Types of optic nerve atrophy, symptoms, course. Congestive optic disc: causes, symptoms and features of the treatment of optic nerve borders are not clear veins are dilated

The most recognized is the retention theory of the pathogenesis of congestive nipple, according to which the disease is caused by a delay in the outflow of tissue fluid along the optic nerve into the cranial cavity. Due to the increase in ICP, a blockade occurs in the area of ​​​​the entrance to the cranial cavity, since the folds of the dura mater are pressed against the intracranial part of the optic nerve.

There are unilateral and bilateral, symmetrical and asymmetric, simple and complicated congestive optic discs. When evaluating unilateral optic disc edema, one should be aware of the possibility of its disc pseudoedema.
According to the degree of severity, five successive stages are distinguished: initial, pronounced, pronounced, congestive nipple in the stage of atrophy and atrophy of the optic nerve.

It should be noted that sometimes it is possible to identify the marginal edema of the optic disc - the optic disc is somewhat hyperemic, the borders are blurred, there is edema along the edges of the optic nerve disc with protrusion into the vitreous body. The veins are slightly dilated, the arteries are not changed.

In the stage of the initial congestive nipple, the edema increases and spreads from the edges of the optic disk to the center, capturing the vascular funnel, the size and degree of prominence of the optic disk into the vitreous body increase; the veins are dilated, tortuous, the arteries are somewhat narrowed.

With a pronounced congestive nipple, the optic disc is hyperemic, significantly enlarged in diameter, protrudes into the vitreous body, its boundaries are blurred. Vessels are sharply changed and covered with edematous tissue of the optic disc. There may be hemorrhages in the disc tissue and the surrounding retina. Whitish foci appear - areas of reborn nerve fibers.

In the stage of a pronounced congestive nipple, the above symptoms increase sharply.

During the transition to the stage of atrophy, first a light, and then a more pronounced grayish hue of the optic disc appears. The phenomena of edema and hemorrhage gradually disappear.

With congestive nipples, visual acuity remains normal for several months, and then begins to gradually decline. With the transition of the process to the stage of atrophy, the decrease in vision progresses rapidly. Changes in the visual field also develop slowly. With atrophy, a concentric uniform narrowing of the visual field develops. It should be noted that with a complicated congestive nipple, which occurs with an increase in intracranial pressure, other changes in the visual field are possible - hemianopsia, central scotomas.

In addition, this type of congestive nipple is characterized by:

• high visual acuity with a pronounced change in the field of view;
• asymmetry of the ophthalmoscopic picture and the degree of visual acuity reduction;
• a more pronounced decrease in vision before the development of optic nerve atrophy.

Myelination of nerve fibers

Normally, the optic nerve fibers inside the eyeball are devoid of myelin. With their myelination, white porous spots form on the fundus, often covering the vessels of the retina and optic nerve and creating a picture of edema of the latter.

Optic disc drusen in both eyes

Drusen are formed by the deposition of hyaline under the retina; there is an impression of disc edema (pseudocongestive disc). If spontaneous pulsation of the retinal veins is visible, then this almost excludes papilledema.

Congestive optic disc (ON) is characterized by its swelling due to increased ICP.

Swelling that is not associated with an increase in ICP is not disc congestion. There are no early symptoms, visual impairment may occur for only a few seconds. When the disc stagnates, it is necessary to immediately diagnose its etiology.

A congestive disc is a sign of increased ICP and is almost always bilateral. Among the reasons are the following:

• GM tumor or abscess,
• brain injury or bleeding,
• meningitis,
• adhesive process of the arachnoid membrane,
• thrombosis of the cavernous sinus,
• encephalitis,
• idiopathic intracranial hypertension (GM pseudotumor) is a state of increased pressure of the cerebrospinal fluid in the absence of focal lesions.

Stages of development of congestive optic disc

In the process of occurrence and course of a stagnant disc, in the dynamics of its development, several stages are clinically determined. However, the opinions of a number of authors about the number of stages in the development of a congestive disc and the characteristics of its clinical manifestations at each stage diverge. E. Zh. Tron distinguishes five stages: the initial stage of edema, the pronounced stage of edema, the pronounced stage of edema, edema with the transition to atrophy and the stage of atrophy after edema. O. N. Sokolova, based on the data of fluorescein angiography, identifies three stages in the development of a congestive disc: the initial stage, the stage of pronounced changes, the stage of transition to optic nerve atrophy.
Usually, in ophthalmological and neuro-ophthalmological practice, depending on the nature of the severity of changes in the fundus, five successive stages of development of a congestive optic disc are used.

Depending on the causes of developmental features and, mainly, on the rate of development of a stagnant disc in the clinical course of the process, five stages are conventionally distinguished:

• initial stage;
• pronounced stage;
• pronounced (far advanced stage);
• pre-terminal stage;
• terminal stage.

The initial stage is characterized by the appearance of a slight marginal edema of the disc, slight blurring of its borders, and a slight protrusion of the disc towards the vitreous body. Edema initially occurs in the upper and lower edges of the disc, then spreads to the nasal side. The high edge of the disc remains free of edema longer, then the edema also captures the temporal disc. Gradually, the edema spreads to the entire surface of the disc, capturing the area of ​​the vascular funnel. As a result of the spread of edema to the layer of nerve fibers of the retina, the retina around the disk acquires a slightly pronounced radial striation. The arteries in the area of ​​the disc are not changed, the veins are slightly dilated, but the tortuosity of the veins is not observed.

The pronounced stage is manifested by a further increase in the size of the disk along the plane of the fundus, its prominence and more pronounced blurring of the boundaries. There is some narrowing of the arteries and a greater expansion of the veins. There is tortuosity of the veins. In places, the vessels are blocked by edematous tissue. Small hemorrhages begin to appear in the marginal zone of the disc, as well as around the disc as a result of venous stasis, compression of the veins and violation of the integrity of the walls of small vessels. The formation of white foci of extravasation in the area of ​​edematous disc tissue is observed.

In a pronounced stage, the phenomena of stagnation continue to grow. The protrusion of the disk continues to increase, sometimes reaching 2-2.5 mm (which corresponds to a hyperopic refraction of 6.0-7.0 diopters, determined refractometrically). Significantly increases the diameter of the disc, there is a pronounced hyperemia of the disc as a result of further deterioration of the outflow of venous blood. Vessels on the disc are poorly visible as a result of immersion in edematous tissue. On the surface of the disk and in its zone, hemorrhages of various sizes appear and less often whitish foci. Whitish foci are a manifestation of the beginning dystrophy of nerve fibers (axons of retinal ganglion cells). Quite rarely, these foci occur in the peripapillary zone of the disc and even in the macular zone of the retina, having a radial orientation like a star figure, as in renal retinopathy. There is a so-called pseudoalbuminuric neuroretinitis.

The pre-terminal stage (edema with the transition to atrophy) with a long-term existence of edema is characterized by the appearance of the first signs of optic nerve atrophy, visible ophthalmoscopically. A grayish tint of the disc appears against the background of decreasing edema. The caliber of the veins becomes smaller, their tortuosity decreases. Hemorrhages resolve, white foci almost completely disappear. The boundaries of the disc are reduced, it acquires a dirty white hue, the boundaries of the disc remain fuzzy. Atrophy of the optic nerve with partially preserved swelling along its borders is determined.

The terminal stage is the stage of secondary atrophy of the optic nerve. The optic disc acquires a pale gray color with fuzzy borders. The arteries on the disk are narrowed, their number is reduced (compared to the norm), the venous network tends to approach the normal state. The degree of blanching of the optic disc depends on the reduction in the number of blood vessels on the disc, as well as on the growth of glial and connective tissue.

Symptoms of congestive optic disc

Initially, visual impairment may not manifest, but there may be short-term blurred vision, glare, blurring of silhouettes, diplopia, or loss of color vision for several seconds. The patient may have other symptoms of increased ICP.

Ophthalmoscopy may show thickened, hyperemic, and edematous optic discs and retinal hemorrhages around the disc, but not in the periphery. Just disc edema, which is not accompanied by changes in the retina characteristic of increased ICP, cannot be considered a congestive phenomenon.

In the early stages of the disease, visual acuity and the reaction of the pupil to light do not suffer, so their changes indicate the neglect of the condition. Examination of the visual fields may reveal extensive blind spot abnormalities (scotomas). In the later stages, perimetry can reveal typical defects associated with damage to nerve fibers (loss of sectors of the visual fields) and loss of peripheral vision.

Diagnosis of congestive optic disc

• Clinical examination.
• Immediate visualization of the GM.

The degree of disc edema can be determined by comparing the optical power of the lenses required to focus the ophthalmoscope on the most elevated area of ​​the disc and on intact areas of the retina.

A thorough ophthalmological examination is essential to differentiate congestion from other causes of ONH edema, such as ON neuritis, ischemic neuropathy, hypotension, uveitis, or disc pseudoedema (eg, ON drusen). If clinical findings suggest congestion, gadolinium MRI or contrast-enhanced CT should be done immediately to rule out intracranial masses. Lumbar puncture and measurement of CVJ pressure can only be done if no intracranial masses have been detected, otherwise there is a high risk of wedging the brainstem. The method of choice for diagnosing disc pseudoedema due to ON drusen is ultrasound in (3-mode.

Treatment of congestive optic disc

Immediate treatment directed at the underlying cause of the disease will help reduce ICP. If it does not decrease, secondary atrophy of the optic nerve and deterioration of vision, as well as other serious neurological disorders, are possible.

Key points

• A congestive ON disc indicates an increase in intracranial pressure.
• In addition to a hyperemic edematous disc, the patient usually has retinal hemorrhages around the disc, but not in the periphery.
• The pathological picture of the bottom of the retina usually precedes visual impairment. Imaging of GM structures is urgently needed.

If no mass is found, a lumbar puncture can be done to measure CSF pressure.

• Therapy is aimed at the root cause of the disease.

optic nerve- This is a segment of the peripheral neuron of the visual pathway, which 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 opening and then both optic nerves converge to the Turkish saddle.

Topographically divided into four sections:

1. Intraocular.

2. Retrobulbar, or orbital.

3. Intratubular.

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

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

Intraocular department 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 near the disc.

Channel shape affects the size of the physiological excavation. It is greater with large scleral canals. The depth of physiological excavation lies within 1 mm. Its bottom is often a lattice 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 called the intraocular part of the optic nerve at the junction of the optical fibers of the retina in the channel formed by the fibrous membrane of the eyeball. The disc is about 1.5-2 mm in diameter, located 2.5-3 mm nasally from the posterior pole of the eye and 0.5-1 mm downward from it.

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

Disc color- pale pink. The temporal half of the disk is paler than the nasal one, since less nerve fibers and vessels are directed towards the yellow spot than into the nasal one.

