Damage to the optic nerve associated with the central divisions. Causes of the development of optic nerve atrophy and methods of treatment

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 or toxic damage to the optic nerve, and nutritional deficiencies.

Causes of optic nerve atrophy

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

In the case of degeneration of fibers in any of the departments of the optic nerve, its ability to transmit signals to the brain is impaired.

Regarding the causes of AD, scientific studies have established that:

• Approximately 2/3 of the cases were bilateral.
• Intracranial neoplasms are the most common cause of bilateral AD.
• The most common cause of unilateral injury is traumatic brain injury.
• Vascular factors are a common cause of AD in people over 40 years of age.

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

Consider the most common causes of AD:

1. Primary diseases affecting the optic nerve: chronic glaucoma, retrobulbar neuritis, traumatic optic neuropathy, formations that compress the optic nerve (eg, tumors, aneurysms).
2. Primary diseases of the retina, for example, occlusion of the central artery or central retinal vein.
3. Secondary diseases of the optic nerve: ischemic optic neuropathy, chronic neuritis or edema of the optic nerve.

Less common causes of AD:

1. Hereditary optic neuropathy (for example, Leber's 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 (for example, 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) atrophy of the optic nerve is distinguished.

The ascending ADS looks like this:

• In diseases with anterograde degeneration (eg, toxic retinopathy, chronic glaucoma), the process of atrophy 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 atrophy is characterized by the fact that the process of atrophy begins in the proximal part of the axon and spreads towards the optic nerve head.

According to the ophthalmoscopic classification, there are:

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

According to the degree of damage to the nerve fibers, there are:

• 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 process of degeneration affects all nerve fibers, leading to blindness.

Symptoms of optic nerve atrophy

Visual impairment is the main symptom of optic nerve atrophy. 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 visual impairment are observed without its complete loss, manifested first by loss of clarity and impaired color perception. When the tumor compresses the optic nerves, the visual fields may decrease. If left untreated, partial atrophy of the optic nerve often progresses to complete loss of vision.

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

Characterization of the clinical picture of AD 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. Even more slowly (over several years) the pathological process develops in compressive and hereditary AD.

If a young patient complains of pain in the eyes associated with their movement, the presence of neurological symptoms (for example, paresthesia, ataxia, weakness in the limbs), this may indicate the presence of demyelinating diseases.

In older people with signs of AD, 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, a recent history of flu-like symptoms or recent vaccination suggests parainfectious or post-vaccination optic neuritis.

Diplopia and facial pain suggest multiple cranial nerve neuropathy seen in inflammatory or neoplastic lesions of the posterior orbit and the anatomical region 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 in AD, but also in other diseases. To establish the correct diagnosis in case of vision problems, you need to consult an ophthalmologist. He will perform a comprehensive eye examination, including ophthalmoscopy, which can be used to examine the optic nerve head. With atrophy, this disc has a pale color, which is associated with a change in blood flow in its vessels.

To confirm the diagnosis, optical coherence tomography can be performed - 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 sharpness and disturbance of the visual fields, and measures intraocular pressure.

It is very important to determine the cause of AD. For this purpose, the patient may undergo computed or magnetic resonance imaging of the orbits and brain, laboratory examination for the presence of genetic abnormalities, or 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, in the presence of any symptoms of optic nerve atrophy, in no case should you resort to treatment with folk remedies on your own, you should immediately contact a qualified ophthalmologist.

It is necessary to start treatment at the stage of partial atrophy of the optic nerve, which allows many patients to maintain 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 nerve atrophy caused by an intracranial tumor or hydrocephalus is aimed at eliminating compression of the nerve fibers by the neoplasm.
• In the case of inflammatory diseases of the optic nerve (neuritis) or ischemic neuropathy, intravenous corticosteroids are used.
• With toxic neuropathy, antidotes are prescribed for those substances that caused damage to the optic nerves. In the event that atrophy is caused by drugs, their administration is stopped or the dose is adjusted.
• Neuropathy due to nutritional deficiencies is treated with dietary modifications and the administration of multivitamin preparations that contain micronutrients necessary for good vision.
• With glaucoma, conservative treatment is possible, aimed at lowering intraocular pressure, or performing a surgical operation.

In addition, there are methods of physiotherapy, magnetic, laser and electrical stimulation of the optic nerve, which are aimed at the maximum possible preservation of the functions of nerve fibers.

There are also scientific works that have shown the effectiveness of the treatment of AD with the introduction of stem cells. With the help of this still experimental technique, it is possible to partially restore vision.

Prognosis for ASD

The optic nerve is part of the central rather than peripheral nervous system, which makes it impossible to regenerate after damage. Thus, AD 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 you can cure this pathology or stop its development is the ophthalmology departments in medical institutions.

The prognosis for vision and life in ADN depends on the cause of the disease 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 AD can be prevented by proper treatment of glaucoma, toxic, alcohol and tobacco neuropathy, and by eating a nutritious and nutritious diet.

Atrophy of the optic nerve is a consequence of the degeneration of its fibers. It can be caused by many diseases, from glaucoma and circulatory disorders (ischemic neuropathy) to inflammation (eg, multiple sclerosis) and nerve-compressing masses (eg, intracranial tumors). Effective treatment is possible only at the stage of partial atrophy of the optic nerve. The choice of method of therapy 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 nerve atrophy

A rapid drop in visual acuity sometimes signals the development of a variety of ophthalmic ailments. But few people think that unpleasant symptoms can be caused by such a dangerous anomaly as optic nerve atrophy. This element of the eye is the main component in the perception of light information. Violation of its functionality can lead to blindness.

This is a pathological condition in which the nervous matter is deficient in nutrients. As a result, it ceases to perform its functions. If left untreated, neurons begin to gradually die off. As the pathology progresses, more and more cells are captured. In severe situations, the nerve trunk is completely damaged. In this case, restoring visual function is almost impossible.

