Neuropathy of the optic nerve to what it will lead. Ischemic neuropathy of the optic nerve. The mechanism of development of optic neuropathy in glaucoma

14.07.2020 Drugs

- defeat optic nerve caused by a functionally significant circulatory disorder in its intrabulbar or intraorbital region. Ischemic neuropathy of the optic nerve is characterized by a sudden decrease in visual acuity, narrowing and loss of visual fields, monocular blindness. Diagnosis of ischemic neuropathy requires visometry, ophthalmoscopy, perimetry, electrophysiological studies, ultrasound scan of the eye, carotid and vertebral arteries, and fluorescence angiography. When ischemic neuropathy of the optic nerve is detected, decongestant, thrombolytic, antispasmodic therapy, anticoagulants, vitamins, magnetotherapy, electro- and laser stimulation of the optic nerve.

General information

Ischemic neuropathy of the optic nerve usually develops between the ages of 40-60, mainly in males. This is a serious condition that can cause severe vision loss and even blindness. Ischemic neuropathy of the optic nerve is not an independent disease of the organ of vision, but serves as an ocular manifestation of various systemic processes. Therefore, the problems associated with ischemic neuropathy are studied not only by ophthalmology, but also by cardiology, rheumatology, neurology, endocrinology, and hematology.

Classification

Damage to the optic nerve can develop in two forms - anterior and posterior ischemic neuropathy. Both forms can proceed as limited (partial) or total (complete) ischemia.

With anterior ischemic neuropathy of the optic nerve, pathological changes are caused by an acute circulatory disorder in the intrabulbar region. Posterior neuropathy develops less frequently and is associated with ischemic disorders that occur along the optic nerve in the retrobulbar (intraorbital) section.

Causes

Anterior ischemic neuropathy is pathogenetically caused by impaired blood flow in the posterior short ciliary arteries and the resulting ischemia of the retinal, choroidal (prelaminar) and scleral (laminar) layers of the optic disc. In the mechanism of development of posterior ischemic neuropathy, the leading role belongs to circulatory disorders in the posterior parts of the optic nerve, as well as stenosis of the carotid and vertebral arteries. Local factors of acute circulatory disorders of the optic nerve can be represented as functional disorders(spasms) of the arteries, and their organic changes (sclerotic lesions, thromboembolism).

The etiology of ischemic neuropathy of the optic nerve is multifactorial; the disease is caused by various systemic lesions and associated general hemodynamic disorders, local changes in the vascular bed, microcirculation disorders. Ischemic neuropathy of the optic nerve most often develops against the background of general vascular diseases - atherosclerosis, hypertension, temporal giant cell arteritis (Horton's disease), periarteritis nodosa, obliterating arteritis, diabetes mellitus, discopathy of the cervical spine with disorders in the vertebrobasilar system, thrombosis of the great vessels. In some cases, ischemic neuropathy of the optic nerve occurs due to acute blood loss with gastrointestinal bleeding, trauma, surgery, anemia, arterial hypotension, blood diseases, after anesthesia or hemodialysis.

Symptoms

With ischemic neuropathy of the optic nerve, one eye is more often affected, but bilateral disorders may be observed in a third of patients. Often, the second eye is involved in the ischemic process after some time (several days or years), usually within the next 2-5 years. Anterior and posterior ischemic neuropathy of the optic nerve is often combined with each other and with occlusion of the central retinal artery.

Optical ischemic neuropathy, as a rule, develops suddenly: often after sleep, physical exertion, or a hot bath. At the same time, visual acuity sharply decreases (up to tenths of light perception or blindness with total damage to the optic nerve). A sharp drop in vision occurs in a period from several minutes to hours, so that the patient can clearly indicate the time of deterioration in visual function. Sometimes the development of ischemic neuropathy of the optic nerve is preceded by precursor symptoms in the form of periodic blurred vision, pain behind the eye, severe headache.

With this pathology, in one form or another, peripheral vision is always impaired. Individual defects (scotomas), loss in the lower half of the visual field, loss of the temporal and nasal half of the visual field, concentric narrowing of the visual fields may be noted.

The period of acute ischemia lasts 4-5 weeks. Then the edema of the optic nerve disc gradually subsides, hemorrhages resolve, and atrophy of the optic nerve occurs varying degrees severity. At the same time, defects in the visual fields remain, but can significantly decrease.

Diagnostics

To clarify the nature and causes of the pathology, patients with ischemic neuropathy of the optic nerve should be examined by an ophthalmologist, cardiologist, endocrinologist, neurologist, rheumatologist, hematologist.

The complex of ophthalmological examination includes functional tests, examination of eye structures, ultrasound, X-ray, electrophysiological studies.

Checking visual acuity reveals its decrease from insignificant values ​​to the level of light perception. When examining the visual fields, defects are determined that correspond to damage to certain parts of the optic nerve.

When ophthalmoscopy reveals pallor, ischemic edema and an increase in the optic disc, its promination in vitreous... The retina around the disc is edematous, a "star figure" is defined in the macula. The veins in the zone of compression by edema are narrow, on the periphery, on the contrary, they are full-blooded and dilated. Sometimes focal hemorrhages and exudation are detected.

Angiography of retinal vessels in ischemic neuropathy of the optic nerve reveals retinal angiosclerosis, age-related fibrosis, uneven caliber of arteries and veins, occlusion of cilioretinal arteries. With posterior ischemic neuropathy of the optic nerve, ophthalmoscopy in the acute period does not reveal any changes in the optic nerve disc. Doppler ultrasonography of the ocular, supra-block, carotid, vertebral arteries often determines changes in blood flow in these vessels.

Electrophysiological studies (determination of the critical flicker fusion frequency, electroretinogram, etc.) demonstrate a decrease in the functional thresholds of the optic nerve. When studying a coagulogram, changes in the type of hypercoagulation are found; when determining cholesterol and lipoproteins, hyperlipoproteinemia is detected. Ischemic optic neuropathy should be distinguished from retrobulbar neuritis, orbital masses, and CNS.

Treatment

Therapy for ischemic neuropathy of the optic nerve should be started in the first hours after the development of the pathology, since long-term impaired blood circulation causes irreversible death of nerve cells. Urgent care with sharply developed ischemia includes immediate intravenous administration aminophylline solution, taking nitroglycerin under the tongue, inhaling ammonia vapors. Further treatment of ischemic neuropathy of the optic nerve is carried out stationary.

Subsequent treatment is aimed at relieving edema and normalizing trophism of the optic nerve, creating bypass pathways for blood supply. The therapy of the underlying disease (vascular, systemic pathology), the normalization of the coagulation system and lipid metabolism, and the correction of blood pressure are of great importance.

With ischemic neuropathy of the optic nerve, the administration and administration of diuretic drugs (diacarb, furosemide), vasodilators and nootropic agents (vinpocetine, pentoxifylline, xanthinol nicotinate), thrombolytic drugs and anticoagulants (phenindione, heparin), corticosteroids, corticosteroids and E. In the future, magnetotherapy, electrical stimulation, laser stimulation of the optic nerve fibers are carried out.

Forecast and prevention

The prognosis of ischemic neuropathy of the optic nerve is unfavorable: despite treatment, there is often a significant decrease in visual acuity and persistent defects in peripheral vision (absolute scotomas) due to optic nerve atrophy. An increase in visual acuity by 0.1-0.2 can be achieved only in 50% of patients. With the defeat of both eyes, the development of low vision or total blindness is possible.

For the prevention of ischemic neuropathy of the optic nerve, the therapy of general vascular and systemic diseases, the timeliness of treatment for medical help... Patients who have undergone ischemic neuropathy of the optic nerve in one eye need dispensary observation ophthalmologist and appropriate preventive therapy.

As a result of a violation of the blood supply, ischemic neuropathy of the optic nerve develops. Pathology is considered secondary and occurs against the background of diseases of the cardiovascular, nervous or endocrine system... Symptoms appear actively, the patient's vision is sharply reduced. Dangers are exposed to males after 40 years. To confirm the diagnosis, it is necessary to study in detail the state of the optic nerves, therefore, a number of instrumental diagnostic procedures are prescribed. Treatment involves the use of conservative methods and physical therapy.

Due to the rapid development and characteristics of pathogenesis, ischemic neuropathy of the optic nerve is often called disc infarction. This condition requires urgent hospitalization.

Etiology and pathogenesis

If the local blood supply is disturbed, the nerve tissues of the eyes do not receive the necessary substances for full functioning. As a result, atrophy of the optic nerve develops, ultimately this process is the cause of the development of blindness. Ischemia appears due to hemodynamic dysfunction. The following factors are capable of provoking such a process:

  • vascular diseases (atherosclerosis, hypertension, Horton's disease, thrombosis);
  • diabetes;
  • neuritis;
  • profuse bleeding;
  • stress and frequent nervous overload.

