Stagnant DN bilateral. What is the optic disc in ophthalmology - the optic disc. Stages of development of the disease

A congestive optic disc is a non-inflammatory edema and in most cases is due to increased intracranial pressure.

Etiology

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

Among diseases of the central nervous system, the most common cause of congestive disc development (64% of cases) are brain tumors. The disease is usually bilateral, unilateral congestive disc occurs with tumors of the orbit and traumatic hypotension of the eyeball.

Diagnostics

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

Classification

The classification is based on the stages of development of the process.

1. Initial congestive optic disc.
2. Pronounced congestive optic disc.
3. Pronounced congestive optic disc.
4. Stagnant disc in the stage of atrophy.
5. Atrophy of the optic nerve after stagnation.

Clinic

In the 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 captures the entire optic disc, its increase 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, an increase in the optic disc, blurring of the boundaries are observed. The veins are dilated, tortuous, hemorrhages appear, white foci 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 an increase in edema, the optic nerve disc protrudes more into the vitreous body. With prolonged existence of a stagnant disc, atrophy gradually begins to develop, a grayish tint appears against the background of hyperemia of the disc, which further intensifies as the edema decreases. With the development of atrophy, the disc acquires a dirty gray color (Fig. 9-9, 9-10, 9-11).

With a stagnant disc, normal discs persist for a long time. visual functions. With a sufficiently long existence of stagnation as a result of the death of peripheral fibers of the optic nerve, the boundaries of the field of view narrow. With the onset of atrophy of the optic disc, the narrowing of the field progresses rapidly. Various forms of hemianoptic visual field defects indicate the impact of the underlying pathological process on one or another part of the visual pathway. The decrease in visual acuity often occurs in parallel with the narrowing of the visual field.

Treatment

Treatment consists in eliminating the cause that caused the stagnation of the optic nerve head.

Literature

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

	Congested optic disc. Edema of the optic disc and peripapillary retina, dilated veins, hard exudate deposits and hemorrhages in the peripapillary region.
	Congested optic disc. FAGD. Late phase, sharply dilated tortuous veins. Hyperfluorescence of the optic disc.
	FAGD of a patient with congestive optic disc. arterial phase. Sharply dilated veins, extravasal hyperfluorescence from dilated papillary and peripapillary vessels.
	Congested optic disc. Sharply dilated tortuous retinal veins and vessels of the papillary and peripapillary regions. The caliber of the retinal arteries is not changed. The disc tissue is edematous, its borders are not clearly contoured.

Under the congestive optic disc (congestive optic nerve disc) in most cases is understood not as a pathology, but as a condition inherent in increased intracranial pressure.

During this violation, several stages are distinguished:

1. Initial stage.

Reduced to swelling on the periphery of the optic disc. At the same time, in the region of the fundus, the fuzziness of the boundaries of the ONH is visualized, which manifests itself from the side of the top. The disc itself is somewhat hyperemic.

2. Second stage.

The pronounced stagnation of the DNZ is called. Edema covers not only the periphery, but also the central sections of the disc. In a healthy person, the disk has a depression in the middle, with swelling it disappears, and this area protrudes towards the vitreous body. Increased hyperemia, redness of the optic disc.

Gradually, it becomes cyanotic, the venous network changes - the vessels expand, bulge onto the swollen disc itself.

In some cases, small hemorrhages are diagnosed in the area of ​​the affected disc.

The visual function at this stage of disc stagnation is still preserved. If the patient continues to see, but the pathological changes are great, then this condition is called "the first scissors of stagnation." Often a person has only migraine-like headaches, or no unusual symptoms at all.

The first 2 phases of OD edema can be corrected if the cause of this condition is removed. Gradually, the clarity of the boundaries of the optic disc will be restored, the swelling will subside.

3. The third stage, or pronounced swelling of the optic disc.

The disk swells even more, bulges into the vitreous body, more extensive hemorrhages appear on the optic disc itself, on the retina of the eye.

The retina also begins to swell, deform, and nerve fibers are compressed. After their death, the optic nerve cannot recover, as it is replaced by connective tissue cells.

4. Fourth stage.

The optic nerve atrophies and dies. The optic disc becomes much smaller, the edema also subsides, the condition of the veins normalizes, and the hemorrhages resolve. This stage is otherwise called the "second scissors of stagnation."

The processes are reduced to an improvement in the visual condition of the fundus, but a sharp drop in visual acuity.

Causes of congestive optic disc

If the reason for which pathological processes occur affects the optic disc for a long time, then vision is irreversibly lost.

Most often, the causes of the above processes are:

• head injuries, especially those that cause displacement of the bones and a decrease in the cranial cavity;
• changes in the state of the bones of the skull;
• edema, dropsy of the brain;
• tumors, aneurysms;
• brain inflammation.

In turn, dropsy of the brain can develop due to severe allergization of the body, against the background of blood pathologies, with kidney damage, and hypertension. Sometimes the onset of optic disc edema starts due to orbital injuries, with various ophthalmic diseases with a drop in the level of intraocular pressure.

