The concept of “primary open-angle glaucoma” unites a large group of eye diseases with different etiologies, which are characterized by:

open anterior chamber angle (ACA) of the eye,
increase in IOP beyond the level tolerant for the optic nerve,
development of glaucomatous optic neuropathy with subsequent atrophy (with excavation) of the optic nerve head,
the occurrence of typical visual field defects.

The tolerant level of ophthalmotonus for the optic nerve is considered to be the level of IOP that is expected to provide the patient with the lowest rate of progression of glaucoma for the duration of his expected life.

Global morbidity statistics among the population indicate an increase in the incidence of POAG: according to WHO estimates, in 2010 the number of patients with glaucoma was about 60 million, and by 2020 it will reach almost 80 million people.

In Russia, glaucoma ranks first in the nosological structure of causes of disability due to ophthalmopathology, and its prevalence is steadily growing: from 0.7 (1997) to 2.2 people (2005) per 10,000 adults. For the period 1994 to 2002. A monitoring analysis carried out in 27 regions of the Russian Federation showed an increase in the incidence of glaucoma on average from 3.1 to 4.7 people per 1000 population.

Primary open angle glaucoma (POAG, simple glaucoma) is a simple chronic glaucoma, usually bilateral, but not always symmetrical, is a neurodegenerative disease and leads to irreversible loss of visual function. The pressure in the eye slowly increases, and the cornea adapts to this without any protrusion. Therefore, most often the disease goes unnoticed.

POAG is a neurodegenerative disease characterized by progressive optic neuropathy and specific changes in visual function associated with a number of factors, of which increased intraocular pressure (IOP) is considered the leading one. That is why normalization of the level of ophthalmotonus plays a leading role in reducing the risk of development and/or progression of the disease.

Although there is ample evidence that oxidative stress plays an important role in the pathogenesis of various types of glaucoma, studies of vitamin levels in the blood of patients with glaucoma are inconclusive and do not correlate with results on the effect of dietary vitamin intake on glaucoma. Moreover, research on the relationship between dietary vitamin intake and glaucoma is sparse. However, vitamin A intake appears to have a protective effect against glaucoma. Vitamin C may also have a comparable effect on glaucoma.

Risk factors

Age - POAG is usually diagnosed after 65 years of age. A diagnosis of glaucoma at age 40 is not typical.
Race - It has been reliably established that in people with black skin, primary open-angle glaucoma develops earlier and is more aggressive than in people with white skin.
Family history and heredity - POAG is often inherited in a multifactorial pattern. Intraocular pressure, ease of aqueous humor outflow, and optic disc size are genetically determined. First-degree relatives are at risk for developing primary open-angle glaucoma, but the degree of risk is unknown, because the disease develops at an older age and requires long-term observation to confirm the fact of inheritance. A conditional risk of developing the disease in siblings (up to 10%) and offspring (up to 4%) is assumed.
Myopia - patients with myopia are more susceptible to the damaging effects of increased levels of ophthalmotonus.
Retinal diseases - Central retinal vein occlusion is often associated with long-term primary open-angle glaucoma. Primary open-angle glaucoma occurs in approximately 5% of patients with retinal detachment and 3% with retinitis pigmentosa.
Risk factors also include a large ratio of the excavation diameter to the diameter of the optic nerve head (E/D > 0.5), and the peripapillary b-zone. b-zone is an uneven, often incomplete ring formed as a result of retraction of the pigment epithelium and atrophy of the peripapillary choroid.

Etiology

Genetic aspects

14 loci (GLC1A-GLC1N) are associated with the development of POAG. In most cases, the molecular mechanism of association is unknown. The most studied genes are MYOC, OPTN and WDR36.

The MYOC gene (myocilin, GLC1A locus, 1q23-q25) encodes myocilin, an intercellular matrix (ECM) protein of unknown function that is expressed in the optic nerve head. The MYOC gene, formerly known as TIGR (trabecular meshwork-inducible glucocorticiod response), was the first gene associated with juvenile and adult open-angle glaucoma, mutations in this gene lead to clinical symptoms. The pathogenic effect of mutant myocilin is the inability of the protein to fold into the correct tertiary structure. Mutant forms of myocilin form aggregates in the endoplasmic reticulum (Russell bodies) and cytoplasm (aggresomes), cause depolarization of mitochondrial membranes, reduce ATP production, increase the generation of oxygen radicals and activate apoptosis, due to their anti-adhesive effect, they disrupt the structure of the MCM trabecular meshwork, which leads to path obstruction outflow of intraocular fluid, intraocular hypertension and glaucoma. Overexpression of myocilin in the trabecular meshwork by the glucocorticoid dexamethasone may cause a structural defect in the trabecular meshwork that damages the optic nerve. Currently, about 80 mutations of the MYOC gene are known. For example, the 1348A/T mutation (replacement of asparagine-450 with tyrosine) is responsible for 8% of severe juvenile glaucoma with incomplete penetrance and 3-4% of early adult POAG. 80% of mutation carriers develop glaucoma or increased IOP. Carriers of this mutation require an intensive therapeutic strategy and constant monitoring.

Mutations of the OPTN gene (optineurin, GLC1E locus, 10p15-14) are associated with hyper-, hypo- and normotensive forms of POAG. Optineurin supports cell survival, protects cells from oxidative damage and apoptosis by blocking the release of cytochrome C from mitochondria. The OPTN gene is activated in response to prolonged increases in IOP and long-term use of dexamethasone, indicating its protective role in the trabecular meshwork. The OPTN 1274A/G (K322Q), 603T/A (M98K) and 1944G/A (R545Q) mutations are responsible for the clinical picture typical of POAG. The most common mutation in the OPTN 458G/A (E50K) gene in patients with glaucoma encodes the replacement of glutamic acid at position 50 with lysine in the optineurin molecule, which disrupts the transport of this protein into the nucleus, leads to oxidative stress and apoptosis of retinal ganglion cells, and imparts a more severe phenotype to hypotensive glaucoma . Overexpression of OPTN in trabecular meshwork cells increases the turnover time of MYOC mRNA, i.e. Optineurin may be involved in the pathogenesis of glaucoma by controlling the stability of myocilin mRNA. Another pathophysiological mechanism is associated with alternative splicing, as a result of which the OPTN gene produces three isoforms of optineurin. An imbalance in their expression can lead to glaucoma. In the Russian population of patients with glaucoma, polymorphisms MYOC 1102C/T, 855G/T, 975G/A, 1041T/C, 1193A/G and OPTN 433G/A, 603T/A were discovered.

The WDR36 gene (WD-40 Repeat Domain 36, GLC1G locus, 5q22.1-q32) is associated with hyper- and normotensive POAG in adult patients. The name of the gene reflects the presence of 36 WD (tryptophan and asparagine) dipeptide repeats in the molecule it encodes. The WDR36 gene is expressed in the lens, iris, sclera, ciliary muscle, ciliary body, trabecular meshwork, retina, and optic nerve. WDR36 is a multifunctional protein involved in the processing of ribosomal RNA, ensuring cellular survival during the development of the brain, eye and intestine. WDR36 has been suggested to be involved in the activation of T lymphocytes, which are involved in glaucoma-associated optic nerve degeneration. WDR36 mutations N355S, A449T, R529Q and D658G were identified in POAG patients with high and low IOP. Mutation 1973A/G (D658G), a substitution of aspartate-658 with glycine, associated with a higher number of relapses, is localized in the cyt cd1 (cytochrome heme cd1) domain, which is part of a bifunctional enzyme with cytochrome oxidase activity. This may explain why mutations of the WDR36 gene, while not being the direct cause of glaucoma, are associated with a more severe course of glaucoma (severe optic nerve degeneration), i.e. WDR36 is a modifier gene.