Disk boundaries Normally, they are clearly defined, the temporal half stands out more clearly than the inner one, since a thinner layer of nerve fibers goes towards the macular zone than into the nasal one (papillomacular bundle).

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

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

In the center of the optic disc there is a deepening of a dull white color of various sizes - physiological excavation. Sometimes physiological excavation occupies a large part of the disk, spreading mainly to the outer half of it. Vessels "excavate" not on the border of the disk, but on its surface.

Orbital or retrobulbar the section of the optic nerve is a small segment from the place of its exit from the eyeball to the entrance to the optic canal, equals 25-35 mm. Here, the diameter of the disk is 4.0-4.5 mm due to the appearance of 3 membranes here - hard, arachnoid and soft, constituting the continuation of the membranes of the brain.

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

intracranial part The optic nerve begins at the cranial foramen 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 on top of the frontal lobe of the brain, and its lateral surface is adjacent to the internal carotid artery.

The space between the arachnoid and soft sheaths 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 and arachnoid meninges and remains covered only by the pia mater.

From the pia mater inside the trunk depart numerous connective tissue septa - septa, with blood vessels embedded in them, dividing the optic nerve into separate bundles. These septa are composed of collagen, elastic tissue and glia.

glia plays the role of a 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 - this is astrocytic glia. In addition to support, glia replaces areas of dead differentiated tissue. Glia, braiding in the form of a clutch a ganglion cell devoid of a myelin sheath, 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 cleaning tissues from decay products (in other tissues, histiocytes do this).

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

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

Nuclei oculomotor nerve located at the bottom of the Sylvius aqueduct at the level of the anterior tubercles of the quadrigemina.

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

From the macrocellular 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 an 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 located in the central part 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 back of the orbital region, the papillomacular bundle moves to the center and goes along its axis. It occupies the same central position before the chiasm and in the chiasm itself.

In the chiasm, there is a partial decussation of the fibers of the papillomacular bundle. Non-crossing fibers are located in the center throughout.

Chiasma, covered with soft and arachnoid membranes, is located on the diaphragm (duplication of the dura mater) of the Turkish saddle and has dimensions of 4-10 mm in length, 9-11 mm in width, and 5 mm in thickness.

Above from the chiasm passes the bottom of the third ventricle, from below under the diaphragm - the pituitary gland, from the sides - the cavernous sinus. Behind it is adjacent funnel (inphundibula), going to the pituitary gland. On both sides of the chiasm are the branches of the internal carotid artery, which take part in the formation of the circle of Willis.

From the posterior surface of the chiasma begin visual tracts and they end in the external geniculate bodies and at the cushion of the visual tubercles. The fibers of the papillomacular bundle occupy most of the lateral 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: in 1, 4, 6, counting from the bottom up, crossing fibers end, in 2, 3, 5 - non-crossing. From the chiasm, the optic tracts go up.

From the ganglion cells of the 1st and 6th layers of the lateral geniculate body, the optic bundle, or the Graziole 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 spur groove.

The upper homonymous quadrants of the retinas are projected in the upper part of the Graziola fasciculus, 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 cortex, the upper lip of the spur sulcus in each hemisphere corresponds to the upper homolateral quadrants of the retinas, the lower lip to the lower ones.

The foveal region of the retina is represented in the most posterior sections of the spur 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 - the middle homolateral sections of both retinas.

The visual zone in the cerebral cortex contains the 17th, 18th and 19th Brodmann fields. 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 - optognostic object, spatial perceptions.

Blood supply to the optic nerve mainly carried out by 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 optical tract is fed by the anterior choroidal artery and its branch arteria communicans posterior. The outer geniculate body and the beginning of Graziole's bundle are from the arteria cerebri media. The visual centers in the brain are fed from the system arteria cerebri posterior - ramus posterior inferior or arteria calcarina.

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

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

Disc involvement may be isolated but is more commonly associated with ametropia, microphthalmos, congenital cataract, and primary persistent hyperplastic vitreous.

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

Hypoplasia of the optic nerve is detected in patients with Warburg's syndrome, in 30-57% of patients with Eicard's 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 (VEP).

When the disc diameter is from 0.1 to 0.25 of the normal radius of the disc, VEP, as a rule, is 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 from 0.6 to normal, VEP is recorded, and vision in such patients is 0.03 to 1.0.

The x-ray often shows a decrease in the visual channels, but CT and MRI or neurosonography are better.

Differential diagnosis of hypoplasia and atrophy of the optic nerve in 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 retinal vessels are always determined, having a normal caliber and corkscrew-like course (Shamshinova A.M., 2002).

An MRI should be done to rule out neonatal hypothyroidism.

In children with hypoplasia and neonatal jaundice or hypoglycemia, as well as with 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 soon as possible, start spectacle or contact correction of ametropia, perform 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. Simultaneously correction of neurosomatic and neuroendocrine disorders.

Optic nerve aplasia

A rare congenital anomaly in which both retinal ganglion cells and their axons and 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 central retinal vessels.

Disk changes are varied:

1. 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, a deep cavity is determined at the site of the optic nerve head, surrounded by a light ring resembling a peripapillary scleral cone. There are no central retinal vessels and no direct pupillary reaction to light.

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

EFI, ERG are not changed, only in some cases subnormal ERG is registered. When recording VEP, there are no bioelectrical responses. With ultrasound and CT of the orbits, a rudimentary optic nerve is sometimes determined, hydroencephaly, anencephaly, and orbital meningoencephalocele are detected.

Differentiate from hypoplasia. With hypoplasia during ophthalmoscopy, the optic disc is practically indistinguishable, convoluted central retinal vessels with a normal caliber are always visible.

Anomalies of the optic nerve excavation

Bindweed Syndrome.Congenital funnel-shaped excavation of the posterior pole with involvement of the optic disc. The disease is most often unilateral, occurs in women 2 times more often than in men. In 60% of patients with 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 cavity, and the area surrounding it has evenly protruding edges.

In the center of the funnel, a “bouquet” of white glial tissue is visible. The macula can be displaced and then located on the wall of the recess. Vessels of the disc in a reduced number appear 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 of the affected eye.

Three-mirror lens biomicroscopy reveals areas of local retinal detachment in most patients, even if no serous retinal detachment is seen on reverse ophthalmoscopy. Quite often, the bindweed syndrome is combined with basal encephalocele in children and anomalies of the facial skeleton (cleft lip and hard palate). There may be kidney anomalies and others. Visual acuity ranges from the correct projection of light to 0.05, cases of 0.8-1.0 are described.

In the field of view, central or centrocecal defects are detected. Color vision in most patients is not changed. The ERG remains normal. With VEP, most patients have a decrease in amplitude and an elongation of the P component.

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

Treatment

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

Children have occlusion and pleoptics. If necessary, surgical correction of strabismus. With retinal detachment - surgical treatment. A new operation, transconjunctival fenestration of the optic nerve sheaths, has been proposed for surgical treatment.

Optic nerve coloboma

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

Coloboma can form at any point along the palpebral fissure and manifests itself from the iris, choroid, retina and optic nerve as a result of incomplete or abnormal matching 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 damage by cytomegalovirus infection. The disease can be both unilateral and bilateral. With ophthalmoscopy: on a slightly enlarged optic disc, there is a spherical depression with clearly defined boundaries, silvery-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. 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 coloboma is often associated with posterior lenticonus, posterior embryotoxon, optic disc fossa, epidermal nevus syndrome, hyaloid artery remnants, and choroidal colobomas. Sometimes rhegmatogenous retinal detachment develops (usually after 20 years).

In patients with a pit of the optic disc, macular edema develops as a result of macular rupture, and then separation of the inner and outer layers of the retina and macular detachment. EFI and ERG are usually not changed.

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

Treatment

In the case of the formation of a subretinal neovascular membrane, laser coagulation is indicated. With macular detachment - surgical treatment: vitrectomy followed by the introduction 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, as a rule, unilateral anomaly, which is characterized by the development of an extensive deep excavation in the region of the posterior pole of the eye, with the optic nerve head 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, an extensive cup-shaped depression is noted, at the bottom of which there is an almost unchanged optic disc. Vessels have a normal course and caliber.

The B-scan can determine the depth of the defect.

Vision ranges from "light projection" to 0.5. Perimetry reveals various defects, 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 in the cribriform plate in the area of ​​the fossa. Some pits are combined with the subarachnoid space.

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

Macular retinoschisis and detachment due to the optic disc pit develop, as a rule, 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.

VEP in the majority is not changed until the development of macular detachment.

Treatment.

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

Syndrome of oblique entry of the optic disc

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

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

This configuration of the disc is combined with the presence of a lower inner scleral cone. There is usually a complex myopic astigmatism with a positive axis oriented parallel to the ectasia. Visual acuity is 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. VVP - within the normal range.

Differentiate with optic nerve hypoplasia. Unlike hypoplasia, the process is usually bilateral and is always associated 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, and 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 - a vertically directed excavation.

The ratio of ED is normal, not more than 0.5 with glaucomatous atrophy, this ratio is significantly reduced.

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

Congenital pigmentation of the optic disc

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

Therapeutic measures are not required.

Doubling 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, congenital cataract.

Visual acuity varies from 0 to 1.0.

Treatment

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

Pseudoneuritis, or pseudostasis of the optic nerve

It is a congenital anomaly resembling optic neuritis. With ophthalmoscopy, the disc has fuzzy boundaries and slightly prominates. 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 a number of cases it is not associated with Druzes.

In atypical cases, myelin fibers can be located along the edges of the optic disc, causing them to prominence, and the boundaries of the disc look scalloped.

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

With ophthalmoscopy of the optic disc, it is pink, slightly prone, the borders seem to be blurred, and the impression of hyperemia of the optic disc is often created.

Drusen are often located in the nasal part 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 upon contact with drusen. For diagnosis, CT and B-sonography are used. Visual acuity and visual field are usually unchanged. But in some cases, especially with pseudostagnation caused by drusen, visual acuity can be reduced, and in the visual fields there is an expansion of the blind spot, central or centrocecal scotomas. Can progress at any age, this leads to diagnostic errors. Sometimes it is difficult to make a differential diagnosis of pseudocongestion and congestive disc. ERG and VEP are normal.

Differential diagnosis. In patients with optic neuritis, visual acuity decreases sharply within a few hours or days, a prodromal period is characteristic, during which subfebrile condition, headache and acute respiratory viral infections are noted. With pseudoneuritis, there is no hyperemia of the optic disc and exudation into the vitreous body.

VEPs change with optic neuritis, with FAH with a congestive disc, vasodilation and pronounced extravasal hyperfluorescence are determined. Sometimes you even have to look at other family members. In doubtful cases, CT and MRI can be used.

Treatment is not required. It is necessary to monitor patients to exclude diagnostic errors.