Stagnation of the ONH develops against the background of a violation of the drainage of interstitial fluid from that area of ​​the nerve that is located in the orbit. In the normal state of the organs of vision, the outflow of excess fluid occurs by directing it into the cranial cavity.

If the pressure in the eyes drops, then the fluid lingers and flows poorly due to insufficient pressure on the nerve in the orbit.

The vision of the patient with optic disc stagnation can be quite normal for a very long time. But if the cause of this condition exists for a long time, and the pressure on the optic nerve itself also increases, then the phenomena of atrophy gradually develop.

Atrophic processes lead to the fact that nerve fibers die off, and connective tissue appears in their place. In this case, blindness occurs.

Treatment of a congested disc

Without the complete elimination of the cause of stagnation of the optic nerve head, this symptom will not be eliminated. Thus, the therapy of congestive optic disc is reduced to the treatment of the underlying disease.

congested optic disc- Edema of the optic nerve of non-inflammatory origin, usually caused by an increase in intracranial pressure. The clinical picture was first described by Graefe in 1860.

Pathogenesis. The following theories of the pathogenesis of congestive disc have been proposed:
inflammatory;
discirculation - the development of a stagnant disc due to circulatory disorders;
transport - the development of a congestive disc with an increase in the pressure of the cerebrospinal fluid on the optic nerve;
retention (currently the most accepted theory).

Retention theory of the development of a stagnant disc (Baer 1912). The optic nerve has sheaths that are a continuation of the meninges of the brain. The cerebrospinal fluid in the intershell spaces of the optic nerve moves towards the third ventricle. In the event of a violation of the outflow of fluid from the optic nerve through the third ventricle (due to increased intracranial pressure or for other reasons), pressure occurs on the cribriform plate of the optic nerve (the fold of the dura mater moves and presses the optic nerve against the underlying bones; it is compressed around the circumference), the displacement of which leads to disruption of the axoplasmic current in the nerve fibers, venous stasis and the development of edema of the optic nerve head, which is clearly visible through the optical media of the eye.

A congestive disc is caused by the retention of tissue fluid, which normally flows freely into the cranial cavity.

The severity of congestive optic discs reflects the degree of increase in intracranial pressure, but does not depend on the size of the mass formation in the cranial cavity. The rate of development of the stagnant disc is largely due to the localization of the neoplasm in relation to the CSF system of the brain and venous collectors, in particular to the sinuses of the brain: the closer the tumor is located to the CSF drainage pathways and sinuses, the faster the congestive optic disc develops.

Clinical picture. The disease is usually bilateral. A unilateral congestive disc is observed with tumors of the orbit, traumatic hypotension of the eyeball. Perhaps a combination of atrophy of the optic nerve head on the side of the brain tumor with congestive optic nerve head on the opposite side (Foster-Kenedy symptom).

Perhaps a combination with other symptoms of increased intracranial pressure: headache, bradycardia, vomiting, dizziness, epileptic seizures. In the clinic of hypertension syndrome, a congestive disc is not an early symptom. Often, brain tumors can proceed without its development.

There are five stages in the development of the congestive optic disc process:

I- initial stagnant disc - hyperemia of the disc, its boundaries are blurred, the veins are dilated, then the edema captures the entire optic disc, its increase is noted, the veins become not only dilated, but also tortuous, the arteries are narrowed;
II- pronounced stagnant disc - increased hyperemia, enlargement of the optic disc, its protrusion (prominence) into the vitreous body, hemorrhages, white foci appear on the disc and around it;
III- a pronounced stagnant disc - the prominence of the disc into the vitreous body increases, small yellow-white foci are found in the area of ​​the macula;
IV- stagnant disc with a transition to atrophy - a gray tint appears against the background of an edematous disc;
V- atrophy of the optic nerve after edema - the disk flattens and acquires a dirty gray tint.

Diagnosis of a congestive optic disc: the disc is enlarged and mushroom-like bulges into the vitreous body; swelling of the surrounding retina is visible; the color of the disk is pinkish-grayish; borders are fuzzy or not visible at all; the veins are sharply dilated, tortuous; there may be hemorrhages; narrow arteries; sometimes the vessels are lost in the edematous tissue.

Visual functions with a stagnant disc remain normal for a long time. Their change is associated with the development of optic nerve atrophy, when visual acuity begins to decline and the boundaries of the visual field narrow. However, a congestive disc is always accompanied by an increase in the size of the blind spot.

According to the peculiarities of the clinical course, a complicated congestive disc is distinguished. It develops in cases where the pathological process that caused an increase in intracranial pressure also has a direct effect on one of the sections of the visual pathway.

With complicated stagnant discs, there are:

Atypical changes in the visual field (hemianopic defects);
a combination of high visual acuity with a sharply narrowed field of view;
significant difference in visual acuity of both eyes;
a sharp decrease in visual acuity that occurs before the onset of atrophy (this symptom is associated with a transient spasm of the arteries that feed the optic nerve; the frequency of such attacks depends on several factors, including the severity of disc edema, and can be up to several attacks within 1 hour );
development of atrophy of one disc with bilateral congestion.

Diagnostics. The diagnosis is based on:
history;
examination of the fundus (ophthalmoscopy);
determination of visual fields (perimetry);
clinical picture of the disease;
results of neurological examination;
X-ray and fluorescent angiographic studies.

