Partial optic nerve atrophy (chazn) causes, diagnosis and treatment. Optic nerve atrophy (partial and complete) - causes, symptoms, treatment and prevention Optic nerve atrophy of both eyes

19-12-2012, 14:49

Description

is not an independent disease. This is a consequence of various pathological processes affecting different parts of the visual pathway. 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, toxins, compression and damage to the optic nerve), diseases of the central nervous system, general diseases of the 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 foci of softening (liquation 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 of the 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 nerve head (congestive papilla), after which atrophy of the optic nerve head 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 of the peripheral neuron of the optic 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 .

In addition, when intraocular pressure increases, collapse of the glial cribriform membrane of the optic disc, which leads to degeneration of nerve fibers in vulnerable areas of the 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 nerve 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 happens more rapidly and in larger 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 glaucomatous (marginal, cavernous, cauldron) atrophy of the optic disc is classified as a separate form. With it, there is practically no proliferation of glia and connective tissue, and as a result of the direct mechanical effect of increased intraocular pressure, depression (excavation) of the optic nerve head occurs 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 site where the central retinal artery enters it (10-12 mm behind the eyeball) causes atrophy of the optic nerve head 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 (with injuries to the optic tract, somewhat faster).

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 the initial stage of bilateral atrophy. In case of impaired blood circulation in the vessels of the optic nerve or 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 with atrophy after a congestive nipple than with 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 no additional resistance is created that prevents 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 altered, and the fundus remains normal for a long time 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 can happen in 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 of intracranial hypertension indicates the post-congestive 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) is of great importance in diagnosis, since 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 ocular symptoms are important: changes in the vessels of the retina, the retina itself, the choroid, as well as the 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 hypermetropics, the optic discs are normally 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 nerve head 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 tumors of the ventricles of the cerebral hemispheres, cerebellum and cerebellopontine angle, and secondary atrophy with tumors of this localization is common. Rarely, simple atrophy of the optic nerves 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, since the increase in intracranial pressure is not so long-lasting, since intracranial hypertension either decreases after surgery, or patients do not live to see the transition of congestive discs 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 the 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. Optic nerve atrophy is more common with tabes 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 in 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 accompanying 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 a 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 atrophy of the optic nerves (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 so for blue than for red and green. 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 optic pathway by the intracranial process, require neurosurgical treatment.

To improve blood supply to the optic nerve use vasodilators, vitamin preparations, biogenic stimulants, neuroprotectors, infusion of 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. With developed atrophy, the prognosis is unfavorable. Treatment of patients with optic atrophy, whose visual acuity has been less than 0.01 for several years, is ineffective.

Article from the book: .

- a process characterized by the gradual death of fibers.

Pathology is often caused by ophthalmological diseases.
The disease is diagnosed when the fibers are damaged. Nerve tissues are located in almost all human organs.

What is it

The optic nerve is a kind of transmission channel. With its help, the image enters the retinal region, then into the brain compartment.

The brain reproduces the signal, turning the description into a clear picture. The optic nerve is connected to many blood vessels from which it receives nutrition.

In a number of processes this relationship is disrupted. The optic nerve dies, which subsequently leads to blindness and disability.

Causes of pathology

During scientific experiments, it was found that 2/3 of cases of optic nerve atrophy were bilateral. The cause is intracranial tumors, edema and disorders of the vascular system, especially in patients aged 42 - 45 years.

The causes of the disease are:

  1. Nerve damage. These include: chronic glaucoma, neuritis, neoplasms.
  2. Neuropathy (ischemic), chronic neuritis, edema is a secondary pathology.
  3. Hereditary neuropathy (Leber).
  4. Neuropathy (toxic). The disease is caused by methanol. This component is found in surrogate alcoholic drinks and medications (Disulfiram, Ethambutol).

The causes of the disease include: retinal damage, TAY-SAXS pathology, syphilis.

The development of atrophy in children is influenced by a congenital anomaly, a negative hereditary factor, and a malnutrition of the optic nerve. Pathology entails disability.

Main classification of the disease

Atrophy of the optic nerve is determined by pathological and ophthalmoscopic signs.

Acquired and congenital form

The acquired form is primary or secondary in nature. Caused by the influence of etiological factors. The process occurs as a result of: inflammation, glaucoma, myopia, and metabolic disorders in the body.

Congenital form: occurs against the background of genetic pathology. There are 6 types of hereditary atrophy: infantile (from birth to 3 years), dominant (juvenile blindness from 3 to 7 years), opto-oto-diabetic (from 2 to 22 years), Beer syndrome (complicated form, appears from 1 year) , increasing (from an early age, gradually progressing), Leicester's disease (hereditary), occurs at the age of 15 - 35 years.

Primary and secondary atrophy

The primary form is localized in a healthy eyeball. Occurs when microcirculation and nutrition of nerve fibers are disrupted.

The occurrence of secondary atrophy is caused by various eye pathologies.

Descending and ascending form

Descending atrophy is characterized by an inflammatory process in the proximal zone of the axon. Retinal disc damage is observed.

In the ascending form, the retina is initially affected. Gradually, the destructive process is directed to the brain. The rate of degeneration will depend on the thickness of the axons.

