Damaged optic nerve. Damage to the optic nerve. Less common causes of AD

The optic nerve (Nervus opticus) is the second pair of twelve cranial nerves. The optic nerve regulates all our activity: it transmits the image to the brain.

The optic nerve is highly sensitive. In the twenty-first century, inflammation of the optic nerve is common, and then damage to the optic nerve, which can lead to loss of vision. The optical apparatus of the eye is damaged. The damaged nerve will no longer function the way it used to. With timely treatment, the nerve can be saved, and its functions can be preserved.

The reasons

The causes of damage to the Nervus opticus (optic nerve) can be various diseases: meningitis, meningoencephalitis, etc. Violation in the functioning of the optic nerve reduces the quality of human life: the patient does not go anywhere because he does not see well. Also one of the main reasons is complications after vision correction surgery.

Signs of damage to the optic nerve

Symptoms occur due to inflammation of the sheaths of nerve fibers. These include: pain in the eyes, which increases with the movement of the eyeballs, edema, photopsia, and others.

The nerve can be affected partially or completely, if the nerve is partially affected, then the outcome of the disease will be favorable. Diseases in which the optic nerve is affected are acute. Clinical manifestations are rapidly growing. A consultation with a neurologist is required.

Patients stop seeing in the dark and are afraid of bright lights.

Symptoms increase and can lead to disability of the sick person (the person will go blind).

Symptoms may vary, depending on the cause of the disease.

Treatment

Treatment includes symptomatic and pathogenetic therapy. After the start of treatment, the patient urgently needs to be hospitalized.

Until the exact cause of the disease is found out, the person receives antimicrobial therapy. After identifying the cause, measures are taken to eliminate the source of infection (in the brain).

Treatment and restoration of the functions of the optic nerve includes the use of corticosteroids and "Prednisolone". Also, patients take "Diakarb", which relieves swelling.

"Panangin" is prescribed to reduce symptoms, nicotinic acid - to improve cerebral circulation. Patients need complete rest and vitamin therapy.

With treatment, the process (more often) does not resume and the person can continue to live his life!

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.

The nerve, called the abducens, plays a small regulatory role in the mobility of the eyes, takes it outward. These nerve fibers enter the oculomotor apparatus of the organ and, together with other nerves, control complex eye movements.

The eye can turn from side to side horizontally, make circular movements, move in a vertical direction.

Ophthalmoplegia is a disease that occurs as a result of damage to the optic nerves and is accompanied by paralysis of the eye muscles. This is a neurological pathology that limits the motor function of the eyeballs.

It can be due to many reasons: infectious diseases. head or eye injuries and poisoning.

The reasons

ZN plays a very important role in the human body. This is a special transmitter that moves signals from the retina to the brain. The optic nerve is made up of millions of fibers, which in total are 50 mm long. This is a very vulnerable, but important structure that can be easily damaged.

As already noted, the most common cause of damage to the optic nerve is head trauma. However, this is far from the only possible factor in the disruption of signal transport. This may be the problem of intrauterine development, when the fetus, under the influence of certain processes, has an incorrect formation of the organs of vision.

In addition, inflammation can lead to damage to the optic nerve, which can concentrate in the area of ​​​​the eyes or brain. Both stagnation and atrophy have a negative impact on the ON. The latter may have a different origin.

Most often, it becomes a complication after a traumatic brain injury. But sometimes atrophic processes in the eyes occur due to poisoning and severe intoxication of the body.

Ophthalmoplegia can occur with congenital or acquired lesions of the nervous system in the region of the nerve roots or trunks, in the area of ​​the nuclei of the cranial nerves. For example, congenital ophthalmoplegia occurs as a result of aplasia of the nuclei of the oculomotor nerves, and in some cases can be combined with changes in the eye muscles and aplasia of the nerve trunks. This pathology is often combined with malformations of the eyeball, can be observed in several members of the same family.

Ophthalmoplegia can also be a sign of such a rare disease as ophthalmoplegic migraine. It is manifested by attacks of severe headaches, accompanied by unilateral ophthalmoplegia (complete or partial). Headaches can last for a long time, while the function of the oculomotor nerves is gradually restored.

In addition, ophthalmoplegia may be a symptom of a rare ophthalmoplegic migraine. After the attack ends, the eye slowly returns to normal.

Oculomotor palsy can result from a number of different conditions. Paralysis of the oculomotor nerve with a non-traumatic middle pupil is often referred to as "medical third" (eng. medical third) for a similar effect on the pupil, known as "surgical third" (eng. surgical third).

The main causes of damage to the oculomotor nerve are:

• trauma;
• neuroinfectious diseases;
• brain tumors of various etiologies;
• pneurism of cerebral vessels;
• diabetes;
• stroke.

However, most often the causes of partial or complete damage to the nuclei or fibers of the oculomotor nerve remain only an assumption. It is impossible to establish them exactly. The human body is a very complex system, and not fully understood, but it is absolutely known that the disruption of one of its components along the chain transmits it to other organs, nerves and muscles.

For example, neuropathy of the oculomotor nerve in an isolated form is very rare and is most often a concomitant manifestation of chronic or congenital diseases, as well as the result of traumatic brain injuries and tumors. With proper and timely treatment, this disease can pass without complications and consequences.

If neuropathy of the oculomotor nerve is suspected, it is imperative to take a whole course of tests, including blood for the presence of neuroinfection in the body. Only after receiving the results and confirming the diagnosis, it is possible to prescribe a course of treatment and be sure to conduct repeated tests.

1. Diseases and damage to the nerve itself (its inflammation, ischemia, compression and swelling).
2. Volumetric processes in the brain tissue (tumor formations, hematomas, aneurysms, tuberculomas, cysts, abscesses).
3. CNS diseases (strokes, multiple sclerosis, inflammation of the meninges and brain tissues).
4. Head injuries (damage or compression of the optic nerve by bone fragments, hematomas).
5. Poisoning and intoxication (lead, chlorophos, carbon disulfide, alcohol, taking certain medications).
6. Pathologies of internal organs leading to vascular disorders ( arterial hypertension, diabetes mellitus, heavy bleeding, anemia, vasculitis, systemic lupus erythematosus, exhaustion, starvation, etc.).
7. Eye diseases (pathology of the retina, its detachment, dystrophy, damage to the retinal vessels, complications of uveitis, glaucoma, eye injuries).
8. Hereditary atrophy of the optic nerves.

Under the influence of the above factors, the destruction of the nerve fibers and their replacement with connective tissue, the desolation of the vessels supplying the nerve, develops. The causes of the disease are many, they can be combined with each other. It is not always possible to identify them.

Clinical picture

In severe forms of the disease, there may be a lack of activity and mobility of the eyeball, a deterioration in the reaction of the pupil to light and its immobility. If ophthalmoplegia develops against the background of other diseases, the clinical picture also includes additional symptoms.

