Optic neuropathy in both eyes. Ischemic optic neuropathy

Disc ischemia is a consequence of circulatory disturbances in the system of arteries supplying the nerve. The disease manifests itself as a sudden loss of vision or a sharp decrease in it, mainly in older people suffering from hypertension or atherosclerosis.

Anterior ischemic neuropathy. Ischemic papilledema with isolated hemorrhages.

The optic disc is swollen, enlarged, prominence in vitreous, its boundaries are blurred. There may be hemorrhages near the disc. Unlike neuritis, the disc vascular pathology pale, arteries sharply narrowed, uneven in caliber. Characteristic changes in the field of vision. Atypical upper or lower hemianopsias occur more often, although central scotomas of various forms are also possible. The process ends with optic nerve atrophy. Sometimes difficulties arise in the differential diagnosis of optic disc ischemia and optic neuritis. Then laboratory immunological studies help in diagnosis. In case of neuritis, immune reactions of the patient's blood serum with an antigen prepared from optic nerve tissue are often positive, and in case of ischemia - negative.

Treatment the same as for acute obstruction of the central retinal artery.

Optic disc drusen

Rare diseases of the optic nerve include optic disc drusen.

Optic nerve drusen with neovascularization

Their peculiarity is grape-shaped elevations of a grayish-white color, consisting of rounded formations, as if covering the surface of the optic nerve head. Drusen consist of hyaline, sometimes lime is deposited in them. With drusen, changes in visual fields are rarely observed. Visual acuity is usually not affected. The appearance of drusen is associated with degenerative processes in damaged optic nerve fibers. Detection of drusen is an indication for a more thorough neurological examination of the patient.

Chapter 15 Pathology of intraocular pressure

Intraocular pressure (IOP) is the pressure exerted by the liquid contents eyeball on its elastic outer shell.

Intraocular pressure

The required level of IOP ensures the spherical shape of the eyeball and the correct topographic relationships of internal structures, and also facilitates metabolic processes in these structures.

The value of IOP depends on the rigidity (elasticity) of the membranes and the volume of the contents of the eyeball. The first factor is relatively stable. Consequently, ophthalmotonus depends on changes in the volume of the eyeball. The contents of the eye consists of a number of components, most of which (lens, vitreous body, inner membranes of the eye) have a relatively constant volume. The degree of blood filling of the intraocular vessels is subject to changes, and mainly the volume of intraocular fluid, which is called aqueous humor (AH).

Eye tone is measured using tonometers. At the time of measurement, the tonometer compresses the eye, as a result of which the IOP in it increases, therefore, true (P 0) and tonometric (P t) pressure are distinguished. Using a Maklakov tonometer, tonometric pressure is determined, and the readings of non-contact pneumotonometers correspond to the true pressure. The normal level of true IOP varies from 9 to 21 mm Hg. Art., on average 14-16 mm Hg. Art.; standards for a Maklakov tonometer weighing 10 g are from 17 to 26 mm Hg. Art.

Measuring intraocular pressure

Recently, the concept of “tolerant IOP” has become increasingly widespread. This term refers to the range of IOP that is safe for a particular person. Pronounced fluctuations in IOP with an amplitude of 4-5 mm Hg. Art. observed throughout the day: as a rule, the maximum value of ophthalmotonus is observed in the early morning hours, in the evening it decreases and reaches a minimum at night.

The IOP level is relatively stable and changes with disturbances in the circulation of aqueous humor. The relative constancy of the IOP level indicates the existence of active mechanisms of its regulation. The rate of EV production appears to be under the control of the hypothalamus and autonomic nervous system. The outflow of fluid from the eye is influenced by fluctuations in the tone of the ciliary muscle. Data were obtained on the existence of biochemical regulation of EV outflow.