According to the generally accepted point of view, primary open-angle glaucoma is a multifactorial disease with a threshold effect and occurs in cases where the combination of unfavorable factors exceeds a certain threshold necessary to trigger the pathophysiological mechanisms of the disease.

Anatomical aspects

To understand the pathophysiology of the eye, it is important to study quantitative features (the so-called endophenotype). The endophenotypes associated with POAG include not only IOP, but also CCT (central corneal thickness - the thickness of the cornea in the central zone), the size and configuration of the optic nerve, in particular the VVR (the ratio of the vertical dimensions of the excavation/disc) and the surface of the optic nerve head, which are structural characteristics of POAG. There is a biological relationship between corneal thickness and the properties of tissues involved in the pathogenesis of glaucoma, such as the lamina cribrosa and trabecular meshwork. Low CCT is considered an important risk factor for elevated IOP and POAG. The FBN1 (fibrillin-1) and PAX6 (paired box 6) genes are associated with abnormal CCT in eye diseases. The FBN1 gene encodes an intercellular fiber glycoprotein, a structural component of the basement membrane, which is expressed in various tissues, including the cornea.

Anatomical factors also include the weak development of the scleral spur and ciliary muscle, the posterior attachment of the fibers of this muscle to the sclera, the anterior position of Schlemm's canal and the small angle of its inclination to the anterior chamber. In eyes with such anatomical features, the “ciliary muscle-scleral spur-trabecula” mechanism, which stretches the trabecular meshwork and maintains Schlemm’s canal open, is ineffective. In addition, in patients with open-angle glaucoma, the outlet canaliculi often originate in the anterior sinus, which leads to a decrease in pressure in the anterior part of Schlemm's canal and facilitates the occurrence of blockade of both the sinus and its outlets.

Another factor is related to the anastomoses between the veins of the ciliary body and the intrascleral venous plexus, the physiological role of which is to maintain pressure in the scleral sinus close to the IOP. With the anterior position of the sinus, which is characteristic of open-angle glaucoma, the anastomoses are lengthened, which cannot but affect their effectiveness.

The larger the size of the optic nerve head, the more sensitive it is to the damaging effects of increased IOP associated with increased excavation. Genetic factors influence both IOP and the sensitivity of the optic nerve to changes in it. Enlargement of the optic disc surface may increase the risk of POAG when combined with risk factors that control SVR. Variability of the surface of the optic nerve head and SVR as a risk factor for POAG is associated with the ATOH7 gene (site rs1900004, S/T), the SIX1/SIX6 gene complex (locus 14q22-23, site rs10483727, S/T), the CDKN2B gene (locus 9p21, site rs1063192, A/G). The ATOH7 gene encodes the Math5 protein, which is involved in the histogenesis of the retinal ganglion.

The role of dystrophic changes. The role of age in the etiology of glaucoma can be explained by dystrophic changes in the trabecular apparatus, iris and ciliary body. In old age, the juxtacanalicular layer thickens, deposits of extracellular material appear in it, the intertrabecular fissures and Schlemm's canal narrow, and pigment granules, tissue decay products and pseudoexfoliative particles are deposited in the trabecular meshwork.

Age-related changes in connective tissue and, consequently, the trabecular diaphragm also include a decrease in its elasticity and the appearance of flabbiness. Age-related dystrophic changes in the anterior part of the choroid consist of focal or diffuse atrophy of the stroma and pigment epithelium of the iris and ciliary body, atrophic changes in the ciliary muscle. Dystrophic changes in the choroid lead to a decrease in the effectiveness of the mechanisms that protect Schlemm's canal from collapse.

Vascular, endocrine and metabolic disorders affect the occurrence of glaucoma, as they change the severity and prevalence of dystrophic changes. The following follows from this concept:

the more pronounced the dystrophic changes in the drainage area of the eye, the lesser the degree of anatomical predisposition is necessary for the occurrence of glaucoma and vice versa;
glaucoma develops earlier and is more severe in those eyes in which the anatomical predisposition and primary dystrophic changes are more pronounced.

Primary open-angle glaucoma is a multifactorial disease with a threshold effect and occurs in cases where the combination of unfavorable factors exceeds a certain threshold necessary to trigger the pathophysiological mechanisms of the disease.

Glucocorticoids and open-angle glaucoma. It has been established that glucocorticoids affect the level of IOP and the hydrodynamics of the eye. In patients with primary open-angle glaucoma, the IOP response to a glucocorticoid test is often increased. The mechanism of action of glucocorticoids on IOP is a progressive deterioration in the outflow of aqueous humor from the eye. Under the influence of glucocorticoids, the content of glycosaminoglycans in trabeculae increases, which apparently occurs due to a decrease in the release of catabolic enzymes from the lysosomes of goniocytes. As a result, the permeability of the trabecular diaphragm decreases slightly, and the pressure difference in the anterior chamber and scleral sinus increases. In anatomically predisposed eyes, especially if the trabecular permeability was previously reduced, a functional sinus block occurs, which leads to an increase in IOP.

The role of heredity, other diseases and the external environment. Both dominant and recessive types of inheritance have been described, but in most cases polygenic transmission of the disease predominates.

Many researchers note that open-angle glaucoma more often occurs in patients with atherosclerosis, hypertension, hypotensive crises, diabetes, as well as Cushing's syndrome and in persons with disorders of lipid, protein and some other types of metabolism.

Primary open-angle glaucoma is much more often combined with myopia than with other types of eye refraction. With emmetropia with myopia, the ease of outflow in the eyes is lower, and the IOP is higher than the average value. The high incidence of open-angle glaucoma in people with myopia may be due to the characteristic anterior position of Schlemm's canal and weakness of the ciliary muscle.

In addition, some racial differences in the incidence of glaucoma and its course have been noted. Thus, in people of the Negroid race, open-angle glaucoma occurs more often at a younger age than in the Caucasian race; and in both races, open-angle glaucoma is noted significantly more often than closed-angle glaucoma. At the same time, the Mongoloid race is characterized by the prevalence of open-angle over open-angle.

Great importance is attached to the acceleration of apoptosis of retinal ganglion cells and loss of axons in its layer of nerve fibers under the influence of risk factors, the main of which is increased IOP.

Classification

The division of the continuous glaucoma process into 4 stages is conditional. In this case, the state of the visual field and optic disc is taken into account.

Stage I (initial) - the boundaries of the visual field are normal, but there are slight changes in the paracentral parts of the visual field. The excavation of the optic disc is expanded, but does not reach the edge of the disc.
Stage II (developed) - pronounced changes in the visual field in the paracentral region in combination with its narrowing by more than 10° in the upper and/or lower nasal segments, the excavation of the optic disc is expanded, but does not reach the edge of the disc, and is of a marginal nature.
Stage III (far advanced) - the border of the visual field is concentrically narrowed and in one or more segments is located less than 15° from the fixation point; the marginal subtotal excavation of the optic disc is expanded, but does not reach the edge of the disc.
Stage IV (terminal) - complete loss of vision or preservation of light perception with incorrect projection. Sometimes a small island of visual field is preserved in the temporal sector

Intraocular pressure level

When making a diagnosis, the following gradations of IOP level are used -

A - IOP within normal values (P 0<22 мм. рт. ст.)
B - moderately increased IOP (P 0<33 мм. рт. ст.)
C - high IOP (P 0 >32 mm Hg)

Dynamics of the glaucomatous process A distinction is made between stabilized and unstabilized glaucoma. In the first case, during long-term observation of the patient (at least 6 months), no deterioration in the state of the visual field and optic disc is detected, and in the second, such changes are recorded during repeated studies.