The manifestations of the disease depend on the severity of the pathological process, the type of atrophy, and its localization. Progressive atrophy can lead to complete loss of vision.

Main symptoms:

1. Decreased visual acuity.

Visual acuity decreases significantly with the defeat of the papillomacular bundle. It practically does not change if only the peripheral part of the nerve is affected. If the lesion is combined, then the changes in vision are moderate.

1. Changing fields of view.

Loss of the central field of vision appears with atrophy of the papillomacular bundle. Damage to the optic chiasm and tracts contributes to bilateral blindness in half of the visual field. The narrowing of the peripheral boundaries of the visual field appears with the involvement of peripheral nerve fibers.

1. Violation of color perception (the perception of green and red colors suffers to a greater extent).

With an atrophic process, changes in the fundus may not correspond to the clinical picture. For example, with descending atrophy, the fundus of the eye remains unchanged for a long time with a pronounced decrease in vision. So, with multiple sclerosis, the optic disc is pale even with a slight deviation from the norm of visual acuity. In addition, if the initial visual acuity was greater than one, then its decrease to this level against the background of disc pathology can already indicate atrophic changes.

Types of atrophic lesions of the optic nerve

The eye is shifted in this case to the zone of action of a healthy or less pathologically affected muscle. The patient has difficulty moving the eyes towards the paralyzed muscles, resulting in double vision.

With complete external ophthalmoplegia, the eyeball is constantly in a static position, which leads to the development of ptosis. Partial internal ophthalmoplegia occurs due to the expansion of the non-reactive pupil.

When the first signs of the disease appear, it is recommended to immediately contact an ophthalmologist.

Ophthalmoplegia can be unilateral or bilateral. External ophthalmoplegia occurs with paralysis of the muscles that are outside the eyeball, and with paralysis of the intraocular muscles, internal ophthalmoplegia occurs. With varying degrees of muscle weakness in paralysis, partial internal or external ophthalmoplegia develops. If both the external and internal muscles of the eye are paralyzed at the same time, then complete ophthalmoplegia occurs. Complete external and complete internal ophthalmoplegia may also occur.

The eyeball with external partial ophthalmoplegia will lean towards a healthy or less paralyzed muscle, and its movement towards the action of the paralyzed muscles will be absent or significantly limited. In this case, doubling of objects will appear. The eyeball with external complete ophthalmoplegia will become immobile and ptosis will develop. Internal partial ophthalmoplegia is characterized only by dilation of the pupil in the absence of a reaction to light, a decrease in convergence and accommodation.

According to the degree of damage to the optic nerves, partial and complete ophthalmoplegia are distinguished. Partial can be external, in which the work of the oculomotor muscle of the eyelid is disrupted and internal, if only the nerve columns are affected by paralysis.

With the full form of the disorder, there is immobility of the eyeball and drooping of the upper eyelid, the inability of the pupil to respond to light.

This pathology can be primary (occurs with an unchanged optic disc) and secondary (develops against the background of inflammation or swelling of the disc), glaucomatous (appears with glaucoma). As well as ascending (the process starts from the disk) and descending (at the beginning, the peripheral neuron is affected). Depending on the severity of atrophy and the degree of color loss, initial, partial, complete atrophy is distinguished.

Provoking pathologies

The key reasons for the development of ophthalmoplegia are pathologies of the nervous tissues. The disease can be congenital or acquired.

The congenital form in most cases occurs with other pathologies in the structure of the eye, is included in the complex of symptoms of various genetic anomalies. There is a hereditary condition of the disease.

The disease can develop against the background of other infectious diseases - tuberculosis or syphilis, as well as tetanus, botulism and diphtheria.

Ophthalmoplegia can be a concomitant symptom of ophthalmoplegic migraine, a rare disease that causes severe headache attacks.

The pathology of the bones of the skull manifests itself in the form of stagnation of the optic disc, as well as nystagmus and divergent strabismus. The symptom of glasses indicates a fracture of the base of the skull. It is manifested by the presence of hemorrhages under the conjunctiva and the skin of the eyelids of both eyes. Perhaps the appearance of a symptom of the upper orbital fissure, which manifests itself in the form of total ophthalmoplegia, ptosis and exophthalmos, impaired sensitivity along the trigeminal nerve. Let us consider in more detail the eye symptoms in pathologies of the central nervous system.

Eye symptoms in cerebrospinal meningitis:

• retrobulbar optic neuritis;
• violation of the reaction of the pupils, more often paralytic immobility of one or both pupils;
• abducens nerve paralysis;
• descending optic nerve atrophy.

What eye symptoms are found in the development of meningitis?

Medical treatment

In order to reduce pain, relieve spasm and strengthen muscles, acupuncture, electrophoresis and phonophoresis with drugs are prescribed.

Damage to the brain tissue in syphilis and brain abscess, in addition to general specific symptoms, can be detected when examining the fundus. With a brain abscess, the following eye symptoms are characteristic:

• bilateral development of stagnation of the optic nerve head;
• the presence of hemianopsia;
• paralysis of the oculomotor and abducens nerves;
• violation of the reaction of the pupils in the form of mydriasis.

Abscess of the cerebellum is manifested by nystagmus. Brain abscess most often develops against the background of carious lesions of the teeth, that is, it has an odontogenic origin.

Brain syphilis has its eye symptoms:

• paralysis of the oculomotor nerve;
• internal unilateral ophthalmoplegia (mydriasis and accommodation paralysis);
• the presence of congestive discs and optic neuritis;
• homonymous hemianopsia.

Late neurosyphilis is manifested by Argyle Robertson's symptom, which looks like the disappearance of the pupillary reaction to light along with the preservation of convergence and accommodation. There is a reflex immobility of the pupils and anisocoria. With syphilis, the field of vision narrows with further loss of vision and paralysis of the oculomotor nerve.

Multiple sclerosis is manifested by certain eye symptoms:

• narrowing of the visual fields;
• emergence of central cattle;
• blanching of the temporal halves of the optic discs;
• horizontal nystagmus;
• remitting visual loss.

An attack of epilepsy is accompanied by constriction of the pupils, which expand at the height of clonic convulsions. The differential diagnostic sign is the absence of pupillary reaction to light. An epileptic attack is always accompanied by a deviation of the eyeballs to the side or upwards.

The development of a brain tumor is manifested by such eye symptoms:

• hemianopsia;
• with tumors of the skull and cerebellum, congestive discs of the optic nerves are observed;
• paralysis of the oculomotor muscles;
• neuritis or atrophy of the optic nerve;
• an attack of neuralgia and headaches with pain points, which are localized at the exit points of the branches of the trigeminal nerve;
• development of neuroparalytic keratitis.

