There are 2 types of MN infarction: caused by arteritis and not caused by arteritis. The second option is much more common, usually among people aged about 50 and older. Vision loss in this case is not as severe as that caused by arteritis. MN infarction caused by arteritis occurs more often in age group from 70 and older.
Ischemic neuropathy ZN is usually unilateral in nature. Simultaneous bilateral lesions are unusual for ischemic neuropathy, and sequential lesions occur only in 20% of cases. Involvement of both optic nerves pathological process most often indicates a connection with arteritis. Atherosclerotic narrowing of the posterior ciliary arteries may predispose to non-arteritis infarction optic nerve, especially against the backdrop of the episode low blood pressure. At the same time, any inflammatory disease vascular wall can provoke an arteritic form of infarction.
Acute ischemia causes swelling of the MN disc, which in turn worsens the ischemia. The small size of the excavation relative to the overall size of the optic disc is a risk factor for the non-arteritic form. Also, all processes that provoke atherosclerosis lead to the development of non-arteritic infarction: diabetes, smoking, hypertension, certain medications (amiodarone and, presumably, phosphodiesterase-5 inhibitors), hypercoagulation. Sharp deterioration vision upon awakening suggests that nocturnal hypotension plays a role in the development of non-arteritic infarction.
Loss of vision in both variants of the development of the disease is rapid and painless. Vision deterioration occurs in a matter of minutes, hours or days. Some patients report worsening vision upon awakening. General malaise, muscle pain, pain when scratching, chronic subluxation lower jaw and tenderness along the temporal artery indicate temporal arteritis, but can occur after vision deterioration. Visual acuity decreases, and an afferent pupillary defect appears. The disc of the optic nerve swells and rises, and small vessels are damaged, leading to the formation of hemorrhages near the disc. The disc of the optic nerve in the arteritic variant has a pale color, and in the non-arteritic variant it is hyperemic. In both variants, when examining the visual fields, a defect is observed in the central and lower fields.
Diagnosis is usually made based on clinical findings, but may also require additional methods examinations. It is very important to diagnose the arterial variant in time, because there is a high probability of developing a pathological process in the other eye. ESR can help with this - in case of arterial infarction it will be greatly increased. OAK in both cases may show thrombocytosis. If giant cell arteritis is suspected, a CRP test and temporal artery biopsy can help confirm it. In some cases of progressive vision loss, a CT or MRI may be recommended to rule out damage due to structural compression.
For nonarteritic ischemic neuropathy of the optic nerve, additional investigations are recommended based on suspected risk factors. For example, if a patient has increased weakness in daytime, snoring or excess body weight, polysomnography is recommended. If vision deterioration occurs upon awakening, continuous monitoring of blood pressure is recommended.
There is no effective treatment. However, up to 40% of patients with nonarteritic infarction experience spontaneous partial restoration functions.
In the arterial variant, it is advisable to prescribe corticosteroids (prednisone 80 mg po once a day, under the control of ESR) to prevent infarction in the second eye. Aspirin or corticosteroids for nonarteritic infarction have been unsuccessful. Risk factors should be controlled. Useful application aids for the visually impaired (magnifying glasses, large print, talking clock).
Ischemic MN neuropathy is usually caused by giant cell arteritis or atherosclerosis.
Acute circulatory disturbance in the optic nerve, it can be in the arterial and venous systems or mixed - simultaneously in the arterial and venous systems.
Reasons. The cause of neuropathy in the optic nerve can be atherosclerosis, hypertension, diabetes mellitus, temporal arteritis, periarteritis nodosa, periarteritis obliterans, circulatory disorders in the vertebrobasilar system, osteochondrosis of the cervical spine, physical and emotional-nervous stress.
The pathogenesis of optic neuropathy lies in vascular obstruction due to spasm or mechanical blockage (thrombosis and embolism) or a combination of both - mechanical blockage and spasm.
Symptoms. With optic neuropathy, patients notice a sudden and significant visual impairment, the presence of defects in the visual field of various shapes, sizes and locations.
If blood circulation in the venous system is impaired, the optic disc is swollen, pink with unclear boundaries and partially protrudes above the surface of the fundus. The veins are dilated, the arteries are not changed. There are streak-like hemorrhages around the disc.