Partial and full degree

Diagnosing the extent of damage:

  • initial (damage to some fibers);
  • partial (diameter damaged);
  • incomplete (the disease progresses, but vision is not completely lost);
  • complete (complete loss of visual functions).

There is unilateral and bilateral atrophy. In the first case, damage to the innervation of one eye is observed, in the second - two.

Localization and intensity of optic disc pathology

Visual acuity is affected by the localization and intensity of the atrophic process:

  1. Modification of the field of view. The disorder is determined by topical diagnostics. The process is influenced by localization, not intensity. Damage to the papillomacular bundle provokes the occurrence of a central scotoma. Damaged optic fiber contributes to a narrowing of the peripheral limits of the visual field.
  2. Violation of color schemes. This symptomatology is clearly expressed in the descending form of the optic disc. The course of the process is determined by previous neuritis or swelling. In the first stages of the disease, the visible outlines of green and red hues are lost.
  3. Pale color of the optic disc. Additional examination using campimetry is required. It is necessary to collect information about the patient's initial visual acuity. In some cases, visual sharpness exceeds one.

If unilateral atrophy is diagnosed, repeated examination will be required to avoid damage to the second eye (bilateral atrophy).

Symptoms of eye disease

The main symptoms of the onset of atrophy are expressed by progressive deterioration of vision in one or both eyes. Vision cannot be treated or improved with ordinary correction methods.

Symptoms are expressed:

  • loss of lateral visibility (fields narrow);
  • the appearance of tunnel vision;
  • the formation of dark spots;
  • decreased pupillary reflex to light rays.

When the optic nerve is damaged, optic neuropathy develops, which leads to partial or complete blindness.

Correct medical diagnosis

An ophthalmological examination determines the presence and extent of the disease. The patient should consult a neurosurgeon and neurologist.

To establish a correct diagnosis you need to go through:

  • ophthalmoscopy (examination of the fundus of the eye);
  • visometry (the degree of damage to visual perception is determined);
  • perimetry (visual fields are examined);
  • computer perimetry (the affected area is determined);
  • evaluation score of color readings (the location of the fiber is determined);
  • video - ophthalmography (the nature of the pathology is revealed);
  • craniography (an X-ray of the skull is taken).

Additional examinations may be prescribed, which include CT scanning, magnetic resonance imaging, and laser Doppler ultrasound.

Treatment of the disease - preventing disability

After diagnosis, the specialist prescribes intensive therapy. The doctor’s task is to eliminate the causes of the pathology, stop the progression of the atrophic process, and prevent complete blindness and disability of the patient.

Effective drug treatment of the patient

It is impossible to restore dead nerve fibers. Therefore, therapeutic measures are aimed at stopping inflammatory processes with the help of drugs.

This ophthalmological disease is treated:

  1. Vasodilators. The drugs stimulate blood circulation. The most effective: No-shpa, Dibazol, Papaverine.
  2. Anticoagulants. The action of the drugs is aimed at preventing blood clotting and the formation of thrombosis. The specialist prescribes: Heparin, Tiklid.
  3. Biogenic stimulants. The metabolic process in nerve tissue structures is enhanced. This group of products includes: Peat, Aloe extract.
  4. Vitamin complex. Vitamins are a catalyst for biochemical reactions that occur in the eye tissue structures. For the treatment of pathology, the following is prescribed: Ascorutin, B1, B6, B12.
  5. Immunostimulants. Promote cell regeneration, suppress inflammatory processes (in case of infection). The most effective: Ginseng, Eleutherococcus.
  6. Hormonal medications. Inflammatory symptoms are relieved. Prescribed: Dexamethasone, Prednisolone individually (in the absence of contraindications).

The patient receives certain results from acupuncture and physiotherapy (ultrasound, electrophoresis).

Surgical intervention - main types of operations

The surgical procedure is indicated for patients with a poor prognosis: optic nerve atrophy with the possibility of blindness.

Types of operations:

  1. Vasoconstructive. The temporal or carotid arteries are ligated, and the blood flow is redistributed. The blood supply to the orbital arteries improves.
  2. Extrascleral. Own tissue is transplanted. An antiseptic effect is created on the affected areas, a healing effect is caused, and blood supply is stimulated.
  3. Decompression. The scleral or bony canaliculus of the optic nerve is dissected. There is an outflow of venous blood. The pressure on the beam section is reduced. Result: the functional abilities of the optic nerve improve.

After drug or surgical treatment, it would be advisable to use alternative medicine.

Traditional medicines stimulate metabolism and increase blood circulation. The use of folk remedies is allowed after consultation with the attending physician (ophthalmologist).

Fighting illness in children

Therapy in children is aimed at saving nerve fibers and stopping the process. Without adequate treatment, the child will become completely blind and disabled.

Despite measures taken at the beginning of treatment, optic atrophy often progresses and develops. In some cases, the duration of therapy will be 1 to 2 months. For advanced forms of atrophy, treatment lasts from 5 to 10 months.

After the examination, the doctor prescribes for the child:

  • magnetic stimulation;
  • electrical stimulation;
  • vasodilators;
  • biostimulating medications;
  • vitamin cocktail;
  • enzymes.