Thus, at an appointment with an ophthalmologist and a neuropathologist, a preliminary diagnosis of damage to the nervous system can be made, which can improve the prognosis for the treatment of this pathology.

It is worth noting that an isolated violation of this nerve is very rare. Here are the main symptoms:

• immobility of the muscles of the upper eyelid and, as a result, its partial or complete omission;
• lack of resistance to the superior oblique and inferior rectus muscles, as a result of which divergent strabismus can be diagnosed;
• immobility of the internal rectus muscle and, as a result, the occurrence of the phenomenon double vision (diplopia);
• lack of pupillary response to light;
• violation of the innervation of the internal muscle and, as a result, the inability of the eye to adapt to objects located at different distances from it;
• lack of contraction of the rectus muscles of both eyes, which makes it impossible to turn the eyeballs inward;
• protrusion of the eyes due to loss of tone of the external muscles, this confirms that there was a lesion of the oculomotor nerve.

Most often, all of these symptoms are combined with concomitant manifestations that cause disruption of the functioning of friendly nerve fibers, nearby muscle groups and organs.

Diagnostics

Despite the presence of pronounced external signs, the following hardware studies are prescribed;

Therapy consists in eliminating the causes of the disease, alleviating the pain syndrome and restoring, if possible, nervous and muscular activity.

Physiotherapy methods

Diagnosis of the type of disease and the causes that cause it is necessary to select a treatment method.

The disease is diagnosed by the initial examination. It has pronounced external manifestations. To establish the nature of the disease and the causes, it is necessary to consult a neurologist and an ophthalmologist.

If neoplasms are detected, an additional consultation with an oncologist may be needed.

After receiving all the necessary data about the disease and determining the causes, treatment is prescribed. It is aimed at eliminating the factors that resulted in the development of ophthalmoplegia, the removal of pain and the maximum restoration of nervous and muscular activity.

Timely and accurate diagnosis is half the success and the secret to a speedy recovery. The ophthalmologist determines the occurrence of defects by checking:

• position of the eyeball, possible downward or outward deviation;
• in what position of the upper eyelid: the presence of ptosis;
• pupil reaction to light;
• the ability to focus, for this the doctor puts his finger to the patient's nose to see the reaction.

Based on the symptoms, the optometrist determines the approximate location where the failure occurred. Next, magnetic resonance imaging is prescribed, an x-ray examination of blood vessels to visualize the lesion and establish the nature of their origin.

Paralysis of the oculomotor nerve is not the only shutdown that causes muscle paresis. Research allows you to exclude other causes of deviation.

The newest method of study is superposition electromagnetic scanning. With the help of it, the time to determine the causes of the disease is significantly reduced.

If there is a suspicion of a violation of the function of the oculomotor nerve, it is possible to confirm or refute this, as well as to identify the real cause of the deviation, only by conducting high-quality professional diagnostics. Most often, this is done by an ophthalmologist, and only in some cases, if the diagnosis is in doubt, an additional consultation of a neurologist is prescribed.

Diagnosis and examination of the organs of vision is carried out on modern computer equipment, as well as by conducting a variety of specialized tests. As a result, after their complex implementation, the patient can be diagnosed.

Also, in addition to the standard procedures carried out to check the condition of the fundus, determine the quality of vision, eye mobility, identify pupil reactions to light, MRI and angiography are performed. If the etiology is not fully identified, and even if the damage to the oculomotor nerve is confirmed, constant monitoring of the patient is mandatory, as well as repeated examinations.

The diagnosis is based on the patient's complaints, a detailed study of the disease, taking into account past and existing diseases, examination and examination by an ophthalmologist. The specialist will determine the visual acuity and fields, conduct color testing and ophthalmoscopy, and measure intraocular pressure. Ophthalmoscopy occupies a special place among all studies, it is with its help that a doctor can assess the condition of the optic nerve head and blood vessels in the fundus.

Features of the ophthalmoscopic picture:

1. With primary atrophy, the disc has clear contours, is white with a bluish or gray tint, and the number of arteries that feed it decreases. The blanching of the disc depends on the severity of the process (at the beginning of the disease, the pallor is slight, at advanced stages it is completely white).
2. The secondary pathology is characterized by: a gray or dirty-gray optic disc with blurred contours, a vascular funnel, which is filled with connective tissue.
3. Glaucomatous atrophy is manifested by a pale disc with an excavation (deepening), which can cover the entire disc.

If necessary, an additional examination may be prescribed: blood and urine tests, biochemistry and blood sugar, computed tomography, MRI of the brain, angiography of retinal vessels, electrophysiological examination. Differential diagnosis is carried out with cataract, amblyopia.

Diagnosis and treatment

Recovery after paralysis takes a long time during the year. A well-known method of treatment is the use of physiotherapy - exposure to pulses of a low-frequency electromagnetic field, stimulation with electric current.

The method of treatment is with analgesic, anti-inflammatory, soothing effect. The disadvantage is that recovery is very slow, and in some cases does not occur at all.

The eye-occipital method of administering a drug (neuromidin) is also used to increase muscle contractility and influence connective muscle defects.

The method of using electrophoresis with a solution of 15% Neuromidin has proven itself well. The duration of the sessions is 15 minutes daily for 15 days. After the procedure is completed, it is recommended to lie down with your eyes closed for 10 minutes.

If the improvement and restoration of the efficiency of the abducens nerve is not observed after the treatment, and the lesion does not go away on its own, surgical intervention is used. The essence of the method is as follows: an injection of ultracaine is made under the conjunctiva, an incision is made in half a circle.

The upper external and lower direct nerves are split into two bundles along and the lower ones are sutured to the upper fibers. This allows you to rotate the eyeball by more than 15–20° already a day after the operation, in some patients up to 25°, binocular vision was restored in every fourth operated patient.

To alleviate the condition in violation of binocular vision, Fresnel prisms are used, which are attached to glasses. Prisms have different angles and are selected individually. Perhaps also the closure of one eye.

Most nerve diseases are associated with a violation of the central nervous system, so the treatment is prescribed accordingly. After past infections and successful treatment, nerve disorders are restored. In rare cases, when an inoperable tumor, serious injuries to the skull and the nerve itself, recovery may not occur.

In order to eliminate the problem with damage to the optic nerve, it is necessary to conduct a comprehensive diagnosis. Based on the data obtained and after identifying the main cause of the pathology, it will be possible to prescribe the correct treatment procedures.

It must be borne in mind that nerve damage is not an independent disease. This problem always has an additional cause that must be eliminated. Otherwise, you should not count on improving visual function.

Experts strongly recommend that at the first deterioration of vision immediately undergo a diagnosis and begin treatment. This is the only opportunity not to miss the moment when you can solve the problem with medication. Most often, therapeutic therapy is aimed at removing puffiness and reducing intracranial pressure.