Anomalies in the development of the optic nerve

pseudoneuritis- a congenital anomaly resembling optic neuritis or congestive disc.

With ophthalmoscopy, there is a fuzzy contour of the disk, the absence of physiological excavation. With pseudoneuritis, developmental anomalies are often observed from the side of the vessels (a large number of vessels with unusual branching and pronounced tortuosity are visible on the disk, they pass from the disk to the retina in all directions).

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

A characteristic feature of pseudoneuritis is the good state of visual functions (visual acuity and visual field, although visual acuity may be reduced) and the lack 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 myelin (fat-like) sheath of white color. It prevents the impulse traveling through the fiber from dissipating to the adjacent axial cylinders.

Myelination of the nerve fibers of the optic nerve breaks, as it were, at the cribriform plate and does not extend to the disc. Occasionally, myelinated fibers extend into the nerve fibers of the disc and the retina adjacent to the disc in about 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 with 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, coloboma of the choroid.

Drusen of disc and retina- These are small single or multiple formations of a gray-white or bluish color, protruding above the level of a normal disk. The size of the drusen is from 1 to 3 diameters of the CVS. They are located on the edge of the disc, so the disc appears uneven. Gradually, the number of drusen can increase and resemble clusters. Physiological excavation disappears, the disk takes on a convex shape. The protrusion into the vitreous body is 2.0-10.0 diopters.

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

Usually there are headaches in the forehead, scattered 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- inflammation of the trunk and sheaths of the optic nerve. It is 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 descendants are classified as retrobulbar.

Diagnosis of bilateral descending neuritis with bilateral disc edema is sometimes very difficult. Fluorescein angiography and complex EPS 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 are varied.

The disease can cause both acute and any chronic infection. Especially frequent are inflammatory diseases of the brain and its membranes (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 be the cause of neuritis.

Of the diseases of the internal organs, diseases of the optic nerve lead to diseases of the kidneys, diabetes, gout, blood diseases, collagen diseases, allergic conditions, diseases associated with malnutrition, beriberi (beri-beri, scurvy).

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

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

A large percentage of cases remain unexplained etiology.

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

Complaints of patients with neuritis: decreased vision, constant or periodic appearance of spots, flickering before the eyes, there may be aching pains behind the eye, in the area of ​​the eyebrow, 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 is reduced, since some patients, bypassing eye institutions, end up in neurological and neurosurgical hospitals.

Atrophy of the optic nerve in its diseases occurs in 40-60% of cases.

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

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

The main manifestations of diseases of the optic pathway are changes in the fundus, a decrease in visual acuity and changes in the visual field. But these changes are not equal.

The study of the visual field is of primary importance for the diagnosis of 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 thorough, pedantic study of the visual field from the periphery to the center, along a larger number of meridians, as well as repeated examinations of the visual field, is needed. The boundaries of the field of view for white color and colors are examined.

Of the known objects in diseases of the visual pathways, only a red mark of 5 mm should be used. On the perimeter of Forster, the boundaries are the norm: 35-40 ° in the temporal half of the field of view 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, there is often a divergence of boundaries between white marks of 5 mm and 2 mm.

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 detect scotomas. However, perimetry is not always able to detect small central scotomas.

The main method for diagnosis is automatic perimetry.

To identify and differential diagnosis of demyelinating processes, VEP is examined in the visual analyzer.

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

An important method in the complex for diagnosing drusen and stagnation of the optic nerve is video ophthalmography.

Used to control the treatment of threshold spatial contrast sensitivity - CSFM.

Neuritis (papillitis)

Neuritis (papillitis) called inflammation of the optic nerve, capturing 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 impairment.

Usually begins with a decrease in vision, which can fall within a few hours, less often a few days.

Loss of vision, which is subjectively felt by the patient, is accompanied by slight headaches and pain when moving the eyes. But these symptoms may or may not be present. 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 dilated. There is a narrowing of the field of view, and with the defeat of the papillomacular bundle - central scotomas. In the field of view, there may also be wedge-shaped loss in the blind spot, arch-like and quadrant, nasal and binasal.

With an increase in the process, hyperemia and edema of the optic nerve increase with its protrusion into the vitreous body. The degree of exposure 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 sweating of exudate from the vessels of the disc, clouding of the vitreous body is observed. Prepapillary vitreous opacities and Tyndall's phenomenon are clearly visible under microscopy in papillitis associated with uveitis.

Previously, when there were frequent diseases of relapsing fever, papillitis due to uveitis was quite common. Full recovery of vision was observed only after 6-8 months, and sometimes vision was restored only to 0.02-0.05.

With injuries of the anterior part of the eye, inflammation often occurs with involvement of the optic nerve in the process.

Damage to the optic nerve occurs with uveo-meningoencephalitic syndromes - Harada's disease (uveitis with spontaneous retinal detachment, meningo-encephalitis, hearing loss, hair loss, graying of hair), Vogt - Kayanagi (baldness, patchy depigmentation of the skin and hair, uveitis, deafness), with syphilitic ophthalmia, Behcet's syndrome, Geerfordt and Ben ye - Beck-Shauman.

Behçet's syndrome is known as ophthalmic-stomatogenital syndrome, Geerfordt's syndrome as subchronic uveoparotitis, and Beck-Schaumann's disease as sarcoidosis syndrome. Geerfordt's syndrome is now also referred to as sarcoidosis.

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

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

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

During surgical interventions, another form of indeterminate uveo-meningitis was revealed, called primary edema of the optic nerve, its intracranial and intracanalicular sections. Edema compresses the optic nerve, which leads to a rapid drop in vision. Emergency opening of the canal leads to a rapid restoration of vision.

The etiology of infectious primary papillitis is most often viral.

Often it is necessary to differentiate with a congestive disc, pseudoneuritis, ischemic conditions of the optic disc, if there is a pronounced edema.

With congestive disc and pseudoneuritis, with a pronounced change in the optic disc, visual functions are preserved. Only with a complicated congestive disc, visual functions are immediately disturbed, but the field of view changes according to the hemianoptic type, which is not typical for neuritis.

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

In the differential diagnosis of neuritis and vascular optic neuropathy, it is necessary to know the onset of the disease: is it gradual or sudden, did the patient suffer from infectious diseases, was there hypothermia, stress, heavy physical exertion. Ophthalmoscopic examination reveals hyperemia of the disc, vasodilation or pale disc, narrow vessels, narrowing of the visual field, scotoma, or hemianopsia.

Optic nerve vasculitis differs from neuritis in a more pronounced swelling of the disc, especially of the retina in the papillary and central zone, often with a "star figure", as well as the presence of accompaniment bands along the vessels on the disc. Visual acuity is higher with retrobulbar neuritis, accompanied by retinal edema in the macular region. It should be differentiated by ophthalmoscopy from central serous chorioretinopathy, in which “transmission points” are detected.

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, 25% of patients have complete atrophy of the optic nerve, and 35% have partial atrophy.

Patients with optic neuritis need urgent referral to a hospital, where they undergo general treatment with broad-spectrum antibiotics with B vitamins, as well as anti-inflammatory, desensitizing, vasodilating and dehydration therapy (hemodez, reopyrin, corticosteroids orally and retrobulbarno, intramuscularly lasix, orally suprastin, furosemide, nicotinic acid preparations), blood transfusions, spinal puncture, corticosteroids are also used. When the cause of the disease is identified, etiotropic therapy is added.

Retrobulbar neuritis (RN)

Inflammatory lesion 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, trauma. Cases caused by chlamydia, brucella, collagenoses and tuberculosis are described. A large percentage remain with an unexplained etiology.

The most common cause of ROP is demyelinating disease: 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) and chronic (toxic). Acute retrobulbar neuritis is usually unilateral, chronic - bilateral.

Retrobulbar neuritis has three clinical forms:

1. Inflammation of only the sheaths of the optic nerve - develops a second time.

2. Inflammation of the peripheral fibers of the nerve trunk - interstitial neuritis, in which the inflammatory process usually begins in the soft sheath 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.

Classical retrobulbar neuritis is characterized by loss of vision, usually unilateral, but bilateral ROP occurs in 19-33% of adults and 60% of children, with impaired color vision with rapid color fatigue. It also shows up:

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

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 visual field, detected during perimetry.

There may be no pathological changes in the fundus, or there may be disturbances characteristic of neuritis and congestive disc. It depends on the intensity of the inflammatory process and its localization. Sometimes there is optic disc edema (5%) with a hemorrhagic component. Children with ROP quickly develop edema and often develop papillitis. After 2-3 months, neuritis resolves, visual acuity is restored, and the central scotoma undergoes regression. On the fundus, blanching of the temporal half or the entire ONH is formed. A repeated attack of ROP over the next 5 years is observed in 12-36% of patients.

Tron E.Zh. (1968) pointed out that the obligatory 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 picture of the fundus and visual functions. At the beginning of the disease, there is a sharp drop in visual acuity; when visual functions are restored, the picture of the fundus worsens, optic disc blanching develops. Paleness of the ONH occurs later if the lesion is located farther from the disc. And sometimes at an early stage, one can observe a pronounced blanching of the optic nerve head in combination with good visual functions. The intensity of blanching of the optic disc is due to the loss of the myelin coating, and good vision is due to the preservation of the axial cylinders. Gradually, complete atrophy of the optic nerve develops. The term "optic nerve atrophy" should be used with a persistent decrease in visual acuity and partial or complete blanching of the ONH. Most patients are characterized by fluctuations in visual acuity after physical exertion (Uthoff's symptom). This symptom can be triggered by taking a hot bath or shower, hot weather, hot food and water, increased lighting, etc. Uthoff's symptom is detected in 32.8-49.5% of patients and has a prognostic value. It is associated with a high risk of developing multiple sclerosis (MS). With a decrease in body temperature, there may be an improvement in vision. With ROP, as a result of demyelination, with long-term preservation of dark adaptation, light adaptation and daytime vision are disturbed: a feeling of blindness occurs, even at moderate brightness. When determining visual acuity, the higher the illumination, the more the patient sees dark spots. Sometimes when the eyes are moved or provoked by sound, flashes of phosphorescent color appear before the eyes - Lhermitte's eye symptom.

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

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

Treatment

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

Antioxidant preparations are necessarily prescribed: emoxipin, vitamin E.

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

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

Dicynon 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.

Apply dikain-adrenaline blockade of the middle nasal passage. Turunda is impregnated with a solution of dicaine 0.5% and adrenaline 0.1% (1 drop of adrenaline per 1 ml of solution). The duration of the procedure is 15-20 minutes. For a course of treatment 5 procedures every other day.

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

Antihistamines are prescribed: astemizole (gistolong), ketotifen (denerel) with a change in the drug. It is possible to use synakten-depot, ACTH, thymus preparations: T-activin, thymalin, interferon and reoferon inducers. Intramuscularly, it is advisable to prescribe delargin 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: anginine, prodectin, doxium.