When assessing the dynamics of the glaucomatous process, the level of IOP and its correspondence to the target pressure are also taken into account. The diagnosis of “unstabilized glaucoma” can be established if the narrowing of the visual field during a given observation period is 10° or more in individual radii in the initial stage of the disease, 5-10° in other stages and 2-3° in tunnel ( up to 10° from the fixation point) field of view. The appearance of marginal excavation where there was none before, obvious expansion and deepening of the previously existing glaucomatous excavation, defects in the axon bundles of retinal ganglion cells indicate an unstabilized glaucomatous process.

Pathogenesis

According to modern concepts, disruption of the structural and biomechanical properties of the sclera in the area of the optic nerve head and the corneoscleral membrane of the eye as a whole can play a significant role in the pathogenesis of POAG.

The central link in the pathogenesis of primary open-angle glaucoma is considered functional blockade (collapse) of the scleral sinus , which occurs as a result of outward displacement of the trabecula into the lumen of Schlemm's canal. Functional blockade of Schlemm's canal in open-angle glaucoma may be due to a decrease in the permeability of the trabecular apparatus, its insufficient rigidity and the ineffectiveness of the ciliary muscle-scleral spur-trabecula mechanism.

It is assumed that the development of POAG is accompanied by a pathological acceleration of natural gerontological processes of changes in the elasticity and firmness of the eye membranes. In turn, increased scleral rigidity, in the absence of stable normalization of IOP, may predispose to the progression of the glaucomatous process.

The etiological and pathogenetic chain of primary open-angle glaucoma is as follows.

Genetic links.
General changes.
Primary local functional and dystrophic changes.
Violations of hydrostatics and hydrodynamics of the eye.
Increased IOP.
Secondary vascular disorders, dystrophy and dystrophic changes in tissues.
Glaucomatous optic neuropathy.

Heredity plays an important role in the occurrence of primary glaucoma. This is evidenced by the results of a survey of the closest relatives of patients with glaucoma, as well as the same prevalence of glaucoma in countries with different climates and living conditions, in urban and rural areas and in different segments of the population.

The genetic influences that cause the occurrence of primary glaucoma are apparently complex in nature and cannot be reduced to the action of a single gene. They determine the intensity of age-related changes in the body, the local reaction in the eye to age-related changes and the anatomical features of the drainage area of the eye and optic disc.

General changes (vascular, endocrine, metabolic, immune) affect the regulation of IOP, homeostasis processes, the severity of age-related disorders in various structures of the eye, primarily in its drainage apparatus, as well as the tolerance of the optic nerve to increased IOP.

Primary dystrophic changes precede the onset of glaucoma and are not associated with the effect of increased IOP on the eye. These include age-related and pathological (with general diseases, pseudoexfoliation and other processes) changes in the trabecular diaphragm, leading to a decrease in its permeability and elasticity.
Local functional disorders include changes in hemodynamics, fluctuations in the rate of formation of aqueous humor, and weakening of the tone of the ciliary muscle. Local functional and trophic disorders create the prerequisites for the development of trabecular and canalicular blocks that disrupt the circulation of aqueous humor in the eye.
Mechanical links in the pathogenesis of primary glaucoma begin with a progressive disturbance of hydrostatic balance. At some stage, this leads to a deterioration in the outflow of aqueous humor, resulting in an increase in IOP. Glaucoma develops only from this moment. A significant role in its occurrence is played by genetically determined features in the structure of the eye, which facilitate the occurrence of a functional block of the scleral sinus.

High IOP and disruption of the relationship between the tissues of the eye (pressing the trabecula against the outer wall of Schlemm's canal) cause secondary circulatory and trophic disorders. The primary glaucomatous process, caused by a functional block of the drainage system of the eye, is essentially superimposed by secondary glaucoma associated with destructive changes in the drainage zone of the sclera.

The development of glaucomatous optic nerve atrophy is associated with an increase in IOP beyond the individual tolerance level. An important feature of glaucomatous atrophy of the optic disc is the slow development of the process, usually over several years. In this case, optic disc atrophy does not begin immediately after the pressure rises to a threshold level, but after a long latent period, calculated in months and years.

The pathogenesis of glaucoma, regardless of its type, includes two mechanisms, separated in space and partly in time.

One of them acts in the anterior part of the eye and ultimately leads to an increase in IOP.
Another mechanism (in the posterior part of the eye) causes optic nerve atrophy.

There are conflicting ideas about the relationship between these pathophysiological mechanisms and the sequence of their development. According to one opinion, the glaucomatous process begins in the anterior part of the eye, and changes in the optic nerve develop as a result of the action of increased IOP on it. Thus, the pathophysiological mechanism caused by changes in the anterior part of the eye precedes the mechanism of development of pathological processes in the posterior part of the eye. In this case, increased IOP serves as the last link in the pathogenetic chain of the anterior mechanism and the first, triggering link of the posterior mechanism.

At the same time, primary damage to the optic disc is sometimes possible, apparently caused by hemodynamic disturbances.

Clinical picture

Primary open-angle glaucoma is asymptomatic until changes in peripheral vision are detected. Damage occurs gradually, and the area of gaze fixation is involved in the process at a later date. Although the disease almost always develops as a bilateral process, asymmetry is often observed, so patients usually exhibit visual field changes in one eye and to a lesser extent in the fellow eye. Even very attentive patients may not notice pronounced perimetric changes, and early defects can only be detected by chance.

Patient's complaints. Subjective symptoms of the disease are either completely absent or mild. About 15% of patients with open-angle glaucoma complain of the appearance of rainbow circles when looking at light and blurred vision. Just as with PACG, these symptoms appear during a period of increased blood pressure. At the same time, the Criminal Procedure Code remains open throughout.

Some patients with primary open-angle glaucoma complain of pain in the eye, brow ridge and head. If the pain is combined with the appearance of rainbow circles, then the diagnosis of PAAG is often mistakenly made.

Other complaints include age-inappropriate weakening of accommodation, flickering before the eyes, and a feeling of tension in the eye.

Anterior part of the eye. When examining the anterior part of the eye, vascular and trophic changes are often detected. Changes in the microvessels of the conjunctiva include uneven narrowing of arterioles and expansion of venules, the formation of microaneurysms, increased capillary permeability, the occurrence of small hemorrhages, and the appearance of granular blood flow.

M.S. Remizov described the “cobra symptom”, which can be observed in any form of glaucoma. Its essence lies in the fact that the anterior ciliary artery, before entering the emissaries, expands, resembling the head of a cobra in appearance. Data on the condition of aqueous veins in eyes with open-angle glaucoma are of interest. Water veins are found less frequently in this disease than in healthy eyes; they are narrower, the fluid flow in them is slower, and the average number of veins in one eye is smaller.

R. Tornquist and A. Broaden (1958) found that the depth of the anterior chamber in patients with open-angle glaucoma is on average 2.42 mm, and in healthy people it is 0.25 mm greater. V.A. Machekhin (1974) found an increase in the anteroposterior axis of the eye by 0.3-0.4 mm in the developed and advanced stages and by 0.66 mm in the terminal stage, which is associated with stretching of the membranes of the posterior part of the eye and an anterior displacement of the eye diaphragm.

Trophic changes in the iris are characterized by diffuse atrophy of the pupillary zone in combination with destruction of the pigment border and penetration of pigment granules into the stroma. In the later stages of the disease, fluorescent iridoangiography detects ischemic zones in the iris, as well as changes in the caliber of blood vessels and microaneurysms. The processes of the ciliary body become thinner, shortened, and their correct location is disrupted. Due to the destruction of the pigment epithelium, the processes “go bald”. Much more often than in healthy individuals of the same age, pseudoexfoliative deposits are visible at the top of the processes, and sometimes between them, having the appearance of grayish-white loose films. Pseudoexfoliation also covers the fibers of the ciliary girdle.