Basically, to stimulate blood circulation in the brain and reduce edema, No-shpu, Papaverine, Eufilin or Galidol are prescribed. In addition, anticoagulants such as Ticlid and Heparin can be used. Vitamin complexes and biogenic stimulants have a positive effect.

However, if the optic nerve lesion was caused by a traumatic brain injury, the patient may need surgery. Without surgery, it is impossible to get rid of a pinched nerve. Also, the problem cannot be solved without surgery if the damage to the optic nerve is caused by pressure on the organs of vision by the tumor.

Any medications for damage to the optic nerve should be prescribed by a doctor only after a thorough examination of the patient. Self-treatment for such a complex problem as visual impairment due to trauma to the optic nerve is categorically unacceptable. You need to be very careful with folk remedies. Their reception may not give the desired result, and the time that could be spent on a full-fledged treatment will be lost.

The treatment of ophthalmoplegia consists of eliminating the causes of the disease, relieving pain, and restoring, as far as possible, muscle and nerve activity.

The earlier the disease is detected, the more likely it is to be successfully cured. Do not ignore visits to the doctor and try to recover on your own.

After establishing an accurate diagnosis - paresis of the oculomotor nerve, the patient remains under the supervision of a specialist. In special cases, a second examination is scheduled to eliminate the possibility of an error. In the vast majority of cases, the treatment of optic nerve paresis gives a positive trend.

At the first suspicion, sometimes even before the final diagnosis is made, the doctor recommends special exercises to strengthen the muscles. The doctor has the right to prescribe taking vitamins and medicines, wearing bandages, glasses, viewing stereo images.

Such things have a healing effect, stimulating the affected eye to active work, improving blood circulation and increasing the tone of the eye muscles. Within six months, there is a complete recovery of mobility. If there is no improvement, then an operation is performed: ptosis is surgically eliminated. But there is a high probability of exposure of the cornea of ​​​​the eye.

Involving folk methods in treatment will not be superfluous, the main thing is to consult a doctor for contraindications and possible individual intolerance. In the reviews they write a lot about decoctions of herbs: garden marjoram, chamomile, wild rose, black elderberry, tannic sumac, evading peony.

You should not assign alternative medicine a major role in the treatment of neuritis. It is here only as an auxiliary element, more suitable for the prevention of the disease.

This is very important, because timely detection of the further progression of the disease, as well as constant monitoring of the treatment prescribed by the doctor, are of great importance for the entire condition of the eye and all further human life. For example, neuritis of the oculomotor nerve in most cases has a positive trend if the patient complies with all prescriptions, but treatment is carried out only with the constant supervision of specialists.

Science does not stand still, and recently one of the innovative diagnostic methods is superposition electromagnetic scanning of the oculomotor muscles to assess their functional activity. Thanks to this method, the time allotted for identifying the cause of the disorder is significantly reduced, and it becomes possible to start treatment much faster and achieve positive results.

As soon as there is a suspicion of a possible violation of the functions of the oculomotor nerve, the patient is immediately recommended to do exercises to strengthen the muscle responsible for the movement of the organs of vision. Of course, trying to strengthen it as much as possible is not bad at all, and not only when problems appear, but even for prevention, but this is only suitable at the very beginning of the violation. If a fairly large part is already affected, these exercises will not help to heal, although they are still an integral part of the treatment.

The next most common recommendation is to take the appropriate vitamins and medications, the action of which is also aimed at strengthening the eye muscle and restoring its work. These can be special vitamins, eye drops, glasses, dressings that make the sore eye work more actively.

Special computer programs are very popular today. Basically, these are the so-called stereo images.

It has been proven that when viewing such pictures, the eye muscles are trained, and, accordingly, blood circulation in them improves. At this time, the nerves responsible for the normal functioning of the eye are in an increased state of tension, and all the reserves of the body are aimed at controlling them, because most of the other organs at the time of viewing are in a relaxed state and do not require such attention.

Stereo pictures do have a very positive result on vision, but they can be used only after consulting a doctor. After all, in some cases they are just a panacea, and in others they can cause irreparable harm.

If, after several complementary diagnostics, it is confirmed that the oculomotor nerve is affected, treatment should begin without delay. One of the positively proven and used in practical ophthalmology for several years now is the treatment with electrophoresis of the affected areas of 1.5% Neuromidin.

It is carried out by applying three round electrodes of different area, two smaller of which are placed on the skin of the orbital region and upper eyelids with closed eyes. They are connected with a forked wire to an electrode of a larger area, which is placed in the cervical-occipital region of the patient's head.

The duration of this procedure with a course of treatment up to 15 sessions carried out daily is 15-20 minutes. The method allows to locally and purposefully influence the defective neuromuscular synapses of the eyeball, as well as the nuclear structures of the oculomotor nerves.

Therapy for optic nerve atrophy directly depends on the cause of its cause. It should begin as early as possible, when it is still possible to stop the process, since changes in atrophy are irreversible. If the cause can be eliminated, then the chances of preserving vision increase. When the nerve is compressed, the treatment is primarily surgical.

Physiotherapy methods

• Ultrasound on an open eye;
• ultraphonophoresis on the eye area with proteolytic enzymes;
• magnetotherapy;
• electrical stimulation of the optic nerves;
• medicinal endonasal electrophoresis with vasodilators (nicotinic acid, drotaverine);
• medicinal electrophoresis on the eye through a bath with potassium iodide, lidase, chymotrypsin;
• laser therapy.

Exposure to physical factors increases the effectiveness of the therapy, stimulates the optic nerves, increases the likelihood of restoration of visual function, provided that treatment is started in a timely manner.

Preventive measures

Ophthalmoplegia can develop against the background of other neurological diseases. A complete preventive examination should be carried out 2 times a year in order to identify them in time and begin treatment.

5-07-2013, 16:28

Description

Inflammatory (neuritis);

Vascular (ischemia of the optic nerve);

Degenerative (atrophy);

There are descending (retrobulbar) neuritis, when the inflammatory process is localized on any part of the optic nerve from the chiasm to the eyeball, and ascending neuritis (papillitis), in which the intraocular and then the intraorbital part of the optic nerve is involved in the inflammatory process.

When the optic nerve is damaged, there are always functional disorders in the form of a decrease in central vision, a narrowing of the visual field, and the formation of absolute or relative scotomas. Changes in the visual field to white and other colors are one of the early symptoms of optic nerve damage.

With a pronounced lesion of the fibers of the optic nerve, amaurotic immobility of the pupil is noted. The pupil of the blind eye is somewhat wider than the pupil of the other, seeing eye.

In this case, there is no direct and indirect (friendly) reaction of the pupil to light is preserved. On the seeing eye, a straight line is preserved, but there is no friendly reaction of the pupil to light. The pupillary response to convergence is preserved.