To clarify the cause of intracranial hypertension, computed (CT) or magnetic resonance (MRI) tomography of the brain is performed.

If signs of a congestive optic disc are found, the patient should immediately be referred for a consultation with a neurosurgeon or neurologist.

Differential Diagnosis. Differential diagnosis is carried out with neuritis and pseudoneuritis. The congestive disc in the initial stage of the disease differs from neuritis in the preservation of visual functions and the presence of partial or complete marginal edema of the optic disc. Pseudoneuritis is a developmental anomaly of the disc and is usually accompanied by abnormal vascular flow with atypical branching and networking of vessels on the surface of the disc. The difference in the caliber of arteries and veins is insignificant. Long-term monitoring of the dynamics of the clinical picture in some cases helps to establish the correct diagnosis. With a complicated congestive disc, the form of hemianopsia allows you to determine the localization of the tumor.

However, in some cases it is very difficult to differentiate a congestive optic disc from diseases such as incipient thrombosis of the central retinal vein, anterior ischemic neuropathy, and optic nerve meningioma. With these diseases, edema of the optic disc also occurs, but its nature is different. It is caused by pathological processes that develop directly in the optic nerve, and is accompanied by a decrease in visual functions of varying severity.

In some cases, due to the difficulties that arise in establishing a diagnosis, it is inevitable to perform a puncture of the spinal cord with a measurement of the pressure of the cerebrospinal fluid and a study of its composition.

Treatment. Etiotropic - elimination of the cause that caused the stagnation of the optic nerve head. To reduce edema, osmotherapy and dehydration therapy are performed. With the development of atrophy of the optic nerve - appropriate treatment. To maintain the nutrition of the nerve, vasodilating drugs (Cavinton, Trental, Sermion) are prescribed, drugs that improve the nutrition of the nervous system (Actovegin, Diavitol, Mexidol, Nootropil).

Course and forecast. With a stagnant disc, normal visual functions are preserved for a long time even with severe edema. In the future, there is a narrowing of the field of view. During the transition to the stage of atrophy, visual acuity quickly falls, the boundaries of the visual fields sharply narrow. The decrease in visual acuity and narrowing of the visual fields often occurs evenly in both eyes. In cases where the underlying pathological process affects the visual pathways, there may be an uneven decrease in visual functions in both eyes (complicated congestive disc). If the cause that caused the stagnation of the optic nerve head is eliminated before the development of the atrophy phase, then the edema regresses and the picture of the fundus returns to normal. However, if atrophic processes have begun, then even after the cause is eliminated, partial or complete atrophy of the optic nerve often develops.

The disc (nipple, head) is part of the optic nerve located inside the eye. Its diameter is approximately 1.2-1.9 mm, on average 1.5-1.6 mm (Linnik P.F. et al., 1994) - two times less than the diameter of the orbital part. The vertical diameter is slightly larger than the horizontal one, by an average of 0.18 mm. Due to the absence of myelin fibers, the ONH occupies the smallest possible area on the fundus - 2 mm 2 (Linnik P.F. et al., 1994). The length of the optic disc is about 1 mm. It is located 2.5-3 mm medially and 0.5-1 mm downward from the posterior pole of the eyeball. Its features include the absence of the meninges and myelin sheaths of nerve fibers. The supporting structures and vascular network in the disc are much more developed than in other parts of the optic nerve. The volume of the optic disc is estimated at 0.51 mm 3 (Linnik P.F. et al., 1994).

The number of nerve fibers in the ONH varies from 800,000 to 1,200,000 and decreases with age (Anderson D. R.). Nerve fibers are grouped into separate bundles (about 400 in number and 35 to 105 microns in diameter), each of which exits the eye through a separate hole in the cribriform plate. The topography of the location of nerve fibers in the optic disc reflects their course in the retina. The papillomacular bundle occupies most of the temporal half of the disc (therefore, the temporal side of the disc is slightly lower and thinner than the nasal one, since the layer of nerve fibers is thinner here). The fibers coming from the temporal half of the retina (arc fibers) are pushed aside to the periphery of the ONH and occupy the upper and lower temporal segments in it. The fibers extending from the nasal regions (radial fibers) occupy the upper and lower nasal segments, respectively. Nerve fibers coming from the nasal half of the retina occupy the superficial parts of the nerve fiber layer, and fibers coming from the temporal half of it occupy deeper parts. The fibers coming from the peripherally located retinal ganglion cells occupy a superficial position in the disk in relation to the fibers coming from the ganglion cells of the central parts of the retina.

Neuroglia in the ONH is represented only by astrocytes that surround each bundle of nerve fibers, separate them from blood vessels, form the supporting structure of the disc and the border tissue that separates the disc from neighboring areas. Astrocytes occupy 23% of the disk volume and only 11% in the orbital part of the optic nerve. The volume of supporting tissue in the disc has significant individual variations.