Anterior chamber angle. The Criminal Procedure Code is always open. However, narrow angles were observed more often (23%) than in the control group (9.5%). It seems that in patients with open-angle glaucoma there is a tendency to reduce the depth of the anterior chamber and narrow its angle. These changes correspond to normal age-related ones, but are expressed, at least in some patients, somewhat more than in healthy eyes and less than in eyes with PACG.

It is known that the transparency of the trabecula decreases with age. In patients with open-angle glaucoma, opacification and thickening of the trabecular apparatus are more pronounced than in healthy people of the same age.

Gonioscopically, trabecular sclerosis is manifested by poorly distinguishable contours of Schlemm's canal: the posterior edge of the optical section is not visible, the trabecula has a tendon or porcelain appearance. Exogenous pigmentation of the trabecula in glaucomatous eyes is observed much more often and is more pronounced. The degree of pigmentation of the UPC increases as open-angle glaucoma develops.

Hydrodynamics of the eye. IOP in patients with open-angle glaucoma gradually increases and reaches a maximum in the advanced or absolute stage of the disease. The amplitude of daily fluctuations is increased in approximately half of the patients. Open-angle glaucoma is characterized by a gradual increase in resistance to the outflow of aqueous humor from the eye.

Deterioration of fluid outflow from the eye precedes an increase in IOP. The disease begins after the coefficient of ease of outflow decreases by approximately 2 times (to 0.10-0.15 mm 3 / min per 1 mm Hg). As the process progresses, the coefficient of ease of outflow and the minute volume of aqueous humor decrease.

Posterior part of the eye. Changes in the retina consist of smoothing and thinning of the layer of nerve fibers in the peripapillary zone, noticeable during ophthalmoscopy in red-free light and especially when photographing the fundus with a blue filter. More noticeable are the banded arcuate defects extending from the optic disc to the paracentral zone. Such defects, characteristic of glaucoma, are also important for diagnosis.

Glaucomatous optic nerve atrophy begins with pallor of the bottom of the physiological excavation and its expansion. Subsequently, a “breakthrough” of the excavation occurs to the edge of the optic nerve, often in the inferotemporal direction. Individual banded hemorrhages are sometimes found on the optic disc or near it, disappearing after a few weeks. In the late stage of primary open-angle glaucoma, the excavation becomes total and deep. The optic disc disappears almost completely, and in its place the cribriform plate of the sclera is visible. Atrophy affects not only the optic nerve, but also part of the choroid around it. With ophthalmoscopy, a white, yellowish or pink ring is visible around the optic disc - halo glaucomatosus.

Dynamics of the peripheral and central visual field. Glaucoma is characterized by both diffuse and focal changes in the visual field. Diffuse changes, indicating a decrease in light sensitivity, in the initial stage of the disease are weakly expressed, low specific and are not used in the early diagnosis of glaucoma.

Focal lesions of the visual field (scotomas) can be relative or absolute. In the initial stage of the disease, they are located in the paracentral part of the field, up to 25° from the point of fixation, especially often in the Bjerrum zone (15-20° from the point of fixation). The appearance of a nasal step on isopters and a narrowing of the visual field on the nasal side occur later. In rare cases, in the early stages of glaucoma, defects also occur on the periphery of the temporal half of the visual field.

The following are typical Central visual field defects:

arcuate scotoma, merging with the blind spot and reaching the meridian 45° above or 50° below;
paracentral scotomas exceeding 5°; nasal protuberance greater than 10°.

Course of primary open-angle glaucoma

Primary open-angle glaucoma occurs unnoticed by the patient and develops slowly, especially in the initial stage of the disease. The approximate duration of the preglaucomatous and initial stages combined is 1-5 years. These figures can only be considered as average, since in some patients the glaucomatous process proceeds mildly and may never leave the latent stage; in others, within 3-5 years the disease goes through all stages up to complete blindness.

Pseudoexfoliation glaucoma

This type of glaucoma is associated with pseudoexfoliation syndrome. This syndrome in patients with glaucoma was first noticed by J. Lindbergh (1917). Pseudoexfoliation syndrome is a systemic disease that occurs in presenile and senile ages and is characterized by the accumulation of a peculiar extracellular material in the tissues of the eye and some other organs.

In most cases, symptoms of pseudoexfoliation syndrome first occur in only one eye. The process may remain one-sided throughout life, but more often after a few months or years the second eye is also affected. In people with pseudoexfoliation syndrome, glaucoma occurs 20 times more often than in the general population of the same age. Approximately half of all patients with open-angle glaucoma exhibit symptoms of pseudoexfoliation syndrome. Glaucoma that occurs with pseudoexfoliation ocular syndrome is called capsular, exfoliative, or pseudoexfoliative.

Clinical symptoms of pseudoexfoliation syndrome are characterized by slowly progressive destruction of the pigment epithelium of the iris, mainly in the pupillary zone. Deposits of pigment granules appear in the stroma of the iris, on the endothelium of the cornea, on the anterior capsule of the lens, in the structures of the trabecular apparatus of the eye and the UPC.

When biomicroscopy, grayish-white scales resembling dandruff are found along the edge of the pupil, as well as characteristic deposits on the anterior capsule of the lens, ciliary girdle, processes of the ciliary body, endothelium of the cornea, in the structures of the UPC and on the anterior membrane of the CT.
As the pathological process develops, a narrowing of the pupil develops, a weakening of its reaction to light, and instillation of drugs that cause mydriasis; sometimes posterior synechiae and/or goniosynechiae are formed.
Vasculopathy occurs in the vessels of the conjunctiva and iris, manifested by uneven lumen of blood vessels, closure of part of the vascular bed, neovascularization of the iris, and increased vascular permeability.

The outflow of aqueous humor from the eye through the drainage system worsens, IOP increases and chronic open-angle (less often closed-angle) glaucoma develops.

The most pronounced clinical symptom of pseudoexfoliation syndrome is the deposits of small grayish scales, reminiscent of dandruff, along the edge of the pupil with simultaneous partial or complete disappearance of the pigment border. Deposits on the anterior capsule of the lens are especially characteristic. When examining the lens with a narrow pupil, pseudoexfoliative deposits may not be detected. With a wide pupil and with a coloboma of the iris, very thin deposits can be seen on the central part of the anterior capsule of the lens, looking like a dull disc with a grayish tint with wavy edges.

Pseudoexfoliation syndrome and glaucoma are considered one of the most important risk factors for the development of ocular hypertension and chronic open-angle glaucoma. This syndrome exceeds the risk of developing glaucoma in eyes without pseudoexfoliation syndrome by a factor of 10. In some cases, pseudoexfoliation syndrome also causes PAOG.

Pigmentary glaucoma

A distinction should be made between pigment dispersion syndrome and pigmentary glaucoma. The first is characterized by progressive depigmentation of the neuroectodermal layer of the iris and dispersion of pigment on the structures of the anterior segment of the eye. Pigmentary glaucoma occurs in some patients with pigment dispersion syndrome. The incidence of pigmentary glaucoma is 1.1-1.5% of all glaucoma cases.

Pigmentary glaucoma was first described by S. Sugar (1940). As subsequent studies have shown, predominantly men (77-90%) fall ill; the age of patients varies from 15 to 68 years: the average age for men is 34 years, for women - 49 years. Among patients, myopes predominate, but there may be emmetropes and hypermetropes. Typically, both eyes are affected. The pathogenesis of glaucoma is only partly associated with pigment dispersion syndrome. In many patients with this syndrome, glaucoma does not develop and IOP remains at a normal level. However, pigmentary and simple open-angle glaucoma are often combined in the same families. Some patients with pigmentary glaucoma showed changes characteristic of goniodysgenesis.