According to the nature of the lesion and clinical manifestations, diseases of the optic nerve are divided into inflammatory (neuritis), vascular (ischemia of the optic nerve), specific (tuberculous, syphilitic), toxic (dystrophic), tumor associated with damage to the optic nerve, anomalies in the development of the optic nerve, lesions, associated with impaired circulation of cerebrospinal fluid in the sheaths of the optic nerve (congestive disc), atrophy of the optic nerve.

To study the morphological and functional state of the optic nerves, clinical, electrophysiological and radiological research methods are used. Clinical methods include the study of visual acuity and field of view (perimetry, campimetry), contrast sensitivity, critical frequency of flicker fusion, color perception, ophthalmoscopy (in direct and reverse form), ophthalmochromoscopy, as well as fluorescein angiography of the fundus, ultrasound examination of the eye and orbit, Dopplerography vessels of the basin of the internal carotid artery (ophthalmic and supratrochlear arteries).

From electrophysiological methods, the study of electrical sensitivity and lability of the optic nerve (ECiL) and the recording of visual evoked potentials (VEP) are used.

X-ray methods for examining the optic nerve include plain radiography of the skull and orbit (face and profile images), examination of the bone canal of the optic nerve, computed tomography and magnetic resonance imaging.

In case of optic nerve disease, comprehensive studies are required with the advice of a general practitioner, neuropathologist, otolaryngologist and other specialists.

INFLAMMATORY DISEASES OF THE OPTIC NERVE

There are more than two hundred different reasons that cause manifestations of the clinical picture of optic neuritis. The clinic has adopted a rather conditional division of neuritis into two groups: intraocular intrabulbar (papillitis) and retrobulbar. Papillitis is characterized by a sharp violation of the function of the papillary system of the hematoophthalmic barrier. With an intrabulbar process (papillitis), the dynamics of the clinical picture is well defined ophthalmoscopically. With retrobulbar neuritis in the diagnosis, the main thing is the symptomatology of visual disturbances and their careful identification, and the ophthalmoscopic picture of the fundus can remain normal for quite a long time.

The main form of retrobulbar neuritis is axial (axial) neuritis, in which the papillomacular bundle is affected. The leading symptom in axial neuritis is the central scotoma, which manifests itself as a relative or absolute scotoma in white or only in red and green.

The optic disc is a small part of a closed system, which is the eyeball, in particular the cavity of the eye. The optic disc is the only part where it is possible to visually observe the state of the anterior end of the optic nerve. Therefore, it is customary to subdivide inflammation of the optic nerve into:

• intrabulbar (papillitis);
• retrobulbar;

Retrobulbar inflammatory diseases of the optic nerve include ophthalmoscopically invisible processes in the initial stage of development.

According to the topographic location, they distinguish:

• orbital;
• intracanalicular;
• intracranial lesions;

The main signs of optic neuritis consist of the appearance of inflammatory exudate, edema, compression of nerve fibers by edema and toxic effects of exudate on them. This is accompanied by small cell lymphoid infiltration and proliferation of neuroglia. In this case, the myelin sheaths and axial cylinders of the optic fibers undergo dystrophy, degeneration and subsequent atrophy. Human optic nerve fibers do not have any regenerative ability. After the degeneration of the nerve fiber (axon), the death of its maternal retinal ganglion cell occurs. When establishing the diagnosis of optic neuritis, it is necessary to urgently use drugs aimed at suppressing the inflammatory process in the affected area of ​​the optic nerve, reducing tissue edema and capillary permeability, limiting exudation, proliferation and destruction.

Treatment of patients with optic neuritis should be urgent in a hospital and directed against the underlying disease that caused neuritis. In recent years, two stages have been outlined in the tactics of treating neuritis: the first stage is the immediate provision of assistance until the etiology of the process is clarified; the second stage - carrying out etiological treatment after establishing the cause of the disease.

Intrabulbar ascending neuritis (papillitis) of the optic nerve

The reason is brucellosis, syphilis, etc.), focal infections (tonsillitis, sinusitis, otitis media, etc.), inflammatory processes in the inner membranes of the eye and orbit, general infectious diseases (blood diseases, gout, nephritis, etc.). With ascending neuritis, the intrabulbar part of the optic nerve (disc) first suffers. In the future, with the spread of the inflammatory process, the retrobulbar part of the optic nerve is affected.

The clinical picture depends on the severity of the inflammatory process. With mild inflammation, the optic disc is moderately hyperemic, its boundaries are indistinct, the arteries and veins are somewhat dilated. A more pronounced inflammatory process is accompanied by a sharp hyperemia of the disc, its borders merge with the surrounding retina. Exudative foci appear in the peripapillary zone of the retina and multiple small hemorrhages, arteries and veins moderately expand. Usually, the disc does not prominate with neuritis. The exception is cases of neuritis with edema.

The main distinguishing feature of optic nerve papillitis from a congestive disc is the lack of protrusion of the disc above the level of the surrounding retina. The appearance of even single small hemorrhages or exudative foci in the disc tissue or the surrounding retina is a sign of optic nerve papillitis.

Papillitis is characterized by an early violation of visual functions - a decrease in visual acuity and a change in the visual field.

The decrease in visual acuity depends on the degree of inflammatory changes in the papillomacular bundle. Usually there is a narrowing of the boundaries of the field of view, which may be concentric or more significant in one of the areas. Central and paracentral scotomas appear. The narrowing of the peripheral boundaries of the visual field is often combined with scotomas. Also characteristic is a sharp narrowing of the field of vision for red and a violation of color perception. There is a decrease in electrical sensitivity and lability of the optic nerve. Dark adaptation is impaired. When neuritis passes into the stage of atrophy, the disc turns pale, the arteries narrow, exudate and hemorrhages resolve.

Treatment should be timely (early) in a hospital setting. When the cause is clarified, the underlying disease is treated. In cases of unclear etiology, broad-spectrum antibiotic therapy is indicated. Ampiox is used 0.5 g 4 times a day for 5-7 days, ampicillin sodium salt 0.5 g 4 times a day for 5-7 days, cephaloridine (ceporin) 0.5 g 4 times a day within 5-7 days, gentamicin, netromycin. Fluoroquinolone preparations are also used - maxakvin, tarivid. Be sure to use vitamins: thiamine (B,) and nicotinic acid (PP). Enter intramuscularly 2.5% solution of thiamine 1 ml daily, for a course of 20-30 injections, 1% solution of nicotinic acid 1 ml daily for 10-15 days. Inside give vitamin B2 (riboflavin) 0.005 g 2 times a day, ascorbic acid (vitamin C) 0.05 g 3 times a day (after meals). Dehydration therapy is indicated: intramuscularly injected with a 25% solution of magnesium sulfate, 10 ml, intravenously - 10% solution of calcium chloride, 10 ml, inside - diacarb, 0.25 g 2-3 times a day, after 3 days of admission, take a break of 2 days; indomethacin 0.025 g. Corticosteroids are used to reduce inflammation. Dexamethasone is given orally at 0.5 mg (0.0005 g), 4-6 tablets per day. After the condition improves, the dose is gradually reduced, leaving a maintenance dose of 0.5-1 mg (0.0005-0.001 g) per day for 2 doses after meals. Retrobulbarno injected 0.4% solution of dexamethasone (dexazone) 1 ml per day for a course of 10-15 injections.

