Home Dental treatment What the fundus shows is normal. Description of the fundus The most common pathologies of the fundus

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What the fundus shows is normal. Description of the fundus The most common pathologies of the fundus

The color is formed by retinal and choroidal pigments and can vary among people of different color types (darker for brunettes and people of the Negroid race, lighter for blonds). Also, the intensity of the fundus coloring is affected by the density of the pigment layer, which can vary. With a decrease in pigment density, even the vessels of the choroid - the choroid of the eye with dark areas between them - become visible (Parkert picture).

The optic disc appears as a pinkish circle or oval up to 1.5 mm in cross section. Almost in its center you can see a small funnel - the exit point of the central blood vessels (central artery and vein of the retina).

Closer to the lateral part of the disc, another cup-like depression can rarely be seen; it represents a physiological excavation. It looks slightly paler than the medial part of the optic disc.

Normal fundus, on which the optic nerve papilla (1), retinal vessels (2), fovea (3) are visualized

The norm in children is a more intense coloration of the optic disc, which becomes paler with age. The same is observed in people with myopia.

Some people have a black circle around the optic disc, which is formed by an accumulation of melanin pigment.

The arterial vessels of the fundus look thinner and lighter, they are more straight. Venous ones are larger in size, in a ratio of approximately 3:2, and more convoluted. After the optic nerve leaves the nipple, the vessels begin to divide according to a dichotomous principle, almost to the capillaries. At the thinnest part that can be determined by fundus examination, they reach a diameter of only 20 microns.

The smallest vessels gather around the macula area and form a plexus here. Its greatest density in the retina is achieved around the macula - the area of best vision and light perception.

The area of the macula (fovea) itself is completely devoid of blood vessels; its nutrition comes from the choriocapillaris layer.

Age characteristics

The fundus of the eye in newborns is normally light yellow in color, and the optic disc is pale pink with a grayish tint. This slight pigmentation usually disappears by the age of two. If a similar pattern of depigmentation is observed in adults, this indicates optic nerve atrophy.

The afferent blood vessels in a newborn are of normal caliber, while the efferent blood vessels are slightly wider. If childbirth was accompanied by asphyxia, then the fundus of the children will be dotted with small pinpoint hemorrhages along the arterioles. Over time (within a week) they resolve.

With hydrocephalus or another cause of increased intracranial pressure in the fundus, the veins are dilated, the arteries are narrowed, and the boundaries of the optic disc are blurred due to its swelling. If the pressure continues to increase, the optic nerve nipple swells more and more and begins to push through the vitreous body.

Narrowing of the arteries of the fundus accompanies congenital atrophy of the optic nerve. His nipple looks very pale (more so in the temporal areas), but the boundaries remain clear.

Changes in the fundus of the eye in children and adolescents can be:

with the possibility of reverse development (no organic changes);
transient (they can only be assessed at the moment of their appearance);
nonspecific (no direct dependence on the general pathological process);
predominantly arterial (without changes in the retina characteristic of hypertension).

With age, the walls of blood vessels thicken, causing small arteries to become less visible and, in general, the arterial network to appear paler.

The norm in adults should be assessed taking into account concomitant clinical conditions.

Research methods

There are several methods for checking the fundus. An ophthalmological examination aimed at studying the fundus of the eye is called ophthalmoscopy.

An examination by an ophthalmologist is performed by magnifying the illuminated areas of the fundus with a Goldmann lens. Ophthalmoscopy can be performed in forward and reverse view (the image will be inverted), which is due to the optical design of the ophthalmoscope device. Reverse ophthalmoscopy is suitable for general examination; the devices for its implementation are quite simple - a concave mirror with a hole in the center and a magnifying glass. Direct is used when a more accurate examination is needed, which is carried out with an electric ophthalmoscope. To identify structures invisible in normal lighting, illumination of the fundus with red, yellow, blue, yellow-green rays is used.

Fluorescein angiography is used to obtain an accurate picture of the retinal vascular pattern.

Why does the fundus of the eye hurt?

The reasons for changes in the fundus picture may relate to the position and shape of the optic disc, vascular pathology, and inflammatory diseases of the retina.

Vascular diseases

The fundus of the eye most often suffers from hypertension or eclampsia during pregnancy. Retinopathy in this case is a consequence of arterial hypertension and systemic changes in arterioles. The pathological process occurs in the form of myeloelastofibrosis, less commonly hyalinosis. The degree of their severity depends on the severity and duration of the disease.

The result of an intraocular examination can establish the stage of hypertensive retinopathy.

First: slight stenosis of arterioles, the beginning of sclerotic changes. There is no hypertension yet.

Second: the severity of stenosis increases, arteriovenous crossovers appear (the thickened artery puts pressure on the underlying vein). Hypertension is noted, but the condition of the body as a whole is normal, the heart and kidneys are not yet affected.

Third: constant vasospasm. In the retina there is effusion in the form of “lumps of cotton wool”, small hemorrhages, swelling; pale arterioles have a “silver wire” appearance. Hypertension levels are high, the functionality of the heart and kidneys is impaired.

The fourth stage is characterized by the fact that the optic nerve swells and the blood vessels undergo critical spasm.

Arterial hypertension can be an indirect cause of thrombosis or spasm of the retinal veins and central retinal artery, ischemia and tissue hypoxia.

Examination of the fundus for vascular changes is also required in case of systemic disturbances in glucose metabolism, which leads to the development of diabetic retinopathy. Excess sugar in the blood is detected, osmotic pressure increases, intracellular edema develops, the walls of the capillaries thicken and their lumen decreases, which causes retinal ischemia. In addition, microthrombi form in the capillaries around the foveola, and this leads to the development of exudative maculopathy.

During ophthalmoscopy, the fundus picture has characteristic features:

microaneurysms of retinal vessels in the area of stenosis;
an increase in the diameter of the veins and the development of phlebopathy;
expansion of the avascular zone around the macula due to capillary closure;
the appearance of a hard lipid effusion and soft cotton-like exudate;
microangiopathy develops with the appearance of couplings on the vessels, telangiectasias;
multiple small hemorrhages at the hemorrhagic stage;
the appearance of an area of neovascularization with further gliosis - the proliferation of fibrous tissue. The spread of this process can gradually lead to tractional retinal detachment.

Pathology of the optic nerve disc can be expressed in the following:

megalopapilla - measurement shows an increase and pallor of the optic disc (with myopia);
hypoplasia – a decrease in the relative size of the optic disc in comparison with the retinal vessels (with hypermetropia);
oblique ascension – the optic disc has an unusual shape (myopic astigmatism), the accumulation of retinal vessels is shifted to the nasal region;
coloboma – a defect of the optic disc in the form of a notch, causing visual impairment;
symptom of “morning glow” – mushroom-shaped protrusion of the optic disc into the vitreous body. Ophthalmoscopy descriptions also indicate chorioretinal pigmented rings around an elevated optic disc;
congestive nipple and edema - enlargement of the optic nerve nipple, its pallor and atrophy with increased intraocular pressure.

Pathologies of the fundus of the eye also include a complex of disorders that occur in multiple sclerosis. This disease has multiple etiologies, often hereditary. In this case, the myelin sheath of the nerve is destroyed against the background of immunopathological reactions, and a disease called optic neuritis develops. An acute decrease in vision occurs, central scotomas appear, and color perception changes.

In the fundus one can detect sharp hyperemia and swelling of the optic disc, its boundaries are erased. There is a sign of optic nerve atrophy - blanching of its temporal region, the edge of the optic disc is dotted with slit-like defects, indicating the onset of atrophy of the retinal nerve fibers. Narrowing of the arteries, formation of couplings around the vessels, and macular degeneration are also noticeable.

Treatment for multiple sclerosis is carried out with glucocorticoid drugs, since they inhibit the immune cause of the disease, and also have an anti-inflammatory and stabilizing effect on the vascular walls. Injections of methylprednisolone, prednisolone, and dexamethasone are used for this purpose. In mild cases, corticosteroid eye drops such as Lotoprednol can be used.

Retinal inflammation

Chorioretinitis can be caused by infectious-allergic diseases, allergic non-infectious, post-traumatic conditions. In the fundus, they appear as many rounded formations of light yellow color, which are located below the level of the retinal vessels. The retina has a cloudy appearance and a grayish color due to the accumulation of exudate. As the disease progresses, the color of inflammatory foci in the fundus may approach whitish, as fibrous deposits form there and the retina itself becomes thinner. The retinal vessels remain virtually unchanged. The outcome of retinal inflammation is cataract, endophthalmitis, exudative, and in extreme cases, atrophy of the eyeball.

Diseases affecting the retinal vessels are called angiitis. Their causes can be very diverse (tuberculosis, brucellosis, viral infections, mycoses, protozoa). The ophthalmoscopy picture shows vessels surrounded by white exudative couplings and stripes, areas of occlusion and cystic edema of the macula area are noted.

Despite the severity of the diseases causing fundus pathologies, many patients initially begin treatment with folk remedies. You can find recipes for decoctions, drops, lotions, compresses from beets, carrots, nettles, hawthorn, black currants, rowan berries, onion peels, cornflowers, celandine, immortelle, yarrow and pine needles.

I would like to draw your attention to the fact that by taking home treatment and delaying a visit to the doctor, you may miss the period of development of the disease at which it is easiest to stop it. Therefore, you should regularly undergo ophthalmoscopy with an ophthalmologist, and if pathology is detected, carefully follow his instructions, which you can supplement with folk recipes.

/ description of the fundus

Depends on the presence of capillaries. The thickness of their layer is equivalent to the thickness of the layer of nerve fibers, therefore, normally the gradation of color is different: from almost red in the nasal part to pale pink in the temporal part. In young people, the color is often yellow-pink; in children under 1 year of age, the color of the disc is pale gray.

In pathology, the optic disc can be decolorized, hyperemic, and bluish-gray. Uniform coloring - abnormal development of the optic disc (often accompanied by amblyopia) is observed with taperetinal dystrophy, in old age.

Clear in normal conditions or blurred in pathology. The ophthalmoscopic border of the disc is the edge of the choroid. When there is underdevelopment of the choroid, an oblique position of the disc, or stretching of the posterior pole of the eye with myopia (myopic cone), the choroid moves away from the edge of the disc.

The senile halo is a peripapillary zone of atrophy without noticeable visual impairment.

Note normal size (true micron size), increased or decreased. In hypermetropic eyes, the discs are usually visually smaller, in emmetropic eyes they are larger. With age, the size of the disc does not change, but part of the supporting tissue atrophies; this atrophy is manifested by flattening of the disc disc.

Form. Normally round or slightly oval.

The central recess (vascular funnel, physiological excavation) is the site of entry and exit of retinal vessels. Formed by 5-7 years. The maximum diameter is normally 60% of the disc diameter (DD), the area is 30% of the total disc area. In some cases, there is no excavation and the central part of the disc is occupied by glial and connective tissue (Kunt's meniscus) and retinal vessels. Sometimes (in 6% of emmetropes) physiological excavation reaches deep into the cribriform plate of the sclera and the latter is visible as a white oval with dark dots.

Pathological excavation (glaucomatous) differs in size, depth, progressive course up to a breakthrough to the edge of the optic disc (E/D diameter ratio from 0.3 to 1.0), and the presence of vascular parallax along the edge of the disc.

Level in relation to the fundus plane.

Normally, the nasal, superior and inferior portions of the optic disc are slightly higher than the surrounding retinal tissue (prominence into the vitreous), and the temporal portion is at the same level as the retina.

Atypical optic disc (“oblique disc”) – occurs in 1% of cases in healthy eyes. Due to the oblique course of the optic disc in the scleral canal, such a disc has a narrowed shape in the horizontal meridian, a flat position of the entire temporal side and an undermined nasal edge of the excavation.

Circulatory (anterior ischemic neuropathy, disc vasculitis - incomplete thrombosis of the central vein),

Hydrodynamic (stagnant disk).

Pseudostagnant disc– in ¼ of patients with hypermetropia, it is also caused by drusen. The reason is the hypertrophy of glial tissue in the central recess of the disc during fetal development. The degree of expression varies. Often this is an increase in the saturation of pink color, some blurring of the nasal, upper and lower borders with the normal state of the retinal vessels. To exclude pathology, dynamic observation is necessary with monitoring of visual functions, monitoring the size of the blind spot (not enlarged here).

Underdevelopment of the papillo-macular sector of the disc: The optic disc has a bean-shaped shape. The temporal sector is absent; pigment deposition is noted in this area.

Coloboma of the disc entrance– in the area of the disk, a wide hole measuring 2-2.5 DD is visible, surrounded by pigment. At the bottom of the hole, which is 3-4 diptres below the level of the retina, a pink disk is visible. The central vessels climb along the lateral surface of this depression to the surface of the retina. Visual functions are usually not impaired.

Myelin sheaths of fibers of the disc area and retina (0.3% of people). Normally, in humans, the border of their distribution is the cribriform plate. Ophthalmoscopically, myelin fibers with clear boundaries come from the depths of the disc and resemble tongues of white flame. The retinal vessels are lost in these tongues. Does not affect vision.

Disc inversion– reverse location, with the retinal vessels located in the temporal half of the disc, and not in the nasal half.

Kestenbaum's symptom– a decrease in the number of vessels on the disc to less than 7 (a symptom of optic nerve atrophy).

Disc drusen– abnormal hyaline bodies in the form of yellowish-white nodules located on the surface of the disc or in its tissue. Discs with drusen are not hyperemic, the borders may be scalloped, there is no exudate or venous stasis. Physiological excavation is smoothed, the edges are blurred and uneven. In doubtful cases, fluorescein angiography is performed.

Evulsion– tearing out the optic nerve from the scleral ring. Ophthalmoscopically, a hole is visible instead of a disc.

Avulsion– rupture, separation of the disc from the scleral ring. The disk remains in place. Visual acuity = 0.

Omnubelation– periodic blurring, transient loss of vision, manifested by increased intracranial pressure.

In newborns it is light yellow, the size corresponds to the area of the optic disc. By 3-5 years of age, the yellowish background decreases and the macular area almost merges with the pink or red background of the central zone of the retina. Localization is determined mainly by the avascular central zone of the retina and light reflexes located approximately 25 0 temporal to the optic disc. The macular reflex is mainly detected until the age of 30, then gradually fades away.

Normally transparent (even the layer of pigment epithelium). The thickness of the optic disc is 0.4 mm, in the area of the macula 0.1-0.03 mm, and at the dentate line 0.1 mm. The fundus background is pink. The near, middle and extreme periphery should be examined.

The first zone, otherwise the posterior pole, is a circle whose radius is equal to twice the distance from the optic disc to the foveola. The second - middle zone - is a ring located outward from the first zone to the nasal part of the dentate line and passing through the temporal part in the equatorial region. The third zone is the rest of the retina anterior to the second. It is most susceptible to retinopathy.

Parquet fundus- unevenly red in color, on which stripes formed by the vessels and darker areas between them are visible. This is due to a small amount of retinal pigment and a large amount of choroidal pigment (normal variant).

Slate fundus– background is slate gray. The norm for people of the dark race.

Albinotic fundus: pale pink color (little pigment in the retinal pigment epithelium layer and choroid and the sclera is visible). The vascular pattern of the choroid is clearly visible.

"Retinal thinning"- this ophthalmological term is incorrect in principle, since even the absence of the retina does not lead to a change in the color of the fundus. If large and medium choroidal vessels are visible through the retina, this means that the retinal pigment epithelium layer and the choriocapillaris vascular layer have died.

Note the condition of the caliber of the vessels (arteries and veins): normal caliber, narrowed, dilated, obliterated. If the arteries are narrowed, note the arteriovenous ratio.

The normal difference in the ratio of caliber A and B is most pronounced in newborns - 1:2, decreases with age - in adults - 2:3 and increases again in the elderly.

Note: normal, pathological tortuosity, arteriovenous crossover.

The CAS and CVS each have 4 branches, supplying blood to 4 quadrants of the retina - the superior and inferior temporal, superior and inferior nasal. Vessels pass through the layer of nerve fibers, small branches branch to the outer mesh layer. Before the first branching, the vessels are called vessels of the first order, from the first to the second - vessels of the second order, etc.

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How is the fundus checked and what does the study show?

A diagnostic examination of the fundus of the eye, carried out to obtain data on the condition of the eyeball (including blood vessels) and identify possible pathologies, is called “Ophthalmoscopy”.

This method is quite informative for the specialist and safe for the patient.

What does the doctor see?

With the help of ophthalmoscopy, you can evaluate the condition of the retina, optic nerve head, and choroid. It makes it possible to determine the functional state of the veins and arteries responsible for the blood supply to the retina.

What diseases can be detected?

This diagnostic procedure can help determine if the following problems exist:

any abnormalities in the structure of the retina (hemorrhage, dystrophy, detachment, swelling, ruptures, foci of inflammation);
the presence of opacities in the vitreous body of the eyeball;
possible deviations of the optic nerve head from the norm, which does not exclude the presence of various brain pathologies (in particular, increased intracranial pressure);
changes in the pattern of blood vessels in the circulatory system in the organ of vision, which indirectly indicates the occurrence of complications in the case of diabetes, as well as the state of blood pressure.

Thus, an ophthalmological examination is a mandatory procedure for people suffering from diseases of the circulatory and nervous systems. It is also indicated for people who have problems with metabolism and endocrine disorders.

How is the research going?

The examination is carried out using special equipment - a fundus lens and a slit lamp or ophthalmoscope. A fundus camera is often used - a highly specialized device that allows you to take photographs of the fundus of the eye.

If necessary, mydriatics can be used - eye drops that help dilate the pupil. When using them, the ability to clearly see objects at various distances is temporarily lost. The duration of action of these drugs is 1 – 1.5 hours, after which visual acuity returns to its original state. It is important for car enthusiasts to remember this, because... Driving vehicles will be difficult for some time.

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Fundus pressure, normal, symptoms.

The phrase fundus pressure is incorrect. In ophthalmology there is no such thing as fundus pressure. This phrase combines two ophthalmological concepts: fundus and intraocular pressure.

The fundus is the inner part of the eye that the doctor sees during a special examination - ophthalmoscopy. Usually, in the fundus of the eye, the doctor normally sees the optic disc, the retina and its vessels. Therefore, fundus pressure loses all meaning, because the image (picture) that the doctor sees cannot have pressure.

In turn, intraocular pressure is the tone of the eye, or the force with which the inner liquid part of the eye presses on the walls of the eye itself.

Normal fundus pressure

Intraocular pressure is measured in millimeters of mercury and is normally mmHg in a standard study according to Maklakov.

In the CIS countries, eye pressure is usually measured using the Maklakov method. An anesthetic (lidocaine, alcaine) is instilled into both eyes, and a special tonometer device is taken. A tonometer is a weight weighing 10g. which has two sites. These areas are lubricated with a special harmless paint and after that the tail is placed on the front part of the eye - the cornea. An imprint remains on the site. The diameter of the imprint determines the amount of eye pressure.

Increased intraocular pressure can lead to changes in the normal fundus of the eye. Usually, changes in the optic nerve occur in the fundus. It turns pale, the number of its vessels decreases and a hole appears in it (pressed by increased pressure) - excavation.

You can often hear the phrase: what are the symptoms of fundus pressure? Most likely these are symptoms of increased intraocular pressure. Typically, in the early stages, increased intraocular pressure is asymptomatic. There may be blurred vision, rainbow circles before the eyes, narrowing of the lateral fields of vision (especially from the side of the nose). With a sharp and strong increase in intraocular pressure, there may be pain in the eye and head, redness of the eye, and blurred vision. Typically, increased eye pressure appears in people after 40 years of age. Therefore, all people over 40 years old must have their eye pressure measured and their fundus examined once every 1-2 years.

With various eye diseases, the picture of the fundus may also change. The fundus of the eye is especially affected by high blood pressure, diabetes, myopia and glaucoma.

So, let's summarize. Fundus pressure is a combined concept of two ophthalmological terms that have a certain connection with each other.

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How to assess intraocular pressure

The fundus is the back part of the inner wall of the eyeball. When examining it with an ophthalmoscope, the doctor sees the condition of the vessels, optic disc (optic nerve head) and retina. The doctor measures intraocular pressure (IOP) with a special tonometer. He then analyzes the results of diagnostic procedures and evaluates the force with which the vitreous body produces fundus pressure. The norm for an adult or a child differs. However, IOP indicators must correspond to the level of mm Hg. Art. (mercury column), then the visual organ will function correctly.

How is intraocular pressure measured?

During tonometry, the ophthalmologist can use one of several contact or non-contact diagnostic methods. This depends on the model of tonometer that the doctor has. Each meter has its own standard IOP norm.

Most often, the fundus is examined using the Maklakov method.

In this case, the person lies down on the couch and is given local anesthesia - an ophthalmic antiseptic drug, for example, Dicaine solution 0.1%, is instilled into the eyes. After removing the tear, a colored weight is carefully placed on the cornea and imprints are made on the tonometer pad. The amount of intraocular pressure is assessed by the clarity and diameter of the remaining pattern. According to Maklakov, for adults and children, normal IOP is a level within the range of mmHg.

Relationship between IOP and fundus pressure

Intraocular pressure is determined by the amount of aqueous humor in the chambers and the volume of circulating blood in the episcleral veins. IOP directly affects all membranes and structures of the visual organ from the inside.

As for such concepts as fundus pressure or its norm, they do not exist in ophthalmology. These phrases mean IOP, its effect on the sclera with the cornea and the vitreous body, which presses on the back of the membrane from the inside. That is, normal, weak (below 10 mm Hg) and high (more than 30 mm Hg) pressure force of the vitreous mass on the retina, vessels, optic disc located in the fundus is possible. The higher or lower the IOP level compared to the norm, the stronger the deformation of the structural elements.

With prolonged high intraocular pressure under continuous pressure, the retina, blood vessels and nerves become flattened and may rupture.

With a low IOP level, the vitreous does not adhere tightly enough to the wall. This can cause shifts in visual fields, retinal detachment and other functional disorders of the organ.

Some subjective symptoms of abnormalities or fluctuations in intraocular pressure can be confused with signs of surges in arterial or intracranial pressure, or spasms of cerebral vessels. For example, migraine, which causes pain in the eye, occurs with vegetative-vascular dystonia, hypertension, and the formation of tumors inside the cranial cavity. To confirm or refute these diseases, ophthalmoscopy and/or tonometry is required.

