Damage to the optic nerve. Optic nerve damage. Types of atrophic lesions of the optic nerve

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Damage to the optic nerve (ON) is an urgent problem at the intersection of neurosurgery and ophthalmology. From 1988 to 1996 at the Institute of Neurosurgery. N.N. Burdenko, 156 patients with damage to the optic nerve during TBI and penetrating wounds of the skull and orbit were observed. The study of such an array of observations showed that in order to improve the diagnosis and choice of tactics for the treatment of damage to the ON, it is obvious that there is a need to create a unified classification that would take into account the nature and mechanism of injury, localization and genesis of the lesion, morphological changes, clinical forms and severity of damage, etc. At the same time, there are only a few reports that present attempts to systematize this pathology. Considering the foregoing, the Institute of Neurosurgery has been working for a number of years to create a classification of ON injuries. Based on the analysis of literature data and our own observations, a classification of AP damage was developed according to the following principles.

I. By the nature of the injury: open and closed.
1) Open damage - damage to the optic nerve with penetrating wounds of the skull and / or orbit.
2) Closed damage - damage to the optic nerve as a result of blunt trauma to the skull and facial skeleton.

P. According to the mechanism of injury: direct and indirect.
1) Direct damage occurs as a result of direct contact of the traumatic agent with the ON.
2) Indirect damage occurs as a result of shock or compression effect of a traumatic agent on distant or surrounding bone structures. Characteristic is the decrease in vision after injury in the absence of signs of damage to the eyeball, which could lead to a decrease in visual functions.

III. According to the genesis of the lesion: primary and secondary.
1) Primary damage - damage in which there are morphological changes caused by mechanical energy, and occurred at the time of injury:
1.1. Hemorrhages in the nerve, membranes and intershell spaces of the nerve;
1.2. Contusion necrosis; 1.3 Gap:
a) anatomical (full or partial);
b) axonal.

Anatomical breaks are characterized by a break in the entire diameter of the nerve or part of it. In this case, the gap extends to all the constituent parts of the nerve - membranes, stroma, visual bundles (axons) and vessels of the nerve, and can be established macroscopically during surgery or autopsy.

Axonal damage to the ON can only be differentiated microscopically: with an outwardly unchanged appearance, axonal ruptures are noted in the depth of the nerve.

2) Secondary damage - damage in which there are morphological changes caused by vascular insufficiency due to intra-, extracranial factors, and developing at any time after the injury.

2.1. Edema;
2.2. Necrosis due to local compression of the vessel or circulatory vascular insufficiency;
2.3. Nerve infarction due to vascular occlusion (spasm, thrombosis).

IV. According to the localization of the lesion: anterior and posterior.
1) Anterior damage - damage to the intraocular region (ON disk) and part of the intraorbital region to the point of entry into it of the central retinal artery (RAS), while pathology is always detected in the fundus.

Clinical forms of anterior injuries:



1.4. Wound.

2) Posterior damage - damage to the optic nerve posterior to the place of entry into the AAS nerve, when there is a clear violation of the function of the optic nerve with delayed changes (atrophy of the optic disc) in the fundus. Clinical forms of posterior injuries:
2.1. Shake;
2.2. Injury;
2.3. compression;
2.4. Wound.

V. By type of damage:
1) Unilateral damage to the AP.
2) Damage to the visual pathway at the base of the brain:
2.1. Bilateral damage to the optic nerve;
2.2. Chiasm damage;
2.3. Combined damage to the ON and chiasm;
2.4. Combined damage to the ON, chiasm and optic tract.

VI. According to the presence of fractures of bone structures:
1) Damage with the presence of a fracture of the walls of the optic canal.
2) Damage with the presence of fractures of adjacent bone structures (the wall of the orbit, the anterior clinoid process, the lesser wing of the sphenoid bone).
3) Damage against the background of fractures of distant bone structures of the skull and facial skeleton.
4) Damage without the presence of fractures of the bone structures of the skull and facial skeleton.

VII According to clinical forms (depending on the location of the lesion).
1) For anterior injuries:
1.1. Violation of blood circulation in PAS;
1.2. Anterior ischemic neuropathy;
1.3. Evulsion (separation of the optic nerve from the eyeball);
1.4. Wound.
2) For posterior injuries:
2.1. Shake;
2.2. Injury
2.3. compression;
2.4. Wound.

Based on the unity of the anatomical structure and blood circulation of the ON and the brain, it can be concluded that damage to the ON is a local injury to the PNS. This gives grounds for using the classification divisions of TBI: concussion, bruise, compression, injury. It should be noted that a number of authors widely use these terms in relation to damage to the optic nerve. However, the content of the above concepts in their morphological, pathophysiological and clinical interpretations is far from the same.

The expediency of isolating the clinical forms of damage to the ON follows from practical considerations. First of all, this is due to the difference in approaches to treatment, including the determination of indications for decompression of the ON. In particular, in case of indirect posterior injuries, which are of the greatest relevance for neurosurgeons, we can talk about at least two clinical forms: compression and contusion of the ON. However, if we proceed from the analogy with the structure of TBI, then it is known that severe forms of traumatic brain injury - contusion, compression - are less common than concussion. The same provision can be quite applicable to the trauma of the ON.