The mechanism of development of pigment dispersion syndrome was studied by O. Campbell (1979). He came to the conclusion that in this syndrome there are conditions for friction between the posterior surface of the iris in the zone of its middle periphery and the bundles of zonular fibers when the pupil width changes. These conditions include the anterior position of the zonular fibers, significant depth of the anterior chamber, and posterior retraction of the periphery of the iris.

Clinically, the disease occurs as open-angle glaucoma. Unlike simple open-angle glaucoma, with pigmentary glaucoma, a common subjective symptom is rainbow circles around the light source, resulting from abundant deposits of pigment dust on the posterior surface of the cornea, so they are constantly noted at any level of IOP. Some patients experience short-term crises, characterized by a sharp increase in IOP, the appearance of a suspension of pigment granules in the moisture of the anterior chamber, blurred vision and an increase in the phenomenon of rainbow circles. Such crises can be caused by the release of a large number of pigment particles during sudden dilation of the pupil, sometimes during intense physical work. They should not be confused with attacks of PAOG.

Pigmentary glaucoma occurs mainly in young and middle-aged people; it is characterized by a deep anterior chamber and an open glaucoma. Pigment granules are deposited on the ciliary band, along the periphery of the lens and on the iris. Pigment deposits on the posterior surface of the cornea usually take the form of a Krukenberg spindle. The latter is located vertically, has a length of 1-6 mm and a width of up to 3 mm. The formation of the spindle is associated with thermal fluid currents in the anterior chamber. The deposition of pigment granules in the CPC is particularly pronounced. They form a continuous ring, completely covering the trabecular tissue. It should be noted that the deposition of a large amount of pigment in the UPC can be detected long before the increase in IOP.

Diagnostics

Signs

Increased IOP level. This objective indicator can have both uncertain and very important significance in the diagnosis of primary open-angle glaucoma. Approximately 2% of the total population over 40 years of age has an intraocular pressure level >24 mmHg. Art. and 7% - >21 mmHg. Art. However, only 1% of them have glaucomatous changes in the visual field. This indicator is not informative in patients with normal intraocular pressure (<22 мм рт. ст.), когда также развиваются характерные изменения зрительного нерва и полей зрения.
Daily fluctuations in IOP within 5 mm Hg. Art. noted normally in approximately 30% of cases. In primary open-angle glaucoma, intraocular pressure fluctuations increase and are detected in approximately 90% of patients. For this reason, the IOP value is 21 mm Hg. Art. or less with a single measurement does not always exclude the diagnosis of primary open-angle glaucoma. If the value of ophthalmotonus with a single measurement is >21 mm Hg. Art., there is a suspicion of primary open-angle glaucoma. To detect daily fluctuations in intraocular pressure, it is necessary to monitor ophthalmotonus at different times of the day. IOP asymmetry in fellow eyes >5 mm Hg. Art. can be considered a suspicion for glaucoma, and eyes with higher IOP are more likely to be involved in the pathological process.
Optic nerve changes. Primary open-angle glaucoma is often diagnosed when characteristic changes in the optic nerves or asymmetry in the ophthalmoscopic picture are detected.
Changes in visual fields- their narrowing is characteristic.
Gonioscopically open CPC is determined

Examination:

Visual acuity
Tonography (decrease in the coefficient of ease of outflow to 0.1–0.2 mm 3 /min per 1 mm Hg).
Biomicroscopy - In the anterior part of the eye, signs of microvascular changes in the conjunctiva and episclera are revealed (uneven narrowing of arterioles, dilation of venules, formation of microaneurysms, small hemorrhages, granular blood flow, cobra symptom, diffuse atrophy of the pupillary zone of the iris and destruction of the pigment border).
Tonometry - the IOP level is above the statistical norm in one or both eyes, the difference in IOP between the left and right eyes is more than 5 mm Hg, the difference between morning and evening IOP is more than 5 mm Hg. It is advisable to carry out tonometry in different positions of the patient (sitting and lying).
Pachymetry
Gonioscopy both eyes - compaction of the trabecular zone, exogenous pigmentation, filling of Schlemm's canal with blood.
Ophthalmoscopy - Thinning and smoothing of the layer of nerve fibers in the peripapillary zone, the development of glaucomatous optic neuropathy - deepening and widening of the optic disc excavation, pallor of the optic disc, banded hemorrhages on or near the optic disc.
Individual disc size varies greatly across populations, with larger discs characterized by larger physiological excavations. The excavation-to-disc ratio varies depending on the individual size of the disc.
To approximate the size of the optic disc relative to the average, the size of the small light spot of a direct ophthalmoscope, approximately equal to it, can be used.
Documenting the condition of the optic disc , preferably using color stereo fundus photography
Perimetry - paracentral relative or absolute Bjerrum scotomas, narrowing of the peripheral boundaries of the visual field mainly in the upper and/or lower nasal segments.

Differential diagnosis

Differential diagnosis is made with normotensive glaucoma and ocular hypertension.

Normal pressure glaucoma is characterized by changes in the visual field typical for glaucoma, glaucomatous optic neuropathy of the optic disc with excavation, IOP within normal values, and an open anterior chamber angle.

Ocular hypertension manifests itself as an increase in IOP without changes in the visual field and optic disc.

Treatment

Achieve a reduction in IOP by 20–30% of the initial value. The greater the damage to the optic nerve, the lower the target pressure level.
In most cases, drug treatment is sufficient.
Argon laser trabeculoplasty may be an acceptable alternative to drug treatment.

Antiglaucoma drugs in the form of eye drops are represented by various groups of drugs, represented by three main types (according to the mechanism of hypotensive action):

Agents that reduce the production of intraocular fluid (adrenoblockers, carbonic anhydrase inhibitors) - for example, Timolol, Betoptik and Trusopt.
Drugs that improve the outflow of intraocular fluid from the eyeball (miotics, lantanoprost) - Pilocarpine, Xalatan, Travatan.
Combined drugs with dual action. These include Fotil (timolol + pilocarpine) and Proxophilin.

Laser treatment allows IOP control without drug treatment for 2 years in less than 50% of patients, i.e. the effect is temporary. However, this makes it possible to delay the prescription of a permanent regimen of medications with their side effects and reduce the subjective attitude of patients to drug therapy (patients do not take from 18 to 35% of prescribed drugs).

Laser treatment may be appropriate for patients who are unable to undergo drug therapy, or as an adjunct to an antihypertensive regimen in patients tolerant to drug treatment.

Despite the obvious successes of drug and laser correction of ophthalmotonus, it is generally accepted that the most effective treatment for POAG is surgery. In some cases, it may be the first choice method immediately after diagnosis.

Filter-type operations are still the main methods of surgical treatment of POAG. Based on the method of formation of outflow tracts, they are conventionally divided into two directions: perforating and non-perforating interventions.

A classic example of a fistulizing operation throughout the world is sinustrabeculectomy (STE) with its numerous modifications, and a non-penetrating technique is sinusotomy, non-penetrating deep sclerectomy (NPDS), and abroad - viscocanalostomy. Numerous domestic and foreign studies have revealed both positive and negative aspects of both directions.

The advantages of perforating interventions, first of all, include a high hypotensive effect, which can be achieved regardless of the stage of the glaucomatous process. Persistent normalization of ophthalmotonus without the use of antihypertensive drugs at different periods of observation ranges from 57 to 88% of all operated patients. The disadvantages are the development of severe intra- and postoperative complications (hyphema, collapse of the anterior chamber, ciliochoroidal detachment (CD), endophthalmitis, induced cataracts and the threat of persistent hypotension) associated with the formation of a macrofistulizing hole, aggressive opening of the eyeball and the inability to dose the volume of intervention, and also by activating the processes of excessive scarring in the surgical area.

