OPTIC NERVE [nervus opticus(PNA, BNA), fasciculus opticus(JNA)] - second pair cranial nerves, representing the initial section of the visual pathway. 3. n. formed by the axons of visual ganglion neurocytes (neurocytus opticoganglionaris, LNH) of the ganglion layer of the retina of the eyeball. Composed of 3. n. Efferent fibers were also found, the origin of which is not precisely established. In terms of development, the 3rd nerve, like the retina, is part of the brain, which makes it different from the rest of the cranial nerves.

Embryogenesis

In human embryos already at the 3rd week. During intrauterine development, optic grooves appear in the wall of the neural plate of the head, which deepen and form optic vesicles, which later represent spherical convexities of the lateral walls of the anterior medullary vesicle. At the beginning of the 5th week. the distal part of the optic vesicles is drawn inward and the optic cups (eye cups) are formed. At the same time, differentiation of the walls of the optic cups occurs: the outer layer turns into a pigment layer, and the inner layer, after complex changes, differentiates into the retina. Invagination, leading to the formation of the optic cup, occurs eccentrically - somewhat closer to its ventral edge, as a result of which the integrity of the optic cup is disrupted and the so-called. vascular fissure (fissura chorioidea). It continues in the form of a groove along the ventral surface of the eyestalk, connecting the optic cup with the medullary vesicle and subsequently forming the 3. n. Along this groove in the stalk, the ophthalmic artery sends a branch through the vascular fissure into the optic cup, which is called the vitreous artery (a. hyaloidea). The proximal part of this artery branches in the retina and is subsequently called the central retinal artery (a. centralis retinae), its distal part later undergoes reverse development. Due to the presence of the vitreous artery and the connective tissue associated with it, the groove in the eyestalk remains open even after the choroidal fissure of the optic cup is closed. At the end of the 6th - beginning of the 7th week. a double-walled epithelial tube is formed from the eyestalk, with vessels lying inside the cut. At the same time, the axons of the visual ganglion neurocytes of the retina grow along the marginal layer and approach the vessels lying in this tube. So, that's it more nerve fibers penetrate the eyestalk. By 8 months intrauterine development of fibers of the intracranial part 3. n. become covered with a myelin sheath, the entire nerve acquires a well-defined connective tissue sheath, and the original tissue of the eyestalk disappears, with the exception of some glia-like elements.

Anatomy

3. n. begins in the area of ​​the visual part of the retina (pars optica retinae) with a disk, or nipple, 3. n. (discus n. optici), leaves the eyeball through the cribriform plate of the sclera, goes back and medially in the orbit, then passes through the bone optic canal (canalis opticus) into the cranial cavity; in the optic canal it is located above and medial to the ophthalmic artery (a. ophthalmica). After leaving the optic canal at the base of the brain, both 3. n. form an incomplete optic chiasm (chiasma opticum - Fig. 1) and pass into the visual tracts (tractus optici). Thus, nerve fibers 3. n. continue continuously to the lateral geniculate body (corpus geniculatum lat.). In this regard, in 3. n. four sections are distinguished: 1) intraocular, or intrabulbar (from the beginning of the 3rd century until it leaves the eyeball); 2) orbital, or retrobulbar (from the exit point from the eyeball to the entrance to the opening of the optic canal); 3) intracanal (corresponding to the length of the optic canal); 4) intracranial (from the place of exit from the optic canal to the chiasma - the visual chiasm of the right and left intracranial parts of the 3rd n.). According to E. Zh. Tron (1955), the total length is 3. n. is 35-55 mm. The length of the intraocular section is 0.5-1.5 mm, orbital - 25-35 mm, intracanal - 5-8 mm and intracranial - 4-17 mm.

Disc 3. n. represents the junction of the optical fibers of the retina in the channel formed by the membranes of the eyeball. It is located in the nasal part of the fundus at a distance of 2.5-3 mm from the posterior pole of the eye and 0.5-1 mm downward from it. The shape of the disc is round or slightly oval, elongated in the vertical direction. Its diameter is 1.5-1.7 mm. In the center of the disc there is a depression (excavatio disci), which has the shape of either a funnel (vascular funnel) or (less often) a cauldron (fiziol, excavation). In the area of ​​this depression, the central retinal artery passes into the retina (tsvetn. Fig. 4) and the vein accompanying it. Disc area 3. n. lacks photosensitive elements and represents a physiologically blind spot (see Field of vision). In the retina in the area of ​​the disk 3. i. Nerve fibers do not have a myelin sheath. Upon exiting the eyeball, nerve fibers 3. n. acquire it, become pulpy. The thickness of the nerve fibers is 3. n. different. Along with thin nerve fibers (diameter 1-1.5 microns), thicker ones (5-10 microns) are also found. The axons of the visual ganglion neurocytes of the retina, forming 3. n., are located in it according to certain areas of the retina. Thus, nerve fibers from the upper parts of the retina are located in the upper (dorsal) side of the 3rd n., fibers from lower sections- in the lower (ventral), from the internal - in the internal (medial), and from the external - in the external (lateral) side 3. n. Coming from the area of ​​the spot (macula) of the retina, the papillomacular bundle (axial, or axial, bundle), consisting of the thinnest optical nerve fibers, in the area of ​​the disk 3. n. located in the inferolateral section. As you remove 3. n. from the eyeball this bundle occupies more and more central position in the nerve. At the entrance to the optic canal, it is located in the center of the nerve and on the section has an o round shape. It retains this position in the intracranial part 3. n. and in the optic chiasm - chiasm.

3. n. in the orbit, optic canal and cranial cavity lies in the external and internal vaginas 3. n., but their structure corresponds to the membranes of the brain (vaginae ext. et int. n. optici). The external vagina corresponds to the dura mater of the brain (color. Fig. 1). The internal vagina limits the intervaginal space from the inside and consists of two membranes: arachnoid and soft. The soft shell directly covers the trunk of the 3rd n., separated from it only by a layer of neuroglia. Numerous connective tissue partitions (septa) extend from it into the trunk, separating the 3. n. into individual bundles of nerve fibers. Intervaginal space 3. n. is a continuation of the intershell (subdural) space of the brain and is filled with cerebrospinal fluid. Violation of the outflow of fluid from it leads to swelling of the disc 3. n. - congestive nipple (see).

At a distance of 7-15 mm from the eyeball in the 3rd n., most often from its lower side, the central retinal artery enters, the edges pass through it, accompanied by a vein and in the area of ​​the 3rd n. disc. is divided into branches that supply blood to the retina. At the exit point 3. n. from the eyeball, the posterior short ciliary arteries (aa. ciliares post, breves) form an arterial plexus in the sclera - the vascular circle 3. n. (circulus vasculosus n. optici), or the arterial circle of Haller - Zinn, due to which the blood supply to the adjacent part of the 3. n. The rest of the orbital section is 3. n. is supplied with blood, according to Hayreh (S. Hayreh, 1963, 1969), Wolff (E. Wolff, 1948), by the branches of the central retinal artery passing through it, and according to Francois (J. Francois et al., 1954, 1956, 1963 ), in a third of cases there is a special axial artery 3. n. Intracranial section 3. n. They supply blood to the branches of the anterior cerebral (a. cerebri ant.), anterior communicating (a. communicans ant.), ophthalmic (a. ophthalmica) and internal carotid (a. carotis int.) arteries. Outflow venous blood carried out into the ophthalmic veins (vv. ophthalmicae) and the cavernous sinus of the dura mater of the brain.

