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Secondary optic nerve atrophy. Optic nerve atrophy: causes of pathology and treatment

Atrophy optic nerve is a pathological process in which nerve fibers are partially or completely destroyed and replaced by connective tissue. As a result, dysfunction of the nervous tissue occurs. Most often, atrophy is a complication of some other eye disease.

As the process progresses, the neurons gradually die off, as a result of which information coming from the retina reaches the brain in a distorted form. As the disease progresses, more and more cells die, eventually affecting the entire nerve trunk.

In this case, it becomes almost impossible to restore visual function. Therefore, treatment should begin at a very early stage, when the first signs of the disease appear.

How is optic nerve atrophy treated, what are the symptoms of this eye disease? We will talk about all this today on this page “Popular about health” with you. But let's start our conversation with the characteristic signs of this pathology:

Symptoms of eye nerve atrophy

It all starts with decreased vision. This process can occur gradually or rapidly, suddenly. It all depends on the location of the nerve lesion and on which segment of the trunk it develops. Depending on the severity of the pathological process, vision loss is divided into degrees:

Uniform decline. Characterized by a uniform deterioration in the ability to see objects and distinguish colors.

Loss of side margins. A person can clearly distinguish objects in front of him, but he sees poorly or does not see at all what is on the side.

Loss of spots. Normal vision is hampered by a spot in front of the eye, which can have different sizes. Within its limits, a person sees nothing; beyond its limits, vision is normal.

In severe cases of complete atrophy, the ability to see is completely lost.

Treatment of optic atrophy

As we already know, this pathological process is often a complication of another eye disease. Therefore, after identifying the cause, prescribe complex treatment underlying disease and take measures to prevent further development of atrophy optic nerve.

In the event that the pathological process has just begun and has not yet developed, it is usually possible to cure the nerve and visual functions are restored within a period of two weeks to several months.

If, by the time the treatment begins, atrophy has already developed sufficiently, it is completely impossible to cure the optic nerve, since destroyed nerve fibers cannot yet be restored in our time. If the damage is partial, rehabilitation to improve vision is still possible. But, in the severe stage of complete damage, it is not yet possible to cure atrophy and restore visual functions.

Treatment of eye atrophy involves the use of medications, drops, injections (general and local), the action of which is aimed at improving blood circulation in the optic nerve, reducing inflammation, as well as restoring those nerve fibers which have not yet been completely destroyed. Additionally, physiotherapy methods are used.

Drugs used in treatment:

To improve blood circulation in the optic nerve, vasodilators are used: Nicotinic acid, No-shpu, Papaverine and Dibazol. Patients are also prescribed Complamin, Eufillin, Trental. And also Galidor and Sermion. For the same purpose, anticoagulant drugs are used: Tiklid and Heparin.

In order to restore metabolic and regenerative processes in the tissues of the affected nerve, patients are prescribed biogenic stimulants, in particular, Vitreous body, Peat and aloe preparations. Vitamins, amino acids, enzymes and immunostimulants are also prescribed.

To stop and reduce the inflammatory process, they are often used hormone therapy with Prednisolone and Dexamethasone.
In addition, complex treatment includes drugs aimed at normalizing the functioning of the central nervous system. nervous system: Cerebrolysin, Phezam, as well as Emoxipin, Nootropil and Cavinton.

The doctor prescribes all of the above and other medications individually, after determining the cause of the pathological process and diagnosing the underlying disease. This takes into account the degree of damage to the optic nerve, the patient’s age, his general condition and the presence of concomitant diseases.

In addition to medications, physiotherapeutic techniques and acupuncture are actively used. Methods of magnetic, laser and electrical stimulation of the optic nerve trunk are used. According to indications, the patient may be recommended surgical treatment.

Complex therapy is prescribed in courses that are repeated every few months.

In conclusion of our conversation, it should be noted that optic nerve atrophy cannot be cured by non-traditional means. You will only waste time. The pathological process will progress, increasingly reducing the chances of successful treatment and restoration of vision.

Therefore, if you have the symptoms described above or other symptoms indicating the development of pathology, do not waste precious time and make an appointment with an experienced ophthalmologist. With timely treatment, the chances of restoring vision increase significantly. Be healthy!

19-12-2012, 14:49

Description

is not an independent disease. This is a consequence of various pathological processes affecting various areas visual path. It is characterized by decreased visual function and blanching of the optic nerve head.

Etiology

Development of optic nerve atrophy cause various pathological processes in the optic nerve and retina(inflammation, dystrophy, edema, circulatory disorders, toxin effects, compression and damage to the optic nerve), diseases of the central nervous system, general diseases body, hereditary causes.

Lead to optic nerve atrophy general diseases. This happens with poisoning with ethyl and methyl alcohols, tobacco, quinine, chlorophos, sulfonamides, lead, carbon disulfide and other substances, with botulism. Vascular diseases can cause acute or chronic circulatory disorders in the vessels of the optic nerve with the development of ischemic foci and areas of softening (colliquation necrosis). Essential and symptomatic hypertension, atherosclerosis, diabetes mellitus, internal profuse bleeding, anemia, diseases of the cardiovascular system, fasting, and vitamin deficiencies can lead to optic nerve atrophy.

In the etiology of optic nerve atrophy, the following are also important: diseases of the eyeball. These are lesions of the retina of vascular origin (with hypertensive angiosclerosis, atherosclerosis, involutional changes), retinal vessels (inflammatory and allergic vasculitis, obstruction of the central artery and central vein retina), dystrophic diseases of the retina (including retinal pigmentary dystrophy), complications of uveitis (papillitis, chorioretinitis), retinal detachment, primary and secondary glaucoma (inflammatory and post-inflammatory, flicogenic, vascular, dystrophic, traumatic, postoperative, neoplastic). Prolonged hypotension of the eyeball after surgery, inflammatory degenerative diseases of the ciliary body, penetrating wounds of the eyeball with the formation of a fistula lead to swelling of the optic disc (congestive papilla), after which atrophy of the optic disc develops.

In addition to Leber's hereditary atrophy and hereditary infantile optic nerve atrophy, hereditary causes are important in the occurrence of atrophy in drusen of the optic nerve head. Diseases and deformations of the skull bones (tower-shaped skull, Crouzon's disease) also lead to atrophy of the optic nerves.

It should be noted that in practice, the etiology of optic nerve atrophy is not always easy to establish. According to E. Zh. Tron, in 20.4% of patients with optic nerve atrophy, its etiology was not established.

Pathogenesis

Nerve fibers peripheral neuron visual pathway can be subject to various influences. This is inflammation, non-inflammatory edema, dystrophy, circulatory disorders, the action of toxins, damage, compression (tumor, adhesions, hematomas, cysts, sclerotic vessels, aneurysms), which leads to the destruction of nerve fibers and their replacement with glial and connective tissue, obliteration of the capillaries that feed them .

Moreover, when increasing intraocular pressure develops collapse of the glial cribriform membrane of the optic disc, which leads to degeneration of nerve fibers in vulnerable places disc, and then to disc atrophy with excavation, resulting from direct compression of the disc and secondary disruption of microcirculation.

