Optic atrophy

Clinically, optic nerve atrophy is a combination of symptoms: visual impairment (decreased visual acuity and development of visual field defects) and pallor of the optic nerve head.

Optic nerve atrophy is characterized by a decrease in the diameter of the optic nerve due to a decrease in the number of axons.

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Causes of optic nerve atrophy

Inflammatory processes, degenerative processes, compression, edema, trauma, diseases of the central nervous system, craniocerebral trauma, general diseases (hypertension, atherosclerosis), intoxication, diseases of the eyeball, hereditary atrophies and resulting cranial deformations. In 20% of cases, the etiology remains unknown.

Among diseases of the central nervous system, the causes of optic nerve atrophy may be:

1. tumors of the posterior cranial fossa, pituitary gland, leading to increased intracranial pressure, nipple congestion and atrophy;
2. direct compression of the chiasm;
3. inflammatory diseases of the central nervous system (arachnoiditis, brain abscess, multiple sclerosis, meningitis);
4. trauma to the central nervous system, leading to damage to the optic nerve in the orbit, canal, cranial cavity in the late period, as a result of basal arachnoiditis, leading to descending atrophy.

Common causes of optic nerve atrophy:

1. hypertension leading to a disturbance in the hemodynamics of the vessels of the optic nerve in the form of acute and chronic circulatory disorders and to atrophy of the optic nerve;
2. intoxication (tobacco and alcohol poisoning with methyl alcohol, chlorophos);
3. acute blood loss (bleeding).

Diseases of the eyeball that lead to atrophy: damage to the retinal ganglion cells (ascending atrophy), acute obstruction of the central artery, degenerative diseases of the artery (retinal pigment dystrophy), inflammatory diseases of the choroid and retina, glaucoma, uveitis, myopia.

Deformities of the skull (tower skull, Paget's disease, in which early ossification of the sutures occurs) lead to increased intracranial pressure, congestion of the optic nerve papilla and atrophy.

With atrophy of the optic nerve, there is a breakdown of nerve fibers, membranes, axial cylinders and their replacement with connective tissue, empty capillaries.

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Symptoms of optic nerve atrophy

1. decreased visual function;
2. changes in the appearance of the optic nerve head;
3. central vision suffers when the maculocapillary bundle is damaged and a central scotoma is formed;
4. peripheral vision changes (concentric narrowing, sector-shaped narrowing), with a focus in the chiasm - loss of peripheral vision;
5. change in color perception (first the perception of green suffers, then red);
6. Tempo adaptation suffers when peripheral nerve fibers are damaged.

There is no dynamics of visual functions observed in atrophy.

With partial atrophy, vision is significantly reduced; with complete atrophy, blindness occurs.

Acquired optic atrophy

Acquired optic atrophy develops as a result of damage to the optic nerve fibers (descending atrophy) or retinal cells (ascending atrophy).

Descending atrophy is caused by processes that damage the optic nerve fibers at various levels (orbit, optic canal, cranial cavity). The nature of the damage varies: inflammation, trauma, glaucoma, toxic damage, circulatory disorders in the vessels that feed the optic nerve, metabolic disorders, compression of the optic fibers by a volumetric formation in the orbit or cranial cavity, degenerative process, myopia, etc.).

Each etiologic factor causes optic nerve atrophy with specific, typical ophthalmoscopic features, such as glaucoma, circulatory disorders in the vessels that feed the optic nerve. However, there are characteristics common to optic nerve atrophy of any nature: pallor of the optic nerve disc and visual impairment.

The degree of visual acuity reduction and the nature of visual field defects are determined by the nature of the process that caused the atrophy. Visual acuity can range from 0.7 to practical blindness.

According to the ophthalmoscopic picture, primary (simple) atrophy is distinguished, which is characterized by paleness of the optic nerve disc with clear boundaries. The number of small vessels on the disc is reduced (Kestenbaum's symptom). The retinal arteries are narrowed, the veins can be of normal caliber or also slightly narrowed.

Depending on the degree of damage to the visual fibers, and consequently on the degree of reduction in visual functions and blanching of the optic nerve disc, a distinction is made between initial, or partial, and complete atrophy of the optic nerve.

The time during which the optic nerve head blanching develops and its severity depend not only on the nature of the disease that led to optic nerve atrophy, but also on the distance of the lesion from the eyeball. For example, in the case of inflammatory or traumatic damage to the optic nerve, the first ophthalmoscopic signs of optic nerve atrophy appear several days to several weeks after the onset of the disease or the moment of injury. At the same time, when a volumetric formation affects the optic fibers in the cranial cavity, only visual disturbances are initially clinically manifested, and changes in the fundus in the form of optic nerve atrophy develop many weeks or even months later.

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Congenital optic atrophy

Congenital, genetically determined optic nerve atrophy is divided into autosomal dominant, accompanied by an asymmetric decrease in visual acuity from 0.8 to 0.1, and autosomal recessive, characterized by a decrease in visual acuity often to the point of practical blindness already in early childhood.

If ophthalmoscopic signs of optic nerve atrophy are detected, a thorough clinical examination of the patient must be performed, including determination of visual acuity and visual field boundaries for white, red and green colors, and examination of intraocular pressure.

In the case of atrophy development against the background of edema of the optic nerve disc, even after the edema disappears, the blurriness of the boundaries and pattern of the disc remains. Such an ophthalmoscopic picture is called secondary (post-edematous) atrophy of the optic nerve. The retinal arteries are narrowed in caliber, while the veins are dilated and tortuous.