Under normal conditions (hydrodynamic equilibrium), the flow of aqueous humor into the eye and its outflow from the eye are balanced. The human eye contains 250-300 mm 3 explosives. It is continuously produced (1.5-4 mm 3 /min) by the epithelium of the processes of the ciliary body, enters the posterior and through the pupil into the anterior (volume 150-250 mm 3) chamber of the eye (Figure 15.1), which serves as its reservoir.

Rice. 15.1 – Cameras of the eye (diagram)

1 – venous sinus of the sclera; 2 – anterior chamber; 3 – anterior section of the posterior chamber; 4 – posterior section of the posterior chamber; 5 – vitreous body.

It flows mainly (85%) into the episcleral veins through the drainage system of the eye (Figure 15.2).

Rice. 15.2 – Diagram of the structure of the anterior chamber angle

1 – Schwalbe border ring; 2 – tenderloin; 3 – venous sinus of the sclera or Schlemm’s canal; 4 – collector tubule; 5 – inner wall of the sinus; 6 – trabecula; 7 – pectineal ligament.

The arrows show the paths of aqueous humor outflow.

The latter is located in the corner of the anterior chamber and is represented by the trabecular apparatus (TA) (Figure 15.3), consisting of connective tissue and having a layered structure.

Rice. 15.3 – Diagram of the structure of the drainage system of the eye

1 – anterior chamber bay; 2 – trabecula; 3 – venous sinus; 4 – collector tubule.

Through numerous holes and cracks, the explosive leaks into the scleral sinus (Schlemm's canal), and then flows through 20-30 collector canaliculi (aqueous veins) into the episcleral veins. About 15% is the uveoscleral pathway of EV outflow - through the stroma of the ciliary body and sclera into the uveal and scleral veins.

The resistance to fluid movement through the drainage system is very significant. It is approximately 100 thousand times greater than the resistance to blood flow throughout the human vascular system. Such a large resistance to the outflow of fluid from the eye at a low rate of its formation ensures the required level of intraocular pressure.

The state of hydrodynamics of the eye is determined by hydrodynamic indicators. The latter include, in addition to intraocular pressure, also outflow pressure, minute volume of aqueous humor, the rate of its formation and the ease of outflow from the eye.

Outflow pressure is the difference between true IOP and pressure in the episcleral veins (Po-Pv), the minute volume of IV (F), expressed in cubic millimeters, characterizes the volumetric rate of production and outflow of IV at stable IOP, the coefficient of ease of outflow (C) is the value , showing how much fluid (in cubic millimeters) flows from the eye in 1 minute per 1 mmHg. Art. outflow pressure. Normally, this indicator ranges from 0.18 to 0.45 mm 3 /min/mmHg. Art., and F – within 1.5-4 mm 3 /min (on average 2 mm"/min).

Glaucoma

The term “glaucoma” unites a large group of eye diseases (about 60) that have the following features: intraocular pressure (IOP) constantly or periodically exceeds the tolerant (individually tolerated) level; a characteristic lesion of the optic nerve head and retinal ganglion cells develops (glaucomatous optic neuropathy - GON); visual disturbances characteristic of glaucoma occur.

Glaucoma can occur at any age, starting from birth, but the prevalence of the disease increases significantly in old age. The incidence of glaucoma is 1 per 1000 population per year.

The main pathogenetic links in the development of various clinical forms of the glaucomatous process include: disturbances in the outflow of aqueous humor from the eye; increase in IOP above the level tolerant for the optic nerve; posterior bending of the cribriform plate of the sclera, ischemia and hypoxia of the head of the optic nerve due to pinching of its fibers and vessels; glaucomatous optic neuropathy with optic nerve atrophy and excavation (Figure 15.4); degeneration (apoptosis) of retinal ganglion cells.

Rice. 15.4 – Glaucomatous excavation of the optic nerve

The head of the optic nerve includes its intraocular part and the section of the nerve adjacent to the eye (1-3 mm in length), the blood supply of which to some extent depends on the level of IOP. The term “optic disc” (ONH) is used to designate the part of the ONH visible under ophthalmoscopy.

The ONH consists of the axons of retinal ganglion cells (RGCs), astroglia, vessels and connective tissue.

