Ischemic optic neuropathy of both eyes in an infant. What is ocular neuropathy? Treatment and prevention

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Ischemic optic neuropathy or ischemic optic disease is characterized by damage to the nerve. This occurs due to circulatory disorders in the intraorbital and intrabulbar region (located within eyeball before exiting the sclera).

The reasons for the development of the disease can be very different. This is one of the most insidious diseases, which at an unexpected moment can deprive a person of his sight.

Causes of ischemic neuropathy

The blood supply to the optic nerve occurs through vascular networks originating from the ophthalmic artery, a branch of the internal carotid artery. Central blood vessel The retina enters the optic nerve about 1 cm behind the eye and supplies the interior of the retina.

The outer part is separated by the choroidal artery, which originates from the posterior ciliary arteries. Its posterior part is located in front and behind the posterior ciliary artery.

Only a small number of capillaries actually penetrate the nerve and spread to its central part. As a result, the center of the posterior optic nerve is relatively poorly vascularized compared with its anterior portion and is therefore susceptible to ischemia with dramatic changes in perfusion.

The head receives its arterial blood supply from the anastomotic arterial circle formed by anastomoses between the lateral branches of the short posterior ciliary arteries, branches from the adjacent pial arterial network, and branches from the choroidal canal.

These very small arteries suffer from a number of local diseases such as atherosclerosis and vasculitis. Emboli usually do not reach them. Hypoperfusion (weak microcirculation) in the area of the ophthalmic artery and its branches causes ischemic optic neuropathy (ION).The non-arteritic form of the disease develops due to:

high blood pressure;
diabetes;
atherosclerosis;
use of certain medications;
blood clots and lower blood pressure overnight.

Arterial ION usually occurs in people over 70 years of age. The blood supply to the optic nerve is blocked due to inflammation of the artery (arteritis), most often giant cell arteritis.

The list of possible risk factors includes severe bleeding, anemia, glaucoma, blood diseases, and arterial hypotension.

Risk group

The risk of developing the disease is increased in patients with diabetes mellitus who abuse alcohol and nicotine. It includes persons with obstructive sleep apnea and constantly elevated blood pressure.

Classification

ION is classified as anterior (AION) or posterior (AION) depending on the optic nerve segment affected. The anterior view accounts for 90% of cases.

Both types are divided into non-arterial (not associated with vasculitis) or arterial.

Anterior ischemic optic neuropathy

PION is the most common cause sudden blindness in people over 50 years of age. The non-arterial form of PION (NPION) often develops due to hypertension and diabetes mellitus.

Thus, hypercholesterolemia, stroke, ischemic disease heart disease, tobacco use, systemic atherosclerosis, and obstructive sleep apnea have been associated with non-arterial anterior ION.

Although NSAID and intracranial cerebrovascular disease share similar risk factors, they are two very different pathologies and do not require the same evaluation.

For example, because of NPION caused by small vessel disease, carotid artery patency studies are not usually indicated. However, the patient has visual symptoms suggestive of ocular hypoperfusion (ie, blurred vision with postural changes in bright light or during exercise) or contralateral neurological symptoms and signs, ipsilateral transient monocular vision loss, Horner's syndrome, or ocular pain.

Thus, hypercoagulability is rarely associated with NPION.

Acute bleeding with anemia and systemic hypotension leads to unilateral or bilateral NPION. Likewise, those with chronic kidney failure who undergo dialysis may precipitate this pathology.

Giant cell arteritis is the most common cause of arterial anterior and posterior ischemic neuropathy, although in rare cases other vasculitides can cause. PION is the most common ocular manifestation of giant cell arteritis.

Arterial PION and ZION are emergency conditions in the ophthalmological field, which must be promptly recognized and treated to prevent complete loss of vision.

Posterior ischemic optic neuropathy

ZIN is a disease characterized by damage to the part of the optic nerve located behind the eye. With posterior ION, a decrease in blood circulation is observed in the areas where the nerve is located or in the intraorbital region.

This disease presents great difficulties for early detection. The pathological process occurs unilaterally.

The therapy is the same as for PION. After treatment, the clarity of visual perception will improve slightly, but it will still remain low.

Even after therapy, patients with posterior ischemic optic neuropathy develop blind spots in the visual field that are not associated with the peripheral boundaries.

Symptoms

Most often, ION affects 1 eye, but some patients develop bilateral damage to the organs of vision. The second eye is involved in pathological process in 2–5 days or 2–5 years.

The clinical picture of PION and ZION is the same. With this disease, peripheral visual perception is always impaired. Visual acuity decreases, and some immediately become blind.

Damage to the optic nerve is preceded by:

cephalgia;
a veil before the eyes;
soreness.

This condition continues for 30 days or longer. Then the symptoms improve.

Diagnostics

Since ION develops against the background of various diseases, consultation with an ophthalmologist, hematologist, neurologist, cardiologist, rheumatologist and endocrinologist will be required.

The following laboratory tests are carried out:

measurement of erythrocyte sedimentation rate;
C-reactive protein level;
general analysis blood and platelet count.

Together, these tests are highly predictive for biopsy-proven giant cell arteritis with a combined sensitivity of 97% for erythrocyte sedimentation rate and C-reactive protein levels.

To determine the disease, ophthalmoscopy is performed. If the patient does not have symptoms of giant cell arteritis, a magnetic resonance imaging (MRI) or computed tomography (CT) scan of the brain is done to make sure the optic nerve is not being compressed by the tumor.

Additional tests may be required depending on the likely causes.. For example, if someone has symptoms of obstructive sleep apnea (such as excessive sleepiness during the day or snoring), a polysomnography is performed. Patients who have had blood clots have their blood tested to diagnose clotting disorders.

Treatment

Giant cell arteritis is responsive to glucocorticoids, with immediate relief of systemic symptoms such as headaches, scalp tenderness, fatigue, fever, and myalgias.

Glucocorticosteroids are used to prevent vision loss in the unaffected eye, but they do not reverse existing pathology. Most neuro-ophthalmologists prescribe high doses of intravenous methylprednisolone to treat patients with acute vision loss.

For ischemic optic neuropathy, diuretics, vasodilators and nootropic medications are prescribed. Additionally - anticoagulants and vitamin complexes, thrombolytic agents - if necessary.

In the future, doctors carry out therapy with magnetotherapy, electrical stimulation and laser stimulation.

Complications

In the absence of therapy, its incorrect implementation or an error in diagnosis, the patient develops complete or partial blindness.

Forecast

In 40% of people, some vision is restored spontaneously. It is estimated that within the next 5 years, 20% of patients will develop disease in the second eye.

No effective treatment arterial ischemic neuropathy, and most of the lost vision cannot be restored. In patients with arterial ION, vision loss occurs in 25–50% within days or weeks without treatment. Non-arterial anterior ION recurs in the affected eye in less than 5% of patients.

Optic atrophy after this disease may reduce crowding and reduce the risk of recurrence.

Bilateral disease is often observed, usually sequentially and not simultaneously. The risk of second eye involvement ranges from 12 to 15% over 5 years and is not associated with age, gender, smoking, or aspirin use.

Information for patients about GLAUCOMA

Definition of glaucoma

What's happened glaucoma ?

