What is optical neuropathy? Features of the clinical course of anterior ischemic optic neuropathies of various origins. Posterior ischemic neuropathy

Ischemic neuropathy of the optic (optic) nerve is a pathology of this area of ​​the eye, occurring due to local circulatory disorders (in the intraorbital and intrabulbar region).

The disease is accompanied by a rapid decline in visual acuity, narrowing of visual fields, and the appearance of blind spots. Methods for diagnosing ischemic neuropathy optic nerve- ophthalmoscopy, visometry, ultrasound, CT and MRI, angiography and others.

Treatment is medicinal, including vitamins, decongestants, antispasmodics, thrombolytics. Treatment is often complemented by physiotherapeutic procedures and laser stimulation of the optic nerve.

The disease is more often observed in the age group of 40-60 years, mostly affecting men. Optic neuropathy is considered a serious pathology, since it can significantly reduce visual acuity, and in some cases threaten its complete loss.

The disease is not considered independent: it is always part of a systemic pathological process(both in the organs of vision and in other parts of the body).

In this regard, ischemic neuropathy is considered not only by ophthalmologists, but also by neurologists, cardiologists, endocrinologists, hematologists, etc.

Types of ischemic optic neuropathy

The disease can occur in two different ways. The first of them is called locally limited ischemic neuropathy, the second is complete, or total ischemic neuropathy. According to the area covered by pathological processes, the disease can be anterior or posterior.

With the development of anterior neuropathy, damage to the optic nerve is observed against the background of acute circulatory disorders in the intrabulbar area.

The posterior form of neuropathy is diagnosed much less frequently. It is caused by ischemia-type damage in the intraorbital region.

Etiology and pathogenesis

Anterior ischemic neuropathy is associated with abnormal changes in blood flow in the ciliary arteries. Due to insufficient oxygen supply to tissues, a state of ischemia (oxygen starvation) of the retinal, prelaminar, and scleral layers of the optic nerve head develops.

Posterior ischemic neuropathy occurs as a result of impaired blood supply to the posterior parts of the optic nerve, often due to stenosis of the carotid and vertebral arteries.

In general, the development of acute circulatory disorders in most cases is provoked by vascular spasms or organic lesion these vessels (for example, thrombosis, sclerosis).

The above conditions, which entail the appearance of signs of ischemic optic neuropathy, may have different prerequisites.

The disease starts against the background of the underlying pathology, mainly vascular disorders - hypertension, vascular atherosclerosis, temporal giant cell arteritis, periarthritis nodosa, obliterating arteritis, thrombosis of arteries and veins. Among the pathologies of metabolic processes, ischemic neuropathy is often accompanied by diabetes mellitus.

The disease can also develop in combination with discopathy of the cervical segment of the spine. Occasionally, pathology can accompany severe blood loss, for example, with perforation of a stomach or intestinal ulcer, injury internal organs, after operation.

Sometimes ischemic neuropathy occurs when serious illnesses blood, anemia, during hemodialysis, after administration of anesthesia, with arterial hypotension.

Clinical picture

In most cases, the symptoms of ischemic neuropathy are unilateral. Less commonly (up to 1/3 of cases), the pathology spreads to the second organ of vision.

Since the course of the disease can be very long, the second eye is affected later - several weeks and even years after the onset of pathological phenomena in the first. Most often, in the absence of treatment, after 3-5 years, both organs of vision become involved in the process.

With the initial occurrence of anterior ischemic neuropathy, posterior ischemic neuropathy may subsequently develop, and signs of occlusion of the central retinal artery may also appear.

Usually the disease starts quickly and suddenly. After waking up in the morning, taking a bath, doing any physical work or playing sports, visual acuity decreases, and in some patients - to the point of blindness or identification of the light source.

In order for a person to feel a deterioration in visual acuity, it sometimes takes from a minute to a couple of hours. In some cases, damage to the optic nerve is preceded by severe headache, the appearance of a veil before the eyes, pain in the orbit on the back side, the occurrence of unusual phenomena in the field of vision.

Ischemic optic neuropathy always leads to deterioration of a person's peripheral vision. Often, vision pathologies come down to the formation of blind spots (scotomas), the disappearance of the image in the lower part of the view or in the nasal and temporal areas.