Fundus changes in hypertension

The pressure will return to normal! Just remember once a day.

With arterial hypertension, damage to small vessels and capillaries is detected during diagnosis in more than 50% of patients. Changes in the fundus of the eye in hypertension are analyzed by severity, degree of tortuosity, ratio of the sizes of veins and arteries, as well as their reaction to light. Their condition depends on the speed of blood flow and the tone of the vascular walls.

Changes in the fundus of the eye with hypertension:

at the site of branching of the retinal arteries, the acute angle disappears, which straightens almost to the point;
small veins around the macula lutea acquire corkscrew tortuosity;
arterioles narrow, the branches of the arterial tree are less noticeable, they are thinner compared to the venous network;
symptoms of Hun-Salus vascular decussation appear (compression of a vein by an artery);
hemorrhages (hemorrhages) in the retina;
the presence of swelling of the nerve fibers, in which characteristic white cotton wool-like lesions appear;
the posterior wall of the eyeball is hyperemic, swollen, the retina and disc are darker in color.

The ophthalmologist also evaluates visual function. With hypertension, dark adaptation decreases, there is an expansion of the area of the blind spot, and a narrowing of the field of view. Fundus examination helps diagnose hypertension at an early stage.

Classification of changes in the organ of vision in hypertension

The systematization of pathological changes in the eyes against the background of hypertension was last carried out by L. M. Krasnov in 1948. It is his classification that is used by ophthalmologists working in countries that were formerly part of the USSR.

Krasnov L.M. divided the development of hypertension into three stages:

Hypertensive angiopathy.
Hypertensive angiosclerosis.
Hypertensive retinopathy.

At the first stage, changes in fundus pressure primarily affect the functioning of retinal vessels, causing spasms, narrowing, partial compression, and increasing tortuosity. With hypertensive angiosclerosis, the symptoms of the previous stage are aggravated, the permeability of the vascular walls increases, and other organic disorders appear. At the third stage, the lesion already covers the retinal tissue. If the optic nerve is damaged in the process, the pathology develops into neuroretinopathy.

Excessively increased IOP significantly reduces the duration of each stage, causing changes in the organ of vision in a short period of time. The process can affect both eyes. Often, laser photocoagulation of the retina is required to eliminate disorders.

Symptoms of fundus pressure

With each disease, certain subjective and objective signs arise that are inherent in a specific pathology.

In the early stages, deviations of IOP from normal for a person may be subtle, or there may be no symptoms at all.

In order not to miss the onset of pathological processes, doctors recommend undergoing ophthalmoscopy once every 12 months, and tonometry every 3 years.

In between examinations, you can do a self-diagnosis of the IOP level, assessing the shape, firmness and elasticity of the eyeball by lightly pressing your finger on it through closed eyelids. If the organ is too hard and does not bend under the hand, or any painful discomfort occurs, then the pressure in it is quite high. The finger seems to have sunk in, and the eye itself is softer than usual - the IOP is too low. In both cases, urgent consultation with an ophthalmologist is required.

Symptoms of high pressure on the fundus:

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bursting pain or discomfort inside the organ of vision;
redness of the sclera;
heaviness of eyelids;
distortion of the picture, loss of several fragments from it, other visual impairments.

Signs of low IOP include sunken eyes into the sockets (as with dehydration), dry conjunctiva, and loss of shine on the white and cornea. With weak pressure on the fundus of the eye, vision is also impaired, and the viewing angle may change. With any deviation in IOP, eye fatigue increases. Other symptoms of disorders and the degree of damage are visible when using ophthalmic devices.

Conclusion

Fundus pressure, normal IOP, optic nerve, choroid, retina, and other structural elements of the sensory organ are closely interconnected. Dysfunction of the ciliary body, impaired blood circulation or aqueous humor can lead to a malfunction of the entire system, disease or irreversible processes. To maintain visual acuity, it is recommended to undergo routine examinations with an ophthalmologist in a timely manner.

Fundus examination - why is such an examination necessary?

Modern medicine refers to fundus examination as ophthalmoscopy. Such an examination allows ophthalmologists to identify a number of pathologies and possible serious diseases. Examination of the fundus can accurately assess the condition of the retina, as well as all its individual structures: the choroid, the macula area, the optic nerve head, etc. This procedure should be carried out regularly, you should not be afraid of it, since it is absolutely painless and does not require long period of time. Moreover, examination of the fundus is mandatory for pregnant women, as well as premature babies in case of manifestation of pathological symptoms of ophthalmological diseases.

Why do you need to perform a fundus examination?

Even if a person does not have any problems with the functioning of the visual system, examination of the fundus must be carried out regularly. This procedure is recommended for pregnant women, as it helps to identify certain ophthalmological diseases that can be transmitted to the baby. It is also necessary to carry out such an examination for people suffering from diabetes mellitus, since this pathological disease can have a very negative effect on the condition of the retina.

Checking the condition of the fundus is also mandatory for people suffering from retinopathy, a non-inflammatory disease, as well as any inflammatory ophthalmological processes. These diseases lead to a sharp deterioration in visual function, since the fundus of the eye during the development of pathologies suffers from an aneurysm, which causes the ability to expand the lumens of the retinal vessels to be impaired.

An examination of the retina is also necessary in order to promptly recognize signs of retinal detachment. With this pathology, a person does not feel any painful symptoms, but his vision gradually deteriorates. The main symptom of retinal detachment is the appearance of a “veil” or “fog” before the eyes. Ophthalmoscopy helps to recognize this pathology in a timely manner, since during this examination it is possible to see all the irregularities in the retina of the eye, leading to its detachment.

Preparation for fundus examination

An ophthalmological examination is carried out only by a medical specialist. Before performing a fundus examination, the patient needs to dilate the pupil. For this, the ophthalmologist uses special medications (usually a 1% solution of tropicamide or drugs such as Irifrin, Midriacil, Atropine).

If the patient wears glasses, they must be removed before the fundus examination procedure. If vision correction is carried out using contact lenses, the issue of the need to remove them is decided by the ophthalmologist individually.

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No other special preparation is required before examining the fundus.

Fundus examination

A medical examination of the fundus of the eye is not difficult. For all adults, as well as for children, the methods of conducting such an examination are the same. How is a fundus examination performed?

As a rule, a mirror ophthalmoscope is used for examination - this is a mirror with a concave lens and a small hole in the center. The ophthalmologist looks into the patient's eye through the device. A thin beam of light passes through a small hole in the ophthalmoscope, which allows the doctor to see the fundus of the eye through the pupil.

How is a fundus examination performed? The procedure for examining the fundus can be direct or reverse. With direct inspection, you can see the main areas of the fundus, as well as their pathologies. A reverse fundus examination is a quick and general examination of all areas of the eye.

The examination procedure must be carried out in a darkened room. The doctor directs a beam of light into the patient's eye, first at a short distance, and then brings the corresponding device closer and closer to the eye. This manipulation allows the ophthalmologist to carefully examine the fundus, lens, and vitreous body. The fundus examination procedure takes about 10 minutes; the ophthalmologist must examine both eyes, even if the patient assures that his vision is absolutely normal.

During the examination, the doctor examines:

the area of the optic nerve is normal when it has a round or oval shape, clear contours, and a pale pink color;
the central region of the retina, as well as all its vessels;
the yellow spot in the center of the fundus is a red oval, along the edge of which there is a light stripe;
pupil - normally, the pupil may become red during examination, but any focal opacities indicate the presence of a certain pathology.

Ophthalmoscopy is also performed using other methods:

Vodovozov technology - during the fundus examination procedure, multi-colored rays are used.
Biomicroscopy or examination of the fundus with a Goldmann lens - a slit light source is used during the examination. This examination method can be carried out even with a constricted pupil.
Laser ophthalmoscopy - the fundus of the eye is examined using a laser.
Examination of the fundus with a fundus lens - the device is used in conjunction with a binocular microscope, which are available in a slit lamp. With this method, all areas of the fundus are scanned, even up to the post-equatorial zone.

Who needs a fundus examination?

An ophthalmological examination is a preventive procedure and should be carried out regularly for every person, but there are a number of diseases for which examination of the fundus is mandatory:

atherosclerosis;
hypertension;
cataract;
diabetes;
increased intracranial pressure;
stroke;
osteochondrosis;
prematurity in children;
retinal dystrophy;
night blindness syndrome;
color vision disorders.

Contraindications to fundus examination

The patient has ophthalmological pathologies with symptoms of photophobia and lacrimation;
Inability to dilate the patient's pupil;
If the patient has a physiological deviation - insufficient transparency of the lens of the eye, as well as the vitreous body.

Precautions when examining the fundus

The ophthalmological procedure should be prescribed by a therapist to people suffering from cardiovascular diseases. In some cases, this procedure is contraindicated for such patients.
You should not drive after having a fundus examination.
After the procedure, you must wear sunglasses.

In order to promptly identify and prevent pathological processes in the eyes, it is necessary to monitor pressure and be able to measure it.

General information and table of eye pressure norms

To maintain blood microcirculation in the eyes, which ensures the functioning of the retina and metabolic processes, normal pressure inside the eyes is necessary. This indicator is individual for each person and is generally considered normal when it does not go beyond the reference indicators. Each age group has its own average parameters. Knowing them, you can understand why vision is deteriorating and what to do about it. A table of intraocular pressure values by age and measurement method will help you monitor the indicators:

IOP in young people

Balanced eye pressure is a sign of the absence of ophthalmological diseases. At a young age without the presence of pathologies, the indicator fluctuates very rarely, most often due to eye strain at work. For everyday intraocular pressure, the norm in adults varies between 10-20 mm. mercury column. Deviations may indicate incipient processes in the retina or optic nerve, the first signs of which are a blurred image, eye pain and headache. If symptoms last more than a week, it is better to be examined by an ophthalmologist.

IOP after 60 years

Until the age of 40, people without ophthalmic pathologies have good vision, but then it begins to gradually deteriorate due to the aging of the body. Anatomical features are such that the eye pressure in women changes faster, and they are exposed to eye ailments more often. Iphthalmotonus and normal eye pressure in men change more smoothly. At the age of 50, the pressure levels out and, in the absence of congenital or acquired eye diseases, reaches the normal level of 10-23 mm. mercury column. The changes are abrupt in nature and are caused by exacerbation of chronic diseases. In women, increased pressure in the eyes occurs after 40 years of age during menopause, when the level of estrogen in the blood drops. At the age of 60, patients' retina transforms, which entails an increase in pressure to 26 mm. mercury column according to Maklakov, the occurrence of cataracts and glaucoma.

Normal for glaucoma

An upward change in IOP indicates processes of changes in blood microcirculation in the eye, and serves as a harbinger of glaucoma. Both at the initial stage of the disease and during its progress, blood pressure readings must be taken twice a day - morning and evening to draw an objective picture. For elderly people with terminal stage, measurements are taken 3-4 times a day. The average norm of eye pressure in glaucoma is fixed in the range from 20 to 22 mmHg. At the last stage, the norm reaches 35 mm Hg.

Methods for measuring pressure

The patient cannot independently determine the norm of intraocular pressure; this requires special medical devices. The most common values in numbers are natural pressure or the result of measurements using Maklakov’s method. In all cases, the reading is based on the response of the eye to the force applied to it. According to the principles of influence, measurement can be different - contact and non-contact. In the first case, the ocular surface comes into contact with the measuring device, in the second, a directed air flow acts on the eye. The hospital may offer the following tonometry methods:

according to Maklakov;
electronograph;
device "Pascal";
non-contact tonometry;
pneumotonometer;
ICare tonometer;
Goldmann device.

The tonometry procedure is painless and causes minimal discomfort. In some cases, an experienced ophthalmologist can determine an increase in pressure by pressing his fingers on the eyeball, but when diagnosing and treating glaucoma, ultra-precise measurements are necessary, because an error of even one millimeter of mercury can have serious consequences.

Daily tonometry

In people suffering from glaucoma or other ophthalmological diseases, IOP monitoring should be regular. Therefore, in order to make an accurate diagnosis and adjust treatment, in some cases patients are prescribed 24-hour tonometry. The procedure is prolonged for 7-10 days and consists of recording eye parameters three times a day, preferably at equal intervals. All marks are recorded in the observation diary, then the doctor displays the maximum and minimum deviation from the norm.

Change indicators

Many patients think about hypertension too late, attributing its primary symptoms to everyday causes - fatigue and overexertion, prolonged exposure to lenses. But timely detection of deviations can serve as evidence of other disease processes in the body. It accompanies hormonal disorders and diseases of the cardiovascular system.

Ocular hypotension

A decrease in IOP is rarely observed in modern medicine and leads to complications including blindness. Low eye pressure is dangerous because it occurs without pronounced symptoms. Patients consult a doctor having already partially lost their vision. You can stop the process of blindness, but you cannot return your vision to its original level. In order to detect low blood pressure in a timely manner, it is necessary to undergo a routine medical examination every 5-6 months. Timely treatment can prevent the development of the disease and maintain visual acuity.

Low eye pressure is no less dangerous than high eye pressure. If it is observed for more than a month, then sudden loss of vision may occur.

Ophthalmohypertension

Increased pressure in the eye is often observed and has different values depending on the gender and age of the patient. The disease can be traced across all ages. Disturbed normal eye pressure manifests itself most aggressively in women, especially in the elderly, causing changes in the fundus of the eye. Children are also susceptible to the disease. They experience headaches, tired eyes syndrome, and sometimes pain when blinking. In the absence of timely treatment, ocular hypertension causes complications on the cardiovascular and hormonal systems, leading to glaucoma and cataracts.

Ways to normalize eye pressure

At an early stage of the disease, Azopt is effective in treatment.

In the chronic stage, hypertension leads to glaucoma and requires surgical intervention, so normalizing intraocular pressure at an early stage of identifying abnormalities is very important. You can achieve a positive effect with the help of special eye drops, such as Azopt, Travatan, Timolol and others. A doctor should prescribe the medicine; it is better not to self-medicate with medications. At home, the patient is able to follow a number of instructions that will help preserve vision by reducing hypertension:

Follow a diet. The diet should contain fewer foods that contribute to the growth of insulin in the blood - potatoes, sugar, rice, pasta and bread, oatmeal and cereal flakes. It is useful to eat dark berries - blueberries, blackberries, as well as lutein-containing vegetables - broccoli, spinach, Brussels sprouts.

Get some exercise. Aerobics, jogging, and cycling are perfect. You need to train for half an hour a day, three to five times a week.

Take fatty acids containing Omega-3 fats. It can be consumed in the form of dietary supplements or obtained naturally - with fish (salmon, salmon, herring, tuna).

There are cases when it is possible to restore normal intraocular pressure in a person only through surgery. Without surgery, the disease will worsen, develop into terminal glaucoma and lead to blindness. One operation is not enough; a number of adjustments are necessary to ensure normal movement of fluids inside the eye and relieve excessive stress on the functional parts of the organ.

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The fundus is normal in adults

The norm of fundus pressure is of great importance for a person. In the structure of the eye, a lot depends on it: very high or low pressure can cause poor vision and other irreversible processes. To understand what eye pressure looks like, you need to imagine a balloon. Pressure is what maintains its shape. In the eye, pressure feeds the spherical shell and thereby maintains its shape. Pressure is formed by the inflow and outflow of fluids. If there are more fluids than needed, the pressure is considered increased. And if on the contrary - reduced.

Normal eye pressure:

In an adult, the pressure is within mm. Mr. Art. This is a normal indicator.

A normal level of eye pressure preserves metabolic processes and microcirculation in the eyes. It maintains the optical properties of the retina.

There are no pressure standards as such. Normal blood pressure depends on the characteristics of the body.

Stabilize blood pressure using special medications.

To rule out problems with eye pressure, visit your ophthalmologist regularly.

Deviations of eye pressure:

Heart disease can cause high eye pressure.

High blood pressure can appear due to the anatomical features of the eye structure.

There are usually no symptoms of high eye pressure. In this case, the disease becomes complicated and develops into glaucoma. The disease cannot be cured. It is possible to maintain development in a certain form. In the vast majority of cases, glaucoma results in blindness.

Various pressure deviations from the norm lead to the disappearance of thin cells of the retina and optic nerve. They also cause disruption of metabolic processes. High blood pressure may be accompanied by a headache, a feeling of heaviness in the pupils, and darkening of the eyes.

It is important to pay attention to the appearance of the disease in a timely manner. Deviations from normal eye pressure may be associated with hormonal disorders. In such cases, it is necessary to undergo examination.

Low blood pressure is a rare occurrence. It is no less dangerous than high. Low blood pressure can cause vision loss.

Eye pressure is measured using a tonometer. The process is unpleasant, but does not cause severe pain.

Eye pressure - norm and measurement. Symptoms and treatment of high eye pressure at home

An important indicator in diagnosing ophthalmological diseases or visual impairment is pressure in the eyes, or intraocular pressure (IOP). Pathological processes cause its decrease or increase. Untimely treatment of the disease can cause glaucoma and vision loss.

What is eye pressure

Ocular pressure is the amount of tone that occurs between the contents of the eyeball and its membrane. About 2 cubic meters enter the eye every minute. mm of liquid and the same amount flows out. When the outflow process is disrupted for a certain reason, moisture accumulates in the organ, causing an increase in IOP. In this case, the capillaries through which the liquid moves are deformed, which increases the problem. Doctors classify such changes as:

transient type – increase for a short period of time and normalization without medications;
labile pressure - periodic increase with independent return to normal;
stable type – constant excess of the norm.

A decrease in IOP (eye hypotony) is a rare phenomenon, but very dangerous. It is difficult to determine the pathology, because the disease is hidden. Patients often seek specialized care when they experience significant vision loss. Possible causes of this condition include: eye injuries, infectious diseases, diabetes mellitus, hypotension. The only symptom of the disorder may be dry eyes and lack of shine.

How is eye pressure measured?

There are several methods that are carried out in a hospital setting to find out the patient's condition. It is impossible to determine the disease on your own. Modern ophthalmologists measure eye pressure in three ways:

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tonometry according to Maklakov;
pneumotonometer;
electronograph.

The first technique requires local anesthesia, since the cornea is affected by a foreign body (weight), and the procedure causes slight discomfort. The weight is placed in the center of the cornea, after the procedure imprints remain on it. The doctor takes prints, measures them and deciphers them. Determination of ophthalmotonus using a Maklakov tonometer began more than 100 years ago, but the method is considered highly accurate today. Doctors prefer to measure indicators with this equipment.

Pneumotonometry operates on the same principle, only the effect is exerted by an air stream. The research is carried out quickly, but the result is not always accurate. Electronograph is the most modern equipment for measuring IOP in a non-contact, painless and safe manner. The technique is based on enhancing the production of intraocular fluid and accelerating its outflow. If equipment is not available, the doctor can check using palpation. By pressing the index fingers on the eyelids, based on tactile sensations, the specialist draws conclusions about the density of the eyeballs.

Eye pressure is normal

Iphthalmotonus is measured in millimeters of mercury. For a child and an adult, the norm of intraocular pressure varies from 9 to 23 mm Hg. Art. During the day, the indicator may change, for example, in the evening it may be lower than in the morning. When measuring ophthalmotonus according to Maklakov, the normal figures are slightly higher - from 15 to 26 mm. Hg Art. This is due to the fact that the weight of the tonometer puts additional pressure on the eyes.

Intraocular pressure is normal in adults

For middle-aged men and women, IOP should range from 9 to 21 mmHg. Art. You should be aware that intraocular pressure in adults may change throughout the day. Early in the morning the indicators are highest, in the evening they are lowest. The amplitude of oscillations does not exceed 5 mmHg. Art. Sometimes exceeding the norm is an individual characteristic of the body and is not a pathology. In this case, there is no need to reduce it.

Normal intraocular pressure after 60 years

With age, the risk of developing glaucoma increases, so after 40 years it is important to undergo a fundus examination, measure ophthalmotonus and take all the necessary tests several times a year. Aging of the body affects every human system and organ, including the eyeball. The norm of intraocular pressure after 60 years is slightly higher than at a young age. A reading of up to 26 mmHg is considered normal. Art., if measured with a Maklakov tonometer.

Increased intraocular pressure

Discomfort and vision problems in most cases are caused by increased intraocular pressure. This problem often occurs in older people, but also young men and women, and sometimes even children can suffer from illnesses with such symptoms. The definition of pathology is available only to a doctor. The patient may only notice symptoms that should prompt a visit to a specialist. This will help to cure the disease in a timely manner. How the doctor will reduce the indicators depends on the degree of the disease and its characteristics.

Increased eye pressure - causes

Before prescribing therapy for the pathology, the ophthalmologist must determine the causes of increased eye pressure. Modern medicine identifies several main factors by which IOP can increase:

a functional disorder in the functioning of the body, as a result of which the secretion of fluid in the organs of vision is activated;
disruptions in the functions of the cardiovascular system, which cause hypertension and increased ophthalmotonus;
heavy physical or psychological stress;
stressful situations;
as a consequence of a previous illness;
age-related changes;
chemical poisoning;
anatomical changes in the organs of vision: atherosclerosis, farsightedness.

Eye pressure - symptoms

Depending on the intensity of the increase in ophthalmotonus, various symptoms may occur. If the increase is insignificant, then it is almost impossible to detect the problem unless an examination is carried out. Symptoms in this case are not expressed. With significant deviations from the norm, symptoms of eye pressure may manifest as follows:

headache localized at the temples;
pain when moving the eyeball in any direction;
high eye fatigue;
feeling of heaviness in the organs of vision;
pressing feeling in the eyes;
visual impairment;
discomfort when working at a computer or reading a book.

Symptoms of eye pressure in men

Deviations from the norm of ophthalmotonus occur equally among the two sexes of the planet's population. Symptoms of eye pressure in men are no different from those characteristic of women. In persistent acute conditions, the patient experiences the following symptoms of intraocular pressure:

twilight vision impairment;
progressive deterioration of vision;
headache with migraine character;
reduction of the radius of vision in the corners;
rainbow circles, spots before the eyes.