Retrobulbar descending optic neuritis

Significant difficulties arise in determining the etiology of retrobulbar neuritis. About half of them are with an unexplained cause. Retrobulbar neuritis often occurs with multiple sclerosis, optomyelitis, and diseases of the paranasal sinuses. The most common causes of neuritis are basal leptomeningitis, multiple sclerosis, paranasal sinus disease, viral (influenza) infection, etc. Sometimes retrobulbar neuritis is the earliest sign of multiple sclerosis. The group of retrobulbar neuritis includes all descending neuritis (regardless of the condition of the optic disc). Compared to inflammation of the optic nerve head (papillitis), inflammation of the optic nerve trunk is observed much more often and manifests itself in the form of interstitial neuritis.

With retrobulbar neuritis, inflammation is localized in the optic nerve from the eyeball to the chiasm.

Cases of primary inflammation of the optic nerve in its orbital part are relatively rare.

Retrobulbar neuritis most often develops in one eye. The second eye becomes ill some time after the first. Simultaneous disease of both eyes is rare. There are acute and chronic retrobulbar neuritis. Acute neuritis is characterized by pain behind the eyeballs, photophobia and a sharp decrease in visual acuity.

In a chronic course, the process increases slowly, visual acuity decreases gradually. According to the state of visual functions (visual acuity and visual field), all descending neuritis is divided into axial neuritis (lesion of the papillomacular bundle), perineuritis and total neuritis.

With ophthalmoscopy at the beginning of the disease with retrobulbar neuritis, the fundus may be normal. The optic disc is normal or more often hyperemic, its boundaries are indistinct. For retrobulbar neuritis is characterized by a decrease in visual acuity, the definition in the field of view of the central absolute scotoma on white and colored objects. At the beginning of the disease, the scotoma is large; later, if visual acuity increases, the scotoma decreases, becomes relative, and disappears with a favorable course of the disease. In some cases, the central scotoma passes into the paracentral annular. The contrast sensitivity of the organ of vision decreases. The disease can lead to descending atrophy of the optic nerve head. Paleness of the optic disc can be different in the degree of distribution and intensity, more often there is a blanching of its temporal half (due to damage to the papillomacular bundle). Less often, with a diffuse atrophic process, a uniform blanching of the entire disc is observed.

Treatment of retrobulbar neuritis depends on the etiology of the inflammatory process and is carried out according to the same principles as the treatment of patients with papillitis. The prognosis for retrobulbar neuritis is always serious and depends mainly on the etiology of the process and the form of the disease. With an acute process and timely rational treatment, the prognosis is often favorable. In chronic course - the prognosis is worse.

VASCULAR DISEASES OF THE OPTIC NERVE

Acute obstruction of the arteries supplying the optic nerve

Vascular pathology of the optic nerve is one of the most difficult problems in ophthalmology due to the extreme complexity of the structural and functional structure and arteriovenous circulation in various parts of the optic nerve. There are two main forms of vascular lesions of the optic nerve: arterial and venous. Each of these forms can occur as an acute or chronic disease. Vascular diseases of the optic nerve are polyetiological disease processes.

The etiology of ischemia - thrombosis, embolism, stenosis and obliteration of blood vessels, protracted spasms, violations of the rheological properties of blood, diabetes mellitus. Basically, these are elderly patients with general vascular diseases, with severe atherosclerosis and hypertension.

Pathogenesis: At the heart of the pathogenesis are violations (decrease) of blood flow in the vessels that feed the optic nerve. Ischemic neuropathy of the optic nerve is a lack of blood supply to the nerve tissue, a decrease in the number of functioning capillaries, their closure, a violation of tissue metabolism, an increase in hypoxia and the appearance of underoxidized metabolic products (lactic acid, pyruvate, etc.).

A. ANTERIOR ISCHEMIC NEUROPATHY OF THE OPTIC NERVE

In the pathogenesis of anterior ischemic optic neuropathy, the main factors are stenosis or occlusion of the arterial vessels that feed the optic nerve, and the resulting imbalance between the perfusion pressure in these vessels and the level of intraocular pressure. The main role is played by circulatory disorders in the system of the posterior short ciliary arteries. There is a rapid (within 1-2 days) decrease in vision up to light perception. Central scotomas appear in the field of view, more often the lower half of the field of view falls out, less often sector-like drops out are observed in the field of view. These changes occur more often in elderly patients due to spasm or are of an organic nature (atherosclerosis, hypertension, endarteritis, etc.).

At the very beginning of the disease, the fundus of the eye may be unchanged, then on the 2nd day there is an ischemic edema of the optic nerve head and a cotton wool-like edema of the retina around it. The arteries are narrowed, in places in the edematous retina (in the area of ​​the disc or around it) are not defined. The area of ​​the yellow spot is not changed. Subsequently, the edema of the optic disc decreases, the disc becomes paler. By the end of the 2-3rd week of the disease, atrophy of the optic nerve of varying severity occurs. Due to the rapid deterioration of visual acuity, early treatment is necessary.

Diagnosis of anterior ischemic neuropathy is facilitated by Dopplerographic detection (about 40% of cases) of stenosing lesions of the carotid arteries using laser Dopplerography, it is possible to determine capillary circulation disorders in the optic nerve head.

Treatment: Urgent hospitalization. Immediately after the diagnosis is established, vasodilators, thrombolytic drugs and anticoagulants are prescribed. Give a tablet of nitroglycerin (0.0005 g). 5-10 ml of a 2.4% solution of aminophylline are injected intravenously together with 10-20 ml of a 40% glucose solution daily, 2-4 ml of a 2% solution of no-shpa (slowly!), 15% solution of xanthinol nicotinate (complamin) - 2 each ml 1-2 times a day (introduced very slowly, the patient is in the supine position). Retrobulbar administration of 0.3-0.5 ml of 0.4% dexazone solution, 700-1000 IU of heparin, 0.3-0.5 ml of 1% emoxipine solution is shown.