Physiology

3. n. is a bundle of fibers (axons) of the third neuron of the visual afferent pathway; the first neuron is photosensory cells; the second - bipolar neurocytes of the retina (see Visual centers, pathways). It receives stimuli from the more peripheral structures of the retina excited by light in the form of slow tonic potentials, which are transformed in the ganglion layer of the retina (see) into fast electrical impulses that transmit incoming visual information to the visual centers along individual fibers 3. n. The study of bioelectric processes occurring in 3. n. is important for understanding physiol, the foundations of a number of visual functions: light perception (see) and color perception (see Color vision), visual acuity (see), etc. Reaction 3. n. to a light stimulus consists of a series of individual rapid changes in potential, recorded on an oscilloscope in the form of the so-called. spikes. Spike duration approx. 0.15 ms, its amplitude and shape for a given nerve fiber are constant, that is, they follow the “All or nothing” law (see). Changing the light intensity only changes the spike frequency; amplitude and shape remain unchanged. The higher the light intensity, the higher the spike frequency. X. Hartline showed that in 3. AD. In vertebrates, there are three types of different fibers: the first type reacts with an explosion of impulse activity when the light is turned on (on-fibers), the second type reacts with such explosions both when the light is turned on and off (on-off fibers), and the third type reacts with increased activity when the light is turned off. (off-fiber). According to the experimental data of Wagner (G. N. Wagner) and others (1963), obtained on fish with color vision, individual visual ganglion neurocytes of the ganglion layer of the retina and, consequently, individual nerve fibers of the 3. n. respond differently to different color stimuli. Thus, short-wave rays cause impulse activity during light stimulation, and maximum activity is observed under the action of green rays (which corresponds to the maximum spectral sensitivity of the eye). Long-wave rays, on the contrary, stop impulse activity, even spontaneous.

One of important features in reactions of fibers 3. n. is that they summarize the activity and interaction of more peripheral structures of the visual pathway. Kuffler (S. W. Kuffler, 1952) established that one visual ganglion neurocyte (and, therefore, one 3rd fiber) transmits along its axon impulses from many receptor cells scattered over a wide area of ​​the retina, the so-called. receptive field; this is due to the presence of extensive horizontal connections between individual nerve elements in different layers of the retina. This transmission is anatomically determined, since the number of individual nerve fibers in 3. n. up to 1 million, and the number of receptors in the retina is approx. 130 million. The size of the receptive fields is different. In mammals, the receptive fields of optoganglionic neurocytes are round in shape; they respond by increasing their impulses when stimulated either at their center or at the periphery. The relationship between the center and the periphery is reciprocal (see Reciprocity). Under conditions of dark adaptation, receptive fields usually do not exhibit such reciprocity. Some receptive fields are particularly sensitive to the movement of stimuli across the retina.

Research methods

When studying 3. n. determine central vision (see Visual acuity), peripheral visual field (see), visual adaptation (see Visual adaptation), visual fields for white, green, blue, red colors (see Color vision), conduct scotometry (see ), ophthalmoscopy (see Fundus, Ophthalmoscopy). Ability 3. n. reproducing the frequency of intermittent current, which irritates the eye (flickering phosphene), makes it possible to determine the rate of occurrence and flow of excitation in the visual neuron (see Electroretinography). In addition, state 3. n. in normal conditions and in pathological conditions, fluorescein angiography methods (see) and rentgenol, examination of the optic canal help to clarify.

X-ray examination of the optic canal. The main research technique is radiography of the skull in an oblique aiming projection, in which the central beam of radiation is combined with the axis of the channel, located perpendicular to the surface of the X-ray film. This method was first used in 1910 by Rhese, and then in a slightly modified form by H. A. Golwin, and therefore this method often bears the name of both authors. There are various modifications of Rezei Golvin's methods. To compare the right and left optic canals, radiography of both orbits is necessary. In this case, a cassette measuring 13 X 18 cm is placed transversely and raised above the table plane at an angle of 10° (Fig. 2). The patient is positioned so that the cassette is adjacent to the orbit under study, and the bridge of the nose is 3-4 cm above the average longitudinal line of the cassette; the vertical diameter of the orbit is aligned with the average transverse line of the cassette. The line passing from the external auditory opening to the corner of the orbit (basal line) forms an angle of 40° with the perpendicular to the horizontal plane, and the sagittal plane of the skull with the same perpendicular forms an angle of 45°. The central beam of radiation is directed to the center of the cassette perpendicular to the horizontal plane.

The optic canal is normally displayed on film as a round or oval hole in diameter. 3-6 mm (Fig. 3), its shape and size depend on projection conditions and focal length. In 33% of cases, there is a discrepancy between the values ​​of both visual channels. The radiograph does not give the absolute dimensions of the diameters of the optic canals.

Pathology

Frequency of diseases 3. n. among others eye diseases the average is 1 -1.5%. Severity of diseases 3. n. determined by the fact that in 19-26% of cases they end in blindness.

Patol, processes 3. n. It is customary to divide into anomalies of disc development 3. p.; damage; circulatory disorders in the blood supply system 3. n.; inflammation; congestive nipple; atrophy (primary and secondary); tumors. Features of the lesion 3. n. for diseases of the nervous system - see Vision.

Developmental anomalies optic nerve head are caused by deviations in the process embryonic development rudiment 3. n. and are relatively rare. These include following forms. Megalopapilla - an increase in the diameter of the disc compared to its normal size. Hypoplasia is a decrease in disc diameter. Coloboma (see) is a defect in the place of which connective or glial tissue is formed, involving only the nerve sheath or the nerve itself, or both the sheath and the nerve at the same time. With ophthalmoscopy - at the site of the disc 3. n. a round or oval depression several times its size. Double disc 3. n. (associated with congenital splitting of the trunk 3. n.); in this case, two discs are visible in the fundus. Disc pigmentation 3. n.; on the fundus of the eye there are nested accumulations of dark pigment at the exit of the vessels, or the dark pigment covers the entire disk. Myelin fibers of the disc 3. i. (normally, the myelin sheath is formed in areas of the 3rd n. after its exit from the eyeball); on the fundus - white shiny spots with uneven edges, emanating from the marginal parts of the disk and spreading to the surrounding parts of the retina. Congenital false neuritis, usually bilateral, - on the fundus there is a picture resembling neuritis of the 3rd disc; congenital false neuritis is associated with excessive development of glia; it is more common in individuals with high hyperopia (see Farsightedness). Differentiate it from true disc neuritis 3. n. the absence of dynamics in the ophthalmoscopic picture of congenital false neuritis helps. Congenital and hereditary atrophies 3. n. are observed in some forms of dysostosis of the skull bones (see Dysostosis) or arise as a result of infectious diseases suffered in utero. A number of anomalies are due to the presence of embryonic tissues of the 3. n. rudiment that have not undergone reverse development: connective tissue film on the 3. n. disc. (the remnant of connective tissue along the embryonic artery of the vitreous body in the form of a film covering the disc and vessels); gray cord coming from disc 3. n. to one of the central vessels of the retina and further forward into the vitreous body (remnants of the embryonic artery of the vitreous body). Anomalies of disc development 3. n. often combined with other anomalies of eye development; as a rule, they are accompanied by incurable loss of vision of varying degrees. Their characteristic feature is the stationarity of the process; any dynamics in the condition of the eye and the ophthalmoscopic picture in case of anomalies are always absent.

