Chronic recurrent inflammatory optic neuropathy. Ischemic optic neuropathy

There are 2 types of MN infarction: caused by arteritis and not caused by arteritis. The second option is much more common, usually among people aged about 50 and older. Vision loss in this case is not as severe as that caused by arteritis. MN infarction caused by arteritis occurs more often in the age group of 70 and older.

Ischemic neuropathy of the optic nerve is usually unilateral. Simultaneous bilateral lesions are unusual for ischemic neuropathy, and sequential lesions occur only in 20% of cases. The involvement of both optic nerves in the pathological process most often indicates a connection with arteritis. Atherosclerotic narrowing of the posterior ciliary arteries may predispose to non-arteritic optic nerve infarction, especially during an episode of low blood pressure. At the same time, any inflammatory disease of the vascular wall can provoke an arterial form of infarction.

Acute ischemia causes swelling of the MN disc, which in turn worsens the ischemia. The small size of the excavation relative to the overall size of the optic disc is a risk factor for the non-arteritic form. Also, all processes that provoke atherosclerosis lead to the development of non-arteritic infarction: diabetes, smoking, hypertension, certain medications (amiodarone and, presumably, phosphodiesterase-5 inhibitors), hypercoagulation. A sharp deterioration in vision upon awakening suggests that nocturnal hypotension plays a role in the development of non-arteritic infarction.

Symptoms and signs of ischemic optic neuropathy

Loss of vision in both variants of the development of the disease is rapid and painless. Vision deterioration occurs in a matter of minutes, hours or days. Some patients report worsening vision upon awakening. General malaise, muscle pain, pain when scratching, chronic subluxation of the lower jaw and pain along the temporal artery indicate temporal arteritis, but can occur after vision deterioration. Visual acuity decreases, and an afferent pupillary defect appears. The disc of the optic nerve swells and rises, and small vessels are damaged, leading to the formation of hemorrhages around the disc. The disc of the optic nerve in the arteritic variant has a pale color, and in the non-arteritic variant it is hyperemic. In both variants, when examining the visual fields, a defect is observed in the central and lower fields.

Diagnosis of ischemic optic neuropathy

  • ESR and SRB.
  • CT or MRI if vision loss progresses.

Diagnosis is usually made based on clinical findings, but additional testing may be necessary. It is very important to diagnose the arterial variant in time, because there is a high probability of developing a pathological process in the other eye. ESR can help with this - in case of arterial infarction it will be greatly increased. OAK in both cases may show thrombocytosis. If giant cell arteritis is suspected, a CRP test and temporal artery biopsy can help confirm it. In some cases of progressive vision loss, a CT or MRI may be recommended to rule out damage due to structural compression.

For nonarteritic ischemic neuropathy of the optic nerve, additional investigations are recommended based on suspected risk factors. For example, if a patient has increased daytime weakness, snoring, or is overweight, polysomnography is recommended. If vision deterioration occurs upon awakening, continuous monitoring of blood pressure is recommended.

Prognosis of ischemic optic neuropathy

There is no effective treatment. However, up to 40% of patients with nonarteritic infarction experience spontaneous partial recovery of function.

Treatment of ischemic optic neuropathy

In the arterial variant, it is advisable to prescribe corticosteroids (prednisone 80 mg po once a day, under the control of ESR) to prevent infarction in the second eye. Aspirin or corticosteroids for nonarteritic infarction have been unsuccessful. Risk factors should be controlled. It is useful to use aids for the visually impaired (magnifying glasses, large print, talking clocks).

Key Points

Ischemic MN neuropathy is usually caused by giant cell arteritis or atherosclerosis.

  • The only obligatory symptom is a sudden painless deterioration in vision.
  • Giant cell arteritis should be excluded to reduce the risk of developing collateral lesions.
  • The prognosis is unfavorable.

Optic neuropathy is a dangerous pathology that can lead to vision loss. The disease is not independent and often becomes a consequence of other diseases. From this article you will learn all the details about this condition: its forms, causes of development, signs, as well as features of diagnosis and further treatment.

In this article

What is optic neuropathy?