If taking medications does not bring results and the disease continues to progress, a course of laser therapy or surgical measures is prescribed.

Tabetic nerve atrophy

Tabes is a disease of the nervous system due to infection with syphilis. If timely treatment is not applied, the disease progresses, causing ocular trophic disorders.

Tabes optic atrophy is the only manifestation of tabes (an early symptom of neurosyphilis). The tabetic form of atrophy is characterized by bilateral vision loss.

A sign of the disease is reflex immobility of the pupils. The optic nerve papilla becomes discolored and becomes gray-white.

There is a sharp decline in vision, the pathology is difficult to treat. Therapy is prescribed by a venereologist and neurologist (treatment of the primary infection is mandatory). Initially, medications and vitamins are prescribed that stimulate metabolic processes in tissue structures.


Prescribed internally:

  • vitamin A;
  • ascorbic acid;
  • nicotinic acid;
  • calcium (pangamate);
  • riboflavin.

After three days, intramuscular injections are prescribed: vitamin B, B6, B12. The drugs are combined with aloe or vitreous extract. Treatment is carried out under the strict supervision of a specialist in a medical institution.

Atrophy due to methyl alcohol poisoning

Methyl alcohol and technical alcohol mixtures can cause serious damage to vision. Pathology sometimes occurs due to methyl alcohol poisoning.

The first sign of poisoning is characterized by: migraine, dizziness, nausea, vomiting, diarrhea. The pupil becomes dilated, the clarity of vision is impaired, and light reflections cannot be distinguished. There is a sharp decrease in vision.

Therapy for this form of atrophy consists of using: alkalizing medications, calcium, B vitamins, ascorbic acid.

In patients diagnosed with methyl arthophy, the prognosis for recovery is pessimistic. Vision restoration is observed in only 15% of patients.

Optic nerve atrophy is damage to nerve fibers. When the process is prolonged, the neurons die, which leads to loss of vision.

Diagnosis of atrophy

When examining patients with optic nerve atrophy, it is necessary to find out the presence of concomitant diseases, the fact of taking medications and contact with chemicals, the presence of bad habits, as well as complaints indicating possible intracranial lesions.

During a physical examination, the ophthalmologist determines the absence or presence of exophthalmos, examines the mobility of the eyeballs, checks the reaction of the pupils to light, and the corneal reflex. Visual acuity testing, perimetry, and color vision testing are required.

Basic information about the presence and degree of optic nerve atrophy is obtained using ophthalmoscopy. Depending on the cause and form of optic neuropathy, the ophthalmoscopic picture will differ, but there are typical characteristics found in various types of optic atrophy.

These include: pallor of the optic disc of varying degrees and prevalence, changes in its contours and color (from grayish to waxy), excavation of the disc surface, a decrease in the number of small vessels on the disc (Kestenbaum’s symptom), narrowing of the caliber of the retinal arteries, changes in the veins, etc. Condition The optic disc is clarified using tomography (optical coherence, laser scanning).

An electrophysiological study (EPS) reveals a decrease in lability and an increase in the threshold sensitivity of the optic nerve. In the glaucomatous form of optic nerve atrophy, tonometry is used to determine an increase in intraocular pressure.

Pathology of the orbit is detected using plain radiography of the orbit. Examination of retinal vessels is carried out using fluorescein angiography. The study of blood flow in the orbital and supratrochlear arteries, the intracranial section of the internal carotid artery is carried out using Doppler ultrasound.

If necessary, the ophthalmological examination is supplemented by a study of the neurological status, including consultation with a neurologist, radiography of the skull and sella, CT or MRI of the brain. If a patient is diagnosed with a brain mass or intracranial hypertension, consultation with a neurosurgeon is necessary.

In the case of a pathogenetic connection between optic nerve atrophy and systemic vasculitis, consultation with a rheumatologist is indicated. The presence of orbital tumors dictates the need to examine the patient by an ophthalmic-oncologist. Therapeutic tactics for occlusive lesions of the arteries (orbital, internal carotid) are determined by an ophthalmologist or vascular surgeon.

For optic nerve atrophy caused by infectious pathology, laboratory tests are informative: ELISA and PCR diagnostics.

The differential diagnosis of optic atrophy should be made with peripheral cataracts and amblyopia.

Forecast

The degree of vision loss in a patient depends on two factors - the severity of damage to the nerve trunk and the time of treatment. If the pathological process has affected only a part of the neurocytes, in some cases it is possible to almost completely restore the functions of the eye with adequate therapy.

Unfortunately, with the atrophy of all nerve cells and the cessation of impulse transmission, there is a high probability of the patient developing blindness. The solution in this case may be surgical restoration of tissue nutrition, but such treatment is not a guarantee of restoration of vision.

Physiotherapy

There are two physiotherapeutic techniques, whose positive effects are confirmed by scientific research:

  1. Pulsed magnetic therapy (MPT) - this method is not aimed at restoring cells, but at improving their functioning. Thanks to the targeted influence of magnetic fields, the contents of neurons are “condensed”, which is why the generation and transmission of impulses to the brain is faster.
  2. Bioresonance therapy (BT) - its mechanism of action is associated with improving metabolic processes in damaged tissues and normalizing blood flow through microscopic vessels (capillaries).

