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Damage to the optic nerve (MN) is an urgent problem at the junction of neurosurgery and ophthalmology. 1988 to 1996 at the Institute of Neurosurgery. N.N. Burdenko observed 156 patients with damage to malignant neoplasms in TBI and penetrating wounds of the skull and orbit. The study of such an array of observations showed that in order to improve the diagnosis and choice of tactics for treating MN damage, it is obvious that it is necessary to create a unified classification that would take into account the nature and mechanism of injury, localization and genesis of the lesion, morphological changes, clinical forms and severity of damage, etc. At the same time, there are only isolated messages, which present attempts to systematize this pathology. Taking into account the above, the Institute of Neurosurgery has been working for a number of years to create a classification of damage to the MN. Based on the analysis of literature data and our own observations, a classification of damage to the ZN was developed according to the following principles.
I. By the nature of the injury: open and closed.
1) Open damage - damage to the MN with penetrating wounds of the skull and / or orbit.
2) Closed injury - damage to the MN as a result of blunt trauma to the skull and facial skeleton.
P. By the mechanism of injury: direct and indirect.
1) Direct damage occurs due to direct contact of the traumatic agent with the MN.
2) Indirect damage occurs as a result of shock or compression action of a traumatic agent on distant or surrounding bone structures. A characteristic feature is a decrease in vision after an injury in the absence of signs of damage to the eyeball, which could lead to a decrease in visual functions.
III. By the genesis of the lesion: primary and secondary.
1) Primary damage - damage in which there are morphological changes caused by mechanical energy, and occurred at the time of injury:
1.1. Hemorrhages in the nerve, sheaths and intershell spaces of the nerve;
1.2. Contusional necrosis; 1.3 Gap:
a) anatomical (full or partial);
b) axonal.
Anatomical breaks are characterized by a break in the entire diameter of the nerve or part of it. In this case, the rupture extends to all components of the nerve — the sheaths, stroma, visual bundles (axons) and vessels of the nerve, and can be established macroscopically at surgery or autopsy.
Axonal damage to the optic nerve can be differentiated only microscopically: when it looks unchanged, there are axonal ruptures in the depth of the nerve.
2) Secondary injury - damage in which there are morphological changes caused by vascular failure caused by intra-, extracranial factors, and developing at any time after injury.
2.1. Edema;
2.2. Necrosis due to local compression of the vessel or circulatory vascular insufficiency;
2.3. Nerve infarction due to vascular occlusion (spasm, thrombosis).
IV. By localization of the lesion: front and back.
1) Anterior injury - lesion of the intraocular section (optic disc) and part of the intraorbital section up to the entry point of the central retinal artery (PAS) into it, while pathology is always detected in the fundus.
Clinical forms of anterior injuries:
1.4. Wound.
2) Posterior damage - damage to the optic nerve posterior to the place of entry into the nerve of the PAS, when there is a clear dysfunction of the optic nerve with delayed changes (atrophy of the optic disc) in the fundus. Clinical forms of posterior lesions:
2.1. Shake;
2.2. Injury;
2.3. Compression;
2.4. Wound.
V. By type of damage:
1) Unilateral damage to the ZN.
2) Damage to the visual pathway at the base of the brain:
2.1. Bilateral damage to ZN;
2.2. Damage to the chiasm;
2.3. Combined damage to MN and chiasm;
2.4. Combined damage to the optic nerve, chiasm and optic tract.
Vi. By the presence of fractures of bone structures:
1) Damage with a fracture of the walls of the optic canal.
2) Damage with the presence of fractures of adjacent bone structures (wall of the orbit, anterior tilted process, small wing of the sphenoid bone).
3) Damage against the background of fractures of distant bone structures of the skull and facial skeleton.
4) Damage without the presence of fractures of the bone structures of the skull and facial skeleton.
VII By clinical forms (depending on the location of the lesion).
1) For front injuries:
1.1. Violation of blood circulation in the PAS;
1.2. Anterior ischemic neuropathy;
1.3. Evulsion (separation of the optic nerve from the eyeball);
1.4. Wound.
2) For back injuries:
2.1. Shake;
2.2. Injury
2.3. Compression;
2.4. Wound.
Based on the unity of the anatomical structure and blood circulation of the MN and the brain, it can be concluded that damage to the MN is a local injury to the PNS. This gives rise to the use of the classification divisions of TBI: concussion, contusion, compression, injury. It should be noted that a number of authors widely use these terms in relation to the damage to the optic nerve. However, the content of the above concepts in their morphological, pathophysiological and clinical interpretations is far from the same.
The expediency of identifying clinical forms of damage to MN follows from practical considerations. This is primarily due to the difference in treatment approaches, including the determination of indications for MN decompression. In particular, in case of indirect posterior injuries, which are of the greatest relevance for neurosurgeons, we can talk about at least two clinical forms: compression and contusion of the MN. However, if we proceed from an analogy with the structure of TBI, it is known that severe forms of traumatic brain injury - contusion, compression, are less common than concussion. The same position can be quite applicable to the injury of the MN.
Below is a clinical interpretation of the terms "concussion", "contusion", "compression" and "injury" in relation to the injury of the ON.
Concussion of the optic nerve
Concussion is defined as "a clinical syndrome characterized by an immediate and transient impairment of neurological function associated with exposure to a mechanical factor."
Concussion is understood as damage to the optic nerve without gross organic changes in its tissues, membranes and surrounding structures.
Concussion of the MN is characterized by transient visual impairment within seconds or minutes, less often hours, followed by its complete restoration. The most common example is the patient's complaints of seeing "stars" or "sparks" in front of the eye for a few seconds after hitting the frontal or temporal region. Apparently, concussion of the MN occurs often, however, due to the transient nature of visual disturbances, it does not attract the attention of both doctors and the patients themselves.
Optic nerve injury
Contusion is histologically defined as "structural tissue damage characterized by blood extravasation and cell death."
Clinically, contusion of the optic nerve is characterized by persistent loss of vision, which develops at the time of injury (an immediate type of visual impairment), which is based on morphological changes. Primary lesions dominate in the structure of the morphological substrate. If the loss of vision is complete, contusion necrosis is likely to occur, much less often a rupture. If the loss of vision is partial and / or there is a restoration of vision, then the area of primary contusional necrosis or rupture did not affect the entire nerve. In addition, hemorrhages (intraneural and meningeal) can also underlie partial vision loss. In these cases, the improvement in vision can be explained by blood resorption and a decrease in the compression of nerve fibers. In most cases, immediate amaurosis is irreversible, although partial or complete restoration of visual function may occur within hours or days after injury.
Compression of the optic nerve
The structure of the morphological substrate is dominated by secondary (ischemic) damage due to mechanical compression of the nerve. Compression of the optic nerve is characterized by progressive or delayed deterioration of visual functions after injury. In the delayed type of vision loss, visual functions are not changed immediately after injury, and their primary deterioration is noted only after some time. With a progressive type of vision loss, the primary deterioration of visual functions is observed immediately after the injury, while there is a partial visual deficit, which increases after a while (secondary deterioration). The period of time from the moment of injury to primary or secondary deterioration of the state of visual functions ("light interval") can take from several minutes and hours to several days after the injury. The "light gap", regardless of its duration, is an indication of the absence of an anatomical break in the MN and the presence of potentially reversible morphological changes.
Compression can occur both against the background of a contusion of the MN, and without it. The reserve spaces of the membranes and the ON canal are extremely limited, therefore, the contusion of the ON, accompanied by its edema and an increase in the transverse size, can lead to compression inside the canal. Considering that in some cases the primary and secondary mechanisms of damage develop in parallel, the immediate type of vision loss is not a reason to exclude compression of the MN, especially if it is not complete, but partial. Loss of vision at the time of injury can occur when compression occurs due to a fracture of the canal walls with displacement of bone fragments.
