Drusen on the fundus. Dominant retinal drusen - causes and treatment

Drusen (from the German "druse" - gland) are yellowish-white deposits localized in Bruch's membrane and pigment epithelium.

The histological picture of drusen was first presented by S. Wedl in 1854, and a little later their clinic was described by F. C. Donders (1855). Later in the literature, dominant hereditary retinal drusen were found under many names: “Hutchinson-Tye choroiditis”, “familial choroiditis”, “Guttata choroiditis”, “superficial Holsous-Batten choiretinitis”, “crystalline retinal degeneration”, “hyaline dystrophy”, “honeycombing” Doine's degeneration", "Leventin's disease", etc.

The similarity of origin and histological findings indicate that this is the same disease. L.G. Hyman et al. (1983), based on the results of a study of patients with drusen and senile macular degeneration, came to the conclusion that there is a significant connection between hereditary drusen and the development of age-related macular degeneration

The term “dominant drusen” can be used only in cases where they are observed in members of the same family and are reliably confirmed when they are detected in individuals in relatively early age, which indicates the hereditary nature of drusen, inherited in an autosomal dominant manner. They usually appear at the age of 20-30 years, but cases of their occurrence have been described at 8-12 years. However, variability in expression and incomplete penetrance of the gene served as the basis for genetic errors when making a diagnosis.

Drusen of Bruch's membrane should not be identified with drusen of the optic disc. According to some researchers, these ophthalmoscopically similar formations differ in structure, as revealed in histological studies. At the same time, no differences were noted between hereditary drusen of Bruch's membrane and drusen visible ophthalmoscopically in senile macular degeneration, which was confirmed by histological, microscopic and ultrastructural studies. In this regard, hereditary drusen are now considered as the initial stage of age-related macular degeneration, previously called senile macular degeneration.

J. Gass (1977) noted that patients with familial drusen have the same hereditary degenerative eye disease, which is often the cause of decreased vision in the sixth and seventh decades of life. Due to variable gene expression and incomplete penetrance, it is sometimes difficult to accurately determine the number of affected individuals in one family. Based on the results of numerous studies of patients 50 years of age and older, it was found that the incidence of drusen increases with age and they are slightly more common in men.

Pathogenesis

According to A.E. Krill (1972), exist three theories of the origin of drusen .

• In the first - transformation - the formation of drusen is considered as a direct transformation of pigment epithelial cells.
• The second, the deposit or secretory theory, suggests that drusen are formed as a result of secretion and deposition of abnormal pigment epithelial cells.
• The third theory is chorovascular: it is assumed that drusen are a product of hyaline degeneration of the chorocapillaries or the organization of chorocapillary hemorrhages. However, the chorovascular theory of the source of drusen did not find histological confirmation.

Histological studies Drusen showed that they consist of two main components: mucopolysaccharide (sialomucin) and lipid - cerebroside. It is believed that these substances are formed in degenerative pigment epithelium. Drusen, which are located in the inner portion of Bruch's membrane, are adjacent to the pigment epithelium and are formed as a result of its autophagic destruction associated with abnormal lysosomal activity. As the process progresses a large number of lysosomes in pigment epithelial cells apparently turn into an amorphous material that fills the inner collagen zone of Bruch's membrane. The size of drusen varies and they can become calcified. The retinal pigment epithelium covering the drusen undergoes a number of changes.

Initially, pigment dissipation occurs in its cytoplasm, accompanied by degeneration of mitochondria and displacement of the nucleus. In the final stage, degenerated pigment epithelial cells fuse with drusen, resulting in the formation of areas where pigment epithelium is absent. Photoreceptors are displaced and exposed dystrophic changes. The formation of drusen in connection with the transformation of pigment epithelial cells is a confirmation of the transformation theory, and the deposition of cells of altered pigment epithelium is a confirmation of the deposit theory.

Further development of drusen leads to either the development of non-exudative predisciform macular degeneration or its exudative disciform form with choroidal or subretinal neovascularization. These transformations occur later, in the fifth to sixth decades of life, while hard drusen contribute to the development of atrophic changes, while soft confluent drusen, especially those located bilaterally, lead to exudative detachment of the pigment epithelium and other complications that determine the further progression of the process.

Clinical picture

In some patients, drusen are asymptomatic, while in others, maculopathy may develop against the background of drusen at a relatively young age. In the fundus, drusen vary in number, shape, size and color, and can be single or multiple. The ophthalmoscopic picture of drusen is very variable among members not only of different families, but also of the same family.

At first these are small round spots, lighter than the surrounding fundus background, which over time acquire a bright yellow color. According to D.A. Newsome (1988), their first diagnosis is possible angiographically rather than ophthalmoscopically. The authors of this chapter do not share this point of view. It is believed that drusen localized medially from the optic nerve head, or multiple ones covering almost the entire fundus of the eye, are dominant drusen. As a rule, they are found in the central zone and in the middle periphery. In rare cases, drusen may be observed only in the middle periphery and absent in the center. Drusen may be peripherally located, sometimes with reticulate pigment, causing them to resemble Sjögren's reticular dystrophy or "bunch of grapes".