The lamina cribrosa of the sclera consists of several perforated sheets of connective tissue separated by astroglial layers. The perforations form 200-400 tubules, through each of which a bundle of nerve fibers passes. In the upper and lower segments, the cribriform plate is thinner, and the openings in it are wider than in its other sections. These segments are more easily deformed when IOP increases.

Changes in visual functions in chronic glaucoma occur unnoticed by the patient and progress slowly; they are detected during examination of the patient, which often happens only after the loss of a significant (30% or more) part of the nerve fibers in the optic optic nerve. This makes it difficult to detect GON at an early stage.

Glaucoma is characterized by the following sequence of changes in the visual field: an increase in the size of the blind spot, the appearance of relative and absolute paracentral scotomas; narrowing of the field of view on the nasal side; concentric narrowing of the visual field - tube vision: the field of vision is so narrowed that the patient looks as if through a narrow pipe (Figure 15.5); light perception with incorrect light projection; in the final stage of the disease, visual functions completely disappear.

Fig. 15.5 – Field of view at various stages of glaucoma

Searches such as “optic neuropathy” are often present on the Internet. In fact, we are talking about optic neuropathy. This is a fairly serious disease, which, most often, is a symptom of another process. The optic nerves, as conductors, perceive all pathological influences and show the doctor a lot when examining the fundus of the eye.

Symptoms of optic nerve damage

It is necessary to immediately distinguish between three concepts, between which confusion constantly occurs when it comes to damage to the optic nerve.

Eyeball – sagittal section

• neuropathy. This is the name for a process that leads to dysfunction of the optic nerves, but without signs of inflammation. An example is acute ischemic optic neuropathy, which can develop with severe atherosclerosis, which leads to thrombosis of the central retinal artery. This serious process can result in blindness in one eye;

• Optic neuritis. This is a process that is characterized by inflammation of the nerve fiber, with a characteristic picture, as well as the addition of pain. Unilateral optic neuritis that develops for no apparent reason may be an important sign multiple sclerosis. Many people with a history of optic neuritis subsequently develop multiple sclerosis;

• congestive optic discs which can be detected by fundus examination. Congestion most likely indicates intracranial hypertension syndrome, and they occur in cases of increased intracranial pressure, especially if this pressure exists for a long period of time.

A clear distinction between these clinical phenomena will allow us to separate neuritis from neuropathy, which allows us to make a correct prognosis for the development of the disease.

Causes of development of neuropathy and optic neuritis

How does neuropathy and optic neuritis develop and for what reasons?

For example, signs of ischemic optic neuropathy include sudden deterioration of vision, usually in one eye. In some cases, ischemic blindness may occur. This is often preceded by specific symptoms such as, for example, blurred vision, the appearance of various spots, sometimes colored.

If incomplete vision loss has developed, then focal loss of visual fields appears, for example, arcuate and sectoral scotomas, that is, areas of the visual fields that do not see anything. A concentric narrowing of the visual fields may appear.

This process is very dangerous due to the so-called sympathetic spread: in some cases, the pathological process from one eye is transferred to the second (after all, the optic nerves form a single whole in the area of ​​the chiasm, or optic chiasm), and as a result, complete blindness can develop.

With ischemic lesions of the nerve, disc swelling also occurs, and the arteries narrow, while the diameter of the veins is normal. This is clearly visible when examining the fundus. Then various hemorrhages occur in the area of ​​the optic nerve head. If intensive treatment is not started (metabolic, vascular drugs, antithrombotic, antiplatelet agents, antioxidants), persistent optic nerve atrophy may develop. It usually occurs 1-3 weeks after the onset of neuropathy.

This lesion (ischemic optic neuropathy) occurs with severe atherosclerosis, systemic vascular lesions - cranial arteritis. Damage to the optic nerve is also possible with obliterating endarteritis, with Buerger's disease (thromboangiitis obliterans).