Damage optic nerve most often occur with traumatic brain injury, accompanied by cracks and fractures of the bones of the base of the skull, spreading to the walls of the 3rd canal, in some cases - only in the area of ​​the canal walls. Violations of integrity 3. n. There are one- and two-sided injuries to the temporal region. The cause of direct damage to 3. n. There are hemorrhages in the intervaginal spaces surrounding the nerve, and in the nerve itself with its pinching in the area of ​​the optic canal.

Clinically damage 3. n. manifested by a sharp decrease in vision or blindness with the absence of a direct reaction of the pupil to light. Immediately after nerve injury, the fundus is normal; Primary disc atrophy develops after 7-10 days. In approximately Ve cases of injuries 3. n. X-rays of the orbits reveal cracks in the walls of the canal 3. n.

Neurosurgical treatment for trauma 3. n. in the area of ​​its canal is reduced to decompression of the canal wall in order to release the nerve from compression. In this case, craniotomy is performed with revision of the optochiasmal area. The operation of decompression of the canal walls is recommended to be carried out in the first 10 days after damage to the 3. n. When a damaging body (stick, ski, knife, pencil, etc.) penetrates into the cavity of the orbit, tears, ruptures and detachments of the 3. n. When pulling out 3. n. from its scleral ring towards the back - eulsion (evulsio n. optici) - blindness suddenly develops with the absence of a direct reaction of the pupil to light. During ophthalmoscopy, a tissue defect surrounded by hemorrhages is determined at the site of the disc; the vessels at the edge of the defect break off. The retina with its vessels is torn off at the edge of the disc. Subsequently, the retinal vessels completely disappear. Over time, hemorrhages in the fundus resolve, and the defect is replaced by connective tissue (see Fundus). Treatment - extraction foreign body followed by symptomatic therapy.

There may be a separation of 3. n. behind the eyeball with preservation of the disc - avulsion (avulsio n. optici). If the nerve ruptures in front of the entry point of the central retinal artery (within 10-12 mm from the eyeball), sharp ischemia of the retina and disc and significant narrowing of the artery are detected ophthalmoscopically; vision drops sharply. If the gap is 3. n. occurs above the entrance of the central retinal artery, blindness suddenly occurs without visible ophthalmoscopic changes and after 2-3 weeks. descending atrophy develops 3. n.

Circulatory disorders optic nerve (syn.: ischemic edema, ischemic neuroopticopathy, vascular pseudopapillitis, apoplexy nipple, opticomalacia). The reasons leading to circulatory disorders 3. n. are circulatory disorders 3. n., caused by atherosclerosis, temporal giant cell arteritis (Horton-Magath-Brown syndrome), diabetic atheromatosis, occlusive endarteritis, periarteritis nodosa, arthrosis cervical spine spine, etc. Structural changes 3. n. in persons old age can also develop as a result of involutional hemodynamic disorders.

Clinically, in patients aged 50 years and older, after prodrochmal transient blurring, vision in one eye suddenly drops sharply, sometimes to light perception. When examining the visual field, central scotomas are determined (see), sectoral prolapses - lower, less often upper hemianopsia (see).

In the fundus, the disc is pale milky in color, edematous, and is slightly protruded with hemorrhages in the disc area. Disc edema develops within 1 - 2 days. after the onset of visual impairment. Very quickly, disc swelling turns into disc atrophy with clear boundaries. A persistent decrease in vision of varying degrees develops, up to blindness. After some time, the other eye may become ill with the same bad outcome.

Treatment - vasodilators, heparin intravenously, intramuscularly and under the conjunctiva; To prevent the same process in the second eye, corticosteroids are used.

Inflammation of the optic nerve They are divided into intrabulbar neuritis (3rd disc neuritis, or papillitis) and retrobulbar neuritis (peri-neuritis, interstitial neuritis, axial neuritis).

• Changes in the fundus of the eye in some diseases of the optic nerve

Intrabulbar neuritis (3rd disc neuritis, or papillitis) occurs due to inflammatory processes in the cornea, iris, ciliary body, choroid and retina (chorioretinal lesions, retinal periphlebitis), and eye injuries. Main symptoms: varying degrees of decrease central vision, limitation peripheral vision, disturbance of color perception, dark adaptation. Intrabulbar neuritis can occur acutely or gradually. The course can be short or longer. Vision functions may not change for some time or temporary deterioration may occur. The pupil's reaction to light is weakened; changes in the pupil's reaction to light occur in parallel with a decrease in visual acuity. Ophthalmoscopic picture (color Fig. 6): disc 3. n. hyperemic, there is a small degree of its protrusion - up to 2.0 diopters (approximately 0.6 mm); very in rare cases- a distance of 5.0-6.0 diopters (1.5-1.8 mm), associated with severe disc swelling. The edges of the disc gradually merge into the edematous peripapillary retina. The arteries are unchanged or narrowed, the veins are dilated. The vascular funnel or fiziol, excavation on the disk is covered with exudate. In the prepapillary area, opacification of the vitreous body is possible.

Treatment of disc neuritis 3. n. should be reduced to antibacterial and desensitizing therapy aimed at eliminating the underlying disease, the use of corticosteroids (orally, retrobulbar osmotherapy, detoxification, vitamin therapy, oxygen therapy, blood transfusions, the use of antispasmodics, etc.

In case of timely treatment and favorable outcome there is a gradual improvement in vision. If the outcome is unfavorable, complete or partial atrophy develops 3. n. with a sharp decrease in vision, sometimes to the point of blindness.

Retrobulbar neuritis. The inflammatory process is localized in area 3. n. between the eyeball and the chiasm, without extending to the disc, changes are not always detected in the fundus. Retrobulbar neuritis is divided into: 1) inflammation of the membranes only 3. n. - perineuritis, which develops secondarily, per continuitatem; 2) inflammation of the peripheral fibers of the nerve trunk - interstitial neuritis; in this case, the inflammatory process usually begins in the soft membrane 3. n. and along connective tissue septa (septa) it passes to the peripheral layers of nerve fibers; 3) inflammation of the papillomacular (axial) bundle of fibers 3. n. - axial neuritis.