The acute condition lasts up to a month (sometimes longer). Further, the swelling of the optic nerve head decreases, hemorrhages gradually resolve, and the nervous tissue atrophies with varying degrees of severity. In many patients, vision is partially restored.

Diagnostics

If any of the above symptoms occur, you must urgently call an ambulance or quickly seek help from an ophthalmologist. The examination program necessarily includes consultations with other specialists - a cardiologist, neurologist, rheumatologist, hematologist, etc. (until the cause of ischemic neuropathy is identified).

Ophthalmological studies include functional testing of the eyes, biomicroscopy, instrumental examinations using ultrasound, x-rays, and various electrophysiological methods. The specialist checks the patient's visual acuity.

With ischemic neuropathy, varying degrees of decrease in this indicator are found - from slight loss of vision to complete blindness. Abnormalities in visual function are also detected depending on the affected nerve area.

During ophthalmoscopy, swelling, pallor, an increase in the size of the optic nerve head, as well as its advancement towards the vitreous body are detected.

In the area of ​​the disc, the retina swells greatly, and a star-shaped figure appears in its central section. The vessels in the area of ​​compression narrow, and at the edges, on the contrary, they become more filled with blood and pathologically expand. In some cases, hemorrhages and exudate are present.

As a result of angiography retina eyes, retinal angiosclerosis, occlusion of cilioretinal vessels, pathological changes in the caliber of veins and arteries are visualized.

Usually, disturbances in the structure of the optic nerve head are not detected in posterior ischemic neuropathy. When performing an ultrasound of the arteries with Doppler sonography, a violation of normal blood flow is recorded.

Electrophysiological examinations include an electroretinogram, calculation of the maximum flicker fusion frequency, etc. Usually there is a decrease in the functional properties of the nerve. A coagulogram reveals hypercoagulation, and a blood test for cholesterol and lipoproteins reveals an increased amount.

Ischemic neuropathy should be differentiated from retrobulbar neuritis, tumors nervous system and orbits of the eye.

Treatment

Treatment should be started as early as possible, optimally in the first hours after the onset of symptoms. This need is due to the fact that long-term disruption of normal blood supply leads to the loss of nerve cells.

From measures emergency care are used intravenous injections aminophylline, taking tableted nitroglycerin, short-term inhalation of ammonia fumes. After emergency treatment, the patient is admitted to the hospital.

In the future, the goal of therapy is to reduce swelling and improve trophism nerve tissue, as well as providing an alternative route of blood circulation. In addition, the underlying disease is treated and normalization of blood clotting, fat metabolism, and blood pressure is ensured.

From vasodilators for ischemic neuropathy, Cavinton, Cerebrolysin, Trental are used, among decongestants - diuretics Lasix, Diacarb, among blood thinners - thrombolytics heparin, phenylin.

Additionally, glucocorticosteroids are prescribed, vitamin complexes, physiotherapy (electrical stimulation, laser nerve stimulation, magnetic therapy, microcurrents).

Forecast

With ischemic optic neuropathy, the prognosis is usually unfavorable. Even with a comprehensive treatment program, visual acuity decreases, a persistent decline in vision and various defects, and loss of areas from vision are often observed, which occurs due to atrophy of nerve fibers.

In half of the patients, vision can be improved by 0.2 units. through intensive treatment. If both eyes are involved in the process, complete blindness often develops.

Prevention

In order to prevent ischemic neuropathy, it is necessary to treat any vascular, metabolic and systemic diseases in a timely manner.

After an episode of ischemic neuropathy occurs in one organ of vision, the patient should be regularly observed by an ophthalmologist, and also follow his advice on preventive therapy.

Ischemic optic neuropathy or ischemic optic disease is characterized by damage to the nerve. This occurs due to circulatory disorders in the intraorbital and intrabulbar region (located within eyeball before exiting the sclera).

The reasons for the development of the disease can be very different. This is one of the most insidious diseases, which at an unexpected moment can deprive a person of his sight.

Causes of ischemic neuropathy

The blood supply to the optic nerve occurs through vascular networks originating from the ophthalmic artery, a branch of the internal carotid artery. Central blood vessel The retina enters the optic nerve about 1 cm behind the eye and supplies the interior of the retina.