When clinical signs of optic nerve atrophy are detected, it is necessary to first establish the cause of this process and the level of damage to the optic fibers. For this purpose, not only a clinical examination is performed, but also CT and/or MRI of the brain and eye sockets.

In addition to etiologically determined treatment, symptomatic complex therapy is used, including vasodilator therapy, vitamins C and group B, drugs that improve tissue metabolism, various types of stimulating therapy, including electrical, magnetic and laser stimulation of the optic nerve.

Hereditary atrophies come in six forms:

1. with a recessive type of inheritance (infantile) - from birth to three years of age, there is a complete decrease in vision;
2. with a dominant type (juvenile blindness) - from 2-3 to 6-7 years. The course is more benign. Vision decreases to 0.1-0.2. Segmental pallor of the optic nerve is noted on the fundus, there may be nystagmus, neurological symptoms;
3. optic-oto-diabetic syndrome - from 2 to 20 years. Atrophy is combined with pigmentary retinal dystrophy, cataracts, diabetes mellitus and diabetes insipidus, deafness, and urinary tract damage;
4. Behr's syndrome - complicated atrophy. Bilateral simple atrophy already in the first year of life, the growth rate drops to 0.1-0.05, nystagmus, strabismus, neurological symptoms, pelvic organ damage, the pyramidal tract suffers, mental retardation joins;
5. gender-related (more often observed in boys, develops in early childhood and increases slowly);
6. Leicester's disease (Lester's hereditary atrophy) - in 90% of cases occurs between the ages of 13 and 30 years.

Symptoms. Acute onset, sudden loss of vision within a few hours, less often - a few days. Retrobulbar neuritis-type lesion. The optic disc is initially unchanged, then blurring of the boundaries and changes in small vessels - microangiopathy - appear. After 3-4 weeks, the optic disc becomes paler on the temporal side. Vision improves in 16% of patients. Often, decreased vision remains for life. Patients are always irritable, nervous, they are bothered by headaches and fatigue. The cause is optochiasmatic arachnoiditis.

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Optic nerve atrophy in some diseases

1. Atrophy of the optic nerve is one of the main signs of glaucoma. Glaucomatous atrophy is manifested by a pale disc and the formation of a depression - excavation, which first occupies the central and temporal sections, and then covers the entire disc. Unlike the above-mentioned diseases leading to disc atrophy, with glaucomatous atrophy the disc is gray, which is associated with the characteristics of the damage to its glial tissue.
2. Syphilitic atrophy.

Symptoms. The optic disc is pale, grey, the vessels are of normal caliber and sharply narrowed. Peripheral vision narrows concentrically, there are no scotomas, colour perception suffers early. There may be progressive blindness, which occurs quickly, within a year.

It proceeds in waves: rapid decrease in vision, then improvement during the remission period, and repeated deterioration during the exacerbation period. Miosis, divergent strabismus, changes in pupils, lack of reaction to light while maintaining convergence and accommodation develop. The prognosis is poor, blindness occurs within the first three years.

1. Features of optic nerve atrophy from compression (tumor, abscess, cyst, aneurysm, sclerotic vessels), which can be in the orbit, anterior and posterior cranial fossa. Peripheral vision suffers depending on the localization of the process.
2. Foster-Kennedy syndrome is an atherosclerotic atrophy. Compression may cause sclerosis of the carotid artery and sclerosis of the ophthalmic artery; ischemic necrosis occurs from softening in arterial sclerosis. Objectively, excavation is caused by the recession of the cribriform plate; benign diffuse atrophy (in sclerosis of small vessels of the pia mater) increases slowly, accompanied by atherosclerotic changes in the retinal vessels.

Optic nerve atrophy in hypertension is the result of neuroretinopathy and diseases of the optic nerve, chiasm and optic tract.

Atrophy of the optic nerve due to blood loss (stomach, uterine bleeding). After 3-10 days, a picture of neuritis develops. The optic disc is pale, the arteries are sharply narrowed, peripheral vision is characterized by concentric narrowing and loss of the lower half of the visual field. Causes - decreased blood pressure, anemia, changes in the disc.

Atrophy of the optic nerve in intoxications (quinine poisoning). General symptoms of poisoning are characteristic: nausea, vomiting, hearing loss. The fundus shows atrophy. In poisoning with male fern, vision decreases, peripheral vision narrows, changes occur quickly and are persistent.

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Diagnosis of optic nerve atrophy

The diagnosis is based on the ophthalmoscopic picture. During examination, the optic nerve disc becomes pale; if the maculocapillary bundle is damaged, the temporal parts of the optic nerve disc become pale (retrobulbar neuritis). The paleness of the disc is caused by a decrease in the number of small vessels, proliferation of glia, and translucency of the cribriform plate. The boundaries of the disc are clear, the caliber and number of vessels decrease (normally 10-12, with atrophy 2-3).

A distinction is made between acquired and congenital atrophy of the optic nerve.

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Treatment of optic nerve atrophy

For diseases of the central nervous system, treatment by a neurologist is necessary. For other diseases, the following is prescribed:

1. stimulant drugs;
2. vasodilators (papaverine, no-shpa, compalamin);
3. tissue therapy (B vitamins, intravenous nicotinic acid);
4. anti-sclerotic drugs;
5. anticoagulants (heparin, ATP subcutaneously);
6. ultrasound;
7. acupuncture;
8. enzymes (trypsin, chymotrypsin);
9. pyrogepal (intramuscular);
10. vagosympathetic blockades according to Vishnevsky (0.5% novocaine solution in the area of the carotid artery), which leads to vasodilation and block of sympathetic innervation.