If we talk about optic neuritis, it occurs due to the appearance of inflammation on the myelin sheath, as well as in the nerve trunk itself. Signs of optic neuritis will be exclusively signs that are noticeable during examination of the fundus:

• hyperemia of the nerve disc, swelling;

• blurred and unclear boundaries of the disc, which indicates inflammation;

• plethora and a sharp expansion of both arteries and veins (and we remember that with neuropathy there is, on the contrary, a narrowing of the arterial network while the venous network is intact. It is clear that plethora is a sign of inflammatory hyperemia);

• foci of hemorrhage in the disc area;

• the appearance of whitish spots on the surface of the disc and retina.

Signs of optic neuritis will also include a variety of visual disturbances, including early loss of acuity, as well as wide and varied changes in visual fields. These disorders occur simultaneously with the appearance of the picture in the fundus.

Neuritis can develop from different reasons. In addition to signs of demyelinating disease, the cause may be:

• meningitis, encephalitis, meningoencephalitis, especially purulent ones;

• general severe infections (malaria, typhus, severe influenza);

• endogenous intoxication and poisoning.

Surrogate poisoning as a cause of optic neuropathy

Classic manifestations of optic neuritis include poisoning with a surrogate of alcohol, such as ingestion of methyl alcohol for the purpose of alcohol intoxication. It is known that the lethal dose of methanol for internal use ranges from 40 to 250 ml, but even the consumption of 5-10 ml of methanol can cause blindness. In addition, when consuming various mixtures containing 1.5% methyl alcohol, cases of toxic blindness also occur.

Typically, visual disturbances when consuming methanol occur 3-6 days after consumption, when, it would seem, everything has already returned to normal. Damage to the optic nerve after taking methanol occurs due to the fact that in the liver it breaks down into toxic products - formic acid and formaldehyde. It is the latter that affects the optic nerve. When drinking regular ethyl alcohol, the products of metabolism in the liver are acetic acid and acetaldehyde, which, despite their harmfulness, do not affect the cells of the optic nerve and retina.

Therefore, in case of sudden visual disturbances, it is necessary to urgently examine the fundus of the eye, and also begin treatment with an ophthalmologist and therapist. This will help not only preserve vision, but also identify the underlying disease, which can harm not only the optic nerve, but the entire body.

Violation of the structure and integrity of the optic nerves under the influence of a number of factors is accompanied by the development of neuropathies. One type of this serious pathology is glaucomatous optic neuropathy.

Perhaps it is one of the most insidious and mysterious eye diseases. While not showing itself at all at first, glaucoma can cause harm as it develops further. general condition person and cause a significant decrease in the quality of life, and subsequently lead to disability. The result of its pathological influence are irreversible changes in the structures of the eye and the main conductor nerve impulses- optic nerve.

The mechanism of development of optical neuropathy in glaucoma

The nerve functions as a kind of “wire” transmitting information from the retina to the corresponding parts of the brain. There it is “processed” and we receive visual images. If the fibers of this conductor are completely or partially damaged, then the signals will not reach in full, reducing visual acuity and color perception. If the nerve fibers are completely damaged, their impulses will be absent and the person will not be able to see at all.

In glaucomatous optic neuropathy, visual neurons are damaged. With untreated glaucoma, pathological processes lead to a sharp decrease in vision up to complete blindness. Ophthalmologists call this form of neuropathy optic nerve atrophy, since it develops as a result of trophic disorders occurring against the background of increased intraocular pressure.

Why does optic nerve atrophy occur? Blood circulation and fluid outflow in the complex structures of the organ of vision are disrupted. This leads to oxygen deficiency in the tissues of the eye, threatening irreversible changes in the retina and the optic nerve itself. All this ultimately ends in damage to the fibers of the main conductor of nerve impulses. The loss of neurons threatens nerve atrophy, a sharp decrease in visual perception and blindness.