Below is a clinical interpretation of the terms "concussion", "bruise", "compression" and "injury" in relation to trauma to the ON.

Concussion of the optic nerve
Concussion is defined as "a clinical syndrome characterized by an immediate and transient impairment of neurological function associated with exposure to a mechanical factor."

Concussion is understood as damage to the optic nerve without gross organic changes in its tissues, membranes and surrounding structures.

Concussion of the ON is characterized by a transient visual impairment within seconds or minutes, less often hours, followed by its complete recovery. The most common example is the patient's complaints of seeing "stars" or "sparks" in front of the eye for a few seconds after a blow to the frontal or temporal region. Apparently, concussion of the ON is common, however, due to the transient nature of visual disturbances, it does not attract the attention of both doctors and the patients themselves.

Optic nerve contusion
Contusion is defined histologically as "a structural tissue injury characterized by extravasation of blood and cell death".

Clinically, contusion of the ON is characterized by a persistent loss of vision that develops at the time of injury (an immediate type of visual impairment), which is based on morphological changes. Primary lesions dominate in the structure of the morphological substrate. If the loss of vision is complete, most likely there is contusion necrosis, much less often - rupture. If the loss of vision is partial and / or there is a restoration of vision, then the area of ​​\u200b\u200bprimary contusion necrosis or rupture did not affect the entire nerve. In addition, hemorrhages (intraneural and meningeal) can also underlie partial loss of vision. In these cases, the improvement in vision can be explained by blood resorption and decreased compression of nerve fibers. In most cases, immediate amaurosis is irreversible, although partial or complete recovery of visual function may occur within hours or days of injury.

Optic nerve compression
The structure of the morphological substrate is dominated by secondary (ischemic) damage due to mechanical compression of the nerve. The compression of the ON is characterized by a progressive or delayed deterioration of visual functions after injury. With a delayed type of vision loss, visual functions are not changed immediately after the injury, and their primary deterioration is noted only after a while. In the progressive type of visual loss, the primary deterioration in visual function is observed immediately after the injury, while there is a partial visual deficit, which increases over time (secondary impairment). The period of time from the moment of injury to the primary or secondary deterioration of visual function (the “luminous gap”) can take from several minutes and hours to several days after injury. A "clear gap" regardless of its duration is an indication of the absence of an anatomical break in the ON and the presence of potentially reversible morphological changes.

Compression can occur both against the background of a contusion of the ON, and without it. The reserve spaces of the membranes and the optic nerve canal are extremely limited; therefore, contusion of the optic nerve, accompanied by its edema and an increase in the transverse size, can lead to compression inside the canal. Considering that in some cases the primary and secondary mechanisms of damage develop in parallel, the immediate type of vision loss is not a reason to exclude compression of the ON, especially if it is not complete, but partial. Loss of vision at the time of injury may occur when compression occurs due to a fracture of the canal walls with displacement of bone fragments.

In the acute period of TBI, massive contusion foci of the frontal lobe, intracranial hematomas of the frontotemporal region, causing displacement of the posterior-basal sections of the frontal lobe into the middle cranial fossa, into the chiasmatic cistern, can lead to compression of the intracranial ON or chiasm at the base of the brain. In these cases, we will talk about a secondary dislocation lesion of the visual pathway.

The following summarizes the main pathological processes that have a compressive effect on the ON throughout its entire length:

I. Deformation and fractures of bone structures surrounding the ON:
1) the upper wall of the orbit;
2) The walls of the visual canal;
3) Anterior inclined process.

II. Hematomas:
1) Intraorbital:
1.1. Retrobulbar hematoma;
1.2. Subperiosteal hematoma of the orbit.
2) Shell hematoma of the ON.
3) Intracranial:
3.1. Frontobasal hematoma;
3.2. Convexital hematoma of the frontotemporal region.

III. Massive foci of contusion and crushing of the frontal lobe of the brain

IV. Arachnoid cyst of GN.

V. Swelling of the ON.

VI. Cicatricial adhesive processes in the remote period:
1) Callus;
2) Scar tissue;
3) Adhesive arachnoiditis.

VII. Traumatic supraclinoid false aneurysm a.carotis interna.

VIII. Expanded cavernous sinus with carotid-cavernous fistula.

Taking into account the presented data, it should be emphasized that the compression of the ON can occur in two ways, both due to external and internal factors. In the first case, it is subjected to external compression due to pathological processes in the orbit (subperiosteal or retrobulbar hematomas, fractures of its walls with displacement of bone fragments), optic canal (fractures with displacement of bone fragments, epidural hemorrhages), cranial cavity (frontobasal or convexital hematomas). , fracture with displacement of the anterior clinoid process, etc.). In the second case, it is subjected to compression “from the inside”, due to pathological processes developing in its parenchyma and membranes (edema, hemorrhages) and exerting a mass effect. In such a situation, in fact, there is a "tunnel" syndrome caused by compression of the ON within the rigid structure of the visual canal with an unchanged lumen or a tightly fitting dural membrane outside the canal.

optic nerve injury
Injury to the optic nerve is a direct injury to the optic nerve resulting from direct contact with a traumatic agent. Wounding of the optic nerve usually leads to its complete irreversible damage, with an anatomical interruption and the development of immediate amaurosis. However, partial damage is also possible. In this case, there is irreversible damage to some of the optic fibers, but intact fibers retain the potential to restore their function. In those cases where the direct impact of a traumatic agent on the ON does not lead to a violation of its integrity, a tangential wound occurs.