Etiology of retrobulbar neuritis: inflammatory processes in the eye, orbit, paranasal sinuses, neuroinfections, multiple sclerosis, optochiasmal arachnoiditis, meningitis of various etiologies, general infections (influenza, tonsillitis, malaria, typhus, syphilis, oral sepsis); Retrobulbar neuritis may also be based on metabolic disorders, patol, pregnancy, hron, intoxication with lead, tobacco, alcohol, quinine.

Changes in visual fields with retrobulbar neuritis vary depending on the form: with peri-neuritis, no visual disturbances may be noted; with interstitial neuritis, these disorders are reduced to incorrect concentric limitation of the field of view; Axial neuritis is characterized by a central scotoma, absolute or relative (green or red). Retrobulbar neuritis most often affects both eyes, although between the lesions of one and the other 3. n. there is a time gap. There are acute and chronic forms of retrobulbar neuritis. At acute form sometimes vision may drop to zero over the course of several hours; in chronic cases, vision loss occurs slowly, over one or several weeks. Retrobulbar neuritis is always detected by disorders color vision(in the earliest stages - a decrease in the color vision threshold), a decrease in dark adaptation, different in different areas mesh shell. Ophthalmoscopically, a picture of 3rd disc neuritis can sometimes be detected.

Treatment of retrobulbar neuritis is the same as intrabulbar neuritis (see above).

The outcome of retrobulbar neuritis with timely treatment can often be favorable - visual functions are restored. In severe cases, the process ends with atrophy 3. n., which is manifested by a decrease in visual acuity and limitations in the visual field, Ch. arr. in the form of a central scotoma; sometimes blindness occurs. Retrobulbar neuritis with disc edema 3. n. prognostically less favorable compared to cases where there are no changes in the disc.

Optic neuropathy- damage to the optic nerve, observed in some patients suffering from hypertension, inflammatory kidney diseases, pathological pregnancy, etc. With optic neuropathy, its disc may be slightly enlarged in size, its tissue is slightly swollen and dull, with a pale pink and yellowish color shade. The boundaries of the disc are unclear. The arteries are most often narrowed, and the veins are dilated (color. Fig. 7). When the peripapillary retina is involved in the process, neuroretinopathy occurs.

Congestive nipple- disc swelling 3. n. without signs of inflammation or with very slight manifestations of secondary inflammation developing due to stagnation (see Congestive nipple, optic nerve).

Optic atrophy may be primary (simple) or secondary. Primary disc atrophy 3. n. formed by compression of 3. n. in any area with tumors, granulomas, sclerotic vessels of the base of the brain, with basal meningitis. Extremely rare disc atrophy 3. n. arises as a result of primary damage to the visual ganglion neurocytes of the ganglion layer of the retina - the so-called. retinal ascending: atrophy 3. n. Secondary atrophies develop after disc swelling 3. n. or neuritis 3. n., with optochiasmal arachnoiditis (see).

With atrophy 3. n., both primary and secondary, vision functions are sharply impaired, sometimes vision is sharply reduced to light perception, dark adaptation worsens, color perception suffers. The degree of disruption varies widely and depends on the location and intensity of the process. With lesions of the papillomacular bundle, a significant decrease in visual acuity is observed. If the nerve fibers coming from the periphery of the retina are damaged and the papillomacular bundle is intact, visual acuity can be satisfactory. The change in the visual field depends on the localization and extent of the atrophic process.

Ophthalmoscopically (tsvetn. fig. 8) with primary atrophy, the borders of the disc are clear, its color is white or grayish-white, bluish or slightly greenish. The blanching may involve the entire disc or just the temporal part. With secondary atrophy 3. n. (color. Fig. 10) the boundaries of the disc are unclear, washed out, its color is gray or dirty gray, a vascular funnel or fiziol, the excavation is filled with connective or glial tissue, the cribriform plate of the sclera is not visible. Disc blanching 3. n. with atrophy, it depends on the desolation of the vessels supplying the disc, on the development of 3. n. glial and connective tissue and the death of a significant part of the nerve fibers. Retinal ascending disc atrophy 3. n. differs from other forms of atrophy by its yellow, waxy color. Arteries and veins with atrophy 3. n., both primary and secondary, are narrowed. There is a decrease in the number small vessels on disk 3. n. (Kestenbaum's symptom). In case of glaucoma as a result of long-term elevated intraocular pressure atrophy of fibers occurs 3. n. with a characteristic excavation of its disk (color fig. 9).

When choosing a treatment method for atrophy 3. n. etiol factor should be taken into account. Vasodilators, antispasmodics, vitamin therapy (especially B complex vitamins), iodine preparations (for atrophy due to sclerosis) are indicated; for atrophy due to optochiasmal arachnoiditis, treatment is anti-inflammatory, surgical (dissection of adhesions and cysts compressing the 3. n.). Physiotherapeutic measures for atrophies of any etiology include pulsed ultrasound on the open eye, endonasal drug electrophoresis(vasodilators); for atrophy due to optochiasmal arachnoiditis - endonasal drug electrophoresis (papain).

Optic nerve tumors in the overwhelming majority of cases they are primary, benign, developing from glia of the nerve or its membranes. Secondary tumors 3. n. often malignant, they grow into the nerve from neighboring tissues or are metastases. Of the primary tumors, the vast majority of cases are gliomas, less often meningiomas and extremely rarely neurofibromas. Gliomas 3. n. usually occur in children under 10 years of age and rarely in adults. Clinically, these tumors, regardless of their histol, structure, proceed in the same way: accompanied by progressive exophthalmos (Fig. 4, a), development of a congestive nipple and decreased visual function. Gliomas 3. n. are divided into orbital and intracranial, they can arise along the entire length of the nerve and through the optic canal grow into the cranial cavity, spread to the optic chiasm, the bottom of the third ventricle of the brain and 3. n. second eye.

Orbital gliomas are approximately one and a half times more common than intracranial ones. Symptoms of orbital gliomas: blindness of the affected eye, exophthalmos - first forward, then with displacement of the eye, obstacles to eye reposition, limitation of its movements. In the orbit, the glioma forms a node, limited from the surrounding tissues by nerve sheaths, which, as a rule, the tumor does not grow. The expansion of the opening of the optic canal, revealed on radiographs of the orbits, is characteristic symptom primary tumors 3. n. (Fig. 4, b) and at the same time an objective sign of tumor spread into the cranial cavity. For early diagnosis primary tumors 3. n. Venography of the orbit is important (Fig. 4, c) and ultrasound examination orbits (see Ultrasound diagnostics). These research methods reveal the presence of a tumor in the orbit, its size and position in the early stage of growth, when there is no expansion of the opening of the 3rd canal. Radical removal of tumors 3. n. It is possible only by excision of the nerve within healthy tissue. For this purpose, A.I. Arutyunov et al. (1970) developed a method for simultaneous cranio-orbital tumor removal (from the orbit and cranial cavity, Fig. 5). The eyeball and its muscular apparatus are preserved during this operation. The radicality of tumor removal can be judged only on the basis of histol data. examination of the intracranial section 3. n., at the intersection of the nerve to the optic chiasm.