What is called today " glaucoma »? Glaucoma (from Greek - the color of sea water, azure) is a serious disease of the organ of vision, named after the greenish color that the dilated and motionless pupil acquires at the stage of the highest development of the disease process - an acute attack of glaucoma. This is also where the second name for this disease comes from – “green water” or “green cataract” (from the German “Grun Star”).

Currently, there are no common ideas about the causes and mechanisms of development of this disease; certain difficulties are encountered even in the very attempt to define the concept “ glaucoma ».

Today glaucoma usually called chronic eye disease . characterized by constant or periodic increase with the development of trophic disorders in the outflow tract intraocular fluid (VGZh, aqueous humor), in retina and in optic nerve . causing the appearance of typical defects in line of sight and development edge excavation (deepening, pushing) optic disc .

Thus, the term " glaucoma ” unites a large group of eye diseases (about 60), which have the following common features:

Intraocular pressure (IOP) constantly or periodically exceeds the individually tolerated (tolerant) level;

A characteristic lesion develops optic nerve fibers – glaucomatous optic neuropathy . leading in its final stage to its atrophy;

Characteristics of glaucoma visual impairment .

Glaucoma can occur at any age, starting from birth, but the prevalence of the disease increases significantly in old age and old age. Thus, the frequency of congenital glaucoma is 1 case per 10-20 thousand newborns; at the age of 40-45 years, primary glaucoma is observed in approximately 0.1% of the population. In the age group of 50-60 years, glaucoma occurs in 1.5% of cases, and in people over 75 years of age, in more than 3%. This disease ranks among the leading causes of incurable blindness and is of great social importance.

Anatomy and physiology of the intraocular fluid outflow tract

Eye cavity contains light-conducting media: aqueous humor, filling its anterior and posterior chambers, lens And vitreous . Regulation of metabolism in intraocular structures . in particular in optical media . and maintaining tone eyeball provided by circulation intraocular fluid V chambers of the eye .

Pathways for the outflow of intraocular fluid (IOH)

Intraocular fluid (IOH) - an important source of nutrition for the internal structures of the eye. Aqueous humor circulates mainly in the anterior segment of the eye. It is involved in the metabolism of the lens, cornea, trabecular apparatus, vitreous body and plays an important role in maintaining a certain level intraocular pressure (IOP) .

Intraocular fluid continuously produced by shoots ciliary body . accumulates in the posterior chamber, which is a slit-like space of complex configuration located posterior to irises . Then most of the moisture flows through the pupil, washing the lens, after which it enters the anterior chamber and passes through the drainage system of the eye, located in the area of the angle of the anterior chamber - trabecula And Schlemm's canal (venous sinus of the sclera ). Out of him intraocular fluid flows through the outlet manifolds (outlets) into the surface scleral veins .

Front wall anterior chamber angle formed at the transition site cornea V sclera . back - formed iris . the vertex of the angle is the front part ciliary body .

Trabecula It is a network-like ring formed by connective tissue plates with many holes and slits. Watery moisture seeps through trabecular meshwork and going to Schlemm's canal . which is a circular slit with a lumen diameter of about 0.3-0.5 mm, and then flows through 25-30 thin tubules (graduates) flowing into episcleral (external) veins of the eye . which are the final point of outflow of aqueous humor.

Trabecular apparatus is a multilayer, self-cleaning filter that ensures one-way movement of fluid from the anterior chamber into the scleral sinus.

The described path is the main one and an average of 85-95% of aqueous humor flows along it. In addition to the anterior path of outflow of intraocular fluid, there is also an additional one: approximately 5-15% of aqueous humor leaves the eye, seeping through ciliary body and sclera in choroid veins And scleral veins . forming the so-called uveoscleral outflow tract .

The condition of the drainage system of the eye can be assessed using a special research method - gonioscopy . Gonioscopy allows you to determine the width anterior chamber angle . as well as the condition trabecular tissue And Schlemm's canal . Anterior chamber angle can be wide, medium and narrow. Data driven gonioscopy distinguish different clinical forms of glaucoma . At open-angle glaucoma gonioscopically all details of the anterior chamber angle are visible, with closed-angle shape angle details are hidden from observation.

Anterior chamber angle during gonioscopy

Between influx And outflow intraocular fluid (IOH) there is a certain balance. If for some reason it is violated, this leads to a change in the level intraocular pressure (IOP) . With a persistent and prolonged increase intraocular pressure Obstacles (blocks) arise that lead to disruption of communications between the cavities of the eyeball or closure of drainage channels. These blocks can be transient (temporary) or organic (permanent).

Causes and mechanisms development of glaucoma

Glaucoma are classified as multifactorial diseases with a threshold effect. This means that for the development of the disease, a number of reasons are necessary, which together lead to its occurrence. Heredity, individual characteristics or abnormalities of the eye structure . pathology of the cardiovascular, nervous and endocrine systems. Currently, scientists suggest that the development and progression of the disease glaucoma – this is a sequential chain of risk factors that are summarized in their action, as a result of which the mechanism leading to the onset of the disease is triggered. However, the mechanisms of visual dysfunction in pathogenesis of glaucoma to date remain insufficiently studied.

The optic disc is normal (left) and in the advanced stage of glaucoma (right). The upper part of the figure shows changes in visual fields. Note the pronounced deflection of the disc in glaucoma (glaucomatous excavation).

The main stages of development of the pathological process with glaucoma can be represented as follows:

disruption and deterioration outflow of aqueous humor from the cavity eyeball . which can be due to a variety of different reasons;
promotion intraocular pressure (IOP) above the level tolerable (tolerable, tolerable) for a given eye;
deterioration of blood circulation in the tissues of the eye;
hypoxia (lack of oxygen) and ischemia (impaired blood supply) to tissues in the exit area optic nerve ;
compression (squeezing) of nerve fibers in the area of their exit from eyeball . which leads to disruption of their function and death;
dystrophy (eating disorder), destruction (destruction) and atrophy optic fibers . their disintegration maternal retinal ganglion cells ;
development of the so-called glaucomatous optic neuropathy and subsequent atrophy (death) optic nerve .

Depending on development glaucomatous process part optic nerve fibers atrophies, and some are in a state of parabiosis (a kind of “sleep”), which allows us to consider possible restoration their functions are influenced by treatment (medical or surgical).

One important postulate follows from the above. Treatment of glaucoma is aimed primarily at normalizing the level of intraocular pressure (IOP) and bringing it to an individual tolerant level – i.e. values carried by the optic nerve of a particular patient (usually 16-18 mm Hg when measured with a standard Maklakov tonometer ). This is the so-called target pressure - that level IOP . which the ophthalmologist who prescribes the drops and the surgeon who performs the antiglaucomatous surgery . The effect of treatment primarily depends on the preservation of the nervous tissue and therefore, as a rule, it can be objectively said that visual functions . who are "caught" glaucoma . they don't come back.

Types of glaucoma

Distinguish congenital glaucoma . juvenile glaucoma (juvenile glaucoma . or young age glaucoma ), primary adult glaucoma And secondary glaucoma .

Congenital glaucoma may be genetically determined (predetermined) or caused by diseases and injuries of the fetus during embryonic development or during childbirth. This type glaucoma manifests itself in the first weeks and months of life, and sometimes several years after birth. This is a fairly rare disease (1 case per 10-20 thousand newborns).

