Optical Neuropathy

Optic neuropathy is the defeat of optic nerve fibers, which is accompanied by its atrophic degeneration with the development of characteristic clinical symptoms. Previously, this condition was designated by the term "optic nerve atrophy", but currently ophthalmologists recommend not using it.

Optical neuropathy is not an independently emerging pathology, but one of the manifestations or consequence of a number of diseases. Therefore, patients with such a diagnosis are found in the practice of doctors of various profiles: the oculist, neurologist, endocrinologist, traumatologists, maxillofacial surgeons and even oncologists.

Content

1Pathogenesis
2What causes degeneration of the optic nerve
3Clinical manifestations
4Features of some forms of optical neuropathy
5Diagnostics
6Principles of treatment
7Forecast

Pathogenesis

Whatever the cause of the damage to the optic nerve, the key pathogenetic factors are ischemia of nerve fibers with a weakening of the antioxidant defense mechanism. This can contribute to various etiological mechanisms:

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compression (squeezing) from the outside of nerve fibers;
lack of blood supply with the development of ischemia, with the importance of violations of arterial and venous blood flow;
metabolic disorders and intoxications accompanied by activation of neurotoxic and peroxide reactions;
inflammatory process;
mechanical damage to nerve fibers (trauma);
violations of central genesis (at the level of the brain);
radiation damage;
congenital anomalies.

If the lesions are irreversible and progressive, the nerve fibers die and are replaced by a gliotic tissue. Moreover, the pathological process tends to spread, so optical neuropathy in most cases tends to increase. The area of the appearance of the primary focus and the rate of degeneration (atrophy) of the nerve depend on the etiology (cause).

What causes degeneration of the optic nerve

There are a lot of diseases that can provoke the development of optical neuropathy. On the mechanism of damage to the optic nerve, they can all be divided into several groups:

Diseases with a predominantly vascular pathogenetic factor. This includes diabetes, hypertension and secondary arterial hypertension of any origin, arterial hypotension, temporal arteritis, generalized atherosclerosis, nodular periarteritis, thrombosis of the main vessels of the cervico-cerebral region and nerve-supplying arteries.
Conditions leading to compression (compression from the outside) of the optic nerve trunk. This is thyrotoxicosis (flowing with endocrine ophthalmopathy), any volumetric formation of the orbit and visual channel (glioma, lymphangioma, hemangioma, cyst, carcinoma), all kinds of pseudotumor orbits. Sometimes there is a compression of fragments after eyebrow injuries, hematomas (including those located between the nerve shells) and foreign bodies. The degeneration of the nervous tissue occurring at the same time is associated not only with direct compression of the fibers. Of great importance is also ischemia (oxygen deficiency) of significant areas of the nerve, which develops as a result of local compression of feeding vessels.
Infiltration of the trunk of the optic nerve. Most often we are talking about germinating tumors, which are primary and secondary (metastatic). To the infiltration of the nerve can also cause foci of inflammation, sarcoidosis, fungal infection.
Demyelinating diseases(multiple sclerosis). Exposure of nerve fibers leads first to a violation of the impulses carried on them, and then to irreversible degeneration.
The toxic form of optical neuropathy.The defeat of the optic nerve can be associated with the impact of a number of industrial toxins, poisonous substances, pesticides, alcohol and its surrogates. The greatest danger is represented by methyl alcohol, the metabolites of which (especially formaldehyde) are highly toxic and tropic to the optic nerve. Optical neuropathy can develop against the background of taking certain drugs: for example, with intolerance to sulfonamides, with severe overdose of cardiac glycosides and amiodarone, during treatment of tuberculosis with ethambutol.
Dystrophy of the optic nerve, due to severe chronic hypovitaminosis,and the long-term vitamin B deficiency is particularly critical. The development of neuropathy can be associated with pronounced disturbances in the absorption process in the small intestine, starvation, and the observance of severe, irrational food restrictions. This mechanism of damage to the optic nerve is also included in chronic alcoholism, along with direct toxic effects of ethanol.
Hereditary Optical Neuropathy. The defeat of the optic nerve in this disease is caused by mutations in the mitochondrial DNA, which leads to defects in the work of the enzymes in the respiratory cycle. A consequence of this is the formation of an excessive amount of toxic molecules of active oxygen and a chronic energy deficit with the disruption of the work of nerve cells and their subsequent death.