Wounds of the ON are observed with penetrating wounds of the skull and/or orbit. However, the latter are not in all cases accompanied by direct injury to the ON itself, despite the presence of symptoms of its damage. When the AP is located in the zone of primary destruction, formed along the path of the projectile, the clinical form of its damage is a wound. If the AP is in the zone of secondary damage caused by the lateral force of the projectile, the clinical form of its damage is a bruise. Thus, in case of open injuries due to gunshot penetrating wounds of the skull and/or orbit, not only direct damage - wound, but also indirect damage - contusion of the ON is possible. As a result of a penetrating gunshot wound of the cranio-orbital region, a combination of clinical forms can be observed: bruising and compression of the optic nerve and wounding it with secondary injuring projectiles (bone fragments).

Direct or lateral (contusion) impact of the projectile not only on the ON, but also on the a.ophthalmica and its branches involved in the blood supply of the ON and the retina, may be accompanied by impaired blood flow in the latter. In such cases, there will also be combined direct and indirect, anterior and posterior lesions of the ON.

It is not always possible to verify the anatomical interruption of the ON due to its injury by CT, especially in the intracranial or intracanalicular regions. In case of contusion of the optic nerve due to injury to the orbit, CT examination allows to detect changes in the intraorbital region (increase in its diameter, change in density), while the presence of a hematoma at the site of its injury may mask a nerve rupture.

VIII. Severity: mild, moderate, severe.
Currently, in most cases, the establishment of clinical forms of damage to the ON is very difficult. There is much in common in the presented characteristics of clinical manifestations. There are certain difficulties in their differentiation. At the same time, for practical purposes (indications for ON decompression, prognosis, rehabilitation potential, expert assessment, determination of the severity of TBI, etc.), clear gradations are required according to unified criteria. As the latter, visual impairments can serve. Considering that they vary widely, all ON injuries are divided into three severity levels according to the severity of visual impairment: mild, moderate, severe (Tables 2—2).

The parameters of visual acuity and field of view are of independent importance in determining the severity of damage to the ON. The latter is evaluated by the worst of two indicators: visual acuity or visual field. In the presence of a central scotoma or the inability to determine the boundaries of the visual field, the severity of the damage is judged by visual acuity. With a combination of normal visual acuity and a visual field defect, the severity is determined by the size of the latter.

Table 2-2

IX. Gradations of disorders of the ON function

1) According to the dynamics of dysfunction:
1.1. Immediate;
1.2. progressive;
1.3. Delayed.

2) According to the degree of violation of the conduction of excitation:
2.1. Partial excitation conduction block;
2.2. Complete excitation conduction block.

3) According to the reversibility of the dysfunction:
3.1. Reversible - functional interruption of the ON;
3.2. Partially reversible - morpho-functional interruption of the ON;
3.3. Irreversible - morphological interruption of the ON.

On fig. 2-28 presents the main provisions of the developed classification.

Rice. 2 - 28. Classification of damage to the optic nerve.

Thus, the developed classification of ON injuries makes it possible to take into account, when making a diagnosis, the nature and mechanism of injury, the genesis and localization of the process, the presence of fractures of bone structures, the types of development of visual impairments, the clinical forms and severity of damage, and thereby contributes to clarifying the diagnosis, determining the prognosis and a differentiated approach to treatment.

DETERMINATION OF THE SEVERITY OF TBI ACCOMPANIED BY DAMAGE TO THE OPTIC NERVE

As is known, the degree of brain damage is the main, but not the only component in determining the severity of TBI. Undoubtedly, damage to the optic nerve is one of the manifestations of brain tissue damage and, in particular, brain contusion. However, for a more detailed solution of the tasks set, it is advisable to take the concept of "damage to the optic nerve" beyond the scope of a brain contusion. This makes it possible to compare the degree of brain damage and ON, but not the severity of TBI and damage to ON, since the latter itself is an important component in determining the severity of TBI. The above judgment is valid for posterior optic nerve injuries. In the presence of anterior injuries of the ON, we will talk about contusion of the orbit combined with TBI.

Damage to the optic nerve can occur with TBI of varying severity: mild, moderate, and severe. The qualification of the severity of TBI, accompanied by damage to the ON, presents certain difficulties, due to the fact that the current classification of TBI does not provide for the dependence of the severity of TBI on the presence or absence of damage to the cranial nerves, and in particular, ON. Meanwhile, damage to the (posterior) ON can make some adjustments in determining the severity of TBI. In some cases, the symptoms of damage to the ON are the only focal manifestation of the trauma, and the clinical picture otherwise fits into the diagnosis of concussion. At the same time, craniography and CT of the brain do not reveal bone-traumatic injuries and changes in the density of the brain tissue. In isolated cases, TBI can be observed without loss of consciousness. However, in these cases, the clinical form of TBI, the degree of brain damage, should be assessed as mild brain contusion.