Congenital glaucoma develops due to developmental anomalies (mainly in anterior chamber angle ), often arising as a result of various pathological conditions of the mother (especially before the 7th month of pregnancy). Towards development congenital glaucoma lead infectious diseases(rubella, mumps, polio, typhus, syphilis, etc.), vitamin deficiency A, thyrotoxicosis, mechanical injuries during pregnancy, poisoning, alcoholism, exposure to ionizing radiation, etc.

In 60% of cases congenital glaucoma are diagnosed with newborns . This condition is sometimes referred to in the medical literature as " hydrophthalmos » ( dropsy of the eye ) or " buphthalmos » ( Bulls-eye ). Cardinal signs congenital glaucoma are high intraocular pressure (IOP) . bilateral magnification cornea . and sometimes that's all eyeball .

Congenital glaucoma . Note the large diameter cornea . On the left eye cornea swollen due to increased intraocular pressure (

35 mmHg)

Juvenile (youthful) glaucoma occurs in children over three years of age. The age limit for this type of glaucoma is 35 years.

Primary adult glaucoma – the most common type of glaucoma associated with age-related changes in the eye. This site focuses on primary adult glaucoma . as the most common disease.

Secondary glaucoma is a consequence of other ocular or common diseases, accompanied by damage to those ocular structures that participate in the circulation intraocular moisture or its outflow from eyes .

Primary adult glaucoma

Primary glaucoma is divided into four main clinical forms: open angle glaucoma . angle-closure glaucoma . mixed glaucoma And glaucoma with normal intraocular pressure . Each form of glaucoma will be discussed in more detail in the corresponding section.

The classification identifies 4 stages of glaucoma: initial stage glaucoma . stage of glaucoma development . advanced stage of glaucoma And end stage glaucoma . Each stage is designated by a Roman numeral I - IV to briefly record the diagnosis. Stages glaucoma determined by state field of view And optic disc .

Optic neuropathy

Images of the surrounding world are transmitted to the brain through the retina and optic nerve, and 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 impairment of vision, up to its complete loss.

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

Kinds

For reasons of occurrence, the disease can be of the following types:

Hereditary;
Food;
Mitochondrial;
Traumatic;
Infiltrative;
Radiation;
Ischemic.

Without proper treatment, all types of the disease can be complicated by optic atrophy and blindness.

Causes

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

Toxic- poisoning by chemicals entering the digestive system, most often it is methyl alcohol, less often - ethylene glycol, medications.

Food- general exhaustion 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 neural 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 direct penetration of a foreign body into the tissue; indirect injury 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, exposure to opportunistic bacteria, viruses and fungi.

Radiation- increased radiation, radiation therapy.

Ischemic Optic nerve neuropathy can be anterior or posterior; the causes of its occurrence differ.

Causes of anterior ischemic neuropathy:

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

Causes of posterior ischemic neuropathy:

Surgical operations on the cardiovascular system;
Spine operations;
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. Often the rate of disease is so high that blindness occurs within a few weeks. With incomplete nerve atrophy, vision is also not completely lost, since the nervous tissue is affected only in a certain area.

The disease is accompanied not only by a decrease, but also by a narrowing of the visual field, part of the picture may disappear from the field of view, the perception of colors is impaired, and tunnel vision develops.

Often darkened areas and blind spots appear in the view; the pathology is accompanied by an afferent pupillary defect, i.e. pathological change response to a light source. Symptoms can appear on one or both sides.

Symptoms of hereditary neuropathy

Most patients do not have associated neuralgic abnormalities, although cases of hearing loss and nystagmus have been reported. The only symptom is bilateral loss of vision, paleness of the temporal part is observed, and the perception of yellow-blue hues is impaired. During diagnosis, a molecular genetic study is performed.

Symptoms of nutritional neuropathy

The patient may notice changes in color perception, the red color is washed out, the process occurs simultaneously in both eyes, there is no pain. In the early stages, the images are blurry and foggy, after which a gradual decrease in vision occurs.

With rapid loss of vision, blind spots appear only in the center; in the periphery, pictures are displayed quite clearly, and the pupils react to light as usual.

Flaw useful substances can negatively affect the entire body, pain and loss of sensation in the extremities occurs in patients with nutritional neuropathies. The disease epidemic occurred during the Second World War in Japan, when soldiers began to go blind after several months of starvation.

Symptoms of toxic neuropathy

Nausea and vomiting are observed in the early stages, followed by headache, symptoms of respiratory distress syndrome, loss of vision are diagnosed 18-48 hours after intoxication. Without taking appropriate measures, complete blindness may occur; the pupils dilate and stop responding to light.

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

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

Diagnostic methods:

Biomicroscopy;
Functional testing of the eyes;
X-ray;
Various electrophysiological methods.

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

Ophthalmoscopy may reveal pallor, swelling, an increase in the size of the optic nerve (disc), as well as its movement towards the vitreous body.

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

Treatment

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

Treatment for ischemic neuropathy

Treatment must begin in the first hours after the onset of symptoms; the need is due to the fact that prolonged circulatory disorders lead to loss of nerve cells.

First aid involves administering aminophylline injections, inhaling ammonia, taking nitroglycerin tablets, further treatment is carried out in a hospital setting.

The goal of therapy is to reduce swelling, provide an alternative route of 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, and blood pressure.

Medications indicated for ischemic neuropathy:

Vasodilators (trental, cerebrolysin, cavinton);
Decongestants medicines(diacarb, lasix);
Blood thinners (phenyline, heparin);
Vitamin complexes;
Glucocorticosteroids.

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

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

With ischemic optic neuropathy, the prognosis is unfavorable; even if all the doctor’s instructions are followed, vision deteriorates, certain areas disappear from view, which leads to atrophy of the fibers of the nerve tissue. In 50% of cases, due to intensive treatment, vision can be improved; when both eyes are involved in the process, complete blindness often develops.

Prevention

In order to prevent the development of the disease, it is recommended to carry out timely treatment any system, exchange and vascular diseases. After the appearance of symptoms of the disease, the patient is recommended to regularly visit an ophthalmologist; the patient must comply with all the doctor’s requirements.

Diagnosis and treatment of ischemic neuropathy

How do we see? Images of the surrounding world fall on the retina and are transmitted along the optic nerve to the brain. There the information received is processed and a picture is formed. When the optic nerve is damaged due to insufficient blood circulation, optical ischemic neuropathy begins. This is a serious disease that causes temporary or permanent vision impairment, including blindness.

Neuropathy or neuropathy is a general name for a variety of diseases that occur due to damage to nerves, including peripheral nerves. These diseases can be grouped according to their causes, such as:

Allergic;
Toxic;

The common cause of diseases of this type is cell injury and disruption of nerve functioning. The most common of them are compression-ischemic neuropathies.

Features of compression-ischemic neuropathy

Long chest;
Suprascapular;
Median;
Ray;
Elbow;
Ilioinguinal, etc.
Lumbar.

For diagnosis, a complete examination of the patient is carried out to identify localization sites. pain syndrome, methods used: electroneuromyography, x-ray, CT scan. Correct diagnosis is difficult due to similar clinical picture with stroke, atherosclerosis, brain tumor and others.

Compression-ischemic neuropathy is treated with medications and physiotherapeutic methods. The entire complex of therapy is aimed at restoring the affected nerve and relieving pain. The desired final result of all treatment is the return of sensitivity and normal functioning of the patient’s body.

Most often, the term “neuropathy” refers to disturbances in the functioning of the optic nerve and the consequences of this. This disease has mixed causes.