One of the most important elements of the structure of the eyeball is the optic nerve. Its anatomy is quite complex and is of great importance in ensuring clear vision. The optic nerve transmits nerve impulses from the eyes to the brain and back. The condition of the intrabulbar region plays an important role in this process. It is located within the eyeball from the vitreous body to the outer layer of the sclera. Due to impaired blood circulation in the intrabulbar region, the optic nerve is damaged. Its tissues receive less nutrients that are necessary for normal functioning. The consequence of this is eye neuropathy.

Pathology usually develops in people aged 50-60 years. Most often, men are affected by this disease. This is a dangerous condition that can lead to decreased vigilance, impaired peripheral vision, “color blindness,” and the formation of scotomas—dark spots that impair visibility. The most serious consequence of the pathology is complete blindness. Optic neuropathy is not an independent ophthalmological disease. This is one of the manifestations of other diseases. Doctors include these:

  • atherosclerosis;
  • diabetes mellitus;
  • cardiac dysfunction;
  • rheumatoid arthritis;
  • hypertension.

The second name for optic neuropathy is neuroopticopathy or ischemic neuropathy. This condition is easily confused with neuritis. In fact, these are different pathologies and it is very important to distinguish them. In order not to confuse ocular neuropathy with other disorders of the visual organs, it is important to know the reasons for the development of this condition, its characteristic signs, methods of diagnosis and treatment.

Symptoms of optic neuropathy

Pathology is characterized by rapid development. It comes suddenly. The main symptom of this disease is decreased vigilance. Visual impairment resulting from neuropathy is usually temporary. Visibility problems can last from 10-15 minutes to several hours. In many people, neuropathy causes impairment of light perception, the main function of the rod apparatus of the retina. This usually happens with mild lesions of the optic nerve. If the damage is more serious, then complete blindness can suddenly occur. The main symptoms of this condition include:

  • eye pain;
  • blurred vision;
  • color vision impairment;
  • tunnel vision;
  • headaches.

Narrowing of the visual field, loss of parts of the image, impaired color perception - all these are symptoms that characterize neuropathy. Integrity is very important to the optic nerve. If it is disrupted, a condition such as atrophy may occur. This is the name for complete or partial destruction of the optic nerve fibers. With incomplete atrophy, vision is not completely reduced. This is due to the fact that the nerve tissue is affected only in a certain area. This condition often leads to problems with peripheral vision - vision outside the focus of attention is impaired. The completeness of the image is interrupted by scotomas - “blind” areas in the field of view.

Anterior ischemic optic neuropathy

Doctors distinguish several types of eye neuropathy. The most common is the ischemic form of this pathology. This condition develops due to damage to the optic nerve, which is a consequence of impaired blood supply. The nerve bundles in the eye area are compressed, which leads to a deficiency of nutritional components. This form of pathology is considered secondary. Usually its development is associated with cardiovascular diseases. Optic neuropathy is often caused by disturbances in the functioning of the endocrine and central nervous systems. Doctors call deterioration of hemodynamics in the area of ​​the eyeballs “anterior neuropathy.” Blood flow disturbance occurs in the anterior segment of the optic nerve.

There are two types of pathology. They differ depending on whether a person suffers from arteritis - inflammation of the arterial walls - or not. Nonarteritic ocular neuropathy usually occurs suddenly. It develops against the background of diseases such as:

  • sleep apnea;
  • coagulopathy;
  • diabetes mellitus;
  • microscopic polyangiitis;
  • microangiopathy;
  • hypertension.

A person usually has vision loss in one eye. Only the top or bottom of the image is clearly visible. Damage to both eyes at the same time does not occur often - in approximately 15% of cases. But vision in the second eye may not deteriorate immediately. Sometimes this happens within 5-7 years. Pathologies are more common in people over 50 years of age. This disorder is extremely rare in children. Against the background of arteritis, this disease develops less frequently. Its symptoms are similar to those of non-arteritic neuropathy. At risk for this pathology are people over 50 years of age who suffer from headaches, jaw muscle spasms, myalgia, alopecia, and loss of appetite. Any changes in the shape of the optic nerve head are also the cause of the development of pathology.