Classification

According to the ophthalmoscopic picture, they distinguish primary (simple) and secondary optic atrophy. Primary atrophy occurs on a previously unchanged disc. With simple atrophy, nerve fibers are promptly replaced by proliferating elements of glia and connective tissue that take their places. The boundaries of the disc remain distinct. Secondary optic disc atrophy occurs on the altered disc due to its swelling (congestive nipple, anterior ischemic neuropathy) or inflammation. In place of dead nerve fibers, as in primary atrophy, glial elements penetrate, but this occurs more rapidly and in large sizes, resulting in the formation of rough scars. The boundaries of the optic disc are not distinct, blurred, and its diameter may be increased. The division of atrophy into primary and secondary is arbitrary. With secondary atrophy, the boundaries of the disc are only unclear at first; over time, the swelling disappears and the boundaries of the disc become clear. Such atrophy is no longer different from simple atrophy. Sometimes in separate form glaucomatous (marginal, cavernous, cauldron) atrophy of the optic disc is distinguished. With it, there is practically no proliferation of glia and connective tissue, and as a result of direct mechanical impact Increased intraocular pressure causes pressing (excavation) of the optic nerve head as a result of the collapse of its glial-cribriform membrane.

Optic disc atrophy, depending on the degree of color loss detected during ophthalmoscopy, is divided into initial, partial, incomplete and complete. With initial atrophy, a slight blanching appears against the background of the pink color of the disc, which later becomes more intense. When not the entire diameter of the optic nerve is affected, but only part of it, partial atrophy of the optic nerve head develops. Thus, when the papillomacular bundle is damaged, blanching of the temporal half of the optic nerve occurs. With further spread of the process, partial atrophy can spread to the entire nipple. With diffuse spread of the atrophic process, uniform blanching of the entire disc is noted. If visual functions are still preserved, then they speak of incomplete atrophy. With complete atrophy of the optic nerve, the disc becomes completely blanched and the visual functions of the affected eye are completely lost (amaurosis). Not only visual but also reflex nerve fibers pass through the optic nerve, therefore, with complete atrophy of the optic nerve, the direct reaction of the pupil to light is lost on the affected side, and the friendly one on the other eye.

Topically isolated ascending and descending optic atrophy. Retinal ascending atrophy (waxy, valerian) occurs during inflammatory and dystrophic processes in the retina due to primary damage to the visual ganglion neurocytes of the ganglion layer of the retina. The optic disc becomes grayish-yellow, the vessels of the disc narrow, and their number decreases. Ascending atrophy does not develop when only the neuroepithelial layer of the retina (rods and cones) is affected. Descending optic atrophy occurs when a peripheral neuron of the optic pathway is damaged and slowly descends to the optic disc. Having reached the optic nerve head, the atrophic process changes it according to the type of primary atrophy. Descending atrophy spreads more slowly than ascending atrophy. The closer the process is to the eyeball, the faster optic disc atrophy appears in the fundus. Thus, damage to the optic nerve at the point where the central retinal artery enters it (10-12 mm behind the eyeball) causes atrophy of the optic disc in 7-10 days. Damage to the intraorbital segment of the optic nerve before the entrance of the central retinal artery leads to the development of optic disc atrophy after 2-3 weeks. With retrobulbar neuritis, atrophy descends to the fundus within 1-2 months. With chiasm injuries, descending atrophy descends to the fundus 4-8 weeks after the injury, and with slow compression of the chiasm by pituitary tumors, optic disc atrophy develops only after 5-8 months. Thus, the rate of spread of descending atrophy is also associated with the type and intensity of the pathological process affecting the peripheral neuron of the visual pathway. They also matter blood supply conditions: the atrophic process develops faster when the blood supply to nerve fibers deteriorates. Atrophy of the optic discs with damage to the optic tract occurs approximately a year after the onset of the disease (slightly faster with injuries to the optic tract).

Optic nerve atrophy may be stationary and progressive, which is assessed during a dynamic study of the fundus and visual functions.

If one eye is affected, it is said unilateral, if both eyes are affected - o bilateral optic atrophy. Atrophy of the optic nerves during intracranial processes is often bilateral, but the degree of its severity varies. Unilateral optic nerve atrophy also occurs in intracranial processes, which is especially common when the pathological focus is localized in the anterior cranial fossa. Unilateral atrophy during intracranial processes can be initial stage bilateral. In case of circulatory disorders in the vessels of the optic nerve, intoxication, the process is usually bilateral. Unilateral atrophy occurs with damage to the optic nerve, pathological processes in the orbit, or is caused by unilateral pathology of the eyeball.

Ophthalmoscopic picture

With optic nerve atrophy there is always optic disc pallor A. There is often, but not always, vasoconstriction of the optic disc.

With primary (simple) atrophy The boundaries of the disc are clear, its color is white or grayish-white, bluish or slightly greenish. In red-free light, the contours of the disc remain clear or become sharper, while the contours of a normal disc are veiled. In red (purple) light, the atrophic disc appears blue. The cribriform plate (lamina cribrosa), through which the optic nerve passes as it enters the eyeball, is very little translucent. Translucency of the cribriform plate is due to a decrease in blood supply to the atrophied disc and less proliferation of glial tissue than with secondary atrophy. Disc blanching can vary in intensity and distribution. With initial atrophy, a slight but distinct blanching appears against the background of the pink color of the disc, then it becomes more intense while the pink tint weakens, which then completely disappears. With advanced atrophy, the disc is white. At this stage of atrophy, vasoconstriction is almost always observed, and the arteries are narrowed more sharply than the veins. The number of vessels on the disc also decreases. Normally, about 10 small vessels pass through the edge of the disc. With atrophy, their number decreases to 7-6, and sometimes to three (Kestenbaum's symptom). Sometimes, with primary atrophy, a slight excavation of the optic nerve head is possible.

With secondary atrophy The boundaries of the disc are unclear and blurred. Its color is gray or dirty gray. The vascular infundibulum or physiological excavation is filled with connective or glial tissue, the lamina cribrosa of the sclera is not visible. These changes are usually more pronounced in atrophy after a congestive nipple than in atrophy after optic neuritis or anterior ischemic neuropathy.

Retinal waxy optic disc atrophy It is distinguished by its yellow waxy color.

For glaucoma Increased intraocular pressure causes the appearance of glaucomatous excavation of the optic nerve head. In this case, first the vascular bundle of the disc shifts to the nasal side, then the excavation of the nipple gradually develops, which gradually increases. The color of the disc becomes whitish and pale. A cauldron-shaped excavation covers almost the entire disc to its edges (cauldron-shaped, marginal excavation), which distinguishes it from physiological excavation, which has the shape of a funnel that does not reach the edges of the disc and does not displace the vascular bundle to the nasal side. The vessels at the edge of the disc bend over the edge of the depression. In advanced stages of glaucoma, the excavation involves the entire disc, which becomes completely white, and the vessels on it are greatly narrowed.

Cavernous atrophy occurs when the optic nerve vessels are damaged. The atrophic optic disc begins to gouge under the influence of normal intraocular pressure with the appearance of excavation, whereas excavation of a normal disc requires increased intraocular pressure. Excavation of the disc in cavernous atrophy is facilitated by the fact that the proliferation of glia is small and therefore does not create additional resistance, preventing excavation.