One of the most common causes of optical neuropathy is glaucoma. Pathogenesis in this disease involves the gradual death of retinal structures due to its chronic compression in the deformed cells of the reference scleral plate and the inclusion of the vascular component. That is, the process of degeneration in this case begins with the periphery, initially the neurons die, then the optic nerve is atrophied. The same mechanism is also characteristic of other pathological conditions that occur with a clinically significant increase in intraocular pressure.

Clinical manifestations

On average, the eye nerve contains about 1-1.2 million neuronal fibers, each of which is covered with myelin sheath. Such a structure provides isolation of the impulses conducted and increases the speed of their transmission. It is the damage to these fibers on any part of the nerve that most often causes the appearance of symptoms, regardless of the etiology of the process and the localization of the primary focus of degeneration.

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The main clinical manifestations of optical neuropathy include:

Reduced visual acuity, and this violation can not be adequately corrected with the help of glasses / lenses. Initially, patients can talk about blurring the vision.
Change in color perception.
Change the fields of view. Divisions and quadrants may fall out, central and paracentral scotomas may appear (defects in the form of blind areas that do not perceive light stimulation). With a pronounced concentric narrowing of the fields, one speaks of the formation of tunnel vision.

These disorders can appear and progress at different rates, and often they are asymmetric or even one-sided. To additional and not always detectable symptoms include pain behind the eyeball or inside it, changing the position and mobility of the eyeball. It should be understood that they are all signs of a primary disease, and not a consequence of damage to the optic nerve.

Features of some forms of optical neuropathy

Despite the uniformity of symptoms, optical neuropathy of various origins has some peculiarities.

With posterior ischemic neuropathy, symptoms usually increase gradually and asymmetrically. Their appearance is associated with a chronic impairment of the blood supply to the intraorbital part of the optic nerve on the background of the defeat of the carotid arteries and their branches. Therefore this variant of optic neuropathy is more common in older people suffering from atherosclerosis, arterial hypertension, diabetes mellitus. There may be other vascular factors. With posterior ischemic neuropathy, fluctuations in the state with a deterioration in visual quality are often noted taking a hot bath, visiting the sauna / bath, immediately after awakening, with excitement and physical exertion. Moreover, an increase in the ischemia of the nerve can cause both an increase and a decrease in total blood pressure.
With anterior ischemic neuropathy, the symptomatology appears acutely and rapidly increases. It is caused by acute hypoxia of the anterior segment of the optic nerve (in the nipple region). The edema and heart attacks develop, and small linear foci of hemorrhages in the retina are also often found. Disorders are usually unilateral and irreversible, after two to three weeks atrophic phenomena are noted in the trunk of the optic nerve.
With endocrine optic neuropathy, visual impairments develop subacute and are associated with decompensated edematous exophthalmos. Venostage, increased intra-orbital pressure, edema of oculomotor muscles and orbital tissue, worsening perfusion of blood along the arteries - all this leads to compression and ischemia of the optic nerve. With an adequate correction of the endocrine status and a decrease in the severity of ophthalmopathy, a partial reduction of symptoms is possible.

Diagnostics

Diagnosis of optic neuropathy is aimed at clarifying the etiology of the severity of the process. But the scope of a doctor-appointed examination often depends not only on the overall clinical picture and the underlying cause, but also on equipping the health facility. And the majority of patients, in addition to consulting an oculist (ophthalmologist), also require an appeal to other specialists.

Diagnosis of optical neuropathy includes the following methods and studies:

Assessment of visual acuity. At the expressed infringements it is possible to spend only the test for light sensation.
Definition of visual fields. Allows to identify their narrowing, the fall of sectors and quadrants, the presence of livestock.
Testing color perception.
Ophthalmoscopy - examination of the fundus with the use of an ophthalmoscope, it is optimal to carry out this examination with a medicamentally dilated pupil. Allows you to assess the condition of the discs of the optic nerves, the retina and its vessels. With optical neuropathy, the pallor of the disc can be detected, its color may change to grayish, streakiness or widening of the borders, vyhubanie in the vitreous. Often, edema of adjacent areas of the retina, expansion or narrowing of the vessels (arteries, veins), sometimes hemorrhages. In the area of the disc, exudate can be seen, which looks like a cotton-like layering. But with posterior ischemic neuropathy, ophthalmoscopy initially does not usually reveal any changes on the fundus.
UZDG arteries: ophthalmic, near-orbital area (especially supra-block), carotid, vertebral. Currently, laser dopplerography is increasingly being used.
Angiography of the vessels of the retina.
Evaluation of the physiological activity of the optic nerves, with the determination of the threshold of their electrical sensitivity, pattern-ERG.
Studies to assess the condition of the bones of the skull and especially the region of the Turkish saddle (radiography, CT, MRI). With their help, you can also identify foreign bodies, signs of voluminous formations and increased intracranial pressure.
Static computer perimetry.
Laboratory diagnostics: a biochemical blood test with an evaluation of the lipid panel and glucose level, a study of the coagulation system. In the presence of clinical signs of the B12-deficient state, the level of the corresponding vitamin in the blood serum is determined.

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Consultations of the neurologist (or neurosurgeon), the vascular surgeon, the endocrinologist, the therapist can be shown.

Principles of treatment

The treatment regimen for optic neuropathy depends on the etiology of optic nerve damage, severity and severity of symptoms. In some cases, emergency hospitalization is indicated, in others the doctor recommends long-term outpatient therapy. And in a number of patients the question of surgical treatment is being solved.

In acute vascular ophthalmopathy therapy should be started as early as possible, this will limit the area of ischemia and improve the prognosis. It is desirable that the scheme of complex drug treatment has been agreed by several specialists, most often requires the joint work of the oculist, neurologist and therapist.

Therapy of vascular ophthalmopathy includes several groups of drugs:

Vasodilators that help reduce reflex spasm of vessels in adjacent areas with ischemia and improve perfusion of blood along the affected arteries.
Decongestants. Their use is aimed at reducing edema in neighboring partially ischemic zones, which will help reduce the compression of the nerve itself and the vessels feeding it.
Anticoagulants for correction of already existing thrombotic disorders and prevention of secondary thrombosis. Of particular importance is heparin, which in addition to direct anticoagulation has also a vasodilator and some anti-inflammatory effects. The drug can be used for systemic and local therapy, it is administered intramuscularly, subcutaneously, subconjunctivally and parabulbar.
Disaggregants for improving the rheological properties of blood and reducing the risk of thrombotic complications.
Vitaminotherapy, it is advisable to use neurotropic vitamins of group B.
Preparations with neuroprotective action.
Glucocorticoids. They are not used by all patients, the decision on their appointment is taken individually.
Metabolic and resorptive therapy.

If possible, also used oxygen therapy. In the recovery period, laser therapy, magnetic and electrical stimulation of the optic nerves are shown. And the revealed vascular factors (atherosclerosis, arterial hypertension, hypotension, etc.) are subject to correction.

In other forms of optical neuropathy also necessarily affect the etiologic factor. For example, with endocrine ophthalmopathy, stabilization of the hormonal status is of paramount importance. With posttraumatic compression, they try to remove foreign bodies and restore the physiological shape of the orbit, to evacuate large hematomas.

Forecast

Unfortunately, the symptoms of optic neuropathy are rarely completely reduced, even with early-initiated adequate therapy. Good results include a partial restoration of vision and a lack of propensity to progression of symptoms in a distant period. In most patients peripheral vision defects and visual acuity are retained, which is associated with the development of irreversible nerve atrophy. And chronic vascular neuropathy is usually prone to a slow and steady progression.

After removing the severity of the condition and stabilizing the symptoms, prevention of repeated ischemic attacks and deterring the process of neurodegeneration are of paramount importance. Most often, long-term maintenance therapy is used to prevent thrombosis, improve the lipid profile of the blood. It is often recommended repeated courses with the use of vascular drugs, and in the case of endocrine ophthalmopathy the patient goes to the endocrinologist to adequately correct the existing disorders.

The doctor-neurologist K. Firsov gives a lecture on the hereditary atrophy of Leber's optic nerves:

Hereditary atrophy of Leber's optic nerves