Apply B vitamins, ascorbic acid, calcium, potassium preparations.

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

Endonasal electrophoresis, phonophoresis, magnetotherapy are widely used. Cerebrolysin intravenously, intramuscularly, retrobulbarno No. 10-15. Locally: a single dose of 0.5 ml.

With atrophy of the optic nerve, 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 their own antigens, including myelin antigens, which leads to blocking of autoimmune reactions.

Multiple sclerosis

Currently, the most common hypothesis is 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 on 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 disturbances in the spinal cord and brain stem; glycoprotein - in the periventricular zone and in the white matter of the cerebellum. To some extent, this also determines the clinical manifestations of MS. Allocate cerebrospinal form (in 50-70%), proceeding with damage to the optical, pyramidal and cerebellar systems; spinal (23%), cerebellar (19%), optic (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 lamina cribrosa to the entry point of the central retinal artery into the optic nerve) and its intracranial part. In the early stages of the disease, only the myelin sheath is affected in the nerve fibers. 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 passes to the axial cylinders, which are little capable of regeneration, persistent lesions of the nervous system develop.

Typical symptoms of MS include:

Movement disorders in the form of a pyramidal syndrome with weakness and spasticity; ataxia (cerebellar, sensitive or vestibular);

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

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

Vegetative disorders: pelvic disorders - imperative urges, increased urination or urinary retention, occasional 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, Lermitte's symptom. Lermitte's symptom is a brief feeling of an electric current passing along the spine, often radiating to the arms and legs, provoked by a forward tilt of the head.

The first clinical manifestations of MS may be symptoms of damage to one or more conduction systems. The most frequently observed polysymptomatic onset, retrobulbar neuritis and pyramidal signs. Other early symptoms of MS include oculomotor disturbances, coordination disorders, facial muscle paresis, mental disturbances, 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 a change in visual fields due to retrobulbar neuritis. Sometimes there is swelling of the eyelid. Pain on eye movement and exophthalmos persist for several days. The diagnosis of MS, or "optic neuritis", is established by the presence of 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.

The characteristic features of retrobulbar neuritis in multiple sclerosis are:

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

2) relapsing 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 eye symptoms: nystagmus, ptosis of the upper eyelid, paresis of the superior rectus muscle of the eye. Visual acuity may decrease after exercise, hot baths. In the evening, vision in such patients is worse than in the morning and after physical activity during the day.

Often there is a narrowing of the field of vision in blue. The picture of the fundus may be different. If there are changes in the optic nerve head (hyperemia, edema), then they are mild. Then comes the period of improvement of visual functions. Visual acuity increases gradually or abruptly, along with this, the central scotoma also disappears. From the beginning of the decrease in visual acuity to the maximum recovery (the duration of the attack), it usually takes 1-3 months. After an attack on the fundus, a simple atrophy of the optic nerve develops, more 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 can not be seen 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 are of great diagnostic value. All these studies objectify the degree of damage to the optic nerves.

Paleness of the ONH occurs later if the lesion is located farther from the disc. Sometimes, even at an early stage, one can observe a pronounced blanching of the optic nerve head in combination with good visual functions. The intensity of blanching of the optic disc is due to the loss of the myelin coating, and good vision is due to the preservation of the axial cylinders. Gradually, complete atrophy of the optic nerve develops.

There are 4 main variants of the course of MS: relapsing (at the beginning of the disease - in 75-85% of patients); primary progredient (in 10% of patients), secondary progredient (initially relapsing course is replaced by progression with or without 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 course.

According to the Poser scale (1983), significant MS is defined in the presence of two exacerbations and clinical data on two separate foci (option A) or two exacerbations, clinical detection of one lesion and identification of another lesion using neuroimaging or EP methods (option B). In this case, 2 exacerbations should affect different areas of the central nervous system, last at least 24 hours, and their appearance should 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. MRI is the most informative for diagnosing a multifocal process in the brain, which provides sufficiently contrasting images of the soft tissues of the orbit, optic nerve, and optic pathway and shows demyelination foci in other parts of the brain.

According to the Fasex criteria, MS typically has at least three areas of increased signal intensity on T2-weighted images, two of them must be in the periventricular space and one infratentorially, and the size of the focus must 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 by isoelectric focusing. In 85-95% of patients with significant MS, oligoclonal IgG groups are detected in the cerebrospinal fluid (but not in plasma). To assess the level of intracerebral production of IgG, 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 To-urtellote 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 patients with MS in the cerebrospinal fluid, there is also an increase in the content of Ig light chains (often λ-type). However, the origin of IgG and Ig light chains and their functional significance in MS has not been elucidated.

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

Treatment

There is no etiotropic treatment to date. Treatment is carried out in conjunction with a neuropathologist. The whole complex of modern therapeutic agents for MS is divided into two groups - pathogenetic and symptomatic.

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

We present the treatment regimen proposed by Guseva M.R. (2001). Corticosteroids and ACTH preparations are used for treatment. Glucocorticoids have an anti-inflammatory effect, and by reducing the permeability of capillaries, they cause a decongestant effect. They are prescribed in shock doses: 1-5th day - 1000 mg of methylprednisolone, which is administered by drip intravenously. Then oral prednisolone is prescribed: 6-8th day - 80 mg, 9-11th day - 60 mg, 12-14th day - 40 mg, 15-17th day - 20 mg, 18-20th day - 10 mg.

Methylprednisolone is used. It is administered intravenously in course doses of 3-7 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 at 15-20 mg every other day and decreasing by 5 mg.

Dexamethasone is administered 1 time per day, 1.0 ml retrobulbarno for 5-10 days. The most effective is the introduction of the drug through the irrigation system into the retrobulbar space. Along with hormonal preparations, Gordox (Kontrykal, Trasylol), which is an enzyme-inhibitor of proteolysis, is administered through the irrigation system. Antioxidant preparations are necessarily prescribed: Essentiale, emoxipin, vitamin E.

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

Dicynone is used in the form of a retrobulbar injection of 0.5 ml No. 10-15, it can be administered intramuscularly and orally in the form of tablets. Dicinone is an angioprotector, has an inhibitory effect on LPO products and the activity of the blood kinin system. It is very good to combine retrobulbar injections of Gordox, Dicinone and Dexamethasone. To reduce edema, dehydration therapy is recommended: diacarb courses for 4-5 days at intervals of 2-3 days. You can enter furosemide 0.5-1.0 ml.

Apply dikain-adrenaline blockade of the middle nasal passage. Turunda is impregnated with a solution of dicaine 0.5% and adrenaline 0.1% (1 drop of adrenaline per 1 ml of solution). The duration of the procedure is 15-20 minutes. For a course of treatment 5 procedures every other day. Of the anti-inflammatory non-steroidal drugs, indomethacin, metindol are prescribed. Antihistamines (pipolphen) are prescribed with a change of the drug after 2 weeks. It is possible to use synakten - ACTH depot, thymus preparations are used: T-activin, thymolin and their analogues, interferon inducers and reoferon.

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

Cerebrolysin intravenously, intramuscularly, retrobulbar No. 10-15, single dose 0.5 ml. Duginov A.G. (2005) performed 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 performed, 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. Half the dose is given for the first 14 days. Due to possible complications, the drug is administered with caution.

With atrophy of the optic nerve, neurotrophic therapy, biostimulants, electrical stimulation of the optic nerve, magnetic stimulation, 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 their own 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 - with hyperreflex bladder syndrome, amitriptyline - with urge to urinate, vasopressin - with frequent nocturnal urination). Tremor is treated with β-blockers, hexamidine.

Acute disseminated encephalomyelitis

In children, the peripheral nervous system is affected.

In the foci of demyelination, gross changes in the axial cylinders are observed until their complete collapse.

Demyelination- this is damage to the nervous tissue as a result of autoallergic reactions. It begins with malaise and catarrhal phenomena from the upper respiratory tract, the temperature rises, chills, paresthesias 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, there is damage to the cranial oculomotor nerves, the bulbar group of nerves with severe dysarthria and dysphagia, in 15-20% of cases - damage to the optic nerve in the form of retrobulbar neuritis, less often congestive discs. A frequent symptom is sensitive disorders in the form of pain, paresthesia.

Patients have 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 disorder, decreased vision with persistent changes in the fundus. In 6.9% - 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 disc

It is a non-inflammatory edema of the optic nerve, in most cases due to an increase in intracranial pressure.

The term "stagnant nipple" was suggested by Grefe A. in 1860.

Initially, it was assumed that the basis of the congestive nipple is edematous impregnation of the nipple of the optic nerve, 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. ophtalmica, before flowing into the cavernous sinus through the orbital veins, anastomoses with a powerful v.facialis anterior u plexus ethmoidalis.

Another theory is inflammatory. According to this theory, disc edema is due to the content of toxins in the cerebrospinal fluid due to diseases of the brain.

Neurotropic theory saw the cause of disc edema in the irritation of the vasomotor centers by the pathological process. She has long since passed away.

Then there was the Schmidt-Mantz transport theory.

Retention theory - the theory of the delay of the centropital tissue current 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 there is an abundance of capillary network on the disk, a weak supporting mesenchymal tissue, and optic fibers are not covered with myelin, the edema of the disk can be more pronounced than the edema of the optic nerve trunk.

Why is a congestive disc the first symptom of increased intracranial pressure in some cases, while in others it is absent with pronounced signs of increased intracranial pressure? This is explained by the fact that stagnant discs occur not just with an increase in intracranial pressure, but in the phase of its decompensation, when all adaptive and compensatory mechanisms have been exhausted.

However, some more 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, the pathological processes that are present in the optic nerve itself play a less significant role than the intracranial factor.

In the etiology of a stagnant disc are important:

1. Tumors of the brain.

2. Abscesses of the brain.

3. Optochiasmatic arachnoiditis.

4. Tuberculomas.

5. Cysticercosis.

6. Echinococcosis.

7. Hemorrhages.

8. Meningitis.

9. Meningo-encephalitis.

10. Syphilis.

11. Diseases of the orbit.

12. Diseases of the kidneys.

13. Hypertension.

14. Traumatic brain injury.

15. Artriovenous aneurysms.

More often, congestive 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 flow of the stagnant disc is different. The speed of development depends on the localization of the process, and not on its size, more often these are tumors. If compression occurs in the region of the basal cisterns, the edema develops earlier.

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

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

Normally, the flow of fluid, the place of formation of which is the plexus chorioideus, from the lateral ventricles through the holes of Monroe goes to the third ventricle and then through the aqueduct of Sylvius to the fourth ventricle. Further, the fluid from the ventricular system through the openings of Luschka and Mogendi enters the subarachnoid space.