Posterior ischemic optic neuropathy

The second form of neuropathy occurs due to hemodynamic disturbances in the posterior parts of the optic nerve. Often this condition develops due to narrowing of the arteries of the eyeball. Research by scientists has led to the conclusion that posterior neuropathy is one of the main causes of decreased vision and complete blindness in people of all ages. Many diseases that are associated with ischemic disorders have become “younger” in recent years. Middle-aged people and young people are increasingly faced with hypertension, hypotension, and atherosclerosis. In the case of acute circulatory disorders of the optic nerve, the factors that precede the onset of pathology are sclerotic lesions and thromboembolism. The main reason for this condition is decreased hemodynamics due to narrowing of the arterial lumen. Doctors call this disorder ischemia. It often leads to dysfunction of the optic nerve. The rate of development of pathology depends on many factors. Among them:

  • atherosclerosis;
  • duration of ischemia;
  • rapid decrease in blood flow;
  • decreased oxygen content in tissues;
  • disorders of the central nervous system;
  • damage to kidney tissue;
  • hypertension.

Unlike the anterior form of eye neuropathy, the posterior form occurs spontaneously. At risk are people who suffer from cardiovascular diseases. But the presence of these ailments in the patient’s medical history is not a prerequisite for the development of visual pathology. Often the posterior form of neuropathy occurs due to damage to the central retinal vein, diabetic angioretinopathy, narrowing of the orbital arteries, and traumatic brain injury. Posterior ischemic optic neuropathy is dangerous because it can lead to complete blindness. Research by scientists has led to the conclusion that posterior neuropathy is one of the main causes of vision decline and loss in people of all ages.

Diagnosis of optic neuropathy

If symptoms of this disease are detected, the patient should make an appointment with an ophthalmologist. An examination by a doctor should include an examination of the structures of the eye, a test of visual acuity, and ophthalmoscopy - examination of the fundus of the eye. Depending on the condition of the eyes, the list of studies may be supplemented. Refraction test, color testing, perimetry - examination of visual fields using a special device - these are the most common procedures that ophthalmologists perform additionally. In severe forms of the disease, the doctor may prescribe an ultrasound of the eye, electrooculography, or rheoophthalmography. These studies allow the ophthalmologist to assess in detail the state of ocular blood flow.

In some cases, the doctor recommends that the patient visit specialized specialists: a neurologist, cardiologist, hematologist, endocrinologist. Consultation with a wide range of professionals allows you to prescribe effective treatment, which should be started immediately.

Treatment of optic neuropathy

A prerequisite for treating a disease is its immediateness. It is important to prevent the death of nerve cells, which occurs as a result of prolonged hemodynamic disturbances. In case of ischemia, it is recommended to call an ambulance. The paramedic will intravenously administer a solution of Eufillin - 5 or 10 ml, depending on the severity of the patient’s condition. Emergency therapy also includes taking Nitroglycerin and, if necessary, inhaling ammonia vapor.

Treatment of optic neuropathy should be carried out in a hospital setting. To treat this condition, doctors use corticosteroid medications, such as:

  • "Kenacort";
  • "Prednisolone";
  • "Hydrocortisone";
  • "Sinaflan";
  • "Lokoid".

Doctors prescribe corticosteroid drugs to relieve swelling. These drugs are hormonal, therefore the admissibility of their use in the treatment of ocular neuropathy should be agreed upon after a complete examination of the patient.

Therapy for pathology must necessarily include the prescription of anticoagulants - drugs that improve blood clotting. They prevent the formation of blood clots and help normalize hemodynamics. These are drugs such as:

  • "Heparin";
  • "Warfarin";
  • "Dicumarin";
  • "Phenilin";
  • "Hirudin".

When treating optic neuropathy, special attention should be paid to the underlying disease against which the ophthalmological pathology developed. To normalize blood pressure, doctors usually prescribe:

  • "Enalapril";
  • "Metoprolol";
  • "Veroshpiron";
  • "Kizinopril";
  • "Verapamil."

When treating the disease, doctors often prescribe nootropic drugs. These are a kind of “pills for the brain”, the use of which improves mental processes. In the treatment of pathology, they help to activate metabolism in nerve cells. Particularly effective:

  • "Glycine";
  • "Piracetam";
  • "Phenotropil";
  • "Pyritinol";
  • "Pantogam".