Clinical manifestations

Optic neuropathy in glaucoma is perhaps one of the most insidious diseases. The main conductor connecting the organ of vision with the brain is under attack. For a long time, the disease can remain unnoticed, and the person can continue to perform his usual functions. All this can be associated with a heavy workload and without resorting to the help of doctors for a long time. Along with manifestations of the underlying disease (pain in the eyes, dizziness, headache, asthenia) visual acuity begins to decrease.

Most often, the disease progresses acutely, but sometimes a latent course is recorded. There are difficulties reading books and watching your favorite TV shows. If this problem is not dealt with closely at this moment, the patient may go blind.

Manifestations of glaucomatous neuropathy:

• expansion of the blind spot and the appearance of uncharacteristic normal vision dark spots - scotoma;
• narrowing of visual fields;
• photophobia;
• pain and redness of the eyes;
• worsening dark adaptation;
• distortion of color perception.

As the disease develops and moves into the next, more severe stage, the patient increasingly feels fatigue and a feeling of fog before the eyes. Attacks of increased intraocular pressure during glaucoma are fraught with severe pain in the eyes, increased headaches and dizziness, which cannot but affect the condition of the optic nerve.

More often, rainbow stains occur when looking at bright light. General weakness and fatigue become constant companions. Often, against the background of increased intraocular pressure, nausea and even vomiting may appear, and the heartbeat may slow down.

Diagnosis of the disease

To diagnose the condition of the fundus and optic nerve, doctors use ophthalmoscopy. A special instrument is used - an ophthalmoscope. It allows you to see the structure of the organ of vision from the inside and assess the condition of the optic nerve head.

Perimetry allows you to determine the field of view and the presence of blind, dark spots. Measurements are made using an arc-shaped device - a perimeter. The patient must fix his gaze on a specific mark. When luminous points appear within the peripheral vision, the patient presses the button of the device, notifying that he has seen objects. Each eye is examined separately, while the other is covered with a bandage. The results are recorded by a computer and displayed on the monitor.

To diagnose glaucoma and the condition of the eye structures, tonometry of the organ of vision (measurement of intraocular pressure with a special tonometer), gonioscopy (examination of the angle of the anterior chamber of the eye), pachymetry (determining the thickness of the cornea) is used.

Treatment and prognosis

Therapeutic measures are aimed at eliminating the cause of the disease - reducing intraocular pressure. They are presented in two versions:

• drug treatment in the form of instilling special drops into the eyes;
• surgical methods to improve the outflow of intraocular fluid, thereby reducing pressure in the eye.

Many patients prefer to use folk methods. At the same time, the disease continues to progress and destroy the optic nerve.

By applying for medical care and receiving adequate treatment, patients will be able to maintain their vision. Let its severity not be one hundred percent, but still, timely treatment measures will allow you to avoid blindness and disability.

The development of ischemic optic neuropathy occurs due to a local change in blood flow, as a result of which local tissues do not receive sufficient nutrients. The formation of pathology is associated with the course of atherosclerosis, hypertension, diabetes or cardiac dysfunction.

Neuropathy is characterized by impaired peripheral vision (narrowing of the visual field), the appearance of blind spots (scotoma). The disease is treated using conservative (drug) therapy and magnetic therapy methods.

Optic nerve ischemia

Ischemic neuropathy (neuropticopathy) of the optic nerve is considered the most common cause of blindness. This pathology is most typical for people over 50 years of age. The disease is more often diagnosed in men.

Pathology does not develop separately, but is a complication of diseases of the eyes or other organs.

In this regard, if ocular nerve ischemia is suspected, comprehensive examination patient in order to identify the cause of nerve fiber damage.

How is it classified?

At the location of the leak pathological process There are anterior and posterior forms of ischemic neuropathy. Depending on the degree of damage to the optic nerve, the disease is divided into local (limited) and total.

The development of anterior ischemic neuroopticopathy is associated with impaired blood flow in the intrabulbar region. Such problems are caused by various forms of vascular lesions: thrombosis, embolism, spasm. With posterior ischemic optic neuropathy, the pathological process is localized in the retrobulbar region (behind the eyeball). The anterior form develops less frequently.