In the acute period of TBI, massive contusion foci of the frontal lobe, intracranial hematomas of the frontotemporal region, causing displacement of the posterior-basal parts of the frontal lobe into the middle cranial fossa, into the chiasmal cistern, can lead to compression of the intracranial part of the malignant neoplasm or chiasm at the base of the brain. In these cases, we will talk about secondary dislocation damage to the visual pathway.
The main pathological processes that exert a compressive effect on the MF along its entire length are summarized below:
I. Deformation and fractures of bone structures surrounding the MN:
1) the upper wall of the orbit;
2) The wall of the optic canal;
3) Anterior inclined process.
II. Hematomas:
1) Intraorbital:
1.1. Retrobulbar hematoma;
1.2. Subperiosteal hematoma of the orbit.
2) Sheath hematoma of the MN.
3) Intracranial:
3.1. Frontal-basal hematoma;
3.2. Convexital hematoma of the frontotemporal region.
III. Massive foci of contusion and crushing of the frontal lobe of the brain
IV. Arachnoid cyst MN.
V. Edema of MN.
Vi. Cicatricial adhesive processes in the long-term period:
1) Callus;
2) Scar tissue;
3) Adhesive arachnoiditis.
Vii. Traumatic supraclinoid false aneurysm a.carotis interna.
VIII. Expanded cavernous sinus with carotid-cavernous anastomosis.
Taking into account the presented data, it should be emphasized that the compression of the ZN can occur in two ways, both due to external and internal factors. In the first case, it is subjected to external compression due to pathological processes in the orbit (subperiosteal or retrobulbar hematomas, fractures of its walls with displacement of bone fragments), the optic canal (fractures with displacement of bone fragments, epidural hemorrhages), cranial cavities (frontal-basal or convexital hematomas , fracture with displacement of the anterior inclined process, etc.). In the second case, he is subjected to compression "from the inside", due to pathological processes developing in his parenchyma and membranes (edema, hemorrhages) and providing a mass effect. In such a situation, there is actually a "tunnel" syndrome caused by compression of the optic nerve within the rigid structure of the optic canal with an unchanged lumen or a tightly fitting dural membrane outside the canal.
Optic nerve injury
MN injury - direct damage to MN, resulting from direct contact with a traumatic agent. MN injury, as a rule, leads to its complete irreversible damage, with an anatomical break and the development of immediate amaurosis. However, partial damage is possible. In this case, there is irreversible damage to part of the optic fibers, but the intact fibers retain the potential for restoration of their function. In those cases when the direct effect of the traumatic agent on the MN does not lead to a violation of its integrity, a tangential injury occurs.
MN injuries are observed with penetrating wounds of the skull and / or orbit. However, the latter are by no means in all cases accompanied by direct injury of the malignant neoplasm itself, despite the presence of symptoms of its damage. When the ZN is located in the zone of primary destruction, formed along the path of the projectile's flight, the clinical form of its damage is injury. If the MN is in the zone of secondary destruction caused by the lateral force of the projectile, the clinical form of its damage is contusion. Thus, in case of open injuries due to gunshot penetrating wounds of the skull and / or orbit, not only direct injury - injury, but also indirect damage - contusion of the MN is possible. As a result of a penetrating gunshot wound to the cranio-orbital region, a combination of clinical forms can be observed: contusion and compression of the MN and wounding it with secondary wounding shells (bone fragments).
Direct or lateral (contusion) impact of the projectile not only on the optic nerve, but also on the a.ophthalmica and its branches, which are involved in the blood supply to the optic nerve and the retina, may be accompanied by impaired blood flow in the latter. In such cases, there will also be combined direct and indirect, anterior and posterior damage to the ZN.
The anatomical break of the MN due to its injury is not always possible to verify by CT, especially in the intracranial or intracanalicular regions. In case of contusion of the malignant neoplasm due to injury to the orbit, CT examination reveals changes in the intraorbital region (an increase in its diameter, changes in density), while the presence of a hematoma at the site of its injury can mask a nerve rupture.
VIII. By severity: mild, moderate, severe.
Currently, in most cases, the establishment of clinical forms of damage to the MN is very difficult. The presented characteristics of clinical manifestations have a lot in common. Certain difficulties arise in distinguishing them. At the same time, for practical purposes (indications for MN decompression, prognosis, rehabilitation potential, expert assessment, determination of the severity of TBI, etc.), clear gradations are required according to unified criteria. Violations of visual functions can serve as the latter. Considering that they vary widely, all damage to the optic nerve is divided into three degrees of severity, according to the severity of visual impairment: mild, moderate, severe (Tables 2–2).
The parameters of acuity and visual field are of independent importance in determining the severity of damage to the MN. The latter is rated according to the worst of two indicators: visual acuity or visual field. In the presence of a central scotoma or the inability to determine the boundaries of the visual field, the severity of the damage is judged by visual acuity. With a combination of normal visual acuity and a visual field defect, the severity is determined by the size of the latter.
Table 2-2
In the case of an immediate type of visual impairment, the severity of damage to the optic nerve is assessed by the initial level of visual functions immediately after the injury. The severity of progressive or delayed types of visual impairment should be assessed over time according to their maximum severity in the acute period of injury.
IX. Grades of functional impairments
1) According to the dynamics of dysfunction:
1.1. Immediate;
1.2. Progressive;
1.3. Delayed.
2) According to the degree of impairment of the conduction of excitation:
2.1. Partial block of excitation conductivity;
2.2. Complete block of excitation conductivity.
3) By reversibility of dysfunction:
3.1. Reversible - functional break of ZN;
3.2. Partially reversible - morpho-functional break of MN;
3.3. Irreversible - morphological break of the MN.
In fig. Figures 2-28 present the main provisions of the developed classification.
Rice. 2 - 28. Classification of optic nerve injuries.
Examples of formulations of the diagnosis in relation to damage to the MN:
- Closed indirect light injury of the right ZN;
- Closed indirect severe injury to the right ZN and chiasm;
- Closed indirect severe damage to ZN from 2 sides;
- Closed indirect severe injury (contusion) of the intracanalicular part of the right optic nerve, linear fracture of the upper wall of the right optic canal;
- Closed indirect severe injury (contusion and compression) of the intracanalicular part of the right MN;
- Closed indirect severe dislocation injury (compression) of the intracranial section of the right malignant neoplasm;
- Open direct severe injury (injury) of the intraorbital part of the right MN with a complete anatomical break;
- Open indirect severe injury (contusion) of the intraorbital section of the right malignant neoplasm.
Thus, the developed classification of MN injuries makes it possible to take into account the nature and mechanism of trauma, genesis and localization of the process, the presence of fractures of bone structures, types of development of visual impairments, clinical forms and severity of damage when constructing a diagnosis, and thus contributes to the specification of the diagnosis, determination of the prognosis and a differentiated approach to treatment.
DETERMINATION OF THE DEGREE OF TBI SEVERITY ACCOMPANIED WITH OPTIC NERVE DAMAGE
As you know, the degree of brain damage is the main, but not the only component in determining the severity of TBI. Undoubtedly, damage to the MN is one of the manifestations of damage to the brain tissue and, in particular, contusion of the brain. However, for a more detailed solution of the set tasks, it is advisable to move the concept of "damage to the MN" outside the framework of brain contusion. This makes it possible to compare the degree of brain injury and MN, but not the severity of TBI and MN damage, since the latter itself is an important component in determining the severity of TBI. The above judgment is valid for posterior damage to the AV. In the presence of anterior damage to the optic nerve, we will talk about the concussion of the orbit combined with head injury.