Symptoms of eye pressure in women

Ophthalmologists do not divide the symptoms of ophthalmotonus into female and male. Symptoms of eye pressure in women do not differ from the signs that signal a violation in men. Additional symptoms that may occur with the problem include:

How to relieve eye pressure at home

Iphthalmotonus is treated in different ways: tablets and eye drops, folk remedies. Your doctor will be able to determine which treatment methods will give good results. You can relieve eye pressure at home and normalize the indicators in a person, provided the degree of the problem is not high and eye function is preserved, using simple measures:

do eye exercises every day;
limit computer work, reduce time spent watching TV and eliminate other activities that strain your eyesight;
use drops to moisturize your eyes;
walk outdoors more often.

Drops to reduce intraocular pressure

Sometimes ophthalmologists suggest lowering the readings with the help of special drops. IOP should be lowered only after consulting a doctor. The pharmacological industry offers a variety of drops for intraocular pressure, the action of which is aimed at the outflow of accumulated fluid. All drugs are divided into the following types:

prostaglandins;
carbonic anhydrase inhibitors;
cholinomimetics;
beta blockers.

Eye pressure tablets

As an additional measure in the treatment of increased ophthalmotonus, specialists prescribe medications for oral administration. The medicine for eye pressure is designed to remove excess fluid from the body, improve blood circulation in the brain and the body's metabolic processes. When using diuretics in therapy, potassium supplements are prescribed, since the substance is washed out of the body when taking such medications.

Folk remedies for eye pressure

Traditional healers also know how to reduce intraocular pressure. There are many recipes made from natural ingredients that help get rid of high IOP. Treatment with folk remedies allows you to bring the levels down to normal and does not allow them to rise over time. Folk remedies for eye pressure include the following measures:

Brew meadow clover and leave for 2 hours. Drink 100 ml decoction at night.
Add 1 pinch of cinnamon to a glass of kefir. Drink if IOP increases.
Freshly brewed eyebright decoction (25 g of herb per 0.5 boiling water) should be cooled and strained through cheesecloth. Apply lotions throughout the day.
Wash 5-6 aloe leaves and cut into pieces. Pour a glass of boiling water over the herbal ingredient and boil for 5 minutes. Use the resulting decoction to wash the eyes 5 times a day.
Natural tomato juice helps get rid of increased ophthalmotonus if you drink it 1 glass a day.
Grate peeled potatoes (2 pcs.), add 1 teaspoon of apple cider vinegar. Mix the ingredients and leave for 20 minutes. Afterwards, put the pulp on gauze and use it as a compress.

Video: how to check eye pressure

The information presented in the article is for informational purposes only. The materials in the article do not encourage self-treatment. Only a qualified doctor can make a diagnosis and make recommendations for treatment based on the individual characteristics of a particular patient.

How to assess intraocular pressure

How is intraocular pressure measured?

During tonometry, the ophthalmologist can use one of several contact or non-contact diagnostic methods. This depends on the model of tonometer that the doctor has. Each meter has its own standard IOP norm.

Most often, the fundus is examined using the Maklakov method.

Relationship between IOP and fundus pressure

With prolonged high intraocular pressure under continuous pressure, the retina, blood vessels and nerves become flattened and may rupture.

With a low IOP level, the vitreous does not adhere tightly enough to the wall. This can cause shifts in visual fields, retinal detachment and other functional disorders of the organ.

Fundus changes in hypertension

The pressure will return to normal! Just remember once a day.

Changes in the fundus of the eye with hypertension:

at the site of branching of the retinal arteries, the acute angle disappears, which straightens almost to the point;
small veins around the macula lutea acquire corkscrew tortuosity;
arterioles narrow, the branches of the arterial tree are less noticeable, they are thinner compared to the venous network;
symptoms of Hun-Salus vascular decussation appear (compression of a vein by an artery);
hemorrhages (hemorrhages) in the retina;
the presence of swelling of the nerve fibers, in which characteristic white cotton wool-like lesions appear;
the posterior wall of the eyeball is hyperemic, swollen, the retina and disc are darker in color.

Classification of changes in the organ of vision in hypertension

Krasnov L.M. divided the development of hypertension into three stages:

Hypertensive angiopathy.
Hypertensive angiosclerosis.
Hypertensive retinopathy.

Symptoms of fundus pressure

With each disease, certain subjective and objective signs arise that are inherent in a specific pathology.

In the early stages, deviations of IOP from normal for a person may be subtle, or there may be no symptoms at all.

In order not to miss the onset of pathological processes, doctors recommend undergoing ophthalmoscopy once every 12 months, and tonometry every 3 years.

Symptoms of high pressure on the fundus:

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bursting pain or discomfort inside the organ of vision;
redness of the sclera;
heaviness of eyelids;
distortion of the picture, loss of several fragments from it, other visual impairments.

Conclusion

Fundus of the eye and its pathologies

In fact, the fundus is what the back of the eyeball looks like when viewed upon examination. Here the retina, choroid and optic nerve nipple are visible.

Closer to the lateral part of the disc, another cup-like depression can rarely be seen; it represents a physiological excavation. It looks slightly paler than the medial part of the optic disc.

Normal fundus, on which the optic nerve papilla (1), retinal vessels (2), fovea (3) are visualized

The norm in children is a more intense coloration of the optic disc, which becomes paler with age. The same is observed in people with myopia.

Some people have a black circle around the optic disc, which is formed by an accumulation of melanin pigment.

The smallest vessels gather around the macula area and form a plexus here. Its greatest density in the retina is achieved around the macula - the area of best vision and light perception.

The area of the macula (fovea) itself is completely devoid of blood vessels; its nutrition comes from the choriocapillaris layer.

Age characteristics

Narrowing of the arteries of the fundus accompanies congenital atrophy of the optic nerve. His nipple looks very pale (more so in the temporal areas), but the boundaries remain clear.

Changes in the fundus of the eye in children and adolescents can be:

with the possibility of reverse development (no organic changes);
transient (they can only be assessed at the moment of their appearance);
nonspecific (no direct dependence on the general pathological process);
predominantly arterial (without changes in the retina characteristic of hypertension).

With age, the walls of blood vessels thicken, causing small arteries to become less visible and, in general, the arterial network to appear paler.

The norm in adults should be assessed taking into account concomitant clinical conditions.

Research methods

There are several methods for checking the fundus. An ophthalmological examination aimed at studying the fundus of the eye is called ophthalmoscopy.

Fluorescein angiography is used to obtain an accurate picture of the retinal vascular pattern.

Why does the fundus of the eye hurt?

The reasons for changes in the fundus picture may relate to the position and shape of the optic disc, vascular pathology, and inflammatory diseases of the retina.

Vascular diseases

The result of an intraocular examination can establish the stage of hypertensive retinopathy.

First: slight stenosis of arterioles, the beginning of sclerotic changes. There is no hypertension yet.

The fourth stage is characterized by the fact that the optic nerve swells and the blood vessels undergo critical spasm.

Arterial hypertension can be an indirect cause of thrombosis or spasm of the retinal veins and central retinal artery, ischemia and tissue hypoxia.

During ophthalmoscopy, the fundus picture has characteristic features:

microaneurysms of retinal vessels in the area of stenosis;
an increase in the diameter of the veins and the development of phlebopathy;
expansion of the avascular zone around the macula due to capillary closure;
the appearance of a hard lipid effusion and soft cotton-like exudate;
microangiopathy develops with the appearance of couplings on the vessels, telangiectasias;
multiple small hemorrhages at the hemorrhagic stage;
the appearance of an area of neovascularization with further gliosis - the proliferation of fibrous tissue. The spread of this process can gradually lead to tractional retinal detachment.

Pathology of the optic nerve disc can be expressed in the following:

megalopapilla - measurement shows an increase and pallor of the optic disc (with myopia);
hypoplasia – a decrease in the relative size of the optic disc in comparison with the retinal vessels (with hypermetropia);
oblique ascension – the optic disc has an unusual shape (myopic astigmatism), the accumulation of retinal vessels is shifted to the nasal region;
coloboma – a defect of the optic disc in the form of a notch, causing visual impairment;
symptom of “morning glow” – mushroom-shaped protrusion of the optic disc into the vitreous body. Ophthalmoscopy descriptions also indicate chorioretinal pigmented rings around an elevated optic disc;
congestive nipple and edema - enlargement of the optic nerve nipple, its pallor and atrophy with increased intraocular pressure.

Treatment for multiple sclerosis is carried out with glucocorticoid drugs, since they inhibit the immune cause of the disease, and also have an anti-inflammatory and stabilizing effect on the vascular walls. Injections of methylprednisolone, prednisolone, and dexamethasone are used for this purpose. In mild cases, corticosteroid eye drops such as Lotoprednol can be used.

Retinal inflammation

OCULAR FUNDUS (fundus oculi) - the inner surface of the eyeball visible during ophthalmoscopy: the optic disc, the retina with the central artery and central vein, and the choroid.

An extremely important area of the retina, which has the function of central vision (the highest vision in the retina), is the macula (s. macula lutea) with the central fovea (fovea centralis). The macula macula is located outward approximately 2 disc diameters from its temporal border; its center is slightly below the horizontal line passing through the middle of the disk. The yellow spot is highlighted in a darker color; it has the shape of a horizontal oval, along the edge of which, especially at a young age, there is often a silvery-white arc or ring - a macular reflex. This light reflex occurs due to the thickening of the retina in the form of a ridge around the macula. In the center of the yellow spot, a darker round spot is visible - a dimple (foveola) with a shiny dot in the middle. In older people, the macula is less clearly visible, and light reflexes are usually weak or completely absent; Its position in this case is judged by its darker color and the absence of vessels.

With conventional ophthalmoscopy, the yellow color of the spot is indistinguishable against the red background of G.D.; it can be seen only with ophthalmoscopy in red-free light, proposed by Vogt (A. Vogt, 1913). This method is used to study the retina and optic nerve head. When examined with a light source, deprived of red rays using a blue-green filter, the retina appears green-blue, the retinal vessels appear almost black, the macula is lemon-yellow, and thin vascular branches that are invisible when examined can be detected in it. conventional ophthalmoscopy (tsvetn. Fig. 5), since short-wave rays are reflected mainly from the surface of the retina. Dimmer (F. Dimmer) established that the yellow color depends on the pigment located in the retina in the area of the macula. In addition to red-free light, variously colored light using light filters is used for ophthalmoscopy.

In 1960, a comprehensive method was developed for studying blood pressure using light of various spectral compositions, including comparative ophthalmoscopy in blue, yellow, red, redless, yellow-green and purple light (see Ophthalmoscopy).

When examining G. in red-free and yellow-green light, one can see the course and distribution of the retinal nerve fibers. These fibers in the form of white stripes start from the disk, bend over its edge and diverge in a fan-shape. Near the disc, the fibers are coarser and more clearly defined than at the periphery. Some of them follow the direction of large vessels and reach the periphery, some go to the macula, forming a papillomacular bundle. In the macula macula, some fibers bend sharply, take a vertical direction and, bordering the macula macula on the temporal side, are lost in it. The fibers coming from the disc up and down do not participate in the formation of the papillomacular bundle; they bend and intersect at an obtuse angle, and partly, without intersecting, they go to the periphery. Blood circulating in the vessels of the retina and choroid can be determined by fluorescein angiography (see). With its help, you can clarify the causes of circulatory failure in the retinal vessels (obstruction, spasm), identify patol processes in the macula and optic nerve that are indistinguishable by ophthalmoscopy, differentiate tumor and inflammatory processes, and early changes in blood vessels in diabetes.

The peripheral border of the G. corresponds to the jagged line (ora serrata); it has a darker color and is visible with a dilated pupil and maximum deviation of the eye in the corresponding direction. The periphery of the eyeball is better visible when using a special research method, which consists of local depression of the eyeball and observation using a slit lamp (see) through a gonioscope with an appropriate mirror (see Gonioscopy).

Pathological changes in blood pressure are caused by damage to the optic nerve, retina and choroid, as well as the limiting membrane of the vitreous body.

Ophthalmoscopically, when the optic nerve is damaged, changes are distinguished that are accompanied by hyperemia and swelling of the optic disc - congestive nipple, ischemic disc edema, pseudocongestive nipple (see Congestive nipple), neuritis; atrophic changes (primary and secondary optic nerve atrophy), tumors of the optic nerve head and developmental abnormalities (see Optic nerve). In some cases, changes are detected ophthalmoscopically only when the process, starting somewhere in the optic nerve behind the eye, reaches the disc (retrobulbar neuritis, descending atrophy).

Patol, changes in the retina are ophthalmoscopically characterized by the appearance in it of diffuse opacities or limited white foci, hemorrhages and dyspigmentation, changes in blood vessels. These changes are based on inflammatory (see Retinitis), circulatory-metabolic (see Retinopathy), dystrophic processes, blood circulation disorders and developmental abnormalities (see Retina).

Changes in the choroid, visible during ophthalmoscopy, are a consequence of inflammatory, dystrophic, sclerotic processes, neoplasms and developmental abnormalities. In most cases, inflammatory processes in the choroid are focal in nature (see Choroiditis). In this case, the retinal pigment epithelium is involved in the process, as a result of which an accumulation of pigment clumps appears in the area of patol changes. Gradually, atrophic changes appear at the site of inflammatory foci, which are the main ophthalmoscopic sign of damage to the choroid. Some changes in blood pressure, for example, disc protrusion with a congestive nipple, a speckled reflex in the arteries with diabetic retinal angiopathy, are better detected by ophthalmochromoscopy. Microaneurysms in diabetic retinal angiopathy are clearly detected by fluorescein angiography.

Clinical and diagnostic characteristics of fundus changes

Illustrations for the table

Rice. 6 - 10. Pathological changes in the fundus. Rice. 6. Neurofibromatosis. Rice. 7. For tuberous sclerosis of the brain. Rice. 8. Multiple retinal angiomas. Rice. 9. With amaurotic idiocy. Rice. 10. Pseudoneuritis of the optic nerve.

Rice. 11 - 26. Rice. 11. Initial congestive nipple (the arrow indicates the arcuate peripapillary light reflex). Rice. 12. Pronounced congestion of the nipple, there is hemorrhage at its upper edge (indicated by the arrow). Rice. 13. Pseudostagnant nipple due to drusen (indicated by arrows). Rice. 14. Pseudo-stagnant nipple due to druses hidden in its depth (indistinguishable from a true stagnant nipple). Rice. 15. Hidden drusen (indicated by an arrow) (visible by ophthalmochromoscopy). Rice. 16. Optic neuritis. Rice. 17. Primary (simple) optic nerve atrophy. Rice. 18. Secondary atrophy of the optic nerve (the arrow indicates the atrophic rim around the disc). Rice. 19. Atrophic optic disc when examined in normal light (enlarged image in Figs. 19 and 20). Rice. 20. An atrophic optic disc appears blue when examined in purple light. Rice. 21. Axial (axial) atrophy of the optic nerve (the arrow indicates blanching of the temporal half of the disc). Rice. 22. Axial atrophy of the optic nerve when examined in purple light (the pale temporal half appears blue). Rice. 23. Axial atrophy of the optic nerve when examined in yellow-green light is a symptom of a break in the pattern of nerve fibers (indicated by an arrow). Rice. 24. Obstruction of the central retinal vein (arrows indicate hemorrhage). Rice. 25. Obstruction of the branch of the central retinal vein (the arrow indicates hemorrhage). Rice. 26. Obstruction of the branch of the central retinal vein when examined in red-free light (the arrow indicates hemorrhage).

Rice. 27 - 42. Rice. 27. Obstruction of the central retinal artery (arrows indicate narrowed arteries). Rice. 28. Hypertensive retinal angiopathy (Gwist's symptom). Rice. 29. Sign of decussation of the first degree (Salus I; indicated by arrows). Rice. 30. Symptom of decussation of the second degree (Salus II; indicated by arrows). Rice. 31. Symptom of chiasm of the third degree (Salus III; indicated by an arrow). Rice. 32. Hypertensive retinopathy. Rice. 33. Hypertensive retinopathy (the arrow indicates the star shape). Rice. 34. Ischemic papilledema. Rice. 35. Dry form of senile macular degeneration. Rice. 36. Wet form of senile macular degeneration (indicated by an arrow). Rice. 37. Ring retinal dystrophy (the arrow indicates the shape of the ring). Rice. 38. Hypertensive neuroretinopathy (the arrow indicates the star shape). Rice. 39. Diabetic retinal angiopathy. Rice. 40. Microaneurysms when examined in normal light. Rice. 41. Microaneurysms when examined in red-free light (the same area as in Fig. 40). Rice. 42. Microaneurysms with fluorescein angiography.. Fig. 6. Neurofibromatosis. Rice. 7. For tuberous sclerosis of the brain. Rice. 8. Multiple retinal angiomas. Rice. 9. With amaurotic idiocy. Rice. 10. Pseudoneuritis of the optic nerve.

Rice. 43 - 58. Rice. 43. Simple diabetic retinopathy. Rice. 44. Proliferating diabetic retinopathy (the arrow indicates the “wonderful network” of newly formed vessels). Rice. 45. Proliferating diabetic retinopathy (the arrow indicates a strand of connective tissue). Rice. 46. Retinopathy due to anemia. Rice. 47. Retinopathy in polycythemia. Rice. 48. Retinopathy in chronic lymphocytic leukemia (the arrow indicates light spots bordered by hemorrhage). Rice. 49. Rheumatic retinovasculitis. Rice. 50. Disseminated tuberculous chorioretinitis (arrow indicates a light focus). Rice. 51. Disseminated tuberculous chorioretinitis when examined in blue light. Rice. 52. Central tuberculous chorioretinitis. Rice. 53. Central tuberculous chorioretinitis when examined in red-free light. Rice. 54. Tuberculous periphlebitis of the retina (arrows indicate couplings on the veins). Rice. 55. Congenital toxoplasmosis chorioretinitis (arrows indicate atrophic foci). Rice. 56 and 57. Congenital syphilitic chorioretinitis. Rice. 58. Diffuse syphilitic neuroretinitis - atrophy of the choroid.