Damage to optic nerve cells, optic neuropathy (ON), leads to their death. The diagnosis is made when the following symptoms are present:

Impaired color perception.
Changes in the optic nerve visible when viewed with an ophthalmoscope.

Optical neuropathy can be caused by:

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Toxic.
Hereditary.

Learn more about optical ischemic neuropathy

Optical ischemic neuropathy is classified according to the site of origin into two types: anterior and posterior. In the first case, POIN affects the head of the optic nerve, which causes swelling in the disc area and blurred vision. This disease also comes in two types:

Arterial. Caused by inflammatory diseases large arteries eg giant arteritis, rheumatoid arthritis and others.
Non-arterial. Often occurs in patients over 50 years of age. The reasons for its appearance are not completely known. It is assumed that diabetes mellitus, glaucoma, high level cholesterol and other conditions accompanied by cerebrovascular accidents lead to ischemia of the optic nerve head, and as a consequence, to POIN.

Posterior (ZOIN) is characterized by the absence of disc edema and the development of optic nerve atrophy and a sharp drop in visual acuity. It occurs in the same situations as POIN, only with more severe circulatory disorders. For example, with a very strong decrease in pressure during surgical operations on the heart. Treatment only helps stop the progression of the disease, but does not restore vision.

Another subtype of SPE is radiation. It occurs on average one and a half years after irradiation of the retina. Exposure to radiation leads to radiation retinopathy and damage to optic nerve cells. Within a few weeks of the onset of the disease, complete loss of vision occurs. When neuropathy begins (the period can range from 3 months to several years), its course and consequences all depend on the radiation dose.

When identifying SPE, an integrated approach is used. Consultations with doctors of the following specialties are required: ophthalmologist, endocrinologist, cardiologist, rheumatologist, neurologist, hematologist. A thorough examination of the patient is carried out to study his complaints and visual defects. An ophthalmoscope examination of the optic disc and fundus of the eye is mandatory. Perimetry, fluorescein angiography, Dopplerography of large arteries, and MRI of the brain are used.

Effective ultrasound diagnostics large arteries: vertebral, ophthalmic, carotid to detect changes in blood flow. After analyzing the coagulogram, a test for blood clotting, hypercoagulation is detected.

With an ophthalmoscope, changes in the optic nerve head are not visible in the first 1–1.5 months after the onset of the disease. This makes diagnosis much more difficult. If this disease is suspected, other methods must be used. When visible signs of optic nerve atrophy appear, irreversible changes will occur.

First aid for this disease can stop damage to the optic nerve and preserve vision. Initially, intravenous aminophylline, sublingual nitroglycerin, and inhalation of ammonia are used. The patient is hospitalized as soon as possible.

Medicines used:

For urgent restoration of blood circulation and normalization of blood pressure.
Decongestants.
Improving metabolism and reducing oxygen starvation.

The treatment further includes physiotherapeutic methods: magnetic therapy, laser and electrical stimulation of the optic nerve. After treatment for OIN, constant monitoring by an ophthalmologist of the condition of the second eye and measures to prevent its disease are required.

DO YOU STILL THINK THAT IT IS IMPOSSIBLE TO GET RID OF HEART DISEASE!?

I constantly feel high blood pressure...
There is nothing to say about shortness of breath after the slightest physical exertion...
And you have been taking a bunch of medications for a long time, going on a diet and watching your weight...

Common types of neuropathies

Compression-ischemic neuropathy;
Inflammatory;
Diabetic;
Mixed.

After compression in the spine or muscle-bone tunnels, the nerve bundles passing there are damaged. Blood circulation is impaired - ischemia. Compression-ischemic neuropathy (tunnel) appears, accompanied by muscle hypertonicity, pain, and loss of sensitivity. The diagnosis is confirmed by an increase in symptoms when exposed to the diseased nerve.

Nerves affected by tunnel neuropathy:

Greater occipital;
Additional;
Axillary;
Musculocutaneous;

Plexus:

Sacral;
Cervical;
Shoulder;

Each type of compression-ischemic neuropathy is characterized by a distinctive location of pain points on the body and a complex of specific syndromes. It is often triggered by being in an uncomfortable, monotonous position or external trauma. The course of the disease is complicated by exposure to alcohol.

Types of Optic Neuropathy

Decrease in visual acuity.

Infiltrative.

Traumatic.

Mitochondrial.

Food.

Also identified are diseases in the ON group: inflammation (neuritis) and compression of the optic nerve. These diseases are not usually accompanied by permanent vision loss.

All types of optic neuropathy, if left untreated, can be complicated by optic atrophy and blindness.

The anterior part of the optic nerve is supplied by the vessels of the eye shell, and the posterior part is connected to the cerebral arteries. Depending on which part of the blood flow is disrupted, different diseases appear.

Lack of nutrition of the optic nerve leads to optical ischemic neuropathy, any type of which is dangerous for humans, as it threatens vision loss. Timely treatment can prevent dire consequences. This requires a quick and correct diagnosis.

Diagnostics

Optical ischemic neuropathy must be differentiated from diseases with similar symptoms: swelling or congestion of the optic nerve head, neuritis.

Treatment and prevention

OIN therapy is carried out under the supervision of an ophthalmologist. It is necessary to achieve remission. Measures are taken to prevent damage to the second eye.

Regenerating biochemical processes.

Optical ischemic neuropathy is most often complicated by decreased or complete loss of vision in the affected eye. Therefore, prevention of this disease is very important: timely treatment for medical care, treatment of diseases that cause circulatory disorders.

Do you often experience discomfort in the head area (pain, dizziness)?
You may suddenly feel weak and tired...

Searches such as “optic neuropathy” are often present on the Internet. In fact, we are talking about optic neuropathy. This is a fairly 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 of the eye.

Symptoms of optic nerve damage

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

Eyeball – sagittal section

neuropathy. This is the name for a process that leads to dysfunction of the optic nerves, but without signs of inflammation. An example is acute ischemic optic neuropathy, which can develop with severe atherosclerosis, which leads to thrombosis of the central retinal artery. This serious process can result in blindness in 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 may be an important sign of multiple sclerosis. Many people with a history of optic neuritis subsequently develop multiple sclerosis;

congestive optic discs which can be detected by fundus examination. Congestion most likely indicates intracranial hypertension syndrome, and they occur in cases of increased intracranial pressure, especially if this pressure exists for a long period of time.

A clear distinction between these clinical phenomena will allow us to separate neuritis from neuropathy, which allows us to make a correct prognosis for the development of the disease.

Causes of development of neuropathy and optic neuritis

How does neuropathy and optic neuritis develop and for what reasons?

For example, signs of ischemic optic neuropathy include sudden deterioration of vision, usually in one eye. In some cases, ischemic blindness may occur. This is often preceded by specific symptoms, such as, for example, “blurred” vision, the appearance of various spots, sometimes colored.

If incomplete vision loss 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. A concentric narrowing of the visual fields may appear.

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

With ischemic lesions of the nerve, disc swelling also occurs, and the arteries narrow, while the diameter of the veins is normal. This is clearly visible when examining the fundus. Then various hemorrhages occur in the area of the optic nerve head. If intensive treatment is not started (metabolic, vascular drugs, antithrombotic, antiplatelet agents, antioxidants), persistent optic nerve atrophy may develop. It usually occurs 1-3 weeks after the onset of neuropathy.