Non-penetrating operations, compared to fistulizing ones, have a greater safety profile, which is expressed in the almost complete absence of intra- and minimal number of postoperative complications. The disadvantages of non-perforating antiglaucomatous interventions are: low duration of the hypotensive effect, caused by rapid scarring in the area of the newly created outflow tracts, especially in advanced stages of POAG, which is confirmed by a large number of modifications, widespread use of laser descemetogoniopuncture (LDG) in the early postoperative period, active use of drainages and cytostatics , as well as technical difficulties that do not guarantee accuracy of performance even by experienced surgeons.

Laser surgery and postoperative management after argon laser trabeculoplasty

Plan before and after laser treatment:

informed consent
at least one preoperative examination by a laser surgeon
at least one IOP measurement between 30 and 120 minutes after surgery
examination 2 weeks after surgery
examination 4–8 weeks after surgery

Surgery and postoperative management after fistulization surgery

Plan before and after surgery:

informed consent
at least one preoperative examination by a surgeon
observation during the first day (12–36 hours after surgery) and at least once from the 2nd to 10th day after surgery
in the absence of complications – 2–5 visits within 6 weeks after surgery
local use of corticosteroids in the postoperative period in the absence of contraindications
more frequent visits for patients with a flat or slit anterior chamber, as needed or in case of complications.

In the last decade, thanks to the introduction of innovative technologies in POAG surgery, a new direction, microinvasive glaucoma surgery (MIGS), has emerged, occupying an intermediate position between fistulizing and non-perforating operations and combining the advantages of both techniques. Modern microinvasive interventions are mainly performed either using special devices or mini-drains and have the following characteristics:

atraumatic (minimization of the volume of intervention, variability of local access, including “ab interno”),
safety,
a small number of intra- and postoperative complications,
high hypotensive effect both in early and long-term follow-up, regardless of the stage of the glaucomatous process,
short rehabilitation periods,
the possibility of performing surgeries on an outpatient basis as an antiglaucomatous component in combination with phacoemulsification of cataracts.

However, an analysis of the literature data showed that the question of a selective approach in choosing one or another microinvasive method of surgical treatment of glaucoma, depending on the stage and degree of the glaucoma process, remains open.

Regardless of the type of antiglaucomatous intervention performed, one of the most common reasons for the failure of surgical treatment of POAG is excessive scarring of the newly created outflow tracts in the early stages after surgery, so assessment of their condition is very relevant. According to modern concepts, disruption of the structural and biomechanical properties of the sclera in the area of the optic nerve head and the corneoscleral membrane of the eye as a whole can play a significant role in the pathogenesis of POAG.

The preferred method of treating patients with PES, cataracts and OAG is simultaneous microinvasive non-penetrating deep sclerectomy and phacoemulsification of cataracts with implantation of a posterior chamber elastic IOL. A persistent decrease in IOP in patients after simultaneous MNGSE + FEC + IOL during postoperative observation from one to three years, the absence of its daily fluctuations, contributes to the stabilization of the glaucomatous process, early, rapid and complete restoration of visual functions. Staged surgery of OAG and cataracts in eyes with manifestations of PES extends the rehabilitation period of patients to two years, causes a persistent loss of the hypotensive effect in 63.3% of cases, requiring additional antihypertensive interventions and leads to a worsening of the stage of the glaucomatous process in every fourth patient. Combined surgical treatment of cataract and glaucoma using MNGSE + FEC + IOL in patients with PES is a safe, effective, low-traumatic intervention that simultaneously improves optical and functional results.

For quotation: Egorov E.A., Alyabyeva Zh.Yu. Glaucoma with normal pressure // Breast cancer. 2000. No. 1. P. 9

Russian State Medical University, Moscow

Recently, ideas about glaucoma have radically changed. If previously the main criterion for glaucoma was an increase in intraocular pressure (IOP), now Glaucoma includes diseases accompanied by characteristic changes in the optic disc and visual field . It has been established that with an increase in IOP to approximately 30 mm Hg. autoregulation of vascular tone is disrupted, which leads to deterioration of optic nerve perfusion. At the same time, the development of glaucoma is possible if the IOP level is within the statistically normal range (average IOP without treatment is less than or equal to 21 mm Hg when measured during daytime hours).

Among a number of factors that determine this course of glaucoma, the disturbance of the hemodynamics of the optic nerve, which reduces the resistance of the optic nerve to increased IOP, is of paramount importance.

Normal tension glaucoma (NTG) is primary open-angle glaucoma with glaucomatous cupping* of the optic nerve and glaucomatous visual field defects, but with IOP levels within normal limits.

According to R. Levene (1980), in European countries, GND ranges from 11 to 30% of all cases of glaucoma. In Japan, in people over 40 years of age, the number of cases of GND is 4 times higher than the number of cases of high-tension glaucoma. GND affects 2% of the Japanese population.

Possible mechanisms for the development of optic neuropathy in GND

The development of glaucomatous neuropathy is promoted by a number of factors that can be divided into those independent of and related to IOP. There is evidence that decreased tolerance optic nerve head (ONH) to IOP may be due to the peculiarities of the architectonics of the cribriform plate. Of particular importance in cases of GND is hemodynamic disturbance in the vessels supplying the optic nerve.

Key factors in the pathogenesis of GND

The vessels supplying the optic nerve may be narrowed due to vasospasm . Convincing evidence has been found for the relationship between GND and Raynaud's syndrome. With GND, there is also an increased frequency of headaches, often migraine-like, and a marked decrease in blood flow in the fingers in response to exposure to cold.

It is assumed that one of the main reasons for the development of GND is violation of autoregulation of hemodynamics in the optic disc. According to some authors, this is due to changes in the endothelin-1-nitric oxide system. The content of endothelin in the blood plasma in some patients with GND is increased compared to the norm, and no systemic vascular pathology or general hemocirculation disorders are noted in these patients.

Impairment of arterial blood flow due to stenosis or diffuse atherosclerotic changes in the main arteries of the head reduces the tolerance of the optic nerve to IOP. The presence of this pathology can be assumed by complaints characteristic of one of the forms of encephalopathy (cephalgia, vestibulopathy, intellectual-mnestic disorders, pyramidal syndrome). No less important venous discirculation . Its cause may be increased intracranial pressure (history of traumatic brain injury), phlebopathy (you need to pay attention to concomitant diseases: varicose veins, hemorrhoids), arterial hypotension (venous stagnation develops due to a decrease in cerebral perfusion pressure). These disorders require consultation with a neurologist and Doppler examination. It is advisable to further jointly manage this group of patients with a neurologist.

In some cases, patients with GND have pronounced decrease in blood pressure (BP) at night and low diastolic pressure. In addition, in patients with glaucoma (both primary open-angle glaucoma and GND) and arterial hypertension taking antihypertensive drugs, with a pronounced decrease in systolic blood pressure at night, there is a tendency to worsen the visual field and progress the disease.

Disorders of hemorheology and fibrinolysis in GND include an increase in plasma and blood viscosity, a tendency to hypercoagulation (in particular, platelet hyperadhesiveness and an increase in the time of euglobulin lysis). However, these disorders are present only in a portion of patients. Considering that changes in the rheological properties of blood in patients with GND are individual, it is necessary to examine each individual patient.

Risk factors for developing GND include hemodynamic crises (episodes of massive blood loss or hypotensive shock), therefore, if GND is suspected, careful collection of anamnestic data is necessary. Patients with GND are characterized by an increased incidence of cardiovascular pathology and the prevalence of a sedentary lifestyle; cerebral infarction is more common (according to magnetic resonance imaging).