In most cases, pathology affects only one visual organ.

The pathology of the optic nerve is more often one-sided, only in 30% of cases ischemia of both eyes is observed. The disease is characterized by a sequence when the symptoms of the disease after a while pass from one eye to the other. Such a process is observed in a third of patients, but it is difficult to predict it. Disease on the second organ can manifest itself in a few days or over 10 years.

Possible Symptoms

Signs depend on the localization and scale of the process. In the first stages, partial or limited damage appears, then the disease turns into a total form. If the process develops in the intrabulbar region, anterior ischemic neuropathy is observed. This is an acute blood circulation disorder localized in the head. The main sign is swelling of the organ, with the following symptoms occurring:

  • a rapid decrease in visual acuity;
  • square loss of sight;
  • headache stupid character;
  • dilated retinal vessels;
  • traces of punctate hemorrhage.

A person completely goes blind with a total form of pathology.

Acute form the disease lasts for a month, then the edema disappears. This means the atrophy of nerve fibers begins. If edema develops in the intraorbital region, posterior ischemic neuropathy is diagnosed. In this case, the damaged nerve is located immediately behind the eyeball. Symptoms are almost identical to the anterior type, but there are some changes in the fundus. The danger is a total form, when all departments are damaged and optic neuropathy develops. This process leads to permanent blindness. Ischemic neuro-opticopathy is rare, but almost impossible to treat.

Ischemia is characterized by rapid development, sometimes the patient remembers the exact time when his vision began to decrease. But the first stages are completely asymptomatic.

Diagnostics

The study is carried out in a comprehensive manner, in addition to an ophthalmological examination, it is necessary to consult a neurologist, endocrinologist, hematologist and rheumatologist. Diagnostics provides a full range of procedures that allow you to determine primary cause... First, the ophthalmologist examines the fundus for signs of edema. It is imperative that both eyes are checked, and the emphasis is on studying the state of the retinas. Then a number of additional procedures are assigned:


An electroretinogram in such a situation is of an auxiliary nature.
  • visual acuity test;
  • X-ray of the head;
  • vascular angiography;
  • electroretinogram;
  • MRI and CT of the skull;
  • kaogulogram.

During the diagnosis, studies are carried out to exclude retrobulbar neuritis. This disease is a formation in the orbital section of the central nervous system. The symptoms of ailments are similar, in addition, active manifestations begin already at the advanced stages of the process. The pathology is very life-threatening and requires urgent surgical intervention.

With the course of the disease, visual acuity is lost rather quickly, the fields of visibility become narrower, completely invisible areas appear. To diagnose this disease, visometry, ophthalmoscopy are used. To clarify the diagnosis and origin, ultrasound, MRI, angiography, etc.

Treatment is carried out immediately, until the diagnosis is confirmed, decongestants, drugs that relieve spasm and thrombolytics are used. An irreplaceable element complex treatment there will be physiotherapy procedures with stimulation of the optic nerve with a laser or other effect, charging for the eyes.

At risk are older people after 40, mostly men. This complex disease does not tolerate delay in treatment, because it threatens not only with loss of visual acuity, but also with complete blindness of a person, disability.

Optical pathology cannot be called an independent disease, since it manifests itself only in the complex of the systemic process of the development of the disease. This applies not only to the visual system, but also to all other parts of the body. Therefore, not only ophthalmologists work on this problem, but also conduct an examination with following doctors: endocrinologists, cardiologists, neurologists and other specialists as needed.

Classification

There are two main forms of development of optical ischemia: anterior and posterior. Both forms can proceed in part or in full.

The main difference between these forms is the location of the pathology. In the process of anterior neuropathy, blood circulation in the intrabulbar region suffers, in the process of the posterior neuropathy, in the retrobulbar region.

Causes

There are many different reasons for the pathological manifestation of optical ischemia, but the main ones can be distinguished, which are more common:

  1. Hereditary predisposition due to the genetic manifestation of the disease.
  2. Traumatic cause. There are two types of injury: direct - an anatomical disorder occurs, an imbalance in the functioning of the optic nerve, which occurs due to the penetration of a foreign body into the tissues of the optical system of vision. An indirect type of injury occurs as a result of violations without damage to the integrity of the nervous tissue.
  3. Toxic. Pathology occurs in the process of poisoning the body with various chemical elements, heavy metal salts, alcohol, drugs that penetrate and poison the body through digestive system.
  4. Food grade. With problems with food assimilation, starvation, problems with the gastrointestinal tract, ischemia of the optic nerve may appear. Due to the depletion of the entire body and a lack of nutrients necessary for the normal functioning of the visual system.
  5. Radiation. Radiation exposure due to radiation therapy.
  6. Infiltration. The reason lies in the infiltration of foreign bodies that are infectious or oncological in origin. It occurs due to the effects of viruses, bacteria, fungal infections.
  7. Another consequence of the onset of the disease is the impact of addictions: smoking, alcoholism, drug addiction.

The causes of the anterior and posterior forms of the disease also differ in the causes of occurrence. The front is provoked by factors:

  • inflammatory processes in the arteries;
  • rheumatoid joint lesions, pain with active movements;
  • Hurga-Strauss syndrome;
  • immunopathological vascular inflammation, for example, arteritis;
  • Wegener's granulomatosis;
  • chronic damage to the arterial walls of blood vessels, which has an acute character and nodes.

Posterior ischemic neuropathy occurs due to other causes:

  • surgical interventions in the spine;
  • low blood pressure and autonomic disorders of the central nervous system;
  • surgical actions on the CVS.

Symptoms

With lesions of the optic nerve, one eye is more often affected, but there are a number of cases in which bilateral visual impairment is detected. A situation may arise when the second eye gradually loses its visibility and is involved in the ischemic process after some time. It can be one hour or several days.

Optic neuropathy occurs unexpectedly and without any foreshadowing signs, this can be after heavy physical exertion, after taking a hot bath or after waking up. Visual acuity decreases suddenly and dramatically over several minutes or hours. The patient may not pay attention to the symptoms that occur on the eve of deterioration in vision, this is temporary blurred eyes, hazy visibility, painful sensations in the eye area, severe and frequent headache.

The first thing that can be noticed in the process of ischemia is a violation of peripheral vision, individual fragments may fall out of the field of vision of a person: the lower half, temporal or nasal. The concentration of vision may decrease, the visible area may narrow.

The acute period of the disease lasts for a month, then the swelling of the DNZ subsides, the hemorrhages gradually dissolve, the muscle tissues of the optic nerve feel complete atrophy. Retinal detachment and other defects do not go away, but are reduced.

Diagnostic methods

At the first suspicions and discomfort, you should consult a doctor. If a person did not manage to prevent the disease in advance, in case of visual impairment, which happened abruptly and unexpectedly, it is important to urgently call ambulance for urgent hospitalization. In the process of finding out the cause of the disease, it is necessary to consult a cardiologist, neurologist, hematologist and other specialists.

The following are used as diagnostic hardware:

  • X-ray examination;
  • biomicroscopy for the study of eyes, structures and the environment using a slit lamp;
  • testing the eyes for the ability to perform functions;
  • other electrophysiological research methods: electroretinogram for calculating the frequency of flickering, checking the functionality of the optic nerve and tissues, coagulogram for examining blood for cholesterol and lipoprotein levels, analyzing their dynamics.

During the diagnosis of vision, the doctor can detect not only a decrease in visual acuity or loss of vision, but also other abnormalities of visual function: an increase in the size of the optic disc, its dislocation, pallor of the nerve, edema.

Treatment

For optimal diagnostics and prompt results, it is necessary to seek medical help in a timely manner, the best option is the first hours after the onset of symptoms, since the blood supply provokes the loss of nerve cells

The ambulance team is taking urgent measures in the form of intravenous injections of aminophylline, bringing the patient to his senses with the help of ammonia, etc. The patient is admitted to the hospital for further therapy.

The first task of the doctor is to remove edema from the nervous tissue of the visual system, to start the process of blood supply, to prevent atrophy of the muscle nervous tissue. In parallel with this, blood pressure is normalized, normal blood clotting is ensured.

An important step in the actions of doctors is vasodilation, which has a positive effect on ischemic neuropathy. To do this, use trental, cavinton. In order to relieve edema, diuretics are used, and thrombolytics are used to thin the blood.

As a complementary therapy to strengthen immune system use vitamin and mineral complexes, physiotherapeutic procedures to stimulate blood supply, glucocorticosteroids to relieve the inflammatory process.

Forecast

Even with the best forecasts of doctors, it is almost impossible to completely restore vision. Full compliance with the entire medical complex, the implementation of all medical prescriptions will not save from a decrease in visual acuity. As a result, vision may still fall, some defects associated with the view and atrophy of nerve fibers will remain. Every second patient manages to improve visual indicators by 0.2 units, such a result is achieved only with intensive treatment in compliance with all necessary measures... If the patient is faced with ischemia in both eyes, there is a risk of complete blindness without the possibility of restoring vision.