Ischemic neuropathy

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

If we talk about optic neuritis, 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 exclusively signs that are noticeable during examination of the fundus:

hyperemia of the nerve disc, swelling;

blurred and unclear 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 while the venous network is intact. It is clear that plethora is a sign of inflammatory hyperemia);

foci of hemorrhage in the disc area;

the appearance of whitish spots on the surface of the disc and retina.

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

Neuritis can develop from various reasons. In addition to signs of demyelinating disease, the cause may be:

meningitis, encephalitis, meningoencephalitis, especially purulent ones;

general severe infections (malaria, typhus, severe influenza);

endogenous intoxication and poisoning.

Surrogate poisoning as a cause of optic neuropathy

Classic manifestations of optic neuritis include poisoning with a surrogate of alcohol, such as ingestion of methyl alcohol for the purpose of alcohol intoxication. It is known that the lethal dose of methanol for internal use ranges from 40 to 250 ml, but even the consumption of 5-10 ml of methanol can cause blindness. In addition, when consuming various mixtures containing 1.5% methyl alcohol, cases of toxic blindness also occur.

Typically, visual disturbances when consuming methanol occur 3-6 days after consumption, 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 using regular ethyl alcohol, the products of metabolism in the liver are acetic acid and acetaldehyde, which, despite all their harmfulness, do not affect the cells of the optic nerve and retina.

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

As the disease progresses, visual acuity is lost quite quickly, the field of vision becomes narrower, and completely invisible areas appear. To diagnose this disease, visometry and ophthalmoscopy are used. To clarify the diagnosis and origin, ultrasound, MRI, angiography, etc. are performed.

Treatment is carried out immediately; until the diagnosis is confirmed, decongestants, anti-spasm drugs and thrombolytics are used. An indispensable element of complex treatment will be physiotherapeutic procedures with stimulation of the optic nerve using a laser or other influence, and eye exercises.

At risk are older people over 40 years of age, mostly men. This complex disease does not tolerate delays in treatment, because it threatens not just loss of visual acuity, but also complete blindness and disability.

Optical pathology cannot be called an independent disease, since it manifests itself only in the complex of the systemic process of 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 examinations with the following doctors: endocrinologists, cardiologists, neurologists and other specialists as necessary.

Classification

There are two main forms of development of optical ischemia: anterior and posterior. Both forms can occur partially or completely.

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 posterior neuropathy, in the retrobulbar region.

Causes

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

Hereditary predisposition due to the genetic manifestation of the disease.
Traumatic cause. There are two types of injury: direct - an anatomical disorder occurs, an imbalance in the functioning of the optic nerve, which occurs as a result of penetration of a foreign body into the tissues of the optical vision system. An indirect type of injury occurs as a result of disturbances without damaging the integrity of the nervous tissue.
Toxic. Pathology occurs in the process of poisoning the body with various chemical elements, salts of heavy metals, alcohol, medicines, which penetrate and poison the body through the digestive system.
Food. If there are problems with digestion of food, fasting, or problems with the gastrointestinal tract, optic nerve ischemia may occur. Due to exhaustion of the entire body and lack of nutrients necessary for the normal functioning of the visual system.
Radiation. Exposure to radiation due to radiation therapy.
Infiltration. The reason is the infiltration of foreign bodies that are infectious or oncological in nature. Occurs due to exposure to viruses, bacteria, fungal infections.
Another consequence of the disease is the impact of harmful habits: smoking, alcoholism, drug addiction.

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

inflammatory processes in the arteries;
rheumatoid joint damage, pain with active movements;
Hurg-Strauss syndrome;
immunopathological inflammation of blood vessels, for example, arteritis;
Wegener's granulomatosis;
chronic damage to the arterial walls of blood vessels, which is acute in nature 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 cardiovascular system.

Symptoms

With lesions of the optic nerve, one eye is most 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 visibility and is involved in the process of ischemia over time. It could be one hour, or it could be several days.

Optic neuropathy occurs unexpectedly and without any warning signs; this may occur after heavy physical exertion, due to taking hot bath or after waking up. Visual acuity decreases suddenly and sharply over several minutes or hours. The patient may not pay attention to the symptoms that occur on the eve of vision deterioration, such as temporary blurred vision, hazy vision, pain in the eye area, severe and frequent headache.

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

The acute period of the disease lasts for a month, then the swelling of the onset disc subsides, the hemorrhages gradually resolve, muscle tissue the optic nerve experiences complete atrophy. Retinal detachment and other defects do not go away, but are reduced.

Diagnostic methods

At the first suspicion and discomfort, you should consult a doctor. If a person did not have time to prevent the disease in advance, in case of visual impairment that occurred suddenly and unexpectedly, it is important to urgently call an ambulance for urgent hospitalization. In the process of finding out the cause of the disease, consultation with a cardiologist, neurologist, hematologist and other specialists is necessary.

The following hardware diagnostic tools are used:

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

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

Treatment

For optimal diagnosis 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 takes urgent measures in the form of intravenous injections of aminophylline, revives the patient with ammonia, etc. The patient is admitted to the hospital for further therapy.

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

An important step in the actions of doctors is the dilation of blood vessels, which has a positive effect on ischemic neuropathy. For this purpose, trental and cavinton are used. In order to relieve swelling, diuretics are used, and thrombolytics are used to thin the blood.

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

Forecast

Even with the best predictions from doctors, it is almost impossible to completely restore vision. Full compliance with the entire treatment complex and compliance with all medical prescriptions will not save you from a decrease in visual acuity. As a result, vision may still decline, and some defects associated with vision and atrophy of nerve fibers will remain. Every second patient manages to improve visual indicators by 0.2 units; this result is achieved only with intensive treatment in compliance with all necessary measures. If the patient is faced with ischemia of 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 promptly contact an ophthalmologist and undergo regular examination by a doctor. Any vascular diseases, metabolic disorders must be examined and treated so that complications do not develop, incl. and before our eyes. After the first symptoms appear, contact a medical institution and comply with all requirements.

Ischemic optic neuropathy. Causes, Symptoms, Treatment

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

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

Treatment is medicinal, including vitamins, decongestants, antispasmodics, thrombolytics. Treatment is often complemented by physiotherapeutic procedures and laser stimulation of the optic nerve.

Ischemic optic neuropathy

The disease is more often observed in the age group, mostly affecting men. Optic neuropathy is considered a serious pathology, since it can significantly reduce visual acuity, and in some cases threaten its complete loss.

The disease is not considered independent: it is always part of a 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 optic neuropathy

The disease can occur in two different ways. The first of them is called locally limited ischemic neuropathy, the second is complete, or total ischemic neuropathy. According to the area covered by pathological processes, the disease can be anterior or posterior.

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

The posterior form of neuropathy is diagnosed much less frequently. It is caused by ischemia-type damage in 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 develops ( oxygen starvation) retinal, prelaminar, scleral layers of the optic nerve head.

Posterior ischemic neuropathy 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 is provoked by vascular spasms or organic lesion these vessels (for example, thrombosis, sclerosis).

The above conditions, which entail the appearance of signs of ischemic optic neuropathy, 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, obliterating arteritis, thrombosis of arteries and veins. Among 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 can accompany severe blood loss, for example, with perforation of a stomach or intestinal ulcer, injury internal organs, after operation.

Sometimes ischemic neuropathy occurs with serious blood diseases, anemia, during hemodialysis, after administration of anesthesia, and with arterial hypotension.