The optic disc is located in the sclerochorioidal canal, the shape and course of which varies, more often the canal has a conical shape, with a wide end facing backwards, a cylindrical shape is less often observed. Even rarer are channels with an expansion in the center and narrowing at the ends. An oblique course of the canal is possible, with a pronounced oblique course during ophthalmoscopy, the optic disc appears to be compressed in the horizontal direction, and its temporal part forms a gentle slope from the periphery to the center, which can be regarded as a flat marginal excavation. The canal is divided into choroidal and scleral parts. The opening in the vitreous membrane of the choroid forms the internal opening of the optic nerve canal, and the openings of the cribriform plate of the sclera form its external opening.

Vessels emerge from the center of the disc, around which you can see a depression - a physiological excavation, or a vascular funnel. Sometimes the vascular funnel is filled with connective tissue and glia that form Kunt's central meniscus. Due to the thinner layer of nerve fibers on the temporal side, the physiological excavation is located closer to the temple. With age, the size of the disk does not change (Armaly, 1967), but part of the supporting tissue atrophies. Since atrophy is diffuse in nature, it manifests itself in most cases not by the expansion of the physiological excavation, but by the flattening of the disc. Individual differences in excavation and protrusion of the disc are determined by the size of the scleral canal and the volume of the supporting tissue. With myopia, especially a high degree, stretching of the sclera to 1/4 of its thickness and expansion of the scleral canal lead to a pronounced flattening of the disc. The small size of the scleral canal and the significant development of the supporting tissue causes the absence of excavation in hypermetropes (Tron E. Zh., 1968).

At the level of the sclera, the disc is surrounded by fibrous tissue (contains many collagen and elastic fibers with a small inclusion of glial tissue and pigment) associated with the sclera (Elschnig's border tissue). This tissue is more strongly developed on the temporal half of the inner surface of the sclera.

Histologically, the ONH consists of several sections (Hayren S. S., 1976; Henkind P., 1976):

1) superficial (internal, retinal) - is a continuation of the layer of nerve fibers of the retina, in this section, the nerve fibers, which are the axons of ganglion cells, turn at an angle of 90 ° and go to the next, prelaminar part. There is no internal limiting membrane in the disk area. This section is separated from the vitreous body by a non-continuous neuroglial membrane of Elschnig (Elschnig). The layers of the retina, except for the layer of nerve fibers and the pigment epithelium, do not reach the edge of the disc. Their place is occupied by a ring of neuroglia - the intermediate tissue of Kuhnt - associated with the glial backbone of the disc. The retinal part of Bruch's membrane also does not reach the edge of the disc, but its choroidal part protrudes into the disc in the form of a visor, which serves as the boundary between the retinal section of the disc and its prelaminar part.

2) prelaminar (choroidal) department, located at the level of the choroid. It consists of bundles of nerve fibers dressed in an astroglial sheath that separates the fibers from the capillaries and glial plates that form the choroidal cribriform plate. A layer of astroglia (Jacoby's border tissue) separates the ONH from the choroid.

3) laminar (scleral) part - consists of the cribriform plate of the sclera (lamina cribrosa), neuroglia, bundles of nerve fibers passing through the holes of the cribriform plate, vessels.

In the lattice plate, there are:

a) posterior "scleral cribriform plate" - represented by several concentric sheets of dense connective tissue containing collagen and elastic fibers. Each sheet has perforations that coincide with each other, forming tubules through which bundles of nerve fibers from the prelaminar part pass. The spaces between the sheets are filled with neuroglia. The posteriormost layer is denser and more massive and merges with the septal system of the intrabulbar part of the optic nerve. The crossbars of the scleral cribriform plate are abundantly vascularized.

b) anterior "glial, or choroidal, cribriform plate" - a multilayer formation located at the level of the choroid, which goes without interruption from the sclera to the anterior edge of the disc and partially continues into the retina. The crossbars of the glial lattices contain capillaries surrounded by a thin layer of collagen fibers.

In the center of the cribriform plate there is a wide canal containing the central vessels of the retina in the connective tissue sheath.

4) retrolaminar section, located behind the cribriform plate and without sharp boundaries passes into the intrabulbar part of the optic nerve. This section is 2 times thicker than the optic disc (diameter 3-4.5 mm), which is due to the myelination of nerve fibers and the appearance of three membranes behind the sclera: soft, arachnoid and hard.

Factors that ensure the mechanical stability of the optic disc to fluctuations in intraocular pressure:

1) the dimensions of the scleral canal are minimal due to the exclusion of myelin sheaths. With an equal IOP, the force acting on the disk is proportional to its area.

2) the rigidity of the structure is facilitated by the axial course of the nerve bundles.

3) the glial cribriform plate acts as a spring, absorbing the fluctuations of the ophthalmotonus.

4) the mechanical structure of the optic disc is strengthened by a rigid central vascular bundle.

In some conditions, such as myopia, the optic nerve head is more prone to glaucomatous changes, due to the fact that compared to the norm it has less connective tissue.

The optic nerve occurs when intracranial pressure (intracranial hypertension) increases due to stenosis or occlusion of the cerebrospinal fluid, or the development of a volumetric pathological process in the cranial cavity, often a tumor, and often a combination of both. An increase in intracranial pressure can also be the result of such volumetric pathological processes as brain abscess, infectious granulomas, parasitic cysts, less often it is due to other causes, in particular craniostenosis, resulting from premature overgrowth of cranial sutures.