Visual functions

Visual acuity of patients with optic atrophy depends on the location and intensity of the atrophic process. If the papillomacular bundle is affected, then visual acuity is noticeably reduced. If the papillomacular bundle is slightly affected, and the peripheral fibers of the optic nerve are more affected, then visual acuity does not decrease much. If there is no damage to the papillomacular bundle, and only the peripheral fibers of the optic nerve are affected, then visual acuity does not change.

Changes in field of view with optic nerve atrophy, they are important in topical diagnosis. They depend to a greater extent on the localization of the pathological process and to a lesser extent on its intensity. If the papillomacular bundle is affected, a central scotoma occurs. If the peripheral fibers of the optic nerve are affected, then narrowing of the peripheral boundaries of the visual field develops (uniform along all meridians, uneven, sector-shaped). If optic nerve atrophy is associated with damage to the chiasm or optic tract, hemianopsia (homonymous and heteronymous) occurs. Hemianopsia in one eye occurs when the intracranial part of the optic nerve is damaged.

Color vision disorders more often occur and are clearly expressed with atrophy of the optic nerve head, occurring after neuritis, and rarely with atrophy after edema. First of all, the color perception of green and red colors suffers.

Often with optic nerve atrophy changes in the fundus correspond to changes in visual functions, but this does not always happen. Thus, with descending atrophy of the optic nerve, visual functions can be greatly changed, and the fundus for a long time remains normal until the atrophic process descends to the optic nerve head. Severe pallor of the optic disc in combination with a slight change in visual functions is also possible. This may be when multiple sclerosis when the death of myelin sheaths in the area of plaques occurs while the axial cylinders of the nerve fibers are preserved. Pronounced blanching of the disc while maintaining visual functions may also be associated with the peculiarity of the blood supply in the area of the cribriform plate of the sclera. This area is supplied with blood from the posterior short ciliary arteries; deterioration of blood flow through them causes intense blanching of the disc. The remaining (orbital) part of the optic nerve is supplied with blood from the anterior and posterior arteries of the optic nerve, that is, from other vessels.

With blanching of the optic nerve head, combined with a normal state of visual functions, it is necessary to study the visual field using campimetry to identify small defects. In addition, you need to collect an anamnesis about the initial visual acuity, since sometimes visual acuity can be above one, and in these cases its decrease to one may indicate the influence of the atrophic process.

With unilateral atrophy a thorough examination of the functions of the second eye is necessary, since unilateral atrophy can only be the beginning of bilateral atrophy, which often happens with intracranial processes. Changes in the visual field of the other eye indicate a bilateral process and acquire important topical and diagnostic significance.

Diagnostics

In severe cases, diagnosis is not difficult. If the pallor of the optic disc is insignificant (especially temporal, since the temporal half of the disc is normally somewhat paler than the nasal half), then a long-term study of visual functions over time helps to establish a diagnosis. In this case it is necessary pay special attention to examining the visual field for white and colored objects. Electrophysiological, radiological and fluorescein angiographic studies facilitate diagnosis. Characteristic changes in the visual field and an increase in the threshold of electrical sensitivity (up to 400 μA when the norm is 40 μA) indicate optic nerve atrophy. The presence of marginal excavation of the optic nerve head and increased intraocular pressure indicate glaucomatous atrophy.

Sometimes it is difficult to determine the type of damage to the optic nerve or the nature of the underlying disease just by the presence of disc atrophy in the fundus. Blurring of the disc boundaries during atrophy indicates that it was the result of edema or inflammation of the disc. It is necessary to study the anamnesis in more detail: the presence of symptoms intracranial hypertension indicates the post-stagnation nature of atrophy. The presence of simple atrophy with clear boundaries does not exclude its inflammatory origin. So, descending atrophy due to retrobulbar neuritis and inflammatory processes of the brain and its membranes, it causes changes in the disc in the fundus similar to simple atrophy. Nature of atrophy(simple or secondary) has great value in diagnostics, because certain diseases lead to certain, “favorite” types of damage to the optic nerves. For example, compression of the optic nerve or chiasm by a tumor leads to the development of simple atrophy of the optic nerves, tumors of the brain ventricles lead to the development of congestive nipples and further to secondary atrophy. However, diagnosis is complicated by the fact that some diseases, for example meningitis, arachnoiditis, neurosyphilis, can be accompanied by both simple and secondary atrophy of the optic discs. In this case, the accompanying eye symptoms: changes in the vessels of the retina, the retina itself, the choroid, as well as a combination of optic nerve atrophy with a disorder of pupillary reactions.

When assessing the degree of color loss and pallor of the optic nerve head it is necessary to take into account the general background of the fundus. Against the parquet background of the fundus of brunettes, even a normal or slightly atrophied disc appears paler and whiter. Against a light background of the fundus, the atrophic nipple may not look so pale and white. In severe anemia, the optic discs are completely white, but more often a faint pink tint remains. In hypermetropes, the optic discs are in in good condition more hyperemic, and with a high degree of hypermetropia there may be a picture of false neuritis (severe hyperemia of the nipples). With myopia, the optic discs are paler than those of emmetropes. The temporal half of the optic disc is normally somewhat paler than the nasal half.

Optic nerve atrophy in some diseases

Brain tumors . Secondary atrophy of the optic nerve in brain tumors is a consequence of congestive nipples. More often it occurs with tumors of the cerebellopontine angle, hemispheres and ventricles of the brain. With subtentorial tumors, secondary atrophy occurs less frequently than with supratentorial ones. The incidence of secondary atrophy is influenced not only by the location, but also by the nature of the tumor. It occurs more often with benign tumors. It develops especially rarely with metastases of malignant tumors in the brain, since death occurs before stagnant nipples turn into secondary atrophy.

Primary (simple) optic nerve atrophy occurs when compression of the peripheral neuron of the optic pathway. Most often, the chiasm is affected, less often the intracranial part of the optic nerve, and even less often the optic tract. Simple atrophy of the optic nerve is characteristic of supratentorial brain tumors; it is especially often caused by tumors of the chiasmal-sellar region. Rarely, primary atrophy of the optic nerves occurs with subtentorial tumors as a symptom at a distance: compression of the peripheral neuron of the optic pathway occurs through the dilated ventricular system or by brain dislocation. Primary optic atrophy rarely occurs with ventricular tumors cerebral hemispheres , cerebellum and cerebellopontine angle, and secondary atrophy with tumors of this localization is common. Simple atrophy of the optic nerves rarely develops with malignant tumors and often with benign ones. Primary atrophy of the optic nerves is usually caused by benign tumors of the sella turcica (pituitary adenomas, craniopharyngiomas) and meningiomas of the lesser wing of the sphenoid bone and olfactory fossa. Optic nerve atrophy develops in Foster Kennedy syndrome: simple atrophy in one eye and a congestive nipple with possible progression to secondary atrophy in the other eye.

Brain abscesses . Congestive discs often develop, but they rarely progress to secondary optic atrophy, as increased intracranial pressure does not last so long, since intracranial hypertension either decreases after surgery, or patients do not live to see the transition of stagnant nipples to secondary atrophy. Foster Kennedy syndrome is rare.