Damage to the MN can occur with TBI of varying severity: mild, moderate, and severe. The qualification of the severity of TBI, accompanied by damage to MN, presents certain difficulties associated with the fact that the current classification of TBI does not provide for the dependence of the severity of TBI on the presence or absence of damage to the cranial nerves, and in particular, MN. Meanwhile, damage to the (posterior) MN can make some adjustments in determining the severity of TBI. In some cases, the symptomatology of MN damage is the only focal manifestation of the trauma suffered, and the clinical picture otherwise fits well with the diagnosis of concussion. At the same time, craniography and CT of the brain do not reveal bone traumatic injuries and changes in the density of brain tissue. In isolated cases, TBI can be observed without loss of consciousness. Nevertheless, in these cases, the clinical form of TBI, the degree of brain damage, should be assessed as mild brain contusion.
It is advisable to determine the severity of TBI, accompanied by damage to the MN, taking into account the principle of mutual burdening, which is presented in the diagram below.
Gradation of TBI severity, accompanied by optic nerve damage
In cases where there is a mild brain contusion and mild damage to the MN, the severity of TBI should be interpreted as mild. If there is a severe damage to the MN, then in terms of the totality of the terms - a mild brain contusion and severe damage to the MN, we should talk about moderate TBI. When determining the severity of TBI in patients with mild brain contusion and moderately severe damage to the malignant neoplasms, as well as in patients with moderate cerebral contusion and severe malignant neoplasm injury, it is necessary to take into account other factors (the presence of subarachnoid hemorrhage, bone traumatic changes, liquorrhea, pneumocephalus, etc.).
The optic nerve (Nervus opticus) is the second pair of twelve pairs of cranial nerves. The optic nerve regulates all our activities: it transmits the image to the brain.
The optic nerve is highly sensitive. In the twenty-first century, inflammation of the optic nerve is common, and then damage to the optic nerve, which can lead to loss of vision. The optical apparatus of the eye is damaged. The damaged nerve will no longer function as it used to. With timely treatment, the nerve can be saved and its functions preserved.
Causes
The causes of damage to the Nervus opticus (optic nerve) can be various diseases: meningitis, meningoencephalitis, etc. A disturbance in the functioning of the optic nerve reduces the quality of human life: the patient does not go anywhere because he does not see well. Also, one of the main reasons is complications after vision correction surgery.
Signs of damage to the optic nerve
Symptoms are due to inflammation of the sheaths of the nerve fibers. These include: pain in the eyes, which increases with the movement of the eyeballs, edema, photopsia, and others.
The nerve can be affected partially or completely, if the nerve is partially affected, then the outcome of the disease will be favorable. Diseases in which the optic nerve is affected are acute. Clinical manifestations are rapidly increasing. Consultation of a neurologist is required.
Patients stop seeing in the dark and are afraid of bright light.
Symptoms increase and can lead to disability of the sick person (the person will go blind).
Symptoms can vary, depending on the cause of the disease.
Treatment
Treatment includes symptomatic and pathogenetic therapy. After starting treatment, the patient urgently needs to be hospitalized.
Until the exact cause of the disease is clarified, the person receives antimicrobial therapy. After identifying the cause, measures are taken to eliminate the focus of infection (in the brain).
Treatment and restoration of the functions of the optic nerve includes the use of corticosteroids and "Prednisolone". Also, patients take "Diakarb", which relieves swelling.
"Panangin" is prescribed to reduce symptoms, nicotinic acid - to improve cerebral circulation. Patients need complete rest and vitamin therapy.
During treatment, the process (more often) does not resume and the person can continue to live his life!
The second pair of cranial nerves is the most important element of the visual system, because the relationship between the retina and the brain is carried out through it. Although the rest of the structures continue to function correctly, any deformations in the neural tissue affect the properties of vision. Atrophy of the optic nerve does not heal without a trace, nerve fibers cannot be restored to their original state, therefore it is better to carry out prevention on time.
Basic information on the disease
Optic atrophy or optic neuropathy is a severe process of destruction of axons (fibers of nerve tissue). Extensive atrophy thinns the nerve column, healthy tissue is replaced by glial tissue, and small vessels (capillaries) are blocked. Each of the processes causes certain symptoms: visual acuity decreases, various defects appear in the field of vision, and the shade of the optic nerve head (optic nerve disc) changes. All pathologies of the optic nerves account for 2% of the statistics of eye diseases. The main danger of optic neuropathy is absolute blindness, which occurs in 20-25% of people with this diagnosis.
Optical neuropathy does not develop by itself, it is always a consequence of other diseases, so a person with atrophy is examined by different specialists. Usually, optic nerve atrophy is a complication of a missed ophthalmic disease (inflammation in the structures of the eyeball, swelling, compression, damage to the vascular or nervous network).
Causes of optic neuropathy
Despite the many causes of optic nerve atrophy known to medicine, in 20% of cases they remain unclear. Usually these are ophthalmic pathologies, diseases of the central nervous system, autoimmune disruptions, infections, trauma, intoxication. Congenital forms of ADS are often diagnosed together with skull defects (acrocephaly, microcephaly, macrocephaly) and hereditary syndromes.
Causes of optic nerve atrophy on the part of the visual system:
- neuritis;
- obstruction of the artery;
- myopia;
- retinitis;
- oncological lesion of the orbit;
- unstable eye pressure;
- local vasculitis.
Injury to nerve fibers can occur at the time of traumatic brain injury or even the mildest trauma to the facial skeleton. Sometimes optic neuropathy is associated with the growth of meningioma, glioma, neuroma, neurofibroma, and similar formations in the thickness of the brain. Optical disturbances are possible with osteosarcoma and sarcoidosis.
Causes from the central nervous system:
- neoplasms in the pituitary gland or cranial fossa;
- squeezing chiasmata;
- multiple sclerosis.
Atrophic processes in the second pair of cranial nerves often develop as a result of purulent-inflammatory conditions. The main danger is brain abscesses, inflammation of its membranes.
Systemic risk factors
- diabetes;
- atherosclerosis;
- anemia;
- avitaminosis;
- hypertension;
- antiphospholipid syndrome;
- Wegener's granulomatosis;
- systemic lupus erythematosus;
- giant cell arteritis;
- multisystem vasculitis (Behcet's disease);
- nonspecific aortoarteritis (Takayasu's disease).
See also: Danger and prognosis with the optic nerve.
Significant nerve damage is diagnosed after prolonged fasting, severe poisoning, and volumetric blood loss. Alcohol and its surrogates, nicotine, chloroform and some groups of medicines have a negative effect on the structures of the eyeball.
Atrophy of the optic nerve in a child
In half of all cases of optic neuropathy in children, the cause is inflammatory infections of the central nervous system, brain tumors and hydrocephalus. Less often, the state of destruction is due to deformation of the skull, cerebral anomalies, infections (mainly "children"), metabolic disorders. Particular attention should be paid to congenital forms of childhood atrophy. They indicate that the baby has brain diseases that have arisen at the stage of intrauterine development.
Optical neuropathy classification
All forms of optic nerve atrophy are hereditary (congenital) and acquired. Congenital are divided according to the type of inheritance, they often indicate the presence of genetic abnormalities and hereditary syndromes that require in-depth diagnosis.
Hereditary forms of ADS
- Autosomal dominant (juvenile). The predisposition to nerve destruction is transmitted in a heterogeneous way. Usually the disease is detected in children under 15 years of age, it is recognized as the most common, but the mildest form of atrophy. It is always bilateral, although sometimes symptoms appear asymmetrically. Early signs are detected by 2-3 years, and functional disorders only at 6-20 years. Possible combination with deafness, myopathy, ophthalmoplegia and distortion.
- Autosomal recessive (infantile). This type of ADS is diagnosed less often, but much earlier: immediately after birth or during the first three years of life. The infantile form is bilateral in nature, it is often detected in Kenny-Coffey syndrome, Rosenberg-Chattorian, Jensen or Wolfram disease.
- Mitochondrial (Leber's atrophy). Mitochondrial optic atrophy is the result of a mutation in mitochondrial DNA. This form is ranked among the symptoms of Leber's disease, it occurs suddenly, resembles external neuritis in the acute phase. Most of the patients are men 13-28 years old.