Over time, the size and number of drusen increase, they merge, calcify, and raise sensory retina. In very rare cases, the number of drusen may decrease. Noticeable changes also occur in the pigment epithelium covering the drusen. It becomes thinner, loses pigment, and pigment accumulations appear around the drusen. These changes in the pigment epithelium are observed in the macula between drusen and can lead to atrophy of pigment epithelial cells.

S.H. Sarks et al. (1996) distinguish two main types of drusen - soft and hard. Hard drusen are small, multiple, hyalinized, crumbly in shape, often calcified, and, as a rule, do not merge. In soft drusen, the hyaline material is destroyed. They are usually larger and tend to merge.

Drusen can be located above and below the basement membrane of the pigment epithelium, and sometimes they are found in the chorocapillary layer. As a rule, drusen are an ophthalmoscopic finding, since they are asymptomatic, even if they are localized in the fovea; in rare cases, patients complain of metamorphopsia. Visual acuity does not decrease, there are no defects in the visual field.

During fluorescein angiography, drusen begin to fluoresce in the early phases with gradually increasing intensity, which quickly decreases in the late venous phase. Typically, angiography reveals a significantly larger number of drusen than with ophthalmoscopy. Hard drusen, even in places of their accumulation and apparent fusion, are visible on FA as individual hyperfluorescent dots. In rare cases, fluorescein angiograms show hypofluorescence of drusen due to their calcification or pigmentation.

Differential diagnosis

Drusen should be differentiated from a number of diseases characterized by yellowish or whitish deposits in the posterior pole of the eye, which, together with hereditary drusen, are attributed to A.E. Krill (1977) on flecked retina syndrome:

1. fundus punctatus albescens - white-spot abiotrophy of the fundus, in which white spots, similar to drusen, are identified in the middle periphery of the fundus. This disease is characterized by a sharp decrease in vision and progressive nyctalopia, similar to early and light forms retinal pigment abiotrophy.
2. fundus albipunctatus, or fundus albuta, a bilateral hereditary pathology, the ophthalmoscopic picture is similar to both the previous disease and hereditary drusen, but differs from them in the non-progressive course and stationary nature of night blindness, occurs without a decrease in vision.
   An ophthalmoscopic examination at the level of the pigment epithelium reveals whitish dotted round spots of the same shape, occupying a large area of ​​the fundus with maximum density in the equatorial and macular areas. In contrast to fundus albipunctatus, dominant drusen are more variable in size and more prominent in the macular area.
3. fundus flavimaculatus, or yellow-spotted fundus, a bilateral disease, which, in contrast to smooth, round, clearly bordered dominant drusen, is characterized by yellowish deposits at the level of the pigment epithelium in the form of spots.
   Angiography often reveals a block of choroidal fluorescence in the posterior field and in the periphery, which is never observed with dominant hereditary drusen. Another difference between fundus flavimaculatus is its frequent combination with bull's-eye macular degeneration, which never occurs with hereditary drusen. Visual acuity decreases when this pathology is combined with Stargardt disease. Fundus flavimaculatus is characterized by a narrowing of the field of vision, which does not happen with drusen.
4. Bietti's dystrophy or crystalline dystrophy, which is also characterized by whitish deposits on the retina, but unlike dominant drusen, they have a polygonal shape with a “diamond-white” sheen and are localized in all layers of the retina. The disease is characterized by a progressive decrease in visual function and marginal corneal dystrophy.

The invention relates to ophthalmology, namely to methods for treating optic disc drusen. Technical result: elimination of compression of nerve fibers by drusen. The essence of the invention: the projection zone of the optic nerve through the closure of the eyelids is exposed to a pulsed electric shock with a pulse voltage from 10 to 500 V with a duration of 80 μs or in bursts in sweep mode with a pulse repetition rate within one systole from 20 to 50 Hz for 10 - 14 days for 15 - 25 minutes. 1 table