They are very specific and are used only in large regional or private ophthalmological centers, due to the need for expensive equipment. As a rule, for most patients these technologies are paid, so BMI and BT are used quite rarely.

Prevention

Optic atrophy is a serious disease.

To prevent it, you need to follow some rules:

  • consultation with a specialist if there is the slightest doubt about the patient’s visual acuity;
  • prevention of various types of intoxication;
  • promptly treat infectious diseases;
  • do not abuse alcohol;
  • monitor blood pressure;
  • prevent eye and traumatic brain injuries;
  • repeated blood transfusion for profuse bleeding.

Timely diagnosis and treatment can restore vision in some cases, and slow or stop the progression of atrophy in others.

Complications

The diagnosis of optic atrophy is very serious. At the slightest decrease in vision, you should immediately consult a doctor so as not to miss your chance of recovery. Without treatment and as the disease progresses, vision may disappear completely, and it will be impossible to restore it.

To prevent the occurrence of pathologies of the optic nerve, it is necessary to carefully monitor your health and undergo regular examinations by specialists (rheumatologist, endocrinologist, neurologist, ophthalmologist). At the first signs of vision deterioration, you should consult an ophthalmologist.

Disability

Disability group I is established with IV degree of impairment of the functions of the visual analyzer - significantly pronounced dysfunction (absolute or practical blindness) and a decrease in one of the main categories of life activity to degree 3 with the need for social protection.

Basic criteria of IV degree of dysfunction of the visual analyzer.

  • blindness (vision equal to 0) in both eyes;
  • visual acuity with correction of the better eye is not higher than 0.04;
  • bilateral concentric narrowing of the boundaries of the visual field to 10-0° from the point of fixation, regardless of the state of central visual acuity.

Disability group II is established in case of III degree of dysfunction of the visual analyzer - pronounced dysfunction (high degree of low vision), and a decrease in one of the main categories of life activity to 2 degree with the need for social protection.

The main criteria for severe visual impairment are:

  • visual acuity of the better eye from 0.05 to 0.1;
  • bilateral concentric narrowing of the boundaries of the visual field to 10-20° from the point of fixation, when work activity is possible only in specially created conditions.

Disability group III is established for degree II - moderate dysfunction (moderate low vision) and a decrease in one of the main categories of life activity to degree 2 with the need for social protection.

The main criteria for moderate visual impairment are:

  • decrease in visual acuity of the better seeing eye from 0.1 to 0.3;
  • unilateral concentric narrowing of the boundaries of the visual field from the point of fixation of less than 40°, but more than 20°;

In addition, when making a decision on the disability group, all diseases that the patient has are taken into account.

The optic nerve (ocular nerve) is a nerve that connects the eye to the gray matter through the nuclei of the diencephalon. This is not a nerve in the usual sense, which is a chain of neurons connected by axons - long processes, but rather a white medulla located outside the skull.

The structure of the optic nerve is a thick bundle of neurons intertwined with the ophthalmic vein and artery, extending directly into the cerebral cortex through the diencephalon. Considering that a person has 2 eyes, he also has 2 optic nerves - 1 for each eye, respectively.

Like any nerve, it is prone to specific diseases and disorders, collectively called neuralgia and neuritis. Neuralgia is a disease that is a long-term painful reaction of the nerve to any irritants without changing the internal structure. And neuritis is the destruction or damage of the nerve fiber under various influences.

Visual neuralgia practically does not occur in humans, since its structure transmits visual signals, analyzing them along the way, which explains its similarity to the brain matter, and other fibers are responsible for tactile or pain sensations. Even if a person develops neuralgia directly from the main optic trunk, he most likely simply will not notice it, which cannot be said about neuralgia of the outgoing lateral branches.

Neuritis is a violation of the structure of the nerve fiber or its damage in some area. In half of the cases, neuralgia turns into neuritis, and in the other, the damage is caused by very real physical reasons, which will be discussed a little later. Optic neuritis is most often called optic atrophy.

The classification of optic atrophy includes: primary, secondary, complete, progressive, partial, complete, bilateral and unilateral, subatrophy, ascending and descending and others.

  • Initial, when only a couple of fibers are damaged.
  • Progressive atrophy is atrophy that continues to progress despite attempts to stop the disease.
  • Completed - a disease that has stopped at some stage.
  • Partial atrophy of the optic nerve is partial destruction of the nerve tissue, while maintaining one or another lobe of vision, sometimes referred to as PAZN.
  • Complete – the nerve is completely atrophied and restoration of vision is impossible.
  • Unilateral – damage to one eye, and bilateral, respectively – damage to the nerves of both eyes.
  • Primary – not associated with other diseases, for example, toxic damage from burnt alcohol.
  • Secondary - atrophy, manifested as a complication after an illness, for example, inflammation of the eyeball, membranes of the brain and other tissues.
  • Subatrophy of the optic nerve is an uneven damage to neurons, as a result of which the perceived information is distorted.
  • Ascending atrophy is a neuronal disorder that begins in the retina and gradually moves upward.
  • Descending optic atrophy is a disease that begins in the brain and gradually spreads to the eyes.
  • Neuropathy is a dysfunction of the nerve fiber without signs of inflammation.
  • Neuritis is inflammation of the optic nerve with pain caused by smaller adnexal optic nerve endings, or the area around the main optic nerve.