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

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

At initial phenomena stagnation, the disc is slightly hyperemic, its borders are washed away, a slight edema 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. Swelling gradually increases, veins writhe, arteries narrow. The edematous disc prominates into the vitreous body. The distance can be 6.0-7.0 diopters. This - pronounced stagnant disc.

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

With the long-term existence of a stagnant disc, atrophy gradually begins to develop. A grayish tint of the disc appears, tissue swelling decreases, the veins become less dilated, and hemorrhages resolve. This stagnant disc in the stage of atrophy. Gradually, the disc becomes even paler, the last phenomena of stagnation disappear, and a typical picture of secondary optic nerve atrophy develops: the disc is pale, its borders are washed away, the outlines of the disc are not quite 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 the stagnant disc.

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

A feature of a congestive disc (with brain tumors) is the normal state of eye functions - visual acuity, visual fields for a long period. However, visual functions can be disturbed: there are attacks of short-term decrease in vision (for 1 minute), at first rare, and then more frequent.

Visual acuity begins to decline with the onset of atrophy, sometimes so rapidly that the patient develops amaurosis within 1–2 weeks.

An increase in the blind spot can already be seen with conventional perimetry, but better with campimetry. The boundaries of the visual field, as well as visual acuity, may 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)

A stagnant disc is usually bilateral, but unilateral stagnant discs may also occur.

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

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

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

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

Diagnostics comes down to a correct differential diagnosis between a congestive disc and neuritis, between a congestive disc and pseudoneuritis, between a congestive disc and optic nerve drusen, between a congestive disc and circulatory disorders in the vascular system that feeds 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 pseudostagnation from stagnation 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 disk:

1. The venous phase lengthens.

2. Large release of matter in the area of ​​the disk.

3. Long-term residual fluorescence.

With pseudostagnation, these changes are not present. Pseudoneuritis is an abnormal development of the disc. Blind spot is normal. The dynamics of the process matter. Most often, a congestive disc has to be differentiated from optic neuritis. A congestive 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 method of studying laser retinotomography is characterized by objective high accuracy of measurements, 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 an increase in 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 effect 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. Big 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 used to be used to make drinks, which led to poisoning. The disease (rarely) can occur by inhalation of methyl alcohol vapor (lacquer, etc.). Methyl alcohol is very toxic and even small doses of it can cause a sharp decrease in vision.

The picture of methyl alcohol poisoning is quite characteristic - on the same day, general symptoms of poisoning develop, varying in intensity: headache, nausea, vomiting, gastrointestinal disorders, 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 develops in both eyes. The pupils are greatly dilated, do not react to light. The fundus of the eye at the onset of the disease is often normal, sometimes there is hyperemia of the disc or a slight phenomenon of neuritis. In rare cases, there is neuritis with edema, resembling a congestive disc, sometimes anemia of the discs: they are pale, the borders are washed away, the arteries are sharply narrowed.

The clinic of the disease can be different - often within the first month after poisoning, vision improves, up to the restoration of the initial one. This disease can be resolved. In especially severe cases, the onset of visual impairment is persistent.

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

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

There are four forms of the course of the disease:

1. Initial deterioration without subsequent improvement.

2. Initial deterioration followed by improvement.

3. Initial deterioration followed by improvement and re-deterioration.

4. Relapsing current with a number of alternating deteriorations and improvements.

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

Sometimes, when the boundaries of the field of view are narrowed, it is not marked by cattle.

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

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

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

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

Alcohol and tobacco intoxication

Alcohol and tobacco intoxication leads to disease of the papillomacular bundle. Alcoholic-tobacco amblyopia develops both on the basis of alcohol abuse and on the basis of tobacco abuse. Most of 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 proceeds according to the type of chronic retrobulbar neuritis, while both eyes are always affected. It begins as a progressive, but not a sharp drop in vision, especially twilight. Decreased vision at the height of the disease can be significant, up to 0.1 or less. There is no complete blindness.

The fundus at the beginning of the disease is mostly normal. Disc hyperemia or neuritis phenomena 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.

Changes in the visual field are characteristic - a relative central scotoma to red and green colors with normal peripheral boundaries of the visual field. These scotomas are in the form of a horizontal oval extending from the point of fixation to the blind spot and extending only a few degrees beyond the vertical meridian into the nasal half of the visual field. They are called centrocecal. Very rarely there is a central absolute scotoma in white.

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

At post-mortem examination in all cases, atrophy of nerve fibers with myelin breakdown is observed throughout the papillomacular bundle.

In areas with atrophy of nerve fibers, the complete disintegration of all the pulpy sheaths has never been noted, some of them have always been preserved.

Along with atrophy, growth of glia and connective tissue is noted. In the connective tissue, there were always no lymphocytes, plasma and other cellular forms characteristic of inflammatory infiltration.

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

In the pathogenesis of diseases of the optic nerves in alcoholic-tobacco amblyopia, hypo- and avitaminosis of the B complex of vitamins is important, therefore, it is better to include preparations containing these vitamins in the treatment.

The disease of the optic nerves in diabetes proceeds according to the type of chronic retrobulbar neuritis and occurs almost exclusively in men. Both eyes are almost always affected.

Anterior ischemic neuropathy- this is an acute circulatory disorder in the arteries that feed the optic nerve, is an eye 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 (polycythemia and chronic leukemia).

It can rarely be after extensive surgical interventions and anesthesia, with thyrotoxic exophthalmos, herpes.

But main reason are hypertension and atherosclerosis, and therefore mainly people of the older age group fall ill. But it can be at the age of 22, and at the age of 30, as there are other causes of the disease.

Approximately in patients the disease is unilateral, in the rest it is bilateral. The process on the second eye can occur in a few days or a few 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 circulatory disorders of the brain - ischemic stroke, confirmed by MRI, ischemic transient attack, myocardial infarction, coronary artery disease.

Kasymova M.S. (2005) in patients with ischemic neuropathy of the optic nerve examined blood and tears for herpes simplex virus, cytomegalovirus, toxoplasmosis, tuberculosis, streptococcus, staphylococcus aureus by polymerase chain reaction. It is believed that the herpes virus is involved in the occurrence of primary inflammation of the vascular wall of the 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 eye disease warning signs- Periodic blurred vision, severe headaches, pain behind the eye.

Visual acuity is reduced until light perception. Central scotomas appear in the field of view, there may be sector-like loss in any part of the field of view, but in 30% of cases the lower half of the field of view falls out, in 18% of cases - the temporal half.

In the acute period, the optic disc is edematous, the boundaries are washed away, there is a prominence of the disc. The edema extends to the peripapillary nerve fibers. On the surface of the disk and in the peripapillary zone, hemorrhages appear in the form of small bands located in the layer of nerve fibers. Sometimes a "soft exudate" forms on the surface of the optic disc.

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

"Star Figure" is an extravasation from the vessels of the optic disc. In patients with hypertension, the retinal vessels are changed, ampulla-shaped expansions alternate with constrictions.

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

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

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 edema and reduce extravasal pressure, which leads to the normalization of perfusion pressure. Moshetova L.K., Koretskaya Yu.M. offer complex treatment in acute situations - Cavinton intravenously, 2 ml No. 10, nicotinic acid intravenously, Mexidol 2 ml intramuscularly No. 15 and 1 ml parabulbarno No. 5, Phezam 1 tablet x 3 times a day. Patients with hypertension receive antihypertensive drugs, the use of Mexidol and Phezam in the treatment is positive. Treatment should begin as soon as possible from the onset of the disease. With temporal arteritis, prednisolone 80 mg is used, and then reduced according to the scheme.

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

The prognosis is unfavorable (defects in the visual field remain, visual acuity behaves differently - it 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.

There is a decrease in vision from 0.9 to 0.01, various defects appear in the field of view. Initially, there are no ophthalmoscopic changes in the optic nerve.

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

On fundus in addition, there are retinal changes depending on the process underlying the vascular lesion of the optic nerve. The process is mostly one-sided. Fluorescent angiogram and ERG are not changed.

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

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

Treatment: local corticosteroids, decongestant treatment, angioprotectors, vasodilator therapy, vitamin therapy. Persistent defects remain in the field of view. Visual acuity increases by 0.1-0.2 only in 50% of patients.

Vasculitis of the optic disc

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

The main complaints that patients present are a small, short-term (transient) blurring of vision, repeated several times during the day, flashing "flies" before the eyes.

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

On the fundus: the optic disc is hyperemic, edematous, the boundaries are not defined due to the pronounced edema of the peripapillary retina. Hemorrhages of various shapes and sizes are ophthalmoscopically scanned on the disk and around; there may be preretinal hemorrhages covering the disk and the posterior pole of the eye. The retinal veins are dilated, plethoric and tortuous, they are determined by exudative clutches. Throughout the fundus — polymorphic hemorrhages.

Due to cystic edema in the macular region, which occurs in patients, visual acuity fluctuates during the day, weeks, months. In the central zone of the fundus, a solid exudate appears in the form of a "star figure" (full or partial); sometimes in the paramacular region, foci of "soft exudate" are determined. In the vitreous body - a cellular reaction that can be seen with biomicroscopy.

For the diagnosis of ZIN, FAG data are important.

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

On the fundus in the macular zone, in some cases, dystrophic changes persist in the form of pathological reflexes, redistribution of pigment, white "clutches" remain along the veins, and single microaneurysms remain on the periphery.

Differentiate with congestive optic disc, CVS thrombosis, optic neuritis, hypertensive neuropathy.

The main differential diagnostic criterion with a congestive disc is the absence of cystic macular edema on carotid angiography.

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

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

CVD thrombosis develops in older patients with atherosclerosis and hypertension. Visual acuity is significantly reduced.

Optic disc vasculitis occurs in young people, with a relatively favorable prognosis. At the heart of it, obviously, is CVS endophlebitis.

Atrophy of the optic nerves in hypertension

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 the atrophy is due to 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 view along all meridians. Rarely there are central scotomas.

The reason for the development of atrophy is a violation of the nutrition of the optic nerve on the basis of the pathology of the blood vessels.

Optic nerve atrophy in 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, aggravated in the evening. Pain can radiate to different parts of the head and face, the temperature rises, hypochromic anemia is observed. The temporal arteries are painful on palpation, compacted, pulsate weakly or do not pulsate at all. Histological examination reveals complete or almost complete obliteration of the arterial 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 complete blindness. Less often vision falls gradually, within several weeks. On the fundus at the beginning of the disease - a picture of ischemic disc edema, then the swelling disappears and atrophy of the optic nerve develops. In most cases, both eyes are affected, but the eyes can be affected at significant intervals.

It is believed that edema and subsequent atrophy are due to malnutrition of the optic nerve due to obliterating arteritis.

Atrophy of the optic nerves with bleeding

It occurs after profuse bleeding of various origins, more often gastrointestinal or uterine, leading to malnutrition 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 there is a picture of neuritis with single hemorrhages in the tissue of the optic disc, there may be ischemic edema, a sharp narrowing of the arteries. In most cases, the disease is bilateral, but the degree of visual acuity decrease can be different. One eye may be affected.