Forms of acquired atrophy
- primary (squeezing of neurons in the peripheral layers, the optic nerve head does not change, the boundaries are clear);
- secondary (swelling and enlargement of the optic nerve disc, blurred boundaries, replacement of axons with neuroglia is quite pronounced);
- glaucomatous (destruction of the ethmoid plate of the sclera due to surges in local pressure).
Destruction is ascending, when the axons of the cranial nerves are affected, and descending, with the involvement of retinal nerve tissues. Symptoms distinguish between unilateral and bilateral ADN, according to the degree of progression - stationary (temporarily stable) and in constant development.
Types of atrophy by optic disc color:
- initial (slight blanching);
- incomplete (noticeable blanching of one segment of the optic disc);
- full (change in shade over the entire area of the optic nerve disc, severe thinning of the nerve pillar, narrowing of the capillaries).
Symptoms of optic nerve atrophy
The degree and nature of optical disorders directly depends on which segment of the nerve is affected. Visual acuity can drop critically very quickly. Complete destruction ends in absolute blindness, blanching of the optic disc with white or gray blotches, narrowing of the capillaries in the fundus. With incomplete ADH, vision stabilizes at a certain time and does not deteriorate anymore, and the blanching of the optic disc is not so pronounced.
If the fibers of the papillomacular bundle are affected, the deterioration of vision will be significant, and the examination will show a pale temporal zone of the optic disc. In this case, optical disturbances cannot be corrected with glasses or even contact lenses. Damage to the lateral zones of the nerve does not always affect vision, which complicates the diagnosis and worsens the prognosis.
ADS is characterized by a variety of visual field defects. The following symptoms allow suspecting optic neuropathy:, concentric narrowing, effect, weak pupil response. In many patients, the perception of colors is distorted, although more often this symptom develops when axons die after neuritis. Often, changes affect the green-red part of the spectrum, but the blue-yellow parts of the spectrum can also be distorted.
Diagnosis of optic nerve atrophy
An expressive clinical picture, physiological changes and functional disorders greatly simplify the diagnosis of ADH. Difficulties can arise when the actual vision does not match the degree of destruction. For an accurate diagnosis, an ophthalmologist must study the patient's history, establish or refute the fact of taking certain medications, contacts with chemical compounds, trauma, bad habits. Differential diagnosis is carried out for peripheral lens opacity and amblyopia.
Ophthalmoscopy
Standard ophthalmoscopy allows to establish the presence of ADS and to accurately determine the degree of its spread. This procedure is available in many conventional clinics and is inexpensive. The results of the study may differ, however, some signs are detected in any form of neuropathy: a change in the shade and contour of the optic disc, a decrease in the number of vessels, narrowing of the arteries, various defects of the veins.
Ophthalmoscopic picture of optic neuropathy:
- Primary: the clarity of the disc boundaries, the optic disc size is normal or reduced, there is a saucer-like excavation.
- Secondary: a grayish tint, blurred disc boundaries, an increase in the optic nerve disc, no physiological excavation, a parasomal reflex to light sources.
Coherent tomography
Optical coherence or laser scanning tomography allows you to study the nerve disc in more detail. Additionally, the degree of mobility of the eyeballs is assessed, the reaction of the pupils and the corneal reflex is checked, carried out with tables, the defects of the visual field are examined, the color perception is checked, and the eye pressure is measured. The oculist visually determines the presence.
Plain radiography of the orbit reveals pathologies of the orbit. Fluorescence angiography shows vasculature dysfunction. Doppler ultrasound is used to study local circulation. If the atrophy is due to an infection, laboratory tests such as an enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) are done.
Electrophysiological tests play a key role in confirming the diagnosis. Atrophy of the optic nerve changes the threshold sensitivity and lability of the nervous tissue. The rapid progression of the disease increases the rates of retino-cortical and cortical time.
The level of reduction depends on the location of the neuropathy:
- when the papillomacular bundle is destroyed, the sensitivity remains at a normal level;
- damage to the periphery causes a sharp increase in sensitivity;
- atrophy of the axial beam does not change the sensitivity, but sharply reduces the lability.
If necessary, check the neurological status (X-ray of the skull, CT or MRI of the brain). When a neoplasm in the brain or unstable intracranial pressure is diagnosed in a patient, a consultation with an experienced neurosurgeon is prescribed. In case of orbital tumors, it is necessary to include in the course of an ophthalmic-oncologist. If the destruction is associated with systemic vasculitis, you need to consult a rheumatologist. Arterial pathologies are dealt with by an ophthalmologist or vascular surgeon.
How is optic atrophy treated?
The treatment regimen for each patient with optic neuropathy is always individual. The doctor needs to get all the information about the disease in order to make an effective plan. People with atrophy require urgent hospitalization, while others are able to support outpatient care. The need for surgery depends on the causes of ADS and symptoms. Any therapy will be ineffective with a weakening of vision to 0.01 units and below.
It is necessary to begin treatment of optic nerve atrophy by identifying and eliminating (or stopping) the root cause. If the cranial nerve injury is due to intracranial tumor growth, aneurysm, or unstable cranial pressure, neurosurgery should be performed. Endocrine factors affect hormonal levels. Post-traumatic compression is surgically corrected by removing foreign bodies, removing chemicals, or limiting hematomas.
Conservative therapy for optic neuropathy is primarily aimed at inhibiting atrophic changes, as well as preserving and restoring vision. Shown are drugs for expanding the vasculature and small vessels, reducing capillary spasm and accelerating blood flow through the arteries. This allows all layers of the optic nerve to be supplied with sufficient nutrients and oxygen.
Vascular therapy for ADN
- intravenously 1 ml of nicotinic acid 1%, glucose for 10-15 days (or orally 0.05 g three times a day after meals);
- one Nikoshpan tablet three times a day;
- intramuscularly 1-2 ml of No-shpy 2% (or 0.04 g orally);
- intramuscularly 1-2 ml of Dibazol 0.5-1% daily (or by mouth at 0.02 g);
- 0.25 g of Nigeksin three times a day;
- subcutaneously, 0.2-0.5-1 ml of sodium nitrate of an ascending concentration of 2-10% in a course of 30 injections (increase every three injections).
Decongestants are needed to reduce swelling, which helps reduce nerve and vascular compression. Anticoagulants are used to prevent thrombosis; the vasodilating and anti-inflammatory Heparin is recognized as the best. It is also possible to prescribe antiplatelet agents (prevention of thrombosis), neuroprotectors (protection of nerve cells), glucocorticosteroids (fight against inflammatory processes).
Conservative treatment of ADS
- To reduce inflammation in the nervous tissue and relieve edema, a dexamethasone solution is prescribed in the eye, intravenous glucose and calcium chloride, and intramuscular diuretics (Furosemide).
- A solution of strychnine nitrate 0.1% in a course of 20-25 subcutaneous injections.
- Parabulbar or retrobulbar injections of Pentoxifylline, Atropine, xanthinol nicotinate. These funds help to accelerate blood flow and improve the trophism of the nervous tissue.
- Biogenic stimulants (FiBS, aloe preparations) in a course of 30 injections.
- Nicotinic acid, sodium iodide 10% or Euphyllin intravenously.
- Vitamins orally or intramuscularly (B1, B2, B6, B12).
- Antioxidants (glutamic acid).
- Oral Cinnarizine, Riboxin, Piracetam, ATP.
- Instillation of Pilocarpine to reduce ocular pressure.
- Nootropic drugs (Lipocerebrin).
- Drugs with antikinin effect (Prodectin, Parmidin) for symptoms of atherosclerosis.
In addition to medications, physiotherapy is prescribed. With ADN, oxygen therapy (use of oxygen) and blood transfusion (urgent blood transfusion) are effective. In the recovery process, laser and magnetic procedures are prescribed, electrical stimulation and electrophoresis (administration of drugs using an electric current) are effective. If there are no contraindications, acupuncture is possible (using needles on active points of the body).