The severity of TBI, accompanied by damage to the optic nerve, should be determined taking into account the principle of mutual aggravation, which is shown in the diagram below.

GRADES OF SEVERITY OF TBI ACCOMPANIED BY DAMAGE TO THE OPTIC NERVE

In cases where there is a mild contusion of the brain and slight damage to the ON, the severity of TBI should be interpreted as mild. If there is severe damage to the ON, then according to the totality of the terms - mild brain contusion and severe damage to the ON, we should talk about moderate TBI. When determining the severity of TBI in patients with mild brain contusion and moderate damage to the ON, as well as in patients with moderate brain contusion and severe damage to the ON, it is necessary to take into account other factors (presence of subarachnoid hemorrhage, bone-traumatic changes, liquorrhea, pneumocephalus, etc.).

Optic nerve atrophy (optic neuropathy) is partial or complete destruction of nerve fibers that transmit visual stimuli from the retina to the brain. During atrophy, the nervous tissue experiences an acute lack of nutrients, which is why 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.

What is the optic nerve?

The optic nerve belongs to the cranial peripheral nerves, but in essence it is not a peripheral nerve, neither in origin, nor in structure, nor in function. This is the white matter of the cerebrum, pathways that connect and transmit visual sensations from the retina to the cerebral cortex.

The optic nerve delivers nerve messages to the area of ​​the brain responsible for processing and perceiving light information. It is the most important part of the whole process of converting light information. Its first and most significant function is to deliver visual messages from the retina to the areas of the brain responsible for vision. Even the smallest injury to this area can have serious complications and consequences.

Optic nerve atrophy according to ICD has ICD code 10

The reasons

The development of optic nerve atrophy is caused by various pathological processes in the optic nerve and retina (inflammation, dystrophy, edema, circulatory disorders, the action of toxins, compression and damage to the optic nerve), diseases of the central nervous system, general diseases of the body, hereditary causes.

There are the following types of disease:

• Congenital atrophy - manifests itself at birth or a short period of time after the birth of a child.
• Acquired atrophy - is a consequence of diseases of an adult.

Factors leading to optic nerve atrophy can be eye diseases, CNS lesions, mechanical damage, intoxication, general, infectious, autoimmune diseases, etc. Optic nerve atrophy appears as a result of obstruction of the central and peripheral retinal arteries that feed the optic nerve, and also it is the main symptom of glaucoma.

The main causes of atrophy are:

• Heredity
• congenital pathology
• Eye diseases (vascular diseases of the retina, as well as the optic nerve, various neuritis, glaucoma, retinitis pigmentosa)
• Intoxication (quinine, nicotine and other drugs)
• Alcohol poisoning (more precisely, alcohol surrogates)
• Viral infections (influenza)
• Pathology of the central nervous system (brain abscess, syphilitic lesion, skull trauma, multiple sclerosis, tumor, syphilitic lesion, skull trauma, encephalitis)
• Atherosclerosis
• Hypertonic disease
• Profuse bleeding

The cause of primary descending atrophy is vascular disorders with:

• hypertension;
• atherosclerosis;
• spinal pathology.

Lead to secondary atrophy:

• acute poisoning (including alcohol surrogates, nicotine and quinine);
• inflammation of the retina;
• malignant neoplasms;
• traumatic injury.

Atrophy of the optic nerve can be provoked by inflammation or dystrophy of the optic nerve, its compression or injury, which led to damage to the nerve tissues.

Types of disease

Atrophy of the optic nerve of the eye is:

• Primary atrophy(ascending and descending), as a rule, develops as an independent disease. Descending optic nerve atrophy is the most commonly diagnosed. This type of atrophy is a consequence of the fact that the nerve fibers themselves are affected. It is transmitted by recessive type by inheritance. This disease is linked exclusively to the X chromosome, which is why only men suffer from this pathology. It manifests itself in 15-25 years.
• Secondary atrophy usually develops after the course of a disease, with the development of stagnation of the optic nerve or a violation of its blood supply. This disease develops in any person and at absolutely any age.

In addition, the classification of forms of optic nerve atrophy also includes such variants of this pathology:

Partial atrophy of the optic nerve

A characteristic feature of the partial form of optic nerve atrophy (or initial atrophy, as it is also defined) is the incomplete preservation of visual function (vision itself), which is important with reduced visual acuity (due to which the use of lenses or glasses does not improve the quality of vision). Residual vision, although it is subject to preservation in this case, however, there are violations in terms of color perception. Saved areas in the field of view remain accessible.

Complete atrophy

Any self-diagnosis is excluded - only specialists with the proper equipment can make an accurate diagnosis. This is also due to the fact that the symptoms of atrophy have much in common with amblyopia and cataracts.

In addition, optic nerve atrophy can manifest itself in a stationary form (that is, in a complete form or a non-progressive form), which indicates a stable state of actual visual functions, as well as in the opposite, progressive form, in which the quality of visual acuity inevitably decreases.