To understand how the anomaly manifests itself, it is necessary to visualize the movement of impulses to the structures of the brain. Conventionally, they can be divided into two types: lateral and medial. In the first part, there is an image of the surrounding objects that the side of the organ of vision, which is closer to the nose, sees. The second area is responsible for the perception of the outer part of the picture (closer to the crown).

As a result, the left tract sees the image from the identical half of the organ of vision, while the right tract sends the image received from the second part of the eye to the brain. For this reason, damage to one of the optic nerves, after leaving the orbit, leads to a violation of the functionality of both eyes.

The reasons

Optic nerve atrophy is not considered an independent pathology. Most often, it is a manifestation of other destructive processes occurring in the eyes. The main reasons provoking the development of the disease include:

• Ophthalmic anomalies (damage to the retina, violation of the integrity of the structures of the organ of vision);
• Destructive processes in the central nervous system (neoplasms, meningitis, encephalitis, skull trauma, inflammation of the brain);
• Abuse for a long time of alcoholic beverages, illegal drugs and tobacco products;
• genetic predisposition;
• Diseases of the cardiovascular system (spasm, atherosclerosis, arterial hypertension).

Damage to the optic nerve can be congenital or acquired. The first occurs as a result of a variety of genetic pathologies (most often due to Leber's disease). In such situations, a person has poor eyesight from the first days of birth. Acquired anomaly develops as a result of past diseases in adulthood.

Classification

Depending on the cause that provoked the development of atrophy, two forms of the disease are distinguished:

• Primary. The appearance of pathology occurs as a result of damage to the X chromosome. Therefore, only young men between the ages of fifteen and twenty-five suffer from it. The disease progresses in a recurrent type and is transmitted at the genetic level;
• Secondary. It manifests itself as a result of an ophthalmic or systemic anomaly associated with a failure in the blood supply to the optic nerve. This form can manifest itself regardless of age and gender.

Depending on the localization of the lesion, the disease is also classified into two types:

• Ascending type. Damage to nerve cells located on the retina. The anomaly progresses towards the brain. This form of the disease is often diagnosed with ophthalmic diseases (for example, glaucoma or myopia);
• descending type. The movement is in the reverse order, i.e. from the optic center to the retina. This form is typical for retrobulbar neuritis and brain damage affecting the area with the optic nerve.

Symptoms

The disease has two main manifestations: loss of visual fields and deterioration in eye acuity. In each patient, they are expressed to varying degrees. It all depends on the cause that provoked the disease and the severity of the course of the disease.

Loss of visual fields (anopsia)

Optical view - this is the area that a person sees. To determine it, just cover one eye with your palm. You will consider only part of the image, since the visual analyzer does not perceive the second area. In other words, the patient falls out of the right or left zone. This is anopia.

Neurologists divide it into two types:

• Temporal. The part of the picture located closer to the temples is visible;
• Nasal. In the field of view, the other half of the image, located from the side of the nose;
• Right or left. Depending on which side the field fell out.

With partial atrophy, there may be no symptoms at all, since the "surviving" neurons transmit enough information to the brain. However, if the damage has affected the entire trunk, then anopia will definitely appear.

Decreased visual acuity (amblyopia)

This symptom is manifested in all patients suffering from atrophy. Only each person has an individual degree of severity:

• Light. It manifests itself at the initial stage of the development of the disease. The deviation in visual acuity is practically not noticeable. The symptom can only make itself felt when looking at distant objects;
• Average. Occurs when a significant part of neurons is damaged. Objects located far away are practically invisible, but at short distances there are no problems;
• Heavy. A clear sign of the progression of the disease. Optical indicators are reduced to such an extent that a person cannot see objects that are at arm's length;
• Complete loss of vision. Blindness results from the death of all neurons.

Amblyopia usually appears suddenly and without treatment progresses rapidly. If symptoms are ignored, the risk of irreversible blindness increases many times over.

Complications

It is important to realize that optic nerve atrophy is a serious disease and an attempt to cure it on your own can lead to sad consequences. The most dangerous complication that can manifest itself as a result of an irresponsible approach to health is a complete loss of vision.

If pathology is ignored, sooner or later all neurons will die. A person will not be able to lead a normal life, as there will be difficulties with vision. Often, when atrophy of the optic nerve is detected at a late stage, the patient is assigned a disability.

Diagnostics

In most cases, there are no difficulties with anomaly detection. A person notes an unexpected drop in visual acuity and goes to an appointment with an optometrist. For the selection of competent therapy, it is important to correctly determine the root cause of the activation of the disease.

To make an accurate diagnosis, the patient is sent for a detailed examination, which includes a number of procedures:

• Visometry. Checking visual acuity using special test tables;
• Spheroperimetry. Allows you to evaluate the optical fields;
• Ophthalmoscopy. It is carried out using a modern apparatus and makes it possible to analyze the condition of the fundus, the initial section of the nerve trunk;
• CT scan. With the help of the procedure, an examination of the brain is carried out. CT helps to identify possible causes that provoked the development of the disease;
• Video ophthalmography. Examination of the relief of the optic nerve;
• Tonometry. Measurement of intraocular pressure indicators;
• Computer perimetry. It is prescribed for the analysis of areas of the damaged nerve.

Treatment

There is an opinion that nerve cells are not restored. This is not entirely true. Neurocytes tend to grow, constantly increasing the number of connections with adjacent tissues. Thus, they take on the functions of comrades who "fell in an unequal battle." However, for full regeneration, they lack one important quality - the ability to reproduce.

Therefore, to the question of whether atrophy can be completely cured, there is an unequivocal answer - no! If the trunk is partially damaged, then with the help of medications there is a chance to increase visual acuity and improve visual fields. If destructive processes have completely blocked the transmission of impulses from the visual apparatus to the brain, then there is only one way out - surgical intervention.

In order for therapy to bring results, it is first necessary to identify the cause that provoked its development. This will help reduce damage to the cell layer and stabilize the course of the disease. If the root cause cannot be eliminated (for example, with a cancerous tumor), doctors immediately begin to restore the functionality of the visual apparatus.