Preventive measures

At the slightest deviation in vision, it is important to consult an ophthalmologist in a timely manner and undergo regular examination by a doctor. Any vascular diseases, disorders metabolic processes must be examined and cured so that complications do not develop, incl. and before our eyes. After the first symptoms appear, go to a medical institution and comply with all requirements.

Ischemic neuropathy of the optic nerve. Causes, Symptoms, Treatment

Ischemic neuropathy of the optic (optic) nerve is a pathology of this part of the eye, occurring due to local circulatory disorders (in the intraorbital and intrabulbar regions).

The disease is accompanied by a rapid drop in visual acuity, narrowing of the visual fields, and the appearance of blind spots. Methods for diagnosing ischemic neuropathy of the optic nerve - ophthalmoscopy, visometry, ultrasound, CT and MRI, angiography and others.

Medication treatment, including vitamins, decongestants, antispasmodics, thrombolytics. Often, treatment is complemented by physiotherapy procedures, laser stimulation of the optic nerve.

Ischemic neuropathy of the optic nerve

The disease is more common in the age group and mostly affects men. Optic nerve neuropathy is considered a serious pathology, since it can significantly reduce visual acuity, and in some cases threatens to completely lose it.

The disease is not considered independent: it is always part of the systemic pathological process (both in the organs of vision and in other parts of the body).

In this regard, ischemic neuropathy is considered not only by ophthalmologists, but also by neurologists, cardiologists, endocrinologists, hematologists, etc.

Types of ischemic neuropathy of the optic nerve

The disease can proceed in two different ways. The first of these is called locally limited ischemic neuropathy, the second is called complete, or total ischemic neuropathy. According to the area of ​​coverage of pathological processes, the disease is anterior, posterior.

With the development of anterior neuropathy, damage to the optic nerve is observed against the background of acute circulatory disorders in the intrabulbar region.

The posterior form of neuropathy is diagnosed much less frequently. It is caused by an ischemic lesion of the intraorbital region.

Etiology and pathogenesis

Anterior ischemic neuropathy is associated with abnormal changes in blood flow in the ciliary arteries. Due to insufficient oxygen supply to tissues, a state of ischemia (oxygen starvation) of the retinal, prelaminar, scleral layers of the optic nerve head develops.

Ischemic neuropathy of the posterior view occurs as a result of impaired blood supply to the posterior parts of the optic nerve, often against the background of stenosis of the carotid and vertebral arteries.

In general, the development of acute circulatory disorders in most cases provoke vasospasm or organic defeat these vessels (for example, thrombosis, sclerosis).

The above conditions, which entail the appearance of signs of ischemic neuropathy of the optic nerve, may have different prerequisites.

The disease starts against the background of the underlying pathology, mainly vascular disorders - hypertension, vascular atherosclerosis, temporal giant cell arteritis, periarthritis nodosa, arteritis obliterans, arterial and venous thrombosis. Of the pathologies of metabolic processes, ischemic neuropathy is often accompanied by diabetes mellitus.

The disease can also develop in combination with discopathy of the cervical segment of the spine. Occasionally, pathology is able to accompany severe blood loss, for example, with perforation of stomach ulcers, intestines, trauma internal organs, after operation.

Sometimes ischemic neuropathy occurs with serious blood diseases, anemia, against the background of hemodialysis, after the introduction of anesthesia, with arterial hypotension.

Clinical picture

In most cases, the symptoms of ischemic neuropathy are unilateral. Less often (up to 1/3 of cases), the pathology extends to the second organ of vision.

Since the course of the disease can be very long, the second eye is affected later - several weeks and even years after the onset of pathological phenomena in the first. Most often, in the absence of treatment, after 3-5 years, both organs of vision become involved in the process.

With the initial onset of anterior ischemic neuropathy, posterior ischemic neuropathy can subsequently develop, and signs of occlusion of the central retinal artery can also be added.

The disease usually starts quickly and suddenly. After waking up in the morning, taking a bath, doing any physical work or playing sports, visual acuity decreases, and in some patients - to blindness or identification of a light source.

In order for a person to feel a deterioration in visual acuity, it sometimes takes from a minute to a couple of hours. In some cases, damage to the optic nerve is preceded by a severe headache, the appearance of a veil before the eyes, pain in the orbit from the back, the appearance of unusual phenomena in the field of vision.

Ischemic neuropathy of the optic nerve always leads to a deterioration in a person's peripheral vision. Often, vision pathologies are reduced to the formation of blind spots (by cattle), the disappearance of the picture in the lower part of the review or in the area of ​​the nasal, temporal part.

The acute condition lasts up to a month (sometimes longer). Further, the puffiness of the optic nerve head decreases, hemorrhages gradually resolve, and the nervous tissue atrophies with varying degrees of severity. In many patients, vision is partially restored.

Diagnostics

If any of the above signs occur, it is necessary to urgently call an ambulance or quickly seek help from an ophthalmologist. The examination program necessarily includes consultations of other specialists - cardiologist, neurologist, rheumatologist, hematologist, etc. (until the cause of ischemic neuropathy is identified).

Ophthalmological examinations include functional testing of the eyes, biomicroscopy, instrumental examinations using ultrasound, X-ray, and various electrophysiological methods. A specialist checks the patient's visual acuity.

With ischemic neuropathy, a different degree of decrease in this indicator is found - from a slight loss of vision to complete blindness. Also, abnormalities of visual function are detected, depending on the affected area of ​​the nerve.

During the performance of ophthalmoscopy, swelling, pallor, an increase in the size of the optic nerve head, as well as its advance towards the vitreous body are detected.

In the region of the disc, the reticular membrane swells strongly, and a star-shaped figure appears in its central part. The vessels in the area of ​​compression narrow, and along the edges, on the contrary, they are more filled with blood, pathologically expanding. In some cases, hemorrhages and exudate are present.

As a result of performing angiography retina eyes visualized retinal angiosclerosis, occlusion of cilioretinal vessels, pathological changes in the caliber of veins and arteries.

Usually, violations of the structure of the optic nerve head in ischemic neuropathy of the posterior type are not detected. When conducting ultrasound of the arteries with Doppler ultrasound, a violation of normal blood flow is recorded.

From electrophysiological examinations, an electroretinogram is prescribed, the calculation of the limiting frequency of flicker fusion, etc. A decrease in the functional properties of the nerve is usually manifested. Performing a coagulogram reveals hypercoagulation, and when blood is tested for cholesterol and lipoproteins, their increased amount is revealed.

Ischemic neuropathy should be differentiated from retrobulbar neuritis, tumors nervous system and the orbit of the eye.

Treatment

Treatment should be started as early as possible, optimally in the first hours after the onset of symptoms. This need is due to the fact that long-term disruption of the normal blood supply leads to the loss of nerve cells.

From the measures of emergency care, intravenous injections of aminophylline, the intake of tableted nitroglycerin, and short-term inhalation of ammonia vapors are used. After performing emergency therapy, the patient is admitted to a hospital.

In the future, the goal of therapy is to reduce swelling, improve the trophism of the nervous tissue, as well as provide an alternative path of blood circulation. In addition, the underlying disease is treated, blood clotting is normalized, fat metabolism, blood pressure.

From vasodilators for ischemic neuropathy, Cavinton, Cerebrolysin, Trental are used, from decongestants - diuretics Lasix, Diacarb, from blood thinners - Thrombolytics heparin, phenylin.

Additionally, glucocorticosteroid preparations are prescribed, vitamin complexes, physiotherapy (electrical stimulation, laser nerve stimulation, magnetotherapy, microcurrents).

Forecast

In ischemic neuropathy of the optic nerve, the prognosis is usually poor. Even with the implementation of a comprehensive treatment program, visual acuity decreases, often there is a persistent drop in vision and its various defects, loss of areas from the view, which occurs due to atrophy of nerve fibers.

In half of the patients, vision can be improved by 0.2 units. through intensive treatment. If both eyes are involved, complete blindness often develops.

Prophylaxis

In order to prevent ischemic neuropathy, it is necessary to treat any vascular, metabolic and systemic diseases in time.

After the onset of an episode of ischemic neuropathy in one organ of vision, the patient should be regularly observed by an ophthalmologist, as well as follow his advice on preventive therapy.