Name of fundus changes	Diseases or conditions that can lead to fundus changes	Ophthalmoscopy data	What fundus pathology needs to be differentiated from?
CHANGES DUE TO VASCULAR PATHOLOGY
Hypertensive retinal angiopathy	Stage I of hypertension	Narrowing of the arteries and dilatation of the retinal veins, moderate unevenness of the caliber of the arteries (functional). A mild symptom of arteriovenous decussation of the first degree (Salus I symptom). Some patients have corkscrew-shaped tortuosity of the veins in the macula area (Gwist's symptom - Fig. 28). Variable: veiling of optic disc contours	Renal angiopathy of the retina. Diabetic retinal angiopathy
Retinal angiopathy, hypertensive, traumatic	Cranial	Enlargement of the retinal veins, unevenness of their caliber, tortuosity of the branches in the area of the macula. The arteries are narrowed, the reflex strip on them is expanded. In some places there are symptoms of arteriovenous crossover. Hemorrhages may occur. As the general condition worsens, a picture of congestive optic disc often develops	Hypertensive angiopathy, hypertensive neuroretinopathy
Retinal angiopathy, hypertensive renal		Narrowing of the arteries, as a rule, without signs of hardening of the vascular wall. Rarely, symptoms of first degree decussation (Salus I). Absence of Gvist's sign. Some patients have constrictions on the arteries, giving them the appearance of rosary beads. Moderate swelling of the peripapillary retina	Hypertensive angiopathy
Hypertensive retinal angiosclerosis	II-III stages of hypertension	Narrowing of the arteries and dilatation of the retinal veins, uneven caliber of the arteries. Symptom of decussation of the first and second degree (Salus I and II - Fig. 29 and 30). Less commonly, Salus III (Fig. 31). Expansion of the reflex strip on the arteries. In some places the reflex strip is yellow (copper wire symptom), in others it is white (silver wire symptom). Along the arteries in limited areas there are lateral accompanying stripes. Dilatation and tortuosity of veins. Variable: retinal edema, hemorrhages in the form of single dots and streaks. Ophthalmochromoscopy: speckled reflex on the arteries when examined in red-free light. In yellow-green light, the unevenness of the caliber and the side accompanying stripes are better revealed. Yellow light reveals hemorrhages that are indistinguishable in normal light	Age-related retinal angiosclerosis
Retinopathy hypertensive	IV stage of hypertension	Narrowing of the arteries, their straightness. Depletion of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Gwist's symptom, a symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Hemorrhages. Large cotton wool-like lesions, as well as small dystrophic white and yellowish lesions in the area of the macula. Retinal swelling around the disc (Fig. 32)	Diabetic retinopathy, retinovasculitis, hypertensive renal retinopathy
Hypertensive neuroretinopathy	IV stage of hypertension (threat of transition to a malignant form)	Narrowing of the arteries, their straightness. Depletion of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Gwist's symptom. A symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Severe swelling of the optic nerve head and retina in the central region. A large number of hemorrhages and cotton wool lesions. Small spots in the macula area can form a star shape (Fig. 33). Ophthalmochromoscopy: in red-free light, a speckled reflex on the arteries. In red light, early signs of macular dyspigmentation	Hypertensive renal neuroretinopathy
Retinopathy hypertensive renal	Acute nephritis, chronic nephritis, toxicosis of pregnant women	Narrowing of the arteries without signs of sclerosis of the vascular wall. Occasionally, symptoms of first degree decussation. Absence of Gvist's sign. Some patients have constrictions on the arteries, giving them the appearance of rosary beads. Moderate swelling of the peripapillary retina. Cotton wool-shaped lesions and degenerative small lesions. Hemorrhages. Severe retinal edema	Hypertensive retinopathy
Hypertensive renal neuroretinopathy	Hypertensive	Narrowing of the arteries without signs of sclerosis of the vascular wall. Occasionally Salus I. Absence of Gvist's symptom. Some patients have constrictions on the arteries, giving them the appearance of rosary beads. Moderate swelling of the peripapillary retina. Cotton wool-shaped lesions and dystrophic small lesions. Hemorrhages. Severe swelling of the retina and optic nerve (congestive nipple). Sharply narrowed arteries in some places disappear into the edematous tissue. Dry patches form a star shape (Fig. 38). Possible retinal detachment	Hypertensive neuroretinopathy, optic disc congestion
Diabetic retinal angiopathy	Diabetes	Predominant changes in the retinal veins: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms are usually in the macula area. The arteries are little changed (damage to the arteries is observed in sclerotic and hypertensive forms of the disease). Single hemorrhages (Fig. 39). Ophthalmochromoscopy: in red-free light, microaneurysms are revealed that are indistinguishable in ordinary light (Fig. 40 and 41). In yellow light, small and deep-seated hemorrhages become visible. Fluorescein angiography reveals a large number of microaneurysms, indistinguishable by ophthalmoscopy (Fig. 42)	Hypertensive angiopathy
Retinopathy diabetic	Diabetes	Predominant changes in the retinal veins: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms, usually in the area of the corpus luteum. The arteries are little changed (damage to the arteries is observed in sclerotic and hypertensive forms of the disease). Waxy lesions of irregular shape (Fig. 43). Yellowish tint of the fundus. In some cases, the lesions form a figure encircling	Hypertensive retinopathy, senile retinopathy
		retinal dystrophy. Some patients have white, cotton wool-like lesions. Major hemorrhages. Thrombosis of the central retinal vein is possible. Ophthalmochromoscopy: in blue light, changes in the color of the fundus of the eye are better revealed, in red-free light - microaneurysms that are indistinguishable in ordinary light. In yellow light, small and deep-seated hemorrhages are visible. Fluorescein angiography reveals a large number of microaneurysms, indistinguishable by ophthalmoscopy
Diabetic proliferative retinopathy	Diabetes	Predominant changes in the retinal veins: the veins are dilated, tortuous, their caliber is uneven. Microaneurysms are usually in the macula area. The arteries are little changed (damage to the arteries is observed in sclerotic and hypertensive forms of the disease). Waxy lesions of irregular shape. Yellowish tint of the fundus. In some cases, the lesions form the figure of encircling retinal dystrophy. Some patients have white cotton wool-like lesions. Major hemorrhages. Thrombosis of the central retinal vein is possible. Newly formed vessels from single branches, loops to the formation of a “wonderful network” (Fig. 44). Light moorings due to proliferation of connective tissue (Fig. 45). Possible: tractional retinal detachment, hemorrhages into the vitreous body. Ophthalmochromoscopy: in red-free light, microaneurysms are revealed that are indistinguishable in ordinary light. In yellow light, small and deep-seated hemorrhages become visible. In blue light, changes in the color of the fundus are better visible. Fluorescein angiography reveals a large number of microaneurysms, small newly formed vessels that are not visible during normal examination	Hypertensive retinopathy, fibroplasia of other etiologies
Angiosclerosis Retina	Universal angiosclerosis	Narrowing of the arteries, their straightness. Depletion of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Gwist's symptom. A symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. Ophthalmochromoscopy: in red-free light - speckled reflex on the arteries. In red light, early signs of macular dyspigmentation	Hypertensive angiosclerosis of the retina
Retinopathy senile	Aging	Narrowing of the arteries, their straightness. Depletion of the vascular tree. Uneven caliber of arteries and reflex bands. Salus I. Symptom of copper, less often silver wire. In some places accompanying stripes along the arteries. In addition, as a result of dispigmentation, the macula acquires a speckled appearance - the dry form of macular degeneration (Fig. 35) or an effusion appears under the retina in the area of the macula - the wet form of macular degeneration (Kunta-Junius discoid dystrophy; Fig. 36). Small lesions can form a figure of ring retinal dystrophy around the altered macula (Fig. 37). Drusen of the vitreous plate are often found. Ophthalmochromoscopy: in red-free light, signs of the senile form of edematous-fibroplastic macular syndrome (stationary reflexes, edema, cystic degeneration, hole in the macula, fibroplasia) are better visible; in indirect red light, retinal drusen, indistinguishable in normal light, become visible	Hypertensive retinopathy, diabetic retinopathy, macular melanoblastoma, transudative macular degeneration with myopia
Retinopathy traumatic	Combination of blunt skull trauma and general contusion, intense compression of the torso	Whitish swelling of the retina. White cotton wool-like lesions of various sizes and shapes, in places overlapping the altered vessels. A large number of hemorrhages located both in the retina and preretinal. The process regresses slowly	Central vein thrombosis, hypertensive neuroretinopathy
Obstruction of the central retinal artery	Vasomotor dystonia, hypertension, endocarditis	Sharp narrowing of the central artery with normal vein caliber. In some places, the collapsed arteries look like white stripes. In some areas, when the lumen of the vessel is not completely closed, intermittent blood flow is visible. Characteristic is clouding of the retina in the central region in the form of a bright field with a cherry-red spot located corresponding to the central fovea (Fig. 27). Obstruction of only one of the branches is possible	Central exudative chorioretinitis, retinovasculitis
Obstruction of the central retinal vein	Hypertension, diabetes mellitus, arteriosclerosis, thrombophlebitis, obliterating endangiitis	The disc is swollen, hyperemic, its boundaries are veiled or almost indistinguishable. The veins are dilated and tortuous. The arteries are narrowed. The retina is swollen, especially around the disc and in the central region. Cyst-like macular edema is possible. A large number of hemorrhages are characteristic: around the disc they can be located like tongues of Flame (Fig. 24), and throughout the rest of the fundus in the form of smears, spots, streaks, splashes and dots. White cotton wool-like lesions are also observed. If one of the branches of the central vein is obstructed, hemorrhages, swelling and white lesions are located according to the affected area (Fig. 25). Ophthalmochromoscopy: in red-free light, retinal edema, cystic macular degeneration and white lesions are better identified (Fig. 26)	Congestive optic disc, hemorrhagic retinovasculitis
Ischemic papilledema	Hypertension, atherosclerosis, obliterating endarteritis, rheumatic vasculitis, cervical osteochondrosis	Pale swelling of the optic disc, giving it the appearance of a moderately erect, stagnant nipple with a milky white or yellowish color (Fig. 34). The arteries are sharply narrowed. The veins are dilated. There may be hemorrhages that are located both on the disc and around it. Characteristic is the absence of an arc reflex near the disc. In case of acute edema, optic nerve atrophy usually develops after 2-3 weeks.	Optic disc congestion, optic neuritis, pseudocongestive optic disc
Congestive nipple	Brain tumor, other diseases c. n. pp., causing an increase in intracranial pressure (inflammatory diseases of the brain and its membranes, deformation of the skull, etc.), general diseases (hypertension, kidney diseases, blood, etc.), diseases of the orbit and eyes	There are initial, pronounced, pronounced stagnant nipples and stagnant nipples in the atrophy stage. In the initial stage, partial veiling of the boundaries of the optic disc, moderate dilatation of the veins, and retinal edema are visible in places. Around the disc there is an arcuate peripapillary light reflex (Fig. 11). A small protrusion of the disc is better detected by ophthalmochromoscopy and biomicroscopy. With pronounced congestive nipple, the disc is enlarged in size and protrudes into the vitreous body by 2-7 D (0.6-2 mm), its borders are veiled, the veins are dilated and tortuous, the arteries are narrowed. The vessels bend over the edge of the disc and in some places seem to be interrupted in the edematous retinal tissue. Hemorrhages on the disc and adjacent retina are possible (Fig. 12). With a pronounced congestive nipple, the distance of the disc reaches 5-7 D (1.5-2 mm) or more, the diameter of the disc is significantly increased, there are more hemorrhages, the boundaries of the disc are blurred. The retina is swollen, small light spots are visible in it, sometimes forming a star shape in the area of the macula. In the atrophy stage, the disc becomes pale, its swelling decreases, the arteries narrow, there are fewer small branches, and hemorrhages resolve. The light reflex near the disc disappears. Subsequently, optic nerve atrophy develops	Pseudocongestive nipple, optic neuritis, ischemic papilledema, central retinal vein obstruction, neuroretinopathy
Optic atrophy	Diseases of the brain and its membranes, multiple sclerosis, intoxication, hypertension, atherosclerosis, trauma, hereditary diseases	A constant sign is pallor of the optic disc. The vessels are narrowed. The boundaries of the disc can be clear - primary (simple) atrophy (Fig. 17) or veiled - secondary atrophy. With secondary atrophy, changes in the fundus around the disc may be observed (Fig. 18). Ophthalmochromoscopy: in purple light, the white disc turns blue (Fig. 19 and 20)	Pallor of the optic disc in blood diseases, constitutional discoloration of the disc
CHANGES DURING INFLAMMATORY PROCESSES
Tuberculous retinal periphlebitis	Unfinished, intrathoracic tuberculosis	Recurrent, often massive hemorrhages into the vitreous body. After the hemorrhages resolve, light, slightly protruding foci, located, as a rule, on the periphery of the fundus, and fibrous strands become visible. White accompanying stripes are marked along the veins. Couplings on veins. Violation of the normal course and caliber of veins. These changes are better visible in red-free light (Fig. 54)	Periphlebitis of various etiologies
Optic neuritis	Inflammatory diseases of the brain and its membranes, general infections (influenza, malaria, tuberculosis, brucellosis), toxicoallergic diseases, local foci of inflammation (paranasal sinuses, nasopharynx, mouth), inflammation of the membranes of the eye and orbit	The optic disc is hyperemic, its borders are veiled. The arteries are not changed, the veins and capillaries are dilated (Fig. 16). There may be hemorrhages on the disc, or, less commonly, white exudative lesions. Hemorrhages and accumulations of exudate are also observed near the disc on the retina. In more rare cases, there may be significant disc swelling	Congestive nipple, pseudoneuritis, ischemic papilledema
Optic neuritis, retrobulbar	Multiple sclerosis, diseases of the paranasal sinuses and orbit, general infectious diseases (influenza, etc.) and intoxications (tobacco-alcohol, etc.)	Characteristic is the absence of changes in the fundus with reduced central vision and the presence of a central scotoma. When examined in red-free light, the contours of the disc are veiled, its swelling and arc reflex are observed. If the focus of inflammation is located near the eyeball, then the process proceeds according to the type of optic neuritis	Congestive nipple, optic neuritis, ischemic edema, onset of descending atrophy of the optic nerve in tumors of the frontal lobe of the brain
Neuroretinitis syphilitic diffuse	Acquired syphilis (stage II-III)	A rough start. Severe diffuse swelling of the retina and optic nerve. Posterior vitreous opacification. Later, extensive atrophy of the choroid, retina and optic nerve develops. The pigment layer is preserved only in the area of the macula (Fig. 58)	Diffuse chorioretinitis of tuberculosis, toxoplasmosis and other etiologies
Chorioretinitis syphilitic congenital	Congenital syphilis	There are three main types of fundus changes. The first, the most common, is characterized by small pigment lumps alternating with small light pockets. Because of its characteristic appearance, it is called “salt and pepper” retinitis (Fig. 56). Ch. is affected. arr. the periphery of the fundus of the eye, but the lesions can also be located in the central region. The second type is large pigmented atrophic foci or light pink atrophic foci, merging with each other in places (Fig. 57). The lesions are located at the extreme periphery of the fundus. The third type occurs as pigmentary dystrophy of the retina	Congenital dystrophies of the fundus of the eye, retinal pigmentary dystrophy of other etiologies
Chorioretinitis toxoplasmosis congenital	Congenital Toxoplasmosis	Mostly in the central region of the fundus of the eye there are light lesions of various sizes, round or oval in shape, with clear boundaries. Characteristic is the accumulation in the lesions, especially at the edges, of a significant amount of dark pigment. A large central lesion resembling a congenital choroidal coloboma is often encountered (Fig. 55). Optic atrophy, retinal fibroplasia, and accumulation of connective tissue in the vitreous called pseudoglioma may also occur.	Disseminated chorioretinitis of tuberculous and other etiologies, retinoblastoma
Chorioretinitis toxoplasmosis acquired	Acquired Toxoplasmosis	The disease can occur as a central retinitis or chorioretinitis with the formation of prominent foci of a grayish color, surrounded by hemorrhages. A course of exudative neuroretinitis or diffuse chorioretinitis is possible. Primary and secondary lesions of retinal vessels are often observed	Chorioretinitis of tuberculous and other etiologies
Tuberculous disseminated chorioretinitis - metastatic focal lesions of the choroid proper with involvement of the retina	Tuberculosis of all localizations	The lesions, as a rule, are of varying age, located in the posterior part of the fundus of the eye outside the macula. Fresh - yellowish or whitish in color with veiled contours and sometimes bordered by hemorrhage. Old ones are lighter with clear boundaries and accumulations of pigment, often forming a corolla. Small lumps of pigment are visible between the lesions (Fig. 50). Ophthalmochromoscopy: in blue light, old lesions are visible less clearly, new ones are detected better (Fig. 51)	Disseminated chorioretinitis of other etiology (Toxoplasmosis, viral and other infections)
Chorioretinitis tuberculous central	Tuberculosis of all localizations	In the area of the macula there is a relatively large, protruding exudative focus of a yellowish or gray-slate color with perifocal edema of the retina (exudative form). Around the lesion, hemorrhages in the form of spots or a rim are possible - exudative-hemorrhagic form (Fig. 52). Perifocal edema and the double-circuit radiation reflexes caused by it are better visible in red-free light (Fig. 53)	Transudative macular degeneration, central granulomatous process in syphilis, brucellosis, malaria, etc.
Retinochoriovasculitis with perivascular infiltration and hyalinosis of the vessel wall	lupus erythematosus	Uneven caliber of the retinal arteries, in some places their obliteration, microaneurysms, hemorrhages, cotton wool lesions, disc edema. The outcome may be retinal fibrosis. Fibrosis of the choroid. Optic atrophy	Hypertensive retinopathy, diabetic retinopathy
Axial optic atrophy	Multiple sclerosis and other diseases c. n. pp., diseases of the paranasal sinuses, general infections and intoxications	Pallor of the temporal half of the optic nerve head with increased clarity of its temporal border (Fig. 21). Narrowing of the arteries. Ophthalmochromoscopic picture: in purple light, blueness of the temporal half of the disc (Fig. 22), in yellow-green - a symptom of a break in the pattern of nerve fibers (Fig. 23). With fluorescein angiography - a symptom of a striped frame	Pronounced physiological excavation of the optic nerve head
Syphilitic optic nerve atrophy	Tabes dorsalis	The optic disc is pale with a characteristic grayish tint. The boundaries of the disc are clear. The arteries are narrowed only in advanced cases. The process is usually two-way	Simple optic atrophy of another etiology
Retinal periarteritis nodosa	Periarteritis nodosa	There are yellowish-brown nodules on the arteries. Hemorrhages. Swelling of the retina and optic nerve head. Some patients have thrombosis of the retinal arteries. In the presence of hypertensive or renal syndrome, the development of malignant neuroretinopathy and serous retinal detachment is possible	Rheumatic retinovasculitis, hypertensive neuroretinopathy
Retinovasculitis rheumatic	Rheumatism	Along the retinal vessels there are lateral accompanying stripes, in places grayish-colored muffs. In the retina along the vessels there are small grayish spots. When multiple vessels are involved, large white foci of effusion are visible at the optic disc, blocking the vascular bundle (Fig. 49). Possible hemorrhages and swelling of the retina	Retinovasculitis with periarteritis nodosa
CHANGES IN BLOOD DISEASES
Retinopathy due to anemia	Anemia: aplastic, hypochromic, pernicious, secondary	The fundus color is pale pink. The optic disc is discolored. The veins are dilated and tortuous. The color difference between veins and arteries is reduced. Variable changes: in purple light, the optic nerve head and fundus turn blue. When the number of red blood cells decreases below 50% of the norm, there are also hemorrhages in the form of streaks, round spots and flames. Hemorrhages with a white center are characteristic (Fig. 46). White cotton wool-like lesions. Peripapillary retinal edema around the disc is possible. With a more severe course of the process, preretinal hemorrhages and hemorrhages into the vitreous body. Congestive nipples, less often neuritis. Optic nerve atrophy. Possible retinal detachment	Optic nerve atrophy of other etiology, congestive nipple, optic neuritis
Retinopathy in chronic myeloid leukemia	Chronic myeloid leukemia	The color of the fundus is orange or yellow. The veins are dilated. In severe cases of hemorrhage, some of them have a white center. Possible hyperemia of the disc, swelling of it and the peripapillary retina. Sometimes cotton wool-like lesions	Optic neuritis
Retinopathy in acute leukemia	Acute leukemia	Pale background of the fundus. The arteries are discolored. The veins are dilated. Polymorphic hemorrhages. The optic disc is pale, the contours of the disc are veiled. Ophthalmochromoscopy: when examined in purple light, the optic disc is blue-purple. When examined in yellow-green light, a preserved pattern of nerve fibers is visible	Stagnant nipple in the atrophy stage
Retinopathy in chronic lymphocytic leukemia	Chronic lymphocytic leukemia	The disk acquires a yellowish tint, its borders are veiled. The arteries are narrowed. The veins are dilated and tortuous. Numerous hemorrhages. Some patients have pale yellow lesions located along the periphery of the fundus. The lesions may be bordered by hemorrhage (Fig. 48)	Ascending optic atrophy, chorioretinitis
Retinopathy due to polycythemia	Polycythemia	The fundus background is dark red with a bluish tint. The veins are cyanotic, sharply dilated and tortuous (Fig. 47), the arteries are almost the same in color as the veins. As the disease progresses, in addition, minor hemorrhages	Pseudoneuritis
CHANGES IN OTHER DISEASES
Choroid angioma	Encephalotrigeminal neuroangiomatosis (Sturge-Weber disease)	Glaucomatous excavation of the optic disc. Myelin fibers are often visible near the disc. The veins are dilated and tortuous. Possible angioma of the choroid. In some cases, peripapillary flat retinal detachment	Primary glaucoma, choroidal melanoblastoma
Retinal angiomatosis	Retino-cerebellovisceral angiomatosis (Hippel-Lindau disease)	Angiomas in the form of rounded glomeruli of various sizes - from small to large nodes exceeding the diameter of the optic nerve head. Each tangle is approached by a pair (vein, artery) of dilated, tortuous vessels (Fig. 8). Newly formed vessels and focal changes in the retina are observed	Racemotic aneurysms of retinal vessels. Proliferating diabetic retinopathy
Retinal dystrophy	Amaurotic	In the early childhood form, characteristic changes in the central part are found at the bottom of the eye in the form of a grayish-white area with a bright red spot in the center, located corresponding to the central fovea (Fig. 9). In the late childhood form, optic nerve atrophy develops	Retina pigmentary dystrophy, changes in the fundus of the eye in reticuloendothelial sphingomyelosis
Atypical retinal pigment dystrophy	Lawrence-Moon-Biedl syndrome	Accumulations of pigment in the form of small round or banded lesions. In 15% there are accumulations of the type of bone bodies typical of pigmentary dystrophy. In most patients, along with pigment accumulations, whitish small lesions are found	Retinal pigmentary dystrophy
Tumor-like formations of the optic nerve head and retina such as hamartomas	Neurofibromatosis (Recklinghausen's disease)	On the optic nerve head, tumor-like formations are whitish or yellowish in color with a shiny surface (Fig. 6). Small nodules and plaques of yellow or white color are visible on the retina	Changes in the fundus of the eye in tuberous sclerosis
	Tuberous sclerosis of the brain (Bourneville disease)	On the retina, mulberry-like formations may cause hemorrhages (Fig. 7). Similar growths are possible on the optic nerve head. There may be obvious or hidden optic disc drusen	Changes in the fundus of the eye in neurofibromatosis
Pseudoneuritis	High farsightedness, delayed embryonic stage of optic nerve development	The optic disc is hyperemic, its borders are veiled. Pronounced tortuosity of blood vessels (Fig. 10). The caliber of the arteries is not changed, atypical course of the vessels and other anomalies of their development are often observed	Optic neuritis
Pseudocongestive nipple	Drusen of the optic nerve head, constitutional features of the structure of the optic nerve head	The pseudocongestive nipple, caused by obvious drusen, has a tuberous appearance, its edges are scalloped, and the caliber of the vessels is not changed (Fig. 13). With a pseudocongestive nipple caused by hidden drusen (Fig. 14), the correct diagnosis can be made by biomicroscopy or ophthalmochromoscopy: in indirect red light, hidden drusen become visible in the form of round luminous formations (Fig. 15)	Congestive nipple, subtraction cones in myopia, ischemic papilledema

Bibliography Arkhangelsky V. N. Morphological foundations of ophthalmological diagnostics, M., 1960; Berezinskaya D. I. Fundamentals of ophthalmoscopic diagnosis, M., 1960; Vodovozov A. M. Ophthalmochromoscopy, Atlas, M., 1969, bibliogr.; Volkov V.V., Gorban A.I. and Dzhaliashvili O.A. Clinical examination of the eye using instruments, L., 1971; Multi-volume guide to eye diseases, ed. V. N. Arkhangelsky, vol. 1, book. 2, p. 16, M., 1962, bibliogr.; Plitas P. S. Ophthalmoscopic Atlas, M., 1960; Radzikhovsky B.A. Ophthalmoscopic diagnostics (with ophthalmoscopic atlas), Chernovitsy, 1957; Radnot M. Atlas of eye diseases, trans. from Hungarian, vol. 2, Budapest, 1963; Shulpina N. B. Biomicroscopy of the eye, M., 1974, bibliogr.; Der Augenarzt, hrsg. u. K. Velhagen, Bd 1, S. 559, Lpz., 1969, Bibliogr.; System of ophthalmology, ed. by S. Duke-Elder, v. 5, L., 1970; Trevor-Roper P.D. The eye and its disorders, Oxford, 1974.

N. K. Ivanov; compiler of the table A. M. Vodovozov.

Normal retina

The color of the retina depends on the blood circulating in the choroid (Fig. 2-1, 2-2). The normal retina is red in color under ophthalmoscopy, but pigment epithelium is located between the choriocapillaris layer and the retina. Depending on the density of the pigment epithelium, the color of the retina can vary from dark red in brunettes, lighter in blonds, to brown in Mongoloid people and dark brown in Negroid people.

With a decrease in the amount of pigment in the pigment epithelium, a pattern of the choroid may be visible in the form of relatively wide stripes - a projection of the choroidal vessels; there may be dark areas between them (the general picture is in the form of the so-called parquet fundus).

Optic disc

The optic disc is the intraocular part of the optic nerve; its length is 1 mm, diameter is from 1.5 to 2 mm. Normally, the optic disc is located 15° medially and 3° superior to the posterior pole of the eye.

The appearance of the optic disc depends on the size of the scleral canal and the angle at which the canal is located in relation to the eye. The size of the physiological excavation depends on the width of the scleral canal.