Modern methods of nerve restoration

About ten years ago, vitamins were mainly used to combat the disease, today they are of secondary importance and are prescribed as additional means. In the first place came medicines aimed at restoring metabolism in neurons and increasing blood flow to them.
The drug therapy regimen is as follows:

• Antioxidants ("Mexidol", "Trimectal", etc.). Medicines regenerate tissues, block the activity of pathological processes, eliminate oxygen deficiency of the optic nerve. In the hospital, they are administered intravenously, on an outpatient basis they are used in the form of tablets;
• Microcirculation correctors ("Actovegin", "Trental"). Drugs normalize metabolism in nerve cells and blood supply. One of the most important elements of conservative therapy. Sold in the form of tablets and injections;
• Nootropics ("Piracetam", "Glutamic acid"). Stimulate blood flow and accelerate the process of neurocyte regeneration;
• Medicines to reduce the degree of permeability of the walls of blood vessels ("Emoxipin"). Creates a protective barrier around the optic nerve, which prevents its further destruction. The injection is carried out in a parabulbar way (a thin needle is inserted along the wall of the orbit into the tissue located around the eye);
• Vitamin and mineral complexes. Auxiliary element of treatment.
  It is important to understand that medications are unable to eliminate the disease, but they significantly improve the condition of nerve cells.

Physiotherapy for optic nerve atrophy

There are two methods that have been proven effective in practice:

• Pulse magnetotherapy. The method does not regenerate nerve fibers, but improves their functionality. Directional magnetic fields give "thickness" to the contents of neurons, as a result of which the formation of impulses and sending them to the brain takes place several times faster;
• bioresonance therapy. The procedure is aimed at normalizing the metabolism in the affected tissues and improving blood flow through the capillaries.

The methods are quite specific and are used only in large medical institutions, since they require expensive equipment. Most often, the procedures are paid, so they are rarely used in practice.

Surgery

There are several operations aimed solely at improving visual acuity in atrophy. Conventionally, they can be divided into two categories:

• Redistributing blood flow in the area of ​​​​the organ of vision. This allows you to activate the supply of useful substances to the damaged element by reducing it in other matters. To do this, part of the vessels on the face is tied up, as a result of the “dead end” that has arisen, the main blood flow is forced to go along the paths leading to the visual apparatus. The operation is used in exceptional cases, since the risk of complications during the recovery period is high;
• Transplantation of revascularizing matter. The essence of the procedure is the transplantation of tissues with increased blood supply (for example, the mucous membrane) to the atrophied area. A new vascular network grows through the implant, which will provide the neurons with the necessary blood flow. This type of operation is used much more often than the first type. Since with it, other matters are practically not affected and not damaged.

This is a condition in which the nervous tissue experiences an acute lack of nutrients, due to which it ceases to perform its functions. If the process continues long enough, neurons begin to gradually die off. Over time, it affects an increasing number of cells, and in severe cases, the entire nerve trunk. It will be almost impossible to restore the function of the eye in such patients.

To understand how this disease manifests itself, it is necessary to imagine the course of impulses to brain structures. They are conditionally divided into two portions - lateral and medial. The first one contains a “picture” of the surrounding world, which is seen by the inner side of the eye (closer to the nose). The second is responsible for the perception of the outer part of the image (closer to the crown).

Both parts are formed on the back wall of the eye, from a group of special (ganglion) cells, after which they are sent to various brain structures. This path is quite difficult, but there is only one fundamental point - almost immediately after leaving the orbit, a crossover occurs with internal portions. What does this lead to?

• The left tract perceives the image of the world from the left half of the eyes;
• The right one carries the "picture" from the right halves to the brain.

Therefore, damage to one of the nerves after it has left the orbit will result in a change in the function of both eyes.

The reasons

One of the factors that can provoke diseases of the optic nerve is multiple sclerosis. This affects the myelin that covers the nerve cells of the spinal cord and brain. Damage to the brain immune system develops. People with brain disorders are at risk. Damage to the optic nerve is caused by autoimmune diseases such as sarcoidosis, lupus erythematosus.

Optic neuromyelitis leads to the development of neuritis. This happens because the disease is accompanied by inflammation of the spinal cord and optic nerve, but damage to brain cells does not occur. The appearance of neuritis is provoked by other factors:

• The presence of cranial arteritis, characterized by inflammation of the intracranial arteries. Violations occur in the blood circulation, the supply of the required amount of oxygen to the cells of the brain and eyes is blocked. Such phenomena provoke a stroke, loss of vision in the future.
• Viral, infectious, bacterial diseases, measles, syphilis, cat scratch disease, herpes, rubella, Lyme disease, neuroretinitis lead to inflammation of the nerve, the development of chronic or purulent conjunctivitis.
• Long-term use of certain drugs that can provoke the development of nerve inflammation (Ethambuton, prescribed in the treatment of tuberculosis).
• radiation therapy. It is prescribed for certain diseases that are difficult.
• A variety of mechanical effects - severe intoxication of the body, tumors, insufficient supply of nutrients to the cornea, retina.

What can provoke the development of eye pathology? By and large, these are both congenital / inherited pathologies, and ordinary trauma in childhood. There are cases when people suffered a certain inflammatory disease, after which atrophy began to develop.

You should not exclude such factors as inflammation of the eyeball and its dystrophy, swelling and congestion, damage and subsequent compression of a certain part of the nerve, unexpected hemorrhage.

Symptoms

The defeat of the optic nerve is a pathology that is characterized by inflammation of the nerve sheaths or fibers. Its symptoms can be: soreness when moving the eyeballs, blurred vision, changes in color perception, photopsia, the eye may swell.

Patients may complain of a decrease in the peripheral field of vision, vomiting, nausea, darkening in the eyes, fever. Each form of damage to the optic nerve has its own symptoms.

Symptoms characteristic of optic nerve atrophy of any etiology:

• decrease in distance visual acuity, and patients note that vision has decreased sharply, more often in the morning, can be reduced to hundredths of a unit, but sometimes remains high;
• loss of visual field, which depends on the localization of the pathological process; central scotomas ("spots"), concentric narrowing of the visual field may be observed;
• violation of the perception of colors;
• complaints characteristic of the underlying disease.