In the medical literature there is some confusion in the concepts of neuritis, neuropathy and atrophy of the optic nerves: somewhere it is said that these are one and the same thing, and somewhere that these are three completely different diseases. However, they certainly have a common essence, symptoms and treatment.

If the definition of neuritis is very broad - a violation of the structure of the nerve, which includes many disorders and inflammations for completely different reasons, then rather atrophy and neuropathy are subtypes of neuritis, and not vice versa.

In medical terminology in the ICD (medical classification of diseases, the latest of which is ICD 10), there are many different names for essentially the same process, depending on the degree of severity, characteristics of the course, method of acquisition, etc. this allows doctors to convey information to each other more informatively, and it is quite difficult for the patient to understand all the intricacies of terminology.

Optic nerve atrophy code according to ICD 10 is H47.2, as indicated in the sick leave certificate, medical reference books or in the patient’s card. The international code is used to maintain medical confidentiality from ignorant strangers. The tenth version of the ICD is the most recent.

Optic nerve atrophy symptoms

Symptoms of optic nerve atrophy look like a rapid decline in vision that cannot be corrected or corrected. The process that has begun can very quickly lead to absolute, incorrigible blindness from just a few days to several months, depending on the cause and severity of the disease.

Signs of optic atrophy may appear as changes in vision without loss of visual acuity. That is:

  • Vision becomes tunnel-like.
  • Changes in visual fields, most often towards their uniform narrowing.
  • The presence of permanent, unchanging dark spots before the eyes.
  • Asymmetric change in visual fields. For example: the side one remains, but the central one disappears.
  • Distortion of color perception or sensitivity to light.

The type of vision change depends on which area is affected, so the appearance of so-called scotomas (dark spots) indicates damage in the central part of the retina, and narrowing of the fields - in the peripheral fibers.

Diagnostics

If a diagnosis of optic nerve atrophy is suspected, diagnosis is carried out primarily by an ophthalmologist, to whom patients come with the first vision problems. The ophthalmologist first conducts a study to separate this disease from peripheral cataracts, as well as amblyopia, which have similar manifestations.

The initial examination carried out to establish a diagnosis is quite simple: examination for acuity with a wide field of view and ophthalmoscopy.

During ophthalmoscopy (a painless examination of the eye itself through a special apparatus directly in the office at the reception), the optic disc is visible; if it turns pale, it means it is atrophied or damaged. If the boundaries of the disc are smooth and normal, the disease is primary, and if the boundaries are violated, it is a secondary consequence of another disease.

Checking the reaction of the pupils: with impaired sensitivity, the pupils contract much more slowly when exposed to light.

After confirming the diagnosis, a neurologist joins the treatment and begins to determine the causes of the degenerative process:

  • General tests for inflammatory processes, as well as viral infections.
  • Tomography.
  • Radiography.
  • electrophysiological study (EPS) – study of the functioning of all eye systems by recording reactions to special impulses.
  • fluorescein angiographic method is a study by introducing a special marker substance into the blood and using it to check the vascular conductivity of the eye.

Causes of the disease

For this diagnosis of optic nerve atrophy, the causes can be so diverse that it is possible to compose an entire scientific treatise on medicine, however, a small circle of the main, most common ones is highlighted.

  • Toxic blindness:

Toxic atrophy of the optic nerve, the causes of which lie in the death of neurons under the influence of poisons. In the nineties in Russia, the first place was toxic damage to visual neurons under the influence of burnt alcohol or even liquids not intended for internal use containing methyl alcohol. It is almost impossible for a non-specialist to distinguish methyl alcohol from ethyl alcohol, however, unlike its cheerful brother, this substance is extremely dangerous to life.

Just 40 to 250 ml of methanol can cause death or very severe disability if resuscitation measures are carried out in time. In order for neurons to die, only 5 to 10 milliliters is enough, even in a mixture with other substances. When it is used, not only the optic nerves die, however, this is not as noticeable to the patient as a sudden loss of vision. In addition, toxic blindness often begins after a long period of time - up to six days after consumption, when methanol breaks down in the liver into its components, one of which is formaldehyde - a terrible poison. By the way, smoking products are also toxic to neurons.

  • Congenital pathologies.

For congenital or hereditary reasons, optic nerve atrophy in children occurs most often due to neglect of the child’s health during the mother’s pregnancy or a genetic failure.

  • Injuries.

Atrophy caused by blows to the head or injuries to the eyeball, as well as brain surgery.

  • Inflammation.

The inflammatory process that leads to the death of visual neurons can occur for many reasons, either simply because of a speck that got into the eye, causing inflammation of the eyeball, or because of previous infectious diseases: meningitis (infectious inflammation of the brain), measles, chickenpox, smallpox, syphilis, encephalitis (viral brain damage), mononucleosis, sinusitis, tonsillitis and even caries.

  • General pathologies of the patient’s entire nervous system.
  • Damage to the eye that provoked nerve atrophy as unnecessary, for example, retinal dystrophy. These two diseases intensify and accelerate each other.
  • Circulatory disorders.