In most cases, but not always, congestive changes in the optic discs appear on both sides. In the process of development, they go through certain stages, while the severity of manifestations of stagnation of the optic nerves changes, with the progression of the underlying disease, it increases.

E. Zh. Tron (1968) considered the congestive optic disc as a certain form of its lesion, which is manifested by a characteristic ophthalmoscopic picture, and a violation of the functions of the eye. With congestive optic discs, there are usually other clinical manifestations characteristic of intracranial hypertension. Of great importance is the nature, localization and dynamics of the development of the underlying pathological process. E. Zh. Tron emphasized the importance of identifying congestive optic discs in the diagnosis of many neurological and neurosurgical diseases, while noting that a congestive disc "is the most common eye symptom in brain tumors."

Intracranial hypertension as the main cause of congestive optic discs and their complications

Intracranial hypertension is usually characterized first by periodic, and then by constant, sometimes aggravated, diffuse, arching headache. Against this background, with an increase in headache (hypertensive crises), cerebral vomiting, a periodic sensation of fog before the eyes, disorders of vestibular functions, bilateral damage to the abducens nerves, pronounced autonomic reactions, and increased mental exhaustion are possible. workload. Against this background, in cases where the patient is not provided with adequate assistance, the development of Bruns' syndrome is possible.

Sometimes there are clinical observations in which congestive optic discs are the main clinical manifestation. First of all, they include the syndrome of primary benign intracranial hypertension.

Theories of pathogenesis

The pathogenesis of congestive optic discs is still debatable. The first hypothesis was proposed in 1866 by A. Grefe (Graefe A., 1828-1870). He believed that the cause of congestion in the fundus is violation of the outflow of venous blood from the eyeball through the central retinal vein into the cavernous sinus. Infiltration of the optic nerve tissue and its disc was explained by stagnation in the central retinal vein. However, this version was later disputed, since venous outflow from the eyeball is possible not only through the central vein, but also through anastomoses between the ophthalmic veins and the veins of the face, as well as through the ethmoid venous plexus, moreover, thrombosis of the central retinal vein is characterized by a different ophthalmoscopic picture.

Concerning T. Leber (German ophthalmologist Leber Th., 1840-1917) in 1877 suggested that ophthalmoscopic changes, interpreted as manifestations of stagnation, are due to inflammation of the optic nerve. He suggested using the terms "papillitis" or "congestive neuritis" in such cases; he was supported by an authoritative at the beginning of the 20th century. ophthalmologist A. Elschnig, who agreed that "congestive nipple is nothing but a special form of inflammation." He recognized such inflammation as a secondary, usually provoked inflammatory focus in the orbit or in the cranial cavity.

Since the essentially different concepts of "congestive nipple" and "neuritis" began to be perceived as the same phenomenon detected during ophthalmoscopy, the English physiologist and ophthalmologist G. Parson in 1908 instead of the term congestive nipple introduced the term "nipple edema" or "papilloedema" ("swelling of the brain") . He used the term "neuritis" in cases where there was a relatively small protrusion of the optic disc in combination with a pronounced visual impairment. The need to differentiate edema of the optic nerve head from its inflammation, i.e. from neuritis was obvious, so Parson's proposal to introduce a new term into practice was supported by many physiologists and clinicians of that period, in particular K. Wilbrand and A. Zenger, authors of the first monograph on neuro-ophthalmology "Neurology of the Eye" (1912-1913). Willingly used this term already in the middle of the 20th century. and well-known domestic neuro-ophthalmologist I.I. Merkulov.

significant certainty in differentiating between congestion and inflammation of the optic disc introduced by V. Gippel (Hippel W., 1923). He emphasized that the congestive papilla of the optic nerve is not its inflammation, but something completely different. The scientist noted that congestive manifestations in the optic nerve papilla usually occur in patients with brain tumors and other diseases, manifested by an increase in intracranial pressure. At the same time, he drew attention to the fact that, in contrast to an inflammatory lesion of the optic nerve, with its congestive nipple (disk), normal or close to normal visual acuity can be maintained for a long time.

Thus, the issue of the pathogenesis of congestive optic discs has been a subject of discussion for a long time and cannot be recognized as absolutely resolved until now. Many theories have fallen into oblivion. And at present, perhaps only two of them are recognized, which today can be considered as the main ones -

• Schmidt-Manz transport theory, recognized as the most probable by R. Bing and R. Bruckner (1959), and
• Baer's retention theory(German ophthalmologist Behr S., born in 1876), which was considered preferable by E. Zh. Tron (1968) and I. I. Merkulov (1979).

According to the transport theory development of a congestive optic disc, the subarachnoid space of the intraorbital optic nerve communicates with the subarachnoid space of the cranial cavity, since it is formed by the meninges penetrating the orbital cavity together with the optic nerve, which consists of brain tissue.