Allocate primary and secondary atrophy of the optic nerves, partial and complete, complete and progressive, unilateral and bilateral.

The main symptom of optic nerve atrophy is a decrease in visual acuity that cannot be corrected. Depending on the type of atrophy, this symptom manifests itself in different ways.

So, with the progression of atrophy, vision gradually decreases, which can lead to complete atrophy of the optic nerve and, accordingly, to complete loss of vision. This process can take from several days to several months.

With partial atrophy, the process stops at some stage and vision ceases to deteriorate. Thus, they distinguish progressive atrophy of the optic nerves and complete.

Visual impairment during atrophy can be very diverse. This can be a change in visual fields (more often narrowing, when “side vision” disappears), up to the development of “tunnel vision”, when a person looks as if through a tube, i.e. sees objects that are only directly in front of him, while scotomas often appear, i.e. dark spots in any part of the field of view; It could also be a color vision disorder.

Since the optic nerve carries visual images, the most common signs of its inflammation are the following phenomena:

• a sharp deterioration in vision in one or both eyes;

• appearance of black and white vision. Color vision, as more perfect, suffers first of all;

• pain when moving the eyes. An optional symptom, may be absent if there are no signs of classic inflammation and swelling of the retrobulbar tissue;

As noted above, the defining symptom here is a sharp decrease in human visual acuity. It can manifest itself in different ways, depending on the type of atrophy. If the form is partial, the deterioration of vision at some stage simply stops, after which it stops falling. Accordingly, the progressive form is characterized by the fact that a person begins to see worse and worse and, in the end, completely loses sight.

Vision in ocular atrophy is impaired in a variety of ways. For example, the field of view changes (as a rule, they begin to narrow), and peripheral vision worsens altogether. A person develops symptoms of "tunnel" vision, when all objects are visible as if through a narrow tube.

The pathogenetic course and symptoms of optic neuropathy directly depend on the etiological factors that caused a particular disorder, and are characterized by some differences in the violation of visual functionality.

So, anterior ischemic optic neuropathy is characterized by:

• gradual painless loss of vision, usually aggravated during morning awakening;
• loss of the lower visual fields in the early stages of the disease, then the process includes the loss of the upper regions.

Posterior optic neuropathy is caused by spontaneous and sudden complete loss of vision at a certain point in the development of the pathological process.

Typical symptoms of optic neuritis are:

• sudden decrease in visual acuity;
• loss of color characteristics;
• pain in the eye sockets;
• photopsies;
• phenomena of visual hallucinations.

Optic neuritis is a curable disease with good remission and prognosis. However, in complicated cases, it is able to leave irreversible traces in the visual neurostructure, which can provoke neuropathic progress.

The toxic etiology of neuropathies usually causes acute loss of vision, but with a favorable prognosis in case of immediate medical attention. Irreversible processes of destructive changes in the neurons of the optic nerve begin 15-18 hours after taking methanol, during which time it is necessary to use an antidote, usually ethyl alcohol.

Other types of neuropathic conditions of the optic nerve have identical symptoms of a gradual loss of visual acuity and color qualities. It is worth noting that in the first place, the perception of red shades always decreases, followed by all other colors.

Regardless of the level of the lesion (above or below the chiasm), there are two reliable signs of optic nerve atrophy - a loss of visual fields ("anopsia") and a decrease in visual acuity (amblyopia). How they will be expressed in a particular patient depends on the severity of the course of the process and the activity of the cause that caused the disease. Let's take a closer look at these symptoms.

Loss of visual fields (anopsia)

What does the term "field of view" mean? In fact, this is just a zone that a person sees. To imagine it, you can close half of the eye on either side. In this case, you see only half of the picture, since the analyzer cannot perceive the second part. We can say that you have “dropped out” one (right or left) zone. This is what anopsia is - the disappearance of the field of vision.

Neurologists divide it into:

• temporal (half of the image, located closer to the temple) and nasal (the other half from the side of the nose);
• right and left, depending on which side the zone falls on.

With partial atrophy of the optic nerve, there may be no symptoms, as the remaining neurons transmit information from the eye to the brain. However, if a lesion occurs through the entire thickness of the trunk, this sign will definitely appear in the patient.

Diagnostics

Methods for detecting inflammation of the optic nerve are based on clinical manifestations, since in most cases the pathology is not detected when examining the fundus. To exclude the presence of multiple sclerosis, a study of cerebrospinal fluid, MRI (magnetic resonance imaging) is performed. With the help of timely diagnosis, you can prevent and cure this disease, otherwise blindness and nerve atrophy will develop.

Fundus fluorescein angiography

This diagnostic method refers to objective research methods when contrasting vessels inside the eye with fluorescein, which is administered intravenously. In pathological conditions, eye barriers that work normally are destroyed, and the bottom of the eye takes on a form that is characteristic of a particular process.

The interpretation of fluorescein angiograms is based on a comparison of the characteristics of the passage of fluorescein through the wall of the retina and choroidal vessels with the clinical picture of the disease. The price of the study is 2500-3000 rubles.

Electrophysiological study

Such a diagnostic procedure is a series of highly informative methods for studying the functions of the retina, optic nerve, and areas of the cerebral cortex. An electrophysiological study of the eye is based on recording its response to specific stimuli.

The ophthalmologist and the doctor who conducts the study work closely with each other to set the right task and decide on the diagnostic method. This study is considered the most informative and effective.

The cost of diagnostics is 2500-4000 rubles.

Diagnosis of this disease is carried out by an ophthalmologist together with other specialists. It is performed in several stages, the first of which is an examination by an ophthalmologist, who will refer the patient for additional examinations.