In the fields of view there is a uniform or uneven narrowing of the boundaries and loss of the lower halves of the field of view.

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

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

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

Optic nerve disease in diabetes mellitus

It proceeds according to the type of chronic retrobulbar neuritis and occurs almost exclusively in men.

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

Gradually, blanching of the temporal half of the optic discs develops.

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

Atrophy of the optic nerves in atherosclerosis

Causes of atrophy: direct compression of the optic nerve by a sclerotic carotid artery and, as a result, a violation of its blood supply due to sclerosis of small arterial branches that feed the optic nerve.

Pressure on the optic nerve is more often 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 chiasm in the area where the internal carotid artery and the anterior cerebral artery cross it from below and above.

In parallel with the atrophy of the nerve fibers in the optic nerve, a slowly progressive secondary proliferation of connective tissue develops. Cicatricial 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 noted at the point where the artery enters the optic nerve trunk through the dura mater. When passing through the lamina cribrosa and in the region of the disk, i.e., in those parts of the blood vessels where their walls are subjected to increased mechanical action from the blood flow, both from vortex blood flows and from the impact of the blood stream on the walls of the vessel.

In the optic nerve on the basis of atherosclerosis as a result of malnutrition, a focus of ischemic necrosis is formed, within which the nerve fibers atrophy and glia grows. Sometimes, as a result of these changes, lamina cribrosa sinks, deep excavation of the optic disc occurs, which leads to the clinical picture of pseudoglaucoma.

On the basis of atherosclerosis, atrophy of peripheral nerve fibers can occur, between which connective tissue grows, and as a result, concentric narrowing of the visual fields is observed in old age. 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.

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

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

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

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

There may be a narrowing of the nasal half of the visual field, which is due to 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 (atrophies) of the optic nerves

Leber's optic nerve 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, more often at the age of 20-30 years, with extreme variants from 5 to 65 years.

In women, it can develop between the ages of 10 and 40 and occurs in 17.5% of cases of the total number of patients.

The disease usually begins with acute bilateral retrobulbar neuritis, rarely with an interval on the second eye of 6 months.

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

On fundus changes may not be, but hyperemia and slight edema of the optic disc are more often detected.

After 3-4 weeks, atrophy begins with predominant blanching of the temporal half of the optic disc. Visual acuity during this period increases to 0.05-0.1. In the field of view - a central or annular paracentral scotoma.

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

In general, in the neurological status at the height of the disease, a normal electroencephalogram is recorded and there are weak signs of damage to the membranes in the diencephalic region of the brain.

Pathological anatomical examination revealed 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. To calculate the probability of inheritance and determine the prognosis for the diseased and the degree of risk for healthy people allows building a pedigree and conducting molecular genetic analysis. 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 atrophy of the optic nerve

They differ from Leberovskaya in early manifestation, clinic 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, achromometry, the field of view is sharply narrowed. Nystagmus.

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

Autosomal dominant form.Develops at an older age, very slowly. Atrophy of this type never ends in blindness. The boundaries of the peripheral visual field remain normal, and visual acuity varies widely. In some patients, it may not be changed, in others it decreases to 0.1-0.2 and below.

In the field of view - central and paracentral scotomas. Color vision is upset by the acquired type.

Complicated infantile atrophy of the optic nerves of the Behr type K.

It is 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 age - visual impairment is detected with further slow progression. It does not reach complete blindness, visual acuity stops at the level of 0.2-0.4.

The fundus of the eye: at the beginning of the disease, hyperemia, then atrophy of the optic disc.

Following the eye, neurological symptoms appear - nystagmus, increased tendon reflexes, positive Babinsky's symptom, spastic muscle hypertension, bladder sphincter disorder, mental retardation. Transmitted as a simple recessive trait.

Drusen of the optic disc

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

These are small single or multiple formations of a 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 the drusen is from 1 to 3 diameters of the CVS. Gradually, the number of drusen can increase and they look like bunches. Physiological excavation disappears, the disk takes on a convex shape. The protrusion into the vitreous can be 2.0-10.0 diopters. The blood vessels on the disc are normal.

Drusen may be associated with retinopathy pigmentosa, Stargardt's macular degeneration, angioid retinal streaks, glaucoma, retinal vascular occlusion, edema, or optic nerve atrophy. Visual acuity may decrease, the blind spot is enlarged. Often there is a prolapse in the nasal half of the visual field.

There are headaches in the forehead, scattered neurological microsymptomatics.

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

It is inherited as an autosomal dominant trait.

Cysticercosis of the brain

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

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

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

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

There may be optic neuritis, rarely simple atrophy (as a symptom at a distance).

The fundus may also be normal.

Treatment of an edematous disc is reduced to the treatment of the underlying disease. In the fight against edema of the optic nerve, intravenous administration of hypertonic solutions, glycerol intake, or surgery are necessary.

Questions:

1. Why is the temporal half of the optic disc (ON) paler than the nasal one?

2. Why is the temporal half of the ONH more clear during ophthalmoscopy than the nasal one?

3. Name the inflammatory diseases of the ONH.

4. Where is inflammation localized in retrobulbar neuritis?

5. What complaints does the patient present with neuritis?

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

7. With what diseases should a congestive disc be differentiated?

8. What is anterior ischemic neuropathy?

9. What is optic disc vasculitis?

10. What diseases of the optic disc differentiate vasculitis?

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

12. What is a congestive optic disc?

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

14. What ophthalmoscopic signs are typical for secondary atrophy of the ONH?

Ophthalmoscopy - examination of the fundus with the help of special instruments (ophthalmoscope or fundus lens), which allows you to evaluate the retina, optic nerve head, fundus vessels. Determine various pathologies: places of retinal breaks and their number; identify thinned areas that can lead to the emergence of new foci of the disease.

Studies can be carried out in various ways: in direct and reverse, with a narrow and wide pupil.

Ophthalmoscopy is included in the standard examination of an ophthalmologist and is one of the most important methods for diagnosing eye diseases.

In addition to eye diseases, ophthalmoscopy helps in the diagnosis of pathologies such as hypertension, diabetes, and many others, because. it is with this study that one can visually assess the state of human vessels.

Fundus examination

An ophthalmologist, by changing the position of the eye relative to the eye of the subject and forcing him to move his gaze in different directions, can also examine the rest of the fundus.

With the maximum dilated pupil, only a small area of ​​the fundus at the limbus 8 mm wide remains inaccessible to research. The general color of the fundus is made up of the color shades of the rays emerging from the examined eye and mainly reflected by the retinal pigment epithelium, the choroid, and partly by the sclera.

1 - uniform coloring of the fundus;
2 - parquet fundus;
3 - fundus with a small amount of pigment

The normal retina, when examined in achromatic light, reflects almost no rays and therefore remains transparent and invisible. Depending on the pigment content in the pigment epithelium and in the choroid, the color and general pattern of the fundus noticeably changes. Most often, the fundus appears uniformly colored red with a lighter periphery. In such eyes, the pigment layer of the retina hides the pattern of the underlying choroid. The more pronounced the pigmentation of this layer, the darker the fundus looks.

The pigment layer of the retina may contain little pigment and then the choroid appears through it. The fundus appears bright red. It shows choroidal vessels in the form of densely intertwined orange-red stripes converging to the equator of the eye. If the choroid is rich in pigment, then its intervascular spaces take the form of elongated spots or triangles. This is the so-called spotty, or parquet, fundus (fundus tabulatus). In cases where there is little pigment in both the retina and the choroid, the fundus of the eye, due to the stronger translucence of the sclera, looks especially bright. Against this background, the optic nerve papilla and retinal vessels are more sharply contoured and appear darker. The choroidal vessels are clearly visible. The macular reflex is poorly expressed or absent.

Weakly pigmented fundus is most common in albinos, which is why it is also called albino. It is similar in color to the albino eye fundus of newborns. But their optic papilla is pale gray with indistinct contours. The veins are wider than usual. Macular reflex is absent. From the second year of life, the fundus of the eye of children almost does not differ from the fundus of adults.

Pathological changes in the vascular and retinal membranes are distinguished by considerable diversity and can manifest themselves in the form of diffuse opacities, limited foci, hemorrhages and pigmentation.

Diffuse opacities of larger or smaller sizes give the retina a dull gray color and are especially pronounced in the region of the optic nerve papilla.

Localized retinal lesions may vary in shape and size and may be light white, light yellow, or bluish yellow in color. Located in the layer of nerve fibers, they take a dashed shape; in the region of the yellow spot form a figure resembling a star.

The round shape and pigmentation of the foci are observed when the process is localized in the outer layers of the retina. Fresh focal changes in the choroid are darker than retinal and less clearly defined. As a result of the subsequent atrophy of the choroid, the sclera is exposed in these areas and they take on the appearance of white, sharply limited foci of various shapes, often surrounded by a pigmented rim. Retinal vessels usually pass over them.

Hemorrhages of the choroid are relatively rare and, being covered by the pigment epithelium, are poorly distinguishable. Fresh retinal hemorrhages have a cherry-red color and vary in size: from small, punctate extravasates to large, occupying a vast area of ​​the fundus. When localized in the layer of nerve fibers, hemorrhages appear as radial strokes or triangles with their apex facing the optic nerve papilla. Preretinal hemorrhages are round or transversely oval. In rare cases, hemorrhages resolve without a trace, but more often they leave behind whitish, gray or pigmented atrophic foci.

Disc (nipple) of the optic nerve during ophthalmoscopy

The most prominent part of the fundus is the nipple (disc) of the optic nerve, and the study usually begins with it. The nipple is located medially from the posterior pole of the eye and enters the ophthalmoscopic field of view if the examined person turns the eye to the nose by 12–15°.

The optic nerve papilla most often has the shape of a circle or a vertical oval and very rarely a transverse oval shape. Astigmatism of the examined eye can distort the true shape of the nipple and give the doctor a false impression of its shape. A similar distortion of the shape of the nipple can also be observed as a result of errors in the examination technique, when, for example, during reverse ophthalmoscopy, the magnifying glass is placed too obliquely to the line of observation.

The horizontal size of the nipple is on average 1.5–1.7 mm. Its visible dimensions, like other elements of the fundus, are much larger during ophthalmoscopy and depend on the refraction of the eye under study and the method of examination. The optic nerve papilla can be located with its entire plane at the level of the fundus of the eye (flat nipple) or have a funnel-shaped depression in the center (excavated nipple). The recess is formed due to the fact that the nerve fibers leaving the eye begin to bend at the very edge of the scleral-choroidal canal. A thin layer of nerve fibers in the central region of the optic papilla makes the underlying whitish lamina cribrosa more visible, and therefore the excavation site appears particularly light. Often here you can find traces of holes in the lattice plate in the form of dark gray dots.