Ischemic neuropathy of the optic nerve

Ischemic neuropathy of the optic nerve is damage to the optic nerve caused by a functionally significant circulatory disorder in its intrabulbar or intraorbital region. Ischemic neuropathy of the optic nerve is characterized by a sudden decrease in visual acuity, narrowing and loss of visual fields, monocular blindness. Diagnosis of ischemic neuropathy requires visometry, ophthalmoscopy, perimetry, electrophysiological studies, ultrasound scan of the eye, carotid and vertebral arteries, and fluorescence angiography. When ischemic neuropathy of the optic nerve is detected, decongestant, thrombolytic, antispasmodic therapy, anticoagulants, vitamins, magnetotherapy, electrical and laser stimulation of the optic nerve are prescribed.

Ischemic neuropathy of the optic nerve

Ischemic neuropathy of the optic nerve usually develops in age, mainly in males. This is a serious condition that can cause severe vision loss and even blindness. Ischemic neuropathy of the optic nerve is not an independent disease of the organ of vision, but serves as an ocular manifestation of various systemic processes. Therefore, the problems associated with ischemic neuropathy are studied not only by ophthalmology, but also by cardiology, rheumatology, neurology, endocrinology, and hematology.

Classification

Damage to the optic nerve can develop in two forms - anterior and posterior ischemic neuropathy. Both forms can proceed as limited (partial) or total (complete) ischemia.

With anterior ischemic neuropathy of the optic nerve, pathological changes are caused by an acute circulatory disorder in the intrabulbar region. Posterior neuropathy develops less frequently and is associated with ischemic disorders that occur along the optic nerve in the retrobulbar (intraorbital) section.

Causes

Anterior ischemic neuropathy is pathogenetically caused by impaired blood flow in the posterior short ciliary arteries and the resulting ischemia of the retinal, choroidal (prelaminar) and scleral (laminar) layers of the optic disc.

In the mechanism of development of posterior ischemic neuropathy, the leading role belongs to circulatory disorders in the posterior parts of the optic nerve, as well as stenosis of the carotid and vertebral arteries.

Local factors of acute circulatory disorders of the optic nerve can be represented by both functional disorders (spasms) of the arteries, and their organic changes (sclerotic lesions, thromboembolism).

The etiology of ischemic neuropathy of the optic nerve is multifactorial; the disease is caused by various systemic lesions and associated general hemodynamic disorders, local changes in the vascular bed, microcirculation disorders. Ischemic neuropathy of the optic nerve most often develops against the background of general vascular diseases - atherosclerosis, hypertension, temporal giant cell arteritis (Horton's disease), periarteritis nodosa, obliterating arteritis, diabetes mellitus, discopathy of the cervical spine with disorders in the vertebrobasilar system, thrombosis of the great vessels. In some cases, ischemic neuropathy of the optic nerve occurs as a result of acute blood loss during gastrointestinal bleeding, trauma, surgery, anemia, arterial hypotension, blood diseases, after anesthesia or hemodialysis.

Symptoms

With ischemic neuropathy of the optic nerve, one eye is more often affected, but bilateral disorders may be observed in a third of patients. Often, the second eye is involved in the ischemic process after some time (several days or years), usually within the next 2-5 years. Anterior and posterior ischemic neuropathy of the optic nerve is often combined with each other and with occlusion of the central retinal artery.

Optical ischemic neuropathy, as a rule, develops suddenly: often after sleep, physical exertion, or a hot bath. At the same time, visual acuity sharply decreases (up to tenths of light perception or blindness with total damage to the optic nerve). A sharp drop in vision occurs in a period from several minutes to hours, so that the patient can clearly indicate the time of deterioration in visual function. Sometimes the development of ischemic neuropathy of the optic nerve is preceded by precursor symptoms in the form of periodic blurred vision, pain behind the eye, severe headache.

With this pathology, in one form or another, peripheral vision is always impaired. Individual defects (scotomas), loss in the lower half of the visual field, loss of the temporal and nasal half of the visual field, concentric narrowing of the visual fields may be noted.

The period of acute ischemia lasts 4-5 weeks. Then the edema of the optic nerve disc gradually subsides, hemorrhages resolve, and atrophy of the optic nerve of varying severity occurs. At the same time, defects in the visual fields remain, but can significantly decrease.

Diagnostics

To clarify the nature and causes of the pathology, patients with ischemic neuropathy of the optic nerve should be examined by an ophthalmologist, cardiologist, endocrinologist, neurologist, rheumatologist, hematologist.

The complex of ophthalmological examination includes functional tests, examination of eye structures, ultrasound, X-ray, electrophysiological studies.

Checking visual acuity reveals its decrease from insignificant values ​​to the level of light perception. When examining the visual fields, defects are determined that correspond to damage to certain parts of the optic nerve.

When ophthalmoscopy reveals pallor, ischemic edema and an increase in the optic disc, its promination into the vitreous body. The retina around the disc is edematous, a "star figure" is defined in the macula. The veins in the zone of compression by edema are narrow, on the periphery, on the contrary, they are full-blooded and dilated. Sometimes focal hemorrhages and exudation are detected.

Angiography of retinal vessels in ischemic neuropathy of the optic nerve reveals retinal angiosclerosis, age-related fibrosis, uneven caliber of arteries and veins, occlusion of cilioretinal arteries. With posterior ischemic neuropathy of the optic nerve, ophthalmoscopy in the acute period does not reveal any changes in the optic nerve disc. Doppler ultrasonography of the ocular, supra-block, carotid, vertebral arteries often determines changes in blood flow in these vessels.

Electrophysiological studies (determination of the critical flicker fusion frequency, electroretinogram, etc.) demonstrate a decrease in the functional thresholds of the optic nerve. When studying a coagulogram, changes in the type of hypercoagulation are found; when determining cholesterol and lipoproteins, hyperlipoproteinemia is detected. Ischemic optic neuropathy should be distinguished from retrobulbar neuritis, orbital masses, and CNS.

Treatment

Therapy for ischemic neuropathy of the optic nerve should be started in the first hours after the development of the pathology, since long-term impaired blood circulation causes irreversible death of nerve cells. Emergency care for sharply developed ischemia includes immediate intravenous administration of aminophylline solution, taking nitroglycerin under the tongue, inhaling ammonia vapors. Further treatment of ischemic neuropathy of the optic nerve is carried out stationary.

Subsequent treatment is aimed at relieving edema and normalizing trophism of the optic nerve, creating bypass pathways for blood supply. The therapy of the underlying disease (vascular, systemic pathology), the normalization of the coagulation system and lipid metabolism, and the correction of blood pressure are of great importance.

With ischemic neuropathy of the optic nerve, the administration and administration of diuretic drugs (diacarb, furosemide), vasodilators and nootropic agents (vinpocetine, pentoxifylline, xanthinol nicotinate), thrombolytic drugs and anticoagulants (phenindione, heparin), corticosteroids, corticosteroids and E. In the future, magnetotherapy, electrical stimulation, laser stimulation of the optic nerve fibers are carried out.

Forecast and prevention

The prognosis of ischemic neuropathy of the optic nerve is unfavorable: despite treatment, there is often a significant decrease in visual acuity and persistent defects in peripheral vision (absolute scotomas) due to optic nerve atrophy. An increase in visual acuity by 0.1-0.2 can be achieved only in 50% of patients. With the defeat of both eyes, the development of low vision or total blindness is possible.

For the prevention of ischemic neuropathy of the optic nerve, the therapy of general vascular and systemic diseases, the timeliness of seeking medical help is important. Patients who have undergone ischemic neuropathy of the optic nerve in one eye need clinical observation by an ophthalmologist and appropriate preventive therapy.

Optic neuropathy

Searches such as "optic neuropathy" are common on the internet. In fact, we are talking about the neuropathy of the optic nerve. This is a rather serious disease, which, most often, is a symptom of another process. The optic nerves, as conductors, perceive all pathological influences, and show the doctor a lot when examining the fundus.

Symptoms of damage to the optic nerve

It is necessary to immediately distinguish between three concepts, between which there is always confusion when it comes to damage to the optic nerve.

Eyeball - sagittal slice

  • neuropathy. This is the name of the process that leads to a disorder of the functions of the optic nerves, but without signs of inflammation. An example is acute ischemic neuropathy of the optic nerve, which can develop with severe atherosclerosis, which leads to thrombosis of the central retinal artery. This serious process can result in the blindness of one eye;
  • optic neuritis. This is a process that is characterized by inflammation of the nerve fiber, with a characteristic picture, as well as the addition of pain. Unilateral optic neuritis that develops for no apparent reason can be an important symptom of multiple sclerosis. Many people with a history of optic neuritis subsequently develop multiple sclerosis;

Central retinal artery thrombosis

  • stagnant discs of the optic nerves, which can be found when examining the fundus. Stagnant phenomena are most likely indicative of a syndrome intracranial hypertension, and they arise in the case of increased intracranial pressure, especially if this pressure exists for a long period of time.

A clear delineation of these clinical phenomena will make it possible to separate neuritis from neuropathy, which makes it possible to make a correct prognosis of the development of the disease.