The disease can cause both obstruction of the supply vessels and their atherosclerosis, high blood pressure or damage with hemorrhage

  • Oncology.

All kinds of tumors with abscesses in the brain compress the nerve itself, destroy the area to which it sends a signal, provoke malfunctions in the functioning of the entire neural system, causing complications in the eyes or even appearing directly in the eyeball.

  • Other diseases: glaucoma, hypertension, atherosclerosis, diabetes, allergic reactions, lack of vitamins or their excess, autoimmune disorders and many others.

Treatment of optic neuritis

Treatment of optic nerve atrophy is carried out by two doctors at once - an ophthalmologist and a neurologist, and in large cities there are neuro-ophthalmological centers specializing in such ailments. Treatment is always carried out inpatiently and urgently already at the stage of a preliminary unconfirmed diagnosis, since the disease is incredibly transient and a person can lose his sight in just a few days.

Can optic nerve atrophy be cured? It is impossible to completely cure the disease. Treatment comes down to stopping the spread of damage and trying to normalize the functioning of surviving neurons as much as possible.

This occurs because neurons lack the ability to divide. The vast majority of neurons in the human nervous system are formed in the mother’s tummy, and increase slightly as the child develops. Neurons themselves cannot divide, their number is strictly limited, new neurons are built only from bone marrow stem cells, which represent the stabilization fund of the body, which has a strictly limited number of cells - lifesavers, laid down during the period of embryonic development and slowly consumed in the process of life. An additional complication is that stem cells can turn into neurons only by forming new chaotic connections, and are unable to become patches for the damaged tissue. This principle of operation is good for renewing the brain, but the body will repair a separate nerve by simply replacing the dead nerve cells with connective tissue cells, which perfectly fill any cellular bald spots in the human body, but are not capable of performing any functions.

Currently, experiments are underway with stem cells obtained from embryos killed during abortions or miscarriages, which give excellent results in the rejuvenation and restoration of various tissues, including nerves, however, in reality this method is not used because it is too fraught with cancer, such as which doctors have not yet figured out to treat.

The place where atrophy can be cured is exclusively in a hospital; in this case, even outpatient (home) treatment is not allowed, during which precious seconds may be lost.

Treatment with folk remedies is not only unacceptable, but simply does not exist. In folk medicine there are no such rigorous effective means for accurate diagnosis and very quick treatment.

With complete or partial atrophy of the optic nerve, treatment begins with diagnosing the causes of the disease, after which the attending physician selects an appropriate course, including surgical intervention.

In addition to the use of special means, the patient is often prescribed a biogenic stimulant, aloe extract, which prevents the replacement of body tissues with connective cells. This drug is given in injections after any operation or after inflammation of the appendages in women as an anti-adhesion drug.

All kinds of pinching, compression, tumors, vascular aneurysms near the optic nerve and other similar causes of atrophy are removed surgically.

The inflammatory process caused by the consequences of an infectious infection is stopped using antibiotics or antiviral and anti-inflammatory drugs.

Toxic visual atrophy. the nerve is treated by removing toxins or neutralizing them, stopping further destruction of neurons. The antidote to methyl alcohol is food grade ethyl alcohol. So, in case of poisoning, it is necessary to rinse the stomach with a solution of sodium bicarbonate (sold in a pharmacy, not to be confused with sodium bicarbonate - baking soda), drink a 30-40% solution, for example, high-quality vodka, in an amount of 100 milliliters and repeat after 2 hours, halving the volume.

Dystrophy and other retinal disorders are treated with ophthalmological methods: laser surgery, vitamin or drug courses, depending on the cause. If the nerve begins to atrophy due to unnecessary use, then it will soon begin to recover after the retina is restored.

Congenital and genetic optic nerve atrophy in children is corrected based on the type of pathology and often surgically.

In addition to specific treatment based on the cause of the disease, treatment includes immunostimulation, vasodilation, biogenic stimulation, hormonal drugs to prevent even the slightest hint of inflammation (prednisolone, dexamethasone), drugs that accelerate resorption (pyrogenal, preductal), some means of maintaining work of the nervous system (emoxipin, fezam, etc.), physiotherapy, laser, electrical or magnetic stimulation of the optic nerve.

At the same time, the body is urgently saturated with vitamins, minerals and nutrients. At this stage, lovers of traditional medicine can choose a remedy to their liking from strengthening, immunostimulating and anti-inflammatory agents. It is only important not to act in secret from the doctor, because everything the patient uses must be correctly combined with a huge number of prescribed drugs, otherwise you risk losing not only your sight, but also your life.

Such a huge set of procedures, sometimes taking more than a year, is necessary not to restore vision, but simply to stop its loss.

Optic nerve atrophy in a child

Optic nerve atrophy in a child is a rather rare disease, characteristic of older people and practically no different from the same disease in an adult. The main difference is that in young children, neurons are still able to partially recover and in the initial stages it is quite possible not only to stop the disease, but also to reverse it. An exception is hereditary atrophy of the optic nerve in children, the treatment of which has not yet been found - Liberov atrophy, transmitted through the male line.