In case of circulatory problems in arterial system The optic disc is swollen and ischemic, partially protrudes, its boundaries are unclear, the arteries are narrowed, the veins are not changed. There may be isolated hemorrhages in the area of the optic nerve head and near its edge.
Treatment. The patient should be given a validol or nitroglycerin tablet under the tongue and inhale amyl nitrite for 2-3 minutes (3-5 drops on a cotton swab).
Inject intravenously 10 ml of a 2.4% solution of aminophylline diluted in 10 ml of a 40% glucose solution.
Inject 1 ml of 1% nicotinic acid solution intramuscularly.
Further treatment similar to acute obstruction in the central retinal arteries and thrombosis central vein retina.
Prescribe vasodilators and improve microcirculation and metabolic processes medicines, anticoagulants and antisclerotic drugs.
For optic neuropathy, dehydration and resorption therapy is also carried out.
of optical neuropathy
A.F. Brovkina, A.G. Schuko
(RMAPO, Moscow, department of FGU MNTK
"Eye Microsurgery" named after acad. Fedorov S.N., Irkutsk)
Authors presented the comparative characteristic of some types of neuropathy (vascular and endocrine genesis). Treatment and prognosis depend on the etiologic and pathogenic factors.
Optic neuropathy (ON) is a collective concept that unites several diseases in which the optic nerve fibers from the retina to the brain are affected. Taking into account the etiological aspects, the mechanism of its development is different.
The causal classification of OH can be presented as follows:
. compression
. ischemic
. inflammatory
. hyperbaric
. traumatic
. radiation
. metabolic
. congenital.
The development of the pathological process of any type of ON is ischemia and hypoxia. nerve fibers with weakening of antioxidant activity, which may be preceded by circulatory disorders, compression of nerve fibers of the optic nerve, blockade of axonal transport, intoxication, activation of peroxide processes and neurotoxic reactions. However, the degree of intensity of these mechanisms, the place of their application and the sequence of appearance vary depending on the underlying pathological process.
For example, when primary glaucoma the main triggering factors for the development of optic neuropathy are an increase in ophthalmotonus or a decrease in cerebrospinal fluid pressure in the retrobulbar portion of the optic nerve. This leads to deformation of the supporting structures (especially the lamina cribrosa) with subsequent pinching of the nerve fiber bundles in the deformed tubules of the lamina cribrosa and/or hypoxia of the optic nerve head.
Anterior ischemic ON develops when acute disorder blood circulation in the anterior segment of the optic nerve. A decrease in perfusion pressure in the posterior short ciliary arteries and ischemia in the prelaminar, laminar and retrolaminar parts of the optic nerve leads to the development clinical picture anterior ischemic neuropathy. Characterized by a rapid and sharp decrease in visual acuity, rapid development optic nerve atrophy.
In patients with edematous exophthalmos, ON develops against the background of an increase in extraocular muscles. The process occurs quickly, before the axoplasmic flow is disrupted, a disruption of blood flow occurs, like arterial flow (as a result of compression by enlarged muscles of the main arterial vessels), and venous.
Having a large own experience and having analyzed the mechanism of development of some forms of optic neuropathy, the authors in this work set themselves the task of studying the features of the clinical picture of ON (vascular) and endocrine (edematous exophthalmos) genesis, as the most common and requiring a fundamentally different therapeutic approach. This is due to the fact that in a number of publications, not only vascular processes, but also thyrotoxic exophthalmos are considered as the basis for the development of anterior ischemic ON. This situation is fundamentally incorrect, since thyrotoxic exophthalmos, although it represents one of the forms of endocrine ophthalmopathy, is never accompanied by organic changes in the soft tissues orbits. A different picture is observed with edematous exophthalmos. Comparison of ophthalmoscopy data and computed tomography conducted by one of us earlier, allowed us to make an opinion about the main mechanisms of ON development. The triggering mechanism for ON in edematous exophthalmos is a sharp increase in the volume of extraocular muscles at the apex of the orbit (Fig. 1). At least two factors take part in the mechanism of its development: mechanical compression of the optic nerve and disruption of the blood-ophthalmic barrier, resulting in edema and tissue hypoxia, and disruption of cellular energy metabolism. The end result of these disturbances is a blockade of axonal transport (Fig. 2).