Taking a whole range of medications has a negative impact on the general condition of the body. Human immunity decreases. Therefore, the immune system should be supported. In order for the treatment of neuropathy to be effective and not cause harm to health, it is recommended to supplement the list of drugs with vitamins B, C and E. They can be prescribed in the form of tablets and intramuscular injections. Any medications should only be prescribed by a doctor.

As a result of impaired blood supply, ischemic optic neuropathy develops. The pathology is considered secondary and occurs against the background of diseases of the cardiovascular, nervous or endocrine systems. Symptoms manifest themselves actively, the patient’s vision sharply decreases. Males over 40 years of age are at risk. To confirm the diagnosis, it is necessary to study the condition of the optic nerves in detail, so 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 optic neuropathy is often called disc infarction. This condition requires urgent hospitalization.

Etiology and pathogenesis

If the local blood supply is disrupted, the nerve tissues of the eyes do not receive the necessary substances for full functioning. As a result, optic nerve atrophy develops, which ultimately causes blindness. Ischemia occurs due to hemodynamic dysfunction. The following factors can trigger this process:

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

In most cases, the pathology affects only one visual organ.

Pathology of the optic nerve is more often unilateral, only in 30% of cases ischemia of both eyes is observed. The disease is characterized by a sequence when the symptoms of the disease pass from one eye to the other after some time. This process is observed in a third of patients, but it is difficult to predict. The disease on the second organ can appear in a few days or over 10 years.

Possible symptoms

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

  • rapid decrease in visual acuity;
  • square loss from the field of view;
  • dull headache;
  • dilated retinal vessels;
  • traces of pinpoint hemorrhage.

A person becomes completely blind in the total form of the pathology.

The acute form of the disease lasts for a month, then the swelling disappears. This means atrophy of nerve fibers begins. If swelling develops in the intraorbital region, posterior ischemic neuropathy is diagnosed. In this case, the damaged nerve is located immediately behind the eyeball. The symptoms are almost identical to the anterior type, but some changes in the fundus are observed. The danger is the total form, when all parts are damaged and optical neuropathy develops. This process leads to irreversible blindness. Ischemic neuroopticopathy is rare, but practically untreatable.

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 comprehensively, in addition to an ophthalmological examination, consultation with a neurologist, endocrinologist, hematologist and rheumatologist is necessary. Diagnostics involves a full range of procedures that allow you to determine the primary cause. First, the ophthalmologist examines the fundus of the eye for signs of swelling. Both eyes must be checked, and the emphasis is on studying the condition of the retinas. Then a number of additional procedures are prescribed:


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

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

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Description

Vascular lesions of the optic nerve occur with changes in the vessels supplying the optic nerve, as well as with pathology of the cerebral vessels. They are described under various names: acute circulatory disturbance in the system of arteries supplying the optic nerve, arteriosclerotic papillitis, ischemic edema, opticomalacia, disc edema due to diseases of the optic nerve arteries, atherosclerotic neuritis, ischemic neuropathy, anterior ischemic neuropathy.

These terms appeared in the early stages of studying vascular pathology of the optic nerve and reflect only one aspect of the disease process. Thus, some of them indicate damage only to the arteries of the optic nerve, while there are also venous disorders, others (ischemic neuropathy, anterior ischemic neuropathy) emphasize the presence of ischemia in the fundus.

But the latter is not always observed with vascular disorders in the optic nerve. In some cases, the optic disc may be hyperemic or remain within normal limits. All these designations cannot be considered sufficiently accurate. S. F. Shereshevskaya et al. (1981) circulatory disorders in the optic nerve are called vascular optic neuropathy. This term, although generalizing, is more objective; in the clinic it is more appropriate to use this definition.

Optic neuropathy.

Etiology .

The causes of damage to the vessels of the optic nerve are mainly general vascular diseases: atherosclerosis, hypertension and hypotension, temporal arteritis, periarteritis nodosa, obliterating arteritis, diabetes mellitus, disorders in the vertebrobasilar system in discopathy of the cervical spine, thrombosis of the great vessels.