Optochiasmal arachnoiditis . More often, primary atrophy of the optic discs occurs in the form of blanching of the entire nipple or its temporal half (partial atrophy). In isolated cases, the upper or lower half of the disc may become pale.

Secondary atrophy of the optic discs in optochiasmal arachnoiditis can be post-neuritic (transition of inflammation from the meninges to the optic nerve) or post-congestive (occurs after congestive nipples).

Arachnoiditis of the posterior cranial fossa . Often lead to the development of pronounced congestive nipples, which then develop into secondary atrophy of the optic discs.

Aneurysms of the vessels of the base of the brain . Aneurysms of the anterior part of the circle of Willis often put pressure on the intracranial part of the optic nerve and chiasm, which leads to the development of simple atrophy of the optic nerve. Simple atrophy due to compression of the optic nerve is unilateral, always located on the side of the aneurysm. When pressure is applied to the chiasm, bilateral simple atrophy occurs, which may first occur in one eye and then appear in the other. Unilateral simple atrophy of the optic nerve most often occurs with aneurysms of the internal carotid artery, less often with aneurysms of the anterior cerebral artery. Aneurysms of the vessels of the base of the brain most often manifest as unilateral paralysis and paresis of the nerves of the oculomotor system.

Thrombosis of the internal carotid artery . The presence of alternating optic-pyramidal syndrome is characteristic: blindness of the eye with simple atrophy of the optic disc on the side of thrombosis in combination with hemiplegia on the other side.

Tabes dorsalis and progressive paralysis . With tabes and progressive paralysis, atrophy of the optic nerves is usually bilateral and has the character of simple atrophy. Atrophy of the optic nerves with tabes is more common than with progressive paralysis. The atrophic process begins with the peripheral fibers and then slowly goes deep into the optic nerve, so there is a gradual decrease in visual functions. Visual acuity gradually decreases with varying degrees of severity in both eyes, up to bilateral blindness. Visual fields gradually narrow, especially to colors, in the absence of scotomas. Optic nerve atrophy with tabes usually develops in the early period of the disease, when other neurological symptoms (ataxia, paralysis) are not expressed or absent. Tabes is characterized by a combination of simple optic atrophy with Argil Robertson's sign. Reflex immobility of the pupils during tabesa is often combined with miosis, anisocoria and pupillary deformation. Argil Robertson's symptom also occurs with syphilis of the brain, but much less frequently. Secondary atrophy of the optic discs (post-congestive and post-neuritic) speaks against tabes and often occurs with syphilis of the brain.

Atherosclerosis . Atrophy of the optic nerve in atherosclerosis occurs as a result of direct compression of the optic nerve by the sclerotic carotid artery or as a result of damage to the vessels supplying the optic nerve. Primary optic nerve atrophy develops more often, and secondary atrophy develops much less often (after disc edema due to anterior ischemic neuropathy). There are often sclerotic changes in the retinal vessels, but these changes are also characteristic of syphilis, hypertension and kidney disease.

Hypertension . Optic nerve atrophy may be a consequence of neuroretinopathy. This is secondary disc atrophy with associated symptoms, characteristic of hypertensive angioretinopathy.

In hypertension, optic nerve atrophy may occur as an independent process not associated with changes in the retina and retinal vessels. In this case, atrophy develops due to damage to the peripheral neuron of the visual pathway (nerve, chiasm, tract) and has the character of primary atrophy.

Profuse bleeding . After profuse bleeding (gastrointestinal, uterine) after more or less long time, from several hours to 3-10 days, anterior ischemic neuropathy may develop, after which secondary atrophy of the optic discs develops. The lesion is usually bilateral.

Leberian optic atrophy . Familial hereditary optic atrophy (Leber's disease) is observed in men 16-22 years old in several generations and is transmitted through the female line. The disease proceeds as bilateral retrobulbar neuritis, starting with a sharp decrease in vision. After a few months, simple atrophy of the optic discs develops. Sometimes the entire nipple turns pale, sometimes only the temporal halves. Complete blindness usually does not occur. Some authors believe that Leber's atrophy is a consequence of optochiasmal arachnoiditis. The type of inheritance is recessive, linked to the X chromosome.

Hereditary infantile optic atrophy . Children aged 2-14 years are affected. Gradually, simple atrophy of the optic nerves develops with temporal blanching of the disc, most rarely the nipple. High visual acuity is often maintained, and blindness in both eyes never occurs. Central scotomas often occur in the field of vision of both eyes. Color perception is usually impaired, more towards blue than red and green colors. The type of inheritance is dominant, that is, the disease is transmitted from sick fathers and sick mothers to both sons and daughters.

Diseases and deformations of the skull bones . In early childhood, with a tower-shaped skull and Crouzon's disease (craniofacial dysostosis), congestive nipples may develop, after which secondary atrophy of the optic discs of both eyes develops.

Principles of treatment

Treatment of patients with optic nerve atrophy is carried out taking into account its etiology. Patients with optic nerve atrophy, which has developed due to compression of the peripheral neuron of the visual pathway by the intracranial process, require neuro surgical treatment.

To improve blood supply to the optic nerve use vasodilators, vitamin preparations, biogenic stimulants, neuroprotectors, infusion hypertonic solutions. It is possible to use oxygen therapy, blood transfusions, and the use of heparin. In the absence of contraindications, physiotherapy is used: ultrasound on the open eye and endonasal medicinal electrophoresis of vasodilators, vitamin preparations, lecozyme (papain), lidase; electrical and magnetic stimulation of the optic nerves is used.

Forecast

Prognosis of optic nerve atrophy always serious. In some cases, you can expect to preserve your vision. If atrophy develops, the prognosis is unfavorable. Treatment of patients with optic nerve atrophy, whose visual acuity has been less than 0.01 for several years, is ineffective.

Article from the book: .

Such a serious ophthalmological disease as descending optic atrophy begins to develop in connection with degenerative processes.

Sclerotic changes occur in the fibers of nerve tissue.

As the disease progresses, vision not only deteriorates, but may even disappear completely. This is due to the death of nerve fibers that carry information about the retinal image to the brain.

Why does descending optic atrophy occur and how to recognize it?

Illness provoke the following reasons:

Consequences glaucoma.
Vasoconstriction, compressing the optic nerve - a tumor appears in the cranial cavity, resulting in the formation brain abscess.
Complications myopia.
Development in blood vessels atherosclerotic plaques — we're talking about about the vessels that supply the optic nerves with blood. Thrombosis begins, the walls become inflamed. Violation of the structure of blood vessels often contributes to syphilis, vasculitis, diabetes mellitus or hypertension.
Injuries eyes.
Intoxication(ARVI, use of alcohol substitutes, narcotic substances, nicotine and quinine).

When the fibers of one optic nerve die, the pathology is considered unilateral. Atrophy in both eyes cause the following disorders and diseases:

syphilis;
intoxication;
tumor in the cavities of the skull;
blood supply disturbance(with atherosclerosis, diabetes mellitus, hypertension).