The outer part is separated by the choroidal artery, which originates from the posterior ciliary arteries. Its posterior part is located in front and behind the posterior ciliary artery.

Only a small number of capillaries actually penetrate the nerve and spread to its central part. As a result, the center of the posterior optic nerve is relatively poorly vascularized compared with its anterior portion and is therefore susceptible to ischemia with dramatic changes in perfusion.

The head receives arterial blood supply from the anastomotic arterial circle formed by anastomoses between the lateral branches of the short posterior ciliary arteries, branches from the adjacent pial arterial network and branches from the choroidal canal.

These very small arteries suffer from a number of local diseases such as atherosclerosis and vasculitis. Emboli usually do not reach them. Hypoperfusion (weak microcirculation) in the area of ​​the ophthalmic artery and its branches causes ischemic optic neuropathy (ION).The non-arteritic form of the disease develops due to:

• high blood pressure;
• diabetes;
• atherosclerosis;
• use of certain medications;
• blood clots and lower blood pressure overnight.

Arterial ION usually occurs in people over 70 years of age. The blood supply to the optic nerve is blocked due to inflammation of the artery (arteritis), most often giant cell arteritis.

The list of possible risk factors includes severe bleeding, anemia, glaucoma, blood diseases, and arterial hypotension.

Risk group

The risk of developing the disease is increased in patients with diabetes mellitus who abuse alcohol and nicotine. It includes persons with obstructive sleep apnea and persistently elevated blood pressure.

Classification

ION is classified as anterior (AION) or posterior (AION) depending on the optic nerve segment affected. The anterior view accounts for 90% of cases.

Both types are divided into non-arterial (not associated with vasculitis) or arterial.

Anterior ischemic optic neuropathy

PION is the most common cause sudden blindness in people over 50 years of age. The non-arterial form of PION (NPION) often develops due to hypertension and diabetes mellitus.

Thus, hypercholesterolemia, stroke, ischemic disease heart disease, tobacco use, systemic atherosclerosis, and obstructive sleep apnea have been associated with non-arterial anterior ION.

Although NSAID and intracranial cerebrovascular disease share similar risk factors, they are two very different pathologies and do not require the same evaluation.

For example, because of NPION caused by small vessel disease, carotid artery patency studies are not usually indicated. However, the patient has visual symptoms suggestive of ocular hypoperfusion (ie, blurred vision with postural changes in bright light or during exercise) or contralateral neurological symptoms and signs, ipsilateral transient monocular vision loss, Horner's syndrome, or ocular pain.

Thus, hypercoagulability is rarely associated with NPION.

Acute bleeding with anemia and systemic hypotension leads to unilateral or bilateral NPION. Likewise, those with chronic renal failure who undergo dialysis may precipitate this pathology.

Giant cell arteritis is the most common cause of arterial anterior and posterior ischemic neuropathy, although in rare cases other vasculitides can cause. PION is the most common ocular manifestation of giant cell arteritis.

Arterial PION and ZION are emergency conditions in the ophthalmological field, which must be promptly recognized and treated to prevent complete loss of vision.

Posterior ischemic optic neuropathy

ZIN is a disease characterized by damage to the part of the optic nerve located behind the eye. With posterior ION, a decrease in blood circulation is observed in the areas where the nerve is located or in the intraorbital region.

This disease presents great difficulties for early detection. The pathological process occurs unilaterally.

The therapy is the same as for PION. After treatment, the clarity of visual perception will improve slightly, but it will still remain low.

Even after therapy, patients with posterior ischemic optic neuropathy develop blind spots in the visual field that are not associated with the peripheral boundaries.

Symptoms

Most often, ION affects 1 eye, but some patients develop bilateral damage to the organs of vision. The second eye is involved in the pathological process after 2–5 days or 2–5 years.

The clinical picture of PION and ZION is the same. With this disease, peripheral visual perception is always impaired. Visual acuity decreases, and some immediately become blind.

Damage to the optic nerve is preceded by:

• cephalgia;
• a veil before the eyes;
• soreness.

This condition continues for 30 days or longer. Then the symptoms improve.