Pathogenesis.

Acute circulatory disorders in the optic nerve can be based on both functional vascular disorders (spasms) and organic changes. Organic changes have been morphologically studied mainly in atherosclerosis and temporal arteritis. M. I. Merkulova (1962), N. Piper and L. Unger (1957), W. Peters (1958), S. DukeElder (1971) showed that against the background of general atherosclerosis, the development of sclerotic changes in the vessels of the optic nerve is possible. Certain disturbances in hemodynamics and coagulation properties of blood can cause the formation of a blood clot.

Thrombosis leads to vascular occlusion, deterioration of the blood supply to the optic nerve and subsequent death of nerve fibers due to the appearance of softening foci, nested gliosis and proliferation of connective tissue.

With temporal arteritis, an inflammatory process is observed in the wall of the temporal artery: giant cell infiltration occurs, which is gradually replaced by connective tissue. S. Heyrch (1974), using the method of fluorescein angiography, came to the conclusion that occlusive processes in the posterior ciliary arteries are of primary importance in the pathogenesis of optic vascular neuropathy.

Partial occlusion of the posterior ciliary arteries, as well as severe general hypotension and large blood losses can lead to a decrease in perfusion pressure. A drop in perfusion pressure causes disruption of hemocirculation, primarily in the vessels of the optic nerve head, in non-ripanillary choroidal vessels, and then in the entire choroidal vascular system.

With temporal arteritis, stenosis of the orbital artery and impaired capillary circulation in the retrobulbar region occur.?

Clinic.

Diagnosis of vascular disorders in the optic nerve is based on anamnestic data, information about the condition of the fundus and the results of functional studies. Among the latter, the determination of the field of view occupies a particularly important place. There are two forms of vascular lesions of the optic nerve - arterial and venous, each of which can occur acutely and chronically.

Acute arterial circulation disorder is characterized by a sudden decrease in visual acuity or the appearance of defects in the visual field, which often occur after sleep, physical or emotional stress, and sometimes in complete well-being.

Visual acuity with arterial dyscirculation can be sharply reduced to the movement of the hand near the face, hundredths, or remain within tenths. In the visual field, changes are detected in the form of prolapse of the lower sections, lower internal quadrants, various defects in the upper halves of the visual field, central and paracentral scotomas, concentric narrowings.

In patients with impaired arterial circulation in the optic nerve, treated in the clinic of eye diseases of the Ukrainian Institute for Advanced Medical Studies, both hemianopic or quadrant restrictions in the lower or upper halves of the visual field, as well as central or paracentral scotomas were equally often observed; concentric narrowing of the visual field was observed less often. In Fig. 102, 103, 104 present variants of visual field defects in patients under our supervision.

In the fundus, swelling and severe ischemia of the optic nerve head, narrowing of arterial vessels, and sometimes accompanying hemorrhages are often detected (Fig. 105). In some patients, the fundus may be normal or there may be mild disc swelling without ischemia.

Yes, from 76 patients who were treated in our clinic for acute arterial circulation disorder in the optic nerve, 19 the optic disc did not present any abnormalities or there was slight swelling without ischemia. Acute arterial circulation disorder in such cases is diagnosed on the basis of a sudden decrease in visual acuity, characteristic defects in the visual field and the result of additional examinations.

Some features of changes in the fundus have been noted in temporal arteritis (Hortop's disease). In the early stage of this disease, congestive hyperemia of the optic nerve head appears, turning into pronounced vitreous edema; the latter is often accompanied by the deposition of a milky-white exudate on the disc.

Quite often, vascular edema of the optic disc with temporal arteritis is combined with obstruction of the central retinal artery or its branches. Usually the pathological process is malignant.?

An acute disturbance of arterial circulation in the optic nerve ends in rapidly developing partial or complete atrophy of the optic nerve. Within a period of several weeks or months to 1-2 years and later, usually similar changes in the optic nerve appear in the other eye.

Since optic nerve atrophy is detected at the bottom of the previously affected eye, and vascular edema resembling a congestive disc is detected at the bottom of the other eye, the disease can be mistakenly regarded as Kennedy syndrome, but a detailed history and general examination data can avoid this mistake.