Location of the optic nerve

Reasons for the development of neuropathy and optic neuritis

How is it manifested and for what reasons can neuropathy and optic neuritis develop?

For example, signs of ischemic optic neuropathy are severe visual impairment, usually in one eye. In some cases, ischemic blindness may occur. Often this is preceded by such specific symptoms as, for example, "blurred" vision, the appearance of various spots, sometimes colored.

If an incomplete loss of vision has developed, then focal loss of visual fields appears, for example, arcuate and sectoral scotomas, that is, areas of the visual fields that do not see anything. Concentric narrowing of the visual fields may appear.

This process is very dangerous by the so-called sympathetic spread: in some cases, the pathological process is transferred from one eye to the other (after all, the optic nerves form a single whole in the area of ​​the chiasm, or optic chiasm), and as a result, complete blindness may develop.

With ischemic lesions of the nerve, disc edema also occurs, and arteries are narrowed, with a normal diameter of the veins. This is clearly visible when examining the fundus. Then, in the area of ​​the optic nerve head, various hemorrhages occur. In the event that intensive treatment is not started (metabolic, vascular drugs, anti-thrombotic, antiplatelet agents, antioxidants), persistent atrophy of the optic nerve may develop. It usually occurs 1–3 weeks after the onset of neuropathy.

This lesion (ischemic neuropathy of the optic nerve) occurs with severe atherosclerosis, systemic vascular lesions - cranial arteritis. It is also possible to damage the optic nerve with obliterating endarteritis, with Buerger's disease (thromboangiitis obliterans).

If we talk about optic neuritis, then it occurs due to the appearance of inflammation on the myelin sheath, as well as in the nerve trunk itself. Signs of optic neuritis will be only the signs that are noticeable when examining the fundus:

  • hyperemia of the nerve disc, edema;
  • blurring and indistinctness of the boundaries of the disc, which indicates inflammation;
  • plethora and a sharp expansion of both arteries and veins (and we remember that with neuropathy there is, on the contrary, a narrowing of the arterial network with intact venous. It is clear that plethora is a sign of inflammatory hyperemia);
  • foci of hemorrhage, in the area of ​​the disc;
  • the appearance of whitish foci on the surface of the disc and retina.

Signs of optic neuritis will also include a variety of visual disorders, including early loss of acuity, as well as wide and varied changes in visual fields. These disorders occur simultaneously with the appearance of a picture in the fundus.

Due to neuritis, acuity may decrease, vision becomes blurry

Neuritis can develop for a variety of reasons. In addition to signs of demyelinating disease, the cause may be:

  • meningitis, encephalitis, meningoencephalitis, especially purulent;
  • endogenous intoxication and poisoning.

Surrogate poisoning as a cause of optic neuropathy

Among the classic manifestations of optic neuritis is poisoning with an alcohol substitute, such as the ingestion of methyl alcohol for the purpose of alcoholic intoxication. It is known that the lethal dose of methanol for internal use ranges from 40 to 250 ml, but even the use of 5-10 ml of methanol can cause blindness. In addition, with the use of various mixtures containing from 1.5% methyl alcohol, there are also cases of toxic blindness.

What is characteristic, visual impairment when using methanol occurs 3-6 days after taking it, when, it would seem, everything has already returned to normal. Damage to the optic nerve after taking methanol occurs due to the fact that in the liver it breaks down into toxic products - formic acid and formaldehyde. It is the latter that affects the optic nerve. When used as usual, ethyl alcohol, the products of metabolism in the liver are acetic acid and acetaldehyde, which, for all their harmfulness, do not affect the cells of the optic nerve and retina.

Therefore, in case of sudden visual impairments, it is necessary to urgently examine the fundus of the eye, as well as begin treatment with an ophthalmologist and therapist. This will help not only preserve vision, but also identify the underlying disease that can harm not only the optic nerve, but the entire body.

Optic neuropathy

Images of the surrounding world are transmitted to the brain through the retina and optic nerve, the information thus obtained is formed into a finished picture.

As a result of insufficient blood circulation or damage to the optic nerve, optic neuropathy begins - a disease that can lead to permanent or temporary visual impairment up to its complete loss.

There are several types of the disease, their symptoms and causes differ.

For the reasons of occurrence, the disease is of the following types:

Causes

Hereditary is caused by a genetic predisposition, four nosological units (Burke-Tabachnik syndrome, Beer's syndrome, dominant optic nerve atrophy, Leber's neuropathy) have been identified as causes.

Toxic - poisoning with chemicals that have entered the digestive system, most often methyl alcohol, less often ethylene glycol, drugs.

Nutritional - general depletion of the body resulting from starvation, as well as diseases that affect the absorption and digestibility of nutrients.

Mitochondrial - smoking, drug addiction, alcoholism, hypovitaminosis A and B, genetic abnormalities in neuronal DNA.

Traumatic - direct or indirect injury, in the first case, there is a violation of the anatomy and functioning of the optic nerve, it can occur as a result of the direct penetration of a foreign body into the tissue; indirect damage involves blunt trauma without compromising the integrity of the nerve tissue.

Infiltration - infiltration of foreign bodies of an infectious nature or oncological structure into the parenchyma of the optic nerve, the effect of opportunistic bacteria, viruses and fungi.

Radiation - increased radiation, radiation therapy.

Ischemic neuropathy of the optic nerve is anterior and posterior, the causes of its occurrence are different.

Causes of anterior ischemic neuropathy:

  • Inflammation of the arteries;
  • Rheumatoid arthritis;
  • Wegener's granulomatosis;
  • Hurga-Strauss syndrome;
  • Polyarteritis nodosa;
  • Giant arteritis.

Causes of posterior ischemic neuropathy:

  • Surgical operations on CVS;
  • Spine surgery;
  • Hypotension.

Symptoms

The most important symptom of all types of disease is considered to be progressive deterioration of vision, which cannot be corrected with glasses and lenses. The rate of illness is often so high that blindness occurs within a few weeks. With incomplete atrophy of the nerve, vision is also not completely lost, since the nerve tissue is affected only in a certain area.

Often in the review there are areas of darkening, blind spots, pathology is accompanied by an afferent defect of the pupil, that is, a pathological change in the response to a light source. Symptoms can occur on one or both sides.

Symptoms of hereditary neuropathy

Most patients do not have concomitant neuralgic abnormalities, although hearing loss and nystagmus are known. The only symptom is bilateral loss of vision, paleness of the temporal part is observed, perception of yellow-blue shades is impaired. During the diagnosis, a molecular genetic study is carried out.

Symptoms of Nutritional Neuropathy

The patient can notice changes in color perception, there is a washout of the red color, the process occurs simultaneously in both eyes, there are no painful sensations. In the early stages, the images are blurry, hazy, after which a gradual decrease in vision occurs.

With a rapid loss of vision, blind spots appear only in the center, at the periphery of the picture are displayed quite clearly, the pupils react to light in the usual way.

Lack of nutrients can negatively affect the entire body, pain and loss of sensation in the limbs is manifested in patients with food neuropathies. The epidemic of the disease fell on the years of the Second World War in Japan, when the soldiers, after a few months of starvation, began to go blind.

Symptoms of toxic neuropathy

In the early stages, nausea and vomiting are observed, after which there is a headache, symptoms of respiratory distress syndrome, vision loss is diagnosed in a few hours. after toxicity. Without appropriate measures, complete blindness can occur, the pupils dilate and stop responding to light.

Diagnostics

When the first symptoms appear, you need to call an ambulance or contact an ophthalmologist.

Before identifying the causes of the onset of the disease, the examination includes examination by a neurologist, cardiologist, rheumatologist and hematologist.

  • Biomicroscopy;
  • Functional eye testing;
  • X-ray;
  • Various electrophysiological methods.

During the examination, a decrease in visual acuity is revealed - from a slight loss to blindness, depending on the area of ​​the lesion, various anomalies of visual function may also appear.

With ophthalmoscopy, pallor, swelling, an increase in the size of the optic nerve (disc), and also its movement in the direction of the vitreous body can be detected.

In the course of electrophysiological examinations, an electroretinogram is usually prescribed, the limiting frequency of flicker fusion is calculated, and a decrease in the functional properties of the nerve is often diagnosed. When conducting a coagulogram, hypercoagulation is detected, when checking blood for lipoprotein and cholesterol, their increase is revealed.

Treatment

With neuropathies, the causes that caused the disease are first of all eliminated. The decision on treatment is made by an ophthalmologist, if necessary, other specialists are involved.

Treatment for ischemic neuropathy

Treatment should be started in the first hours after the onset of symptoms, the need is due to the fact that prolonged circulatory disturbance leads to the loss of nerve cells.

The goal of therapy is to reduce swelling, provide an alternative pathway for blood circulation, and improve the trophism of nervous tissue. It is also necessary to take measures to treat the underlying disease, to ensure the normalization of fat metabolism, blood clotting, blood pressure.

