Mart, 2025-Yil
316
PATHOGENETIC MECHANISMS OF OPTIC NERVE DAMAGE IN ISCHEMIC
NEUROPATHY
Jalalova Dilfuza Zuhridinovna
Scientific supervisor.
Department of Ophthalmology, Samarkand State Medical University
Yaxshinorov Islombek
Samarkand State Medical University, Department of Ophthalmology, 1st year clinical ordinator
https://doi.org/10.5281/zenodo.15072867
Abstract. Optic neuritis (optic neuritis) is an inflammatory lesion of the optic nerve. This
disease also includes nerve damage in demyelinating diseases. Within the framework of optic
neuritis, intra- and retrobulbar neuritis are distinguished, which differ significantly in the
ophthalmoscopic picture. Common symptoms: decreased vision and the appearance of scotomas;
In some forms, pain in the eye may occur. Ophthalmoscopy plays a key role in diagnosis.
Treatment is based on a combination of anti-edema, anti-inflammatory, desensitizing,
antibacterial or antiviral, immunocorrective, detoxifying and metabolic therapy.
Keywords: Causes, Pathogenesis, Classification, Symptoms of intrabulbar neuritis,
Symptoms of retrobulbar neuritis, Diagnosis of optic neuritis, Treatment and prognosis of optic
neuritis.
Introduction:
The optic nerve (n. opticus) consists of processes (axons) of retinal neurons.
The latter perceive the image and transmit information about it in the form of nerve
impulses that travel along the axons to the visual centers of the brain. Each optic nerve consists of
more than 1 million axons. It begins in the optic disc, which is located in the retina and can be
examined by ophthalmologists. The part of n. opticus located inside the orbit is called intrabulbar
(intraorbital). After leaving the orbit, the optic nerve passes into the cranial cavity, this part of
which is called the retrobulbar part. In the area of \u200b\u200bthe sella turcica, the optic nerves
intersect (chiasm), where they partially exchange their fibers. The optic nerves end in the visual
centers of the midbrain and diencephalon.
The optic nerve is surrounded along its entire length by a sheath that is closely connected
to the orbit and adjacent structures of the brain, as well as to the membranes of the brain. This
leads to the frequent occurrence of optic neuritis in inflammatory diseases of the eye socket, brain,
and its membranes.
Mart, 2025-Yil
317
Research methods and materials:
Among the factors provoking optic neuritis, the most
common are inflammatory processes in the orbit (periostitis, phlegmon), eyeball (iridocyclitis,
retinitis, keratitis, panophthalmitis) and brain (arachnoiditis, meningitis, encephalitis); infectious
processes in the nasopharynx (ethmoiditis, sinusitis, frontal sinusitis, chronic tonsillitis, sore throat,
pharyngitis). Common infections can lead to the development of optic neuritis: tuberculosis,
malaria, typhoid, brucellosis, acute respiratory viral infections, diphtheria, gonorrhea, etc. Other
causes include alcoholism, traumatic brain injury, complicated pregnancy, systemic blood diseases,
autoimmune diseases (gout, diabetes mellitus). Often optic neuritis manifests itself multiple
sclerosis.
The inflammatory process (neuritis) can develop both in the sheath of the optic nerve and
in its div. In this case, inflammatory edema and infiltration lead to compression of the optic fibers
with subsequent degeneration, which leads to a decrease in visual acuity. After the acute
inflammation subsides, some fibers can restore their function, which is clinically manifested by an
improvement in vision. Severe optic neuritis often leads to the destruction of nerve fibers and the
growth of glial tissue in their place. Atrophy of the optic nerve develops with irreversible loss of
visual acuity.
In multiple sclerosis, neuritis is based on the process of demyelination of nerve fibers - the
destruction of their myelin sheath. Although demyelination is not an inflammatory process, in the
medical literature and practice demyelinating lesions of n. opticus are classified as retrobulbar
neuritis, since their clinical symptoms are the same.
Optic neuritis can be classified according to its etiology and the location of the lesion.
Depending on the etiological factor, infectious, parainfectious, demyelinating, ischemic,
toxic and autoimmune neuritis are distinguished. Parainfectious types include optic neuritis
resulting from vaccination or previous viral infection. Ischemic neuritis can occur as a result of a
stroke. The classic type of toxic optic neuritis is damage to the optic nerve due to methyl alcohol
poisoning.