With an increase in intracranial pressure, cerebrospinal fluid penetrates into the subarachnoid space of the optic nerve, accumulates in it, and gradually forms a club-shaped expansion that compresses its fibers.In the nerve, compression occurs primarily of those fibers that make up its outer sections.In parallel, in the optic nerve there is a difficulty in blood circulation. All this provokes swelling of this nerve and its disc. version is attractive. However, the presence of communication between the intershell spaces in the cranial cavity and the retrobulbar intraocular part of the optic nerve turned out to be not indisputable, since experimental work appeared that disproved the connection between them.

At the heart of Bohr's retention theory (1912) lies the idea that the aqueous tissue fluid formed mainly in the ciliary body normally flows along the optic nerve into its intracranial part, and then into the subarachnoid space. According to this theory, a congestive optic disc with an increase in intracranial pressure is due to a delay in the outflow of tissue fluid along the optic nerve into the cranial cavity. This is due to the fact that with an increase in intracranial pressure, there is a difficulty, and then a blockade of the movement of tissue fluid, as Behr believed, mainly at the exit of the optic nerve through the bone hole (optic canal) into the cranial cavity.

The fibrous (intracranial) part of the optic canal is formed by a fold of the dura mater stretched between the anterior inclined process and the upper edge of the opening of the optic canal. This fold partially covers the top of the optic nerve at its exit from the bone canal into the cranial cavity. With an increase in intracranial pressure, the fold of the dura mater is pressed against the optic nerve, and the nerve itself is pressed against the underlying bone structures. As a result, the tissue fluid of the eye flowing along the nerve is retained in its orbital and intraocular regions, including in the optic nerve head. The fibers of the optic nerve are gradually squeezed by it along the entire circumference of the nerve and, in parallel, its swelling develops and progresses, primarily swelling of the bundles of its fibers located along the periphery. Over time, usually after weeks, sometimes many months, the pupillomacular bundle, which occupies a central position at this level of the optic nerve, is also involved in the process.

In the optic disc, the pupillomacular bundle is located in its temporal part, and this explains why, with congestive optic disc, edema of the temporal edge of the disc usually develops later than its other departments. The edema of the optic disc is manifested more often, starting from its upper edge. The relatively late involvement of the pupillomacular bundle in the pathological process makes it possible to understand the often long-term preservation of visual acuity in a patient with congestive phenomena in the fundus.

In 1935, Baer wrote that in the initial stage of a congestive optic disc, tissue fluid accumulates between the bundles of its fibers, which leads to the development of intrafascicular edema of the optic nerve. In the future, it also appears in the nerve fibers themselves, spreads along the nerve, penetrating at the same time into the surrounding subpial space. Baer suggested that the spread of edema of the optic nerve occurs from its disk to the bone canal. Reaching the optic nerve canal, the disc edema terminates at this level.

Most of the authors who conducted morphological studies of the optic nerve with congestion in its disk (Hippel E., 1923; Schick F., Bruckner A., ​​1932; and others) came to the conclusion that the edema of the optic nerve is especially pronounced in the perivascular spaces of the branches central vessels of the retina (arteries and veins), as well as in the optic nerve head and its proximal sections, in which these vessels pass.

I. I. Merkulov (1979) adhered to the retention theory of the development of congestion in the fundus and at the same time recognized that disc edema, or congestive optic disc, is the result of a violation of the circulation of aqueous tissue fluid in its subpial space and in the perineural fissures, as well as disorders of microcirculation in the optic nerve. He also noted that the pressure of tissue fluid, which accumulates in the event of a violation of its outflow in the subpial space, on the optic nerve occurs evenly, in accordance with Pascal's law, according to which pressure on any part of the fluid surface is transmitted in all directions with the same force.

E. Zh. Tron (1968) recognized the great advantage of Beer's retention theory that it explains not only the pathogenesis, but also a number of clinical features of the state of visual functions in congestive optic disc. At the same time, he noted that not one of the existing theories, including the retention one, can be considered definitively proven. He believed that when studying the pathogenesis of congestive optic discs, one should clarify the degree of edema distribution along the optic nerve and find out whether the nerve edema, as Behr argued, does not go beyond its intraorbital segment, breaking off at the level of the bony optic foramen. In addition, E.Zh. Tron noted that from the standpoint of this theory, such facts as a one-sided congestive disc, a different frequency of congestion of the optic nerve discs in intracranial volumetric pathological processes of different localization, and the possible absence of congestion in the optic nerve discs in some cases of brain tumors cannot be satisfactorily explained. accompanied by an increase in CSF pressure.

Ophthalmoscopic picture

The ophthalmoscopic picture with a congestive optic disc depends on the stage of the process. According to E. Zh. Throne, there are five of them:

1. initial stagnant disc
2. pronounced stagnant disc
3. pronounced stagnant disc
4. stagnant disc in the stage of atrophy;
5. atrophy of the optic disc after stagnation.

These stages do not have a clear distinction and gradually pass into each other. The development of congestive optic discs and their progression largely depends on the duration and severity of intracranial hypertension, and due to their certain variability, the dynamics of ophthalmoscopic changes in the fundus is not identical either. However, such a separation of the stages of development of a congestive optic disc still has practical meaning, since it contributes to the characterization of the patient's set of ophthalmoscopic signs and creates opportunities for judgments about the severity of intracranial pressure and, therefore, allows predicting further dynamics of the clinical picture.