The invention relates to medicine and can be used for the treatment of optic disc drusen. There is a known method of treating optic disc drusen with a therapeutic method, including detoxification agents, desensitizing and vitamin therapy (Spencer, Tso, Am. J. Ophthalmol. Vol. 85, No. 1, 1978, pp. 1-12). Considering that the presence of optic disc drusen is accompanied by the development and progression of atrophy of nerve fibers, and acute circulatory disorders in the retinal vessels are also possible, which leads to a decrease or loss of visual functions, the issue of timely and adequate treatment of optic disc drusen remains relevant to this day. por (Harris M.J., Fine S.J., Owens S.L., Am J Ophthalmol 1981, 92. p. 70 - 72). The objective of the invention is to create a method for treating optic disc drusen in order to improve visual function in case of optic nerve atrophy caused by compression of nerve fibers by drusen and preventing irreversible acute disorders blood circulation in the optic nerve head through electrical stimulation treatment. The technical result achieved by using the invention is the restoration of visual functions by eliminating compression of nerve fibers by drusen. The technical result is achieved by the fact that in the method of treating drusen of the optic nerve head through the skin of the eyelids, the projection area of ​​the optic nerve is exposed to a pulsed electric current with a voltage in the pulse from 10 to 500 V with a duration of 80 μs in batches in the “sweep” mode with a pulse repetition frequency within 1 th systole from 20 - 50 Hz and the duration of the "sweep" pack within 0.3 s for 10 - 14 days for 15 - 25 minutes. When using an electric charge of less than 20 Hz and less than 10 V, a weak stimulating effect is noted, which does not lead to an increase in blood supply to the vessels, a change in nerve conduction. The use of an electric charge of more than 50 Hz and more than 500 V leads to loosening and fiberization nerve tissue. To achieve a stimulating effect, the session time should not exceed 25 minutes, as this can lead to microhemorrhages in the choroid. The stimulation time should not be less than 15 minutes, since this is the time required to achieve a stimulating effect in neuroglial tissue. The treatment period is at least 10 days, since this time is necessary for full recovery biochemical processes of neuroglia, more than 14 days is impractical, it can cause damage to the nervous tissue. For an objective assessment of quantitative changes occurring in the optic nerve head under the influence of an electric field, visometry, computer perimetry, determination of electrical lability, computed tomography. The examination was carried out before electrical stimulation, after the first and tenth sessions, and also 3, 6, 12 months after treatment. The method was carried out as follows. The patient was treated in a sitting position. The active electrode was placed on the eye, the other electrode was placed on the eye, and the patient held the other electrode in his hand. Electrical stimulation parameters (voltage, procedure duration and number of sessions) were selected individually for each patient depending on the initial condition. The proposed method allows, without direct contact with the posterior pole of the eye, to non-invasively treat optic disc drusen, increasing visual acuity, expanding the boundaries of the visual field and reducing the number of absolute scotomas in the visual field, increasing foveal photosensitivity. Comparative data from examining the eyes of patients after electrical stimulation are given in the table. There were no adverse events in any case6 positive result was received in 97%. Clinical example. Patient Z., 66 years old, a/k 256254. Diagnosis: Optic disc drusen, partial atrophy optic nerve of both eyes. I completed a course of electrical stimulation of the optic nerve of both eyes for 10 days for 20 minutes with a pulse voltage of 100 V, in the “sweep” mode with a pulse repetition rate within the first systole of 20 Hz and a “sweep” duration of 0.3 seconds. Visual acuity of the right eye before treatment was 0.9 with correction, of the left eye 0.4 with maximum correction. After a course of electrical stimulation, the patient noted a significant improvement. Objectively: visual acuity of the right eye is 1.0, the left eye is 0.7 with correction. Computer perimetry determined positive dynamics: the number of absolute scotomas on the right eye decreased from 59 to 50, on the left from 61 to 42 out of 120 examined points.

Claim

A method of treating optic disc drusen, characterized in that the area of ​​projection of the optic nerve through closed eyelids is exposed to a pulsed electric current with a pulse voltage of 10,500 V, a duration of 80 μs, or in bursts in a “sweep” mode with a pulse repetition frequency within one systole 20-50 G for 10-14 days for 15-25 minutes.

Dry macular degeneration is chronic disease which leads to a decrease or loss central vision. The dry form of macular degeneration of the retina is the most common, its symptoms varying degrees severity are diagnosed in 90% of patients with macular degeneration. Dry macular degeneration occurs when the retinal pigment epithelium is damaged or thinned. The retinal pigment layer is located directly below the light-sensitive layers of the retina of the eye, its functions primarily include feeding the photoreceptors.

The death of these retinal cells is called atrophy, as a result of which the dry form of macular degeneration of the retina is often called atrophic. Dry macular degeneration is characterized by the presence of drusen (point deposits under the retina yellow color, crystalline structure) and thinning of the photoreceptors of the macular zone.

Macular degeneration of the retina. What are retinal drusen?

Drusen are nothing more than deposits colloidal substances, the accumulation occurs in the space between Bruch's membrane and the retinal pigment epithelium. According to the classification, drusen are divided into hard and soft. They are the most common early sign of dry macular degeneration. Histologically, drusen are composed of lipids. The main reason for their occurrence in macular degeneration of the retina is a violation of the excretion of waste products due to the death of retinal photoreceptors.

Dry macular degeneration. Symptoms

In the early stages, dry macular degeneration may be asymptomatic, at least until it affects both eyes. The first symptom of macular degeneration is usually distortion of straight lines.