Medications indicated for ischemic neuropathy:

  • Vasodilator drugs (Trental, Cerebrolysin, Cavinton);
  • Decongestants medicines(diacarb, lasix);
  • Blood thinners (phenylin, heparin);
  • Vitamin complexes;
  • Glucocorticosteroids.

Treatment also involves the use of physiotherapeutic methods (microcurrents, magnetotherapy, laser nerve stimulation, electrical stimulation).

There is no effective treatment for hereditary neuropathies, drugs in this case are ineffective, it is recommended to refrain from alcoholic beverages and smoking. In the presence of neuralgic and cardiac abnormalities, patients are recommended to be referred to an appropriate specialist.

With ischemic optic neuropathy, the prognosis is poor, even when all the doctor's prescriptions are followed, vision deteriorates, individual areas fall out of the review, which leads to atrophy of nerve tissue fibers. In 50% of cases, due to intensive treatment, vision can be improved, with the involvement of both eyes in the process, complete blindness often develops.

Prophylaxis

In order to prevent the development of the disease, it is recommended to carry out timely treatment of any systemic, metabolic and vascular diseases. After the onset of symptoms of the disease, the patient is recommended to regularly visit an ophthalmologist, the patient must comply with all the requirements of the doctor.

Ischemic neuropathy of the optic nerve: anterior, posterior

At the heart of ischemic neuropathy of the optic nerve is an acute disturbance of the arterial circulation in the vascular system that feeds the optic nerve.

ICD-10 code

Causes of ischemic neuropathy of the optic nerve

In the development of this pathology, the following three factors play the main role: violation of general hemodynamics, local changes in the vascular wall, coagulation and lipoprotein shifts in the blood.

Violations of general hemodynamics are most often caused by hypertension, hypotension, atherosclerosis, diabetes, the occurrence of stressful situations and profuse bleeding, atheromatosis of the carotid arteries, occlusive diseases of the brachiocephalic arteries, blood diseases, the development of giant cell arteritis.

Local factors. At present, great importance is attached to local local factors that cause the formation of blood clots. Among them are changes in the endothelium of the vascular wall, the presence of atheromatous plaques and areas of stenosis with the formation of a vortex of blood flow. The presented factors determine the pathogenetically oriented therapy of this serious disease.

Symptoms of ischemic optic neuropathy

There are two forms of ischemic neuropathy - anterior and posterior. They can manifest as partial (limited) or complete (total) damage.

Anterior ischemic neuropathy

Acute circulatory disorders in the intrabulbar part of the optic nerve. Changes in the optic nerve head are detected by ophthalmoscopy.

With total damage to the optic nerve, vision decreases to hundredths and even to blindness, with partial damage it remains high, but characteristic wedge-shaped scotomas are noted, and the top of the wedge is always facing the gaze fixation point. Wedge-shaped loss is explained by the sectoral nature of the blood supply to the optic nerve. Wedge-shaped defects, merging, cause a quadrant or half loss in the field of view. Defects in the visual field are more often localized in its lower half. Vision decreases within minutes or hours. Usually, patients accurately indicate the day and hour when their vision has sharply decreased. Sometimes there may be precursors in the form of headache or transient blindness, but more often the disease develops without precursors. On ophthalmoscopy, a pale edematous disc of the optic nerve is visible. The vessels of the retina, primarily the veins, change for the second time. They are wide, dark, twisted. There may be hemorrhages on the disc and in the parapapillary zone.

The duration of the acute period of the disease is 4-5 weeks. Then the edema gradually decreases, the hemorrhages resolve, and atrophy of the optic nerve of varying severity is manifested. Defects in the visual field persist, although they can be significantly reduced.

Posterior ischemic neuropathy

Acute ischemic disorders develop along the optic nerve behind the eyeball - in the intraorbital region. These are posterior manifestations of ischemic neuropathy. Pathogenesis and clinical course diseases are identical to those of anterior ischemic neuropathy, but in the acute period there are no changes in the fundus. The optic disc is natural in color with clear boundaries. Only after 4-5 weeks disc decoloration appears, partial or complete atrophy begins to develop. With total damage to the optic nerve central vision can decrease to hundredths or to blindness, as in the case of anterior ischemic neuropathy, with partial visual acuity, it can remain high, but characteristic wedge-shaped loss is revealed in the field of view, more often in the lower or lower nasal regions. Diagnosis at an early stage is more difficult than with ischemia of the optic nerve head. Differential diagnosis carried out with retrobulbar neuritis, masses of the orbit and central nervous system.

In 1/3 of patients with ischemic neuropathy, the second eye is affected, on average after 1-3 years, but this interval can vary from several days.

Optic neuropathy

Optical neuropathy is called damage to the fibers of the optic nerve, which is accompanied by its atrophic degeneration with the development of characteristic clinical symptoms... Previously, this condition was denoted by the term "optic nerve atrophy", but now ophthalmologists recommend not to use it.

Optical neuropathy is not an independently occurring pathology, but one of the manifestations or a consequence of a number of diseases. Therefore, patients with such a diagnosis are found in the practice of doctors of various profiles: an ophthalmologist, neurologist, endocrinologist, traumatologists, maxillofacial surgeons and even oncologists.

Pathogenesis

Whatever the cause of damage to the optic nerve, the key pathogenetic moments are ischemia of nerve fibers with a weakening of the antioxidant defense mechanism. This can be facilitated by various etiological mechanisms:

  • compression (squeezing) from outside the nerve fibers;
  • insufficiency of blood supply with the development of ischemia, while impairments of arterial and venous blood flow are important;
  • metabolic disorders and intoxication, accompanied by the activation of neurotoxic and peroxide reactions;
  • inflammatory process;
  • mechanical damage to nerve fibers (trauma);
  • disorders of central genesis (at the level of the brain);
  • radiation damage;
  • congenital anomalies.

If the damage is irreversible and progressive, the nerve fibers die and are replaced by gliosis tissue. Moreover, the pathological process tends to spread, therefore, optic neuropathy in most cases tends to increase. The area of ​​appearance of the primary focus and the rate of degeneration (atrophy) of the nerve depend on the etiology (cause).

What leads to optic nerve degeneration

There are a lot of diseases that can provoke the development of optic neuropathy. According to the mechanism of damage to the optic nerve, all of them can be divided into several groups:

  • Diseases with a predominantly vascular pathogenetic factor. This includes diabetes mellitus, hypertension and secondary arterial hypertension of any genesis, arterial hypotension, temporal arteritis, generalized atherosclerosis, periarteritis nodosa, thrombosis of the great vessels of the cervicocerebral region and arteries feeding the nerve.
  • Conditions leading to compression (squeezing from the outside) of the optic nerve trunk. This is thyrotoxicosis (occurring with endocrine ophthalmopathy), any volumetric formations of the orbit and optic canal (gliomas, lymphangiomas, hemangiomas, cysts, carcinomas), all types of pseudotumor of the orbit. Sometimes there is compression by fragments after trauma to the orbit, hematomas (including those located between the sheaths of the nerve) and foreign bodies. The degeneration of the nervous tissue that occurs in this case is associated not only with direct compression of the fibers. Ischemia (oxygen deficiency) of significant parts of the nerve, which develops as a result of local compression of the supplying vessels, is also of great importance.
  • Infiltration of the optic nerve trunk. Most often we are talking about germinating tumors, which are primary and secondary (metastatic). Infiltration of the nerve can also lead to foci of inflammation, sarcoidosis, fungal infection.
  • Demyelinating diseases (multiple sclerosis). Exposure of nerve fibers leads first to a violation of the conduction of impulses along them, and then to irreversible degeneration.
  • Toxic form of optic neuropathy. Damage to the optic nerve can be associated with exposure to a number of industrial toxins, toxic substances, pesticides, alcohol and its surrogates. The greatest danger is methanol, the metabolites of which (especially formaldehyde) are highly toxic and have a tropism for the optic nerve. Optical neuropathy can develop while taking certain drugs: for example, with intolerance to sulfonamides, with severe overdose with cardiac glycosides and amiodarone, during treatment of tuberculosis with ethambutol.
  • Dystrophy of the optic nerve caused by severe chronic hypovitaminosis, and a long-term deficiency of B vitamins is especially critical. The development of neuropathy may be associated with severe disorders of the absorption process in small intestine, fasting, adherence to strict irrational food restrictions. This mechanism of damage to the optic nerve is included in chronic alcoholism, along with direct toxic effect ethanol.
  • Leber's hereditary optic neuropathy. Damage to the optic nerve in this disease is caused by mutations in mitochondrial DNA, which leads to defects in the functioning of the enzymes of the respiratory cycle. The consequence of this is the formation of an excessive amount of toxic molecules of active oxygen and chronic energy deficit with disruption of the functioning of nerve cells and their subsequent death.