Bibliography: Averbakh M. I. Ophthalmological essays, M., 1949; Arutyunov A.I. et al. On the surgical treatment of optic nerve gliomas, Vopr, neurokhir., No. 2, p. 8, 1970; Bogoslovsky A. I. and Zhdanov V. K. Basic principles of clinical electrophysiology of the visual system, Scientific. works Moscow. scientific research, Institute of Eye Diseases, V. 22, p. 6, 1976; Merkulov I.I. Clinical ophthalmology, book. 2, Kharkov, 1971, bibliogr.; Merkulov I. I., Vinetskaya M. I. and Babich S. B. On the biochemistry of the optic nerve, in the book: Vopr., neuroophthalm., ed. I. I. Merkulova, vol. 9, p. 39, Kharkov, 1962, bibliogr.; Polyak B. L. Damage to the organ of vision, L., 1972; Sokolova O. N. and Volynskaya Yu. N. Tumors of the optic nerve and chiasm, M., 1975, bibliogr.; Tron E. Zh. Diseases of the visual pathway, L., 1968, bibliogr.; Shlykov A. A., Sokolova O. N. and Osipova I. L. On visual impairment in traumatic brain injury and indications for neurosurgical treatment, in the book: Severe traumatic brain injury, ed. A. I. Arutyunov and N. D. Leibzon, p. 192, M., 1969; S o g a n D. G. Neurology of the visual system, Springfield, 1967, bibliogr.; Medical ophthalmology, ed. by F. C. Rose, L., 1976; Neuroophthalmologie, hrsg. v. R. Sachsenweger, Lpz., 1975, Bibliogr.; System of ophthalmology, ed. by S. Duke-Elder, v. 12, L., 1971; Walsh F. B. Clinical neuroophthalmology, Baltimore, 1947.

I. I. Merkulov, O. N. Sokolova; B. A. Vorobyova (an.), V. G. Ginzburg (rent.).

Date: 02/11/2016

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• Structure of the optic nerve
• Functions of the optic nerve
• Treatment of the optic nerve
• Disease Prevention

Everything in the structure of the human body is important, irreplaceable and performs a specific task. The optic nerve is no exception. The main task it performs is the provision and transmission of nerve impulses. These impulses are caused by light stimulation. Even seemingly minor violations in this area can lead to quite serious consequences. The main ones are a low level of visual acuity, impaired color perception and more.

Structure of the optic nerve

The location and course of nerve fibers has a clearly defined structure. The total number of these fibers can reach 1 million. Over the years a person lives, the total amount of his fibers can decrease.
The nerve begins from the disc and ends at the place where the optic fibers of both eyes enter the cranial cavity and connect in the area of ​​the sella turcica. This place is called chiasmus. In this place, partial interweaving of the main components of the optic nerve occurs. The structure of the nerve is quite complex.

This part of the body combines the nerve fibers of the retina. The presented nerve consists of 4 sections:

1. Intracanalicular (meaning the optic nerve canal).
2. Intraocular. It is a disk with a diameter. The length of this disc is approximately 1.5 mm.
3. Intraorbital. The orbital part reaches a size of about 3 mm.
4. Intracranial. The length of the nerve in the intracranial canal can be from 4 mm to 17 mm.

The optic nerve of an adult can reach sizes from 35 to 55 mm. There are 3 optic nerve sheaths: soft, hard and arachnoid. The spaces between these shells contain a liquid with complex chemical composition. It has a hook-like bend. This anatomy of the optic nerve allows tension to be freely produced at the moment of movement of the eyeball.

A special place is occupied by the blood supply to the optic nerve. This action is carried out thanks to the ophthalmic artery. It enters the orbit and adheres to the surface of the nerve. The blood supply to the optic nerve is carried out by two vascular systems.

1. Using the choroid plexus system of the pia mater.
2. Due to the blood supply system of the optic nerve, powered by the branches and twigs of the central retinal artery.

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Functions of the optic nerve

In the presented part of the body, three main functions are distinguished: visual acuity, color perception, field of vision. Each of these functions operates separately from each other.

Visual acuity is the ability of the eye to clearly recognize small objects. It is considered normal when two luminous points are recognized separately at a viewing angle of one minute. Acuity is diagnosed using special tables (Photo 1). This table consists of rows that are arranged horizontally. They depict letters and special characters different sizes. From a distance of 5 m, the patient must reproduce the symbols within a few seconds. The pathology of this function is expressed in a decrease in visual acuity to varying degrees or in the onset of complete blindness.
Color perception is expressed in the ability to identify all primary colors and their shades. The pathology of this function is considered to be the inability to distinguish certain colors or shades. This deviation from the norm is called color blindness or color blindness, and by medical definition it is called achromatopsia.
The visual field is the portion of space that the eye can track when stationary. Failure in this area can lead to changes in the form of central scotoma, concentric narrowing of the visual field, or hemianopsia.

The presented list means that the role of the nerve is very high in difficult human body. That's why minor violations This part cannot be ignored.

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Treatment of the optic nerve

The most common diseases associated with the optic nerve include glaucoma, neuritis and atrophy. The good news is that some diseases can be treated if the stage is not too severe.

Neuritis is an inflammation of the optic nerve, which is accompanied by decreased vision. Many reasons can cause this disease: acute and chronic infections, alcohol intoxication, injuries and more. The disease can have an acute and chronic form. In the acute form, vision may sharply decrease over 2 or 3 days. In the case of chronic form With this disease, visual acuity may gradually decrease.

In the acute course of the disease, the patient must be hospitalized and diagnosed as much as possible. After this, a course of broad-spectrum antibiotics will be prescribed. After a course of antibiotics, it is imperative to take B vitamins. After determining the etiology, treatment will be prescribed, which is aimed at eliminating the underlying cause.

Complete or partial destruction of the optic nerve fibers with their replacement by connective tissue is called atrophy. The main causes of this disease include dystrophy, trauma, toxic damage, swelling, etc. Self-diagnosis and self-medication is unacceptable for such a disease. If you feel that your vision is beginning to rapidly deteriorate or dark spots begin to appear before your eyes, then in this case it is necessary to mandatory consult a doctor.

It is impossible to restore destroyed fibers. You can only pause this process, but if you miss this moment, you can lose your sight forever. Atrophy is a consequence past diseases that affected various departments visual pathways. The main treatment is aimed at eliminating the cause that caused the disease.

High intraocular pressure that causes damage to nerve fibers is called glaucoma. This disease is very insidious and dangerous. It can bring quite serious consequences. Glaucoma, like atrophy, is almost impossible to cure. You can use special drops, neuroprotectors, prostaglandins and more that can stop this disease. Remember that all diseases associated with the organ of vision cannot be treated independently. All medications should be taken as prescribed by specialists in this field.