Sometimes physiological excavation is located paracentrally, somewhat closer to the temporal edge of the nipple. From pathological types of excavations, it is distinguished by a small depth (less than 1 mm) and the main obligatory presence of a rim of normally colored nipple tissue between its edge and the excavation edge. A pronounced depression at the site of the optic nerve papilla can be observed in congenital colobomas. In such cases, the nipple is often surrounded by a white rim with pigment inclusions and seems somewhat enlarged. A significant difference in the level of the nipple and the retina leads to a sharp bending of the vessels and creates the impression that they do not appear in the middle of the nipple, but from under its edge.

Rarely encountered defects (pits) in the tissue of the nipple and pulpy, myelinated fibers, which look like bright white shiny elongated spots, are also associated with an anomaly of development. They can sometimes be located on the surface of the nipple, cover it; with inattentive examination, they can be mistaken for a bizarre nipple.

Against the red background of the fundus, the optic nerve papilla stands out with its clear boundaries and pink or yellowish-red color. The color of the nipple is determined by the structure and ratio of the anatomical elements that form it: arterial capillaries, grayish nerve fibers and the whitish cribriform plate underlying them. The nasal half of the nipple contains a more massive papillomacular bundle of nerve fibers and is better supplied with blood, while in the temporal half of the nipple the layer of nerve fibers is thinner and the whitish tissue of the cribriform plate is more visible through it. Therefore, the outer half of the optic papilla almost always looks lighter than the inner half. For the same reason, due to the greater contrast with the background of the fundus, the temporal edge of the nipple is outlined more sharply than the nasal one.

However, the color of the nipple and the clarity of its borders vary markedly. In some cases, only extensive clinical experience and dynamic monitoring of the state of the fundus make it possible to distinguish the normal variant from the pathology of the optic nerve papilla. Such difficulties arise, for example, with the so-called false neuritis, when the normal nipple has fuzzy contours and appears to be hyperemic. Pseudoneuritis mostly occurs in moderate and high hypermetropia, but can also be observed in myopic refraction.

Often, the optic nerve papilla is surrounded by a white (scleral) or dark (choroidal, pigmented) ring.

The first ring, also called the cone, is usually the rim of the sclera, visible as a result of the hole in the choroid through which the optic nerve passes is wider than the hole in the sclera. Sometimes this ring is formed by glial tissue surrounding the optic nerve. The scleral ring is not always complete and may be sickle or crescent shaped.

As for the choroidal ring, it is based on the accumulation of pigment along the edge of the hole in the choroid. In the presence of both rings, the choroidal ring is located more peripherally than the scleral one; often it occupies only part of the circumference.

Changes in the optic disc in various diseases

For diseases of the optic nerve , mainly proceeding in the form of inflammation or stagnation, the nipple may become red, grayish-red or cloudy red in color and the shape of an elongated oval, irregular circle, kidney-shaped or hourglass. Its dimensions, especially with stagnation, often exceed the usual 2 times or more. The borders of the nipple become fuzzy, blurry. Sometimes the outlines of the nipple cannot be caught at all, and only the vessels emerging from it make it possible to judge its location in the fundus.

Atrophic changes optic nerve accompanied by whitening of the nipple. A gray, grayish-white or grayish-blue nipple with sharp borders is observed with primary atrophy of the optic nerve; a dull white nipple with fuzzy contours is characteristic of secondary optic nerve atrophy.

There are 2 types of pathological excavation of the optic nerve papilla

1. atrophic, characterized by a whitish color, regular shape, slight depth, gentle edges and a slight bend in the vessels at the edge of the nipple.
2. glaucomatous, characterized by a grayish or grayish-green color, it is much deeper, with undermined edges. Bending over them, the vessels seem to break off and at the bottom of the excavation, due to the deep occurrence, they are less distinguishable. They are usually displaced to the nasal edge of the nipple. Around the latter, a yellowish rim (halo glaucomatosus) is often formed.

In addition to excavations of the nipple, there is also a bulging, protrusion of it into the vitreous body. Particularly pronounced bulging of the nipple is with congestion in the optic nerve (the so-called mushroom nipple).

Vessels visible in the fundus

From the middle of the nipple of the optic nerve or a little medially from the middle comes out central retinal artery(a. centralis retinae). Next to her, laterally, enters the nipple central retinal vein(v. centralis retinae).

On the surface of the nipple, the artery and vein divide into two vertical branches - top And lower(a. et v. centralis superior et inferior). Each of these branches, leaving the nipple, again divides into two branches - temporal And nasal(a. et v. temporalis et nasalis). In the future, the vessels tree-like break up into smaller and smaller branches and spread along the fundus of the eye, leaving a yellow spot free. The latter is also surrounded by arterial and venous branches (a. et v. macularis), directly extending from the main vessels of the retina. Sometimes the main vessels divide already in the optic nerve itself, and then several arterial and venous trunks immediately appear on the surface of the nipple. Occasionally, the central retinal artery, before leaving the nipple and making its usual path, twists in a loop and protrudes somewhat into the vitreous body (prepapillary arterial loop).

Distinguishing arteries from veins with ophthalmoscopy

arteries thinner, lighter than them and less crimped. Light stripes stretch along the lumen of larger arteries - reflexes formed due to the reflection of light from a column of blood in a vessel. The trunk of such an artery, as if divided by the indicated stripes, seems to be double-circuit.

Vienna wider than arteries (their calibers are respectively 4:3 or 3:2), painted in cherry red, more convoluted. The light strip along the course of the veins is much narrower than along the course of the arteries. On large venous trunks, the vascular reflex is often absent. Often there is a pulsation of the veins in the region of the nipple of the optic nerve.

In the eyes with high hypermetropia, the tortuosity of the vessels is more pronounced than in the eyes with myopic refraction. Astigmatism of the examined eye, not corrected with glasses, can create a false impression of the uneven caliber of the vessels. In many parts of the fundus of the eye, a decussation of arteries with veins is visible, and both an artery and a vein can lie in front.

Vascular changes in various diseases

A change in the caliber of blood vessels occurs as a result of violations of vascular innervation, pathological processes in the walls of blood vessels and varying degrees of their blood supply.

1. For inflammation of the retina: vasodilatation, especially veins.
2. With arterial thrombosis: the veins are also dilated, while the arteries are constricted.
3. With spasm of the arteries: the transparency of their walls is not violated
4. With sclerotic changes: along with the narrowing of the lumen of the vessels, there is a decrease in their transparency. In severe cases of such conditions, the vascular reflex acquires a yellowish tint (a symptom of copper wire). Along the edge of vessels that reflect light more strongly, white stripes appear. With a significant narrowing of the arteries and compaction of their walls, the vessel takes the form of a white thread (a symptom of a silver wire). Often, small vessels become more tortuous and uneven in thickness. Corkscrew-shaped tortuosity of small veins occurs in the region of the macula (Relman-Guist symptom). In places where the vessels cross, compression of the underlying vein by the artery can be observed (a symptom of Gunn-Salus).

Pathological phenomena also include the occurrence of arterial pulsation, especially noticeable at the site of the bending of the vessels on the papilla of the optic nerve.

Yellow spot on ophthalmoscopy

In the posterior pole of the eye lies the most functionally important region of the retina - the yellow spot (macula lutea). It can be seen if the subject directs his gaze to the light "flare" of the ophthalmoscope.

But at the same time, the pupil narrows sharply, which makes it difficult to study. It is also interfered with by light reflexes that occur on the surface of the central part of the cornea.

Therefore, when examining this area of ​​the retina, it is advisable to use non-reflex ophthalmoscopes, resort to pupil dilation (where possible) or direct a less bright beam of light into the eye.

With conventional ophthalmoscopy (in achromatic light), the yellow spot looks like a dark red oval, bordered by a shiny stripe - the macular reflex. The latter is formed due to the reflection of light from a roller-like thickening of the retina along the edge of the macula.

The macular reflex is better expressed in young people, especially in children, and in eyes with hyperopic refraction.

The macula lutea is surrounded by separate arterial branches, somewhat reaching its periphery.

The size of the yellow spot varies markedly. So, its larger horizontal diameter can have a value from 0.6 to 2.9 mm. In the center of the yellow spot is a darker round spot - the central fossa (fovea centralis) with a shiny bright dot in the middle (foveola). The diameter of the central fossa averages 0.4 mm.

Under optic nerve atrophy is understood as a gradual process of the death of the optic nerve fibers with their subsequent replacement with connective tissue, while the light signal received by the retina of the eye is converted into an electrical signal, after which it is transmitted to the posterior lobes of the brain with various disorders, resulting in a narrowing of the fields and a decrease in visual acuity.

Causes of atrophy

In most cases, optic nerve atrophy is the result of a whole group of pathological processes occurring in the body, although in some cases doctors have to deal with hereditary optic nerve atrophy, which can occur both immediately after birth and after a certain period of time.

Diseases of the retina and diseases of the eyeball, as well as its structures, can lead to atrophy.
Diseases of the optic nerve leading to its atrophy:

• inflammation
• stagnation
• injury
• circulatory disorders
• toxic damage

Diseases of the central nervous system leading to atrophy of the optic nerve:

• chronic diseases
• brain injury
• multiple sclerosis
• meningitis
• encephalitis
• syphilitic brain injury
• tumors

In addition, optic nerve atrophy can develop as a result of diseases of the cardiovascular system (arterial hypertension), atherosclerosis, beriberi, and massive and profuse blood loss.

Disease classification

To date, there are several types of optic nerve atrophy.

It is customary to distinguish between congenital and acquired atrophy of the optic nerve.

Under congenital atrophy of the optic nerve refers to atrophy due to genetic diseases in which the patient and vision suffer from birth. The most common disease in this group is Leber's disease.

Under acquired optic nerve atrophy refers to atrophy resulting from damage to the optic nerve fibers (so-called descending atrophy) or retinal cells (so-called ascending atrophy).

The causes of acquired atrophy of the optic nerve can be inflammation, trauma, toxic damage or circulatory disorders in the vessels of the optic nerve, compression of the optic nerve fibers by a tumor, metabolic disorders.

In addition, it is customary to further distinguish between primary and secondary atrophy of the optic nerve, which is detected during ophthalmoscopy.

With primary (the so-called simple) atrophy, the disc is pale, while its boundaries are clear, narrowing of the retinal vessels, flat excavation is possible.

With secondary atrophy, which develops as a result of inflammation of the optic nerve or its stagnation, there are signs characteristic of primary atrophy, with the only difference being that in this case the boundaries of the optic nerve head are fuzzy.

In addition to this, it is customary to distinguish partial and complete atrophy of the optic nerve, which depends on the amount of damaged nerve tissue.