Symptoms of complete and partial atrophy

Symptoms of the disease depends on the type atrophy. The main sign of pathology is decreased visual acuity.

Important! Improve vision in case of atrophy glasses or contact lenses it won't work.

Another characteristic symptom of the disease is visual field change. During the diagnosis of the disease, the patient describes in detail his feelings, according to which the doctor determines at what stage the disease is. The patient may observe the following phenomena:

you can see everything as if through a tube - tunnel vision;
before my eyes regularly spots appear, reminiscent of a mosaic;
image fragment, which is located in the bow, absent, the same thing is noticed from the side of the temples.

In patients disturbances are observed in color vision. A person does not distinguish the color red and does not perceive green shades.

A characteristic sign of the disease is slow recovery of vision when leaving the dark into the light and vice versa. This symptom often appears at the beginning of the disease, after which it actively progresses.

Reference. Atrophy may be partial, in this case vision remains relatively sharp.

Diagnostic methods

As diagnostic measures are carried out:

fundus analysis— the examination is carried out through the pupil; for convenience, it is first dilated with special drops;
acuity test vision;
calculation of the boundaries of the field of view ( spheroperimetry);
grade correct color perception;

Photo 1. You can check color perception using Rabkin’s polychromatic tables. Normally, the eye distinguishes all numbers.

perimetry using a computer, through which the affected areas of the optic nerve are identified;
videoophthalmography— determination of the nature of damage to nerve fibers;
x-ray skulls;
computed and magnetic resonance imaging;
dopplerography using a laser is an optional, additional diagnostic method.

Treatment. Is it possible to avoid disability?

During the treatment process, doctors do everything to “revitalize” nerve fibers in maximum quantities.

Important! The earlier the disease was identified and treatment started, the more chances for successful correction of the disease.

Nerves are stimulated by laser, alternating magnetic fields, electric current .

Also used as therapy:

medicinal impact;
blood transfusion;
taking B vitamins and special tonics, promoting vasodilation;
surgery in severe cases.

Reference. Even if partial optic atrophy is diagnosed, disability must be registered. The purpose of the group depends on the stage of the pathology and the possibility of its correction.

Acquired optic atrophy develops as a result of damage to the optic nerve fibers (descending atrophy) or retinal cells (ascending atrophy).

Descending atrophy is caused by processes that damage the optic nerve fibers at different levels(orbit, optic canal, cranial cavity). The nature of the damage is different: inflammation, trauma, glaucoma, toxic damage, circulatory disorders in the vessels supplying the optic nerve, metabolic disorders, compression of the optic fibers by a space-occupying formation in the orbital cavity or in the cranial cavity, degenerative process, myopia, etc.).

Every etiological factor cause atrophy of the optic nerve with certain typical ophthalmoscopic features, for example glaucoma, circulatory disorders in the vessels supplying the optic nerve. However, there are characteristics common to optic atrophy of any nature: blanching of the optic disc and impaired visual function.

The degree of decrease in visual acuity and the nature of visual field defects are determined by the nature of the process that caused the atrophy. Visual acuity can range from 0.7 to practical blindness.

Based on the ophthalmoscopic picture, primary (simple) atrophy is distinguished, which is characterized by pallor of the optic nerve head with clear boundaries. The number of small vessels on the disc is reduced (Kestenbaum's symptom). The retinal arteries are narrowed, the veins may be of normal caliber or also slightly narrowed.

Depending on the degree of damage to the optic fibers, and therefore on the degree of decrease in visual functions and blanching of the optic nerve head, initial, or partial, and complete atrophy of the optic nerve is distinguished.

The time during which pallor of the optic nerve head develops and its severity depend not only on the nature of the disease that led to optic nerve atrophy, but also on the distance of the source of damage from the eyeball. So, for example, with inflammatory or traumatic injury optic nerve, the first ophthalmoscopic signs of optic nerve atrophy appear several days to several weeks after the onset of the disease or the moment of injury. At the same time, when a space-occupying lesion affects the optic fibers in the cranial cavity, at first only visual disorders are clinically manifested, and changes in the fundus in the form of optic nerve atrophy develop after many weeks and even months.

Congenital optic atrophy

Congenital, genetically determined optic nerve atrophy is divided into autosomal dominant, accompanied by an asymmetric decrease in visual acuity from 0.8 to 0.1, and autosomal recessive, characterized by a decrease in visual acuity, often to the point of practical blindness already in early childhood.

If ophthalmoscopic signs of optic nerve atrophy are detected, it is necessary to conduct a thorough clinical examination patient, including determination of visual acuity and the boundaries of the visual field for white, red and green colors, and examination of intraocular pressure.

If atrophy develops against the background of papilledema, even after the edema disappears, the boundaries and pattern of the disc remain unclear. This ophthalmoscopic picture is called secondary (post-edema) optic nerve atrophy. The retinal arteries are narrowed in caliber, while the veins are dilated and tortuous.

When found clinical signs optic nerve atrophy, it is necessary to first establish the cause of the development of this process and the level of damage to the optic fibers. For this purpose, not only a clinical examination is carried out, but also CT and/or MRI of the brain and orbits.

In addition to etiologically determined treatment, symptomatic complex therapy is used, including vasodilator therapy, vitamins C and B, drugs that improve tissue metabolism, various options stimulating therapy, including electrical, magnetic and laser stimulation of the optic nerve.

Hereditary atrophies come in six forms:

with a recessive type of inheritance (infantile) - from birth to three years of age there is a complete decrease in vision;
with the dominant type (juvenile blindness) - from 2-3 to 6-7 years. The course is more benign. Vision decreases to 0.1-0.2. In the fundus there is segmental blanching of the optic disc; there may be nystagmus and neurological symptoms;
opto-oto-diabetic syndrome - from 2 to 20 years. Atrophy is combined with retinal pigmentary dystrophy, cataracts, sugar and diabetes insipidus, deafness, urinary tract damage;
Beer's syndrome is a complicated atrophy. Bilateral simple atrophy already in the first year of life, reggae drops to 0.1-0.05, nystagmus, strabismus, neurological symptoms, damage pelvic organs, suffers pyramidal path, joins mental retardation;
associated with gender (more often observed in boys, develops in early childhood and increases slowly);
Leicester's disease (Lester's hereditary atrophy) - in 90% of cases occurs between the ages of 13 and 30 years.

Symptoms Acute onset, a sharp drop in vision over several hours, less often - several days. The lesion is a type of retrobulbar neuritis. The optic disc is initially unchanged, then blurring of the boundaries and changes in small vessels appear - microangiopathy. After 3-4 weeks, the optic disc becomes paler on the temporal side. In 16% of patients, vision improves. Most often, reduced vision remains for life. Patients are always irritable, nervous, and worried headache, fatigue. The cause is optochiasmatic arachnoiditis.

Optic nerve atrophy in some diseases

Optic nerve atrophy is one of the main signs of glaucoma. Glaucomatous atrophy is manifested by paleness of the disc and the formation of a depression - an excavation, which first occupies the central and temporal sections, and then covers the entire disc. Unlike the above diseases leading to disc atrophy, with glaucomatous atrophy the disc has gray, which is associated with the characteristics of the damage to its glial tissue.
Syphilitic atrophy.