Causes of ischemic neuropathy

The disease develops against the background of systemic pathologies that affect the vascular bed and cause a disorder of blood microcirculation. At the same time, the influence of local disturbances cannot be excluded. The latter include spasms ( functional disorders) And organic lesions(thrombosis, sclerotization) of local arteries.

Systemic vasculopathies lead to the development of ocular ischemia:

• hypertonic disease;
• atherosclerosis;
• diabetes;
• thrombosis of the great vessels;
• systemic lupus erythematosus;
• arterial hypertension.

The appearance of anterior ischemic neuropathy may be associated with the course of vasculitis:

• syphilis;
• damage to the carotid arteries of an occlusive nature;
• giant cell temporal arteritis;
• allergic vasculitis;
• other vasculitis.

To the number possible causes The occurrence of this pathology of the optic nerve includes:

• heavy blood loss (including during surgery);
• anemia
• discopathy of the cervical spine;
• glaucoma;
• surgery for cataract removal.

Damage to the cervical spine and carotid arteries mainly causes the development of posterior ischemic optic neuropathy.

Symptoms

The course of ischemic optic neuropathy is often unilateral. Only in 30% of cases the disease affects both eyes. Moreover, bilateral eye damage is usually observed in those patients who did not undergo timely treatment for anterior ischemic neuropathy (neuropticopathy).

Most patients are diagnosed with both forms of the disease simultaneously.

Along with this pathology, lesions of the retinal vessels are noted.

Symptoms of optic nerve ischemia appear suddenly. Initially noted:

• a sharp decrease in visual acuity;
• impaired light perception;
• complete blindness (in case of total defeat).

These phenomena are temporary, and after a few minutes or hours, visual functions are restored on their own. In some cases, before the appearance of these signs, warning symptoms are noted:

• blurred vision;
• pain behind the eyeball;
• intense headaches.

Regardless of the form of the pathology, with ischemic neuropathy of the optic nerve, the quality of peripheral vision decreases, manifested in the form of:

• scotomas (blind spots in the field of vision);
• concentric narrowing of vision;
• loss of the lower, temporal or nasal region of the visual field (the patient does not see objects from the side of the temples, jaw or near the nose).

Clinical phenomena characteristic of the acute stage of the disease develop for about 4-5 weeks. At the end of this period, the swelling of the optic nerve subsides, and internal hemorrhages in the eyeball area resolve without intervention.

At this stage, optic nerve atrophy of varying severity develops and visual acuity (especially peripheral) is not restored. Often, after the acute period ends, the disease progresses.

Diagnostics

Due to the fact that ischemic neuropathy develops against the background various diseases Diagnosis of this disease is carried out by:

• ophthalmologist;
• endocrinologist;
• neurologist;
• rheumatologist;
• cardiologist;
• hematologist.

If ischemic optic neuropathy is suspected, the following studies are prescribed:

• functional tests;
• ophthalmological examination of the intraocular fundus;
• electrophysiological studies;
• radiography.

Studies in anterior ischemic neuropathy show varying degrees of decreased visual acuity.

Ophthalmoscopy can reveal swelling of the optic nerve and the location of its damage.

The veins in the central part are narrowed and widened at the edges. In rare cases, the examination reveals internal hemorrhages.

The following studies are considered important from the point of view of making a diagnosis and determining the causes of damage:

• color Doppler mapping of the eye;
• ultrasound duplex scanning of the carotid arteries;
• daily monitoring of blood pressure indicators;
• temporal artery biopsy;
• MRI of the brain.

In addition to these techniques, angiography of retinal vessels is often used, through which the nature of their damage is determined. Doing an ultrasound scan helps to identify features of changes in blood flow in the arteries.

Using electrophysiological techniques, the nature of the decrease in the functionality of the optic nerve is diagnosed. In order to identify the causes of the disease, these studies are supplemented by a coagulogram, which helps determine the level of cholesterol and lipoproteins.