Anterior ischemic ON is characterized by a sudden sharp decrease in visual function as a result of ischemic infarction of the optic nerve and its head. This definition is confirmed by J.D. Gass with the following phrase: “Anterior ischemic optic neuropathy is swelling, ischemia and varying degrees infarctions of the anterior part of the optic nerve caused by a reduction in blood flow in the nerve.” Persons aged 45 years and older are affected ( middle age 69 years old). The process is often unilateral, but in 40% of cases, damage to the optic nerve on the opposite side is possible with a fairly significant time interval.
Ophthalmoscopically, the optic disc is grayish-white or yellowish color with a sharp swelling of its tissue. Prominence is more pronounced in the upper half of the disc. IN acute stage streak-shaped hemorrhages on the disc or along its edge are possible (Fig. 3). The swelling also extends to the peripapillary nerve fibers (Fig. 4). Cotton-like exudate in separate foci is located juxtapapillary. Swelling occurs in the macular area. Arteries and veins are narrowed. Go to chronic stage, when regression of disc edema occurs with transition to atrophy (secondary), it occurs quickly (after 2-3 weeks). During this period, cystic degeneration or its fibrotic changes develop in the macular zone.
In cases where it is possible to examine the visual field, prolapses are detected in the lower half (1/3 of cases); in 12% of patients, absolute scotoma in Bjerrum's space, less often (about 6%) it is possible to detect a central scotoma and a concentric narrowing of the visual field.
In patients with edematous exophthalmos in the stage of subcompensation or decompensation (more often) of the pathological process, when the manifestation intensifies clinical symptoms, venous stasis occurs in the orbital tissues and in the optic nerve. Early sign disruption of the compensation process and the appearance of ON - dilation of the retinal veins, which leads to hypoxia primarily of the retinal ganglion cells (Fig. 5). Early visual impairment is characteristic. Initially, most patients develop peripheral scotomas with normal visual acuity; they are detected at the extreme periphery of the outer and upper sections fields of view.
According to ophthalmoscopy data (the condition of the optic nerve head and retinal vessels), two forms of ON were identified: initial (57%) and developed (43% of patients).
Initial ON was characterized by the presence of dilated and tense retinal veins (Fig. 6). The optic disc remains normal with subcompensated edematous exophthalmos. In the stage of its decompensation, blurring of the boundaries of the optic nerve head and its swelling appear. In contrast to anterior ischemic ON, vision in patients with edematous exophthalmos and ON worsens gradually to 0.1-0.7. A sharp deterioration in vision (before light projection) occurs with the appearance of hyperemia and swelling of the optic nerve head (Fig. 7). However, the process is reversible: against the background of the basic intensive care when decreasing clinical symptoms Visual acuity increases, changes in the visual field decrease or disappear. This confirms the hypothesis of the development of ON during tissue compression at the apex of the orbit against the background of a hypoxic state, which has a detrimental effect on ganglion cells.
Each of these factors (or both together) leads to disruption of axoplasmic transport connecting the body of the retinal ganglion cell with its terminals.
Thus, ON, taking into account pathogenetic factors, has its own clinical differences, differs in the nature of the pathological process and its outcome.
Comparative characteristics of the analyzed types of OH are presented in Table 1.
The differences presented in the table confirm the possibility of clinical differentiation of ON depending on etiopathogenetic factors, which determines the planning of medication or surgical treatment and visual forecast in each specific case.
Literature
1. Brovkina A.F. Endocrine ophthalmopathy//Moscow: GOETAR, 2004.
2. Katsnelson L.A., Forofonova T.I., Bunin A.Ya. Vascular diseases eyes //Moscow: Medicine, 1990. - 269 p.
3. Nesterov A. P. Glaucomatous optic neuropathy // Vestn. ophthalmol., 1999, No. 1. - P. 3-6
4. Barch A., Bosahard C., Burgi U., Burgi H. Severe endocrine ophthalmopathy. A revive with case reports.- Schweiz Med. Wochenachr. - 1991. - V.121. - S. 3-9
5. Gass J.D. Stereoscopic Atlas of Macular Diseases: diagnosis and treatment.// The C.V. Mosby Company.-St.Louis.-1987. - V. 1. - P. 69
6. Kritzinger E.. Beaumont H., Optic discrepancies, -Wolfe Medical Publications Ltd. - USA. - 1987. - 118 P.
7. Shine B., Fells P., Edwards O., Weetman A. Association between Graves? ophthalmopathy and smoking. - Lancet. - 1990. - V. 335. - P. 1261-1263.