Stages of diagnostics in the office of an ophthalmologist:

1. Determination of visual acuity - the study is carried out using special tables or a projector of signs. In rare cases, visual acuity remains within 0.8-0.9, more often there is a decrease to hundredths of a unit.
2. Kinetic perimetry: in case of optic nerve disease, there will be a narrowing of the visual field to green and red.
3. Computer perimetry: carried out to more accurately determine the presence of livestock ("blind spots"), their number and properties. The light sensitivity and threshold sensitivity of the retina are examined.
4. Examination of the reaction of pupils to light: in the presence of a disease on the side of the lesion, the reaction to light decreases.
5. Tonometry (determination of intraocular pressure) is performed to exclude the glaucomatous process.
6. EFI (electrophysiological examination of the eyes): during this examination, visual evoked potentials are examined; these are signals generated in the nervous tissue in response to stimulation, and with atrophy of the optic nerves, their intensity decreases.
7. Ophthalmoscopy: examination of the fundus and optic disc. During this procedure, the ophthalmologist sees:

• with primary atrophy, the disc is white or grayish-white, the boundaries are clear, a decrease in the number of small vessels on the disc, narrowing of the circumdiscal vessels and thinning of the retinal nerve fiber layer;
• with secondary atrophy, the disc is gray, the boundaries are fuzzy, a decrease in the number of small vessels on the disc;
• with glaucomatous atrophy, the disc is white or gray, the boundaries are clear, pronounced excavation (deepening of the central part of the disc), shift of the vascular bundle.

Consultations of related specialists:

1. A consultation with a therapist is carried out to identify diseases that can cause disturbances in the optic nerve and lead to its atrophy.
2. Consultation with a neurologist to rule out multiple sclerosis.
3. A consultation with a neurosurgeon is prescribed if an increase in intracranial pressure is suspected.
4. A consultation with a rheumatologist is indicated in the presence of complaints characteristic of vasculitis.

The diagnosis of toxic damage to the optic nerve is established on the basis of anamnestic data, studying the reaction of pupils to light, ophthalmoscopy, visometry, perimetry, computed tomography (CT). In most patients, it is possible to confirm the relationship between the development of symptoms and exposure to toxins.

Ophthalmoscopy can determine the stage of the disease. At stage I, slight hyperemia of the optic nerve head (OND) and vascular injection are visualized.

At stage II, edema of the optical fibers joins. Stage III is characterized by severe ischemia.

Stage IV is considered as terminal, manifested by degenerative and atrophic changes in nerve fibers.

In the acute course of the disease, the reaction to the pupils to light is sluggish. Conducting visiometry indicates a decrease in visual acuity.

The method of ophthalmoscopy allows visualizing the swelling of the ONH. With a complete loss of vision, the white color of the optic disc, vasospasm are determined.

The method of perimetry makes it possible to establish concentrically narrowed visual fields and to uncover central scotomas. In the chronic form of the disease, there is a moderate decrease in visual acuity (0.2-0.3).

Ophthalmoscopically confirmed the waxy hue of the optic disc, pronounced spasm of arterioles. Conducting perimetry indicates a concentric narrowing of the visual field.

On CT, small-focal atrophic changes in the optic nerve head are visualized.

The diagnosis of optic neuropathy includes a sufficient set of methods and tools to determine the nature of the course of the pathology and the prognosis of its cure. As you know, neuropathy is more often a secondary disease caused by individual diseases, so the anamnesis plays a leading role in diagnosing types of neuropathy.

Outpatient ophthalmological examinations include a range of procedures.

• Examination of the fundus.
• Classic visual acuity test.
• Spheroperimetric diagnostics, which allows to determine the boundaries of the visual fields.
• Assessment of color perception.
• X-ray examination of the skull with the obligatory inclusion of the hypothalamic region in the image.
• The methods of computed tomography and cerebral magnetic resonance are of decisive importance in clarifying the local causes that caused the development of optic neuropathy.

Treatment

Treatment of atrophy of the optic nerve drug and physiotherapy:

• Drug treatment is effective only in case of compensation of the underlying disease and visual acuity of at least 0.01. If the cause of atrophy is not eliminated, a decrease in visual functions will also be observed against the background of neuroprotective therapy.
• Physiotherapy is carried out in the absence of contraindications to this type of treatment. Main contraindications: stage 3 hypertension, severe atherosclerosis, fever, neoplasms (tumors), acute pyoinflammatory processes, condition after a heart attack or stroke within 1-3 months.

Stages of treatment:

1. Treatment of the underlying disease, if detected, is carried out by an appropriate specialist, more often in a hospital setting. The prognosis of the course of optic nerve atrophy depends on the timely detection of the disease.
2. Refusal of bad habits allows you to stop the progression of the disease and preserve the visual functions of the patient.
3. Direct acting neuroprotective agents protect the axons (fibers) of the optic nerve. The choice of a specific drug is carried out taking into account the leading role of one or another pathological factor (hemodynamic disturbance or regional ischemia).
4. Neuroprotective agents of indirect action affect the risk factors that contribute to the death of optic nerve cells. The choice of the drug is carried out individually.
5. Magnetotherapy.
6. Electro-laser stimulation of the optic nerve.
7. Acupuncture.

The last three items are physiotherapy procedures. They are prescribed to improve blood circulation, stimulate reduced metabolic processes, increase tissue permeability, improve the functional state of the optic nerve, which ultimately corrects the state of visual functions. All treatment is carried out in a hospital setting.

Neuroprotective agents of direct action:

• methylethylpyridinol (Emoxipin) 1% injection;
• pentahydroxyethylnaphthoquinone (Histochrome) 0.02% injection.

Neuroprotective agents of indirect action:

• Theophylline tablets 100 mg;
• Vinpocetine (Cavinton) 5 mg tablets, injection;
• Pentoxifylline (Trental) injection 2%, tablets 0.1 g;
• Picamilon tablets 20 mg and 50 mg.

Treatment of optic nerve atrophy is a very difficult task for physicians. You need to know that destroyed nerve fibers cannot be restored.

One can hope for some effect from the treatment only when the functioning of nerve fibers that are in the process of destruction, which still retain their vital activity, is restored. If you miss this moment, then the vision in the sore eye can be lost forever.

When treating atrophy, it must be borne in mind that this is often not an independent disease, but a consequence of other pathological processes affecting various parts of the visual pathway. Therefore, the treatment of optic nerve atrophy must be combined with the elimination of the cause that caused it.