The given examination methods help to differentiate this pathology from tumors of the central nervous system and.

Treatment

If ischemic optic neuropathy is detected, treatment should begin immediately.

Long-term circulatory disorders cause the death of nerve fibers, which is irreversible and cannot be eliminated even through surgical intervention.

Immediately after detection of pathology, the following are prescribed:

• intravenous infusion of Eufillin solution;
• taking nitroglycerin (put under the tongue);
• inhalation over ammonia vapor.

The main goal of treatment is to ensure stable remission of the disease and prevent the spread of neuropathy to the second eye. In this regard, pathology therapy is carried out in a hospital setting.

After elimination acute form diseases, measures are taken to restore blood flow. For this purpose, the following drugs are prescribed intramuscularly or intravenously, as well as in tablet form:

• vasodilators (“Papaverine”, “Benziclan”, “Xanthinol nicotinate”, “Nikoshpan”);
• vasoactive (“Vinpocetine”, “Nicergoline”, “Vazorbal”);
• anticoagulants (“Heparin sodium”, “Nadroparin calcium”);
• antiplatelet agents (acetylsalicylic acid, Pentoxifylline, Dipyridamole);
• hemocorrectors (intravenous infusion of Dextran).

If necessary, treatment is supplemented with antihypertensive drugs (Timolol, Dorzolamide), which normalize intraocular pressure. Depending on the indications, the treatment regimen includes:

• osmotic agents;
• antioxidants (ascorbic acid, Taurine, Inosine, Rutoside and others);
• anti-sclerotic drugs (statins).

It is necessary to take diuretics, which eliminate the swelling of the affected tissues. At the same time, vitamins B, C, and E are prescribed.

If the disease is caused by vasculitis, glucocorticoids are used. Over time, it is recommended to reduce the dosage of these drugs.

For posterior ischemic neuropathy the following are prescribed:

• antispasmodic drugs (“Sermion”, “Cavinton”, “Trental”);
• thrombolytic agents (“Urokinase”, “Gemaza”, “Fibrinolysin”);
• decongestant medications (Lasix, Diacarb, GSK).

At the end drug treatment sessions of laser and electrical stimulation, magnetic therapy are carried out. These procedures are necessary to restore the conductivity of the optic nerve.

During the treatment of ischemic neuropathy, it is necessary to take measures aimed at eliminating concomitant pathologies. In particular, it is important to suppress the activity of vasculitis. If necessary, drug therapy is supplemented surgical intervention. Similar procedures are performed to eliminate stenosis or thrombosis of the arteries.

Forecast and prevention

Ischemic optic neuropathy is dangerous disease, provoking irreversible changes. The course of the pathology is accompanied by atrophy of nerve fibers, as a result of which a decrease in visual acuity and scotomas become persistent (cannot be corrected). Only in 50% of cases is it possible to slightly restore the functioning of the affected eye. Visual acuity in such situations improves by no more than 0.1-0.2.

If the pathology affects both eyes, chronic ischemic ocular neuropathy and total blindness are highly likely to develop.

Prevention of neuropathy involves timely treatment vascular and systemic pathologies. People who have previously been treated for this disease in one eye should undergo regular ophthalmological examinations of the healthy organ of vision.

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 antioxidant activity, which may be preceded by circulatory disorders, compression of the 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, in primary glaucoma, the main triggering factors for the development of optical 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. end result of these disorders is a blockade of axon transport (Fig. 2).
Anterior ischemic ON is characterized by a sudden sharp decrease in visual function 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 infarctions 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 on the opposite side is possible with a fairly significant time interval.
Ophthalmoscopically, the optic disc has a grayish-white or yellowish color with sharp swelling of its tissue. Prominence is more pronounced in the upper half of the disc. 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. The transition to the chronic stage, when regression of disc edema occurs with the transition to atrophy (secondary), 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). Early visual impairment is characteristic. 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 of the eye //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.