Possible consequences and forecasts

Should I panic after hearing such a diagnosis? At the initial stages there is no particular reason for panic; at this time the disease is quite easily controlled. And neurons that are not severely damaged even restore their functions. With improper treatment, self-medication and an irresponsible attitude, there is another possible outcome: in addition to vision, in some cases a person can lose his life, since the optic nerve is very large and is directly connected to the brain. Along it, like a bridge, inflammation from the eye can easily spread to brain tissue and cause irreversible consequences. It is even more dangerous when atrophy is caused by inflammation of the brain itself, tumors or problems with blood vessels. Complete or partial atrophy of the optic nerves may also occur, with atrophy of the optic nerve (main trunk).

When the first symptoms occur, you need to remember that a person builds his own future, and his correct actions will determine whether he will be healthy, whether his vision will be restored, whether the normal functioning of the entire nervous system of the body will be maintained, or whether he will prefer to spend invaluable time on not the most important things. activities, for example, being afraid to leave work, trying to save on treatment by ignoring some prescriptions, or wasting time on long-term rehabilitation.

This condition is the final stage of damage to the optic nerve. This is not a disease, but rather a sign of a more serious disease. Possible causes include direct trauma, pressure on the optic nerve or toxic damage, and nutritional deficiencies.

Causes of optic nerve atrophy

The optic nerve is made up of nerve fibers that transmit impulses from the eye to the brain. It contains approximately 1.2 million axons that originate in retinal cells. These axons have a thick myelin sheath and cannot regenerate after injury.

If fibers in any part of the optic nerve degenerate, its ability to transmit signals to the brain is impaired.

Regarding the causes of ASD, scientific studies have found that:

  • Approximately 2/3 of cases were bilateral.
  • The most common cause of bilateral ADN is intracranial neoplasms.
  • The most common cause of unilateral damage is traumatic brain injury.
  • Vascular factors are a common cause of AD after the age of 40 years.

In children, causes of AUD include congenital, inflammatory, infectious, traumatic and vascular factors, including perinatal strokes, mass lesions and hypoxic encephalopathy.

Let's look at the most common causes of ASD:

  1. Primary diseases affecting the optic nerve: chronic glaucoma, retrobulbar neuritis, traumatic optic neuropathy, formations compressing the optic nerve (for example, tumors, aneurysms).
  2. Primary retinal diseases, such as occlusion of the central retinal artery or central vein.
  3. Secondary diseases of the optic nerve: ischemic optic neuropathy, chronic neuritis or papilledema.

Less common causes of ASD:

  1. Hereditary optic neuropathy (eg, Leber optic neuropathy).
  2. Toxic neuropathy, which can be caused by exposure to methanol, certain drugs (disulfiram, ethambutol, isoniazid, chloramphenicol, vincristine, cyclosporine and cimetidine), alcohol and tobacco abuse, metabolic disorders (eg, severe renal failure).
  3. Retinal degeneration (eg, retinitis pigmentosa).
  4. Retinal storage diseases (eg, Tay-Sachs disease)
  5. Radiation neuropathy.
  6. Syphilis.

Classification of optic nerve atrophy

There are several classifications of ADS.

According to the pathological classification, ascending (anterograde) and descending (retrograde) optic nerve atrophy is distinguished.

The ascending ADS looks like this:

  • In diseases with anterograde degeneration (for example, toxic retinopathy, chronic glaucoma), the atrophy process begins in the retina and spreads towards the brain.
  • The rate of degeneration is determined by the thickness of the axons. Larger axons decay faster than smaller ones.

Descending optic nerve atrophy is characterized by the fact that the atrophy process begins in the proximal part of the axon and spreads towards the optic nerve head.

According to ophthalmoscopic classification there are:

  • Primary ADS. In diseases with primary atrophy (for example, pituitary tumor, optic nerve tumor, traumatic neuropathy, multiple sclerosis), degeneration of optic nerve fibers leads to their replacement by columns of glial cells. On ophthalmoscopy, the optic disc appears white and has clear edges, and the retinal blood vessels are normal.
  • Secondary ADS. In diseases with secondary atrophy (eg, papilledema or inflammation of the optic disc), degeneration of nerve fibers is secondary to papilledema. On ophthalmoscopy, the optic disc has a gray or dirty gray color, its edges are unclear; retinal blood vessels may be altered.
  • Sequential ADS. With this form of atrophy (for example, with retinitis pigmentosa, myopia, central retinal artery occlusion), the disc has a waxy pale color with clear edges.
  • Glaucomatous atrophy is characterized by a cup-shaped optic disc.
  • Temporary optic disc pallor can occur with traumatic neuropathy or nutritional deficiencies, and is most common in patients with multiple sclerosis. The disc is pale in color with clear edges and normal vessels.

According to the degree of damage to nerve fibers, they are distinguished:

  • Partial atrophy of the optic nerve - the process of degeneration affects not all fibers, but a certain part of them. This form of optic nerve subatrophy is characterized by incomplete loss of vision.
  • Complete atrophy of the optic nerve - the degeneration process affects all nerve fibers, leading to blindness.

Symptoms of optic atrophy

The main symptom of optic atrophy is blurred vision. The clinical picture depends on the cause and severity of the pathology. For example, with partial atrophy of the optic nerves of both eyes, bilateral symptoms of vision deterioration are observed without complete loss, manifested first by loss of clarity and impaired color perception. When the optic nerves are compressed by the tumor, the visual field may decrease. If partial optic atrophy is left untreated, visual impairment often progresses to complete loss.