Symptoms of atrophy

The main sign of optic nerve atrophy is a decrease in visual acuity that cannot be corrected with glasses and lenses.

• With progressive atrophy, a decrease in visual function develops over a period of several days to several months and may result in complete blindness.
• In the case of partial atrophy of the optic nerve, pathological changes reach a certain point and do not develop further, and therefore vision is partially lost.

With partial atrophy, the process of vision deterioration stops at some stage, and vision stabilizes. Thus, it is possible to distinguish progressive and complete atrophy.

Alarming symptoms that may indicate that optic nerve atrophy is developing are:

• narrowing and disappearance of visual fields (lateral vision);
• the appearance of "tunnel" vision associated with color sensitivity disorder;
• the occurrence of livestock;
• manifestation of the afferent pupillary effect.

The manifestation of symptoms can be unilateral (in one eye) and multilateral (in both eyes at the same time).

Complications

The diagnosis of optic nerve atrophy is very serious. At the slightest decrease in vision, you should immediately consult a doctor so as not to miss your chance for recovery. In the absence of treatment and with the progression of the disease, vision may disappear completely, and it will be impossible to restore it.

In order to prevent the occurrence of pathologies of the optic nerve, it is necessary to carefully monitor your health, undergo regular examinations by specialists (rheumatologist, endocrinologist, neurologist, ophthalmologist). At the first sign of visual impairment, you should consult an ophthalmologist.

Diagnostics

Optic nerve atrophy is a rather serious disease. In case of even the slightest decrease in vision, it is necessary to visit an ophthalmologist so as not to miss precious time for the treatment of the disease. Any self-diagnosis is excluded - only specialists with the proper equipment can make an accurate diagnosis. This is also due to the fact that the symptoms of atrophy have much in common with amblyopia and.

An examination by an ophthalmologist should include:

• visual acuity test;
• examination through the pupil (expand with special drops) of the entire fundus;
• spheroperimetry (accurate determination of the boundaries of the field of view);
• laser dopplerography;
• assessment of color perception;
• craniography with a picture of the Turkish saddle;
• computer perimetry (allows you to identify which part of the nerve is affected);
• video ophthalmography (allows you to identify the nature of damage to the optic nerve);
• computed tomography, as well as magnetic nuclear resonance (clarify the cause of the disease of the optic nerve).

Also, a certain information content is achieved to compile a general picture of the disease through laboratory research methods, such as a blood test (general and biochemical), testing for or for syphilis.

Treatment of atrophy of the optic nerve of the eye

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.

In the treatment of optic nerve atrophy, the following actions are performed:

1. Biogenic stimulants are prescribed (vitreous body, aloe extract, etc.), amino acids (glutamic acid), immunostimulants (eleutherococcus), vitamins (B1, B2, B6, ascorutin) to stimulate the restoration of altered tissue, as well as to improve metabolic processes are prescribed
2. Vasodilators are prescribed (no-shpa, diabazol, papaverine, sermion, trental, zufillin) - to improve blood circulation in the vessels that feed the nerve
3. Phezam, emoxipin, nootropil, cavinton are prescribed to maintain the work of the central nervous system.
4. To accelerate the resorption of pathological processes - pyrogenal, preductal
5. Hormonal drugs are prescribed to stop the inflammatory process - dexamethasone, prednisone.

Drugs are taken only as directed by a doctor and after an accurate diagnosis has been established. Only a specialist can choose the optimal treatment, taking into account concomitant diseases.

Patients who have completely lost their sight or have lost it to a significant extent are assigned an appropriate course of rehabilitation. It is focused on compensating and, if possible, eliminating all the restrictions that arise in life after suffering atrophy of the optic nerve.

The main physiotherapeutic methods of therapy:

• color stimulation;
• light stimulation;
• electrical stimulation;
• magnetic stimulation.

To achieve a better result, magnetic, laser stimulation of the optic nerve, ultrasound, electrophoresis, oxygen therapy can be prescribed.

The earlier treatment is started, the better the prognosis of the disease. Nervous tissue is practically unrecoverable, so the disease cannot be started, it must be treated in a timely manner.

In some cases, with atrophy of the optic nerve, surgery and surgery may also be relevant. According to research, the optic fibers are not always dead, some may be in a parabiotic state and can be brought back to life with the help of a professional with extensive experience.

The prognosis of optic nerve atrophy is always serious. In some cases, you can count on the preservation of vision. With developed atrophy, the prognosis is unfavorable. Treatment of patients with atrophy of the optic nerves, whose visual acuity was less than 0.01 for several years, is ineffective.

Prevention

Optic nerve atrophy is a serious disease. To prevent it, you need to follow some rules:

• Consultation with a specialist at the slightest doubt in the visual acuity of the patient;
• Prevention of various types of intoxication
• timely treat infectious diseases;
• do not abuse alcohol;
• monitor blood pressure;
• prevent eye and craniocerebral injuries;
• repeated blood transfusion for profuse bleeding.

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

Diseases of the optic nerve can be congenital and acquired, be inflammatory, degenerative, allergic. There are also tumors of the optic nerve and anomalies of its development.