Clinical picture

In most cases, the symptoms of ischemic neuropathy are unilateral. Less commonly (up to 1/3 of cases), the pathology spreads 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 occurrence of anterior ischemic neuropathy, posterior ischemic neuropathy may subsequently develop, and signs of occlusion of the central retinal artery may also appear.

Usually the disease 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 the point of blindness or identification of the 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 on the back side, and the occurrence of unusual phenomena in the field of vision.

Ischemic optic neuropathy always leads to deterioration of a person's peripheral vision. Often, vision pathologies come down to the formation of blind spots (scotomas), the disappearance of the image in the lower part of the view or in the nasal and temporal areas.

The acute condition lasts up to a month (sometimes longer). Further, the swelling 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 symptoms occur, you must urgently call an ambulance or quickly seek help from an ophthalmologist. The examination program necessarily includes consultations with other specialists - a cardiologist, neurologist, rheumatologist, hematologist, etc. (until the cause of ischemic neuropathy is identified).

Ophthalmological studies include functional testing of the eyes, biomicroscopy, instrumental examinations using ultrasound, x-rays, and various electrophysiological methods. The specialist checks the patient's visual acuity.

With ischemic neuropathy, varying degrees of decrease in this indicator are found - from slight loss of vision to complete blindness. Abnormalities in visual function are also detected depending on the affected nerve area.

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

In the area of the disc, the retina swells greatly, and a star-shaped figure appears in its central section. The vessels in the area of compression narrow, and at the edges, on the contrary, they become more filled with blood and pathologically expand. In some cases, hemorrhages and exudate are present.

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

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

Electrophysiological examinations include an electroretinogram, calculation of the maximum flicker fusion frequency, etc. Usually there is a decrease in the functional properties of the nerve. A coagulogram reveals hypercoagulation, and a blood test for cholesterol and lipoproteins reveals an increased amount.

Ischemic neuropathy should be differentiated from retrobulbar neuritis, tumors nervous system and orbits 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 normal blood supply leads to the loss of nerve cells.

Emergency measures include intravenous injections of aminophylline, taking tableted nitroglycerin, and short-term inhalation of ammonia fumes. After emergency treatment, the patient is admitted to the hospital.

In the future, the goal of therapy is to reduce swelling, improve the trophism of nervous tissue, and also provide an alternative route of blood circulation. In addition, the underlying disease is treated and normalization of blood clotting, fat metabolism, and blood pressure is ensured.

Vasodilators for ischemic neuropathy include Cavinton, Cerebrolysin, Trental, decongestants - diuretics Lasix, Diacarb, blood thinners - thrombolytics heparin, phenylin.

Additionally, glucocorticosteroids are prescribed, vitamin complexes, physiotherapy (electrical stimulation, laser nerve stimulation, magnetic therapy, microcurrents).

Forecast

With ischemic optic neuropathy, the prognosis is usually unfavorable. Even with a comprehensive treatment program, visual acuity decreases, a persistent decline in vision and various defects, and loss of areas from vision are often observed, 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 in the process, complete blindness often develops.

Prevention

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

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

Ischemic optic neuropathy

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

Ischemic optic neuropathy

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

Classification

Optic nerve damage can develop in two forms - anterior and posterior ischemic neuropathy. Both forms can occur as limited (partial) or total (complete) ischemia.

In anterior ischemic optic neuropathy, pathological changes are caused by 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) region.

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 presented as functional disorders(spasms) of the arteries, as well as their organic changes (sclerotic lesions, thromboembolism).

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

Symptoms

With ischemic optic neuropathy, one eye is most often affected, but a third of patients may experience bilateral impairment. 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 optic neuropathy are often combined with each other and with occlusion of the central retinal artery.

Optical ischemic neuropathy usually develops suddenly: often after sleep, physical exertion, or a hot bath. In this case, visual acuity sharply decreases (down to tenths of light perception or blindness with total defeat optic nerve). A sharp drop in vision occurs over a period of several minutes to hours, so the patient can clearly indicate the time of deterioration in visual function. Sometimes the development of ischemic optic neuropathy is preceded by warning symptoms in the form of periodic blurred vision, pain behind the eye, and severe headache.

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

The period of acute ischemia lasts for 4-5 weeks. Then the swelling of the optic disc gradually subsides, hemorrhages resolve, and optic nerve atrophy occurs varying degrees expressiveness. In this case, visual field defects remain, but can be significantly reduced.

Diagnostics

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

Complex ophthalmological examination includes functional tests, examination of eye structures, ultrasound, x-ray, electrophysiological studies.

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

Ophthalmoscopy reveals pallor, ischemic edema and enlargement of the optic disc, its prominence into the vitreous body. The retina around the disc is swollen, and a “star shape” is visible in the macula. The veins in the area 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 optic neuropathy reveals retinal angiosclerosis, age-related fibrosis, uneven caliber of arteries and veins, occlusion of cilioretinal arteries. With posterior ischemic optic neuropathy, ophthalmoscopy in the acute period does not reveal any changes in the optic disc. Doppler ultrasound of the ophthalmic, supratrochlear, carotid, and vertebral arteries often reveals changes in blood flow in these vessels.

Electrophysiological studies (determining the critical frequency of flicker fusion, electroretinogram, etc.) demonstrate a decrease in the functional thresholds of the optic nerve. When examining a coagulogram, changes in the type of hypercoagulation are detected; When determining cholesterol and lipoproteins, hyperlipoproteinemia is detected. Ischemic optic neuropathy should be distinguished from retrobulbar neuritis, space-occupying lesions of the orbit and the central nervous system.

Treatment

Therapy for ischemic optic neuropathy should be started in the first hours after the development of the pathology, since prolonged disruption of blood circulation causes irreversible death of nerve cells. Urgent Care in case of sharply developed ischemia, includes immediate intravenous administration aminophylline solution, taking nitroglycerin under the tongue, inhaling ammonia vapor. Further treatment of ischemic optic neuropathy is carried out inpatiently.

Subsequent treatment is aimed at relieving swelling and normalizing the trophism of the optic nerve, creating bypass blood supply routes. Treatment of the underlying disease (vascular, systemic pathology), normalization of coagulation system parameters and lipid metabolism, and correction of blood pressure levels are important.

For ischemic optic neuropathy, the use and administration of diuretics (diacarb, furosemide), vasodilators and nootropics (vinpocetine, pentoxifylline, xanthinol nicotinate), thrombolytic drugs and anticoagulants (phenindione, heparin), corticosteroids (dexamethasone), vitamins B, C are prescribed and E. In the future, magnetic therapy, electrical stimulation, and laser stimulation of the optic nerve fibers are performed.

Prognosis and prevention

The prognosis of ischemic optic neuropathy is unfavorable: despite treatment, a significant decrease in visual acuity and persistent peripheral vision defects (absolute scotomas) caused by optic nerve atrophy often persist. An increase in visual acuity of 0.1-0.2 can be achieved only in 50% of patients. If both eyes are affected, low vision or total blindness may develop.

For the prevention of ischemic optic neuropathy, therapy of general vascular and systemic diseases, timeliness of seeking medical help. Patients who have suffered ischemic optic neuropathy of one eye require clinical observation by an ophthalmologist and appropriate preventive therapy.