Diagnostics

Since ION develops against the background various diseases, you will need to consult an ophthalmologist, hematologist, neurologist, cardiologist, rheumatologist and endocrinologist.

The following laboratory tests are carried out:

• measurement of erythrocyte sedimentation rate;
• C-reactive protein level;
• general analysis blood and platelet count.

Together, these tests are highly predictive for biopsy-proven giant cell arteritis with a combined sensitivity of 97% for erythrocyte sedimentation rate and C-reactive protein levels.

To determine the disease, ophthalmoscopy is performed. If the patient does not have symptoms of giant cell arteritis, a magnetic resonance imaging (MRI) or computed tomography (CT) scan of the brain is done to make sure the optic nerve is not being compressed by the tumor.

Depending on the probable causes Additional tests may be required. For example, if someone has symptoms of obstructive sleep apnea (such as excessive sleepiness during the day or snoring), a polysomnography is performed. Patients who have had blood clots have their blood tested to diagnose clotting disorders.

Treatment

Giant cell arteritis is responsive to glucocorticoids, with immediate relief of systemic symptoms such as headaches, scalp tenderness, fatigue, fever, and myalgias.

Glucocorticosteroids are used to prevent vision loss in the unaffected eye, but they do not reverse existing pathology. Most neuro-ophthalmologists prescribe high doses Intravenous methylprednisolone for the treatment of patients with acute vision loss.

For ischemic optic neuropathy, diuretics, vasodilators and nootropic medications are prescribed. Additionally - anticoagulants and vitamin complexes, thrombolytic agents - if necessary.

In the future, doctors carry out therapy with magnetotherapy, electrical stimulation and laser stimulation.

Complications

In the absence of therapy, its incorrect implementation or an error in diagnosis, the patient develops complete or partial blindness.

Forecast

In 40% of people, some vision is restored spontaneously. It is estimated that within the next 5 years, 20% of patients will develop disease in the second eye.

No effective treatment arterial ischemic neuropathy, and most of the lost vision cannot be restored. In patients with arterial ION, vision loss occurs in 25–50% within days or weeks without treatment. Non-arterial anterior ION recurs in the affected eye in less than 5% of patients.

Optic nerve atrophy after of this disease may reduce crowding and reduce the risk of relapse.

Bilateral disease is often observed, usually sequentially and not simultaneously. The risk of second eye involvement ranges from 12 to 15% over 5 years and is not associated with age, gender, smoking, or aspirin use.

of optical neuropathy
A.F. Brovkina, A.G. Schuko
(RMAPO, Moscow, department of FGU MNTK
"Eye Microsurgery" named after acad. Fedorov S.N., Irkutsk)

Authors presented the comparative characteristic of some types of neuropathy (vascular and endocrine genesis). Treatment and prognosis depend on the etiologic and pathogenic factors.