Surgical treatment of optic neuropathy
One of the methods of surgical treatment of the optic nerves is hemodynamic correction. The procedure can be performed under local anesthesia: a collagen sponge is placed in the sub-Tenon space, which stimulates aseptic inflammation and dilates blood vessels. Thus, it is possible to provoke the proliferation of connective tissue and new vascular network. The sponge dissolves on its own after two months, but the effect lasts for a long time. The operation can be performed several times, but at intervals of several months.
New branches in the vascular network improve the blood supply to nerve tissues, which stops atrophic changes. Correction of blood flow allows you to restore vision by 60% and eliminate up to 75% of visual field defects with a timely visit to the clinic. If the patient has severe concomitant disorders or atrophy has developed to a late stage, even hemodynamic correction will be ineffective.
With partial atrophy of the optic nerve, a collagen implant is used. It is impregnated with antioxidants or drugs to expand the capillaries, and then injected into the eyeball without seams. This method is only effective when the eye pressure is stable. The operation is contraindicated in patients over 75 years old, with diabetes mellitus, severe somatic disorders and inflammation, as well as vision less than 0.02 diopters.
Prognosis for optic nerve atrophy
To prevent ADH, it is necessary to regularly check the state of those organs that regulate the functioning of the visual system (central nervous system, endocrine glands, joints, connective tissue). In a severe case of infection or intoxication, as well as in severe bleeding, urgent symptomatic therapy should be carried out.
It is impossible to completely regain your vision after neuropathy even in the best clinic. A successful case is when the patient's condition has stabilized, ADS does not progress for a long time, and vision is partially restored. For many people, visual acuity remains permanently impaired, and there are also defects in lateral vision.
Some forms of atrophy continue to progress even with adequate treatment. The ophthalmologist's task is to slow down atrophic and other negative processes. Having stabilized the symptoms, it is necessary to constantly carry out the prevention of ischemia and neurodegeneration. For this, long-term supportive therapy is prescribed, which helps to improve the lipid profile of the blood and prevent the formation of blood clots.
The course of treatment for optic nerve atrophy must be repeated regularly. It is very important to eliminate all factors that can affect the axons of the optic nerve. A patient with optic neuropathy should have regular specialist appointments as indicated. It is necessary to constantly carry out the prevention of complications and improve the way of life. Refusal of therapy for optic neuropathy inevitably leads to disability due to total death of nerves and irreversible blindness.
Any changes in the layers of the optic nerve negatively affect a person's ability to see. Therefore, it is necessary to undergo examinations in time for people with a predisposition and treat all diseases that contribute to atrophy of the optic nerve. Therapy will not help restore vision to 100% when optic neuropathy is already well developed.
5-07-2013, 16:28
Description
Diseases of the optic nerve are classified into three main groups:Inflammatory (neuritis);
Vascular (optic nerve ischemia);
Degenerative (atrophies);
There are descending (retrobulbar) neuritis, when the inflammatory process is localized in any part of the optic nerve from the chiasm to the eyeball, and ascending neuritis (papillitis), in which the intraocular and then the intraorbital part of the optic nerve is involved in the inflammatory process.
With damage to the optic nerve, functional disorders always take place in the form of a decrease in central vision, a narrowing of the visual field, the formation of absolute or relative cattle. Changes in the visual field to white and other colors are one of the early symptoms of optic nerve damage.
With pronounced damage to the fibers of the optic nerve, amaurotic immobility of the pupil is noted. The pupil of the blind eye is somewhat wider than the pupil of the other seeing eye.
At the same time, there is no direct and indirect (friendly) reaction of the pupil to light is preserved. In the seeing eye, a direct, but no friendly, pupil response to light is retained. The pupil response to convergence is preserved.
By the nature of the lesion and clinical manifestations of the optic nerve diseases, they are subdivided into inflammatory (neuritis), vascular (ischemia of the optic nerve), specific (tuberculous, syphilitic), toxic (dystrophic), tumor associated with damage to the optic nerve, anomalies in the development of the optic nerve, lesions, associated with impaired circulation of cerebrospinal fluid in the sheaths of the optic nerve (stagnant disc), optic atrophy.
To study the morphological and functional state of the optic nerves, clinical, electrophysiological and radiological research methods are used. Clinical methods include the study of visual acuity and field (perimetry, campimetry), contrast sensitivity, critical flicker fusion frequency, color perception, ophthalmoscopy (forward and backward), ophthalmochromoscopy, as well as fundus fluorescence angiography, ultrasound of the eye and orbit, Doppler vessels of the basin of the internal carotid artery (ocular and above the block arteries).
From electrophysiological methods, the study of electrical sensitivity and lability of the optic nerve (ECHL) and recording of visual evoked potentials (VEP) are used.
X-ray methods for examining the optic nerve include a general X-ray of the skull and orbit (frontal and profile images), examination of the bone canal of the optic nerve, computed tomography and examination by magnetic resonance imaging.
In case of optic nerve disease, comprehensive studies are required with the consultation of a therapist, neuropathologist, otolaryngologist and other specialists.
INFLAMMATORY OPTICAL NERVE DISEASES
There are more than two hundred different reasons that cause manifestations of the clinical picture of optic neuritis. The clinic has adopted a rather conventional division of neuritis into two groups: intraocular intrabulbar (papillitis) and retrobulbar. Papillitis is characterized by a sharp dysfunction of the papillary system of the blood-ophthalmic barrier. With an intrabulbar process (papillitis), the dynamics of the clinical picture is well defined ophthalmoscopically. With retrobulbar neuritis, the main thing in diagnosis is the symptomatology of visual disturbances and their careful identification, and the ophthalmoscopic picture of the fundus can remain normal for a long time.
The main form of retrobulbar neuritis is axial (axial) neuritis, in which the papillo-macular bundle is affected. The leading symptom in axial neuritis is a central scotoma, which manifests itself in the form of a relative or absolute scotoma in white or only in red and green.
The optic disc is a small part of the closed system, which is the eyeball, in particular the eye cavity. The optic disc is the only part where it is possible to visually observe the condition of the anterior end of the optic nerve. Therefore, it is customary to subdivide inflammation of the optic nerve into:
- intrabulbar (papillitis);
- retrobulbar;
Retrobulbar inflammatory diseases of the optic nerve include ophthalmoscopically invisible processes at the initial stage of development.
According to the topographic location, they are distinguished:
- orbital;
- intracanalicular;
- intracranial lesions;
The main signs of optic neuritis consist of the appearance of inflammatory exudate, edema, compression of nerve fibers by edema and the toxic effects of exudate on them. This is accompanied by small cell lymphoid infiltration and proliferation of neuroglia. In this case, the myelin sheaths and axial cylinders of the optic fibers undergo dystrophy, degeneration and subsequent atrophy. The fibers of the human optic nerve do not possess any regenerative ability. After degeneration of a nerve fiber (axon), its maternal retinal ganglion cell dies. When establishing the diagnosis of optic neuritis, it is necessary to urgently use drugs aimed at suppressing the inflammatory process in the affected area of the optic nerve, reducing tissue edema and capillary permeability, limiting exudation, proliferation and destruction.
Treatment of patients with optic neuritis should be urgent in a hospital setting and directed against the underlying disease that caused the neuritis. In recent years, two stages have been outlined in the tactics of treating neuritis: the first stage is immediate assistance until the etiology of the process is clarified; the second stage is carrying out etiological treatment after establishing the cause of the disease.
Intrabulbar ascending neuritis (papillitis) of the optic nerve
The reason is brucellosis, syphilis, etc.), focal infections (tonsillitis, sinusitis, otitis media, etc.), inflammatory processes in the inner membranes of the eye and orbit, general infectious diseases (blood diseases, gout, nephritis, etc.). With ascending neuritis, the intrabulbar part of the optic nerve (disc) first suffers. In the future, with the spread of the inflammatory process, the retrobulbar part of the optic nerve is affected.