One of the most common causes of optic neuropathy is glaucoma. The pathogenesis in this disease includes the gradual death of the retinal structures due to its chronic compression in the deformed cells of the supporting lattice plate of the sclera and the inclusion of the vascular component. That is, the process of degeneration in this case begins from the periphery, initially neurons die, then the optic nerve atrophies. The same mechanism is characteristic of other pathological conditions occurring with a clinically significant increase in intraocular pressure.

Clinical manifestations

Average optic nerve contains about 1-1.2 million neuronal fibers, each of which is covered with a myelin sheath. This structure provides isolation of the conducted pulses and increases the speed of their transmission. It is the defeat of these fibers in any part of the nerve that most often causes the appearance of symptoms, regardless of the etiology of the process and the localization of the primary focus of degeneration.

To the main clinical manifestations optic neuropathy includes:

  • Decreased visual acuity, and this impairment does not lend itself to adequate correction with glasses / lenses. Initially, patients may report blurred vision.
  • Change in color perception.
  • Change in visual fields. Sections and quadrants may fall out, central and paracentral scotomas appear (defects in the form of blind spots that do not perceive light stimulation). With a pronounced concentric narrowing of the fields, one speaks of the formation of tunnel vision.

These disorders can appear and progress at different rates, and they are often asymmetric or even one-sided. Additional and not always detectable symptoms include pain behind or inside the eyeball, change in position and mobility eyeball... It should be understood that they are all signs of a primary disease, and not a consequence of damage to the optic nerve.

Features of some forms of optic neuropathy

Despite the uniformity of symptoms, optic neuropathy of various origins has some features.

  • In posterior ischemic neuropathy, symptoms usually increase gradually and asymmetrically. Their appearance is associated with chronic disorder blood supply to the intraorbital part of the optic nerve against the background of damage to the carotid arteries and their branches. Therefore, this variant of optic neuropathy is more common in older people suffering from atherosclerosis, arterial hypertension, diabetes mellitus. Other vascular factors are also possible. With posterior ischemic neuropathy, fluctuations in the state are often noted with a deterioration in the quality of vision after taking a hot bath, visiting a sauna / bath, immediately after waking up, with excitement and physical activity... Moreover, both an increase and a decrease in total blood pressure can provoke an increase in nerve ischemia.
  • With anterior ischemic neuropathy, the symptoms appear acutely and increase rapidly. It is caused by acute hypoxia of the anterior optic nerve (in the nipple area). Edema and heart attacks develop, and small linear foci of hemorrhage in the retina are often found. Violations are most often one-sided and irreversible, after 2-3 weeks atrophic phenomena are noted in the optic nerve trunk.
  • With endocrine optic neuropathy, visual impairments develop subacutely and are associated with decompensated edematous exophthalmos. Venostasis, increased intraorbital pressure, edema of the oculomotor muscles and orbital tissue, deterioration of blood perfusion through the arteries - all this leads to compression and ischemia of the optic nerve. With adequate correction of the endocrine status and a decrease in the severity of ophthalmopathy, partial reduction of symptoms is possible.

Diagnostics

Diagnosis of optic neuropathy is aimed at clarifying the etiology of the severity of the process. But the scope of the examination prescribed by the doctor often depends not only on the general clinical picture and the alleged root cause, but also from the equipment of the medical facility. Moreover, most patients, in addition to consulting an ophthalmologist (ophthalmologist), also need to contact other specialists.

Diagnosis of optic neuropathy includes the following methods and studies:

  • Assessment of visual acuity. With pronounced violations, it is possible to carry out only a test for light perception.
  • Determination of visual fields. Allows you to identify their narrowing, the loss of sectors and quadrants, the presence of livestock.
  • Color perception testing.
  • Ophthalmoscopy - examination of the fundus using an ophthalmoscope, it is optimal to carry out this examination with a medically dilated pupil. Allows you to assess the condition of the optic nerve discs, retina and its vessels. With optic neuropathy, disc pallor, discoloration to grayish, blurred or widened boundaries, bulging into the vitreous body can be detected. Edema of adjacent areas of the retina, dilation or narrowing of blood vessels (arteries, veins), and sometimes hemorrhage are often detected. In the area of ​​the disc, exudate can be seen, which looks like cotton-like layers. But with posterior ischemic neuropathy, ophthalmoscopy at first usually does not reveal any changes in the fundus.
  • Doppler ultrasonography of arteries: ocular, periorbital region (especially supra-block), carotid, vertebral. Currently, laser Doppler ultrasonography is increasingly used.
  • Retinal angiography.
  • Assessment of the physiological activity of the optic nerves, with the determination of the threshold of their electrical sensitivity, pattern-ERG,.
  • Studies to assess the condition of the bones of the skull and especially the area of ​​the sella turcica (X-ray, CT, MRI). They can also be used to identify foreign bodies, signs of masses and increased intracranial pressure.
  • Static computer perimetry.
  • Laboratory diagnostics: biochemical analysis blood with an assessment of the lipid panel and glucose levels, study of the coagulation system. In the presence of clinical signs of a B12-deficiency state, the level of the corresponding vitamin in the blood serum is determined.

Consultations of a neurologist (or neurosurgeon), vascular surgeon, endocrinologist, therapist may be shown.

Treatment principles

The treatment regimen for optic neuropathy depends on the etiology of optic nerve damage, the severity and severity of symptoms. In some cases, emergency hospitalization is indicated, in others, the doctor recommends long-term outpatient therapy. And in a number of patients, the issue of surgical treatment is being resolved.

In acute vascular ophthalmopathies, therapy should be started as early as possible, this will limit the ischemic zone and improve the prognosis. It is desirable that the scheme of a complex drug treatment was agreed by several specialists, most often the joint work of an ophthalmologist, neurologist and therapist is required.

Therapy for vascular ophthalmopathy includes several groups of drugs:

  • Vasodilators that reduce reflex vasospasm in areas adjacent to ischemia and improve blood perfusion through the affected arteries.
  • Decongestants. Their use is aimed at reducing edema in neighboring partially ischemic zones, which will help to reduce the compression of the nerve itself and the vessels feeding it.
  • Anticoagulants for the correction of existing thrombotic disorders and the prevention of secondary thrombosis. Of particular importance is heparin, which, in addition to direct anticoagulant action, also has vasodilating and some anti-inflammatory effects. The drug can be used for systemic and local therapy, it is administered intramuscularly, subcutaneously, subconjunctivally and parabulbar.
  • Disaggregants to improve the rheological properties of blood and reduce the risk of thrombotic complications.
  • Vitamin therapy, the use of neurotropic B vitamins is advisable.
  • Drugs with neuroprotective action.
  • Glucocorticoids. They are not used in all patients; the decision on their appointment is made individually.
  • Metabolic and resorption therapy.

Oxygen therapy is also used whenever possible. In the recovery period, laser therapy, magnetic and electrical stimulation of the optic nerves are indicated. And the identified vascular factors (atherosclerosis, arterial hypertension, hypotension, etc.) are subject to correction.

In other forms of optic neuropathy, the etiological factor is also necessarily affected. For example, in endocrine ophthalmopathy, the stabilization of the hormonal status is of paramount importance. In case of post-traumatic compressions, they try to remove foreign bodies and restore the physiological shape of the orbit, and evacuate large hematomas.

Forecast

Unfortunately, symptoms of optic neuropathy are rarely completely reduced even with early adequate therapy. Good results include partial restoration of vision and the absence of a tendency to progression of symptoms in the long term. In most patients, peripheral vision defects and a decrease in visual acuity persist, which is associated with the development of irreversible nerve atrophy. Chronic vascular neuropathy tends to progress slowly and steadily.

After removing the severity of the condition and stabilizing the symptoms, the prevention of repeated ischemic attacks and inhibition of the neurodegeneration process. Most often, long-term maintenance therapy is prescribed, aimed at preventing thrombosis, improving the lipid profile of the blood. Repeated courses with the use of vascular drugs are often recommended, and in the case of endocrine ophthalmopathy, the patient is referred to an endocrinologist for adequate correction of existing disorders.

Neurologist K. Firsov lectures on hereditary atrophy of Leber's optic nerves.

of optical neuropathy
A.F. Brovkina, A.G. Schuko
(RMAPO, Moscow, department of FGU MNTK
"Eye Microsurgery" named after acad. Fedorov S.N., Irkutsk)

Authors presented the comparative characteristic of some types of neuropathy (vascular and endocrine genesis). Treatment and prognosis depend on the etiologic and pathogenic factors.