GND is characterized by severe loss of neuroglial ring tissue and an extensive area of peripapillary atrophy. This may be due to the relatively late diagnosis of this type of glaucoma, since the diagnosis is often made only when a central scotoma appears. Patients with GND have a higher incidence of hemorrhages on the optic nerve head. The prognostic value of hemorrhages in favor of the progression of GND has been established.

H. Geijssen and E. Greve (1995) identified three groups of patients with GND according to optic disc status:

1st - with focal ischemic glaucoma;

2nd - with senile sclerosis;

3rd - with glaucoma with myopia.

All these groups differ in etiology and prognosis. In connection with the increased frequency of excimer laser operations for myopia, it is necessary to keep in mind that a decrease in the thickness of the cornea in the central zone leads to an underestimation of IOP compared to the real one when measured by routine methods.

Optic disc excavation in GND often exceeds what would be expected based on the size and depth of the defects in the visual field. A very deep excavation and gray color of the disc (“failed” optic disc) with GND should be alarming in terms of the presence of stenosis of the main arteries. In this case, defects in the visual field often reach the point of fixation, while at the same time the peripheral temporal boundaries may remain practically unchanged. GND is characterized by a deeper and steeper decrease in photosensitivity, in addition, visual field defects are located closer to the fixation point compared to the high-tension glaucoma group. These differences may be related to differences in patient age and IOP level, since, for example, more diffuse visual field defects are characteristic of younger patients with higher IOP.

Determining the progression of NHL

Unlike high-tension glaucoma, which can cause rapid loss of visual function (within a few hours in an acute attack), with GND, visual field deterioration usually occurs gradually . According to the experience of D. Kamal and R. Hitchings (1998), the rate of decrease in retinal light sensitivity can vary from undetectable changes over a period of 10 years or more, to a loss of 5 dB* per year. Treatment is necessary if the disease progresses and the rate of progression in a given patient is such that, taking into account the patient’s age, he is at risk of visual impairment.

Differential diagnosis

GND is differentiated from glaucoma with large daily fluctuations in IOP , when its increase occurs outside the doctor’s office (i.e., these increases cannot be registered). High IOP may spontaneously normalize (one example is pigmentary glaucoma , in which IOP often normalizes with age).

It is also necessary to differentiate GND from the initial condition existing optic nerve atrophy (with loss of visual field), in which even IOP in the high normal zone often causes progression of the process. It is important to exclude non-glaucomatous changes in the optic disc.

IOP is usually measured during the daytime, mainly with non-contact tonometers with the patient in a sitting position. At the same time, it has been shown that some patients with glaucoma are characterized by pressure rises in the early morning hours. The dependence of the IOP value on the patient’s position is also known (in particular, a decrease when measuring pressure in a sitting position). Therefore, if GND is suspected, IOP should be measured early in the morning before the patient rises in a supine position.

According to the summary table given by H. Geijssen (1991), differential diagnosis for GND should be carried out with the following conditions:

1. Increase in IOP within the statistical norm.

2. Undetected rises in IOP, dependent on body position. Cavity and/or visual field defects not associated with IOP elevation.

3. Changes in the optic nerve head:

Large physiological excavation;

Myopia with peripapillary atrophy;

Colobomas and pits of the optic nerve head;

Optic disc inversion.

4. Neurological diseases:

Meningioma of the optic foramen;

Meningioma of the dorsum sella;

Pituitary adenoma;

Optico-chiasmatic arachnoiditis;

Empty saddle syndrome.

With optochiasmal arachnoiditis A consultation with a neuro-ophthalmologist and a neurosurgeon is indicated to resolve the issue of neurosurgical treatment. If neurosurgical treatment is not indicated and there is a threat to central vision, then an attempt to improve the perfusion of the optic nerve by fistulizing surgery is possible.

An issue that concerns all ophthalmologists without exception who are faced with GND is the need to use neurological imaging methods in the general examination of patients. If IOP is normal, it is necessary to exclude neurological causes of changes in the optic nerve. Although the presence of excavation is not typical for optic nerve pathology caused by its compression, there are reports of this in the literature. Computed tomography (CT) and magnetic resonance imaging (MRI) are expensive tests, so there is no need to use them routinely. According to CT and MRI data, the frequency of volumetric processes in patients with GND was the same as in the general population, as for diffuse ischemic pathology at the level of small vessels of the brain, it is more often observed in GND. In our opinion, this indicates the need for a more detailed study of the vascular status in patients with GND.

For further examination regarding suspected space-occupying processes, it is advisable to refer patients only if there is no correlation between the condition of the optic disc and changes in the visual field, i.e., in the presence of pale optic discs without typical excavation or visual field, suspicious for existing neurological pathology (for example , homonymous visual field defects with a clear boundary along the midline), and also if the patient’s complaints are not explained by loss of vision.

Measures aimed at reducing IOP

Antihypertensive treatment that reduces IOP by more than 25% effectively slows the progression of NPH.

Currently, in patients with GND who initially have IOP at the lower limit of normal values, fistulizing operations with intraoperative use of cytostatics are more effective. Although in this case, a 25% decrease in IOP is fraught with the development of postoperative hypotension. Because of this complication, D. Kamal and R. Hitchings (1998) recommend surgical treatment in patients with undoubted deterioration of the visual field, in whom a 25-30% reduction in IOP is possible when medications are ineffective. In such cases, almost immediate surgical treatment is required. Perhaps in GND, one of the most important effects of antihypertensive drugs is to improve perfusion of the optic nerve head. With a wide angle of the anterior chamber, but its coracoid profile, laser iridectomy is indicated to exclude a rise in IOP at night.

Correction of hemodynamic disorders

Drug therapy for hemodynamic disorders in GND is currently quite limited and includes oral administration calcium antagonists and antiplatelet agents , as well as local remedies such as betaxolol .

Data on the effectiveness of calcium channel blockers in GND are conflicting. According to J. Flammer (1993), calcium channel blockers can be effective in patients with vasospastic syndrome, as well as in those in whom a short course of treatment has improved or stabilized the visual field. Particularly promising nilvadipine And nimodipine , having tropism to the vessels of the brain. These drugs should be used in cases where a reduction in IOP by 25-30% cannot be achieved or if, despite a decrease in IOP, there is a deterioration in the visual field.

Considering the effect of disturbances of venous outflow on the blood supply to the optic nerve in patients with venous discirculation, it is advisable to use drugs venotonic series (aescin, diosmin, etc.).

A very important aspect is treatment available to the patient cardiovascular pathology or a condition affecting the blood coagulation system (for example, gastrointestinal diseases, anemia, congestive cardiovascular failure, transient circulatory disorders, cardiac arrhythmias) to ensure maximum perfusion of the optic nerve head. If central hemodynamics are impaired due to cardiac disease (previous myocardial infarction, arterial hypertension, circulatory failure, etc.), the patient must be managed together with a cardiologist. Appointment possible antiplatelet agents from the group of ticlopidine, pentoxifylline and dipyridamole.

Blood pressure monitoring in patients with progressive GND allows us to detect a significant decrease in it at night in patients taking systemic antihypertensive drugs and adjust the drug regimen. It is recommended to use only mild antihypertensive therapy and avoid taking antihypertensive drugs in the evening. In patients not taking antihypertensive drugs, it is difficult to adjust blood pressure at night. You should try to pick local antihypertensive therapy , aimed at reducing IOP during hours coinciding with the peak fall in blood pressure in order to improve perfusion pressure (for example, instilling latanoprost once a day). Latanoprost effectively reduces IOP even at low levels during both daytime and nighttime, which is especially important in the case of GND, when impaired perfusion of the optic disc often occurs at night. The use of betaxolol is preferable to timolol, given the hemodynamic impairment in GND.