Optic neuropathy (ON) is a collective concept that unites several diseases in which the optic nerve fibers from the retina to the brain are affected. Taking into account the etiological aspects, the mechanism of its development is different.
The causal classification of OH can be presented as follows:
. compression
. ischemic
. inflammatory
. hyperbaric
. traumatic
. radiation
. metabolic
. congenital.
The development of the pathological process of ON of any type is based on ischemia and hypoxia of nerve fibers with weakening of antioxidant activity, which may be preceded by circulatory disorders, compression of nerve fibers of the optic nerve, blockade of axonal transport, intoxication, activation of peroxide processes and neurotoxic reactions. However, the degree of intensity of these mechanisms, the place of their application and the sequence of appearance vary depending on the underlying pathological process.
For example, when primary glaucoma the main triggering factors for the development of optic neuropathy are an increase in ophthalmotonus or a decrease in cerebrospinal fluid pressure in the retrobulbar portion of the optic nerve. This leads to deformation of the supporting structures (especially the lamina cribrosa) with subsequent pinching of the nerve fiber bundles in the deformed tubules of the lamina cribrosa and/or hypoxia of the optic nerve head.
Anterior ischemic ON develops with acute circulatory disturbance in the anterior segment of the optic nerve. A decrease in perfusion pressure in the posterior short ciliary arteries and ischemia in the prelaminar, laminar and retrolaminar parts of the optic nerve leads to the development clinical picture anterior ischemic neuropathy. Characterized by a rapid and sharp decrease in visual acuity, rapid development of optic nerve atrophy.
In patients with edematous exophthalmos, ON develops against the background of an increase in extraocular muscles. The process occurs quickly, before the axoplasmic flow is disrupted, a disturbance in blood flow occurs, both arterial (as a result of compression of the main arterial vessels by enlarged muscles) and venous.
Having extensive personal experience and having analyzed the mechanism of development of some forms of optic neuropathy, the authors in this work set themselves the task of studying the features of the clinical picture of ON (vascular) and endocrine (edematous exophthalmos) genesis, as the most common and requiring a fundamentally different therapeutic approach. This is due to the fact that in a number of publications, not only vascular processes, but also thyrotoxic exophthalmos are considered as the basis for the development of anterior ischemic ON. This situation is fundamentally incorrect, since thyrotoxic exophthalmos, although it represents one of the forms of endocrine ophthalmopathy, is never accompanied by organic changes in the soft tissues orbits. A different picture is observed with edematous exophthalmos. Comparison of ophthalmoscopy data and computed tomography conducted by one of us earlier, allowed us to make an opinion about the main mechanisms of ON development. The triggering mechanism for ON in edematous exophthalmos is a sharp increase in the volume of extraocular muscles at the apex of the orbit (Fig. 1). At least two factors take part in the mechanism of its development: mechanical compression of the optic nerve and disruption of the blood-ophthalmic barrier, resulting in edema and tissue hypoxia, and disruption of cellular energy metabolism. The end result of these disturbances is a blockade of axonal transport (Fig. 2).
Anterior ischemic ON is characterized by sudden sharp decline visual functions as a result of ischemic infarction of the optic nerve and its head. This definition is confirmed by J.D. Gass with the following phrase: “Anterior ischemic optic neuropathy is swelling, ischemia and varying degrees of infarction of the anterior part of the optic nerve, caused by a reduction in blood flow in the nerve.” Persons aged 45 years and older are affected ( average age 69 years old). The process is often unilateral, but in 40% of cases damage to the optic nerve is possible opposite side with a fairly significant time interval.
Ophthalmoscopically, the optic disc is grayish-white or yellowish color with a sharp swelling of its tissue. Prominence is expressed in to a greater extent in the upper half of the disk. In the acute stage, streak-shaped hemorrhages on the disc or along its edge are possible (Fig. 3). The swelling also extends to the peripapillary nerve fibers (Fig. 4). Cotton-like exudate in separate foci is located juxtapapillary. Swelling occurs in the macular area. Arteries and veins are narrowed. Go to chronic stage, when regression of disc edema occurs with the transition to atrophy (secondary), it occurs quickly (after 2-3 weeks). During this period, cystic degeneration or its fibrotic changes develop in the macular zone.
In cases where it is possible to examine the visual field, prolapses are detected in the lower half (1/3 of cases), in 12% of patients an absolute scotoma is recorded in Bjerrum's space, less often (about 6%) it is possible to identify a central scotoma and a concentric narrowing of the visual field.
In patients with edematous exophthalmos in the stage of subcompensation or decompensation (more often) of the pathological process, when the manifestation of clinical symptoms intensifies, venous stasis occurs in the orbital tissues and in the optic nerve. Early sign disruption of the compensation process and the appearance of ON - dilation of the retinal veins, which leads to hypoxia primarily of the retinal ganglion cells (Fig. 5). Characteristic early disorder visual functions. Initially, most patients develop peripheral scotomas with normal visual acuity; they are detected at the extreme periphery of the outer and upper parts of the visual field.
According to ophthalmoscopy data (the condition of the optic nerve head and retinal vessels), two forms of ON were identified: initial (57%) and developed (43% of patients).
Initial ON was characterized by the presence of dilated and tense retinal veins (Fig. 6). The optic disc remains normal with subcompensated edematous exophthalmos. In the stage of its decompensation, blurring of the boundaries of the optic nerve head and its swelling appear. In contrast to anterior ischemic ON, vision in patients with edematous exophthalmos and ON worsens gradually to 0.1-0.7. A sharp deterioration in vision (before light projection) occurs with the appearance of hyperemia and swelling of the optic nerve head (Fig. 7). However, the process is reversible: against the background of basic intensive therapy with a decrease clinical symptoms Visual acuity increases, changes in the visual field decrease or disappear. This confirms the hypothesis of the development of ON during tissue compression at the apex of the orbit against the background of a hypoxic state, which has a detrimental effect on ganglion cells.
Each of these factors (or both together) leads to disruption of axoplasmic transport connecting the body of the retinal ganglion cell with its terminals.
Thus, ON, taking into account pathogenetic factors, has its own clinical differences, differs in the nature of the pathological process and its outcome.
Comparative characteristics of the analyzed types of OH are presented in Table 1.
The differences presented in the table confirm the possibility of clinical differentiation of ON depending on etiopathogenetic factors, which determines the planning of medication or surgical treatment and visual forecast in each specific case.