The optic nerve occupies the most important place in the eye. He has complex structure and serious importance for the visual process, performs the functions of transmitting nerve impulses from the eye to the brain and to reverse side. But due to congenital pathologies, neurotic diseases and inflammatory processes, nerve function deteriorates. Without treatment, this leads to atrophy and vision loss. Therapy is carried out in a hospital setting under the supervision of an ophthalmologist.

Anatomy and structure of the nerve

The optic nerve (ON) is made up of nerve fibers that extend from the retina of the eye.

The anatomy of a nerve is quite complex and takes up a lot of space. The nervous system of the eye is formed from 1 million fibers, but with age their number decreases. The beam is located 3 mm from the back of the eye. The origin is located in the optic nerve head (OND), passes through the optic canal, and ends its path in the chiasm. The organ is supplied with blood by the ophthalmic artery. It is also needed for conductivity nutrients. A network of vessels also emerges from the orbital disc. The fibers that enter the ONH are denser than those near the retina. This is the orbital part of the organ. The normal disc diameter is about 2 millimeters and the thickness is 3 mm. The optic nerve has a duration from 34 to 55 millimeters.

The beam has an S-shaped structure, which allows it to be flexible during eye movement. The branches are divided into the following sections: peripheral (papillomacular bundle) and central. Nerve fibers pass from both eyes into the cranial membrane and form a chiasma near the exit of the optic nerve. Clusters of neurons are located in the center of the organ. In this part, in addition to the intersection, there are also the optic tracts and the external geniculate body, which consists of 6 layers.

The neuronal circuit is divided into 4 main branches:

• intraocular;
• intraorbital - the space from the pupil to the optic canal;
• intracanalicular, which creates a course in the canal;
• intracranial - the location of the space that includes the vagina of the brain with cerebrospinal fluid.

Functions of ZN

Everything we see is impossible without the participation of the optic nerve.

The main task of the organ is considered to be the transmission of primary nerve impulses from the brain. It performs important functions so that the body responds to external stimuli in a timely manner. The optic nerve serves to respond to threats that come from the environment. The optic nerve sends signals to the brain and receives them back. In this way, a reflection of external reality is formed. Due to disruptions in the functioning of this organ, visual abilities deteriorate, hallucinations appear and fields narrow, and poor vision develops.

The chiasm is a chiasm of the optic nerves, which is formed as a result of their conjugation in the prophase of meiosis.

Lesions: types

Diseases of this organ are divided into congenital anomalies and acquired ailments. Thus, some people from birth suffer from a pathology in the development of the system, there is a fossa in the disc or megalopopilla. At a conscious age, atrophy of the optic nerve or neuritis may develop due to injuries. All these deviations lead to complete or partial loss of vision, as well as deterioration in color perception.

The following violations are distinguished:

• increase in the diameter of the DNZ (megalopopilla);
• aplasia;
• hypoplasia;
• neuritis;
• atrophy;
• drusen DNZ;
• dilatation or constriction of blood vessels.

Causes and symptoms of damage

Inflammatory processes

Most common inflammatory diseases optic nerve. Most often, doctors diagnose neuritis. There are papillary and retrobulbar types of the disease. The first type affects the area near the optic disc, and the second - near the intersection of the nerve and the apple of the eye. White spots or flashes of light appear before the eyes. Some patients complain of headaches. This disease occurs against the background of tonsillitis, meningitis, brain abscess, encephalitis and inflammation of the vascular system. Pseudoneuritis is also distinguished. Features of the disease are a large tortuosity of the fibers that extend from the disc to the retina. So, doctors note the passage of fibers past the retina or its overlap.

Spasms in the eyes can be a signal of neuritis.

Symptoms of neuritis include:

• unexpected decrease in the quality of vision;
• spasms in the eyes;
• decreased ability to project light and color perception;
• swelling of the intrathecal spaces of the nerve.

In addition, neuritis is caused by:

• bacterial or viral infections;
• caries;
• otitis;
• flu;
• inflammation of the sinuses.

Atrophy of the optic nerve

Another dangerous abnormality that affects this orbital nerve is called atrophy. This is a progressive pathology that eventually leads to complete blindness. Atrophy is caused by neuritis, damage to the facial part, viral infections, and hypertension. At the same time, the nerve endings gradually die off, thereby developing weak visual abilities. This process takes place slowly and unnoticed by a person, which is why few people turn to a doctor for help. In addition, patients complain of headaches, spasms in the eyes when moving, and decreased color vision.

There are 2 types of atrophy:

• Primary. Evolving in the background hypertension, atherosclerosis, deterioration of circulation in the optic nerve.
• Secondary. The causes are tumors, inflammation of the retina and the nerve itself.

TO congenital pathologies refers to the doubling of the DND. Upon examination, two discs are noticeable, which are formed by fibers and have an independent blood supply. The circle of the blind spot is enlarged. Typically, such damage to the optic nerve is accompanied by congenital glaucoma. Megalopopilla is considered a common disease. This is an anomaly in which the diameter of the disc is significantly larger than normal. Upon examination, one gets the impression that there are few vessels in the disc. The disease, expressed by such symptoms, resembles clinical picture atrophy of the optic nerve. But megalopopilla causes slight visual impairment. Intrathecal hemorrhages indicate a disruption of brain function.

Optic nerve (n.opticus)- begins with a disk, which is formed by the axons of retinal ganglion cells, and ends in the chiasm. The optic nerve has four sections: intraocular (with prelaminar, intralaminar and postlaminar parts), orbital, intracanalicular and intracranial. The total length of the optic nerve varies in adults from 35 to 55 mm. A significant part of it is the orbital process (25 - 30 mm), which in the horizontal plane has an S-shaped bend and thanks to this the optic nerve does not experience tension when the eyeball moves. The axons of all retinal ganglion cells ultimately gather at the posterior pole of the eye into the optic nerve, the initial (intraocular) part of which is called the disc. Since the layer of nerve fibers and the entire retina protrude into the eye in the form of a papilla, hence its former name - papilla n.optici (papilla of the optic nerve).

Total number of nerve fibers components of the optic nerve head (OND), reaches 1200000 , but with age their number gradually decreases. The topography of this zone is distinguished by a strict pattern. From the macular region of the retina to the middle-temporal part of the optic disc there is a short but dense bundle of axons, which pushes the arc fibers emanating from the superior and inferior temporal quadrants of the retina into its corresponding segments. Radial fibers extending from the superior and inferior nasal quadrants of the retina occupy segments of the same spatial orientation in the optic nerve head. Then the fibers collected in it make an arcuate bend (at 900) and form the initial part of the optic nerve in the form of separate bundles.