If the optic nerve enters the sclera at an acute angle, the retinal pigment epithelium ends in front of the edge of the canal, forming a semiring of the choroid and sclera. If the angle exceeds 90°, then one edge of the disk appears steep and the opposite edge appears flat.

With ophthalmoscopy, the optic disc appears as a pink, almost circular spot on the red background of the fundus. Its temporal half is normally always paler than the nasal half. The color of the disc is determined by the number of capillaries feeding it. A more intense color of the optic disc is observed in children and young people

people, it fades with age. The color of the optic disc is also paler in people with myopic refraction. If the choroid is distant from the edge of the optic disc, it is surrounded by a scleral semiring. Sometimes the edge of the disc has a black border due to the accumulation of melanin. The basis of the optic disc is made up of nerve fibers, the posterior surface is represented by the cribriform plate. The central retinal artery and vein pass through the center of the optic nerve head.

Retinal vessels

The main branches of the central arteries and veins pass from the optic disc to the periphery superficially, at the level of the nerve fiber layer. Here, the retinal vessels divide dichotomously up to the precapillaries, forming arterioles of the 1st and 2nd order. According to a number of authors, the proximal segment of arterioles and venules of the 1st order has a diameter, respectively, of about 100 and 150 µm, the middle segment of vessels (arterioles and venules of the 2nd order) - about 40-50 µm, the smallest visible vessels (arterioles and venules of the 3rd order) - about 20 µm.

From the inferior and superior temporal vascular arcades, thin vascular branches pass to the macular region, where they end in the capillary plexus. This capillary plexus forms arcades around the foveola. An avascular foveal area with a diameter of about 0.3-0.4 mm is visible, supplied with blood from the choriocapillaris layer.

Macula

The most important area of the retina is the macular region, or macula, the central part of which is called the fovea (diameter 1.85 microns). In the center of the fovea there is a small darkish depression - the foveola (diameter 0.3 µm). The macula (diameter 2.85 µm) and foveola are normally surrounded by light reflexes, which are more pronounced in children and young people.

Optic nerve is a segment of a peripheral neuron of the visual pathway that begins in the fundus and ends in the middle cranial fossa.

It is formed by the axial cylinders of retinal ganglion cells and contains about 1,000,000 nerve fibers. The optic nerve leaves the orbit through the optic foramen and then both optic nerves converge to the sella turcica.

Topographically divided into four sections:

1. Intraocular.

2. Retrobulbar, or orbital.

3. Intratubular.

4. Intracranial (intracranial) section (up to the chiasm).

total length the optic nerve varies between 35-55 mm depending on the structure of the skull.

Intraocular section The optic nerve consists of the optic disc itself and its scleral part, localized in the canal. The canal is a junction of Foramen opticum chorioideae and Foramen opticum sclerae. Its length in this area is approximately 0.5 mm. In relation to the sclera, the direction of the walls of the scleral canal can be vertical or oblique. If it is oblique, then the retina and choroid end before reaching the edge of the canal, which is automatically perceived as the presence of a cone at the disc.

Channel shape influences the size of physiological excavation. It is greater with large scleral canals. The depth of physiological excavation is within 1 mm. Its bottom is often a cribriform plate. Most often, physiological excavation is observed with emmetropia (73-86%), less often with hypermetropia (22-34%) and rarely with myopia (5%).

The optic disc is the intraocular part of the optic nerve at the junction of the optical fibers of the retina in the canal formed by the fibrous membrane of the eyeball. The diameter of the disc is about 1.5-2 mm across, located 2.5-3 mm nasally from the posterior pole of the eye and 0.5-1 mm inferior to it.

Disk has the shape of a fairly regular circle, and with astigmatism it appears elongated in the form of an oval.

Disc color- pale pink. The temporal half of the disc is paler than the nasal half, since fewer nerve fibers and vessels are directed towards the macula than to the nasal half.

Disk Boundaries Normally, they are clearly defined, the temporal half stands out more clearly than the inner half, since a thinner layer of nerve fibers goes towards the macular zone than to the nasal one (papillo-macular fascicle).

Vessels come out in the center of the disk or slightly inward from the center. With congenital cones and colobomas of the optic nerve, the exit site of the vessels sharply shifts towards the defect.

The arteries are narrower, light red in color, the veins are darker, thicker and more tortuous. Each artery and vein begins in the center of the optic disc with one trunk, then splits into two main branches running up and down. Often the upper and lower branches of the vessel appear separately on the disc.

In the center of the optic nerve head there is a dull white depression of varying sizes - a physiological excavation. Sometimes physiological excavation occupies a large part of the disc, spreading mainly to the outer half of it. The vessels “excavate” not at the border of the disc, but on its surface.

Orbital or retrobulbar the section of the optic nerve is a small segment from the place where it exits the eyeball to the entrance to the optic canal, equal to 25-35 mm. Here, the diameter of the disc is 4.0-4.5 mm due to the appearance of 3 membranes - hard, arachnoid and soft, which form a continuation of the membranes of the brain.

Intratubular part The optic nerve is enclosed in a bone canal located in the lesser wing of the main bone, here the optic nerve passes along with the ophthalmic artery. The bony canal is located among the cells of the ethmoid and main nasal sinuses. Its length is 4-6 mm, diameter 4-8 mm.

Intracranial part The optic nerve begins at the cranial opening of the optic canal and ends at the chiasm. The length of this section varies between 3-16 mm (average 10 mm). This part of the optic nerve borders above the frontal lobe of the brain, and its lateral surface is adjacent to the internal carotid artery.

The space between the arachnoid and pia mater of the optic nerve is a continuation of the intervaginal space of the brain and is filled with cerebrospinal fluid.

In the intracranial part, the optic nerve loses the dura mater and arachnoid mater and remains covered only by the pia mater.

Numerous connective tissue partitions - septa, with blood vessels embedded in them, dividing the optic nerve into separate bundles extend from the pia mater into the trunk. These septa are composed of collagen, elastic tissue and glia.

Glia plays the role of connective, supporting tissue of the central nervous system. It consists of process cells, which are smaller than nerve cells, almost devoid of protoplasm and have the shape of round nuclei.

The thinnest processes are densely attached - these are astrocytic glia. In addition to support, glia replace areas of dead differentiated tissue. Glia, entwining a ganglion cell devoid of a myelin sheath in the form of a coupling, plays the role of an insulator.

There are also oligodendroglia and microglia. These cells with long branching processes are capable of movement and phagocytosis. They play a role in clearing tissues of decay products (in other tissues this is done by histiocytes).

Optic nerve fibers are divided into groups: visual afferent, pupillary afferent, afferent of unknown function. The largest number of visual fibers end in the primary visual centers - the external geniculate bodies.

Pupillary fibers in the region of the posterior third they branch from it and go to the pupillary nuclei of the oculomotor nerve.

Cores oculomotor nerve located at the bottom of the Sylvian aqueduct at the level of the anterior tubercles of the quadrigeminal.

The nuclei consist of two outer large cell nuclei, two small cell nuclei (Yakubovich's nucleus) and one internal unpaired small cell nucleus (Perlea's nucleus).

From the magnocellular nucleus fibers go to the five external oculomotor muscles.

From the paired small cell nucleus, the fibers go to the smooth internal muscles of the sphincter of the pupil and to the accommodative muscle (m. ciliaris). They are interrupted in the ganglion ciliare, while the act of convergence is associated with the unpaired small cell nucleus.

The visual fibers on the disk are located as follows: the main number of fibers going to the periphery of the retina are located on the periphery, and those coming from the central section are in the central section of the nerve. The papillomacular bundle, coming from the macular region, is located in the lower outer part of the temporal sector of the disc.

The papillomacular bundle maintains a peripheral position throughout the anterior segment of the orbital part of the optic nerve, and the retinal vessels occupy a central position in the nerve trunk.

In the posterior part of the orbital region, the papillomacular bundle moves to the center and runs along its axis. It occupies the same central position before the chiasmus and in the chiasmus itself.

In the chiasm, partial crossover of the fibers of the papillomacular bundle occurs. Non-crossing fibers are located in the center throughout.

Chiasma, covered with soft and arachnoid membranes, is located on the diaphragm (duplicate dura mater) of the sella turcica and measures from 4-10 mm in length, 9-11 mm in width, and 5 mm in thickness.

The bottom of the third ventricle runs above the chiasm, the pituitary gland below the diaphragm, and the cavernous sinus on the sides. Adjacent to it is a funnel (inphundibula), which goes to the pituitary gland. On both sides of the chiasma there are branches of the internal carotid artery, which take part in the formation of the circle of Willis circulation.

The chiasmata begin from the posterior surface optic tracts and they end in the external geniculate bodies and at the cushion of the visual tuberosities. The fibers of the papillomacular bundle occupy most of the external geniculate body, the peripheral fibers occupy a smaller part. The total length of the optic tracts is approximately 4-5 cm.

The outer geniculate body consists of 6 layers: 1, 4, 6, counting from bottom to top, end with intersecting fibers, 2, 3, 5 - non-intersecting ones. From the chiasm, the optic tracts go upward.

From the ganglion cells of the 1st and 6th layers of the external geniculate body, the optic bundle, or Graziole's bundle (the central neuron of the visual pathway) originates. It passes through the lenticular part of the posterior femur of the internal capsule and is located along the posterior horn of the lateral ventricle towards the inner surface of the occipital cortex, where it ends in the upper and lower lips of the calcarine groove.

The upper homonymous quadrants of the retinas are projected in the upper part of the Graziole bundle, and the lower homonymous quadrants are projected in the lower part.

The papillomacular section is projected in the middle parts of the stratum sagittale externum.

In the visual cortical area, the upper lip of the calcarine sulcus in each hemisphere corresponds to the upper homolateral quadrants of the retinas, and the lower lip corresponds to the lower ones.

The foveal region of the retina is represented in the most posterior parts of the calcarine sulcus.

In the most anterior sections, the extreme peripheral sections of the nasal half of the retina of the opposite side are projected (the so-called temporal crescents of the visual field). In the middle sections are the middle homolateral sections of both retinas.

The visual area in the cerebral cortex contains the 17th, 18th and 19th Brodmann areas. In the 17th field, the perception of light and color, shape and localization is carried out, in the 18th field - the act of convergence and accommodation and combined eye movement, in the 19th field - opticognostic object, spatial perceptions.

Blood supply to the optic nerve mainly carried out by the branches of the ophthalmic artery.

IN blood supply to the chiasm The internal carotid arteries, anterior cerebral, posterior communicating, anterior choroidal and unpaired communicating arteries take part, and are supplied with blood from the arteria cerebri posterior system, the posterior part of the bundle and also the branches of the posterior cerebral artery. The optic tract is fed by the anterior choroidal artery and its branch arteria communicans posterior. The external geniculate body and the beginning of the Graziole bundle are from the arteria cerebri media. The visual centers in the brain are fed from the arteria cerebri posterior - ramus posterior inferior or arteria calcarina system.

Optic nerve hypoplasia- reduction in disk diameter. The anomaly is associated with a decrease in the number of axons of the affected nerve with normal development of supporting tissue. Hypoplasia can be either unilateral or bilateral.

Visual acuity varies from 1.0 to “no light perception.” In the visual field, changes can be in the form of local central and/or peripheral loss. On examination, the macula appears flat, the foveal reflex is absent or weakly expressed. The retinal vessels have a corkscrew appearance, the caliber is not changed.

Disc damage can be isolated, but more often in combination with ametropia, microphthalmos, congenital cataracts and primary persistent hyperplastic vitreous.

Neurological symptoms are observed in every fifth patient with optic nerve hypoplasia. 23-43% of children have endocrine disorders: growth hormone deficiency, less commonly hypothyroidism, diabetes insipidus.

Optic nerve hypoplasia is detected in patients with Warburg syndrome, in 30-57% of patients with Eickard syndrome, which is characterized by underdevelopment of the corpus callosum, muscle spasms or myoclonic convulsions, and the presence of lacunar chorioretinal foci.

The most informative test for assessing visual functions in children with this pathology is the registration of visual evoked potentials (VEPs).

When the disc diameter is from 0.1 to 0.25 of the normal disc radius, VEP, as a rule, are not recorded and visual acuity in such children ranges from 0 to light perception with the correct projection. If the disc diameter is 0.3-0.5 of the normal disc radius, VEP is recorded and vision in such patients is from 0.005 to 0.04. When the disc size exceeds 0.6 to normal, VEP is recorded, and vision in such patients is 0.03 to 1.0.

X-rays often show a decrease in the optic canals, but it is better to perform CT and MRI or neurosonography.

Differential diagnosis of hypoplasia and atrophy of the optic nerve with bilateral lesions is difficult: with hypoplasia of the optic nerve, the disc may have a white or gray color, but it is always reduced in size; with aplasia of the disc, the central vessels of the retina are always identified, having a normal caliber and a corkscrew-like course (Shamshinova A. M., 2002).

An MRI must be performed to rule out neonatal hypothyroidism.

In children with hypoplasia and neonatal jaundice or hypoglycemia, as well as symptoms of posterior pituitary ectopia detected on MRI, hormonal insufficiency of the anterior pituitary gland is possible. A thorough endocrinological examination is required.

Treatment

Carrying out measures to prevent the development of amblyopia (refractive, dysbinocular) and its treatment. As early as possible, begin spectacle or contact correction of ametropia, carry out dosed occlusion of the better-seeing eye, laser pleoptics and transcutaneous stimulation of the optic nerve of the affected eye. In some cases, surgical treatment of strabismus is performed. Simultaneously correction of neurosomatic and neuroendocrine disorders.

Optic aplasia

A rare congenital anomaly in which both retinal ganglion cells and their axons and the central retinal vessels are absent in the affected eye.

There is a frequent combination of damage to the optic nerve with damage to the central nervous system (anencephaly, hydroencephaly).

The most constant and fundamental sign is the absence of the central vessels of the retina.

Disc changes are varied:

1. The optic disc, central vessels and macular differentiation are absent.

2. A rudimentary white optic disc is visualized, devoid of central retinal vessels, macular reflexes are not detected.

3. With ophthalmoscopy, at the site of the optic nerve head, a deep cavity is determined, surrounded by a light ring resembling a peripapillary scleral cone. The central vessels of the retina and the direct reaction of the pupil to light are absent.

Optic nerve aplasia can be unilateral or bilateral and combined with other developmental anomalies (cornea, UPC, cataracts, iris, ciliary body, choroid and retina, vitreous), with microphthalmia, ptosis, orbital underdevelopment and congenital defects of the central nervous system. Microphthalmos is observed in almost all patients with optic aplasia.

EPI and ERG are not changed, only in some cases a subnormal ERG is recorded. When recording VEP, there are no bioelectrical responses. Ultrasound and CT of the orbits sometimes reveal a rudimentary optic nerve, hydroencephalia, anencephaly, and orbital meningoencephalocele.

Differentiate from hypoplasia. With hypoplasia, the optic disc is practically invisible during ophthalmoscopy; tortuous central retinal vessels with normal caliber are always visible.

Abnormalities of optic nerve excavation

Convolvulus syndrome.Congenital funnel-shaped excavation of the posterior pole with involvement of the optic nerve head. The disease is most often unilateral and occurs in women 2 times more often than in men. In 60% of cases of unilateral pathology, the right eye is affected.

With ophthalmoscopy, the disc looks pink or orange, significantly enlarged and is located, as it were, in a funnel-shaped depression, and the surrounding area has uniformly protruding edges.

In the center of the funnel, a “bouquet” of white glial tissue is visible. The macula may be displaced and then located on the wall of the recess. Disc vessels appear in reduced numbers closer to the edges of the funnel. Arterioles are often difficult to distinguish from venules. Almost all patients with unilateral pathology have strabismus, high myopia, often with astigmatism in the affected eye.

When biomicroscopy with a three-mirror lens is found, the majority show areas of local retinal detachment, even if reverse ophthalmoscopy does not reveal serous retinal detachment. Quite often, bindweed syndrome is combined with basal encephalocele in children and anomalies of the facial skeleton (cleft lip and hard palate). There may be kidney and other abnormalities. Visual acuity ranges from correct light projection to 0.05, cases of 0.8-1.0 have been described.

The field of view reveals central or centrocecal defects. Color vision is unchanged in most patients. The ERG remains normal. With VEP, most patients experience a decrease in amplitude and lengthening of the P component.

On CT scan, at the site of contact of the optic nerve with the sclera, a funnel-shaped expansion of the distal part of the optic nerve is detected.

Treatment

Spectacle or contact correction of ametropia. If anisometropia is high, photorefractive keratectomy, keratomileusis, or keratotomy are possible.

In children - occlusion and pleoptics. If necessary, surgical correction of strabismus. For retinal detachment - surgical treatment. For surgical treatment, a new operation has been proposed - transconjunctival fenestration of the optic nerve sheaths.

Coloboma of the optic nerve

A congenital non-progressive anomaly, which looks like a depression of various sizes in the optic disc area, filled with retinal cells.

Coloboma can form at any point along the palpebral fissure and manifests itself on the side of the iris, choroid, retina and optic nerve as a result of incomplete or abnormal alignment of the proximal ends of the embryonic fissure, which normally closes at 4-5 weeks of gestation. Etiology: cases of autosomal dominant inheritance are known, sometimes as a result of intrauterine infection with cytomegalovirus infection. The disease can be both unilateral and bilateral. With ophthalmoscopy: on the optic nerve disc, slightly enlarged in diameter, there is a spherical depression with clearly defined boundaries, silver-white in color, several times larger than the size of the disc. Almost all patients have high myopia and myopic astigmatism, as well as strabismus. A B-scan or CT scan reveals a deep defect in the posterior pole of the eye, and MRI often reveals epilateral hypoplasia of the intracranial part of the optic nerve. Optic nerve coloboma is often associated with posterior lenticonus, posterior embryotoxon, optic disc fossa, epidermal nevus syndrome, hyaloid artery remnants, and choroidal colobomas. Rhegmatogenous retinal detachment sometimes develops (usually after age 20).

In patients with a pitted optic disc, as a result of macular edema, a macular hole appears, followed by separation of the inner and outer layers of the retina and macular detachment. EPI and ERG are usually not changed.

In children, coloboma is often combined with epidermal nevus syndrome, focal Goltz skin hypoplasia, oculoauriculovertebral dysplasia (Goldenhaar syndrome), Down, Edwards, and Warburg syndromes.

Treatment

In case of formation of a subretinal neovascular membrane, laser coagulation is indicated. For macular detachment - surgical treatment: vitrectomy followed by injection of gas into the eye and krypton laser coagulation of the retina, with visual acuity below 0.3.

Congenital peripapillary staphyloma

This is an extremely rarely observed, usually unilateral anomaly, which is characterized by the development of an extensive deep excavation in the posterior pole of the eye, with the optic disc located at its bottom. The etiology is not clear.

On examination, deviation of the affected eye is noted. Ophthalmoscopically, in the region of the posterior pole, a large cup-shaped depression is noted, at the bottom of which there is an almost unchanged optic disc. The vessels have a normal course and caliber.

With a B-scan, the depth of the defect can be determined.

Vision ranges from “light projection” to 0.5. Perimetry reveals various defects and expansion of the blind spot. ERG is normal.

Treatment

Spectacle correction, pleoptics, orthoptics.

Optic disc fossa

A congenital anomaly that looks like a limited depression in the optic nerve head.

The pathogenesis is not clear. Histologically, there is a defect of the cribriform plate in the area of the fossa. Some fossae are combined with the subarachnoid space.

Ophthalmologically, the optic disc fossa looks like a round or oval-shaped depression that is white, gray or yellow. Diameter from to RD. The usual location is the temporal half of the disc, but it can also be located in other sectors. Most often the disease is unilateral, but in 15% it can be bilateral. Serous retinal detachment develops in 45-75% of eyes with a congenital optic disc pit.

Macular retinoschisis and detachment caused by the optic disc fossa usually develop at the age of 20-40 years. The risk of developing macular complications is higher if the fossa is large and localized in the temporal half of the disc.

The ERG remains normal in most patients.

The majority of VEPs are not changed until macular detachment develops.

Treatment.

Currently, vitrectomy followed by intravitreal tamponade with expanding perfluorocarbon gas and barrier laser coagulation.

Oblique optic disc entry syndrome

This is a congenital pathological condition in which the abnormal disc is a secondary manifestation in relation to ectasia of the inferior nasal region of the posterior pole of the eyeball.

Symptoms: the upper outer part of the disc is slightly protruding, and the lower inner segment is, as it were, shifted back, resulting in the impression of an oval shape of the optic disc with an obliquely oriented long axis.

This disc configuration is combined with the presence of an inferior internal scleral cone. Typically there is complex myopic astigmatism with the positive axis oriented parallel to the ectasia. Visual acuity ranges from 0.05 to 1.0 and depends on the severity of refractive amblyopia.

Color vision is not impaired. ERG and EOG are not changed. VEP is within normal limits.

Differentiate with optic nerve hypoplasia. Unlike hypoplasia, the process is usually bilateral and is always combined with complex myopic astigmatism.

Treatment

Optical correction.

Megalopapilla

A congenital condition in which the optic disc has an unusually large diameter.

The anomaly can be either unilateral or bilateral. Visual acuity is usually normal. In the field of view there is an expansion of the blind spot, but ERG, PERG, EOG, VEP are normal.

Differentiate between megalopapilla and low-pressure glaucoma.

With megalopapilla, the excavation has a round shape or a horizontal oval, and with glaucoma, it has a vertically directed excavation.

The ED ratio is normal, no more than 0.5; with glaucomatous atrophy, this ratio decreases significantly.

With megalopapilla, there are no changes in visual acuity or field of vision (except for the expansion of the blind spot).

Congenital optic disc pigmentation

It is characterized by the deposition of dark pigment on the surface of the unchanged disc. True pigmentation of the optic disc is extremely rare. Ophthalmoscopy reveals slight prominence and unclear boundaries of the disc, which is gray in color. Visual acuity, color perception, visual fields are normal.

No therapeutic measures are required.

Duplication of the optic disc

Associated with congenital splitting of the optic nerve trunk. In most cases, the process is one-way. Ophthalmoscopy reveals two optic discs, each of which has an independent blood supply; both discs can be connected by a common artery and vein.

Often combined with high ametropia, iris coloboma, and congenital cataracts.

Visual acuity varies from 0 to 1.0.

Treatment

Correction of ametropia, occlusion of the better seeing eye and pleoptic eye. With high visual acuity, surgical correction of strabismus is possible.