Literature
1. Brovkina A.F. Endocrine ophthalmopathy //Moscow: GOETAR, 2004.
2. Katsnelson L.A., Forofonova T.I., Bunin A.Ya. Vascular diseases eyes //Moscow: Medicine, 1990. - 269 p.
3. Nesterov A. P. Glaucomatous optic neuropathy // Vestn. ophthalmol., 1999, No. 1. - P. 3-6
4. Barch A., Bosahard C., Burgi U., Burgi H. Severe endocrine ophthalmopathy. A revive with case reports.- Schweiz Med. Wochenachr. - 1991. - V.121. - S. 3-9
5. Gass J.D. Stereoscopic Atlas of Macular Diseases: diagnosis and treatment.// The C.V. Mosby Company.-St.Louis.-1987. - V. 1. - P. 69
6. Kritzinger E.. Beaumont H., Optic discriminatory abnormalities,-Wolfe Medical Publications Ltd. - USA. - 1987. - 118 P.
7. Shine B., Fells P., Edwards O., Weetman A. Association between Graves? ophthalmopathy and smoking. - Lancet. - 1990. - V. 335. - P. 1261-1263.

Ischemic optic neuropathy is a lesion caused by functional disorder blood supply to the optic nerve in its intrabulbar or intraorbital sections. The pathology is characterized by a sudden decrease in visual acuity, loss or narrowing of its fields, and monocular blindness.

As a rule, ischemic neuropathy affects the optic nerve in people 40-60 years old, mainly men. This is a serious condition that can cause significant visual impairment and even blindness. Pathology is not an independent disease, but arises as an ocular manifestation of some system processes. Therefore, the treatment of the problem is carried out not only by ophthalmologists, but also by cardiologists, rheumatologists, neurologists, endocrinologists or hematologists.

Classification of lesions

Damage to the optic nerve develops in the form of ischemic neuropathy of two forms - anterior and posterior. Each of the forms occurs as partial (limited) or complete (total) ischemia.

Anterior ischemic neuropathy occurs due to acute circulatory disorder of the intrabulbar part of the optic nerve. Posterior neuropathy is less common and is caused by ischemic circulatory disorders of the retrobulbar (intraorbital) region.

Causes

Anterior ischemic neuropathy occurs when blood flow in the posterior ciliary short arteries is disrupted, causing ischemia of the retinal, choroidal (prelaminar) or scleral (laminar) layers of the optic nerve head.

Posterior ischemic neuropathy develops as a result of circulatory disorders of the posterior parts of the optic nerve or stenosis of the vertebral and carotid arteries.

In acute circulatory disorders of the optic nerve, local factors include arterial spasms, as well as their organic changes - sclerotic lesions or thromboembolism.

Various predisposing factors for the occurrence of ischemic neuropathy in parts of the optic nerve systemic lesions, as well as the general hemodynamic disorders caused by them. In addition, local changes in the vascular bed or microcirculation disorders can lead to ischemia.

Especially often, such damage to the optic nerve develops against the background of diabetes mellitus, hypertension, atherosclerosis, arteritis, discopathy in cervical spine spine, thrombosis of the great vessels.

Sometimes ischemic neuropathy develops when acute blood loss, due to gastrointestinal bleeding, injuries, surgical interventions, anemia, arterial hypotension, blood diseases, and also after hemodialysis or anesthesia.