In the early stage of stagnant disc development (initial congestive optic disc) is characterized by venous hyperemia in the region of the disc and the fuzziness of its boundaries. A small uneven swelling of its tissue gradually develops along the edge of the disc, and a slight protrusion of the disc appears. At first, the edema does not capture the entire circumference of the disc, but only its individual sections, more often these are its upper and lower edges and the place where large vessels pass over the edge of the disc. The edema then spreads to the inner (nasal) edge of the disc. The outer (temporal) edge of the optic disc remains free of edema for the longest time, and this is recognized by almost all authors. In the zone of marginal edema of the disc, its tissue acquires a whitish tint, due to the fact that the accumulation of tissue fluid between the nerve fibers at the edge of the disc to some extent hides its usual color. In addition, at the site of the marginal edema of the disc, one can note a radial striation caused by the expansion of the nerve fibers by the edematous fluid. The venous vessels of the fundus in the initial stage of the congestive disc gradually expand, while the caliber of the arteries remains the same.

Further marginal edema of the optic disc increases and gradually spreads throughout the disc, last of all, the depression of the disc is filled with edematous tissue (physiological excavation). Before filling it, for some time at the bottom of the depression, one can see the central vessels of the retina. With an increase in edema of the optic nerve tissue, an increase in the size of the disc, its diameter, as well as the degree of disc protrusion above the level of the surrounding retina towards the vitreous body occurs. The veins become not only dilated, but also tortuous, the arteries narrow somewhat. With the spread of edema to the physiological disc excavation, according to E. Zh. Tron, the stage of the initial congestive optic disc can be considered completed.

With a pronounced stagnant disc of the optic nerve, more significant hyperemia and an increase in the disc, as well as an increase in the blurring of its borders, attract attention. Swelling of the borders of the disk is observed along its entire circumference, while the disk is already significantly out in the direction of the vitreous body. The veins are wide and tortuous. The underlying edematous retinal tissue overlaps fragments of blood vessels in places. The edematous disc tissue becomes cloudy. In the fundus, hemorrhages and white foci may appear. Hemorrhages can be multiple, different in size, are more often linear in shape and are located mainly along the edges of the disc, as well as in adjacent parts of the retina. They are usually recognized as a consequence of obstruction of blood circulation in the veins of the disc and rupture of small venous vessels. There is an opinion that the role of toxic factors (I. I. Merkulov, 1979) or concomitant manifestations of aseptic inflammation is also possible in the origin of hemorrhages. However, even when in a pronounced congestive optic disc, hemorrhages in the fundus may not be for a long time. The appearance in the edematous tissue of the disk of white foci of various sizes and outlines is usually explained by the degenerative degeneration of sections of the nervous tissue. They occur in the congestive optic disc less often than hemorrhages, and when they occur, they are usually combined with foci of hemorrhages.

Pronounced stagnant discs are usually characterized by the same ophthalmoscopic signs detected during ophthalmoscopy, however, the degree of their severity by this time is much greater. Due to the intense edema of the disc, it will stand considerably and protrude into the adjacent vitreous body. This distance can be up to 2.5 mm. Particularly noteworthy is the increase in the diameter of the disk, it is sometimes so significant that during ophthalmoscopy the disk does not fit into the field of view of the fundus even after medical dilation of the pupil, and then the disk has to be studied in parts. Hyperemia of the disk at this stage of its stagnation becomes so pronounced that upon examination, its almost complete fusion in color with the surrounding retina is noted. The vessels in this case can be almost completely immersed in the edematous tissue of the disc and become visible only before they go beyond it.

The entire surface of the disc is dotted with small and large hemorrhages and white foci. Multiple foci of hemorrhage are often found in the retina. Then they are located mainly around the congestive optic disc, some of them merge with each other, forming blood "puddles". Sometimes, with severe stagnation of the optic nerve head, foci of hemorrhage can occur between the optic nerve head and the macular zone, and they may also appear at a distance from the disk. In such cases (in 3-5%), they can form small white foci in the form of a half-star or star, known as pseudoalbuminuric (or stellar) retinitis, which can also extend to the macula. Similar changes in the retina are observed in the area of ​​the macular zone in hypertension and kidney diseases, complicated by arterial hypertension. A rapid decrease in visual acuity with congestive optic discs usually occurs during their transition from the stage of pronounced congestive discs to the stage of atrophy.

Long-term signs of a pronounced congestive optic disc gradually pass into the next stage of its development, known as stagnant disc in the stage of atrophy . At this stage, attention is drawn to the fact that the hyperemic congestive disc is covered with a gray coating, while the severity of the degree of disc edema gradually decreases. If during the period of the culmination of the stagnant disc, foci of hemorrhage and white foci were detected in it, then during the transition of the stagnant disc to its atrophy, they gradually resolve and disappear, while the disc gradually turns pale. As a result, it acquires a white color with a dirty tint, its boundaries remain indistinct, the dimensions decrease, but remain somewhat larger than normal. In some places, a small, uneven protrusion of the optic nerve head remains for some time. His veins at this stage of the process are still dilated and tortuous, his arteries are narrowed.