The clinical picture depends on the severity of the inflammatory process. With mild inflammation, the optic nerve head is moderately hyperemic, its borders are indistinct, the arteries and veins are somewhat dilated. A more pronounced inflammatory process is accompanied by a sharp hyperemia of the disc, its borders merge with the surrounding retina. Exudative foci appear in the peripapillary zone of the retina and multiple small hemorrhages, arteries and veins are moderately dilated. Usually the disc will not dominate with neuritis. The exception is cases of neuritis with edema.
The main distinguishing feature of papillitis of the optic nerve from a stagnant disc is the lack of standing of the disc above the level of the surrounding retina. The appearance of even single small hemorrhages or exudative foci in the tissue of the disc or the surrounding retina is a sign of papillitis of the optic nerve.
For papillitis, early visual impairment is characteristic - a decrease in visual acuity and a change in the visual field.
Decrease in visual acuity depends on the degree of inflammatory changes in the papillomacular bundle. Usually, there is a narrowing of the boundaries of the field of view, which can be concentric or more significant in one of the areas. Central and paracentral scotomas appear. Narrowing of the peripheral boundaries of the visual field is often combined with scotomas. Also characteristic are a sharp narrowing of the field of vision to red and a violation of color perception. There is a decrease in electrical sensitivity and lability of the optic nerve. Dark adaptation is impaired. With the transition of neuritis to the stage of atrophy, the disc turns pale, the arteries narrow, exudate and hemorrhages resolve.
Treatment should be timely (early) in a hospital setting. If the reason is found out, the underlying disease is treated. In cases of unclear etiology, broad-spectrum antibiotic therapy is indicated. Apply ampiox 0.5 g 4 times a day for 5-7 days, ampicillin sodium salt 0.5 g 4 times a day for 5-7 days, cephaloridin (seporin) 0.5 g 4 times a day within 5-7 days, gentamicin, netromycin. Fluoroquinolone preparations are also used - maksaquin, tarivid. The use of vitamins is mandatory: thiamine (B,) and niacin (PP). A 2.5% solution of thiamine is injected intramuscularly, 1 ml daily, for a course of 20-30 injections, 1% solution of nicotinic acid, 1 ml daily for 10-15 days. Inside, vitamin B2 (riboflavin) is given 0.005 g 2 times a day, ascorbic acid (vitamin C) 0.05 g 3 times a day (after meals). Dehydration therapy is shown: a 25% solution of magnesium sulfate is injected intramuscularly, 10 ml, intravenously - 10% solution of calcium chloride, 10 ml, inside - diacarb, 0.25 g 2-3 times a day, after 3 days of administration, take a break for 2 days; indomethacin 0.025 g. In order to reduce inflammation, corticosteroids are used. Dexamethasone is given orally at 0.5 mg (0.0005 g), 4-6 tablets per day. After improvement of the condition, the dose is gradually reduced, leaving a maintenance dose of 0.5-1 mg (0.0005-0.001 g) per day for 2 doses after meals. A 0.4% solution of dexamethasone (dexazone) 1 ml per day is injected retrobulbar, for a course of 10-15 injections.
Retrobulbar descending optic neuritis
Significant difficulties arise in determining the etiology of retrobulbar neuritis. About half of them end up with an unexplained reason. Retrobulbar neuritis often occurs with multiple sclerosis, opticomyelitis, and diseases of the paranasal sinuses. The most common causes of neuritis are basal leptomeningitis, multiple sclerosis, sinus disease, viral (influenza) infection, etc. Sometimes retrobulbar neuritis is the earliest sign of multiple sclerosis. The group of retrobulbar neuritis includes all descending neuritis (regardless of the state of the optic nerve head). Compared to inflammation of the optic nerve head (papillitis), inflammation of the optic nerve trunk is observed much more often and manifests itself in the form of interstitial neuritis.
With retrobulbar neuritis, inflammation is localized in the optic nerve from the eyeball to the chiasm.
Cases of primary lesions by the inflammatory process of the optic nerve in its orbital part are relatively rare.
Retrobulbar neuritis most often develops in one eye. The second eye gets sick some time after the first. The simultaneous disease of both eyes is rare. Distinguish between acute and chronic retrobulbar neuritis. Acute neuritis is characterized by pain behind the eyeballs, photophobia and a sharp decrease in visual acuity.
In a chronic course, the process grows slowly, visual acuity decreases gradually. According to the state of visual functions (visual acuity and visual field), all descending neuritis are divided into axial neuritis (lesions of the papillomacular bundle), perineuritis and total neuritis.
With ophthalmoscopy at the onset of retrobulbar neuritis, the fundus may be normal. The optic disc is normal or, more often, hyperemic, its borders are indistinct. For retrobulbar neuritis, a decrease in visual acuity is characteristic, the definition of a central absolute scotoma in the field of vision for white and colored objects. At the beginning of the disease, the scotoma is large, later, if the visual acuity increases, the scotoma decreases, becomes relative and disappears with a favorable course of the disease. In some cases, the central scotoma becomes paracentral annular. The contrast sensitivity of the organ of vision decreases. The disease can lead to descending atrophy of the optic nerve head. The blanching of the optic nerve head can be different in the degree of distribution and intensity, the blanching of its temporal half is more often noted (due to the defeat of the papillomacular bundle). Less often, with a diffuse atrophic process, a uniform blanching of the entire disc is observed.
Treatment of retrobulbar neuritis depends on the etiology of the inflammatory process and is carried out according to the same principles as the treatment of patients with papillitis. The prognosis for retrobulbar neuritis is always serious and depends mainly on the etiology of the process and the form of the disease. With an acute process and timely rational treatment, the prognosis is often favorable. In chronic course, the prognosis is worse.
VASCULAR DISEASES OF THE OPTIC NERVE
Acute obstruction of the arteries feeding the optic nerve
Vascular pathology of the optic nerve is one of the most difficult problems in ophthalmology due to the extreme complexity of the structural and functional structure and arteriovenous circulation in various parts of the optic nerve. There are two main forms of vascular lesions of the optic nerve: arterial and venous. Each of these forms can proceed as an acute or chronic disease. Vascular diseases of the optic nerve refer to polietiologic disease processes.
The etiology of ischemia is thrombosis, embolism, stenosis and obliteration of blood vessels, prolonged spasms, impaired rheological properties of blood, diabetes mellitus. These are mainly elderly patients with general vascular diseases, severe atherosclerosis and hypertension.
Pathogenesis: The pathogenesis is based on violations (decrease) of blood flow in the vessels feeding the optic nerve. Ischemic neuropathy of the optic nerve is a lack of blood supply to the nerve tissue, a decrease in the number of functioning capillaries, their closure, a violation of tissue metabolism, an increase in hypoxia and the appearance of under-oxidized metabolic products (lactic acid, pyruvate, etc.).
A. Anterior ischemic neuropathy of the optic nerve
In the pathogenesis of anterior ischemic neuropathy of the optic nerve, the main factors are stenosis or occlusion of the arterial vessels supplying the optic nerve, and the resulting imbalance between the perfusion pressure in these vessels and the level of intraocular pressure. The main role is played by circulatory disorders in the posterior short ciliary arteries. There is a rapid (within 1-2 days) decrease in vision up to light perception. Central scotomas appear in the field of view, more often the lower half of the field of view falls out, less often sector-shaped losses are observed in the field of view. These changes occur more often in elderly patients on the basis of spasm or are organic in nature (atherosclerosis, hypertension, endarteritis, etc.).