In case of timely elimination of the cause and if atrophy has not yet developed, within 2-3 weeks to 1-2 months, the fundus picture normalizes and visual functions are restored.

The treatment is aimed at eliminating edema and inflammation in the optic nerve, at improving its blood circulation and trophism (nutrition), restoring the conductivity of incompletely destroyed nerve fibers.

But it should be noted that the treatment of optic nerve atrophy is lengthy, the effect of it is weak, and sometimes completely absent, especially in advanced cases. Therefore, it should be started as early as possible.

As mentioned above, the main thing is the treatment of the underlying disease, against which complex treatment is carried out directly for atrophy of the optic nerve. To do this, prescribe various forms of drugs: eye drops, injections, both general and local; tablets, electrophoresis. Treatment is aimed at

The tactics of treating toxic damage to the optic nerve depends on the stage and characteristics of the course of the disease. At stage I, patients are shown detoxification therapy.

Intensive dehydration and the appointment of anti-inflammatory drugs are recommended at stage II. At stage III, it is advisable to introduce antispasmodics.

With the development of stage IV, in addition to vasodilators, the complex of therapeutic measures should include immunomodulators, multivitamin complexes and physiotherapeutic methods of treatment (magnetotherapy, physioelectrotherapy in combination with electrolaser therapy).

The most difficult task for the attending physician is competently prescribed treatment. This is due to the fact that it is no longer possible to restore dead nerve fibers, although a certain effect in this area can be achieved. We are talking about fibers that are in the active stage of destruction.

All methods of treatment can be divided into three types:

• Conservative. The doctor prescribes a whole series of drugs with a different spectrum of effects. For example, papaverine and no-shpa improve blood circulation in the affected nerve, nootropil improves the functions of the nervous system, hormonal drugs stop the inflammation process.
• Therapeutic. Patients are prescribed a fairly wide range of procedures, including magnetic stimulation, acupuncture, laser or electric current stimulation. As a rule, patients undergo such treatment every few months in separate courses.
• Surgical. It involves the elimination of pathological formations that compress the patient's nerve, the implantation of biogenic materials and the subsequent ligation of the temporal artery. This improves the overall circulation of the nerve and its further vascularization.

The main direction of therapeutic schemes for the treatment of optic neuropathy is the inhibition of pathological processes developing in the parenchyma of the optic trunk, if possible, their complete exclusion, as well as the restoration of lost visual qualities.

As already mentioned, optic neuropathy is a secondary pathology initiated by other diseases. Proceeding from what, first of all, the treatment of primary diseases is carried out under regular monitoring of the state of the optic nerve and attempts to restore its organic characteristics.

Several methods are available for this purpose.

• Magnetic stimulation of optic nerve neurons using an alternating electromagnetic field.
• Electrical stimulation of the nerve trunk by conducting currents of a special frequency and strength through the parenchyma of the optic nerve. This method is invasive and requires a highly skilled specialist.

The essence of both methods is to stimulate the metabolic processes of the optic nerve fibers, which partially contributes to their regeneration due to the body's own forces.

One of the most effective treatments for optic neuropathy is autologous stem cell transplantation therapy.

The common background of every therapeutic regimen is the traditional conservative support.

• Vasodilator drugs.
• Tonics.
• B group vitamins.
• In some cases, especially in toxic neuropathy, blood transfusions are used.

Surgical treatment is the main method of therapy for squeezing the optic nerve, its traumatism or infiltration.

It is widely believed in society that "nerve cells do not regenerate." This is not entirely correct. Neurocytes can grow, increase the number of connections with other tissues and take on the functions of dead "comrades". However, they do not have one property that is very important for complete regeneration - the ability to reproduce.

Can optic nerve atrophy be cured? Definitely not. With partial damage to the trunk, medications can improve visual acuity and visual fields. In rare cases, even virtually restore the patient's ability to see to normal levels. If the pathological process has completely disrupted the transmission of impulses from the eye to the brain, only surgery can help.

Complications of optic nerve atrophy

Timely diagnosis of optic neuropathy allows you to start treatment at an early stage. This makes it possible to prevent destructive processes in the optic nerve, maintain and even increase visual acuity. However, it is impossible to fully restore visual function due to damage and death of nerve cells.

Late treatment can lead to threatening consequences: not only loss of visual acuity, color sensitivity, but also the development of complete blindness.

In order to prevent

Prevention of this disease consists in maintaining a healthy lifestyle, timely treatment of concomitant diseases, and avoiding hypothermia.

To prevent the death of the optic nerve, it is necessary:

• prevent the development of inflammatory processes in the body, infectious diseases, stop them;
• avoid eye damage and brain injury;
• regularly visit an oncologist and conduct appropriate studies for the timely diagnosis of the disease and treatment;
• do not drink alcohol, stop smoking;
• monitor daily blood pressure;
• monitor proper nutrition;
• lead a healthy lifestyle with sufficient physical activity.

Forecast and consequences

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

Unfortunately, with atrophy of all nerve cells and the cessation of impulse transmission, the patient is likely to develop blindness. The way out in this case may be surgical restoration of tissue nutrition, but such treatment is not a guarantee of restoration of vision.

Atrophy of any organ is characterized by a decrease in its size and loss of functions due to lack of nutrition. Atrophic processes are irreversible and speak of a severe form of any disease. Optic nerve atrophy is a complex pathological condition that is almost untreatable and often ends in loss of vision.

In this article

Functions of the optic nerve

The optic nerve is the white matter of the large brain, as if brought to the periphery and connected with the brain. This substance conducts visual images from the retina, on which light rays fall, to the cerebral cortex, where the final image is formed, which the person sees. In other words, the optic nerve plays the role of a message provider to the brain and is the most important component of the entire process of converting the light information received by the eyes.