Pseudoneuritis, or pseudocongestion of the optic nerve

This is a congenital anomaly resembling optic neuritis. On ophthalmoscopy, the disc has unclear boundaries and is slightly protruding. The anomaly is often bilateral.

The most common cause is optic disc drusen. Drusen are hyaline-like material with calcium inclusions.

The anomaly is explained by the structural features of the scleral canal, which leads to the development of axoplasmic stasis and the formation of drusen. But in some cases it is not associated with drusen.

In atypical cases, myelin fibers may be located at the edges of the optic disc, causing prominence, and the boundaries of the disc appear scalloped.

Elevation in hypermetropia is likely due to narrowing of the scleral canal or hyperplasia of glial tissue.

On ophthalmoscopy, the optic disc is pink, slightly protruding, the boundaries seem blurred, and the optic disc often appears hyperemic.

Drusen are often located on the nasal portion of the disc. Sometimes in patients with pseudostagnation, small hemorrhages in the disc tissue are detected, the cause of which is mechanical damage to the walls of small vessels in contact with drusen. CT and B-sonography are used for diagnosis. Visual acuity and visual field are usually unchanged. But in some cases, especially with pseudocongestion caused by drusen, visual acuity may be reduced, and in the visual fields there may be an expansion of the blind spot, central or centrocecal scotomas. They can progress at any age, this leads to diagnostic errors. It is sometimes difficult to differentiate between pseudocongestion and stagnant disc. ERG and VEP are normal.

Differential diagnosis. In patients with optic neuritis, visual acuity sharply decreases over several hours or days; a prodromal period is characteristic, during which low-grade fever, headache, and ARVI symptoms are noted. With pseudoneuritis, there is no hyperemia of the optic disc and no exudation into the vitreous body.

VVP changes with optic neuritis; with FA with a congestive disc, vasodilation and pronounced extravasal hyperfluorescence are determined. Sometimes you even have to examine other family members. In doubtful cases, CT and MRI can be used.

No treatment required. Monitoring of patients is necessary to exclude diagnostic errors.

Optic nerve development abnormalities

Pseudoneuritis- a congenital anomaly resembling optic neuritis or congestive disk.

Ophthalmoscopy reveals blurred disc contours and lack of physiological excavation. With pseudoneuritis, developmental anomalies are often observed on the part of the vessels (a large number of vessels with unusual branching and pronounced tortuosity are visible on the disc; they pass from the disc to the retina in all directions).

In most cases, pseudoneuritis is bilateral, often observed with high hypermetropia, but can occur with any refraction of the eye.

A characteristic feature of pseudoneuritis is a good state of visual functions (visual acuity and visual field, although visual acuity may be reduced) and the absence of dynamics in the ophthalmoscopic picture. ERG and VEP are normal.

Myelinated fibers of the optic disc and retina

All axons soon after leaving the cell body are covered with a white myelin (fat-like) sheath. It prevents the dissipation of the impulse traveling along the fiber to adjacent axial cylinders.

Myelination of the nerve fibers of the optic nerve breaks off at the cribriform plate and does not extend to the disc. Sometimes myelinated fibers extend into the nerve fibers of the disc and the retina adjacent to the disc in approximately 0.3% of people.

Depending on the number of myelin fibers, the retinal vessels either pass over them, or in places, or are completely covered by them. They are observed in all types of refraction and, as a rule, do not affect the functions of the eye.

They can be combined with other developmental anomalies - microphthalmos, choroidal coloboma.

Disc and retinal drusen- these are small single or multiple formations of gray-white or bluish color, protruding above the level of the normal disc. The size of drusen is from 1 to 3 diameters of the central vein. They are located along the edge of the disk, so the disk appears uneven. Gradually, the number of drusen may increase and resemble clusters. Physiological excavation disappears, the disc takes a convex shape. The distance into the vitreous body is 2.0-10.0 diopters.

Drusen may be associated with pigmentary degeneration, Stargardt macular degeneration, retinal angioid streaks, glaucoma, retinal vascular occlusion, optic edema, or optic atrophy. Vision may decrease.

Usually there are headaches in the forehead and diffuse neurological symptoms. Some believe that this disease is an erased form of Bourneville tuberous sclerosis.

Inflammatory diseases of the optic nerve

Currently, inflammatory diseases of the optic nerve are divided into optic neuritis and retrobulbar neuritis.

Neuritis- inflammatory process of the optic nerve trunk and sheaths. Characterized by pronounced changes in the optic nerve head.

Retrobulbar neuritis- inflammation of the optic nerve behind the eyeball.

Inflammatory diseases of the optic nerve are divided into descending and ascending neuritis. All descending ones belong to the retrobulbar group.

Diagnosis of bilateral descending neuritis with bilateral disc edema is sometimes very difficult. Fluorescein angiography and complex EPI do not provide clear differential criteria for the diagnosis of neuritis and congestive discs, accompanied by a rapid decline in visual function.

Etiological factors inflammation of the optic nerve is varied.

The disease can be caused by either acute or any chronic infection. Inflammatory diseases of the brain and its membranes are especially common (cerebrospinal meningitis, serous meningitis, meningitis due to syphilis and tuberculosis, encephalitis - viral, bacterial, rickettsia, protozoal), influenza, typhus, erysipelas, syphilis, tuberculosis, brucellosis, smallpox, local foci of inflammation (diseases of the paranasal sinuses, diseases of the teeth, tonsils).

Retrobulbar infections, poisons from snake and insect bites can also cause neuritis.

Diseases of the internal organs that lead to diseases of the optic nerve include kidney disease, diabetes, gout, blood diseases, collagen diseases, allergic conditions, diseases associated with malnutrition, vitamin deficiency (beriberi, scurvy).

Many intoxications can cause inflammation of the optic nerve, in particular tobacco and alcohol intoxication (10%), lead and methyl alcohol intoxication.

The etiological factor may be diseases of the eyeball and orbit, as well as trauma and pregnancy pathology.

A large percentage of cases of the disease remain of unknown etiology.

Neuritis should be treated by neurologists, and optic neuritis should be treated by ophthalmologists.

Patients' complaints with neuritis: decreased vision, constant or periodic appearance of spots, flickering before the eyes, there may be aching pain behind the eye, in the eyebrow area, headache.

Allergic poison can cause allergic conditions in the body, as well as exacerbation of other allergic diseases, including rheumatism. One patient had neurorheumatism (chorea minor) and a bee sting caused toxic-allergic neuritis.

Pathology of the optic nerve in relation to the total number of eye diseases is 1-3%. But this figure has been reduced, since some patients, bypassing eye institutions, end up in neurological and neurosurgical hospitals.

Optic nerve atrophy in diseases of the optic nerve occurs in 40-60% of cases.

Pathology of the optic nerve as a cause of blindness is 6.6-15.2% (disability).

Practically blindness due to damage to the optic nerve is 21%.

The main manifestations of diseases of the visual pathway are changes in the fundus, decreased visual acuity and changes in the visual field. But these changes are not equivalent.

Visual field testing is of fundamental importance for making a diagnosis in diseases of the visual pathways. In the field of view there may be central scotomas, various types of narrowing of peripheral vision, hemianopic loss of visual fields.

The most careful, pedantic examination of the visual field from the periphery to the center, along a larger number of meridians, as well as repeated studies of the visual field are required. The boundaries of the visual field are examined for white and colors.

Of the known objects for diseases of the visual pathways, only a red mark of 5 mm should be used. On the Forster perimeter, the norm is: 35-40° in the temporal half of the visual field and 25-30° in other directions.

Minor changes in the visual field may not be detected with more intense stimuli, but are easily noted with weaker ones. Therefore, in diseases of the visual pathways, a divergence of boundaries between the white marks of 5 mm and 2 mm is often observed.

Therefore, perimetry in patients with diseases of the visual pathways should be carried out with white marks of 5 mm and 2 mm and a red mark of 5 mm.

A 2 mm mark can identify scotomas. However, perimetry is not always able to detect small central scotomas.

The main method for diagnosis is automatic perimetry.

To identify and differentially diagnose demyelinating processes, VEP are examined in the visual analyzer.

For early diagnosis of space-occupying formations, demyelinating processes of the brain, traumatic damage to the bone structures of the orbit and optic nerve, CT, MRI, and angiography are important.

An important method in the complex diagnosis of drusen and optic nerve congestion is video ophthalmography.

Threshold spatial contrast sensitivity (TSCS) is used to monitor treatment.

Neuritis (papillitis)

Neuritis (papillitis) called inflammation of the optic nerve, involving its intraocular part.

The inflammatory process can affect the peripheral or central fibers of the optic nerve, which is manifested by a variety of visual impairments.

It usually begins with decreased vision, which can decrease within a few hours, less often within a few days.

The loss of vision, which the patient subjectively feels, is accompanied by minor headaches and pain when moving the eyes. But these symptoms may not exist. Simultaneously with the loss of vision, and sometimes preceding it, ischemia of the optic disc and its edema appear. Its borders become blurred, veins and arteries are slightly expanded. There is a narrowing of the field of view, and if the papillomacular bundle is damaged, central scotomas occur. In the field of view there may also be wedge-shaped loss in the area of the blind spot, arch-like and quadrant, nasal and binasal.

As the process increases, hyperemia and swelling of the optic nerve increase with its protrusion into the vitreous body. The degree of retention can be from 2.0 diopters to 5.0-6.0 diopters. Hemorrhages may appear around the disc - point and linear.

The vessels are sharply dilated and tortuous; often, due to exudation of exudate from the vessels of the disc, clouding of the vitreous body is observed. Prepapillary vitreous opacities and the Tyndall phenomenon are clearly visible under microscopy in papillitis associated with uveitis.

Previously, when relapsing fever was common, papillitis due to uveitis was quite common. Complete restoration of vision was observed only after 6-8 months, and sometimes vision was restored only to 0.02-0.05.

With injuries to the anterior part of the eye, inflammation often occurs, involving the optic nerve.

Damage to the optic nerve occurs with uveo-meningoencephalitic syndromes - Harada disease (uveitis with spontaneous retinal detachment, meningo-encephalitis, hearing loss, hair loss, graying of hair), Vogt - Kayanagi (baldness, patchy depigmentation of skin and hair, uveitis, deafness), with syphilitic ophthalmia, Behçet, Heerfordt and Besnier-Beck-Schaumann syndrome.

Behçet's syndrome is known as ophthalmo-stomatogenital syndrome, Heerfordt's syndrome is known as subchronic uveoparotitis, and Beck-Schaumann disease is known as sarcoidosis syndrome. Heerfordt syndrome is now also classified as sarcoidosis.

The inflammatory process of the optic nerve head also spreads to its trunk, turning into retrobulbar neuritis with changes in the fundus.

There are also unspecified latent forms of uveo-meningoencephalitis, which are combined with damage to the intracranial part of the optic nerve and the optic disc. These are neuropapillitis, which can be diagnosed by examining cerebrospinal fluid, EEG, studying the vestibular system, taking an audiogram, and also by surgical intervention.

Neuropapillitis can occur in isolation or together with neurological symptoms - headaches, pain when moving the eyes, vomiting, redness of the neck, indicating the involvement of the meningeal membranes in the process, oculomotor paralysis, indicating the presence of encephalitis.

During surgical interventions, another form of vague uveo-meningitis was identified, called primary edema of the optic nerve, its intracranial and intracanalicular sections. The swelling puts pressure on the optic nerve, causing rapid loss of vision. Emergency opening of the canal leads to rapid restoration of vision.

The etiology of infectious primary papillitis is most often viral.

Often it is necessary to differentiate with congestive disc, pseudoneuritis, ischemic conditions of the optic disc, if there is severe swelling.

With congestive disc and pseudoneuritis, with pronounced changes in the optic disc, visual functions are preserved. Only with a complicated stagnant disc are visual functions impaired immediately, but at the same time the field of vision changes according to the hemianoptic type, which is not typical for neuritis.

With pseudoneuritis there is no dilation of the veins, hemorrhages, and there is no dynamics of the process.

When differentially diagnosing neuritis and vascular optic neuropathy, it is necessary to know the onset of the disease: is it gradual or sudden, whether the patient has had infectious diseases, whether there has been hypothermia, stress, or heavy physical activity. Ophthalmoscopic examination reveals disc hyperemia, vascular dilation or pale disc, narrow vessels, narrowing of the visual field, scotoma or hemianopsia.

Optic nerve vasculitis differs from neuritis by more pronounced swelling of the disc, especially of the retina in the papillary and central zones, often with a “star figure,” as well as the presence of accompanying stripes along the vessels on the disc. Visual acuity is higher with retrobulbar neuritis, accompanied by retinal edema in the macular area. It should be differentiated using ophthalmoscopy from central serous chorioretinopathy, in which “transillumination points” are identified.

The course and prognosis of neuritis are determined by the etiology, severity of the inflammatory process, timely and rational therapy. With proper treatment, vision can be completely or significantly restored.

With infectious viral papillitis, complete atrophy of the optic nerve occurs in 25% of patients, and partial atrophy in 35%.

Patients with optic neuritis need urgent referral to hospital, where they undergo general treatment with broad-spectrum antibiotics with B vitamins, as well as anti-inflammatory, desensitizing, vasodilating and dehydration therapy (hemodesis, reopirin, oral and retrobulbar corticosteroids, intramuscular Lasix, oral suprastin, furosemide, nicotinic acid preparations), blood transfusions, spinal tap, and corticosteroids are also used. When the cause of the disease is identified, etiotropic therapy is added.

Retrobulbar neuritis (RN)

Inflammatory lesion of the area of the optic nerve located behind the eyeball and not extending to the optic nerve head. The causes of ROP can be infectious diseases (viral and bacterial), including diseases of the paranasal sinuses, intoxication, allergies, and injuries. Cases caused by chlamydia, brucella, collagenosis and tuberculosis have been described. A large percentage remains with unknown etiology.

The most common cause of ROP is demyelinating diseases: in 80% of cases it is one of the first signs of multiple sclerosis, first unilateral, rapidly transient, alternating, and then bilateral.

Retrobulbar neuritis can be acute (infectious) or chronic (toxic). Acute retrobulbar neuritis is usually unilateral, chronic - bilateral.

Retrobulbar neuritis has three clinical forms:

1. Inflammation of the optic nerve sheath only—develops secondary.

2. Inflammation of the peripheral fibers of the nerve trunk - interstitial neuritis, in which the inflammatory process usually begins in the soft shell of the optic nerve and passes through the connective tissue septa (septa) to the peripheral layers of the nerve fibers.

3. Inflammation of the papillomacular (axial) bundle of the optic nerve - axial neuritis.

Classic retrobulbar neuritis is characterized by vision loss, usually unilateral, but bilateral ROP occurs in 19-33% of adults and 60% of children, with impaired color vision with rapid color fatigue. In addition, it manifests itself:

Pain behind the eye, aggravated by eye movement, especially when looking up. There may be aching pain when moving the eyeball, pain may occur simultaneously with or precede loss of vision;

Headache in the fronto-parietal or fronto-occipital regions;

Central scotoma (relative or absolute for all colors, including white, as well as peripheral scotomas, narrowing or loss of the visual field, detected by perimetry.

There may be no pathological changes in the fundus or disturbances characteristic of neuritis and congestive disc may occur. This depends on the intensity of the inflammatory process and its location. Sometimes there is swelling of the optic disc (5%) with a hemorrhagic component. In children with ROP, swelling quickly occurs and papillitis often develops. After 2-3 months, the neuritis resolves, visual acuity is restored, and the central scotoma undergoes reverse development. In the fundus, blanching of the temporal half or the entire optic disc develops. A repeated attack of ROP over the next 5 years is observed in 12-36% of patients.

Tron E.Zh. (1968) pointed out that a mandatory sign of retrobulbar neuritis is the presence of a central scotoma, and changes in the fundus can be very diverse. ROP is characterized by dissociation of symptoms: discrepancy between the fundus picture and visual functions. At the onset of the disease, there is a sharp drop in visual acuity; When visual functions are restored, the fundus image deteriorates and discolouration of the optic disc develops. Optical disc pallor occurs later if the lesion is located further from the disc. And sometimes in the early stage one can observe pronounced blanching of the optic disc in combination with good visual functions. The intensity of blanching of the optic disc is explained by the death of the myelin coating, and good vision is due to the preservation of the axial cylinders. Complete atrophy of the optic nerve gradually develops. The term “optic nerve atrophy” should be used when there is a persistent decrease in visual acuity and partial or complete blanching of the optic disc. Most patients are characterized by fluctuations in visual acuity after physical activity (Utgoff's symptom). This symptom can be triggered by taking a hot bath or shower, hot weather, eating hot food and water, increased lighting, etc. Utgoff's symptom is detected in 32.8-49.5% of patients and has prognostic significance. It is associated with a high risk of developing multiple sclerosis (MS). When body temperature decreases, vision may improve. In ROP, as a result of demyelination while dark adaptation persists for a long time, light adaptation and daytime vision are disrupted: a feeling of blindness occurs, even at moderate brightness. When determining visual acuity, the higher the illumination, the more dark spots the patient sees. Sometimes, when moving the eyes or provoking a sound, phosphate-color flashes appear before the eyes - Lhermitte's eye sign.

At the beginning of the disease, pathology may not be visible in the fundus. Therefore, functional research methods are used, such as static and computer perimetry, color campimetry, visocontrastometry, and the study of electrical sensitivity and lability of the optic nerve. Visual evoked potentials have great diagnostic value. All these studies objectify the degree of damage to the optic nerves.

In case of ROP, even in the absence of neurological symptoms, one should first think about multiple sclerosis and perform an MRI of the brain.

Treatment

Dexamethasone 1.0 ml retrobulbar x 1 time per day for 5-10 days. The most effective administration of drugs is through the irrigation system into the retrobulbar space.

Antioxidant drugs must be prescribed: emoxypine, vitamin E.

With a pronounced hemorrhagic component, exudative retinovasculitis, uveitis - dicynon.

Dicynone is used as a retrobulbar injection of 0.5 ml No. 10-15; it can also be administered intramuscularly and orally.

Dicinone is an angioprotector and also has an inhibitory effect on lipid peroxidation products and the activity of the blood kinin system.

It is very good to combine retrobulbar injections of gordox, dicinone and dexamethasone.

For the purpose of desensitization, use chloropyramine (suprastin) 25 mg x 3 times a day, clemastine (tavegil) 1 mg x 2 times a day.

Antihistamines are prescribed: astemizole (Histolong), ketotifen (Denerel) with a change in drug. It is possible to use synacthen depot, ACTH, thymus preparations: T-activin, thymalin, interferon and reoferon inducers. It is advisable to prescribe delargin intramuscularly in a single dose of 1 mg, per course - 30-40 mg. It stimulates tissue regeneration and normalizes microcirculation in the area of inflammation.

To reduce tissue hypoxia, angioprotectors are prescribed: anginin, prodectin, doxium.

B vitamins, ascorbic acid, calcium and potassium supplements are used.

After acute inflammatory phenomena have subsided, drugs that improve trophism, as well as blood circulation in the optic nerve and retina, should be used in the early stages. 4% taufon is used.

Endonasal electrophoresis, phonophoresis, and magnetic therapy are widely used. Cerebrolysin intravenous, intramuscular, retrobulbar No. 10-15. Locally: single dose 0.5 ml.

For optic nerve atrophy, neurotrophic therapy, biostimulants, electrical stimulation of the optic nerve, and magnetic stimulation are indicated. Acupuncture is widely used.

One of the promising methods of immunocorrection is bone marrow cell transplantation. It is believed that newly developing T cells acquire tolerance to self-antigens, including myelin antigens, which leads to blocking of autoimmune reactions.

Multiple sclerosis

Currently, the most common hypothesis is about the multifactorial etiology of the disease, in the origin of which a number of factors are important - viral, endocrine, allergic, geographical. It is assumed that a combination of external factors acts against the background of a genetically determined defective immune system, causing chronic inflammation, autoimmune reactions and demyelination. Depending on the location of the damaged myelin, different brain structures are affected. Thus, proteolipid myelin causes disorders in the spinal cord and brain stem; glycoprotein - in the periventricular zone and in the white matter of the cerebellum. This to some extent determines the clinical manifestations of MS. There is a cerebrospinal form (in 50-70%), which occurs with damage to the optical, pyramidal and cerebellar systems; spinal (23%), cerebellar (19%), optical (6%), pseudotabetic and some other forms. The favorite localization of plaques in MS is the anterior part of the orbital part of the optic nerve (from the cribriform plate to the entry point of the central retinal artery into the optic nerve) and its intracranial part. In the first stages of the disease, only the myelin sheath in the nerve fibers is affected. At the same time, their conductivity does not completely disappear and their function is restored during remyelination. This explains the remissions during the course of the disease, which are very characteristic of multiple sclerosis. Further, when the process moves to the axial cylinders, which are poorly capable of regeneration, persistent damage to the nervous system develops.

Typical symptoms of MS include:

Motor disorders in the form of pyramidal syndrome with weakness and spasticity; ataxia (cerebellar, sensory or vestibular);

Sensory disorders: paroxysmal pain of the type of neuralgia or chronic (dysesthesia in the extremities), impaired deep sensitivity with ataxia or a disorder of two-dimensional spatial sense;

Brainstem symptoms: vestibular dizziness, dysarthria, damage to the III, V, VI, VII cranial nerves, visual disturbances (retrobulbar neuritis);

Autonomic disorders: pelvic disorders - urgency, increased frequency of urination or urinary retention, periodic urinary incontinence, constipation, sexual disorders;

Nonspecific symptoms: general weakness, impaired memory, attention, thinking, increased weakness when exposed to high temperature (bath, weather);

Paroxysmal symptoms: short-term motor and sensory disturbances, attacks of desarthria, ataxia, epileptic seizures, Lhermitte's symptom. Lhermitte's sign is a brief sensation of electric current passing along the spine, often radiating to the arms and legs, provoked by tilting the head forward.

The first clinical manifestations of MS may be symptoms of damage to one or more conduction systems. The most commonly observed symptoms are polysymptomatic onset, retrobulbar neuritis and pyramidal signs. Other early symptoms of MS include oculomotor disorders, coordination problems, facial paresis, mental disorders and pelvic organ dysfunction.