Symptoms The optic disc is pale, gray, the vessels are of normal caliber and sharply narrowed. Peripheral vision narrows concentrically, there is no scotoma, color perception suffers early. There may be progressive blindness that occurs quickly, within a year.

It occurs in waves: a rapid decrease in vision, then during the period of remission - improvement, during the period of exacerbation - repeated deterioration. Miosis develops, divergent strabismus, changes in pupils, lack of reaction to light while maintaining convergence and accommodation. The prognosis is poor, with blindness occurring within the first three years.

Features of optic nerve atrophy from compression (tumor, abscess, cyst, aneurysm, sclerotic vessels), which can be in the orbit, anterior and posterior cranial fossa. Peripheral vision suffers depending on the location of the process.
Foster-Kennedy syndrome - atherosclerotic atrophy. Compression can cause sclerosis of the carotid artery and sclerosis of the ophthalmic artery; Ischemic necrosis occurs from softening during arterial sclerosis. Objectively - excavation caused by retraction of the cribriform plate; benign diffuse atrophy (with sclerosis of small vessels of the pia mater) increases slowly and is accompanied by atherosclerotic changes in the vessels of the retina.

Optic nerve atrophy in hypertension is the outcome of neuroretinopathy and diseases of the optic nerve, chiasm and optic tract.

Optic nerve atrophy is clinically a set of symptoms: visual impairment (decreased visual acuity and development of visual field defects) and blanching of the optic nerve head. Optic nerve atrophy is characterized by a decrease in the diameter of the optic nerve due to a decrease in the number of axons.

Optic nerve atrophy occupies one of the leading places in the nosological structure, second only to glaucoma and degenerative myopia. Optic nerve atrophy is considered to be the complete or partial destruction of its fibers with their replacement by connective tissue.

According to the degree of decrease in visual functions, atrophy can be partial or complete. According to research data, it is clear that 57.5% of men and 42.5% of women suffer from partial atrophy of the optic nerve. Most often, bilateral damage is observed (in 65% of cases).

The prognosis for optic atrophy is always serious, but not hopeless. Due to the fact that pathological changes are reversible, treatment of partial atrophy of the optic nerve is one of the important areas in ophthalmology. With adequate and timely treatment, this fact makes it possible to achieve an increase in visual functions even with a long-term existence of the disease. Also in recent years the number of this pathology of vascular origin has increased, which is associated with an increase in the overall vascular pathology- atherosclerosis, coronary heart disease.

Etiology and classification

By etiology
- hereditary: autosomal dominant, autosomal recessive, mitochondrial;
- non-hereditary.
According to the ophthalmoscopic picture - primary (simple); secondary; glaucomatous.
According to the degree of damage (preservation of functions): initial; partial; incomplete; complete.
According to the topical level of the lesion: descending; ascending.
By degree of progression: stationary; progressive.
According to the localization of the process: one-sided; bilateral.

There are congenital and acquired optic atrophy. Acquired optic atrophy develops as a result of damage to the optic nerve fibers (descending atrophy) or retinal cells (ascending atrophy).

Descending acquired atrophy is caused by processes that damage the fibers of the optic nerve at various levels (orbit, optic canal, cranial cavity). The nature of the damage is different: inflammation, trauma, glaucoma, toxic damage, circulatory disorders in the vessels supplying the optic nerve, metabolic disorders, compression of the optic fibers by a space-occupying formation in the orbital cavity or in the cranial cavity, degenerative process, myopia, etc.).

Each etiological factor causes optic nerve atrophy with certain ophthalmoscopic features typical for it. However, there are characteristics common to optic atrophy of any nature: blanching of the optic disc and impaired visual function.

The etiological factors of optic nerve atrophy of vascular origin are diverse: these are vascular pathology, acute vascular neuropathies (anterior ischemic neuropathy, occlusion of the central artery and vein of the retina and their branches), and a consequence of chronic vascular neuropathies (with general somatic pathology). Optic nerve atrophy occurs as a result of obstruction of the central and peripheral retinal arteries that supply the optic nerve.

Ophthalmoscopically, narrowing of the retinal vessels and blanching of part or all of the optic nerve head are detected. Persistent blanching of only the temporal half occurs with damage to the papillomacular bundle. When atrophy is a consequence of disease of the chiasm or optic tracts, then there are hemianopic types of visual field defects.

Diagnostics

Complaints: gradual decrease in visual acuity ( varying degrees severity), changes in the visual field (scotomas, concentric narrowing, loss of visual fields), impaired color vision.

Anamnesis: availability volumetric formations brain, intracranial hypertension, demyelinating lesions of the central nervous system, lesions of the carotid arteries, systemic diseases(including vasculitis), intoxication (including alcohol), history of optic neuritis or ischemic neuropathy, occlusion of retinal vessels, taking medications that have neurotoxic effect, within the last year; head and neck injuries, cardiovascular diseases, hypertension, acute and chronic cerebrovascular accidents, atherosclerosis, meningitis or meningoencephalitis, inflammatory and volumetric processes paranasal sinuses, profuse bleeding.

Physical examination :

external examination of the eyeball (limited mobility of the eyeball, nystagmus, exophthalmos, ptosis upper eyelid)
study of the corneal reflex - may be reduced on the affected side

Laboratory research

biochemical blood test: blood cholesterol, low-density lipoproteins, high-density lipoproteins, triglycerides; ·
coagulogram;
ELISA for herpes simplex virus, cytomegalovirus, toxoplasmosis, brucellosis, tuberculosis, rheumatic tests (if indicated, to exclude an inflammatory process)

Instrumental studies

visometry: visual acuity can range from 0.7 to practical blindness. When the papillomacular bundle is damaged, visual acuity is significantly reduced; with minor damage to the papillomacular bundle and involvement of peripheral nerve fibers of the optic nerve in the process, visual acuity decreases slightly; when only peripheral nerve fibers are affected, it does not change. ·
refractometry: the presence of refractive errors will allow differential diagnosis with amblyopia.
Amsler test - distortion of lines, clouding of the pattern (damage to the papillomacular bundle). ·
perimetry: central scotoma (with damage to the papillomacular bundle); various shapes narrowing of the visual field (with damage to the peripheral fibers of the optic nerve); with damage to the chiasm - bitemporal hemianopsia, with damage to the optic tracts - homonymous hemianopsia. When the intracranial part of the optic nerve is damaged, hemianopia occurs in one eye.
- Kinetic perimetry for colors - narrowing the field of vision to green and red, less often to yellow and blue.
- Computer perimetry - determination of the quality and quantity of scotomas in the field of view, including 30 degrees from the point of fixation.
Dark Adaptation Study: Dark Adaptation Disorder. · study of color vision: (Rabkin tables) - disturbance of color perception (increased color thresholds), more often in the green-red part of the spectrum, less often in the yellow-blue.
tonometry: possible increase in IOP (with glaucomatous optic atrophy).
biomicroscopy: on the affected side - afferent pupillary defect: decreased direct pupillary reaction to light while maintaining a friendly pupil reaction.
ophthalmoscopy:
- initial atrophy of the optic disc – against the background of the pink color of the optic disc, blanching appears, which subsequently becomes more intense.
- partial atrophy of the optic disc – pallor of the temporal half of the optic disc, Kestenbaum’s symptom (decrease in the number of capillaries on the optic disc from 7 or less), arteries are narrowed,
- incomplete atrophy of the optic disc – uniform blanching of the optic nerve, moderately expressed Kestenbaum’s symptom (reduction in the number of capillaries on the optic disc), arteries are narrowed,
- complete atrophy of the optic nerve – total pallor of the optic nerve, vessels are narrowed (arteries are narrowed more than veins). Kestenbaum's symptom is pronounced (reduction in the number of capillaries on the optic disc - up to 2-3 or capillaries may be absent).