With partial (initial) atrophy of the optic nerve, partial preservation of vision is observed, while visual acuity is reduced (it cannot be increased by the selection of glasses or lenses), although residual vision is preserved, color perception suffers, and intact areas of vision remain in the field of view.

Meanwhile, atrophy of the optic nerve can be stationary (stable visual functions are noted) or progressive (a steady decrease in visual acuity is noted), as well as unilateral or bilateral.

Symptoms

The clinical picture of optic nerve atrophy consists of the following symptoms:

• central and sector-shaped scotomas
• field of view is concentrically narrowed
• decreased central vision
• constriction of retinal arteries
• flat excavation formation
• pale optic disc

With secondary atrophy of the optic nerve during ophthalmoscopy, it is additionally possible to identify:

• vasoconstriction
• smoothing the borders of the optic nerve head
• varicose veins
• light disc prominence
• disc blanching

It should be noted that for nerve atrophy caused by sclerosis of the internal carotid artery, nasal or binasal hemianopsia is characteristic.

Diagnosis of the disease

Diagnosis of optic nerve atrophy should be comprehensive and include the following diagnostic methods:

• ophthalmoscopy
• perimetry
• visometry
• color vision test
• X-ray of the skull (optional Turkish saddle)
• fluorescein angiography
• CT scan
• NMR scan of orbit, brain

Treatment of optic nerve atrophy is a rather complicated and time-consuming process for doctors, since it must be remembered that it is impossible to restore dead optic nerve fibers. In addition, there are many causes of optic nerve atrophy, so the diagnostic search can take a long time.

Treatment of the disease can be carried out in three directions:

• conservative treatment
• physiotherapy treatment
• surgery

Conservative therapy implies the appointment of symptomatic treatment, including:

• vasodilators;
• drugs that improve the blood supply to the optic nerve (eufillin, trental, no-shpa, nicotinic acid, papaverine)
• anticoagulants (tiklid, heparin)
• drugs that improve metabolic processes in nerve tissues (biogenic stimulants, enzymes, amino acids, immunostimulants)
• drugs whose action is aimed at stimulating metabolic processes and resolving pathological processes (preductal), stopping the inflammatory process (hormones), improving the functioning of the nervous system (cavinton, nootropil, emoxipin)

Electro-, magneto- and laser stimulation of the optic nerve are prescribed as physiotherapeutic procedures.

Surgical treatment of optic nerve atrophy involves surgery to remove formations that compress it, ligate the temporal artery, and implant various biogenic materials that improve blood circulation and vascularization of the nerve.

Treatment with folk remedies

When treating optic nerve atrophy with folk methods, it should be remembered that as a result of such treatment, precious time can be lost in diagnosing the disease and prescribing adequate and timely treatment. With atrophy of the optic nerve, folk remedies are ineffective.

Disease prognosis

With timely treatment, it is possible to completely restore vision and stop the pathological process, while in advanced cases, the development of partial or complete blindness is observed.

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 lutea (s. macula lutea) with the central fovea (fovea centralis). The yellow spot is located outside approximately 2 diameters of the disk from its temporal border; its center is slightly below the horizontal line passing through the middle of the disc. The yellow spot stands out in a darker color; it has the form of a horizontally located oval, along the edge of which often, especially at a young age, a silvery-white arc or ring is noted - a macular reflex. This light reflex occurs due to the thickening of the retina in the form of a roller 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 yellow spot stands out less clearly, while light reflexes are usually weakly expressed or completely absent; its position in this case is judged by a darker color and the absence of blood vessels.

With conventional ophthalmoscopy, the yellow color of the spot is indistinguishable against the red background of G.; it can be seen only with ophthalmoscopy in redless light, proposed by Vogt (A. Vogt, 1913). This method is used to study the retina and optic disc. When examining with a light source devoid of red rays using a blue-green light filter, G. appears to be colored green-blue, the retinal vessels appear almost black, the yellow spot is lemon-yellow, and thin vascular branches can be found in it, invisible during conventional ophthalmoscopy (printing. Fig. 5), since short-wave rays are reflected mainly from the surface of the retina. Dimmer (F. Dimmer) found that the yellow color depends on the pigment located in the retina in the macula. In addition to redless, for ophthalmoscopy, light colored differently with the help of light filters is used.

In 1960, a comprehensive method for the study of G. by light of various spectral compositions was developed, including comparative ophthalmoscopy in blue, yellow, red, redless, yellow-green and purple light (see Ophthalmoscopy).

In the study of G. in redless and yellow-green light, you can see the course and distribution of the nerve fibers of the retina. These fibers in the form of white stripes start from the disk, bend over its edge and diverge in a fan-like fashion. 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. At the macula, some fibers are steeply bent, take a vertical direction, and, bordering the macula from the temporal side, are lost in it. The fibers going up and down from the disc do not participate in the formation of the papillomacular bundle; they bend and cross at an obtuse angle, and partly, without crossing, go to the periphery. The blood circulating in the vessels of the retina and choroid can be determined by fluorescein angiography (see). With its help, it is possible to clarify the causes of circulatory insufficiency in the vessels of the retina (obturation, spasm), to identify patol, processes in the macula and optic nerve that are indistinguishable during ophthalmoscopy, to differentiate tumor and inflammatory processes, early vascular changes in diabetes.

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

Pathological changes in G. are caused by damage to the optic nerve, the retina and vascular membranes of the eye, as well as the boundary membrane of the vitreous body.

Ophthalmoscopically, with damage to the optic nerve, there are changes accompanied by hyperemia and edema of the optic disc - congestive nipple, ischemic disc edema, pseudocongestive nipple (see Congestive nipple), neuritis; atrophic changes (primary and secondary atrophy of the optic nerve), tumors of the optic disc and developmental anomalies (see Optic nerve). In some cases, changes are detected ophthalmoscopically only when the process, having begun 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 of diffuse opacities in it or limited white foci, hemorrhages and dyspigmentations, vascular changes. These changes are based on inflammatory (see Retinitis), circulatory-metabolic (see Retinopathy), dystrophic processes, circulatory disorders and developmental anomalies (see Retina).

Changes in the choroid, visible during ophthalmoscopy, are the result of inflammatory, degenerative, sclerotic processes, neoplasms and developmental anomalies. In most cases, inflammatory processes of the choroid are focal in nature (see Choroiditis). At the same time the pigment epithelium of a retina is involved in process owing to what in the field patol, changes there is an accumulation of lumps of a pigment. Gradually, on the site of inflammatory foci, atrophic changes occur, which are the main ophthalmoscopic sign of damage to the choroid. Some changes in G.'s, for example, the protrusion of the disc with a congestive nipple, a mottled reflex on the arteries with diabetic retinal angiopathy, are better detected with ophthalmochromoscopy. Microaneurysms in diabetic retinal angiopathy are well detected by fluorescein angiography.

Clinical and diagnostic characteristics of fundus changes

Rice. 6 - 10. Pathological changes in the fundus. Rice. 6. Neurofibromatosis. Rice. 7. With 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. The initial congestive nipple (the arrow indicates the arc around the nipple light reflex). Rice. 12. A pronounced congestive nipple, at the upper edge of its hemorrhage (indicated by an arrow). Rice. 13. Pseudocongestive nipple on the basis of drusen (indicated by arrows). Rice. 14. Pseudo-congestive nipple on the basis of drusen hidden in its depth (indistinguishable from a true congestive nipple). Rice. 15. Hidden druse (indicated by an arrow) (distinguishable with ophthalmochromoscopy). Rice. 16. Optic neuritis. Rice. 17. Primary (simple) atrophy of the optic nerve. Rice. 18. Secondary atrophy of the optic nerve (arrow indicates an atrophic corolla around the disc). Rice. Fig. 19. Atrophic optic disc when examined in normal light (Fig. 19 and 20 the image is enlarged). Rice. 20. An atrophic optic disc appears blue when examined in purple light. Rice. 21. Axial (axial) atrophy of the optic nerve (arrow indicates blanching of the temporal half of the disc). Rice. 22. Axial atrophy of the optic nerve when examined in purple light (pale temporal half appears blue). Rice. 23. Axial atrophy of the optic nerve when examined in yellow-green light - 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 (arrow indicates hemorrhage). Rice. 26. Obstruction of the branch of the central retinal vein when examined in redless light (arrow indicates hemorrhage).

Rice. 27-42. Rice. 27. Obstruction of the central retinal artery (arrows indicate narrowed arteries). Rice. 28. Hypertensive angiopathy of the retina (Gwist symptom). Rice. 29. Symptom 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 decussation of the third degree (Salus III; indicated by the arrow). Rice. 32. Hypertensive retinopathy. Rice. 33. Hypertensive retinopathy (the arrow indicates the figure of a star). Rice. 34. Ischemic edema of the optic disc. Rice. 35. Dry form of senile macular degeneration. Rice. 36. Wet form of senile macular degeneration (indicated by an arrow). Rice. 37. Ring dystrophy of the retina (the arrow indicates the shape of the ring). Rice. 38. Hypertensive neuroretinopathy (the arrow indicates the figure of a star). Rice. 39. Diabetic angiopathy of the retina. Rice. 40. Microaneurysms on examination in normal light. Rice. 41. Microaneurysms on examination in redless light (the same area as in Fig. 40). Rice. Fig. 42. Microaneurysms in fluorescein angiography. Fig. 42. 6. Neurofibromatosis. Rice. 7. With 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 in anemia. Rice. 47. Retinopathy in polycythemia. Rice. 48. Retinopathy in chronic lymphocytic leukemia (arrow indicates light foci bordered by hemorrhage). Rice. 49. Rheumatic retinovasculitis. Rice. 50. Disseminated tuberculous chorioretinitis (arrow indicates a light focus). Rice. 51. Disseminated tuberculous chorioretinitis on examination in blue light. Rice. 52. Central tuberculous chorioretinitis. Rice. 53. Central tuberculous chorioretinitis on examination in redless light. Rice. 54. Tuberculous retinal periphlebitis (arrows indicate muffs on veins). Rice. 55. Congenital toxoplasmic chorioretinitis (arrows indicate atrophic foci). Rice. 56 and 57. Congenital syphilitic chorioretinitis. Rice. 58. Diffuse syphilitic neuroretinitis - atrophy of the choroid.

Bibliography Arkhangelsky VN Morphological bases of ophthalmic 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 with the help of instruments, L., 1971; Multi-volume guide to eye diseases, ed. V. N. Arkhangelsky, vol. 1, book. 2, p. 16, M., 1962, bibliography; Plitas P. S. Ophthalmoscopic atlas, M., 1960; Radzikhovsky B.A. Ophthalmoscopic diagnostics (with an ophthalmoscopic atlas), Chernivtsi, 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. y. 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.

H. K. Ivanov; tabular compiler. A. M. Vodovozov.