Our doctors who will solve your vision problems:

Symptoms

As a rule, ischemic neuropathy affects one eye, but in almost a third of patients there are also bilateral lesions. The second eye becomes involved in the process after some time, often in the next 2-3 years. Anterior and posterior forms of optic neuropathy are often combined, both with each other and with blockage of the central artery of the retina.

The development of optical ischemic neuropathy occurs suddenly: after sleep, physical activity or a hot bath. In this case, visual acuity drops sharply (down to tenths of light perception and even blindness, with complete damage to the optic nerve). A decrease in visual function develops over several minutes or hours and the patient is able to clearly indicate when this happened. Sometimes the development of the condition is preceded by certain symptoms - periodic blurred vision, severe headache, pain behind the eye.

Any form of this pathology is accompanied by impaired peripheral vision. These can be either individual defects (scotomas), or loss of parts of the visual fields or their concentric narrowing.

Acute ischemia lasts at least 4-5 weeks. Next, swelling of the optic disc slowly subsides, hemorrhages resolve, and partial or complete atrophy of the optic nerve occurs. In this case, visual field defects are significantly reduced, but do not completely disappear.

Diagnostics

In order to clarify the nature of the pathology and its causes, patients should be examined by an ophthalmologist, endocrinologist, neurologist, cardiologist, rheumatologist and hematologist.

An ophthalmological examination includes examining the ocular structures, performing functional tests, as well as conducting other studies - x-ray, ultrasound, electrophysiological.

When checking visual acuity, it is revealed that it decreases from insignificant to the level of light perception. Examination of visual fields reveals their defects, which corresponds to damage to various parts of the optic nerve.

Ophthalmoscopy reveals pallor, swelling caused by ischemia and an increase in the size of the optic nerve head, its protrusion into the vitreous. Swelling of the retina around the optic disc is observed; the macular area is characterized by a “star shape”. In the compression zone, narrow veins are identified, in contrast to the periphery, where they are full-blooded. Sometimes exudation and focal hemorrhages are detected.

With angiography of retinal vessels, ischemic optic neuropathy is manifested by retinal angiosclerosis, age-related fibrosis, unequal size of arteries and veins, occlusion of cilioretinal arteries. Ultrasound examinations carotid, supratrochlear and vertebral arteries often determine blood flow disturbances.

Electrophysiological studies show decreased function of optic nerve thresholds. A coagulogram reveals hypercoagulability. Determination of cholesterol and lipoproteins shows hyperlipoproteinemia.

Differential diagnosis of ischemic optic neuropathy is carried out with retrobulbar neuritis, space-occupying formations of the orbit and the central nervous system.

Treatment

Ischemic optic neuropathy is an emergency condition, since prolonged disruption of blood circulation leads to irreversible death of nerve cells. Help with the sudden development of ischemia includes the immediate administration of aminophylline solution intravenously, nitroglycerin under the tongue, ammonia on a cotton swab for inhalation.

To treat ischemic neuropathy, the patient must be hospitalized.

Therapy in a hospital is aimed at relieving edema, improving trophism of the optic nerve, and organizing additional blood supply routes. Treatment of the underlying disease, bringing blood coagulation and lipid metabolism to normal, and stabilizing blood pressure are very important.

For this purpose, the intake or administration of diuretics, vasodilators, thrombolytic, nootropic drugs, and anticoagulant drugs is prescribed. Therapy is carried out with corticosteroids, vitamins B, C, E are prescribed. Further treatment includes the use of physiotherapeutic methods - magnetic therapy, electrical stimulation, laser stimulation of undead fibers of the optic nerve of the eye.

Prognosis and prevention

With the development of ischemic optic neuropathy, the prognosis is unfavorable. Even with timely treatment, a significant decrease in vision often persists, and peripheral vision defects remain, which is caused by optic nerve atrophy. Only in 50% of patients is it possible to improve vision by 0.1 or 0.2. Damage to both eyes often results in further low vision or complete blindness.

Prevention of ischemic optic neuropathy should include timely treatment of vascular and systemic pathologies. For those who have suffered ischemic neuropathy of one eye, follow-up with an ophthalmologist and regular preventive therapy are indicated.

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