With primary atrophy of the optic disc, the boundaries of the optic disc are clear, its color is white, grayish-white, bluish or slightly greenish. In red-free light, the contours remain clear, whereas the contours of the optic disc normally become blurred. In red light, with atrophy of the optic disc disc, it is blue. With secondary atrophy of the optic disc, the boundaries of the optic disc are unclear, blurred, the optic disc is gray or dirty gray, the vascular infundibulum is filled with connective or glial tissue (in the long term, the boundaries of the optic disc become clear).

optical coherence tomography of the optic disc (in four segments - temporal, superior, nasal and inferior): reduction in the area and volume of the neuroretinal rim of the optic disc, reduction in the thickness of the layer of nerve fibers of the optic disc and in the macula.
Heidelberg retinal laser tomography – decreasing the depth of the optic nerve head, the area and volume of the neuroretinal belt, increasing the excavation area. With partial atrophy of the optic nerve, the depth range of the optic nerve head is less than 0.52 mm, the rim area is less than 1.28 mm 2, the excavation area is more than 0.16 mm 2.
fluorescein angiography of the fundus: hypofluorescence of the optic nerve head, narrowing of the arteries, absence or decrease in the number of capillaries on the optic disc;
electrophysiological studies (visual evoked potentials) - decreased VEP amplitude and prolonged latency. When the papillomacular and axial bundles of the optic nerve are damaged, electrical sensitivity is normal; when peripheral fibers are damaged, the electrical phosphene threshold is sharply increased. Lability decreases especially sharply with axial lesions. During the period of progression of the atrophic process in the optic nerve, the retino-cortical and cortical time increases significantly;
Doppler ultrasound of the vessels of the head, neck, eye: decreased blood flow in the orbital, supratrochlear artery and intracranial part of the internal carotid artery;
MRI of brain vessels: foci of demyelination, intracranial pathology (tumors, abscesses, brain cysts, hematomas);
MRI of the orbit: compression of the orbital part of the optic nerve;
X-ray of the orbit according to Riese - a violation of the integrity of the optic nerve.

Differential diagnosis

Optic atrophy with tabes develops in both eyes, but the extent of damage to each eye may not be the same. Visual acuity decreases gradually, but because... The process with tabes is always progressive, then ultimately bilateral blindness occurs at different times (from 2-3 weeks to 2-3 years). The most common form of change in the visual field in tabetic atrophy is a gradually progressive narrowing of the boundaries in the absence of scotomas within the remaining areas. Rarely, with tabesa, bitemporal scotomas, bitemporal narrowing of the boundaries of the visual field, as well as central scotomas are observed. The prognosis for tabetic optic atrophy is always poor.

Optic nerve atrophy can be observed with deformations and diseases of the skull bones. Such atrophy is observed with a tower-shaped skull. Decreased vision usually develops in early childhood and rarely after 7 years. Blindness in both eyes is rare; sometimes blindness in one eye is observed with a sharp decrease in vision in the other eye. From the side of the visual field, there is a significant narrowing of the boundaries of the visual field along all meridians; there is no scotoma. Atrophy of the optic nerve with a tower-shaped skull is considered by most to be a consequence of congestive nipples, developing due to increased intracranial pressure. Among other deformations of the skull, atrophy of the optic nerves is caused by dysostosis craniofacialis (Crouzon's disease, Apert's syndrome, marble disease, etc.).

Optic nerve atrophy can occur due to poisoning with quinine, plasmacide, fern when expelling worms, lead, carbon disulfide, botulism, and methyl alcohol poisoning. Methyl alcohol optic atrophy is not so rare. After drinking methyl alcohol, within a few hours paralysis of accommodation and dilation of the pupils appears, central scotoma occurs, and vision sharply decreases. Then vision is partially restored, but atrophy of the optic nerve gradually increases and irreversible blindness occurs.

Optic nerve atrophy can be congenital and hereditary, due to birth or postpartum head injuries, prolonged hypoxia, etc.