Optical neuropathy (OH) is a collective concept that unites several diseases in which the fibers of the optic nerve from the retina to the brain are affected. Taking into account the etiological aspects, the mechanism of its development is different.
The causal classification of OH can be represented as follows:
... compression
... ischemic
... inflammatory
... hyperbaric
... traumatic
... radiation
... metabolic
... congenital.
The development of the pathological process of OH of any type is based on ischemia and hypoxia of nerve fibers with weakening of antioxidant activity, which may be preceded by impaired blood circulation, compression of nerve fibers of the optic nerve, blockade of axonal transport, intoxication, activation of peroxide processes and neurotoxic reactions. However, the degree of intensity of these mechanisms, the place of their application and the sequence of their appearance are different depending on the main pathological process.
For example, for primary glaucoma the main triggering factors for the development of optic neuropathy are an increase in ophthalmotonus or a decrease in cerebrospinal fluid pressure in the retrobulbar part of the optic nerve. This leads to deformation of the supporting structures (especially the ethmoid plate of the sclera) with subsequent infringement of the bundles of nerve fibers in the deformed tubules of the ethmoid plate of the sclera and / or hypoxia of the optic nerve head.
Anterior ischemic OH develops in acute circulatory disorders in the anterior segment of the optic nerve. A decrease in perfusion pressure in the posterior short ciliary arteries and ischemia in the prelaminar, laminar and retrolaminar parts of the optic nerve leads to the development of a clinical picture of anterior ischemic neuropathy. Characterized by a rapid and sharp decrease in visual acuity, fast development optic nerve atrophy.
In patients with edematous exophthalmos, OH develops against the background of an increase in extraocular muscles. The process occurs quickly, before the axoplasmic current is disturbed, blood flow is disturbed, both arterial (as a result of compression by enlarged muscles of the main arterial vessels) and venous.
Having extensive personal experience and analyzing the mechanism of development of some forms of optic neuropathy, the authors in this work set themselves the task of studying the features of the clinical picture of OH (vascular) and endocrine (edematous exophthalmos) genesis, as the most common and requiring a fundamentally different therapeutic approach. This is due to the fact that in a number of publications, not only vascular processes, but also thyrotoxic exophthalmos are considered as the basis for the development of anterior ischemic OH. This position is fundamentally wrong, since thyrotoxic exophthalmos, although it represents one of the forms of endocrine ophthalmopathy, is never accompanied by organic changes in soft tissues orbits. A different picture is observed with edematous exophthalmos. Comparison of the data of ophthalmoscopy and computed tomography, carried out by one of us earlier, allowed us to make a judgment about the main mechanisms of development of OH. The triggering mechanism of OH in edematous exophthalmos is a sharp increase in the volume of extraocular muscles at the apex of the orbit (Fig. 1). At least two factors are involved in the mechanism of its development: mechanical compression of the optic nerve and violation of the blood-ophthalmic barrier, resulting in edema and tissue hypoxia, and energy cellular metabolism is disrupted. The end result of these disorders is blockade of axon transport (Fig. 2).
Anterior ischemic OH is characterized by a sudden sharp decrease in visual functions as a result of ischemic infarction of the optic nerve and its head. This definition is confirmed by J.D. Gass with the following phrase: "Anterior ischemic optic neuropathy is edema, ischemia and varying degrees of infarction of the anterior part of the optic nerve, caused by a reduction in blood flow in the nerve." Persons aged 45 and over are affected (mean age 69). The process is often one-sided, but in 40% of cases, damage to the optic nerve on the opposite side with a fairly significant time interval is possible.
Ophthalmoscopically, the optic disc has a grayish-white or yellowish color with a sharp swelling of its tissue. Prominence is more pronounced in the upper half of the disc. In the acute stage, streak-like hemorrhages are possible on the disc or along its edge (Fig. 3). The edema extends to the peripapillary nerve fibers (Fig. 4). Cotton-wool exudate with separate foci is located juxtapapillary. There is edema in the macular area. Arteries and veins are narrowed. The transition to the chronic stage, when the regression of disc edema with the transition to atrophy (secondary) occurs, occurs quickly (after 2-3 weeks). During this period, cystic dystrophy or its fibrotic changes develop in the macular zone.
In those cases when it is possible to examine the field of vision, loss is detected in the lower half (1/3 of cases), in 12% of patients an absolute scotoma is recorded in the Bjerrum space, less often (about 6%) it is possible to identify a central scotoma and concentric narrowing of the field of vision.
In patients with edematous exophthalmos in the stage of subcompensation or decompensation (more often) of the pathological process, when the manifestation of clinical symptoms increases, venous stasis occurs in the tissues of the orbit, in the optic nerve. An early sign of a violation of the compensation process and the appearance of OH is the expansion of the retinal veins, which leads to hypoxia, primarily of the retinal ganglion cells (Fig. 5). Early impairment of visual functions is characteristic. Initially, most patients develop peripheral scotomas with normal visual acuity, they are detected in the extreme periphery of the outer and upper parts of the visual field.
According to ophthalmoscopy data (the state of the optic nerve head and retinal vessels), two forms of OH were identified: initial (57%) and developed (43% of patients).
The initial OH was characterized by the presence of dilated and tense retinal veins (Fig. 6). The optic disc remains normal with subcompensated edematous exophthalmos. In the stage of its decompensation, blurring of the boundaries of the optic nerve head appears, its edema. Unlike anterior ischemic OH, vision in patients with edematous exophthalmos and OH deteriorates gradually to 0.1-0.7. Sharp deterioration vision (before light projection) occurs when hyperemia and edema of the optic nerve head appear (Fig. 7). However, the process is reversible: against the background of basic intensive therapy, with a decrease in clinical symptoms, visual acuity increases, and changes in the field of vision decrease or disappear. This confirms the hypothesis of the development of OH during compression of tissues at the apex of the orbit against the background of a hypoxic state, which has a detrimental effect on the ganglion cells.
Each of these factors (or both together) leads to a disturbance in axoplasmic transport connecting the body of the retinal ganglion cell with its terminals.
Thus, OH, taking into account pathogenetic factors, has its own clinical differences, differs in the nature of the course of the pathological process and its outcome.
Comparative characteristics of the analyzed types of OH are presented in Table 1.
The differences presented in the table confirm the possibility of clinical differentiation of OH depending on etiopathogenetic factors, which determines the planning of drug or surgical treatment and visual prediction in each case.

Literature
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And one of the most insidious. Starting sometimes imperceptibly, gradually, it strikes a blow to the eyesight at the most unexpected moment. And it is a companion of many other diseases that, for the time being, do not manifest themselves in any way.

Our expert is an ophthalmologist, senior researcher at the Research Institute of Eye Diseases of the Russian Academy of Medical Sciences, Candidate of Medical Sciences Natalia Sheremet.

Dangerous failure

Optical neuropathy is targeted by the optic nerve, which transmits all visual information obtained by the retina of the eye. When, for one reason or another, a part of the optic nerve fibers, resembling a telephone wire in a dense braid, dies, incomplete information reaches our main "control panel", as a result of which one or another sector of the visual field (in the center or on the periphery) falls out, decreases visual acuity, its color characteristics change.

Most often, the disease begins acutely. But there is also a more hidden course of it, when the victim of neuropathy may not notice any vision problems. Until it decreases so much that it becomes difficult for a person to watch TV, read ... Experts warn: if the problem is not dealt with, the case may end in complete blindness.

It is also important to consult an ophthalmologist in time and undergo an examination because optical neuropathy, like diabetes mellitus, arterial hypertension or hypotension, atherosclerosis, pathology of the blood coagulation system, multiple sclerosis, which at first may no longer manifest themselves.

One hundred troubles - one answer

Brain tumors are often the cause of optic neuropathy (including in young people). In this case, early diagnosis is not only a guarantee of saving vision, but sometimes life itself.

A special article - patients who received other diseases as a result of treatment. According to our expert, women who have developed optic neuropathy after the use of hormonal contraceptives and hormone replacement therapy, which affects the coagulation properties of the blood, and hence the nutrition of the optic nerve, often turn to her.

In some patients, due to the individual characteristics of their body, some drugs for the treatment of cardiac arrhythmias can also impair vision, which is why, on the recommendation of an ophthalmologist, the cardiologist often selects another drug for them.

That's just with timely diagnosis neuropathy, which is early stages is successfully treated, with us, alas, big problems... Sometimes even experienced doctors cannot identify this diagnosis for a long time. Therefore, the specialists of the Research Institute of Eye Diseases of the Russian Academy of Medical Sciences recommend: at the first suspicion of visual impairment (decrease in visual acuity, change in color perception, change in the field of vision, etc.), contact an ophthalmologist.

And go through a comprehensive examination, which, if you suspect optic neuropathy, must necessarily include: a study of visual acuity, fundus, eye pressure, visual fields (perimetry), color vision, structure of the optic nerve (optical coherence tomography), electrophysiological methods. Otherwise, the problems will not be long in coming.