At the very beginning of the disease, the fundus of the eye may be unchanged, then on the 2nd day ischemic edema of the optic nerve head and cotton-like edema of the retina around it appear. The arteries are narrowed, in places in the edematous retina (in the area of the disc or around it) are not defined. The macular area is not changed. Subsequently, the edema of the optic nerve head decreases, the disc becomes paler. By the end of the 2-3rd week of the disease, atrophy of the optic nerve of varying severity occurs. Due to the rapid deterioration in visual acuity, early treatment is necessary.
The diagnosis of anterior ischemic neuropathy is facilitated by Doppler identification (about 40% of cases) of stenosing lesions of the carotid arteries using laser Doppler ultrasonography, it is possible to determine capillary circulatory disorders in the optic nerve head.
Treatment: Urgent hospitalization. Immediately after the diagnosis is made, vasodilators, thrombolytic drugs and anticoagulants are prescribed. Give a nitroglycerin tablet (0.0005 g). Intravenously, 5-10 ml of a 2.4% solution of aminophylline is injected together with 10-20 ml of a 40% glucose solution daily, 2-4 ml of a 2% solution of no-shpa (slowly!), 15% solution of xanthinol nicotinate (Complamin) - 2 each ml 1-2 times a day (injected very slowly, the patient is in the supine position). Shown retrobulbar injection of 0.3-0.5 ml of 0.4% dexazone solution, 700-1000 U of heparin, 0.3-0.5 ml of 1% emoxypine solution.
During the period of development of edema of the optic nerve head, patients must be prescribed thiazide 0.05 g once a day before meals for 5-7 days, followed by a break of 3-4 days, furosemide 0.04 g once a day, brinaldix 0 , 02 g 1 time per day, 50% glycerin solution at the rate of 1-1.5 g / kg, ethacrynic acid 0.05 g each. Treatment is continued for 1.5-2 months. Patients should be consulted by a therapist and neuropathologist
B. Posterior ischemic optic nerve neuropathy
Posterior ischemic neuropathy of the optic nerve occurs mainly in the elderly and occurs against the background of general (systemic) diseases such as hypertension, atherosclerosis, diabetes mellitus, collagenosis, etc. As with anterior ischemic neuropathy, the main factor in the development of this disease is narrowing , stenosis, spasm or occlusion of arterial vessels supplying the posterior optic nerve. Doppler ultrasound in such patients often reveals stenosis of the internal and common carotid arteries.
The disease begins acutely. Patients complain of a sharp decrease in visual acuity. In the field of vision, various defects are determined: sectoral loss mainly in the lower nasal region, concentric narrowing of the fields. Ophthalmoscopic examination during this period does not reveal any changes in the optic nerve head.
Electrophysiological studies help diagnose the disease, revealing a decrease in electrical sensitivity and lability of the optic nerve and an increase in the transit time of a nerve impulse along the visual pathway.
Doppler studies of the carotid, ocular and supra-block arteries often reveal changes in the parameters of blood flow in these vessels. After 4-6 weeks, the optic nerve head starts to turn pale in the sector that corresponds to the dropped out area in the field of view. Then a simple descending atrophy of the optic nerve gradually develops. Excavation of the optic nerve head with this pathology is not detected.
This pathology presents great difficulties for early diagnosis. It is much less common than anterior ischemic neuropathy. At the same time, venous circulation in the optic nerve is disturbed to one degree or another. This process is in the overwhelming majority of cases one-sided.
Treatment is similar to that for anterior ischemic neuropathy. Despite the treatment, visual acuity often remains low, and persistent defects - absolute scotomas - are determined in the field of vision in patients.
Article from the book:.
The nerve, called the abducens, plays a small regulatory role in the mobility of the eyes, taking it outward. These nerve fibers enter the oculomotor apparatus of the organ and, together with other nerves, control complex eye movements.
The eye can turn from side to side horizontally, make circular movements, move in a vertical direction.
Ophthalmoplegia is a disease that occurs as a result of damage to the optic nerves and is accompanied by paralysis of the ocular muscles. This is a neurological pathology that limits the motor function of the eyeballs.
It can be due to many reasons: infectious diseases. head or eye injuries and poisoning.
Causes
ZN plays a very important role in the human body. It is a special transmitter that transports signals from the retina to the brain. The optic nerve is made up of millions of fibers, with a total length of 50 mm. It is a very vulnerable but important structure that can be easily damaged.
As noted, the most common cause of optic nerve damage is head injury. However, this is far from the only possible factor in disrupting signal transport. This may be the problem of intrauterine development, when the fetus, under the influence of certain processes, has an abnormal formation of the organs of vision.
In addition, inflammation, which can concentrate in the eye or brain, can damage the optic nerve. Both congestion and atrophy have a negative effect on MN. The latter can have various origins.
Most often it becomes a complication after traumatic brain injury. But sometimes atrophic processes in the eyes arise due to poisoning and severe intoxication of the body.
Ophthalmoplegia can occur with congenital or acquired lesions of the nervous system in the area of nerve roots or trunks, in the area of the nuclei of the cranial nerves. For example, congenital ophthalmoplegia occurs as a result of aplasia of the nuclei of the oculomotor nerves, and in some cases can be combined with changes in the eye muscles and aplasia of the nerve trunks. This pathology is often combined with malformations of the eyeball, it can be observed in several members of the same family.
Ophthalmoplegia can also be a symptom of a rare condition such as ophthalmoplegic migraine. It is manifested by attacks of severe headaches, accompanied by unilateral ophthalmoplegia (complete or partial). Headaches can last for a long time, while the function of the oculomotor nerves is gradually restored.
In addition, ophthalmoplegia can be a symptom of a rare ophthalmoplegic migraine. After the end of the attack, the eyes slowly return to normal.
Oculomotor palsy can result from a number of different conditions. Oculomotor nerve palsy with a non-traumatic middle pupil is often referred to as the "medical third" because of a similar effect on the pupil known as the "surgical third".
The main causes of damage to the oculomotor nerve are:
- trauma;
- neuroinfectious diseases;
- brain tumors of various etiologies;
- cerebral vascular pneumism;
- diabetes;
- stroke.
However, most often the causes of partial or complete damage to the nuclei or fibers of the oculomotor nerve remain only a guess. It is impossible to establish them exactly. The human body is a very complex system, and it is not fully understood, but it is absolutely certain that the disruption of the work of one of its components along the chain transfers this to other organs, nerves and muscles.
For example, neuropathy of the oculomotor nerve in an isolated form is very rare and is most often a concomitant manifestation of chronic or congenital diseases, as well as the result of craniocerebral trauma and tumors. With proper and timely treatment, this disease can go away without complications and consequences.
If neuropathy of the oculomotor nerve is suspected, it is imperative to take a whole course of tests, including blood for the presence of neuroinfection in the body. Only after receiving the results and confirming the diagnosis can a course of treatment be prescribed and it is imperative to conduct repeated tests.
- Diseases and damage to the nerve itself (inflammation, ischemia, compression and edema).
- Volumetric processes in the brain tissue (tumor formations, hematomas, aneurysms, tuberculomas, cysts, abscesses).
- Diseases of the central nervous system (strokes, multiple sclerosis, inflammation of the meninges and brain tissue).
- Head trauma (damage or compression of the optic nerve by bone fragments, hematomas).
- Poisoning and intoxication (lead, chlorophos, carbon disulfide, alcohol, taking certain medications).
- Pathologies of internal organs leading to vascular disorders ( arterial hypertension, diabetes mellitus, profuse bleeding, anemia, vasculitis, systemic lupus erythematosus, exhaustion, starvation, etc.).
- Diseases of the eye (pathology of the retina, its detachment, dystrophy, damage to the vessels of the retina, complications of uveitis, glaucoma, eye injuries).
- Hereditary atrophy of the optic nerves.
Under the influence of the above factors, the destruction of nerve fibers and their replacement by connective tissue develops, the desolation of the vessels supplying the nerve develops. There are many causes of the disease, they can be combined with each other. It is not always possible to identify them.