Anatomical parameters of the optic disc: length about 1 mm, diameter 1.75-2.0 mm, area - 2-3 mm2 (more detailed parameters of the optic disc are given in the section "24 mm"). The optic disc is slightly displaced towards the nose from the posterior pole of the eye (4 mm) and slightly below it. According to the projection of the optic disc into space, there is a blind spot (physiological scotoma) in the temporal half of the visual field of each eye. It was first discovered in 1668 by the physicist E. Mariotte (when examining the visual field, a physiological negative absolute scotoma is diagnosed, which is a projection of the optic nerve head. The reason for the occurrence of scotoma is that the area of ​​the disc is devoid of light-receiving elements). According to the tissue structure of the optic disc, it belongs to the so-called non-pulp nerve fibers, i.e. it itself is deprived of all meninges, and the nerve fibers that make it up - myelin fibers - have a myelin sheath. There are also no oligodendroglia and microglia in it. But the optic disc is richly equipped with vessels and supporting elements. Its neuroglia consists exclusively of astrocytes with long processes that surround all bundles of fibers and, penetrating into them, accompany each fiber. Astrocytes also take part in the formation of the lattice support structure of the optic disc and separate it from neighboring tissues. The border between the pulpless and pulpal sections of the optic nerve coincides with the outer surface of the lamina cribrosae, i.e. still located inside the eye. The non-pulpal portion of the optic nerve is divided into three parts(according to Salzmann M., 1913): retinal, choroidal and scleral. The retinal part of the optic disc is a ring, the temporal half of which is lower than the nasal half, since it has a thinner layer of nerve fibers. The latter, after the above-mentioned arcuate bend, form a depression in its middle either in the form of a funnel (called vascular) or in the form of a ring (physiological excavation). The retinal vessels passing here are covered with a thin sheath of glia, which forms a connecting cord at the bottom of the physiological excavation. The retinal part of the optic disc is separated from the vitreous body by a non-continuous glial membrane, described by A. Elshning (Elshning A., 1899). The main layers of the retina - from the layer of ganglion cells to the layer of rods and cones inclusive - end at the edge of the optic disc, and the inner layers end before the outer ones, which is due to the passage of ganglion cell axons into them. The choroidal part of the optic disc consists of the above-mentioned bundles of nerve fibers, covered with astroglial tissue with transverse branches that form a lattice structure. The basal lamina of the choroid has a rounded hole in this place (for. optica choroideae), which is connected by a channel to the cribriform plate of the sclera (lamina cribrosa). The length of this chorioscleral canal is 0.5 mm, the diameter of the internal opening is about 1.5 mm, and the external one is slightly larger. This layer of the optic disc is equipped with a dense network of capillaries.

The scleral part of the optic disc is represented, as can be seen from the above, only with fibers passing through the cribriform plate of the sclera. The blood supply to the optic disc is carried out, mainly due to the posterior short ciliary arteries with insufficiently developed anastomoses. For this reason, the nutrition of its tissue is segmental in nature, which immediately manifests itself when blood flow in one of the arteries is disrupted. According to some data, the central retinal artery is involved in the blood supply to the retinal part of the optic nerve head. Over a considerable distance (from the exit from the eyeball to the entrance to the canalis opticus), the nerve, like the brain, has three membranes: the hard arachnoid and the soft. Together with them, its thickness is 4 -4.5 mm, without them - 3 -3.5 mm. At the eyeball, the dura mater fuses with the sclera and Tenon's membrane, and at the optic canal with the periosteum. The intracranial segment of the nerve and the chiasm are located in the subarachnoid chiasmatic cistern, dressed only in a soft shell. The intrathecal spaces of the orbital part of the nerve (subdural and subarachnoid) are connected to similar spaces in the brain, but are isolated from each other. They are filled with liquid complex composition(intraocular, tissue, cerebrospinal fluid). Since intraocular pressure is normally twice the intracranial pressure (10 -12 mm Hg), the direction of fluid flow coincides with the pressure gradient. The exception is cases when the intracranial pressure or the tone of the eye sharply decreases.

Subdural space The optic nerve looks like a narrow gap with crossbars running from the hard shell to the soft shell. Subarachnoid space somewhat wider than the subdural and includes complex system from crossbars that connect the soft and arachnoid membranes. From the soft membrane covering the orbital part of the optic nerve, numerous processes (septa) extend into it, which create a connective tissue base and divide the nerve fibers into separate bundles. At a distance of 7-12 mm from the eye and below, the central connecting cord enters the trunk of the optic nerve, which is a tube-shaped continuation of the soft shell. It bends almost at a right angle towards the axis of the nerve and reaches its disc. The cord includes the central arteries and veins of the retina and is connected to them by loose tissue. The bulk of the optic nerve consists of centrifugal fibers - the axons of retinal ganglion cells already mentioned above. The total number of them according to P. Eisler (1930) reaches 1 million. The cross-sectional diameter of one fiber is 0.002 -0.01 mm. All nerve fibers that make up the optic nerve are grouped into three main bundles. The axons of ganglion cells extending from the central (macular) region of the retina constitute the papillo-macular fascicle, which enters the temporal half of the optic nerve head. Fibers from the ganglion cells of the nasal half of the retina go along radial lines to the same half. Similar fibers, but from the temporal half of the retina, along the path of the optic nerve head, “flow around” the papillo-macular bundle above and below. In the orbital segment of the optic nerve near the eye, the relationships between nerve fibers remain the same as in its disc. Next, the papillo-macular one moves to the axial position, and the fibers from the temporal quadrants of the retina move to the entire corresponding half of the optic nerve. Thus, the optic nerve is clearly divided into right and left halves. Its division into upper and lower halves is less pronounced. Clinically important is the fact that that the nerve is devoid of sensory endings. In the cranial cavity, the optic nerves connect above the area of ​​the sella turcica, forming chiasmus. In the area of ​​the chiasm, the fibers of the optic nerve partially intersect due to portions associated with the nasal halves of the retinas. Moving to the opposite side, they connect with fibers from the temporal halves of the retinas of the other eye and form visual track - tr.opticum. The papillo-macular bundles also partially intersect here. It should be emphasized once again that in the optic nerve, optic tract and in visual radiance - radiato optica, starting from the neurons of the lateral geniculate body, the fibers are located in a strict retinotypic order. A similar order is observed in the cortical visual field, located in the occipital lobe, in the area of ​​the calcarine groove - sulcus calcarinus.

1. Afferent fibers. The optic nerve contains about 1.2 million afferent nerve fibers coming from retinal ganglion cells. Most of the fibers form synapses in the lateral geniculate body, although some of them enter other centers, mainly the pretectal nuclei of the midbrain. About 1/3 of the fibers correspond to the central 5th field of vision. Fibrous septa arising from the pia mater divide the fibers of the optic nerve into approximately 600 fascicles (each containing 2000 fibers).
2. Oligodendrocytes provide myelination of axons. Congenital myelination of retinal nerve fibers is explained by the abnormal intraocular distribution of these cells.
3. Microglia are immunocompetent phagocytic cells, possibly regulating apoptosis (“programmed” death) of retinal ganglion cells.
4. Astrocytes line the space between axons and other structures. When axons die during optic atrophy, astrocytes fill the resulting spaces.
5. Surrounding shells
   • pia mater - soft (inner) meninges containing blood vessels;
   • the subarachnoid space is a continuation of the subarachnoid space of the brain and contains cerebrospinal fluid;
   • the outer shell is divided into the arachnoid and dura mater, the latter continuing into the sclera. Surgical fenestration of the optic nerve involves making incisions in the outer sheath.