According to the site of defeat n. opticus distinguish intrabulbar and retrobulbar optic
neuritis. Intrabulbar neuritis (papilitis) occurs with changes in the optic nerve head and is the most
common form of optic neuritis in children. The combination of papillitis with damage to the retinal
nerve fiber layer is classified as neuroretinitis. The latter is very rare and can be a consequence of
viral diseases, cat scratch disease, Lyme disease and syphilis. Retrobulbar neuritis is a term used
to describe damage to the optic nerve after it leaves the orbit. Often associated with multiple
sclerosis.
Mart, 2025-Yil
318
In retrobulbar neuritis, ophthalmoscopy does not reveal changes in the optic nerve head,
they can appear only in the late stages of the disease, when the process spreads to the intraorbital
part of the nerve; Due to the prevalence of inflammation and degenerative changes n. opticus
during the course of the disease, the division of neuritis into intra- and retrobulbar is very arbitrary.
Typically, the onset of visual impairment is acute. Their severity and nature depend on the
degree of damage to the optic nerve head. In the general process, visual acuity decreases to the
level of complete blindness (amaurosis). In partial cases, visual acuity may even remain at 1.0. At
the same time, spots appear in the field of vision - paracentral or central scotomas, which have an
arched or rounded shape; There is a decrease in color perception and dark adaptation, a low level
of optic nerve lability, and a critical flicker fusion frequency.
Results:
From the first days of neuritis, a pathognomonic picture of changes in the optic
nerve head is determined: hyperemia, blurred boundaries, exudative-type edema, moderate
vasodilation, the presence of linear hemorrhages in the disc tissue and in the peridiscal region. If
the exudate fills the vascular funnel and absorbs the adjacent layers of the vitreous div, then the
fundus is not clearly visible. Unlike congestive discs associated with intracranial hypertension and
hydrocephalus, with optic neuritis there is no pronounced protrusion of the disc, and the changes
are usually unilateral.
The acute period lasts from 3 to 5 weeks. Then the hyperemia and swelling of the disc
gradually disappear, the hemorrhages disappear, and the disc boundaries again acquire clear
contours. More rarely, with severe optic neuritis, atrophy of n. optic. In this case, ophthalmoscopy
reveals a pale disc with narrowed, thread-like vessels and clear boundaries.
In the clinical presentation of retrobulbar optic neuritis, 3 types of inflammatory changes
are distinguished: axial, peripheral, and transverse.
Axial inflammation primarily affects the bundle of axons that run in the optic nerve. It is
characterized by the formation of central scotomas in the visual field and a significant decrease in
functional tests, leading to impaired central vision.
The peripheral type of retrobulbar neuritis is associated with the onset of the inflammatory
process in the nerve sheath and its subsequent spread deep into the nerve trunk. In this case, a
significant accumulation of exudate occurs under the optic nerve membranes, which causes
patients to experience the so-called "membranous" pain in the eye, which is aggravated by
movement of the eyeball. Typically, there is a concentric narrowing of the visual fields, while
maintaining central vision. The results of functional tests may be within normal limits.
Mart, 2025-Yil
319
The most severe type is the transverse type of retrobulbar neuritis, in which inflammation
affects all tissues of the optic nerve. Visual acuity is reduced to the point of blindness. Functional
tests show very poor results.
All types of retrobulbar neuritis are characterized by the absence of changes in the optic
nerve head. Only a month after the onset of the disease, ophthalmoscopy can detect signs of disc
discoloration and general or partial atrophy of the optic nerve.
Discussion:
Since optic neuritis is an interdisciplinary pathology, its diagnosis often
requires the joint participation of specialists in the fields of neurology and ophthalmology. Usually,
a consultation with an ophthalmologist is sufficient to confirm the diagnosis, during which the
patient's complaints, visual acuity test data, perimetry and ophthalmoscopy results are compared.
The most important task is to differentiate disc changes in optic neuritis from disc
congestion. This is especially true in cases of mild neuritis with minimal visual impairment and in
cases of neuritis combined with disc swelling. In such cases, the detection of foci of exudation and
small hemorrhages in the disc tissue indicates neuritis. Fundus fluorescein angiography helps to
differentiate these conditions. In complex cases, consultation with a neurologist,
echoencephalography, or lumbar puncture may be required to exclude a herniated disc.