Among the various manifestations of optical disorders, the most common is a sharp decrease in visual acuity to light perception (less often to hundredths) and changes in visual fields due to retrobulbar neuritis. Sometimes there is swelling of the eyelid. Pain when moving the eye and exophthalmos last for several days. The diagnosis of MS, or “optic neuritis,” is established when there is an acute or subacute decrease in visual acuity, more often than one eye, accompanied by pain when moving the eyeballs, lasting at least 24 hours and usually with complete or partial restoration of vision.

Characteristic features of retrobulbar neuritis in multiple sclerosis are:

1) the coincidence of the onset of pallor of the optic nerve head with the onset of restoration of visual functions;

2) remitting course with relapses;

3) tendency to spontaneous healing;

4) discrepancy between the picture of the fundus and the state of visual functions at the end of the attack (high visual acuity and normal field of vision with severe atrophy of the optic disc).

Retrobulbar neuritis in multiple sclerosis can be combined with other ocular symptoms: nystagmus, ptosis of the upper eyelid, paresis of the superior rectus muscle of the eye. Visual acuity may decrease after physical activity or a hot bath. In the evening, vision in such patients is worse than in the morning and after physical activity during the day.

There is often a narrowing of the field of vision to blue. The fundus picture may be different. If there are changes in the optic nerve head (hyperemia, edema), they are mild. Then comes a period of improvement in visual functions. Visual acuity increases gradually or abruptly, and at the same time the central scotoma disappears. From the onset of a decrease in visual acuity to maximum recovery (duration of attack) it usually takes 1-3 months. After an attack on the fundus, simple atrophy of the optic nerve develops, most often in the form of blanching of the temporal half of the optic disc associated with damage to the papillomacular bundle. Rarely, after an attack, the fundus of the eye remains unchanged.

Since pathology may not be visible in the fundus at first, functional research methods are used: static and computer perimetry, color campimetry, visocontrastometry, determination of electrical sensitivity and lability of the optic nerve. Visual evoked potentials have great diagnostic value. All these studies objectify the degree of damage to the optic nerves.

Optical disc pallor occurs later if the lesion is located further from the disc. Sometimes, even at an early stage, pronounced pallor of the optic disc can be observed in combination with good visual functions. The intensity of blanching of the optic disc is explained by the death of the myelin coating, and good vision is due to the preservation of the axial cylinders. Complete atrophy of the optic nerve gradually develops.

There are 4 main variants of the course of MS: relapsing-remitting (at the onset of the disease - in 75-85% of patients); primary progressive (in 10% of patients), secondary progressive (initially remitting course is replaced by progression with or without the development of exacerbations and minimal remissions), progressive course with exacerbations (in 6% of patients). In 20% of cases, it is difficult to determine the type of MS.

According to the Poser scale (1983), reliable MS is determined by the presence of two exacerbations and clinical evidence of two separate lesions (option A) or two exacerbations, clinical detection of one lesion and determination of the other lesion using neuroimaging or EP methods (option B). In this case, 2 exacerbations must affect different areas of the central nervous system, last at least 24 hours, and their appearance must be separated by an interval of at least one month. In addition, the Poser scale determines the criteria for probable (2 exacerbations and clinical signs of two separate foci) and possible (2 exacerbations) MS. The most informative method for diagnosing a multifocal process in the brain is MRI, which provides sufficiently contrast images of the soft tissues of the orbit, optic nerve and visual pathway and shows foci of demyelination in other parts of the brain.

According to the Phazex criteria, it is typical for MS to have at least three areas of increased signal intensity on T2-weighted images, two of which should be in the periventricular space and one infratentorial, and the size of the lesion should be more than 5 mm in diameter. It should be noted that in MS, new lesions in the brain occur more often than clinical exacerbations.

Characteristic of MS is an increase in the content of immunoglobulins (IgG) and the detection of oligoclonal antibodies of the IgG group in the cerebrospinal fluid using the isoelectric focusing method. In 85-95% of patients with significant MS, oligoclonal IgG groups are detected in the cerebrospinal fluid (but not in the plasma). To assess the level of intracerebral IgG production, simultaneous determination of the levels of albumin and IgG in the cerebrospinal fluid and blood is used with the calculation of the IgG index in the Tourtellote formula:

From 65 to 85% of patients with clinically significant MS have an IgG index above 0.7.

The level of IgG production in the brain is directly related to the total area of demyelination foci recorded by MRI.

In 80-90% of MS patients, there is also an increase in the content of Ig light chains (usually λ-type) in the cerebrospinal fluid. However, the origin of IgG and Ig light chains and their functional significance in MS are not clear.

The use of VP and other methods (T-cell markers, etc.) are not specific tests for MS.

Treatment

There is no etiotropic treatment to date. Treatment is carried out jointly with a neurologist. The entire range of modern therapeutic agents for MS is divided into two groups - pathogenetic and symptomatic.

Pathogenetic therapy is aimed at preventing the destruction of optic nerve and brain tissue by activated cells of the immune system and toxic substances, restoring myelin, the pathways of retinal neurons, and improving the trophism of brain tissue.

Here is the treatment regimen proposed by Guseva M.R. (2001). Corticosteroids and ACTH drugs are used for treatment. Glucocorticoids have an anti-inflammatory effect, and by reducing capillary permeability, they cause an anti-edematous effect. They are prescribed in loading doses: days 1-5 - 1000 mg of methylprednisolone, which is administered intravenously. Then prednisolone is prescribed orally: days 6-8 - 80 mg, days 9-11 - 60 mg, days 12-14 - 40 mg, days 15-17 - 20 mg, days 18-20 day - 10 mg.

Methylprednisolone is used. It is administered intravenously in course doses for 3 to 7 days, followed by a course of oral prednisolone. Methylprednisolone is administered intravenously at a dose of 0.5-1 g daily, after a short maintenance course of oral prednisolone, starting with 15-20 mg every other day and decreasing by 5 mg.

Dexamethasone is administered once a day, 1.0 ml retrobulbarly for 5-10 days. The most effective administration of the drug is through the irrigation system into the retrobulbar space. Along with hormonal drugs, gordox (contrical, trasylol), which is an enzyme inhibitor of proteolysis, is administered through the irrigation system. Antioxidant drugs must be prescribed: Essentiale, emoxipine, vitamin E.

ACTH normalizes the permeability of the BBB, has an immunosuppressive effect, suppresses the activity of cellular and humoral immunity (40-100 units intramuscularly for 10-14 days).

Dicinone is used in the form of a retrobulbar injection of 0.5 ml No. 10-15, it can be prescribed intramuscularly and orally in the form of tablets. Dicinone is an angioprotector, has an inhibitory effect on lipid peroxidation products and the activity of the blood kinin system. It is very good to combine retrobulbar injections of gordox, dicinone and dexamethasone. To reduce swelling, dehydration therapy is recommended: Diacarb in courses of 4-5 days at intervals of 2-3 days. You can administer furosemide 0.5-1.0 ml.

Dicaine-adrenaline blockades of the middle nasal passage are used. Turunda is soaked in a solution of 0.5% dicaine and 0.1% adrenaline (1 drop of adrenaline per 1 ml of solution). The duration of the procedure is 15-20 minutes. The course of treatment consists of 5 procedures every other day. Anti-inflammatory non-steroidal drugs include indomethacin and methindole. Antihistamines (pipolfen) are prescribed and the drug is changed after 2 weeks. It is possible to use synacthen - an ACTH depot; thymus preparations are used: T-activin, thymolin and their analogues, interferon inducers and rheoferon.

It is advisable to prescribe delargin intramuscularly in a single dose of 1 mg, for a course of 30-40 mg. It stimulates tissue regeneration and normalizes microcirculation in the area of inflammation. To reduce tissue hypoxia, angioprotectors such as anginin, prodectin, and doxium are prescribed. With a pronounced hemorrhagic component, exudative retinovasculitis, uveitis, dicinone is better. B vitamins, ascorbic acid, calcium and potassium supplements are used. After acute inflammatory phenomena have subsided, drugs that improve trophism, as well as blood circulation in the optic nerve and retina, should be used in the early stages. Taufon, nicotinic acid, and vitamin therapy are prescribed. Electrophonophoresis, magnetic therapy, and endonasal electrophoresis are widely used.

Cerebrolysin intravenously, intramuscularly, retrobulbarly No. 10-15, single dose 0.5 ml. Duginov A.G. (2005) carried out catheterization of the retrobulbar space with the introduction of a catheter into the lower outer or upper outer quadrant. Then, for 7-10 days, retrobulbar infusions of drug solutions were carried out, followed by electrical stimulation and laser stimulation, and an improvement in such indicators as EOG, ERG, and EC was noted.

Immunocorrection with β-interferons is carried out subcutaneously at a dose of 8 million IU every other day. In the first 14 days, half the dose is administered. Due to possible complications, the drug is administered with caution.

For optic nerve atrophy, neurotrophic therapy, biostimulants, electrical stimulation of the optic nerve, magnetic stimulation, and acupuncture are recommended. One of the promising methods of immunocorrection is bone marrow cell transplantation.

It is believed that newly developing T cells acquire tolerance to self-antigens, including myelin antigens, which leads to blocking of autoimmune reactions.

Symptomatic therapy is aimed at maintaining and correcting the functions of the damaged system, compensating for existing disorders. It includes the fight against spasticity (baclofen, mydocalm, sirdalud), pain (NSAIDs), bladder dysfunction (detrusiol - for hyperreflex bladder syndrome, amitriptyline - for urinary urgency, vasopressin - for frequent night urination). For tremor, β-blockers, hexamidine, are prescribed.

Acute disseminated encephalomyelitis

In children, the peripheral nervous system is affected.

In foci of demyelination, gross changes in the axial cylinders are observed until they completely disintegrate.

Demyelination is damage to nervous tissue as a result of autoallergic reactions. It begins with malaise and catarrhal symptoms in the upper respiratory tract, the temperature rises, chills and paresthesia appear in the body. On the 2-7th day from the onset of the disease, focal neurological symptoms develop. In 100% of cases, motor disorders, paresis and paralysis are observed, more often in the legs, less often of a spastic nature, and more often mixed paresis and paralysis (central and peripheral motor neurons).

In many cases, damage occurs to the cranial oculomotor nerves, the bulbar group of nerves with severe dysarthria and dysphagia, in 15-20% of cases there is damage to the optic nerve in the form of retrobulbar neuritis, and less commonly the phenomenon of congestive discs. Sensory disorders in the form of pain and paresthesia are common symptoms.

Patients exhibit meningeal symptoms with inflammatory changes in the cerebrospinal fluid.

The outcome is favorable in 76.4%, but in 16% there are paresis or paralysis of the legs, sensitivity disorders, decreased vision with persistent changes in the fundus. In 6.9% there was death.

The clinical picture of acute and chronic forms of disseminated encephalomyelitis is based on remissions with dissociation syndrome in the optical, motor, sensory, cochleovestibular spheres and cerebrospinal fluid, which is not typical for acute primary encephalitis.

Stagnant disk

It is a non-inflammatory swelling of the optic nerve, in most cases caused by increased intracranial pressure.

The term “stagnant nipple” was proposed by A. Graefe in 1860.

It was initially assumed that the basis of the congestive nipple was edematous impregnation of the optic nerve nipple, caused by obstruction of the venous outflow from the optic nerve. But even with bilateral thrombosis of the cavernous sinus, accompanied by obliteration of most of the orbital veins, congestive nipples may be absent.

These observations find their anatomical explanation in the fact that v. ophthalmica, before its entry into the cavernous sinus through the orbital veins, anastomoses with the powerful v.facialis anterior u plexus ethmoidalis.

Another theory is inflammatory. According to this theory, disc swelling is caused by toxins in the cerebrospinal fluid due to brain diseases.

The neurotropic theory saw the cause of disc swelling in irritation of the vasomotor centers by a pathological process. She has long gone into eternity.

Then there was the Schmidt-Mantz transport theory.

Retention theory is a theory of delay in the centropital tissue flow of the optic nerve due to increased intracranial pressure.

It has now been established that edema and swelling of the brain and optic nerve are a single pathological process.

But since the disc has an abundance of capillary network, weak supporting mesenchymal tissue, and optic fibers are not covered with myelin, disc edema can be more pronounced than edema of the optic nerve trunk.

Why is it that in some cases a stagnant disc is the first symptom of increased intracranial pressure, while in others, with pronounced signs of increased intracranial pressure, it is not? This is explained by the fact that congestive discs arise not simply when intracranial pressure increases, but in the phase of its decompensation, when all adaptation and compensatory mechanisms are exhausted.

However, some pathoanatomical and pathogenetic details regarding the origin of the congestive disc remain controversial.

But there is no doubt that in the pathogenesis of a congestive disc, pathological processes that exist in the optic nerve itself play a less significant role than the intracranial factor.

In the etiology of a stagnant disc, the following are important:

1. Brain tumors.

2. Brain abscesses.

3. Optochiasmal arachnoiditis.

4. Tuberculomas.

5. Cysticercosis.

6. Echinoccocosis.

7. Hemorrhages.

8. Meningitis.

9. Meningo-encephalitis.

10. Syphilis.

11. Diseases of the orbit.

12. Kidney diseases.

13. Hypertension.

14. Traumatic brain injury.

15. Artriovenous aneurysms.

More often, a stagnant disc occurs with brain tumors (70-96%), inflammatory diseases of the brain and its membranes with hypertensive syndrome (21.4%), with traumatic brain injury (10-20%), arteriovenous aneurysms (25%) . The time of appearance and progression of a stagnant disc varies. The speed of development depends on the localization of the process, and not on its size; most often these are tumors. If compression occurs in the area of the basal cisterns, edema develops earlier.

A stagnant disc appears very quickly if the tumor is located near the Sylvian aqueduct.

If the tumor is located close to the cerebrospinal fluid outflow pathways and venous drainage of the brain, then stagnant discs occur early.

Normally, the flow of fluid, the place of formation of which is the plexus chorioideus, from the lateral ventricles through the foramina of Monroy goes into the third ventricle and then through the aqueduct of Sylvius into the fourth ventricle. Next, fluid from the ventricular system through the holes of Luschka and Mozhandi enters the subarachnoid space.

The ophthalmoscopic picture of a congestive disc is extremely diverse and highly dynamic.

During a congestive disc, 5 stages are distinguished: initial, pronounced, pronounced, congestive disc in the stage of atrophy and atrophy after a congestive disc.

At initial phenomena stagnation, the disc is slightly hyperemic, its borders are washed away, and slight swelling is observed along the edge of the disc. The veins are somewhat dilated, but not tortuous. The caliber of the arteries is not changed.

In rare cases, there are single small banded hemorrhages along the edge of the disc and in the surrounding retina. The swelling gradually increases, the veins twist, and the arteries narrow. The edematous disc protrudes into the vitreous body. The distance can be 6.0-7.0 diopters. This - pronounced congestive disc.

At pronounced stagnant disc there is its hyperemia, it is significantly increased in size, the boundaries are washed away, and protrudes into the vitreous body. The veins are dilated and tortuous. Hemorrhages are small and larger along the edge of the disc and in the surrounding retina. Hemorrhages are associated with venous stagnation. White spots of various sizes and shapes (degenerated areas of nerve fibers); white spots can also be observed in the macula. In some cases, they resemble the shape of a star or half-star.

With prolonged existence of a stagnant disc, atrophy phenomena gradually begin to develop. A grayish tint of the disc appears, tissue swelling decreases, veins become less dilated, and hemorrhages resolve. This stagnant disc in the atrophy stage. Gradually, the disc becomes even more pale, the last signs of stagnation disappear, and a typical picture of secondary optic nerve atrophy develops: the disc is pale, its boundaries are washed away, the outline of the disc is not entirely correct, the arteries and veins are narrow.

Then the boundaries become clear and a picture of primary atrophy is observed, i.e. This the last stage during a stagnant disk.

But the stagnant disk does not necessarily go through all stages; sometimes, already at the initial stage, the process undergoes reverse development. In other cases, a stagnant disc moves from one stage to another very quickly, and sometimes it happens gradually. The faster the intracranial pressure increases, the faster the congestive disc develops.

A feature of a stagnant disc (with brain tumors) is the normal state of eye functions - visual acuity, visual fields for a long period. However, visual functions may be impaired: attacks of short-term decreased vision (for 1 minute) occur, at first rare, and then more frequent.

Visual acuity begins to decline with the appearance of atrophy, sometimes so quickly that the patient experiences amaurosis within 1-2 weeks.

An increase in the blind spot can already be noticed with conventional perimetry, but better with campimetry. The boundaries of the visual field, as well as visual acuity, can remain normal for a long time. Then the boundaries of the visual fields begin to narrow, sometimes unevenly in different meridians.

More often there is a parallelism between the state of visual acuity and visual field. Less common are hemianopic defects (this is the effect of the main pathological process on one or another part of the visual pathway)

Stagnant disks are usually bilateral, but unilateral stagnant disks can also be observed.

A unilateral congestive disc may be a temporary stage in the development of the disease, and then develops in the second eye. It also occurs with orbital tumors and traumatic hypotony of the eyeball.

But the mechanism of unilateral congestive disk in diseases of the brain and general diseases of the body is not clear.

At Foster-Kennedy syndrome atrophy of the optic nerve on the side of the tumor (usually the frontal lobe) and a congestive disc on the opposite side are observed.

If a mechanical obstacle of a pathological nature completely blocks the communication between the subarachnoid spaces in the cranial cavity and the intershell space of the optic nerve, then with increased intracranial pressure, congestive discs do not develop. Often, with tuberculous and purulent meningitis, the formation of meningeal adhesions leads to separation of the cerebrospinal fluid pathways and thereby makes it impossible for the development of stagnant discs even in cases where there is a significant increase in intracranial pressure.

Diagnostics comes down to making a correct differential diagnosis between a congestive disc and neuritis, between a congestive disc and pseudoneuritis, between a congestive disc and drusen of the optic nerve, between a congestive disc and circulatory disorders in the vascular system supplying the optic nerve.

The protrusion of the optic nerve head is determined using skiascopy (3.0 diopters = 1 mm; 4.0 diopters = 1.33 mm, maybe 2 mm or more).

It is possible to differentiate pseudocongestion from congestion using fluorescein angiography.

Fine:

1. Early arterial phase - after 1 second.

2. Late arterial phase - after 2-3 seconds.

3. Early venous phase - after 10-14 seconds.

4. Late venous phase - after 15-20 seconds.

For a stagnant disc:

1. The venous phase lengthens.

2. Large output of substance in the disk area.

3. Long-term residual fluorescence.

With pseudostagnation, these changes do not occur. Pseudoneuritis represents an abnormal development of the disc. The blind spot is normal. The dynamics of the process matter. Most often, a congestive disc must be differentiated from optic neuritis. A congested optic disc cannot be differentiated from neuritis using fluorescein angiography.

An X-ray of the skull is required, followed by a CT scan of the head. The modern research method of laser retinotomography is characterized by objective high accuracy of measurements and the possibility of dynamic monitoring of the state of the congestive optic disc. High-resolution MRI makes it possible to study radiography of the orbital segment of the optic nerve with congestive disc. MRI shows increased intracranial pressure in the subarachnoid space of the optic nerve, its expansion and possible compression of the optic fibers.

Those forms of congestive discs, in which, along with the influence of increased intracranial pressure, there is also an impact of the main pathological process on the visual pathway, are designated by the term “complicated congestive discs.” They occur in approximately 18-20% of cases and are characterized by:

1. Unusual changes in visual fields.

2. High visual acuity with greatly altered visual fields.

3. A sharp decrease in vision without visible atrophy.

4. Large difference in visual acuity of both eyes.

5. Bilateral congestive disc with atrophy in one eye.

In malignant tumors, congestive discs develop earlier and faster than in benign ones.

Degenerative diseases of the optic nerve of toxic origin

In case of poisoning with methyl alcohol Poisoning occurs not only with pure methyl alcohol, but also with liquids containing methyl alcohol (denatured alcohol, some alcohol mixtures intended for technical purposes). It was previously used to make drinks, which led to poisoning. The disease (rarely) can occur when inhaling vapors of methyl alcohol (varnish, etc.). Methyl alcohol is very toxic and even small doses can cause a sharp decrease in vision.

The picture of methyl alcohol poisoning is quite typical - on the same day, general symptoms of poisoning develop, varying in intensity: headache, nausea, vomiting, gastrointestinal disorders, and in more severe cases, unconsciousness or coma.

But visual impairment may not be preceded by general symptoms of poisoning.

A few hours or days after poisoning, more often after 1-2 days, a sharp, rapidly progressive decrease in vision in both eyes develops. The pupils are greatly dilated and do not react to light. The fundus of the eye at the onset of the disease is often normal, sometimes there is disc hyperemia or a slight phenomenon of neuritis. In rare cases, there is neuritis with edema, reminiscent of a congestive disc, sometimes anemia of the discs: they are pale, the boundaries are washed away, the arteries are sharply narrowed.

The clinical picture of the disease can be different - often during the first month after poisoning, vision improves, up to the restoration of the original vision. This may resolve the disease. In especially severe cases, the resulting deterioration in vision is permanent.

More often, after improvement, deterioration occurs again, and often the patient becomes blind in both eyes or very low visual acuity remains.

A remitting course of the disease has been noted - in the late period after poisoning, a series of successive improvements and deteriorations occurs, which ultimately leads to a sharp decrease in visual acuity.

There are four forms of the disease:

1. Initial deterioration without subsequent improvement.

2. Initial deterioration followed by improvement.

3. Initial deterioration followed by improvement and repeated deterioration.

4. Remitting course with a number of alternating deteriorations and improvements.

From the visual field, absolute central scotomas are more often observed with normal boundaries or with their narrowing.

Sometimes, when the boundaries of the visual field are narrowed, scotoma is not noted.

By the end of the first month of the disease, simple atrophy of the optic nerve is detected in the fundus of the eye in most cases; rarely the fundus remains normal.

A characteristic feature of methyl alcohol poisoning is pronounced differences in individual tolerance to this poison.

Pathological studies in humans show that degenerative decay of nerve fibers develops in the optic nerve without inflammation.