Axoplasmic transport

Axoplasmic transport is the movement of cytoplasmic organelles in a neuron between the cell body and the synaptic terminal. Orthograde transport involves movement from the cell body to the synapse, and retrograde transport in the opposite direction. Rapid axoplasmic transport is active process, requiring oxygen and ATP energy. Axoplasmic flow can be interrupted for a variety of reasons, including hypoxia and toxins that interfere with ATP production. Retinal cotton wool lesions result from accumulation of organelles when axoplasmic flow between retinal ganglion cells and their synaptic terminals is interrupted. A congestive disc also develops when axoplasmic flow stops at the level of the lamina cribrosa.

The optic nerve is covered by three meninges: the dura mater, the arachnoid membrane, and the pia mater. In the center of the optic nerve, in the closest segment to the eye, there passes the vascular bundle of the central vessels of the retina. Along the axis of the nerve, a connective tissue cord surrounding the central artery and vein is visible. The optic nerve itself does not have half frequencies of the central vessels of any branch.

The optic nerve is like a cable. It consists of the axial processes of all ganglion cells of the retinal rim. Their number reaches approximately one million. All fibers of the optic nerve exit the eye into the orbit through a hole in the cribriform plate of the sclera. At the exit site, they fill the opening of the sclera, forming the so-called optic nerve papilla, or optic disc, because in in good condition The optic disc lies at the same level with the retina. Only the congestive papilla of the optic nerve protrudes above the level of the retina, which is pathological condition- a sign of increased intracranial pressure. In the center of the optic nerve head, the exit and branches of the central retinal vessels are visible. The color of the disc is paler than the surrounding background (during ophthalmoscopy), since there is no choroid and pigment epithelium in this place. The disc has a lively pale pink color, more pink on the nasal side, from where the vascular bundle often emerges. Pathological processes developing in the optic nerve, as in all organs, are closely related to its structure:

1. the many capillaries in the septa surrounding the optic nerve bundles and its special sensitivity to toxins create conditions for the optic nerve fibers to be affected by infections (for example, influenza) and a number of toxic substances (methyl alcohol, nicotine, sometimes plasmacide, etc.);
2. with increases in intraocular pressure the most weak point it turns out that the optic nerve disc (it, like a loose plug, closes the holes in the dense sclera), therefore, with glaucoma, the optic nerve disc is “pressed in” and a fossa is formed.
3. excavation of the optic nerve head with atrophy from pressure;
4. increased intracranial pressure, on the contrary, delaying the outflow of fluid through the interthecal space, causes compression of the optic nerve, stagnation of fluid and swelling of the interstitial substance of the optic nerve, which gives the picture of a stagnant nipple.

Hemo- and hydrodynamic shifts also have an adverse effect on the optic nerve head. They lead to a decrease in intraocular pressure. Diagnosis of diseases of the optic nerve is based on data from fundus ophthalmoscopy, perimetry, fluorescein angiography, and electroencephalographic studies.

A change in the optic nerve is necessarily accompanied by dysfunction of central and peripheral vision, limitation of the field of vision for colors and a decrease twilight vision. Diseases of the optic nerve are very numerous and varied. They are inflammatory, degenerative and allergic in nature. There are also developmental anomalies of the optic nerve and tumors.

Symptoms of optic nerve damage

1. A decrease in visual acuity when fixating near and far objects is often observed (may occur in other diseases).
2. Afferent pupillary defect.
3. Dychromatopsia (impaired color vision, mainly red and green). A simple way to identify unilateral color vision deficiency is to ask the patient to compare the color of a red object seen in each eye. A more accurate assessment requires the use of Ishihara pseudoisochromatic tables, the City University test, or the Farnsworth-Munscll 100-shade test.
4. Decreased light sensitivity, which may persist after restoration of normal visual acuity (for example, after optic neuritis). This is best defined as follows:
   • light from an indirect ophthalmoscope is illuminated first on a healthy eye, and then on an eye with suspected damage to the optic nerve;
   • the patient is asked whether the light is symmetrically bright for both eyes;
   • the patient reports that the light seems less bright in the affected eye;
   • The patient is asked to determine the relative brightness of the light seen by the affected eye compared to the healthy eye.
5. Reduced contrast sensitivity is defined as follows: the patient is asked to identify gratings of gradually increasing contrast of different spatial frequencies (Arden tables). This is a very sensitive, but not specific for optic nerve pathology, indicator of vision loss. Contrast sensitivity can also be examined using Pelli-Robson charts, in which letters of gradually increasing contrast (grouped in groups of three) are read.
6. Visual field defects that vary depending on the disease include diffuse depression in the center of the visual field, central and centrocecal scotomas, bundle defects, and altitudinal defects.

Optic disc changes

There is no direct correlation between the appearance of the optic disc and visual functions. In acquired diseases of the optic nerve, 4 main conditions are observed.

1. A normal disc appearance is often characteristic of retrobulbar neuritis, initial stage Leber optic neuropathy and compression.
2. Disc edema is a sign of disc congestion” in anterior ischemic optic neuropathy, papillitis and the acute stage of Leber optic neuropathy. Disc edema may also occur with compression lesions before optic atrophy develops.
3. Optociliary shunts are retino-choroidal venous collaterals on the optic nerve, which develop as a compensatory mechanism for chronic venous compression. This is often caused by meningioma and sometimes by optic nerve glioma.
4. Optic atrophy is the outcome of almost any of the above-mentioned clinical conditions.

Special studies

1. Manual Goldmann kinetic perimetry is useful for diagnosing neuro-ophthalmic diseases because... allows you to determine the state of the peripheral visual field.
2. Automatic perimetry determines the threshold sensitivity of the retina to a static object. The most useful programs are those that test the central 30", with objects spanning the vertical meridian (for example, Humphrey 30-2).
3. MPT is the modality of choice for imaging the optic nerves. The orbital part of the optic nerve is better visible when the bright signal from adipose tissue is eliminated on T1-weighted tomograms. The intracanalicular and intracranial parts are visualized better on MRI than on CT, since there are no bone artifacts.
4. Visual evoked potentials are recordings of electrical activity in the visual cortex caused by stimulation of the retina. The stimuli are either a flash of light (flash VEPs) or a black and white chess pattern reversing on the screen (VEP pattern). Several electrical responses are obtained, which are averaged by a computer, and both the latency (increase) and amplitude of the VEP are assessed. In optic neuropathy, both parameters are changed (latency increases, VEP amplitude decreases).
5. Fluorescein angiography may be useful in differentiating between disc congestion, in which there is dye leakage on the disc from disc drusen when autofluorescence is observed.