Optic nerve atrophy: a general description

With atrophy of the optic nerve, its fibers are completely or partially destroyed. They are subsequently replaced by connective tissue. The death of the fibers causes the light signals received by the retina to be converted into electrical signals that are transmitted to the brain. For the brain and eyes, this process is pathological and very dangerous. Against its background, various disorders develop, including a decrease in visual acuity and narrowing of its fields. Optic nerve atrophy is quite rare in practice, although even the most minor eye injuries can provoke its onset. However, approximately 26% of cases of diseases end with the fact that the patient completely loses sight in one eye.

Causes of optic nerve atrophy

Optic nerve atrophy is one of the symptoms of various eye diseases or a stage in the development of any disease. There are a lot of reasons that can lead to this pathology. Among the ophthalmic diseases that can provoke atrophic changes in the optic nerve, the following ailments:

• glaucoma;
• retinitis pigmentosa;
• myopia;
• uveitis;
• retinitis;
• optic neuritis,
• damage to the central artery of the retina.

Also, atrophy can be associated with tumors and diseases of the orbit: optic nerve glioma, neurinoma, orbital cancer, meningioma, osteosarcoma, and others.
All kinds of diseases of the brain and central nervous system in some cases lead to atrophic processes in the eyes, affecting primarily the optic nerves. These diseases include:

• multiple sclerosis;
• pituitary tumors;
• meningitis;
• brain abscess;
• encephalitis;
• traumatic brain injury;
• damage to the skeleton of the face with a wound in the optic nerve.

Types and forms of optic nerve atrophy

This pathological condition is congenital and acquired. Acquired atrophy is divided into descending and ascending. In the first case, the fibers of the optic nerve directly are affected. In the second, the cells of the retina are hit.
According to another classification, acquired atrophy can be:

1. Primary. It is also called a simple form of atrophy, in which the optic disc turns pale, but has clear boundaries. The vessels in the retina narrow in this type of pathology.
2. Secondary, which develops due to inflammation of the optic nerve or its stagnation. The boundaries of the disk become fuzzy.
3. Glaucomatous, accompanied by increased intraocular pressure.

According to the scale of damage to the optic nerve fibers, atrophy is divided into partial and complete. The partial (initial) form is manifested in a severe deterioration in vision, which cannot be corrected with contact lenses and glasses. At this stage, you can save the remaining visual functions, but color perception will be severely impaired. Complete atrophy is a lesion of the entire optic nerve, in which a person no longer sees anything with a sore eye. Atrophy of the optic nerve manifests itself in a stationary form (does not develop, but remains at the same level) and progressive. With stationary atrophy, visual functions remain in a stable state. The progressive form is accompanied by a rapid decrease in visual acuity. Another classification divides atrophy into unilateral and bilateral, that is, with damage to one or both organs of vision.

Symptoms of optic nerve atrophy

The first and main symptom that manifests itself in any form of optic nerve atrophy is visual impairment. However, it cannot be corrected. This is a sign by which the atrophic process can be distinguished from ametropia - a change in the ability of the human eye to correctly refract light rays. Vision may deteriorate gradually and rapidly. It depends on the form in which atrophic changes occur. In some cases, visual functions decrease within 3-4 months, sometimes a person becomes completely blind in one or both eyes in a few days. In addition to a general decrease in visual acuity, its fields narrow.


The patient almost completely loses peripheral vision, which leads to the development of the so-called "tunnel" type of perception of the surrounding reality, when a person sees everything as if through a pipe. In other words, only what is directly in front of the person is visible, and not to the side of him.

Another common sign of optic nerve atrophy is the appearance of scotomas - dark or blind areas that occur in the field of vision. By the location of the scotoma, it is possible to determine the fibers of which area of ​​the nerve or retina are damaged the most. If spots appear right in front of the eyes, then the nerve fibers located closer to the central section of the retina or directly in it are affected. Disorder of color perception becomes another problem that a person faces with atrophy. Most often, the perception of green and red shades is disturbed, rarely the blue-yellow spectrum.

All these symptoms are signs of the primary form, that is, its initial stage. They can be noticed by the patient himself. Symptoms of secondary atrophy are visible only during examination.

Symptoms of secondary optic nerve atrophy

As soon as a person goes to the doctor with symptoms such as reduced visual acuity and narrowing of its fields, the doctor conducts an examination. One of the main methods is ophthalmoscopy - examination of the fundus with the help of special instruments and devices. During ophthalmoscopy, the following signs of optic nerve atrophy are revealed:

• vasoconstriction;
• varicose veins;
• disc blanching;
• decreased pupillary response to light.

Diagnostics

As already described above, the first method used to detect pathology is ophthalmoscopy. However, the symptoms that can be detected with this study do not allow for an accurate diagnosis. Deterioration of vision, lack of pupillary response to light, vasoconstriction of the eye are signs of many eye ailments, for example, a peripheral form of cataract. In this regard, many different methods are used to diagnose atrophy:

Laboratory studies are also carried out. The patient donates blood and urine for analysis. Tests for syphilis, borreliosis and other non-ophthalmic diseases are prescribed.

How is optic nerve atrophy treated?

It is impossible to restore fibers that have already been destroyed. Treatment helps stop atrophy and save those fibers that are still functioning. There are three ways to deal with this pathology:

• conservative;
• therapeutic;
• surgical.

With conservative treatment, the patient is prescribed vasoconstrictor drugs and drugs, the actions of which are aimed at normalizing the blood supply to the optic nerve. The doctor also prescribes anticoagulants, which inhibit the activity of blood clotting.


Drugs that stimulate metabolism and drugs that relieve inflammation, including hormonal ones, help stop the death of fibers.

Physiotherapeutic effect involves the appointment of:

The surgical method of treatment is focused on the removal of formations that put pressure on the optic nerve. During the operation, the surgeon can implant the patient with biogenic materials that will help improve blood circulation in the eye and in the atrophied nerve, in particular. The transferred pathology in most cases leads to the fact that a person is assigned a disability. Blind or visually impaired patients are sent to rehabilitation.

Prevention

To prevent atrophy of the optic nerve, it is necessary to start treating ophthalmic diseases in a timely manner.