The development of ischemic optic neuropathy occurs due to a local change in blood flow, as a result of which local tissues do not receive enough nutrients. The formation of pathology is associated with the course of atherosclerosis, hypertension, diabetes mellitus or cardiac dysfunction.
Neuropathy is characterized by a disorder peripheral vision(narrowing of the field of vision), the appearance of blind spots (scotoma). The disease is treated using conservative (drug) therapy and magnetic therapy methods.
Ischemic neuropathy (neuropticopathy) of the optic nerve is considered the most common cause of blindness. This pathology is most typical for people over 50 years of age. The disease is more often diagnosed in men.
Pathology does not develop separately, but is a complication of diseases of the eyes or other organs.
In this regard, if ocular nerve ischemia is suspected, comprehensive examination patient in order to identify the cause of nerve fiber damage.
Based on the location of the pathological process, anterior and posterior forms of ischemic neuropathy are distinguished. Depending on the degree of damage to the optic nerve, the disease is divided into local (limited) and total.
The development of anterior ischemic neuroopticopathy is associated with impaired blood flow in the intrabulbar region. Such problems are caused various forms vascular lesions: thrombosis, embolism, spasm. With posterior ischemic optic neuropathy, the pathological process is localized in the retrobulbar region (behind the eyeball). The anterior form develops less frequently.
The disease develops against the background systemic pathologies, which affect the vascular bed and cause a disorder of blood microcirculation. However, one cannot exclude the influence local violations. The latter include spasms ( functional disorders) And organic lesions(thrombosis, sclerotization) of local arteries.
Systemic vasculopathies lead to the development of ocular ischemia:
The appearance of anterior ischemic neuropathy may be associated with the course of vasculitis:
To the number possible reasons The occurrence of this pathology of the optic nerve includes:
Defeat cervical regions spine and carotid arteries mainly causes the development of posterior ischemic optic neuropathy.
The course of ischemic optic neuropathy is often unilateral. Only in 30% of cases the disease affects both eyes. Moreover, bilateral eye damage is usually observed in those patients who did not undergo timely treatment for anterior ischemic neuropathy (neuropticopathy).
Most patients are diagnosed with both forms of the disease simultaneously.
Along with this pathology, lesions of the retinal vessels are noted.
Symptoms of optic nerve ischemia appear suddenly. Initially noted:
These phenomena are temporary, and after a few minutes or hours visual functions recover on their own. In some cases, before the occurrence indicated signs warning signs are noted:
Regardless of the form of the pathology, with ischemic neuropathy of the optic nerve, the quality of peripheral vision decreases, manifested in the form of:
Clinical phenomena characteristic of the acute stage of the disease develop for about 4-5 weeks. At the end of this period, the swelling of the optic nerve subsides, and internal hemorrhages in the area eyeball resolve without intervention.
At this stage, optic nerve atrophy of varying severity develops and visual acuity (especially peripheral) is not restored. Often, after the acute period ends, the disease progresses.
Due to the fact that ischemic neuropathy develops against the background various diseases Diagnosis of this disease is carried out by:
If ischemic optic neuropathy is suspected, the following studies are prescribed:
Studies in anterior ischemic neuropathy show varying degrees of decreased visual acuity.
Ophthalmoscopy can reveal swelling of the optic nerve and the location of its damage.
The veins in the central part are narrowed and widened at the edges. In rare cases, the examination reveals internal hemorrhages.
The following studies are considered important from the point of view of making a diagnosis and determining the causes of damage:
In addition to these techniques, angiography of retinal vessels is often used, through which the nature of their damage is determined. Carrying out ultrasound examination helps to identify features of changes in blood flow in the arteries.
Using electrophysiological techniques, the nature of the decrease in the functionality of the optic nerve is diagnosed. In order to identify the causes of the disease, these studies are supplemented by a coagulogram, which helps determine the level of cholesterol and lipoproteins.
The given examination methods help to differentiate this pathology with tumors of the central nervous system and.
If ischemic optic neuropathy is detected, treatment should begin immediately.
Long-term circulatory disorders cause the death of nerve fibers, which is irreversible and cannot be eliminated even through surgical intervention.
Immediately after detection of pathology, the following are prescribed:
The main goal of treatment is to ensure stable remission of the disease and prevent the spread of neuropathy to the second eye. In this regard, pathology therapy is carried out in a hospital setting.