Symptoms of macular degeneration:

• Straight lines in the central field of vision are distorted
• Dark or white, blurry areas in the central field of vision are distorted
• Impaired perception of colors or their shades
• Distortions on the Amsler test

Dry macular degeneration. Prevention and treatment

There are a number preventive measures aimed at reducing the risk of developing macular degeneration, as well as aimed at slowing its progression. Clinical studies carried out around the world have identified a number of risk factors. If you have macular degeneration, there are a number of medications that can slow the progression of the disease by as much as 25%.

Macular degeneration. Initial stage.

Currently, in the arsenal of ophthalmologists there are no methods or drugs aimed at treating the early stages of dry macular degeneration. However, if you find initial manifestations Macular degeneration of the eye requires a complete ophthalmological examination once a year. This frequency of examinations will allow us to assess the degree of progression and take the necessary steps. therapeutic measures already in the early stages.

As for prevention, quitting smoking and eating vegetables, salads and seafood can prevent the progression of the disease.

Macular degeneration. Intermediate and late stage.

Research by the National Eye Institute (USA) aimed at identifying a pattern between the intake of dietary supplements and the progression of macular degeneration has been carried out in the last few years. According to their data, daily consumption of certain vitamins and minerals in high doses can slow the progression of dry macular degeneration.

According to the AREDS study, a combination of vitamin C, vitamin E, beta-carotene, zinc and copper can reduce the risk of developing and developing macular degeneration by 25 percent. The AREDS2 study aimed to identify the positive effects of adding lutein, zeaxanthin and omega-3 to previously described microelements. fatty acids. According to the authors, the inclusion of lutein and zeaxanthin or omega-3 fatty acids in the drug does not affect the risk of progression of macular degeneration. However, the same study showed that replacing beta-carotene in the original drug with lutein and zeaxanthin helps reduce the risk of developing and progressing the disease. In addition, a pattern of influence of beta-carotene on an increased risk of developing lung cancer in former and current smokers was identified, while no connection was found with the intake of lutein and zeaxanthin.

Clinically effective dosages:

1. 500 milligrams (mg) vitamin C
2. 400 international units of vitamin E
3. 80 mg zinc as zinc oxide
4. 2 mg copper as copper oxide
5. 15 mg beta-carotene or 10 mg lutein and 2 mg zeaxanthin

A number of dietary supplements based on these studies are labeled "AREDS" or "AREDS2" on their labels.

Dry macular degeneration. Treatment

If you have an intermediate or late stage of the disease, take biological active additives may have a positive effect on the course of the disease. However, when choosing a drug, you must check the composition on the label. Many of the supplements have different composition and different dosages that do not always correspond to those tested in clinical studies. In addition, it is necessary to consult a doctor before taking it to exclude side effects.

If there is a risk of developing late stage macular degeneration of the retina, you must take dietary supplements tested in studies, even if you take a daily multivitamin. Such preparations contain much higher doses of vitamins and minerals.

However, as you already understood, currently specific treatment does not exist. Macular degeneration is a natural process of aging of the eye. In order to prevent this process from affecting you or to slow it down, you must at least change your daily lifestyle. Quitting smoking, wearing sunglasses is healthy balanced diet, rich in antioxidants. It should be remembered that dry macular degeneration, as a rule, if it leads to vision loss, it is gradual. The development of visual impairment occurs over many years.

The term "druze" translated from German language means iron. This formation is a deposit in the pigment epithelium and Bruch's membrane and has a yellowish-white color.

Drusen were first described in 1854 by the histologist Veld, and a little later Donders described their clinical picture. In the literature, hereditary dominant drusen are described under different names (Holsous-Batten superficial choroiditis, Guttata choroiditis, familial choroiditis, Hutchinson-Tye choroiditis, Doine honeycomb degeneration, hyaline dystrophy, Leventin's disease, crystalline retinal degeneration).

Due to similar histological and clinical picture it was found that all these diseases represent the same pathology. Back in 1983, Hyman et al established that there is a significant association between age-related macular degeneration and hereditary drusen.

The term dominant drusen refers only to those changes that are detected in members of the same family, as well as those detected at an early age, which indicates the hereditary nature of the formation. The type of inheritance of drusen is autosomal dominant. Most often, the disease is diagnosed in young people aged 20-30, but there are cases of more early diagnosis(8-12 years old). At the same time, when making a diagnosis, genetic errors cannot be excluded, which can be explained by incomplete pentrance of the gene or variability of its expression.

Bruch's drusen and optic disc drusen are various diseases. Externally, with ophthalmoscopy, both of these formations are similar, but upon histological evaluation, differences are revealed. At the same time, Bruch's drusen and formations that are detected against the background of senile macular degeneration are similar in both macroscopic and histological structure. In this regard, hereditary drusen are considered the initial stage of age-related macular degeneration.

In 1977, scientist Gass discovered that patients in whom familial drusen were detected during ophthalmoscopy also suffered from another hereditary degenerative eye disease. This is the cause of vision loss at older ages (60-70 years). Due to the characteristics of the gene, it can be difficult to establish the true number of affected people within one family. Based on data obtained from numerous studies, it was determined that the likelihood of drusen formation increases with age, and men are more prone to this disease.