To determine the etiology of optic neuritis, an MRI scan of the brain, blood culture for
sterility, PCR studies, ELISA, RPR test, consultation with an infectious disease specialist,
rheumatologist, immunologist, etc. may be necessary.
Etiotropic therapy is determined by the cause of the development of neuritis. Treatment is
carried out urgently in a hospital setting. Until the etiology of the disease is determined, anti-
inflammatory, rehydration, antibacterial, metabolic, desensitizing and immunocorrective
treatment methods are usually used. Broad-spectrum antibiotics (except for the aminoglycoside
group), corticosteroids, acetazolamide with potassium preparations, intravenous glucose infusions,
intramuscular magnesium sulfate, piracetam and B vitamins are prescribed (for example, after
determining the nature of the optic nerve damage). lithitis and sinusitis).
Conclusion
: Emergency therapy for optic neuritis resulting from methyl alcohol poisoning
consists of immediate gastric lavage and oral administration of 30% ethyl alcohol (vodka). The
latter acts as an antidote that displaces methyl alcohol from the div. A single dose is 100 g and
is administered every 2-3 hours.
If signs of optic nerve atrophy are detected, antispasmodics and drugs to improve
microcirculation (nicergoline, pentoxifylline, nicotinamide, nicotinic acid) are additionally
recommended.
Mart, 2025-Yil
320
The outcome of intra- and retrobulbar forms of optic neuritis depends on the type and
severity of the lesion. It varies from complete restoration of visual function to the development of
atrophy and amaurosis.
REFERENCES
1.
БЕЛКА, F. S. Р. С. Р. (2022). В ПАТОГЕНЕЗЕ СОСУДИСТЫХ ЗАБОЛЕВАНИЙ
ОРГАНА ЗРЕНИЯ У БОЛЬНЫХ АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИЕЙ.
2.
Жалалова, Д. З., Кадирова, А. М., & Хамракулов, С. Б. (2021). Исходы герпетических
кератоувеитов на фоне лечения препаратом «офтальмоферон» в зависимости от
иммунного статуса пациентов. междисциплинарный подход по заболеваниям
органов головы и шеи, 103.
3.
ЖД, З., and А. БС. "РЕЗУЛЬТАТЫ ОЦЕНКИ УРОВНЯ ЭНДОТЕЛИНА-1 И Д-
ДИМЕРОВ В СЛЕЗНОЙ ЖИДКОСТИ У ПАЦИЕНТОВ С АРТЕРИАЛЬНОЙ
ГИПЕРТЕНЗИЕЙ." SCIENTIFIC JOURNAL OF APPLIED AND MEDICAL
SCIENCES 3.3 (2024): 300-307.
4.
Zhalalova, D. Z. OCT angiography in the assessment of retinal and choreoretinal
microcirculation in patients with uncomplicated arterial hypertension International
Ophthalmological Congress IOC Tashkent 2021.
5.
Zhalalova, D. Z. Evaluation of markers of endothelial dysfunction in tear fluid in patients
with arterial hypertension. Journal of Biomedicine in Amaliet. Tashkent-2022, Volume
No., No. WITH.
6.
Жалалова, Д. З. (2021). Эндотелин-1 ва гомоцистеин даражасини артериал
гипертензия фонида тур пардв узгаришларида эндотелиал дисфункциянинг
маркерлари сифатида текшириш. Биомедицина ва амалиет журнали, 6(5), 203-210.
7.
Jalalova, D., Axmedov, A., Kuryazov, A., & Shernazarov, F. (2022). Combined dental and
eye pathology. Science and innovation, 1(8), 91-100.
8.
Zhalalova, D. Z. (2022). Pulatov US MICROCIRCULATORY DISORDERS IN THE
VASCULAR SYSTEM OF THE BULBAR CONJUNCTIVA WITH INITIAL
MANIFESTATIONS OF INSUFFICIENT BLOOD SUPPLY TO THE BRAIN. European
journal of molecular medicine, 2(5).
9.
Жалалова, Д. З. (2021). ОКТ-ангиография при оценке сосудистого русла сетчатки и
хориоидеи. Биология ва тиббиет муаммолари, 6(130), 211-216.
Mart, 2025-Yil
321
10.
Жалалова, Д. З. (2022). Классификационые критерии изменений сосудов сетчатки
при артериальной гипертензии. In Международная научная конференция
Университетская наука: взгляд в будущее (pp. 56-64).
11.