After elimination acute form diseases, measures are taken to restore blood flow. For this purpose, the following drugs are prescribed intramuscularly or intravenously, as well as in tablet form:
If necessary, treatment is supplemented antihypertensive drugs(“Timolol”, “Dorzolamide”), which normalize intraocular pressure. Depending on the indications, the treatment regimen includes:
It is necessary to take diuretics, which eliminate the swelling of the affected tissues. At the same time, vitamins B, C, and E are prescribed.
If the disease is caused by vasculitis, glucocorticoids are used. Over time, it is recommended to reduce the dosage of these drugs.
For posterior ischemic neuropathy the following are prescribed:
Upon completion drug treatment sessions of laser and electrical stimulation, magnetic therapy are carried out. These procedures are necessary to restore the conductivity of the optic nerve.
During the treatment of ischemic neuropathy, it is necessary to carry out measures aimed at eliminating accompanying pathologies. In particular, it is important to suppress the activity of vasculitis. If necessary drug therapy supplemented surgical intervention. Similar procedures are carried out to eliminate stenosis or thrombosis of the arteries.
Ischemic optic neuropathy is dangerous disease, provoking irreversible changes. The course of the pathology is accompanied by atrophy of nerve fibers, as a result of which a decrease in visual acuity and scotomas become persistent (cannot be corrected). Only in 50% of cases is it possible to slightly restore the functioning of the affected eye. Visual acuity in such situations improves by no more than 0.1-0.2.
If the pathology affects both eyes, chronic ischemic ocular neuropathy and total blindness are highly likely to develop.
Prevention of neuropathy involves timely treatment vascular and systemic pathologies. People who have previously received therapy of this disease on one eye, should be checked regularly ophthalmological examination healthy organ vision.
And one of the most insidious. Starting sometimes imperceptibly, gradually, it strikes a blow to vision at the most unexpected moment. And it is a companion to many other diseases that for the time being do not manifest themselves in any way.
Our expert is an ophthalmologist, senior researcher at the Research Institute of Eye Diseases of the Russian Academy of Medical Sciences, candidate medical sciences Natalia Sheremet.
Targeted by Optic Neuropathy - optic nerve, which transmits to the brain all visual information received by the retina. When, for one reason or another, part of the fibers of the optic nerve, which resembles a densely braided telephone wire, dies, incomplete information reaches our main “control panel”, as a result of which one or another sector of the visual field (in the center or on the periphery) drops out and decreases visual acuity, its color characteristics change.
Most often, the disease begins acutely. But there is also a more hidden course, when the victim of neuropathy may not notice any problems with vision. Until it decreases so much that it becomes difficult for a person to watch TV, read... Experts warn: if the problem is not dealt with, the matter may end in complete blindness.
It is also important to consult an ophthalmologist in a timely manner and undergo an examination because optical neuropathy, such as diabetes mellitus, arterial hypertension or hypotension, atherosclerosis, pathology of the blood coagulation system, multiple sclerosis, which at first may not show themselves in any way.
Optic neuropathy (including in young people) is often caused by brain tumors. In this case early diagnosis- not only the key to saving vision, but sometimes life itself.
A special article is for patients who received other diseases as a result of treatment. According to our expert, she is often approached by women who have developed optic neuropathy after using hormonal contraceptives and hormone replacement therapy, which affects the coagulation properties of the blood, and therefore the nutrition of the optic nerve.
In some patients, due to the individual characteristics of their body, some drugs for the treatment of cardiac arrhythmia can worsen their vision, which is why, on the recommendation of an ophthalmologist, the cardiologist often selects another drug for them.
That's just with timely diagnosis neuropathy, which early stages successfully treated, with us, alas, big problems. Sometimes even experienced doctors cannot identify this diagnosis for a long time. Therefore, specialists from the Research Institute of Eye Diseases of the Russian Academy of Medical Sciences recommend: at the first suspicion of visual impairment (decrease in visual acuity, change in color perception, change in field of vision, etc.), consult an ophthalmologist.
And undergo a comprehensive examination, which, if you suspect optic neuropathy, must include: examination of visual acuity, fundus, eye pressure, visual fields (perimetry), color vision, structure of the optic nerve (optical coherence tomography), electrophysiological methods. Otherwise, problems will not keep you waiting long.