In the future, the consequences of stagnant phenomena in the disk finally disappear, and a typical final phase of the stagnant disk is formed - stage of secondary disc atrophy optic nerve after stagnation. It is characterized by pallor of the disc, some irregularity of its outlines and indistinct boundaries, while the veins and arteries of the disc become narrow. Signs of this stage of development of a congestive optic disc can persist for a very long time, sometimes a year or more. However, over time, its boundaries become more and more clear, the color is white (the color of the foil or muscle tendon), the size of the disc reaches its original (normal) size. At this stage, secondary atrophy of the optic disc after stagnation is difficult, and sometimes impossible, to distinguish from its primary atrophy, if only ophthalmoscopic data are used. Clarification of the origin of the atrophy of the optic nerve head in such cases is possible only taking into account carefully collected anamnestic data, as well as comparing the existing state of the fundus with the results of previous ophthalmoscopy and other methods of neuro-ophthalmological, as well as neurological examination.

If the cause of the congestive disc is eliminated during the treatment, but before that, secondary atrophy of the optic disc after stagnation has already developed, then in this case, the disappearance of the remnants of ophthalmoscopic signs of stagnation in the fundus and the development of an ophthalmoscopic picture that mimics a condition characteristic of simple atrophy of the optic disc, happens faster. A congestive optic disc usually develops simultaneously on both sides, but exceptions to this rule are possible.

Single sided stagnant disc of the optic nerve is possible with a tumor of the orbit, traumatic damage to intraorbital tissues and, in some cases, supratentorial localization of volumetric pathological processes (tumor, abscess, etc.). A unilateral congestive disc is also characteristic of Föster Kennedy syndrome, in which, first, on one side (usually on the side of the pathological focus), primary atrophy of the optic nerve head is detected, and then signs of a congestive disc appear on the other side. This syndrome is more common with intracranial neoplasms growing in the middle cranial fossa, sometimes with tumors of the lower back sections of the frontal lobe.

Thus, the identification of a particular stage of a congestive optic disc in a patient often does not in itself make it possible to judge the duration and outcome of the underlying pathological process.
The rate of formation and change of stages of a congestive optic disc usually corresponds to the rate of development and localization of the cause that caused it. If a patient develops occlusive hydrocephalus, manifestations of intracranial hypertension, including the development of congestive optic discs, may develop rapidly. Sometimes manifestations of the initial congestive disc are transformed into a pronounced congestive disc within 1-2 weeks. However, the ophthalmoscopic picture of a congestive optic nerve head can stabilize for several months, and in some cases even regress, as happens, for example, with primary benign intracranial hypertension.

visual functions

Visual acuity and visual fields during the development of congestive optic discs in typical cases may remain unchanged for some time, sometimes for a long time (correspond to a premorbid state). The first clinical sign of the development of a congestive optic disc is usually an enlargement of the physiological scotoma, a blind spot most easily detected by campimetry. Edema of the optic disc tissue extends to the adjacent parts of the retina and affects its function. The increase in signs of stagnation and the size of the disc leads to a further increase in the size of the blind spot.

In 1953-55. S. N. Fedorov, using campimetry data and strictly standardized photographs of the fundus in patients with intracranial tumors, in the process of completing his Ph.D. thesis, showed that an increase in the size of the blind spot outstrips the appearance and subsequent development of ophthalmoscopic signs of congestive optic discs, primarily changes in their diameter . If, however, in a patient with congestive optic discs, the tumor was removed before their atrophy, then the decrease in the blind spot began to decrease earlier than the ophthalmoscopic picture, indicating a tendency towards normalization of the discs.

The first visual disturbances subjectively perceived by patients with congestive optic discs are usually short-term episodic sensations of fog before the eyes. These short-term but significant visual disturbances occur, usually during periods of physical exertion or being in a stooping position. K. Baer considered it possible to explain such periodic blurring of vision by a deterioration in the conductivity of nerve fibers in the region of the optic nerve canal as a result of a temporary increase in intracranial pressure in a patient.

The boundaries of the visual fields with a congestive optic disc can remain within the normal range for a long time. However, after months, sometimes after a year or more, a narrowing of the visual fields of the concentric type, detected during perimetry, occurs and gradually increases, while first their boundaries narrow to colors, and then to white light, in most cases evenly along all meridians.

With an increase in the severity of atrophy of the optic discs, a decrease in visual acuity is manifested and rather rapidly increases. Sometimes the loss of vision in this case can develop catastrophically: with rapidly progressive atrophy of the optic nerves, blindness may occur in 2-3 weeks.

However, if a patient with congestive optic discs undergoes a radical neurosurgical operation or palliative intervention aimed at reducing intracranial pressure, congestion in the fundus begins to regress after a few weeks and this process continues for 2-3 months, and sometimes longer. The development of signs of regression of congestion in the optic nerve head is usually preceded by a gradual decrease in the size of the blind spot. Preservation of vision is more likely if neurosurgical intervention was performed before the advent of ophthalmoscopic signs of secondary atrophy of the optic discs. In such cases, one can hope for the possibility of normalizing the state of the fundus and an almost complete or complete restoration of visual function.