In acute venous circulation disorders, visual acuity, as in arterial disorders, is reduced to varying degrees (from tenths to light perception). But the dynamics of vision loss with changes in the venous system differs from those with arterial disorders. According to our observations, in cases of venous circulation disorders, a mild decrease in visual functions may initially be observed, but after 1-2 day there is a progressive deterioration to stable limits.

With arterial dyscirculation, as mentioned above, a decrease in visual acuity appears suddenly. This position can be used as one of the differential diagnostic signs of impaired arterial and venous circulation in the optic nerve. Typical visual field defects in venous circulation disorders are central or paracentral scotomas, concentric narrowing of the visual field, horizontal hemia-type loss

On ophthalmoscopy, the optic disc appears slightly edematous, maintaining a pink color, or hyperemic (there are streak-like retinal hemorrhages around it). The veins are often dilated, and there may also be hemorrhages along their course (Fig. 106). The arteries are of normal caliber or narrowed. The process ends with optic nerve atrophy.

Chronic vascular insufficiency is characterized by a slow gradual development of the disease and is manifested by a decrease in visual acuity, often pronounced swelling of the optic disc, and narrowness of the arteries. The disease ends with atrophy of the optic nerves.

S. Heureh (1976) considers optic nerve atrophy in low-pressure glaucoma as chronic vascular insufficiency. It occurs as a result of discirculation in the posterior ciliary arteries due to an imbalance between perfusion and intraocular pressure. A drop in perfusion pressure in the posterior ciliary arteries may be associated with local or systemic vascular disorders, such as arterial hypotension, embolic phenomenon, and hematogenous disorders.

Optic nerve vasculitis.

Among vascular pathologies, vasculitis, described by S. Heyreh (1972) and others, deserves attention.

Etiology

The disease has not been precisely elucidated. It is believed that it is based on an inflammatory-allergic reaction to bacteria, viruses and various substances of an antigenic nature. This assumption is confirmed by the effectiveness of corticosteroids.

Clinic .

Vasculitis of the optic nerve occurs at a young age and is unilateral. Visual acuity does not decrease sharply. Peripheral vision is not affected. Ophthalmoscopically it can appear in two forms. In the first form, the picture resembles a congestive disc, but the lack of data indicating liquor hypertension and the one-sidedness of the disease do not confirm this diagnosis.

In the second form, multiple hemorrhages are observed in the fundus along the vessels, as with thrombosis of the central retinal vein, but not as extensive. There are “couplings” along the vessels and small “lumps” of white exudate. The development of the first form is explained by vasculitis of the disc vessels, which leads to increased capillary permeability and swelling.

In the second form, phlebitis of the central retinal vein develops in the area of ​​the head of the optic nerve or the retrobulbar part, which causes localized thrombosis of the central vein; in such cases, stasis phenomena prevail over disc edema. The prognosis is favorable. V. I. Kobzeva and M. P. Pronin (1976) described 5 patients with optic nerve vasculitis.

Lesions of the optic nerve caused by pathology of intracranial vessels include its changes in amaurotic-hemiplegic Elynnig-Merkulov syndrome, which is quite common in clinical practice.

The syndrome consists of amaurosis or decreased vision in one eye and movement disorders (hemiplegia, hemiparesis) on the opposite side. It is observed in patients with atherosclerosis, hypertension, and rheumatism. Amaurotic-hemiplegic syndrome develops when there is a violation of blood circulation in the central retinal and middle cerebral arteries.

The cause of the development of Elynig-Merkulov syndrome is most often thrombosis of the internal carotid artery. At the same time, blood flow in the arterial circle of the cerebrum increases, near the thrombus in the internal carotid artery, vortex juices are created, which contribute to the separation of pieces from the thrombus. The latter can close the lumen of the central retinal or middle cerebral arteries.

The clinical picture of crossed amaurotic-hemiplegic syndrome may be due to overirritation of the carotid sinus located in the area of ​​the bifurcation of the common carotid artery. In this case, visual and motor disturbances develop as a result of vascular spasms or regional hypotension and are transient.