Neuritis.

Acute inflammation of the optic nerve is called neuritis.

The reasons.
It can develop due to the introduction of microbes or viruses that can cause an inflammatory process (during the transition of inflammation from the membranes of the brain, eyeball, paranasal sinuses, teeth, after influenza, etc.), or exposure to neurotropic poisons.

Clinic.
The main symptom of acute optic neuritis is visual impairment up to blindness. In some cases, there is pain behind the eye. These pains are intermittent. They occur when the eye moves.

Diagnosis optic neuritis is diagnosed by an ophthalmologist by a characteristic inflammatory change in the nerve, which is visible when examining the fundus.

Emergency first aid if neuritis is suspected, the patient is sent to the hospital.

Treatment neuritis is carried out jointly by oculists and neuropathologists.

• Applies Etiotropic therapy (depending on the etiology of neuritis) in combination with anti-inflammatory and desensitizing:
  • antibiotics,
  • 40% solution of hexamethylenetetramine (urotropine) intravenously,
  • corticosteroids topically and orally,
  • diprazine (pipolphen),
  • diphenhydramine,
  • vitamins C, B.
• Detoxification:
  • 40% glucose solution intravenously,
  • spinal punctures,
  • blood transfusion.
• Dehydration:
  • magnesium sulfate intramuscularly,
  • furosemide (lasix),
  • calcium chloride intravenously,
  • diacarb (fonurite),
  • glycerin inside.
• Reflex therapy:
  • epinephrine-cocaine tamponade of the middle nasal passage,
  • epinephrine electrophoresis,
  • leeches, mustard plasters on the occipital region.

In severe cases, neuritis ends with atrophy of the optic nerve, which is accompanied by a persistent decrease in visual acuity and narrowing of the visual field.

Stagnant papilla (disc) of the optic nerve.

The reasons.
It develops as a result of increased intracranial pressure, which can be caused by tumors, brain abscess, inflammation of the meninges, skull injuries and cerebral aneurysms, liver and blood diseases.

Clinic.
Patients with congestive optic papilla rarely complain about the state of visual functions. Sometimes they note a short-term blurred vision or even a temporary complete loss of it. More often, patients pay attention only to the headache.

Diagnosis congestive nipple puts the ophthalmologist according to typical changes in the fundus (the disk is enlarged, protrudes into the vitreous body, its borders are blurred, hemorrhages are possible), very similar to neuritis, but with preserved visual functions.

Treatment It is aimed at lowering intracranial pressure and treating the underlying disease that caused the congestion.

visual atrophynerve.

The reasons.
It occurs as a result of inflammation or stagnation in the optic nerve and is always accompanied by a decrease in visual acuity up to blindness and narrowing of the boundaries of the visual field.

atrophy may be congenital and acquired as a result of damage to the central nervous system, with tumors, syphilis, brain abscesses, encephalitis, multiple sclerosis, skull trauma, intoxication, alcohol poisoning with methyl alcohol, etc.

Optic atrophy may be preceded by hypertonic disease and atherosclerotic vascular changes. Often, atrophy of the optic nerve is observed with quinine poisoning, beriberi, starvation. It can also develop in diseases such as obstruction of the central retinal artery and the arteries that feed the optic nerve, with uveitis, pigmentary retinal degeneration, etc.

Clinic.
The clinical picture of atrophy is always characterized by dilated pupils and an almost complete absence of their reaction to light, lack of tracking and fixation. The gaze of such patients is wandering. When examining the fundus of the eye, atrophy of the optic nerve is manifested primarily by blanching of the disc and narrowing of the arterial vessels. According to the state of the borders of the disk, optic nerve atrophy is divided into primary, or simple (the borders of the disk are clear), and secondary (the borders of the disk are smeared).

Treatment.

Optic nerve atrophy is treated by ophthalmologists and neuropathologists.

Apply vasodilators, vitamins, etc. .

• To the group vasodilators includes:
  • amyl nitrite,
  • nicotinic acid (subcutaneous injections of 1 ml of a 1% solution), santhinol nicotinate (complamin),
  • cinnarizine (stugeron),
  • but-shpa,
  • dibazole;
• Use intravenous infusions 10% sodium chloride solution, 40% glucose solution.
• Appoint adenosine triphosphoric acid (ATP), cocarboxylase, as well as vitamins - ascorutin, B „ B 6 and B 12.
• Useful 0.1% solution of strychnine nitrate and 1-2% solution of sodium nitrite under the skin of the temple.
• The use of tissue preparations according to Filatov is shown (in the form of subcutaneous injections preparations of aloe, FIBS, peat).
• Appoint pyrogenal, ginseng, eleutherococcus.
• Possible effect of application ultrasound, reflexology (acupuncture).

Thanks

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Diseases of the optic nerve

Neuritis

• pain with eye movements, and sometimes without them,
• decreased visual acuity,
• decreased color perception
• blind spot in the center
• narrowing of the area of ​​peripheral vision,
• fever,
• deterioration of vision after physical exertion, hot showers, baths or baths.