During the development of edema of the optic nerve head, patients must be prescribed thiazide 0.05 g 1 time per day before meals for 5-7 days, followed by a break of 3-4 days, furosemide 0.04 g 1 time per day, brinaldix 0 02 g 1 time per day, 50% solution of glycerin at the rate of 1-1.5 g / kg, ethacrynic acid 0.05 g each. Treatment is continued for 1.5-2 months. Patients should be consulted by a general practitioner and a neurologist

B. POSTERIOR ISCHEMIC NEUROPATHY OF THE OPTIC NERVE

Posterior ischemic optic neuropathy occurs mainly in the elderly and occurs against the background of general (systemic) diseases such as hypertension, atherosclerosis, diabetes mellitus, collagenosis, etc. As with anterior ischemic neuropathy, the main factor in the development of this disease is narrowing , stenosis, spasm or occlusion of arterial vessels supplying the posterior optic nerve. Ultrasound dopplerography in such patients often detects stenosis of the internal and common carotid arteries.

The disease begins acutely. Patients complain of a sharp decrease in visual acuity. Various defects are determined in the field of view: sectoral loss mainly in the lower nasal region, concentric narrowing of the fields. Ophthalmoscopic examination during this period does not reveal any changes in the optic nerve head.

Diagnosis of the disease is helped by electrophysiological studies that reveal a decrease in electrical sensitivity and lability of the optic nerve and an increase in the time it takes the nerve impulse to travel along the optic pathway.

Doppler studies of the carotid, ophthalmic and supratrochlear arteries often reveal changes in blood flow parameters in these vessels. After 4-6 weeks, pallor of the optic disc begins to appear in the sector that corresponds to the dropped out area in the field of view. Then, simple descending atrophy of the optic nerve gradually develops. Excavation of the optic disc in this pathology is not detected.

This pathology presents great difficulties for early diagnosis. It is much less common than anterior ischemic neuropathy. In this case, to some extent, venous circulation in the optic nerve is disturbed. This process is in most cases one-sided.

Treatment is similar to that for anterior ischemic neuropathy. Despite the treatment, visual acuity often remains low, and patients have persistent defects in the field of vision - absolute scotomas.

Article from the book: .

Optic nerve atrophy (synonym: optic neuropathy) is an organic damage to the optic nerve, characterized by irreversible processes in its parenchyma and often leading to incurable visual impairment, including complete blindness. The definition of "atrophy" is outdated and is not recommended for use in modern ophthalmology. The process of atrophy implies a violation of the cellular structure of the organ with the possible reversibility of pathological processes. This phenomenon is not correct in relation to the optic nerve. In relation to damage to this organ, the term "optic neuropathy" is recommended.

Anatomy and physiology of the optic nerve

The optic nerve belongs to the second pair of cranial nerves, which ensures the transmission of bioelectric potentials generated by the retina from the light spectrum of exposure to the occipital region of the brain, which organizes the mental perception of these signals.

Optic nerve its structure is somewhat different from other pairs of cranial nerves. Its fibers with their neural structure are more consistent with the parenchyma of the white matter of the brain. This feature provides an unhindered and very high speed of transmission of bioelectric impulses.

The path of the optic nerve starts from retinal ganglion cells - neurons of the third type, a bundle of which is collected in the so-called papilla of the optic nerve, located in the region of the posterior eye pole, forming the optic disc. Subsequently, the common bundle of optic fibers passes through the sclera and, overgrown with meningeal tissue, resembling the tissues of the meninges in its structure, merges into a single optic trunk. The optic nerve contains about 1.2 million individual fibers.

Between the bundles of nerve fibers of the optic nerve is the central retinal artery, together with the vein of the same name, which provide nutrition to all the structures of the organ of vision of the corresponding side. The optic nerve enters the cranial cerebral space through the optic opening located under the lesser wing of the sphenoid bone, after which chiasma - a rather unique anatomical feature characteristic of all representatives of the living world with bipolar vision.

Chiasma or optic chiasm , is an area of ​​incomplete intersection of nerve fibers within one optic nerve, located at the base of the brain, under the hypothalamus. Thanks to the chiasm, part of the image entering the nasal part is transmitted to the opposite side of the brain, and the second part, from the temporal region of the retina, to the same side.

As a result, visual information from one eye, divided into two halves, is processed by different sides of the brain. This phenomenon gives the effect of combining the sides of vision - each half of the field of view of one eye is processed by one half of the brain. The right halves of the right and left eyes are processed by the left side of the brain, and the left halves of both eyes are processed by the right. This unique phenomenon allows you to look at the same point with both eyes without the effect of a split image.

After decussation, each half of the optic nerve continues its path, bending around the cerebral stalk from the outside, dissipates in the primary visual centers of the subcortex, located in the thalamus. In this place, the primary processing of visual impulses occurs and pupillary reflexes are formed.

Further, the optic nerve reassembles into a bundle - the central visual pathway (or Graziola's visual radiance), passes to the internal capsule and impregnates the visual region of the cortex of the cerebral hemispheres of the occipital lobe of its side with individual fibers.

Etiology of the disease and classification - causes of optic nerve atrophy

Considering the complex anatomical structure of the optic nerve and the high physiological loads placed on it by nature, the organ is very delicate in relation to various pathological disorders that may occur in its environment. And this causes quite a wide range of reasons contributing to its possible damage.

Ischemic optic neuropathy

Pathology occurs due to insufficient blood flow to the fibers of the optic nerve, which inevitably leads to malnutrition of its neurons. The anterior part of the optic nerve, up to the optic disc, is fed by the ciliary arteries of the choroid, while the posterior part is fed by branches of the ophthalmic, carotid, and anterior cerebral arteries. Depending on the localization of malnutrition of the optic nerve, there are several varieties of its ischemic neuropathies.

Anterior ischemic optic neuropathy

Pathology limited to the area of ​​the optic nerve papilla, which often leads to disc edema. Often the primary causes of anterior ischemic neuropathy are inflammation of the arteries that feed this part of the optic nerve.

• Giant arteritis.
• Nodular polyarteritis.
• Hurg-Strauss syndrome.
• Wegener's granulomatosis.
• Rheumatoid arthritis.

This type of ischemic neuropathy often occurs in people over the age of 50.

Posterior ischemic optic neuropathy

More common without manifestation of pathological phenomena in the region of the optic disc. In addition, it practically does not manifest itself due to the pathology of the blood vessels that feed the optic nerve in its back. This phenomenon is due to a large number of vessels, which provides sufficient compensatory replacements.

Often the cause of posterior optic neuropathy is atrophic phenomena of the nerve trunk due to the genetic predisposition of patients to this type of pathology. This process is due to the suppression of the nutritional functionality of individual neurons, followed by the generalization of inflammatory processes.

Posterior ischemic optic neuropathy does not depend on the age of the patient, in addition, it may be congenital. Modern ophthalmology has data on the dependence of the development of posterior ischemia of the optic nerve on a number of factors.

• Hypotension.
• Operations on the cardiovascular system.