In the group with vasospasm, it is possible to carry out carbogen therapy courses. An increase in the amplitude of the ocular pulse and an improvement in visual fields after inhalation of air enriched with carbon dioxide is explained by the removal of the primary vasospasm that exists with GND. There is experience in using magnesium , which also reduces the severity of peripheral vasospasm. Currently, attempts to use neuroprotectors at GND. Neuroprotective effects of ginkgo biloba preparations have been reported. Reception is carried out in courses of 2 months 2-3 times a year. There is no doubt the feasibility of a course of use of antioxidants and antihypoxants (emoxipine, histochrome, etc.) parabulbarly or in eye films.

Thus, the problem of diagnosing and treating GND is not purely ophthalmological, but affects a wide range of medical problems and requires the participation of a therapist, cardiologist, and neurologist.

Literature

1. Kamal D., Hitchings R. Normal tension glaucoma - a practical approach.// Br. J. Ophthalmol. 1998; 82 (7): 835-40.

2. Nesterov A.P. Basic principles for diagnosing primary open-angle glaucoma. Vestn. ophthalmol. 1998; 114 (2): 3-6.

3. Geijssen H.C., Greve E.L. Vascular concepts in glaucoma // Curr. Opin. Ophthalmol. 1995; 6:71-7.

4. Egorov E.A., Alyabyeva Zh.Yu. Glaucoma with normal pressure: pathogenesis, clinical features and treatment. // Proceedings of the conference “Glaucoma. Results and prospects at the turn of the millennium”: M., 1999 (in press).

5. Krasnov M.M. About intraocular blood circulation in glaucoma. Vestn. ophthalmol. 1998; 114 (5): 5-7.

6. Geijssen H.C. Studies on normal pressure glaucoma. Amsterdam: Kugler. 1991; 240.

7. Textbook of glaucoma. 3-d ed. M. Bruce Shields, Williams & Wilkins, Baltimore. 1992; 682.

Diagnostic criteria for GND

(R.Hitchings, D.Kamal, 1998)

The average IOP (true intraocular pressure) without treatment is less than or equal to 21 mmHg. Art. when measured during daylight hours

Open angle of the anterior chamber during gonioscopy

Absence of any reasons for the development of secondary glaucoma (increased intraocular pressure in the past due to trauma, long-term use of corticosteroids, uveitis)

Changes in the optic disc (ONH) typical for glaucoma with the presence of glaucomatous excavation and loss of neuroglial ring tissue

Defects in the visual field corresponding in severity to changes in the optic disc

Progression of visual field and optic disc changes

Frequently asked questions about IOP

Purchasing all-terrain track kits for your vehicle is quite a responsible process. First of all, this is due to the considerable cost of VGD tracks. Therefore, potential buyers are intensively looking for answers to their questions, which, as usual, arise quite a few, especially if we are talking about an expensive purchase. To make things easier for everyone and save your and our time, we suggest that you familiarize yourself with the most common questions that interest consumers.

What is the maximum depth of snow that a vehicle can move through on VOP?

We can say with full confidence that a vehicle with caterpillar propulsion feels confident on virgin snow up to 90 cm deep, which has been confirmed by repeated tests. The value of 90 cm is not the limit of possibilities, since it was not situationally possible to test the car in deeper snow.

What is the service life of VGD tracks in the winter and summer seasons?

According to information received directly from the manufacturer, with reasonable operation in winter, caterpillar tracks can travel on snow on average 15,000 km. The use of caterpillar tracks in the summer season reduces this figure to 10,000 km according to information.

What is the maximum speed allowed when driving on IOP?

The maximum permissible speed of a vehicle with installed All-Terrain Tracked Propulsors, which is recommended by the manufacturer, is up to 60-70 km/h on an asphalt road, and on snow cover – 20-30 km/h. These restrictions are primarily due to the safety of the driver and passengers.

Is it possible to install an IOP on a front- or rear-wheel drive car?

All-terrain tracked engines can only be used on off-road vehicles with a 4x4 wheel arrangement, and must have a differential lock. All-terrain propulsion systems are not produced for front-wheel drive or rear-wheel drive vehicles.

Why is it not allowed to use IOP without rollover stops?

The operation of all-terrain vehicles without rollover limiters is prohibited for a simple reason. If the caterpillar hits a high obstacle, especially at speed, for example, hidden under snow cover, then you can say goodbye to the suspension of your car and not only... The engine can twist in such a way that the car body is seriously damaged.

When and under what conditions is VOP supplied?

Sales of All-Terrain Tracked Kits are carried out on a 100% prepayment basis after concluding an agreement for the supply of CFD. The order processing time is 10-12 days (a delay of 3-5 days is possible), plus the time spent on the monetary transaction and on delivery of the order by the transport company named by the buyer or suggested by the seller.

Is a vehicle with VOP allowed to drive on public roads?

Unfortunately, the current Russian Road Traffic Regulations (SDR) restrict the movement of vehicles on public roads using all-terrain tracked VGD propulsion systems. If you have tracks installed on your car, then the car automatically falls under the category of low-speed vehicles. If you want to drive a VGD on city streets and on highways, then you will have to register the car as a tractor (slow-moving vehicle), and then move on a tracked vehicle on public roads in compliance with all established norms and rules for this type of vehicle .

All-Russian family tree (IOP) - one of the largest Russian Internet projects for genealogy(primarily covering the territory of the former USSR). Founded in 1999 Sergei Kotelnikov And Lyudmila Biryukova. Currently, it combines a guide to genealogical searches, a large genealogical forum, and a genealogy database. The site host (administrator) is Julia Zabello.

Site description

The VGD website is a constantly growing genealogical database where visitors can add information themselves, that is, in essence, it is a “people's project” in the field of genealogy. With the help of IOP you can find lost relatives, friends and acquaintances, create clubs of namesakes and explore your own family tree.

The site contains the following main sections:

genealogical dictionary
tips for aspiring genealogists
genealogical forum VGD is the largest section of the site with a large selection of topics based on search methods, various historical eras and geographic regions, with advertisements for searching for relatives and namesakes, etc. (as of March 2009 - 18,365 topics, 332,984 messages, 31,789 users, as of March 2012 - 30988 topics, 796053 messages, 100200 users)
genealogical knowledge base: alphabetical lists of personalities, geographical index, chronology of events
celebrity genealogy
paid services (genealogical research, production of noble coats of arms, photo restoration)
genealogy digital goods store
short english version

Research and publishing

In addition to Internet activities, the founders of the site and many of its visitors are engaged in scientific activities. In total, over the years of the project’s existence, more than 300 studies have been carried out, one of which is to clarify family tree Vladimir Putin.

In 2006, the first project was launched to publish a book based on materials collected by site users. As of 2009, there were already two such projects:

Trial

The preliminary hearing on November 25 and December 11 was postponed due to the failure of the parties to appear, the next hearing was scheduled for January 19, 2011.

On the evening of January 13, 2011, a message from the site’s host, Yu. V. Zabello, appeared on the VGD website forum, from which forum participants first learned about the lawsuit. An open letter in defense of the site was posted in the system Democrat January 15 and already in the first two days it collected more than 2,500 signatures; the letter is addressed to the President of the Russian Federation D. A. Medvedev, Chairman of the Government of the Russian Federation V. V. Putin, His Holiness Patriarch of Moscow and All Rus' Kirill, Chairman Commission under the President of the Russian Federation to counter attempts to falsify history to the detriment of the interests of Russia