Diagnosis	Rationale for differential diagnosis	Surveys	Diagnosis exclusion criteria
Amblyopia	Significant decrease in vision in the absence of pathology from the anterior segment of the eye and retina.	Physical examinations	U small child- the presence of strabismus, nystagmus, inability to clearly fix the gaze on a bright object. In older children - decreased visual acuity and lack of improvement from its correction, impaired orientation in an unfamiliar place, squint, the habit of closing one eye when looking at an object or reading, tilting or turning the head when looking at an object of interest.
		Refractometry	Anisometropic amblyopia develops with uncorrected high degree anisometropia in the eye with more pronounced refractive errors (myopia more than 8.0 diopters, hyperopia more than 5.0 diopters, astigmatism more than 2.5 diopters in any meridian), refractive amblyopia - with prolonged absence optical correction hyperopia, myopia or astigmatism with a difference in refraction of both eyes: hyperopia more than 0.5 diopters, myopia more than 2.0 diopters, astigmatic 1.5 diopters.
		HRT OCT	According to NRT: the depth range of the optic nerve head is more than 0.64 mm, the area of the optic nerve rim is more than 1.48 mm 2, the excavation area of the optic nerve is less than 0.12 mm 2.
Hereditary atrophy Leber	Sharp decline vision of both eyes in the absence of pathology from the anterior segment of the eye and retina.	Complaints and anamnesis	The disease develops in male members of the same family aged 13 to 28 years. Girls get sick very rarely and only if the mother is a proband and the father suffers from this disease. Heredity is associated with the X chromosome. A sharp decrease in vision in both eyes over several days. The general condition is good, sometimes patients complain of headache.
		Ophthalmoscopy	Initially, hyperemia and slight blurring of the optic disc borders appear. Gradually, the optic discs become waxy and pale, especially in the temporal half.
		Perimetry	In the field of view there is a central absolute scotoma, white, the peripheral borders are normal.
Hysterical amblyopia (amaurosis)	Sudden deterioration of vision or complete blindness in the absence of pathology from the anterior segment of the eye and retina.	Complaints and anamnesis	Hysterical amblyopia in adults is a sudden deterioration of vision that lasts from several hours to several months, developing against the background of severe emotional shocks. It is more often observed in women aged 16-25 years.
		Physical examinations	There may be a complete lack of reaction of the pupils to light.
		Visometry	Reduced visual acuity to varying degrees, up to blindness. With repeated studies, the data may be completely different from previous ones.
		Ophthalmoscopy	The optic disc is pale pink, the contours are clear, the Kestenbaum sign is absent.
		Perimetry	Concentric narrowing of the visual field, characteristic disturbance normal type borders - the widest field of vision for red; less commonly, hemianopsia (homonymous or heteronymous).
		VEP	VEP data is normal.
Optic nerve hypoplasia	Bilateral decrease or complete loss of vision in the absence of pathology from the anterior segment of the eye and retina.	Visometry	Optic nerve hypoplasia is accompanied by bilateral vision loss (in 80% of cases from medium degree until complete blindness).
		Physical examinations	The afferent pupillary reflex is absent. Unilateral optic disc changes are often associated with strabismus and can be seen by a relative afferent pupillary defect and unilateral weak or absent fixation (instead of positional nystagmus).
		Ophthalmoscopy	The optic disc is reduced in size, pale, surrounded by a faint pigment ring. The outer ring (about the size of a normal disc) consists of the lamina cribrosa, pigmented sclera and choroid. Options: yellow-white, small disc with a double ring or complete absence of nerve and vascular aplasia. With a bilateral process, the disc is often difficult to detect; in this case, it is determined along the course of the vessels.
		Perimetry	If central vision is preserved, defects in the visual fields may be detected.
		Consultation with a neurologist, endocrinologist, laboratory tests	Optical hypoplasia of the nerve is rarely combined with septo-optic dysplasia (Morsier syndrome: absence of the transparent septum (septum pellucidum) and pituitary gland, which is accompanied by disorders of the thyroid gland and other hormonal disorders: possible growth retardation, hypoglycemia attacks, combination with mental retardation and malformations of brain structures).
Coloboma of the optic nerve head	Pathology of the optic nerve	Ophthalmoscopy	With ophthalmoscopy, the optic disc is enlarged in size (elongation of the vertical size), deep excavation or local excavation and increased crescent-shaped pigmentation with partial involvement of the lower nasal part of the optic disc in the process. When the choroid is also involved in the process, a line of demarcation appears, represented by bare sclera. Lumps of pigment may mask the boundary between normal tissue and coloboma. There may be glial tissue on the surface of the optic disc.
Coloboma of the optic nerve head	Pathology of the optic nerve	MRI	MRI - the membranes of the optic canal are weakly expressed or absent.
Morning glow syndrome	Pathology of the optic nerve	Physical examinations	Almost all patients with unilateral pathology have strabismus and high myopia in the affected eye.
		Visometry	Visual acuity is often reduced, but can also be very high.
		Refractometry	Often with a unilateral process there is high myopia of the affected eye.
		Ophthalmoscopy	On ophthalmoscopy, the optic disc is enlarged and appears to be located in a funnel-shaped cavity. Sometimes the head of the optic disc is raised; it is also possible to change the position of the head of the optic disc from a staphylomatous depression to its prominence; Around the nerve there are areas of transparent grayish retinal dysplasia and pigment clumps. The demarcation line between the optic disc tissue and the normal retina is indistinguishable. Many abnormally branching vessels are identified. Most patients have areas of local retinal detachment and radial retinal folds within the excavation.
		Perimetry	Possible defects in the visual field: central scotomas and enlargement of the blind spot.
		Consultations with an otolaryngologist	Morning glow syndrome occurs as an independent manifestation or can be combined with hypertelorism, cleft lip, palate and other anomalies.

Treatment

Treatment of optic nerve atrophies is a very difficult task. Except pathogenetic therapy tissue therapy, vitamin therapy, spinal puncture in combination with osmotherapy, vasodilators, B vitamins, especially B1 and B12, are used. Currently, magnetic, laser and electrical stimulation are widely used.

In the treatment of partial optic nerve atrophy, pharmacotherapy is usually used. The use of drugs makes it possible to influence various parts of the pathogenesis of optic nerve atrophy. But do not forget about physical therapy methods and various routes of drug administration. The issue of optimizing routes of drug administration has also become relevant in recent years. Thus, parenteral (intravenous) administration of vasodilators can promote systemic vasodilation, which, in some cases, can lead to steal syndrome and impair blood circulation in the eyeball. It is generally accepted that the therapeutic effect is greater when drugs are used topically. However, in diseases of the optic nerve local application medication is associated with certain difficulties caused by the existence of a number of tissue barriers. Creation of a therapeutic concentration of a drug in a pathological focus is achieved more successfully with a combination of drug therapy and physical therapy.

Drug treatment (depending on the severity of the disease)
Conservative (neuroprotective) treatment is aimed at increasing blood circulation and improving the trophism of the optic nerve, stimulating vitally active nerve fibers that have survived and/or are in the stage of apoptosis.
Drug treatment includes direct (directly protect the retinal ganglia and axons) and indirect (reduce the effect of factors that cause death) neuroprotective drugs nerve cells) actions.

Retinoprotectors: ascorbic acid 5% 2 ml intramuscularly once a day for 10 days, in order to reduce the permeability of the vascular wall and stabilize endothelial cell membranes
Antioxidants: tocopherol 100 IU 3 times a day – 10 days, in order to improve oxygen supply to tissues, collateral circulation, strengthening vascular wall
Drugs that improve metabolic processes(direct neuroprotectors): retinalamin for intramuscular 1.0 ml and/or parabulbar administration 5 mg 0.5 ml parabulbar once a day for 10 days
List of additional medicines:
- vinpocetine – adults 5-10 mg 3 times a day for 2 months. Has vasodilating, antihypoxic and antiplatelet effects
- cyanocobalamin 1 ml intramuscularly once a day for 5/10 days

Electrical stimulation is also used - it is aimed at restoring the function of nerve elements that were functional, but did not perform visual information; the formation of a focus of persistent excitability, which leads to the restoration of the activity of nerve cells and their connections, which were previously weakly functioning; improvement metabolic processes and blood circulation, which contributes to the restoration of the myelin sheath around the axial cylinders of the optic nerve fibers and, accordingly, leads to the acceleration of the action potential and the revival of the analysis of visual information.

Indications for consultation with specialists:

consultation with a therapist - to assess the general condition of the body;
consultation with a cardiologist – high level blood pressure is one of the main risk factors for the development of vascular occlusions of the retina and optic nerve;
consultation with a neurologist - to exclude demyelinating disease of the central nervous system and clarify the topical affected area visual pathways;
consultation with a neurosurgeon - if the patient develops signs of intracranial hypertension or symptoms characteristic of volumetric education brain;
consultation with a rheumatologist - if there are symptoms characteristic of systemic vasculitis;
consultation with a vascular surgeon to decide on the need for surgical treatment if there are signs of an occlusive process in the system of the internal carotid and orbital arteries (the appearance of scotoma fugax in the patient);
consultation with an endocrinologist – in the presence of diabetes mellitus/other pathology of the endocrine system;
consultation with a hematologist (if blood diseases are suspected);
consultation with an infectious disease specialist (if vasculitis of viral etiology is suspected).
consultation with an otolaryngologist - if inflammation or neoplasm is suspected in the maxillary or frontal sinus.

Indicators of treatment effectiveness:

an increase in the electrical sensitivity of the optic nerve by 2-5% (according to computer perimetry),
increase in amplitude and/or decrease in latency by 5% (according to VEP data).