Долиев, М. Н., Тулакова, Г. Э., Кадырова, А. М., Юсупов, З. А., & Жалалова, Д. З.
(2016). Эффективность комбинированного лечения пациентов с центральной
серозной
хориоретинопатией.
Вестник
Башкирского
государственного
медицинского университета, (2), 64-66.
12.
Жалалова, Д. З. Оценка маркеров эндотелиальной дисфункции в слезной жидкости
у пациентов с артериальной гипертензиейЖурнал «Биомедицина ва амалиет».
Тошкент-2022, Том №, №. С.
13.
Жалалова, Д. З. (2021). ОКТ-ангиография в оценке ретинальной и хореоретинальной
микроциркуляции у пациентов с неосложненой артериальной гипертензией/I
Международный офтальмологческий конгресс IOC Uzbekistan, 2021 г. Ташкент, с,
96.
14.
Shernazarov, F., Jalalova, D., Azimov, A., & CAUSES, S. A. (2022). SYMPTOMS,
APPEARANCE, TREATMENT OF VARICOSE VEINS.
15.
Жалалова, Д. З. (2021). Эндотелин-1 ва гомоцистеин даражасини артериал
гипертензия фонида тур пардв узгаришларида эндотелиал дисфункциянинг
маркерлари сифатида текшириш. Биомедицина ва амалиет журнали, 6(5), 203-210.
16.
Shernazarov, F., Tohirova, J., & Jalalova, D. (2022). Types of hemorrhagic diseases,
changes in newboens, their early diagnosis. Science and innovation, 1(D5), 16-22.
17.
Zhalalova, D. Z. (2022). The content of endothelin and homocysteine in blood and lacrimal
fluid in patients with hypertensive retinopathy Web of Scientist: International Scientific
Research Journal. ISSUE, 2, 958-963.
18.
Shernazarov, F., & Zuhridinovna, J. D. (2022). Microcirculation disorders in the vascular
system of the bulbar conjunctiva in the initial manifestations of cerebral blood supply
deficiency. Science and innovation, 1(Special Issue 2), 515-522.
19.
Zhalalova, D. Z. (2022). Modern aspects of neuroprotektive treatment in hypertensive
retinopathy Web of Scientist: International Scientific Research JournalVolume 3. ISSUE,
2, 949-952.
20.
Жалалова, Д. З. (2009). Метод комбинированного лечения диабетической
ретинопатии. Врач-аспирант, 37(10), 864-868.
Mart, 2025-Yil
322
21.
Жалалова, Д. З. (2023). Результаты оценки эффективности комплексного лечения у
пациентов с 3-4 стадиями гипертонической ангиоретинопатии. Miasto Przyszłości, 41,
33-36.
22.
ЖД, З., & ИЖ, Ж. (2024). КЛАССИФИКАЦИЯ ГИПЕРТОНИЧЕСКОЙ
РЕТИНОПАТИИ НА ОСНОВЕ ДАННЫХ ОПТИЧЕСКОЙ КОГЕРЕНТНОЙ
ТОМОГРАФИИ. SCIENTIFIC JOURNAL OF APPLIED AND MEDICAL SCIENCES,
3(3), 336-342.
23.
ЗЖД, Ж. (2024).
КЛИНИКО-ФУНКЦИОНАЛЬНЫЕ ПОКАЗАТЕЛИ ОРГАНА ЗРЕНИЯ У
ПАЦИЕНТОВ С ИШЕМИЧЕКИМИ ИЗМЕНЕНИЯМИ СОСУДОВ СЕТЧАТКИ.
SCIENTIFIC JOURNAL OF APPLIED AND MEDICAL SCIENCES, 3(3), 286-293.
24.
ЖД, З. (2024). ОЦЕНКА КЛИНИЧЕСКИХ И ФУНКЦИОНАЛЬНЫХ
ПОКАЗАТЕЛЕЙ ЭНДОТЕЛИАЛЬНОЙ ДИСФУНКЦИИ В СЛЕЗНОЙ ЖИДКОСТИ
У ПАЦИЕНТОВ С АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИЕЙ. SCIENTIFIC JOURNAL
OF APPLIED AND MEDICAL SCIENCES, 3(3), 330-335.
25.
Жалалова, Д. З. (2023). Актуальность проблемы изменений глазного дна при
артериальной гипертензии. Miasto Przyszłości, 41, 37-40.