Our doctor's video about drusen

Pathogenesis

There are three known theories that explain the formation of drusen:

• The transformation hypothesis is based on the fact that drusen are formed from pigment epithelial cells that undergo transformation.
• The depository (secretory) theory explains the formation of drusen by the deposition of abnormal pigment epithelial cells, which appear through secretion.
• The choriovascular theory suggests that drusen are a product of hyaline degeneration that affects the choriocapillaris, as well as the organization of choriocapillary hemorrhages. This theory, unlike others, has no histological evidence.

Histological analysis of drusen revealed that it contains two main components: cerebroside, which is a lipid, and sialomucin, which is a mucopolysaccharide. Scientists believe that these substances are formed during the degeneration of pigment epithelial cells. Drusen on the inner part of Bruch's membrane are adjacent to the pigment epithelium and are formed during autophagic destruction, which is associated with increased lysosomal activity. As it progresses pathological process Most of the lysosomes, which are located in the pigment epithelium, gradually turn into an amorphous material. This substance fills the internal collagen zone in the area of ​​Bruch's membrane. The size of drusen may vary and they may become calcified.

At the same time, epithelial pigment cells also undergo transformation. First, the pigment disperses in the cytoplasm, which leads to mitochondrial degeneration and nuclear translocation. Ultimately, pigment epithelial cells fuse with drusen, that is, areas devoid of pigment epithelium are formed. Photoreceptor cells are displaced and also suffer from dystrophy. The formation of drusen against the background of transformation of pigment epithelial cells speaks in favor of the transformation theory, while the deposition of altered pigment cells speaks in favor of the secretory theory.

With further growth of drusen, either non-exudative predisciform macular degeneration or exudative disciform form occurs, accompanied by subretinal or choroidal neovascularization. Typically, such changes are formed by the age of 50-60 years. Hard drusen lead to the development of cell atrophy, and soft or confluent drusen lead to exudative detachment of the pigment epithelium.

Clinical picture

Sometimes drusen may not be accompanied by any symptoms, but in some cases maculopathy develops, including in young patients. With ophthalmoscopy, you can identify different numbers of drusen, which differ in shape, color, and size. External manifestations very diverse.

Most often, in the early stages, drusen appear as small round spots that are lighter than the surrounding fundus tissue. Over time, the drusen become yellow. Some authors believe that it is easier to identify early signs drusen with angiography than with ophthalmoscopy. However, not all scientists adhere to this point of view. Typically, drusen located medially to the optic disc are dominant. Also called dominant are multiple drusen that cover most of the fundus. They can usually be identified in the central region and mid-periphery. It is extremely rare that drusen are absent in the center, but are located only in the middle periphery. With peripheral localization of drusen and reticular pigment, changes in the fundus resemble a bunch of grapes or Sjögren's reticular dystrophy.

As the process progresses, the number of drusen and their size increase, they are prone to fusion and calcification. The sensory area of ​​the retina gradually rises. Very rarely the number of drusen decreases. Changes also affect the pigment epithelium located on top of the drusen. It becomes noticeably thinner, the amount of pigment decreases, and islands of pigment can be detected around the drusen. Such changes can occur in the macula and are often accompanied by degeneration of epithelial cells.

According to the Sarks classification (1996), two types of drusen are distinguished:

• Solid drusen are small, multiple, hyalinized lesions that are often calcified, crumbly, and non-confluent.
• Soft drusen are large, tend to fuse, and the hyaline material in them is usually destroyed.

Drusen are located above or below the basement membrane, less often they are detected in the choriocapillaris layer. Typically, drusen are not accompanied by symptoms and are an incidental finding during ophthalmoscopy. Rarely, patients complain of metamorphopsia (with foveal drusen location). Visual field defects or decreased visual acuity are usually not detected.

With fluorescein angiography, drusen glow even in the early phases. The intensity of the glow gradually increases. During the venous phase, the fluorescence intensity decreases rapidly. Most often, angiography can detect more drusen than ophthalmoscopy. On angiography, hard drusen appear as separate hyperfluorescent dots, even if they appear to merge. Very rarely, calcification or pigmentation of drusen leads to their hypofluorescence.