Optic neuropathy

Symptoms of optic nerve damage

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

Eyeball - sagittal section

neuropathy. This is the name for a process that leads to dysfunction of the optic nerves, but without signs of inflammation. An example is acute ischemic optic neuropathy, which can develop with severe atherosclerosis, which leads to thrombosis of the central retinal artery. This serious process can result in blindness in 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 may be an important sign of multiple sclerosis. Many people with a history of optic neuritis subsequently develop multiple sclerosis;

Thrombosis of the central retinal artery

congestive optic discs, which can be detected during fundus examination. Congestion most likely indicates intracranial hypertension syndrome, and they occur in cases of increased intracranial pressure, especially if this pressure exists for a long period of time.

A clear distinction between these clinical phenomena will allow us to separate neuritis from neuropathy, which allows us to make a correct prognosis for the development of the disease.

Location of the optic nerve

Causes of development of neuropathy and optic neuritis

How does neuropathy and optic neuritis develop and for what reasons?

For example, signs of ischemic optic neuropathy include sudden deterioration of vision, usually in one eye. In some cases, ischemic blindness may occur. This is often preceded by specific symptoms such as, for example, blurred vision, the appearance of various spots, sometimes colored.

hyperemia of the nerve disc, swelling;

blurred and unclear 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 while the venous network is intact. It is clear that plethora is a sign of inflammatory hyperemia);

foci of hemorrhage in the disc area;

the appearance of whitish spots on the surface of the disc and retina.

Due to neuritis, acuity may decrease and vision becomes blurred.

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

meningitis, encephalitis, meningoencephalitis, especially purulent ones;

general severe infections (malaria, typhus, severe influenza);

endogenous intoxication and poisoning.

Surrogate poisoning as a cause of optic neuropathy

Typically, visual disturbances when consuming methanol occur 3-6 days after consumption, 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 drinking regular ethyl alcohol, the products of metabolism in the liver are acetic acid and acetaldehyde, which, despite their harmfulness, do not affect the cells of the optic nerve and retina.

Optic neuropathy

Images of the surrounding world are transmitted to the brain through the retina and optic nerve, and 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 impairment of vision, up to its complete loss.

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

For reasons of occurrence, the disease can be of the following types:

Causes

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

Toxic - poisoning by chemicals that enter the digestive system, most often methyl alcohol, less often - ethylene glycol, medications.

Nutritional - general exhaustion 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 neural 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 direct penetration of a foreign body into the tissue; indirect injury 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, exposure to opportunistic bacteria, viruses and fungi.

Radiation - increased radiation, radiation therapy.

Ischemic neuropathy of the optic nerve can be anterior or posterior, the causes of its occurrence differ.

Causes of anterior ischemic neuropathy:

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

Causes of posterior ischemic neuropathy:

Surgical operations on the cardiovascular system;
Spine operations;
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. Often the rate of disease is so high that blindness occurs within a few weeks. With incomplete nerve atrophy, vision is also not completely lost, since the nervous tissue is affected only in a certain area.

Often, darkened areas and blind spots appear in the view; the pathology is accompanied by an afferent pupillary defect, i.e., a pathological change in the response to the light source. Symptoms can appear on one or both sides.

Symptoms of hereditary neuropathy

Symptoms of nutritional neuropathy

With rapid loss of vision, blind spots appear only in the center; in the periphery, pictures are displayed quite clearly, and the pupils react to light as usual.

A lack of nutrients can negatively affect the entire body; pain and loss of sensation in the extremities manifests itself in patients with nutritional neuropathies. The disease epidemic occurred during the Second World War in Japan, when soldiers began to go blind after several months of starvation.

Symptoms of toxic neuropathy

In the early stages, nausea and vomiting are observed, followed by headache, symptoms of respiratory distress syndrome, and loss of vision is diagnosed after a period of time. after toxicity. Without taking appropriate measures, complete blindness may occur; the pupils dilate and stop responding to light.

Diagnostics

When the first symptoms appear, you should call an ambulance or consult an ophthalmologist.

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

Biomicroscopy;
Functional testing of the eyes;
X-ray;
Various electrophysiological methods.

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

Ophthalmoscopy may reveal pallor, swelling, an increase in the size of the optic nerve (disc), as well as its movement towards the vitreous body.

Treatment

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

Treatment for ischemic neuropathy

Treatment must begin in the first hours after the onset of symptoms; the need is due to the fact that prolonged circulatory disorders lead to loss of nerve cells.

Medications indicated for ischemic neuropathy:

Vasodilators (trental, cerebrolysin, cavinton);
Decongestants (diacarb, lasix);
Blood thinners (phenyline, heparin);
Vitamin complexes;
Glucocorticosteroids.

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

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

Prevention

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 appearance of symptoms of the disease, the patient is recommended to regularly visit an ophthalmologist; the patient must comply with all the doctor’s requirements.

Ischemic optic neuropathy: anterior, posterior

Ischemic optic neuropathy is based on an acute disturbance of arterial circulation in the vascular system supplying the optic nerve.

ICD-10 code

Causes of ischemic optic neuropathy

In the development of this pathology, the main role is played by the following three factors: disturbance of general hemodynamics, local changes in the vascular wall, coagulation and lipoprotein changes in the blood.

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

Local factors. Currently, great importance is attached to local local factors causing the formation of blood clots. Among them are changes in the endothelium of the vessel wall, the presence of atheromatous plaques and areas of stenosis with the formation of turbulence in the blood flow. The presented factors determine pathogenetically oriented therapy for this serious disease.

Symptoms of ischemic optic neuropathy

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

Anterior ischemic neuropathy

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

With total damage to the optic nerve, vision is reduced to hundredths and even blindness; with partial damage, vision remains high, but characteristic wedge-shaped scotomas are noted, with the apex of the wedge always facing the point of gaze fixation. Wedge-shaped loss is explained by the sectoral nature of the blood supply to the optic nerve. Wedge-shaped defects, merging, cause quadrant or half loss in the field of view. Visual field defects are most often localized in the lower half. Vision decreases over several minutes or hours. Usually, patients accurately indicate the day and hour when their vision sharply decreased. Sometimes there may be warning signs in the form of headache or transient blindness, but more often the disease develops without warning. Ophthalmoscopy reveals a pale, swollen optic disc. The vessels of the retina, primarily the veins, change secondaryly. They are wide, dark, convoluted. 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 swelling gradually decreases, the hemorrhages resolve and optic nerve atrophy of varying severity appears. Visual field defects persist, although they may 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. The pathogenesis and clinical course of the disease are identical to those of anterior ischemic neuropathy, but in the acute period there are no changes in the fundus. The optic disc is a natural color with clear boundaries. Only after 4-5 weeks does decolorization of the disc appear and partial or complete atrophy begins to develop. With total damage to the optic nerve, central vision may be reduced to a hundredths or to blindness, as with anterior ischemic neuropathy; with partial damage, visual acuity may remain high, but characteristic wedge-shaped loss is detected in the visual field, more often in the lower or lower nasal regions. Diagnosis in the early stage is more difficult than with ischemia of the optic nerve head. Differential diagnosis is carried out with retrobulbar neuritis, space-occupying formations of the orbit and the 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 to years.

Optic neuropathy

Optic 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 referred to as “optic atrophy,” but ophthalmologists now recommend against using it.