Toxic defeat

Damage to the optic nerve can lead to:

• methyl and ethyl alcohols,
• substances found in tobacco smoke
• lead,
• quinine,
• antihelminthic drugs.

With the use of methyl alcohol, toxic damage begins with nausea, vomiting, and sometimes loss of consciousness. Large doses of methyl alcohol can also be fatal. Visual disturbances occur a few hours after the use of methanol. In the optic nerve, an inflammatory process develops quite quickly, leading to atrophy of the optic nerves and death of nerve fibers.

Treatment of toxic damage to the optic nerve should begin with the termination of the further action of the toxin and the appointment of detoxification therapy to remove the hazardous substance from the body. Diuretics and anti-inflammatory drugs are prescribed to reduce swelling. In order to maintain the function of the optic nerve, drugs that improve the nutrition of the nervous tissue, as well as antioxidants and vitamins, are used.

neuropathy

There are the following types of neuropathies:

• compression ( nerve compression),
• ischemic ( disruption of oxygen delivery to the nerve),
• inflammatory,
• traumatic,
• radiation,
• congenital.

Optical neuropathy is manifested primarily by a violation of central vision. For early recognition, the following method is recommended: alternately closing your eyes, read small text or evaluate the intensity of colors, for example, on a TV screen.
Visual acuity in neuropathies is reduced, but is reversible. A weakened reaction of the pupil to light, a deterioration in light and color perception are also characteristic.

In the treatment of optic neuropathy, drugs are used that protect nerve fibers and improve their nutrition and blood supply, biostimulants, and physiotherapy methods. Sometimes operations are performed to reduce pressure on the optic nerve.

glioma

Surgical treatment of optic nerve glioma. The best results are achieved with surgical interventions at an early stage, when the tumor has not yet had time to spread into the cranial cavity.

Hypoplasia (underdevelopment)

Unfortunately, there are currently no truly effective methods of therapy for this pathology. Drugs that improve nerve nutrition, laser stimulation of the retina, transcutaneous electrical stimulation of the optic nerves and light stimulation are used.

Atrophy

Disorders of the circulation of aqueous humor in the eye (Glaucoma)

What is glaucoma?

Any glaucoma is characterized by a triad of symptoms: increased intraocular pressure, changes in the fundus and limited visual field.

In addition, there are also the following symptoms:

• blurred vision,
• pain, pain and a feeling of heaviness in the eyes,
• blurred vision at night,
• the appearance of "rainbow circles" when looking at a bright light.

congenital glaucoma

The basis of this pathology is a congenital anomaly of the eye, which creates obstacles and difficulties in the outflow of intraocular fluid, which leads to an increase in intraocular pressure.

Causes of congenital glaucoma in the fetus- various pathological conditions of a woman, especially in the first months of pregnancy:

• infections ( influenza, measles rubella, etc.),
• ionizing radiation, etc.

• increased intraocular pressure,
• lacrimation,
• photophobia,
• rapidly progressive increase in the size of the eyeball,
• an increase in the diameter of the cornea,
• corneal edema,
• slow pupil reactions
• changes in the optic disc.

Secondary glaucoma

Angle-closure glaucoma

Open angle glaucoma

Acute attack of glaucoma

• rapid loss of vision up to blindness,
• sharp pain in the eye and half of the head,
• vomit,
• corneal edema,
• pupil dilation,
• no pupillary response to light
• redness of the eye.

Glaucoma treatment

With closed-angle form, the method of removing the lens with the implantation of an intraocular lens is more often used.

Diseases of the oculomotor apparatus

Ophthalmoplegia

Ophthalmoplegia is divided into complete and partial. With complete, both external and internal muscles of the eye are affected. Partial ophthalmoplegia can be external, in which only the external muscles are paralyzed, and internal, in which only the internal muscles of the eye are paralyzed. With external ophthalmoplegia, the immobility of the eyeball is observed, and the reaction of the pupil to light is preserved. With the internal - the movements of the eyeball are preserved, but there is no reaction of the pupil to light, and convergence and accommodation are also disturbed.

In the treatment of ophthalmoplegia, the main emphasis is on the treatment of the underlying disease - it is necessary to eliminate the cause that caused ophthalmoplegia. In the primary form of ophthalmoplegia, vitamins of groups E and B, the introduction of prozerin and dibazol are also used.

Strabismus

The cause of this pathology can be:

• developmental defects, paralysis and damage to the oculomotor muscles,
• diseases of the nervous system,
• childhood infectious diseases
• head injury,
• nerve tissue tumors
• multiple sclerosis,
• wearing glasses with incorrect centering,
• long bang.

Ways to treat strabismus
1. Plenoptic therapy - increased visual load on the affected eye. In this case, various methods of stimulation are used with the help of a therapeutic laser and medical computer programs.
2. Orthoptic Therapy – treatment with the use of computer programs and synoptic devices that restore binocular vision.
3. Diplomatic therapy – restoration of stereoscopic and binocular vision in natural conditions.
4. Convergence trainer workouts is a method that improves convergence ( reduction to the nose) eye.
5. To surgical intervention resorted to in cases where conservative therapy is ineffective and does not give a result within 1.5 - 2 years. Surgery cures strabismus, but special exercises to restore normal eye function will still be needed.