Differential diagnosis

It is necessary to distinguish drusen from a number of diseases that are accompanied by white or yellow deposits in the posterior pole eyeball. All these diseases are united by Flecked retina syndrome:

• Fundus punctatus albescens is a white-spot abiotrophy of the fundus, which is accompanied by the formation of white foci, according to appearance resembling druses. They are located in the middle periphery of the eye. The disease is accompanied by a sharp decrease in visual acuity, progressive nyctalomia, which has similar features to lungs and early forms retinal pigment abiotrophy.
• Fundus albipunctatus (spotted fundus) is a bilateral hereditary pathology that has similarities with the previous disease. The main difference is a non-progressive course, no decrease in visual function and stationary night blindness. With ophthalmoscopy, you can detect whitish round spots that are located at the level of the pigment epithelium and cover the entire fundus of the eye, especially the macula and equatorial region. Dominant drusen have a different size and are more dominant in the macula area.
• Fundus flavimaculatus (yellow-spotted fundus) is a bilateral process in which there are yellowish macular deposits in the pigment epithelium. Angiography may reveal blockade of choroidal fluorescence in the periphery and posterior pole. With dominant drusen, such changes are not recorded. Also, this pathology is often combined with bull’s eye macular degeneration. Visual acuity decreases with the development of Stargardt disease. There is also a narrowing of the field of vision, which does not happen with drusen.
• Bietti's dystrophy (crystalline dystrophy) is accompanied by whitish deposits in the retinal area, which have a polygonal shape and a brilliant-white shine. At the same time, vision loss and marginal retinal dystrophy are progressive.

DRUSINS OF THE OPTIC NERVE

Optic disc drusen, or hyaline bodies, ophthalmoscopically they look like lesions 1-2 times the diameter of a vein with white or yellowish-pinkish opalescence. Later they may undergo calcification. Drusen most often appear along the periphery of the disc, but they also occur in its center, and are also located in groups away from the blood vessels. There are superficial and deep drusen. Deep drusen are better identified with lateral illumination and may resemble papilledema. Surrounding the optic nerve head, they usually do not extend beyond its limits by more than 1/2 DD and are never pigmented. Disc drusen do not combine with Bruch's membrane drusen. The changes can be unilateral or bilateral, sometimes the fellow eye is affected after a few years. Visual functions are not reduced or reduced slightly.

Histologically, drusen are deposits of hyaline and are most often localized in front of the cribriform plate, but can also be located behind it.

FAHD plays an important role in the diagnosis of optic disc drusen, especially in differential diagnosis drusen and papilledema. With drusen, a fluorescein angiogram shows scalloped marginal hyperfluorescence of the disc, there is no contrasting of tissues outside it, and no changes in the retinal and papillary vessels are observed, as is the case with edema (Fig. 9-1-9-4).

The pressure of drusen on the tissue of the optic nerve head can lead to atrophy of nerve fibers and cause expansion of the blind spot. In some cases, there are hemorrhages in the retina and vitreous.

They can also be observed in Grönblad-Strandberg syndrome, retinal pigmentary abiotrophy and tuberous sclerosis.

Literature

Seitz R.: Die intraokularen Drusen. Klin. WE. Augenheilk 152. - 1968. - P. 203-211.

ANTERIOR ISCHEMIC NEUROPATHY

Epidemiology

The disease is eye symptom various system processes. Average age patients 50-60 years old.

Etiology and pathogenesis

The disease is polyetiological. In particular, they note the role hypertension, generalized atherosclerosis, diabetes mellitus, rheumatism, temporal arteritis. In isolated cases, anterior ischemic neuropathy can develop after significant blood loss, anesthesia, surgical interventions, and is sometimes observed against the background of optic disc drusen, after cataract extraction. The disease usually develops in one eye, but involvement of the fellow eye is possible at varying intervals, up to 10 years.

In the pathogenesis of anterior ischemic neuropathy, the leading role belongs to circulatory disorders in the posterior short ciliary arteries.

Clinic

Anterior ischemic neuropathy develops acutely, more often in the morning after sleep, less often after lifting weights and hot bath. Precursors of the disease: slight periodic blurring of vision, severe headache, pain behind the eye. Anterior ischemic neuropathy can also develop without preliminary symptoms. Visual acuity is reduced. Defects are often found in the lower half of the visual field, and the temporal and nasal half of the visual field may also be lost. Ophthalmoscopic

The picture is varied. In the acute period, the optic disc is swollen, its boundaries are not differentiated, and hemorrhages may appear on its surface and in the peripapillary zone. Sometimes a soft exudate forms on the surface of the optic nerve head. In some cases, occlusion of the cilioretinal artery or central retinal artery occurs simultaneously with anterior ischemic neuropathy.

FAGD at early stage V acute phase process: the optic nerve head in the ischemic zone is not contrasted. The capillaries of its intact part are ectatic, their walls are highly permeable, which leads to hyperfluorescence of the healthy part of the disc at the late stage of FAHD. Concomitant changes on FAGD include uneven caliber of arteries, unevenness of their contours (atherosclerotic changes in blood vessels) (Fig. 9-5-9-8).

Treatment

Corticosteroids are used locally. Dehydration therapy is carried out, vasodilators, disaggregation drugs and fibrinolytics are prescribed. Installation of b-blockers at night to increase perfusion pressure in the eye is indicated.

Literature

1.

2. Hayreh S. Anterior ischemic optic neuropathy. - Berlin-Heidelberg-New-York. - 1975. - 145 p.

STAGNESS OPTIC NERVE DISC

Congestive optic disc is swelling of non-inflammatory origin and in most cases is caused by increased intracranial pressure.