Optic neuropathy is not a self-occurring pathology, but one of the manifestations or consequences of a number of diseases. Therefore, patients with this diagnosis are encountered in the practice of doctors of various profiles: ophthalmologist, neurologist, endocrinologist, traumatologists, maxillofacial surgeons and even oncologists.

Pathogenesis

Whatever the cause of damage to the optic nerve, the key pathogenetic aspects are ischemia of nerve fibers with a weakening of the antioxidant protective mechanism. Various etiological mechanisms may contribute to this:

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

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

What Causes 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 origin, arterial hypotension, temporal arteritis, generalized atherosclerosis, periarteritis nodosa, thrombosis of the great vessels of the cervicocerebral region and arteries supplying the nerve.
Conditions leading to compression (external pressure) of the optic nerve trunk. This is thyrotoxicosis (occurring with endocrine ophthalmopathy), any space-occupying formations of the orbit and optic canal (gliomas, lymphangiomas, hemangiomas, cysts, carcinomas), all types of orbital pseudotumor. Sometimes compression occurs due to fragments after injuries to the orbit, hematomas (including those located between the nerve sheaths) and foreign bodies. The degeneration of nervous tissue that occurs is associated not only with direct compression of the fibers. Ischemia (oxygen deficiency) of large areas 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). Foci of inflammation, sarcoidosis, and fungal infection can also lead to nerve infiltration.
Demyelinating diseases (multiple sclerosis). The exposure of nerve fibers first leads to disruption of the conduction of impulses through them, and then to irreversible degeneration.
A toxic form of optic neuropathy. Damage to the optic nerve can be associated with exposure to a number of industrial toxins, poisonous substances, pesticides, alcohol and its surrogates. The greatest danger is methyl alcohol, the metabolites of which (especially formaldehyde) are highly toxic and have a tropism for the optic nerve. Optic neuropathy can develop while taking certain drugs: for example, with intolerance to sulfonamides, with a severe overdose of cardiac glycosides and amiodarone, during treatment of tuberculosis with ethambutol.
Dystrophy of the optic nerve caused by severe chronic hypovitaminosis, and long-term deficiency of B vitamins is especially critical. The development of neuropathy may be associated with severe disturbances in the absorption process in small intestine, fasting, compliance with strict irrational dietary restrictions. This mechanism of damage to the optic nerve is also activated when chronic alcoholism, along with the direct toxic effects of 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 respiratory cycle enzymes. The consequence of this is the formation of an excess amount of toxic active oxygen molecules and chronic energy deficiency 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 of this disease includes the gradual death of retinal structures due to its chronic compression in the deformed cells of the supporting cribriform plate of the sclera and the inclusion of the vascular component. That is, the degeneration process in this case begins from the periphery, neurons initially 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

On average, the optic nerve contains about 1–1.2 million neuronal fibers, each of which is covered by a myelin sheath. This structure ensures isolation of conducted pulses and increases the speed of their transmission. It is the defeat of these fibers on any part of the nerve that most often causes the appearance of symptoms, regardless of the etiology of the process and the location of the primary focus of degeneration.

To the main clinical manifestations Optic neuropathy includes:

Decreased visual acuity, and this disorder cannot be adequately corrected with glasses/lenses. Initially, patients may report blurred vision.
Change in color perception.
Changes in visual fields. Sections and quadrants may fall out, and central and paracentral scotomas may appear (defects in the form of blind areas that do not perceive light stimulation). With a pronounced concentric narrowing of the fields, they speak of the formation of tunnel vision.

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

Features of some forms of optic neuropathy

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

With posterior ischemic neuropathy, symptoms usually increase gradually and asymmetrically. Their appearance is associated with a chronic disruption of the 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. There may be other vascular factors. With posterior ischemic neuropathy, fluctuations in the condition are often observed with deterioration in the quality of vision after taking a hot bath, visiting a sauna/bath, immediately after waking up, during anxiety 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, symptoms appear acutely and increase rapidly. It is caused by acute hypoxia of the anterior portion of the optic nerve (in the nipple area). Edema and infarctions develop, and small linear foci of hemorrhages in the retina are often found. The disorders are most often unilateral and irreversible; after 2-3 weeks, atrophic phenomena are observed in the optic nerve trunk.
With endocrine optic neuropathy, visual impairment develops subacutely and is associated with decompensated edematous exophthalmos. Venostasis, increased intraorbital pressure, edema 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, a partial reduction of symptoms is possible.

Diagnostics

Diagnosis of optical 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 presumed root cause, but also on the equipment of the medical institution. Moreover, most patients, in addition to consulting an ophthalmologist (ophthalmologist), also need to consult other specialists.

Diagnosis of optic neuropathy includes the following methods and studies:

Assessment of visual acuity. In case of severe disturbances, only a light perception test can be performed.
Determination of visual fields. Allows you to identify their narrowing, loss of sectors and quadrants, and the presence of scotomas.
Color perception testing.
Ophthalmoscopy is an examination of the fundus of the eye 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 discs, retina and its vessels. With optical neuropathy, pallor of the disc, a change in its color to grayish, fading or widening of the boundaries, and bulging into the vitreous can be detected. Swelling of adjacent areas of the retina, dilation or narrowing of blood vessels (arteries, veins), and sometimes hemorrhages are often detected. Exudate may be visible in the disc area, which looks like cotton wool-like layers. But with posterior ischemic neuropathy, ophthalmoscopy initially usually does not reveal any changes in the fundus.
Doppler ultrasound of arteries: ophthalmic, periorbital region (especially supratrochlear), carotid, vertebral. Currently, laser Doppler ultrasound is being increasingly used.
Angiography of retinal vessels.
Assessment of the physiological activity of the optic nerves, with determination of the threshold of their electrical sensitivity, pattern ERG, .
Studies to assess the condition of the skull bones and especially the area of the sella turcica (radiography, CT, MRI). They can also be used to identify foreign bodies, signs of space-occupying formations and increased intracranial pressure.
Static computer perimetry.
Laboratory diagnostics: biochemical analysis blood with an assessment of the lipid panel and glucose level, study of the coagulation system. If there are clinical signs of B12 deficiency, the level of the corresponding vitamin in the blood serum is determined.

Consultations with a neurologist (or neurosurgeon), vascular surgeon, endocrinologist, and therapist may be indicated.

Principles of treatment

The treatment regimen for optic neuropathy depends on the etiology of damage to the optic nerve, 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 decided.

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

Therapy for vascular ophthalmopathy includes several groups of drugs:

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

Oxygen therapy is also used whenever possible. During 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, they also necessarily affect etiological factor. For example, with endocrine ophthalmopathy, stabilization of hormonal status is of paramount importance. With post-traumatic compressions, they try to remove foreign bodies and restore the physiological shape of the orbit, and evacuate large hematomas.

Forecast

Unfortunately, the symptoms of optic neuropathy are rarely completely reduced even with early adequate therapy. Good results include partial restoration of vision and no tendency to progression of symptoms in the long term. Most patients retain peripheral vision defects and decreased visual acuity, which is associated with the development of irreversible nerve atrophy. And chronic vascular neuropathy usually tends to progress slowly and steadily.

After the severity of the condition has been relieved and symptoms have stabilized, the prevention of repeated ischemic attacks and curbing the process of neurodegeneration becomes of paramount importance. Most often, long-term maintenance therapy is prescribed, aimed at preventing thrombosis and improving the blood lipid profile. Repeated courses using 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 gives a lecture on Leber's hereditary optic atrophy.