It is wrong to assume that strabismus can go away by itself. Moreover, if left untreated, it threatens to develop serious complications. Therefore, an ophthalmologist should be consulted immediately after the appearance of its first signs.

Amblyopia

There are the following types of amblyopia, depending on the causes of its occurrence:
1. Anisometropic amblyopia develops with significant differences in the refractive power of the eyes.
2. obscurative, or deprivation, - is a consequence of the suppression of visual activity in one eye, which is caused by congenital anomalies such as cataracts or corneal clouding. This species is characterized by the persistence of reduced vision even after the elimination of opacification.
3. Dysbinocular amblyopia, which develops with strabismus: the brain, in order to suppress double vision, perceives information coming from only one eye.
4. Hysterical (psychogenic blindness) - occurs with hysteria, often in combination with other functional visual disorders ( violation of color perception, photophobia, narrowing of the field of view, etc.).
5. Refractive amblyopia can develop with untreated refractive errors that lead to blurry focusing of objects with one eye.

Therapy of the disease that underlies amblyopia should be started as early as possible. Amblyopia does not go away on its own, does not disappear as the child grows older, and in all cases requires treatment. In the treatment of amblyopia, several areas are usually involved: the elimination of strabismus, the correct correction of defects in the optical system of the eye, and the training of the amblyopic eye.

nystagmus

Bilateral nystagmus is much more common than unilateral. Depending on the direction of movement of the eyeballs, horizontal, vertical, rotational and diagonal nystagmus is distinguished.
This pathology can be congenital and be accompanied by a fairly strong decrease in visual acuity.

The cause of nystagmus almost always lies in various diseases of the areas of the brain that are responsible for eye movements and their coordination. In addition, nystagmus can develop with pathologies of the organ of balance and areas of the brain associated with its activity, in case of poisoning with drugs or narcotic substances.

Treatment of nystagmus lies in the treatment of the underlying disease, but pathological nystagmus is practically not amenable to complete cure. Symptomatically used vitamin therapy and antispasmodics, which can temporarily improve the condition.

Spasm of accommodation

Reasons for the development of accommodation spasm:

• poor illumination of the workplace;
• excessive eye strain computer, TV, doing homework in the evening);
• insufficient duration of night sleep, lack of walks in the fresh air and sports;
• discrepancy between the height of the chair and the desk height of the child;
• violation when reading the optimal distance to the book, which should be 30 - 35 cm;
• weakness of the back and neck muscles;
• circulatory disorders of the cervical spine;
• hypovitaminosis, malnutrition.

• feeling of pain and burning, redness of the eyes;
• eyes get tired quickly when working at short distances;
• near the picture becomes less clear, and far away the image blurs;
• sometimes there is double vision;
• the appearance of a headache, sometimes taken for age-related restructuring of the body.

Diseases of the orbit

exophthalmos

This condition occurs when:

• tumors of the orbit located behind the eyeball,
• tissue swelling,
• aneurysms and thrombosis of cerebral vessels,
• inflammatory processes in the orbit and paranasal sinuses,
• traumatic injuries of the eye.

enophthalmos

Refractive errors (ametropia)

Myopia

Myopia most often develops during school years, and in most cases is associated with prolonged work of the visual apparatus at close distances ( writing, reading, drawing). Such activity is especially dangerous in case of improper, insufficient lighting. In addition, the weakening of the eye muscles also contributes to the development of myopia.

Currently, there are 7 officially recognized methods for correcting myopia:

• wearing glasses,
• wearing contact lenses,
• laser vision correction ,
• lens replacement,
• lens implantation,
• radial keratotomy,
• corneal plastic.

If measures are not taken to correct myopia, then myopia can progress, which can lead to irreversible changes in the eye and significant loss of vision.

farsightedness

One of the types of this pathology is presbyopia - age-related farsightedness. With age, vision deteriorates more and more due to a decrease in the accommodative abilities of the eye - the elasticity of the lens decreases, and the muscles that hold it weaken. Therefore, presbyopia is diagnosed in almost all people over the age of 50 years.

Farsightedness can be corrected with glasses or contact lenses. In addition, laser eye surgery methods are also used in its treatment.

Astigmatism

In the treatment of astigmatism, special glasses with cylindrical glasses or contact lenses are used, since optical lenses of a spherical shape are not able to fully compensate for this defect. Also, on the recommendation of an ophthalmologist, surgical treatment can also be used.

Untreated astigmatism can lead to the development of strabismus and a sharp decrease in vision. In addition, uncorrected astigmatism often causes headaches and pain in the eyes.

Anisometropia

The treatment of anisometropia lies in the systematic application of correct and methodical exercises for the eyes. Therapy should be carried out under the mandatory supervision of an ophthalmologist.

asthenopia

• burning, stinging and pain in the eyes,
• marked increase in lacrimation,
• headache,
• feeling of general fatigue.

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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 RNP in the fundus reveals a pathology that fits into the pattern of CAS 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 vision 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 no 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 radiological 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 noticeable 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 a few hours or days after the 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.