Etiology

Diseases of the central nervous system, general diseases, diseases of the eyeball and orbit, skull deformation.

Among diseases of the central nervous system, the most common cause of the development of a congestive disc (64% of cases) is tumors

brain. The disease is usually bilateral; unilateral congestive disc occurs with orbital tumors and traumatic hypotony of the eyeball.

Diagnostics

In the diagnosis of congestive optic disc, anamnesis, visual field examination, ophthalmoscopy and FAHD are important.

Classification

The classification is based on the stages of process development:

1. Initial congestive optic disc.

2. Severe congestive optic disc.

3. Pronounced congestive optic disc.

4. Stagnant disc in the atrophy stage.

5. Optic nerve atrophy after stagnation.

Clinic

On initial stages The optic disc is hyperemic, its boundaries are blurred, the veins are dilated, but not tortuous. Hemorrhages at this stage, as a rule, are not observed. Then the edema covers the entire optic nerve head, and its enlargement is noted. The veins are not only dilated, but also tortuous, the arteries are somewhat narrowed. At this stage, the vascular funnel is still preserved.

With pronounced congestive discs, hyperemia, enlargement of the optic disc, and blurred boundaries are observed. The veins are dilated, tortuous, hemorrhages and white spots appear.

At the stage of a pronounced congestive disc, the ophthalmoscopic picture consists of the same details as at the previous stage, but due to increased edema, the optic disc protrudes more into the vitreous body. With the long-term existence of a stagnant disc, atrophy gradually begins to develop, a grayish tint appears against the background of disc hyperemia, which further intensifies as the edema decreases. As atrophy develops, the disc becomes a dirty gray color (Fig. 9-9-9-12).

With a stagnant disc, normal visual functions are maintained for a long time. If stagnation persists for a sufficiently long time as a result of the death of peripheral fibers of the visual non-

the ditch narrows the boundaries of the field of vision. With the onset of optic disc atrophy, the narrowing of the field rapidly progresses. Various shapes hemianoptic visual field defects indicate the impact of the underlying pathological process on a particular area visual pathway. A decrease in visual acuity often occurs in parallel with a narrowing of the visual field.

Treatment

Treatment consists of eliminating the cause of optic disc congestion.

Literature

Tron E. Zh. Diseases of the visual pathway. - L.: Medgiz, 1955. - P. 35-108.

OPTIC NEURITIS

Optic neuritis is an inflammatory process in the optic nerve. In most cases, the disease affects both the trunk and the nerve sheaths.

Etiology

Etiological factors are very numerous. They are combined into 5 main groups:

1. Inflammatory diseases brain.

2. Acute and chronic infections.

3. Local foci of inflammation.

4. Diseases of internal organs of non-infectious origin ( diabetes, blood diseases).

5. Inflammatory diseases of the eyeball and orbit.

Most common reasons Optic neuritis is a disease of the brain and kidneys.

Pathogenesis

Development mechanism pathological changes fundus in optic neuritis is caused by an inflammatory process. Hyperemia of the optic disc is caused by vasodilation; hemorrhages and exudation are associated with increased permeability of the vascular wall. Exudation leads to inflammatory swelling of the optic disc tissue and causes blurring of its boundaries.

Diagnostics

Diagnosis is based on the results of ophthalmoscopy and visual field examination

and FAGD.

Clinic

The course of optic neuritis is varied and is determined by both the severity and causes of the inflammatory process. With mild inflammation, the optic disc is hyperemic, its boundaries are blurred, and the papillary arteries and veins are dilated.

With a more intense inflammatory process, all of the above changes increase, hemorrhages and exudate deposits appear.

With pronounced neuritis, the hyperemia of the disc and blurring of its boundaries are so significant that it merges with the surrounding retina. On the surface of the optic nerve head, as well as in the area of ​​the peripapillary retina, there are many hemorrhages and white patches of exudate. In most cases, neuritis is not characterized by protrusion of the optic nerve head above the level of the retina.

Typically, early visual impairment parallels the development of the ophthalmoscopic picture. This is observed in relation to both acuity and visual field. The severity of the decrease in visual function correlates with the intensity of the inflammatory process and mainly depends on the degree of damage to the papillomacular bundle.

Changes in the visual field are often manifested by a narrowing of its boundaries, and the deeper the inflammation penetrates into the optic nerve trunk, the more pronounced the narrowing of the visual field boundaries. If the inflammatory process involves nerve fibers running in the center of the optic nerve trunk, a central scotoma is observed. With the transition of neuritis to optic nerve atrophy, first of all, hyperemia decreases and first a weak and then more intense blanching of the optic nerve head develops. Over time, a typical picture of secondary atrophy forms. The vessels become narrow, hemorrhages and exudate resolve.

With FAGD, at the onset of the disease, intense hyperfluorescence of the visual disc is noted.

body nerve, increasing in the later phases of FAHD (Fig. 9-13).