The disease often manifests itself as changes in the organ of vision. After a few days or months, movement disorders appear. Motor and then visual disturbances appear. Only occasionally do visual and movement disorders develop simultaneously.

As a rule, patients note primarily unilateral vision loss to varying degrees. Various changes are detected in the field of view depending on the location and severity of the process. Ophthalmoscopically, the main picture observed is vascular optic neuropathy or acute obstruction of the central retinal artery, leading to optic nerve atrophy.

There are known cases of transient visual impairment from several seconds to several minutes with normal fundus. A short-term decrease in vision can be explained by the occurrence of a spasm in the vessels supplying the retina or optic nerve. Movement disorders are observed (from minor hemiparesis to complete hemiplegia), which may decrease over time.

Treatment.

Patients with vascular pathology of the optic nerve need emergency care. Their treatment should be comprehensive and agreed upon with a therapist and neurologist. The use of vasodilators, decongestants, and anticoagulants is indicated. Among the latter, heparin deserves special attention.

Being a direct anticoagulant, it simultaneously produces a vasodilator, anti-inflammatory and hyposensitizing effect. Heparin can be administered bulbarly, subconjunctivally, as well as intramuscularly or subcutaneously. Antisclerotic agents (diasponin, cetamifene, iodine preparations, etc.), vitamin therapy (B vitamins), ATP, distraction and resorption therapy, oxygen therapy are recommended.

Along with this, for vascular processes caused by temporal arteritis and for vasculitis of the optic nerve, corticosteroids and hyposensitizing agents are indicated.

Forecast

in case of vascular diseases of the optic nerve, it is always serious, but not hopeless. In some cases, under the influence of treatment, improvement or stabilization of the disease process may occur. However, it is not always persistent, so repeated treatment in the form of regular courses is required.

Vascular pathology of the optic nerve is one of the pressing problems in ophthalmology, due to the complexity of arteriovenous circulation in various parts of the optic nerve. Recently, the incidence of vascular diseases of the optic nerve, leading to low vision and blindness, has increased, including in young people. The causes of vascular pathology are varied. The most common diseases that cause circulatory disorders in the optic nerve are atherosclerosis and hypertension. Circulatory disorders in the vessels of the optic nerve develop with occlusive lesions of the carotid arteries, against the background of diabetes mellitus and other endocrine pathologies. Vascular pathology of the optic nerve is possible in case of systemic diseases, vasculitis, cerebrovascular accidents, and glaucoma. Depending on the etiology of the disease, the clinical course of ischemic neuropathies has its own characteristics, which makes it possible to select adequate treatment. The terminology of vascular diseases of the optic nerve is very diverse, however, most authors consider the most acceptable term to be ischemic optic neuropathy, which, according to the location of the lesion, is divided into anterior (damage to the optic nerve head) and posterior (damage to the postlaminar part of the optic nerve).

Anterior ischemic optic neuropathy (AION) can be a bilateral process characterized by acute loss of visual function. In the pathogenesis of PION, the main role is played by circulatory disorders in the system of the posterior short ciliary arteries.

Target— identification of features of the clinical course of PION depending on the etiology of the disease.

Material and methods. We observed 34 patients aged from 45 to 77 years (20 men, 14 women). To assess visual functions, the following techniques were used: visometry, computer perimetry, tonometry, biomicroscopy, ophthalmoscopy, electron tonography, ultrasound biomicroscopy, laser scanning retinal tomography (HRT), laser Dopplerography. The patients were examined by a therapist, a neurologist, an endocrinologist, and, if indicated, by a cardiologist and an angiosurgeon. Diagnoses were established: arterial hypertension - in 13 patients, glaucoma - in 10, diabetes mellitus - in 8, atherosclerosis - in 3 patients. Diagnoses of hypertension, atherosclerosis, and diabetes mellitus were established by a therapist and an endocrinologist.