Depending on the etiological factors, patients with AD may also exhibit other symptoms that are not directly related to this pathology. For example, with glaucoma, a person may suffer from eye pain.

Characterizing the clinical picture of ADN is important in determining the cause of neuropathy. Rapid onset is characteristic of neuritis, ischemic, inflammatory and traumatic neuropathy. Gradual progression over several months is characteristic of toxic neuropathy and atrophy due to nutritional deficiencies. The pathological process develops even more slowly (over several years) with compressive and hereditary ADN.

If a young patient complains of eye pain associated with eye movement and the presence of neurological symptoms (eg, paresthesia, ataxia, limb weakness), this may indicate the presence of demyelinating diseases.

In older adults with signs of ADN, the presence of temporary vision loss, double vision (diplopia), fatigue, weight loss, and muscle pain may suggest ischemic neuropathy due to giant cell arteritis.

In children, the presence of flu-like symptoms in the recent past or recent vaccination indicates parainfectious or post-vaccination optic neuritis.

Diplopia and facial pain suggest multiple neuropathy of the cranial nerves, observed with inflammatory or neoplastic lesions of the posterior orbit and the anatomical area around the sella turcica.

Short-term blurred vision, diplopia and headaches indicate the possibility of increased intracranial pressure.

Diagnosis of optic nerve atrophy

The described clinical picture can be observed not only with ADN, but also with other diseases. To establish the correct diagnosis, if vision problems occur, you need to consult an ophthalmologist. He will perform a comprehensive eye examination, including an ophthalmoscopy, which can be used to examine the optic disc. With atrophy, this disc has a pale color, which is associated with a change in blood flow in its vessels.

To confirm the diagnosis, you can perform optical coherence tomography, an examination of the eyeball that uses infrared light waves for visualization. The ophthalmologist also evaluates color vision, the reaction of the pupils to light, determines the acuity and impairment of visual fields, and measures intraocular pressure.

It is very important to determine the cause of ADN. For this purpose, the patient may undergo computed or magnetic resonance imaging of the orbits and brain, laboratory testing for the presence of genetic abnormalities, or a diagnosis of toxic neuropathy.

How to treat optic nerve atrophy?

How to treat optic nerve atrophy? The importance of vision for a person cannot be overestimated. Therefore, if you have any symptoms of optic nerve atrophy, you should never resort to treatment with folk remedies on your own; you should immediately contact a qualified ophthalmologist.

It is necessary to begin treatment at the stage of partial atrophy of the optic nerve, which allows many patients to retain some vision and reduce the degree of disability. Unfortunately, with complete degeneration of nerve fibers, it is almost impossible to restore vision.

The choice of treatment depends on the cause of the disorder, for example:

  • Treatment of descending optic atrophy caused by an intracranial tumor or hydrocephalus is aimed at eliminating compression of the nerve fibers by the tumor.
  • In the case of inflammatory diseases of the optic nerve (neuritis) or ischemic neuropathy, intravenous corticosteroids are used.
  • For toxic neuropathy, antidotes are prescribed to those substances that caused damage to the optic nerves. If atrophy is caused by drugs, their use is stopped or the dose is adjusted.
  • Neuropathy due to nutritional deficiencies is treated by adjusting the diet and prescribing multivitamins that contain the microelements necessary for good vision.
  • For glaucoma, conservative treatment aimed at reducing intraocular pressure or surgery is possible.

In addition, there are methods of physiotherapeutic, magnetic, laser and electrical stimulation of the optic nerve, which are aimed at preserving the functions of the nerve fibers as much as possible.

There are also scientific works that have shown the effectiveness of treating ADN using the introduction of stem cells. Using this still experimental technique, it is possible to partially restore vision.

Prognosis for ADN

The optic nerve is part of the central, not the peripheral, nervous system, which makes it impossible to regenerate after damage. Thus, ADN is irreversible. Treatment of this pathology is aimed at slowing down and limiting the progression of the degeneration process. Therefore, every patient with optic nerve atrophy should remember that the only place where this pathology can be cured or its development stopped is the ophthalmology departments in medical institutions.

The prognosis for vision and life with AD depends on the cause of it and the degree of damage to the nerve fibers. For example, with neuritis, after the inflammatory process subsides, vision may improve.

Prevention

In some cases, the development and progression of ADN can be prevented by proper treatment of glaucoma, toxic, alcohol and tobacco neuropathy, and eating a nutritious and nutrient-rich diet.

Optic nerve atrophy is a consequence of degeneration of its fibers. It can be caused by many diseases, from glaucoma and blood supply disorders (ischemic neuropathy) to inflammatory processes (for example, multiple sclerosis) and formations that compress the nerve (for example, intracranial tumors). Effective treatment is possible only at the stage of partial atrophy of the optic nerve. The choice of treatment method depends on etiological factors. In this regard, it is necessary to establish the correct diagnosis in time and direct all efforts to preserve vision.

Useful video about optic atrophy

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 are talking 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(for atherosclerosis, diabetes, 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.