Treatment: quick and abundant gastric lavage with 1% sodium bicarbonate solution. As an antidote, ethyl alcohol is used, 100 ml of a 30% solution orally, then every 2 hours, 50 ml, the next day, 100 ml 2 times a day. In case of coma - intravenously, drip 5% solution (up to 1 ml/kg per day) based on 96° alcohol, administered with ascorbic acid. Lumbar puncture, cardiovascular stimulants. Repeated lumbar punctures are performed in combination with intravenous infusion of glucose and vitamin B1, and blood transfusion. To combat developing acidosis, a soda solution is injected intravenously or administered orally (initially 30-60 g, then 5-10 g every hour until the urine reaction becomes alkaline).

Alcohol and tobacco intoxication

Alcohol and tobacco intoxication leads to papillomacular bundle disease. Alcohol-tobacco amblyopia develops both due to alcohol abuse and tobacco abuse. In most cases, these factors operate simultaneously. Strong varieties of tobacco (cigars, pipe tobacco) are especially harmful.

It is observed mainly in men aged 30-50 years, less often in women. It occurs as a chronic retrobulbar neuritis, and both eyes are always affected. It begins in the form of a progressive, but not sharp decline in vision, especially twilight vision. The decrease in vision at the height of the disease can be significant, up to 0.1 or less. Complete blindness is not observed.

The fundus at the onset of the disease is mostly normal. Disc hyperemia or neuritis are rarely observed. In later stages, simple atrophy of the optic nerve develops in the form of blanching of the temporal half of the disc.

Characteristic changes in the visual field are a relative central scotoma in red and green colors with normal peripheral boundaries of the visual field. These scotomas have the shape of a horizontal oval, running from the point of fixation to the blind spot and only passing a few degrees beyond the vertical meridian to the nasal half of the visual field. They are called centrocecal. Very rarely, a central absolute white scotoma is observed.

With complete abstinence from drinking alcohol and smoking, significant improvement occurs, although blanching of the temporal half of the disc remains.

At pathological examination in all cases, atrophy of nerve fibers with myelin disintegration is observed throughout the entire papillomacular bundle.

In areas with atrophy of nerve fibers, complete disintegration of all pulpy sheaths was never observed; some of them were always preserved.

Along with atrophy, proliferation of glia and connective tissue is noted. The connective tissue always lacked lymphocytes, plasma cells and other cellular forms characteristic of inflammatory infiltration.

The absence of inflammatory infiltration both in the walls of blood vessels and in the vicinity of them also speaks against the inflammatory nature of the process.

In the pathogenesis of optic nerve disease in alcohol-tobacco amblyopia, hypo- and avitaminosis of the B vitamin complex is important, therefore, during treatment it is better to include drugs containing these vitamins.

Disease of the optic nerves in diabetes occurs as chronic retrobulbar neuritis and occurs almost exclusively in men. Both eyes are almost always affected.

Anterior ischemic neuropathy- this acute circulatory disorder in the arteries supplying the optic nerve is an ocular symptom of various systemic processes.

It can be functional (spasm) and organic (generalized atherosclerosis, hypertension, diabetes mellitus).

In addition, anterior ischemic neuropathy can be a symptom of diseases such as rheumatism, temporal arteritis, blood diseases (polycethemia and chronic leukemia).

It can rarely occur after extensive surgery and anesthesia, with thyrotoxic exophthalmos, herpes.

But main reason are hypertension and atherosclerosis, and therefore mainly people in the older age group get sick. But it can happen at the age of 22 or at the age of 30, since there are other causes of the disease.

Approximately in patients the disease is unilateral, in the rest it is bilateral. The process in the second eye can occur after a few days or several weeks, months and even years, on average after 2-4 years. But he was observed after 3 days, and after 20 years.

The disease develops acutely, more often in the morning after sleep, less often after lifting weights and taking hot baths. Patients often have a history of acute cerebral circulatory disorders - ischemic stroke confirmed by MRI, transient ischemic attack, myocardial infarction, coronary artery disease.

Kasymova M.S. (2005) examined blood and tears for herpes simplex virus, cytomegalovirus, toxoplasmosis, tuberculosis, streptococcus, and staphylococcus in patients with ischemic optic neuropathy using the polymerase chain reaction method. It is believed that the herpes virus is involved in the occurrence of primary inflammation of the vascular wall of arteries or arterioles, followed by their obliteration. Therefore, it is advisable to include antiviral, nonspecific anti-inflammatory and immunomodulatory drugs in the course of treatment of patients with ischemic neuropathy.

Sometimes there are warning signs of eye disease- periodic blurred vision, severe headaches, pain behind the eye.

Visual acuity decreases down to light perception. Central scotomas appear in the field of view; there may be a sector-shaped loss in any part of the visual field, but in 30% of cases the lower half of the visual field is lost, in 18% of cases - the temporal half.

In the acute period, the optic disc is swollen, the boundaries are washed away, and prominence of the disc is noted. The swelling extends to the peripapillary nerve fibers. On the surface of the disc and in the peripapillary zone, hemorrhages appear in the form of small stripes located in the layer of nerve fibers. Sometimes a “soft exudate” forms on the surface of the optic nerve head.

In some cases, simultaneously with the ischemic process in the optic nerve head, occlusion of the central retinal artery (CRA) and occlusion of the cilioretinal arteriole develop. Ischemic oculopathy may occur (ischemic uveitis with conjunctival hyperemia, corneal edema, folds of Descemet's membrane, precipitates on the posterior surface of the cornea, exudate in the humor of the anterior chamber and in the vitreous, with posterior synechiae). A “star figure” may form in the macular area, which disappears 2-3 months after the disc edema resolves.

"Star Figure"- This is a transudation from the vessels of the optic nerve head. In patients with hypertension, the retinal vessels are changed, ampulla-shaped expansions alternate with narrowings.

After 3-4 weeks or 2-3 months, swelling of the optic disc decreases and sectoral or total atrophy of the optic nerve develops. In some cases, as a consequence of severe disc edema, a posterior detachment of the vitreous plate is formed. In patients with diabetes mellitus, the symptom of preproliferative diabetic retinopathy is determined in the fundus.

With long-term observation, severe hypertensive patients continue to experience a progressive gradual decrease in vision, a narrowing of the visual field, that is, chronic ischemic neuropathy.

It is very important to study the features of fluorescein angiograms, which differ in the acute and chronic stages of the process.

Treatment

Local and general use of corticosteroids, hyperosmotic agents to reduce swelling and reduce extravasal pressure, which leads to normalization of perfusion pressure. Moshetova L.K., Koretskaya Yu.M. They offer complex treatment in acute situations - Cavinton intravenous drip 2 ml No. 10, nicotinic acid intravenous drip, Mexidol 2 ml intramuscular No. 15 and 1 ml parabulbar No. 5, Fezam 1 tablet x 3 times a day. Patients with hypertension receive antihypertensive drugs; the use of Mexidol and Fezam in treatment is positive. Treatment should begin as early as possible from the onset of the disease. For temporal arteritis, prednisolone 80 mg is used, and then reduced according to the scheme.

Argon laser coagulation of the peripapillary area is used (Kishkina V.Ya., 1983).

The prognosis is unfavorable (defects in the visual field remain, visual acuity behaves differently - increases, does not change, decreases).

Posterior ischemic neuropathy (PIN)

The causes are similar to those causing anterior ischemic neuropathy. The onset of the disease is always acute: often the first symptoms appear in the morning. Prodromal symptoms are rare.

A decrease in vision occurs from 0.9 to 0.01, and various defects appear in the visual field. Initially, there are no ophthalmoscopic changes in the optic nerve.

After 6-8 weeks, blanching of the optic disc appears and simple descending atrophy gradually develops.

On fundus In addition, there are retinal changes that depend on the process underlying the vascular lesion of the optic nerve. The process is in most cases one-sided. Fluorescein angiogram and ERG were unchanged.

Katsnelson L.A., Farafonova T.I., Bunin A.Ya. (1999) give the following figures: in 50% the second eye is healthy, in 25%, after 1-15 years, PIN develops in the fellow eye, in 25%, occlusion of the central sac.

In 23% of patients with ZIN, they also noted conduction disturbances in the homolateral carotid artery.

Treatment provided: topical corticosteroids, decongestant treatment, angioprotectors, vasodilator therapy, vitamin therapy. Persistent defects remain visible. Visual acuity increases by 0.1-0.2 only in 50% of patients.

Optic disc vasculitis

This is incomplete thrombosis of the central retinal vein (CRV). It develops in young people, in most cases the process is one-sided. The disease usually begins acutely.

The main complaints that patients make are a slight, short-term (transient) blurred vision, repeated several times during the day, and the flickering of “spots” before the eyes.

Visual acuity may not decrease in most people, but it can be 0.6-0.8 and in some cases less.

On the fundus: the optic disc is hyperemic, swollen, the boundaries are not defined due to pronounced edema of the peripapillary retina. Hemorrhages of various shapes and sizes can be seen on the disc and around it, and there may be preretinal hemorrhages covering the disc and the posterior pole of the eye. The retinal veins are dilated, full-blooded and tortuous, with exudative couplings visible on them. There are polymorphic hemorrhages throughout the fundus.

Due to cystic edema in the macular area, which occurs in patients, visual acuity fluctuates over the course of a day, weeks, or months. In the central zone of the fundus, a hard exudate appears in the form of a “star figure” (full or partial); sometimes pockets of “soft exudate” are identified in the paramacular region. In the vitreous body there is a cellular reaction that can be seen during biomicroscopy.

To make a diagnosis of ZIN, FA data are important.

Regression occurs after 6-8 months, visual acuity in most patients is restored to 1.0.

In the fundus of the eye in the macular zone, in some cases, dystrophic changes persist in the form of pathological reflexes, redistribution of pigment, white “couplings” remain along the veins, and isolated microaneurysms remain on the periphery.

Differentiate with congestive optic disc, thrombosis of the central vein, optic neuritis, hypertensive neuropathy.

The main differential diagnostic criterion for patients with disc congestion is the absence of cystoid macular edema on carotid angiography.

With a stagnant disc, hemorrhages are localized mainly in the peripapillary zone and do not spread to the extreme periphery.

With neuritis, there is an early and significant decrease in vision, swelling in the disc and in the peripapillary region, there is no such pronounced dilatation of the veins and increased permeability of the retinal vessels.

Thrombosis of the central vein develops in older patients who suffer from atherosclerosis and hypertension. Visual acuity decreases more significantly.

Optic disc vasculitis occurs in young people, with a relatively favorable prognosis. It is obviously based on endophlebitis of the central vein.

Atrophy of the optic nerves in hypertension

They may be a consequence of neuroretinopathy or develop independently of changes in the retina. As with atherosclerotic atrophy, with arterial hypertension there is a sharp narrowing and uneven caliber of the arteries. Changes in the field of view are varied. If atrophy is caused by a disease of the chiasm or optic tracts, then bitemporal or binasal hemianopsia is observed. In all other cases, there is a narrowing of the boundaries of the field of vision along all meridians. Central scotomas are rare.

The cause of atrophy is a malnutrition of the optic nerve due to pathology of the blood vessels.

Optic nerve atrophy with arteriitis temporalis

Arteriitis temporalis is a peculiar form of obliterating inflammation of the temporal arteries. It is observed in old age, more often in women. It is characterized by sharp headaches in the temporal region, intensifying in the evening. The pain can radiate to different parts of the head and face, the temperature rises, and hypochromic anemia is observed. The temporal arteries are painful on palpation, hardened, pulsate weakly or do not pulsate at all. Histological examination reveals complete or almost complete obliteration of the artery lumen by granulation tissue with inflammatory infiltration and partial necrosis of the arterial wall.

Ocular symptoms include central retinal artery embolism and optic nerve disease. A sharp drop in visual acuity, often to the point of complete blindness. Less commonly, vision decreases gradually over several weeks. In the fundus at the beginning of the disease there is a picture of ischemic edema of the disc, then the edema disappears and atrophy of the optic nerve develops. In most cases, both eyes are affected, but eyes can be affected at significant intervals.

It is believed that edema and subsequent atrophy are explained by impaired nutrition of the optic nerve due to obliterating arteritis.

Optic nerve atrophy due to bleeding

Occurs after profuse bleeding of various origins, most often gastrointestinal or uterine, leading to disruption of the optic nerve. Decreased vision occurs at different times: during bleeding and within 10 days after it due to thrombosis of the vessels supplying the optic nerve.

Sometimes a picture of neuritis is observed with isolated hemorrhages into the tissue of the optic nerve head, there may be ischemic edema, a sharp narrowing of the arteries. In most cases, the disease is bilateral, but the degree of visual acuity loss may vary. One eye may be affected.

In the visual fields, a uniform or uneven narrowing of the boundaries and loss of the lower halves of the visual field occurs.

Pathogenesis: optic nerve atrophy develops if, during bleeding or immediately after it, a decrease in blood pressure occurs, which leads to disruption of the nutrition of the optic nerve.

In the late period, 3-10 days after the start of bleeding, when the person gets better, blood clots form in the vessels supplying the optic nerve, which is caused by damage to the endothelium, this explains the development of atrophy in only one eye. It is not clear why this rarely occurs after injury.

The prognosis of the disease is serious - complete blindness may occur.

Disease of the optic nerves in diabetes mellitus

It occurs as a chronic retrobulbar neuritis and occurs almost exclusively in men.

Both eyes are almost always affected. Vision declines slowly and can reach a significant decrease. The boundaries of the visual field are normal, absolute or relative scotomas are noted. Less often paracentral. Sometimes scotomas have the shape of a horizontal oval. There may be scotomas in red, green and white colors.

Pallor of the temporal half of the optic discs gradually develops.

It is considered as a primary degenerative process of the papillomacular bundle, arising under the influence of toxic substances.

Atrophy of the optic nerves in atherosclerosis

Causes of atrophy: direct compression of the optic nerve by the sclerotic carotid artery and, as a consequence, disruption of its blood supply due to sclerosis of small arterial branches supplying the optic nerve.

Pressure on the optic nerve most often occurs in the fibrous part of the canal, and then in the pointed edge of the fibrous canal and between the exit of the optic nerve into the cranial cavity and the chiasma in the area where the internal carotid artery and the anterior cerebral artery cross it below and above.

In parallel with the atrophy of nerve fibers, a slowly progressive secondary proliferation of connective tissue develops in the optic nerve. Scar areas in the optic nerve, formed as a result of partial or complete obliteration of blood vessels, are most often observed in the segment of the nerve located near the eyeball.

The most severe sclerotic changes in the wall of the central retinal artery are observed at the site where the artery enters through the dura mater into the optic nerve trunk. When passing through the lamina cribrosa and in the disc area, i.e. in those parts of the blood vessels where their walls are subject to increased mechanical stress from the blood flow, both from vortex blood flows and from the impact of the blood stream on the vessel walls.

In the optic nerve, due to atherosclerosis as a result of a nutritional disorder, a focus of ischemic necrosis is formed, within which nerve fibers atrophy and glial proliferation occurs. Sometimes, as a result of these changes, the lamina cribrosa sinks, a deep excavation of the optic nerve head occurs, which leads to the clinical picture of pseudoglaucoma.

Due to atherosclerosis, atrophy of the peripheral nerve fibers can occur, between which the connective tissue grows, and as a result, in old age, a concentric narrowing of the visual fields is observed. Changes in the visual field such as nasal hemianopsia and central scotoma are observed with sclerosis of the internal carotid artery and are not characteristic of optic nerve atrophy due to hypertension.

Atrophy of the optic nerve with atherosclerosis can be combined with changes in the retina and blood vessels in the form of white and pigmented spots and hemorrhages, as with atrophy of the optic nerve due to syphilis, hypertension, and kidney disease.

Visual acuity can vary from blindness to 100% vision. And there may be a sharp difference in the visual acuity of one eye and the other. The latter can be explained by the fact that the vessels of both eyes can be affected by sclerosis to an unequal extent.

Despite the atrophy, visual acuity can be high, since atherosclerosis sometimes leads to atrophy of predominantly peripheral fibers of the optic nerve.

In the field of view, central scotomas and narrowing of the peripheral borders, in combination or separately, are more often detected.

There may be a narrowing of the nasal half of the visual field, which is caused by sclerosis of the internal carotid artery, nasal and binasal narrowing, bitemporal and homonymous hemianopsia.

Central scotomas are caused by pressure from the internal carotid artery.

Hereditary diseases (atrophy) of the optic nerves

Leberian optic atrophy

The disease was first described by Leber in 1871, 1874 in members of the same family. It develops, as a rule, in men of puberty, most often at the age of 20-30 years, with extreme variants from 5 to 65 years.

It can develop in women between the ages of 10 and 40 years and occurs in 17.5% of cases of the total number of patients.

The disease usually begins with acute bilateral retrobulbar neuritis, rarely at an interval of 6 months in the other eye.

Central vision drops to hundredths, sometimes over a period of several hours, but usually within a few days. In the field of view are central scotomas. The peripheral boundaries of the visual field may be normal or concentrically narrowed.

On fundus There may be no changes, but hyperemia and slight swelling of the optic disc are more often detected.

After 3-4 weeks, atrophy begins with predominantly blanching of the temporal half of the optic nerve head. Visual acuity during this period increases to 0.05-0.1. In the field of view there is a central or ring-shaped paracentral scotoma.

After 3-4 months, the process stabilizes, and temporal or complete atrophy of the optic disc is determined in the fundus.

In general, the neurological status at the height of the disease shows a normal electroencephalogram and mild signs of damage to the membranes in the diencephalic region of the brain.

A pathological examination reveals the death of retinal ganglion cells and optic nerve fibers (primary degeneration) and secondary degeneration of the rest of the optical system, in addition, arachnoid adhesions were found in the optochiasmal zone.

This is a hereditary disease. The construction of a pedigree and molecular genetic analysis can be used to calculate the probability of inheritance and determine the prognosis for sick people and the degree of risk for healthy people. The presence of a genetic factor has been proven by the manifestation of this disease in identical twins.

It is inherited in two ways: transmission occurs by inheritance of a sex-linked recessive trait and very rarely inheritance is autosomal dominant.

Infantile hereditary optic atrophies

They differ from Leberovskaya in early manifestation, clinical picture and type of inheritance.

Autosomal recessive form.Atrophy of the optic nerve is present at birth or develops before 3 years of age. The disc is pale, often with deep excavation. Visual acuity is very low, achrometry, field of vision is sharply narrowed. Nystagmus.

Differentiate with ascending and descending atrophies, taperetinal degeneration, underdevelopment of the ganglion layer of the retina. The electroretinogram is flattened or absent; with descending optical atrophy, it is not changed.

Autosomal dominant form.Develops at an older age, very slowly. This type of atrophy never results in blindness. The boundaries of the peripheral visual field remain normal, and visual acuity varies widely. In some patients it may not change, in others it decreases to 0.1-0.2 or lower.

In the field of view are central and paracentral scotomas. Color vision is disordered according to the acquired type.

Complicated infantile optic atrophy of the Beer type K.

Inherited in an autosomal recessive manner. It begins in early childhood and is characterized by cardinal signs: bilateral temporal blanching, less often complete blanching of the optic disc, neurological symptoms with a predominant lesion of the pyramidal system, progression of the process over several years.

The first symptoms appear suddenly at 3-10 years of life - visual impairment with further slow progression is detected. It does not reach complete blindness; visual acuity stops at 0.2-0.4.

Fundus of the eye: at the beginning of the disease there is hyperemia, then atrophy of the optic disc.

Following the ocular symptoms, neurological symptoms appear - nystagmus, increased tendon reflexes, positive Babinski's sign, spastic muscle hypertension, bladder sphincter disorder, mental retardation. It is transmitted as a simple recessive trait.

Optic disc drusen

They were first described in 1858 by histologist Muller, and in 1868 by A.V. Ivanov.

These are small single or multiple formations of gray-white or bluish color, located along the edge of a normal disc and protruding above its level, so the disc appears uneven. The size of drusen is from 1 to 3 diameters of the central vein. Gradually, the number of drusen may increase and they resemble clusters. Physiological excavation disappears, the disc takes a convex shape. The distance into the vitreous can be 2.0-10.0 diopters. The blood vessels on the disc are normal.

Drusen may be associated with pigmentary retinopathy, Stargardt macular degeneration, retinal angioid streaks, glaucoma, retinal vascular occlusion, optic edema, or optic atrophy. Visual acuity may decrease, the blind spot is enlarged. There is often loss in the nasal half of the visual field.

Headaches in the forehead and scattered neurological microsymptoms are observed.

It is believed that this pathology of the optic nerve is a disease from the group of neuroectodermal dysplasias or phacomotosis (an erased form of Bourneville tuberous sclerosis).

Inherited as an autosomal dominant trait.

Cysticercosis of the brain

Cysticerci in humans are localized in the brain and eye. Congestive discs are the most common ocular symptom and are more common in basal cysticercosis meningitis, cysticercosis of the fourth ventricle and less often in the substance of the brain.

The main factor in increasing intracranial pressure is hydrocele of the cerebral ventricles due to compression of the intracranial part of the optic nerves.

As a result of venous stagnation or stasis, hemorrhages often develop in the disc tissue. Rarely, a unilateral congestive disc is observed; there are complicated congestive discs. Stagnant discs often lead to secondary optic nerve atrophy.

Spontaneous reverse development of stagnant discs occurs, which may be due to the death of cysticerci and their calcification, accompanied by a decrease in intracranial pressure.

Optic neuritis and, rarely, simple atrophy (as a symptom in the long term) may be observed.

The fundus may be normal.

Treatment of an edematous disc is limited to treating the underlying disease. To combat papilledema, intravenous administration of hypertonic solutions, glycerol intake, or surgery are necessary.

Questions:

1. Why is the temporal half of the optic nerve head (ONH) paler than the nasal half?

2. Why is the temporal half of the optic disc more distinct during ophthalmoscopy than the nasal half?

3. Name the inflammatory diseases of the optic disc.

4. Where is inflammation localized in retrobulbar neuritis?

5. What complaints does a patient have with neuritis?

6. What will the doctor see during ophthalmoscopy in the fundus of a patient with neuritis?

7. What diseases should a congestive disc be differentiated from?

8. What is anterior ischemic neuropathy?

9. What is optic disc vasculitis?

10. What diseases of the optic disc are differentiated from vasculitis?

11. Through which opening does the optic nerve leave the orbit?

12. What is optic disc congestion?

13. What ophthalmoscopic signs are characteristic of primary atrophy of the optic disc?

14. What ophthalmoscopic signs are characteristic of secondary atrophy of the optic disc?

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