 component increased from

11.7 ± 4.7 to 14.3 + 5.1 pV.

We are inclined to believe that a more pronounced

therapeutic effect in patients of the 1st group is due to the
action of gliatilin. This assumption is confirmed by the
observation of a large number of patients who periodically
receive similar therapy at the institute.

Conclusion

Thus, the inclusion of gliatilin in the complex of ther-

apeutic measures aimed at maintaining visual functions in
patients with unstabilized glaucoma, aimed at various links
in the pathogenesis of glaucoma optical neuropathy, makes
it possible to achieve stabilization of the process in 89% of
patients with far-reaching unstabilized glaucoma for 6
months.

Thus, the inclusion of gliatilin in the complex of ther-

apeutic measures aimed at maintaining visual functions in
patients with unstabilized glaucoma, aimed at various links
in the pathogenesis of glaucoma optical neuropathy, makes
it possible to achieve stabilization of the process in 89% of
patients with far-reaching unstabilized glaucoma for 6
months.

The frequency of the course of stabilizing therapy

depends on the effectiveness of the previous therapy and the
clinical manifestation of the glaucoma process.

List of sources used

1.

Егоров

E.A.,

Алексеев

B.H.,

Мартынова Е.Б., Харьков

-

ский А.О. Патогенетические аспекты лечения первичной

открытоугольной глаукомы.

-

М., 2001.

-

118 с.

2.

Ермакова В.Н. О воздействии инстилляций эмокси

-

пина на циркуляцию водянистой влаги и состояние поля

зрения больных первичной открытоугольной глаукомой

//

Глаукома: проблемы

и решения: Материалы Всерос. на

-

уч.

-

практ. конф.

-

М., 2004.

-

С. 197

-201.

3.

Курышева Н.И. Механизмы

снижения зрительных

функций при первичной

открытоугольной

глаукоме и

пути

их предупреждения: Автореф.

дис. ... д

-

ра мед. наук.

-

М„

2001. -

47 с.

4.

Flammer J. Glaucomatous optic

neuropathy: a reperfusion

injury

//

Klin. Monatsbl. Augenbeilkd. -

2001.

-

Bd. 218, №5.

-S.

290-291.

5.

Hasler P.W., Orgul S., Gugleta K. et al.

Vascular

dysregulation in the choroid of subjects with

acral vasospasm

//

Arch. Ophthalmol. - 2002.

-

Vol. 120.

-

P. 302-307.

6.

Pache M., Krauchi K., Cajochen C. et al. Cold feet

and

prolonged sleep-onset latency in vasospastic syndrome

//

Lancet. - 2001. - Vol. 358. - P. 125-126.

7.

Satilmis M.,

Orgul

S., Doubler B., Flammer

J.

Rate

of

progression ofglaucoma correlates with retrobulbar circulation

and intraocular pressure

//

Amer. ]. Ophthalmol. - 2003.

-

Vol.

135. - P. 664-669.

8.

Schwartz M., Yoles E. Optic nerve degeneration and

potential neuroprotection: implications for glaucoma.

Department of Neurobiology, Weizmann Institute of Science,

Rehovot, Israel // Europ. J. Ophthalmol. - 1999. - Vol. 9. - P. 9-11.

ESTIMATION OF EFFICIENCY OF COMPLEX THERAPY
OF PROGRESSING GLAUCOMA NEUROPATHY

Mirbabaeva F.A., Yangieva N.R.

To evaluate the therapeutic efficacy of gliatilin for stabilizing

visual functions after complex treatment of patients with

progressive glaucoma-optical neuropathy with "normalized"

pressure. Gliatilin is a nootropic drug, a central cholinomimetic

with a primary effect on the central nervous system. The inclusion

of gliatilin in the complex of therapeutic measures aimed at

maintaining visual functions in patients with unstabilized

glaucoma, aimed at various

links in

the pathogenesis ofglaucoma

optical neuropathy, makes it possible to achieve stabilization of

the process in 89% of patients with far-reaching unstabilized

glaucoma for 6 months.

Key words:

primary glaucoma, glaucoma-optical neuropathy,

gliatilin, nootrope.


Библиографические ссылки

Егоров Е.А., Алексеев В.Н., Мартынова Е.Б., Харьковский А.О. Патогенетические аспекты лечения первичной открытоугольной глаукомы. - М., 2001. - 118 с.

Ермакова В.Н. О воздействии инстилляций эмокси-пина на циркуляцию водянистой влаги и состояние поля зрения больных первичной открытоугольной глаукомой // Глаукома: проблемы и решения: Материалы Всерос. на-уч.-практ. конф. - М., 2004. - С. 197-201.

Курышева Н.И. Механизмы снижения зрительных функций при первичной открытоугольной глаукоме и пути их предупреждения: Автореф. дис. ... д-ра мед. наук. -М„ 2001. -47 с.

Flammer J. Glaucomatous optic neuropathy: a reperfusion injury // Klin. Monatsbl. Augenbeilkd. - 2001. - Bd. 218, №5. -S. 290-291.

Hasler P.W., Orgul S., Gugleta K. et al. Vascular dysregulation in the choroid of subjects with acral vasospasm // Arch. Ophthalmol. - 2002. - Vol. 120. - P. 302-307.

Pache M., Krauchi K., Cajochen C. et al. Cold feet and prolonged sleep-onset latency in vasospastic syndrome // Lancet. - 2001. - Vol. 358. - P. 125-126.

Satilmis M., Orgul S., Doubler B., Flammer J. Rate of progression ofglaucoma correlates with retrobulbar circulation and intraocular pressure // Amer. ]. Ophthalmol. - 2003. - Vol. 135. - P. 664-669.

Schwartz M., Yoles E. Optic nerve degeneration and potential neuroprotection: implications for glaucoma. Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel // Europ. J. Ophthalmol. -1999. - Vol. 9. - P. 9-11.

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