Radiation optic neuropathy

An organic lesion of the optic nerve of a dystrophic type, characterized by an extremely slow course of pathological processes as a result of exposure to an increased level of radiation or radiation therapy. The average period from the onset of radiation exposure to the appearance of clinical signs of neuropathy is about 1.5 years, the maximum period known to science is 8 years.

The pathological process in radiation visual neuropathy is initiated by the destructive effect of gamma rays on the outer shell of neurons, which reduces its trophic properties.

pathological process, characterized by the development of inflammatory processes in the parenchyma of the optic trunk. Organic destruction of neurons is initiated by edema and destruction of myelin formations, which have protective functions for nerve fibers, due to their inflammatory destruction.

In addition to direct demyelination of the optic nerve trunk, other etiological factors that destroy its myelin sheaths can be:

• progressive meningitis;
• inflammation of the contents of the orbit;
• inflammation of the canals of the posterior ethmoid cells.

Until the beginning of the 21st century, it was believed that the primary causative factors of optic neuritis were the destruction of the myelin sheaths. However, histopathological studies conducted in the 2000s made it possible to judge about the primacy of destruction of neurons of the optic nerve, followed by the transition to myelin. It should be noted that to date, the genesis of this approach has not been studied enough.

Compression of the optic nerve

Organic damage with subsequent destruction of optic nerve neurons is caused by banal compression of the nerve trunk by pathological formations in the orbital region and less often in the optic canal. These pathologies often cause swelling of the optic disc, which causes a partial loss of visual functions in the early stages of the disorder. Such formations can include various types and degrees of complications.

• Gliomas.
• Hemangiomas.
• Lymphangiomas.
• Cystic formations.
• Carcinomas.
• Orbital pseudotumor.
• Some disorders of the thyroid gland that determine the development of pathological processes in the orbital region, for example, ophthalmopathy of the thyroid gland.

Infiltration optic neuropathy

Destructive changes in the neurons of the optic nerve are caused by infiltration into its parenchyma of foreign bodies, usually of an oncological structure or an infectious nature. Formed on the surface of the optic nerve, atypical neoplasms grow with their roots into the interfiber spaces of the nerve trunk, thereby causing irreparable damage to its functionality, and contributes to an increase in size.

Other reasons Infiltration of the optic nerve trunk can be progressive effects of opportunistic fungi, viruses and bacteria that have penetrated into the peripheral regions of the optic nerve. The creation of favorable conditions for their further development (for example, a cold factor or a decrease in immune defense) provokes their transition to a pathogenic state with a subsequent increase in the population area, including in the interfiber spaces of the nerve.

Traumatic optic neuropathy

The traumatic effect on the optic nerve can be direct or indirect.

• Direct exposure is due to direct damage to the optic nerve trunk. This phenomenon is observed with bullet wounds, erroneous actions of a neurosurgeon, or with craniocerebral injuries, of moderate and high severity, when fragments of the bones of the skull physically damage the parenchyma of the optic nerve.
• Indirect factors include injuries formed at the time of blunt trauma to the frontal region of the skull, when the impact energy is transmitted to the optic nerve, causing it to concussion and, as a result, myelin rupture, stretching of individual fibers, and bundle divergence.
• Factors of the second series of indirect damage to the optic nerve may be fractures of the orbital bones of the skull or persistent prolonged vomiting. Such phenomena can contribute to the suction of air into the orbital spaces, which increases the risk of damage to the optic nerve.

Mitochondrial optic neuropathy

Mitochondria of the neuronal layer of the retina are highly active, providing nerve cells with the necessary amount of trophic resources. As already mentioned, the processes of visual innervation are highly energy dependent due to high loads on the optical organs. Therefore, any deviations in the activity of mitochondria immediately affect the overall quality of vision.

The main causes of mitochondrial dysfunction are:

• genetic mutations in neuronal DNA;
• hypovitaminosis A and B;
• chronic alcoholism;
• addiction;
• nicotine addiction.

Nutritional optic neuropathies

The food etiology of optic neuropathy is based on the general depletion of the body caused by voluntary or forced starvation, or diseases that affect the digestibility and assimilation of nutrients. Optic neuropathy is an exceptional companion of patients suffering from anorexia or general cachexia. The genesis of this type of disorder is especially acutely affected by the deficiency of B vitamins and proteins.

Toxic optic neuropathies

Toxic optic neuropathy occurs due to poisoning with chemicals that have entered the digestive tract. Methyl alcohol poisoning is the most common when patients mistakenly take it instead of the ethyl counterpart.

Half a glass of methanol is enough to start the processes of loss of visual functionality already 15 hours after ingestion.

In addition to methyl alcohol, ethylene glycol poisoning is often recorded - the main component of the coolant for complex mechanical systems. Ethylene glycol has a dual neuropathic effect on the optic nerve:

• direct destructive effect on myelin sheaths and neurons;
• compression of the optic nerve caused by high intracranial pressure due to poisoning.

Some drugs increase the risk of optic neuropathy.

• Ethambutol is an anti-tuberculosis drug.
• Amiodarone is an antiarrhythmic drug with a fairly effective targeted therapeutic effect.

Tobacco smoking, especially in middle-aged and elderly people, is often the cause of toxic optic neuropathy. The loss of visual functionality occurs gradually, from the loss of a separate color spectrum and ending with complete blindness. The genesis of the phenomenon is practically not studied.

hereditary optic neuropathy

This type of neuropathy is characterized by pathology resistant to treatment, symmetry in the organs of vision, and a characteristic progression of symptoms. As the causes of this type of disorder, several separate nosological units have been identified.

• Leber's optic neuropathy.
• Dominant atrophy of the optic nerve.
• Ber's syndrome.
• Burke-Tabachnik syndrome.

All diseases are the result of genetic mutational changes.

Symptoms of optic nerve atrophy

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 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 due to spontaneous and sudden complete loss of vision at a certain point in the development of the pathological process.

characteristic symptoms with 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.

Toxic etiology of neuropathies causes, as a rule, 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.

Modern methods for diagnosing optic nerve atrophy

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, therefore 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.

One of the cutting-edge diagnostic tools for optic neuropathy is laser dopplerography circulatory microcirculatory network of the fundus and peripheral areas of the optic nerve. The method is respected in ophthalmology due to its non-invasive qualities. Its essence lies in the ability of a laser beam of a certain wavelength to penetrate the surrounding tissues without harming them. Based on the indicators of the returning wavelength, a graphical scheme of the movement of blood cells in the studied area of ​​the vascular bed is built - the Doppler effect.

Treatment of optic nerve atrophy and prognosis

Main stream therapeutic regimens for the treatment of optic neuropathy is inhibition of pathological processes developing in the parenchyma of the optic trunk, if possible, their complete exclusion, as well as in 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.