At the first sign of a decrease in visual acuity, you should immediately make an appointment with an ophthalmologist. With the onset of atrophy, not a minute can be lost. If at the initial stage it is still possible to preserve most of the visual functions, then as a result of further atrophic changes, a person may become disabled.

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Optic nerve damage (OPD) occurs in 5-5% of cases with TBI, and the intracanal part of the nerve is predominantly affected. Usually this injury is the result of a blow, most often inflicted in the frontal, orbital, less often in the frontotemporal region. ZNP are observed in severe TBI, craniobasal fractures, extending to the bone structures surrounding the optic nerve (ON): the optic canal, the anterior sphenoid process, the roof of the orbit. The severity of MN lesions does not always correlate with the severity of TBI. Vision loss up to amaurosis can sometimes occur after trauma to the fronto-orbital region without loss of consciousness, when no other neurological disorders are noted.

According to the localization of damage can be divided into anterior and posterior. Anterior optic nerve damage is extremely rare. With this pathology, the lesion of the intraocular department (disk) and part of the intraorbital department of the optic nerve containing the central retinal artery (CAS) is determined. Posterior NNPs are more common (between the CAC nerve entry and the chiasm). Due to the anatomical features, the intracanal department of the ON is most susceptible to traumatic effects. In contrast to the mobile intraorbital and intracranial sections, in the bone canal the nerve is tightly fixed by the dura mater. The blood supply of the intracanal section is carried out by small branches of the ophthalmic and internal carotid arteries, which form the pial vascular network surrounding the ON. At the time of injury, abrupt displacements of the brain and/or fracture of the canal can cause stretching and rupture of the axons of the ON and the vessels that feed it. NRPs are rarely the result of direct compression by bone fragments in the canal. Compression due to reactive nerve edema and secondary ischemic disorders are considered to be the main mechanism of injury. It should be emphasized that the force of the inflicted frontal impact can directly propagate to the ON and the presence of a canal fracture is not a prerequisite for an intracanal lesion.

Pathological changes in the optic nerve can be divided into primary and secondary. The primary ones include injuries that occurred during the impact: intershell and intraneural hemorrhages, contusions, nerve ruptures. Secondary damage occurs delayed and is the result of vascular disorders: edema, ischemic necrosis of the ON.

Clinic of damage to the optic nerve.

ZNP are manifested by a sharp decrease in visual acuity up to blindness. Violations of the visual fields are defined as central and paracentral scotomas, concentric narrowing, sector-like loss. The most reliable sign is a decrease or absence (with amaurosis) of a direct pupillary reaction to light with a preserved friendly reaction. On the opposite (healthy) side, the direct reaction of the pupil to light will be preserved, and the friendly one will be weakened. Ophthalmoscopy in all cases of anterior NAP in the fundus reveals a pathology that fits into the pattern of CAC occlusion, anterior ischemic neuropathy, or avulsions of varying severity with hemorrhages along the edge of the disc. In posterior NRPs, including intracanal ones, the ON disk and fundus generally appear normal. After 2-4 weeks. blanching of the disc appears. The closer anteriorly the ON is affected, the faster its atrophy is detected. To clarify the localization of damage, radiography of the openings of the optic canal according to Reze is used, which makes it possible to identify fractures of the canal walls. In most cases, linear fractures occur, less often with displacement of fragments. However, radiography often does not reveal a crack in the canal. Intracanal fractures are more often detected by CT of the orbit. At the same time, changes in the ON and soft tissues of the orbit are also determined (shell hematoma of the ON, retrobulbar hemorrhage, the ratio of ON to bone fragments in the orbit, hemorrhage into the sphenoethmoid sinus). At the same time, the absence of traumatic changes on radiographs and CT is not a basis for excluding intracanal damage.

Treatment of damage to the optic nerve.

Currently, there is no generally accepted tactic for the treatment of intracanal CNS. Surgical treatment is aimed at eliminating compression of the ON and consists in removing one of the walls of the canal, depending on the access, as well as bone fragments and sheath hematoma of the ON (if any).

2 surgical approaches are used:

1. intracranial transfrontal (with resection of the upper wall of the canal and dissection of the dura mater in the region of the internal visual aperture);
2. extracranial transethmoidal (with resection of the medial wall of the canal). Usually, ON decompression is performed within a few hours. Up to 7-10 days. after injury. The shorter the time interval between TBI and surgery, the better the results of surgical treatment. Indications for ON decompression and timing of its implementation are not unified.

The problem is that the same clinical data may have different morphological substrates in different patients. When deciding on surgical intervention, one should take into account the severity and time of onset of visual impairment. If visual loss develops some time after the injury, or if there is a progressive deterioration of vision despite medical treatment, decompression of the ON is indicated. If the loss of vision occurred during the injury, is complete, with the absence of a direct reaction of the pupil to light, this, as a rule, indicates severe morphological damage, in most cases leading to persistent visual deficit. In such cases, the effect of the operation is doubtful. It is inappropriate to perform surgery on patients with partial loss of vision, if the visual acuity is above 0.1 and the visual field defect is less than 1/4, without observation and an attempt at conservative treatment. The presence of radiographic and CT signs of a canal fracture is not a prerequisite for surgical intervention. Data on the effectiveness of ON decompression remain controversial. This is due to the fact that often operations are performed with irreversible damage. At the same time, some neurosurgeons believe that surgical intervention has no significant advantages over conservative treatment and use ON decompression only as an adjunct to other skull surgeries. Drug treatment includes the use of decongestants (mannitol, lasix) and vasoactive agents (trental, sermion, complamin, cavinton), corticosteroids, drugs that improve microcirculation (reopoliglyukin, etc.).

The prognosis for visual recovery in optic nerve injury is poor when visual loss occurs at the time of injury. In most cases, amaurosis is irreversible, although occasionally some improvement may occur within hours or days after injury, regardless of the type of treatment performed. Better results can be expected with delayed vision loss or when the initial visual defect is partial and diagnosis is timely and therapy is adequate. The prognosis depends on the severity of the damage to the ON and is largely predetermined at the time of the traumatic impact.