At the final stage of the process, with the development of optic nerve atrophy, persistent hypofluorescence of the disc is observed on a fluorescein angiogram.

Treatment

Treatment is most effective when the etiology of the disease is determined and should be etiotropic. Prescription of antibiotics is mandatory. Corticosteroids are also used locally and orally, and B vitamins.

Literature

1. Tron E.Zh. Diseases of the visual pathway. - L.: Medgiz, 1955. - P. 109-124.

2. Spar T., Rockwell D. Treatment of optic neuritis with intrevenous megadose corticosteroids: a consecutive series/Ophthalmol. - Vol. 95. - 1988. - P. 131-134.

PITSA OF THE OPTIC DISC

NERVA

Optic disc pits are a rare congenital disease that manifests itself between the ages of 20 and 40 years as decreased vision caused by serous macular detachment.

Diagnostics

The main diagnostic methods are ophthalmoscopy and FAHD.

Clinic

Oval grayish-white depressions measuring from 1/8 to 1/2 DD are detected in the temporal sector of the optic nerve head. In the macular area there is edema (detachment of the neuroepithelium), sometimes cystic degeneration of the retina. FAGD detects late fluorescence of the optic disc pits. Detachment of the neuroepithelium in the macular area in this pathology is not contrasted in the early and late phases of FAHD (Fig. 9-17-9-24).

Treatment

Laser coagulation along the edge of the optic nerve head and barrier laser coagulation, delimiting the zone of neuroepithelial detachment.

Literature

1. Katsnelson L. A., Forofonova T. I., Bunin A. Ya. Vascular diseases of the eyes. - M.: Medicine, 1990. - P. 217-226.

2. Gass J.D. Stereoscopic atlas of macular diseases. -St. Louis, etc.: CV Mosby Co., 1977. - P. 368-410.

Rice. 9-1. Superficial drusen of the optic disc.

Rice. 9-2. Deep drusen of the optic nerve head.

Rice. 9-3. Optic disc drusen. Uneven scalloped hyperfluorescence of the optic disc. FAGD. Arteriovenous phase.

Rice. 9-4. Optic disc drusen. FAGD. Late phase. More intense hyperfluorescence of the optic disc, scalloped coloring of its borders remains.

Rice. 9-5. Anterior ischemic neuropathy. Ischemic edema of the optic disc with isolated hemorrhages.

Rice. 9-6. Anterior ischemic neuropathy. Sectoral hyperfluorescence of the inner half of the optic disc (from ectatic papillary capillaries). FAGD. Late phase.

Rice. 9-7. Optic disc atrophy after anterior ischemic neuropathy.

Rice. 9-8. Hypofluorescence of the optic nerve head after anterior ischemic neuropathy. FAGD. Arteriovenous phase.

Rice. 9-9. Congestive optic disc. Edema of the optic disc and peripapillary retina, dilated veins, hard exudate deposits and hemorrhages in the peripapillary area.

Rice. 9-10. Congestive optic disc. FAGD. Late phase, sharply dilated, tortuous veins. Hyperfluorescence of the optic disc.

Rice. 9-11. FAGD of a patient with stagnant disk optic nerve. Arterial phase. Sharply dilated veins, extravasal hyperfluorescence from dilated papillary and peripapillary vessels.

Rice. 9-12. Congestive optic disc. Sharply dilated convoluted retinal veins and vessels of the papillary and peripapillary areas. The caliber of the retinal arteries is not changed. The disc tissue is swollen, its boundaries are not clearly contoured.

Rice. 9-13. Optic neuritis. Hyperfluorescence of the optic nerve head as a result of increased permeability of papillary vessels. FAGD. Late phase.

Rice. 9-14. Optic neuritis. The optic disc is hyperemic, its boundaries are blurred. Retinal veins and papillary vessels are dilated.

Rice. 9-15. Optic neuritis with initial atrophy of nerve fibers.

Rice. 9-16. A small pit in the form of a rounded grayish depression in the temporal half of the optic nerve.

Rice. 9-17. FAGD. Arteriovenous phase. Hyperfluorescence of the optic disc fossa without secondary focal changes in the center.

Rice. 9-18. The fossa of the optic nerve occupies 1/4 of the DD.

Rice. 9-19. Large fossa of the optic nerve head.

Rice. 9-20. Non-fluorescent optic disc fossa. Hyperfluorescence in the central zone of the fundus in the form of small foci as a result of disorganization of the pigment epithelium. FAGD. Arteriovenous phase.

Rice. 9-21. FAGD of the same patient as in Fig. 9-20. Late phase. Bright hyperfluorescence of the optic disc fossa with secondary changes in the center.

Rice. 9-22. Glaucomatous excavation in the differential diagnosis of the large fossa of the optic nerve head.

Rice. 9-23. A unique case - foreign body on the optic nerve head, simulating the optic disc fossa.