Results and discussion. PION in arterial hypertension was characterized by a sudden decrease in visual acuity, the appearance of a central scotoma, loss of the lower half of the visual field or sector 8-24 hours after the hypertensive crisis. Visual acuity decreased on average to 0.02-0.04. During biomicroscopy, all patients showed a decrease in the pupillary reaction on the affected side. In the fundus of the eye, in 89.0% of cases the Solyus-Hun symptom of the 2nd-3rd degree was visualized, in 43.0% the presence of streak-shaped hemorrhages, in 85.6% - swelling and prominence of the optic nerve head, in 38.5% - cotton-like exudates. With significant blood pressure levels, 77.9% of patients had ischemic edema of the peripapillary zone of the retina involving the macular region and ischemic exudate on the optic nerve head. Computed retinotomography (HRT) revealed unclear boundaries of the optic disc, its prominence by 1-2 mm, banded hemorrhages, pale optic disc and an average increase in area of ​​1.8 times, narrowing of the arteries and slight dilatation of the veins of the fundus.

For PION due to glaucoma, vision loss was characteristic for 5-7 hours. All patients had an open-angle form with stages 1-3 of the disease, the level of intraocular pressure on average was 22 mm. rt. Art. against the background of antihypertensive therapy. Visual acuity in the affected eye averaged 0.02. In the other eye, 8 (80%) patients had glaucomatous atrophy of the optic nerve head; visual acuity averaged 0.2. During biomicroscopy, dystrophic changes in the iris, baldness of the pigmented pupillary border, initial signs of cataracts, and a decrease in the reaction of the pupil to light on the affected side were observed. During perimetry, 80% of patients had loss of the nasal and lower half of the visual field, and 20% had arcuate scotomas with concentric narrowing. In the fundus there is blurred boundaries, prominence of the optic disc in 90% of patients, swelling of the peripapillary layer of nerve fibers in 80%, cotton wool-like exudates in 45%, hemorrhages on the optic disc in 90% of patients. The color of the optic nerve disc was pale, glaucomatous excavation, atrophic changes in the deep layers of the retina, significant narrowing of the arteries and veins. On HRT - prominence of the optic disc by 0.5-1.0 mm, an increase in its size by 1.1 times, unclear boundaries, an increase and deepening of the excavation area by an average of 0.78 mm. In the other eye, a decrease in the visual field on the nasal side was recorded, the presence of various scotomas, and low vision with glaucomatous changes in the optic nerve head was noted.

In 8 patients, PION occurred against the background of diabetes mellitus. An ophthalmoscopic picture of diabetic angioretinopathy of varying severity was revealed in both eyes. A gradual decrease in visual acuity was noted against the background of an increase in blood sugar levels within 16-24 hours to 0.08, a concentric narrowing of the visual field with loss of the lower sector. In the lens there are opacities of varying severity, destruction of the vitreous body. In the fundus there was pallor and prominence of the optic disc, blurred boundaries, peripapillary edema of the retina in 87.5%, cotton wool-like and hard exudates in 75%, hemorrhages in 87.5% of patients, narrowing of the arteries and significant dilatation of the veins of the fundus . Computed retinotomography (HRT) revealed prominence of the optic disc into the vitreous body by an average of 0.9-1.0 mm, an increase in optic disc size by 1.2 times, unclear boundaries, and stagnant veins. In the fellow eye, visual acuity is 0.4-0.5.

Anterior optic neuropathy in atherosclerosis developed in elderly and old patients due to sclerosis and was organic in nature. There was a decrease in vision within 410 hours to 0.02. In the field of view there is prolapse of the lower half with paracentral scotomas. Dystrophic changes in the stroma of the iris and pigment border, decreased reaction of the pupil to light on the affected side. In the fundus there is a pale coloration of the optic disc, unclear boundaries, slight prominence, single streak-shaped hemorrhages in 52.7% of patients, peripapillary retinal edema in 71.5%, pronounced narrowing of the arteries and slight narrowing of the veins. HRT shows blurred boundaries and prominence of the optic nerve head by 0.5 mm, an increase in size by 1.1 times.

Conclusions. Anterior ischemic optic neuropathy occurs in elderly patients with general vascular diseases, severe atherosclerosis, hypertension, and has its own course characteristics depending on the etiology of the disease. The most severe form of the course is anterior ischemic optic neuropathy against the background of glaucoma and atherosclerosis. With diabetes mellitus and arterial hypertension, with adequate treatment, the prognosis is more favorable.