Clinical picture
In severe forms of the disease, there may be a lack of activity and mobility of the eyeball, a deterioration in the reaction of the pupil to light and its immobility. If ophthalmoplegia develops against the background of other diseases, the clinical picture also includes additional symptoms.
The manifestations of the disease depend on the severity of the pathological process, the type of atrophy, and its localization. Progressive atrophy can lead to complete loss of vision.
The main symptoms are:
- Decreased visual acuity.
Visual acuity decreases significantly when the papillomacular bundle is damaged. It practically does not change if only the peripheral part of the nerve is affected. If the lesion is combined, then the changes in vision are moderate.
- Change in visual fields.
Loss of the central visual field appears with atrophy of the papillomacular bundle. Damage to the optic chiasm and tracts contributes to bilateral blindness in half of the visual field. Narrowing of the peripheral boundaries of the visual field appears when peripheral nerve fibers are involved.
- Violation of color perception (the perception of green and red is more affected).
With an atrophic process, changes in the fundus may not correspond to the clinical picture. For example, with descending atrophy, the fundus of the eye remains unchanged for a long time with a pronounced decrease in vision. So, in multiple sclerosis, the optic disc is pale even with a slight deviation from the norm of visual acuity. In addition, if the initial visual acuity was more than one, then its decrease to this level against the background of disc pathology may already indicate atrophic changes.
Types of atrophic lesions of the optic nerve
In this case, the eye is displaced into the zone of action of a healthy or less affected muscle. The patient has difficulty moving the eyes in the direction of the paralyzed muscles, which leads to double vision.
With complete external ophthalmoplegia, the eyeball is constantly in a static position, which leads to the development of ptosis. Partial internal ophthalmoplegia occurs due to the expansion of the pupil that does not respond to light.
When the first signs of the disease appear, it is recommended to immediately consult an ophthalmologist.
Ophthalmoplegia can be unilateral or bilateral. External ophthalmoplegia occurs with paralysis of the muscles that are outside the eyeball, and with paralysis of the intraocular muscles, internal ophthalmoplegia occurs. With various degrees of muscle weakening with paralysis, partial internal or external ophthalmoplegia develops. If both the external and internal muscles of the eye are paralyzed at the same time, then complete ophthalmoplegia occurs. Complete external and complete internal ophthalmoplegia can also occur.
With external partial ophthalmoplegia, the eyeball will lean towards the healthy or less paralyzed muscle, and its movements towards the action of the paralyzed muscles will be absent or significantly limited. In this case, doubling of objects will appear. The eyeball with external complete ophthalmoplegia will acquire immobility and ptosis will develop. Internal partial ophthalmoplegia is characterized only by dilatation of the pupil in the absence of a response to light, a decrease in convergence and accommodation.
According to the degree of damage to the optic nerves, partial and complete ophthalmoplegia are distinguished. Partial can be external, in which the work of the oculomotor muscle of the eyelid and the internal muscle is disrupted, if only the nerve columns are paralyzed.
With the full form of the disorder, there is an immobility of the eyeball and a drooping of the upper eyelid, the inability of the pupil to respond to light.
This pathology can be primary (occurs with an unchanged optic nerve head) and secondary (develops against the background of inflammation or edema of the disc), glaucomatous (appears with glaucoma). And also ascending (the process begins with the disc) and descending (at the beginning, the peripheral neuron is affected). Depending on the severity of atrophy and the degree of color loss, an initial, partial, complete atrophy is distinguished.
Provoking pathologies
The key reasons for the development of ophthalmoplegia are pathologies of nerve tissues. The disease can be congenital or acquired.
The congenital form in most cases meets with other pathologies in the structure of the eye, is included in the complex of symptoms of various genetic abnormalities. There is a hereditary condition for the disease.
The disease can develop against the background of other infectious diseases - tuberculosis or syphilis, as well as tetanus, botulism and diphtheria.
Ophthalmoplegia can be an accompanying symptom of ophthalmoplegic migraine, a rare condition that causes severe headache attacks.
The pathology of the bones of the skull manifests itself in the form of stagnation of the optic disc, as well as nystagmus and divergent strabismus. The eyeglass symptom indicates a fracture of the base of the skull. It is manifested by the presence of hemorrhages under the conjunctiva and skin of the eyelids of both eyes. Perhaps the appearance of a symptom of the superior orbital fissure, which manifests itself in the form of total ophthalmoplegia, ptosis and exophthalmos, impaired sensitivity along the trigeminal nerve. Let us consider in more detail the eye symptoms in pathologies of the central nervous system.
Eye symptoms with cerebrospinal meningitis:
- retrobulbar optic neuritis;
- violation of the reaction of the pupils, more often paralytic immobility of one or both pupils;
- abducens nerve paralysis;
- descending atrophy of the optic nerve.
What eye symptoms are found in the development of meningitis?
Drug treatment
In order to reduce pain, relieve spasm and strengthen muscles, acupuncture, electrophoresis and phonophoresis with drugs are prescribed.
Damage to brain tissue in syphilis and brain abscess, in addition to general specific symptoms, can be detected by examining the fundus. With an abscess of the brain, the following eye symptoms are characteristic:
- bilateral development of stagnation of the optic nerve head;
- the presence of hemianopsia;
- paralysis of the oculomotor and abducens nerves;
- violation of the reaction of the pupils in the form of mydriasis.
A cerebellar abscess is manifested by nystagmus. A brain abscess most often develops against the background of carious lesions of the teeth, that is, it has an odontogenic origin.
Syphilis of the brain has its own eye symptoms:
- paralysis of the oculomotor nerve;
- internal unilateral ophthalmoplegia (mydriasis and accommodation paralysis);
- the presence of stagnant discs and optic neuritis;
- homonymous hemianopsia.
Late neurosyphilis is manifested by Argyll Robertson's symptom, which looks like the disappearance of the pupil response to light, along with the preservation of convergence and accommodation. There is a reflex immobility of the pupils and anisocoria. With syphilis, the field of vision is narrowed with further loss of vision and paralysis of the oculomotor nerve.
Multiple sclerosis is manifested by certain eye symptoms:
- narrowing of the visual fields;
- the emergence of central cattle;
- blanching of the temporal halves of the optic discs;
- horizontal nystagmus;
- remitting decrease in vision.
An epileptic seizure is accompanied by constriction of the pupils, which dilate at the height of the clonic seizures. Differential - diagnostic sign is the lack of reaction of the pupils to light. An epileptic seizure is always accompanied by a deviation of the eyeballs to the side or upward.
The development of a brain tumor is manifested by the following eye symptoms:
- hemianopsia;
- with tumors of the skull and cerebellum, stagnant discs of the optic nerves are observed;
- paralysis of the oculomotor muscles;
- optic neuritis or atrophy;
- an attack of neuralgia and headaches with painful points, which are localized in the places where the branches of the trigeminal nerve exit;
- development of neuroparalytic keratitis.
Thus, at an appointment with an ophthalmologist and neuropathologist, it is possible to make a preliminary diagnosis of a lesion of the nervous system, which can improve the prognosis of the treatment of this pathology.
It should be noted that an isolated violation of this nerve is very rare. Here are the main symptoms:
- immobility of the muscles of the upper eyelid and, as a result, its partial or complete omission;
- lack of resistance for the superior oblique and inferior rectus muscles, as a result of which divergent strabismus can be diagnosed;
- immobility of the internal rectus muscle and, as a result, the occurrence of the phenomenon double vision (diplopia);
- lack of reaction of the pupil to light;
- violation of the innervation of the internal muscle and, as a result, the inability of the eye to adapt to objects located at different distances from it;
- lack of contraction of the rectus muscles of both eyes, which makes it impossible to turn the eyeballs inward;
- bulging of the eyes due to loss of tone of the external muscles, this confirms that the oculomotor nerve has been damaged.
Most often, all of the listed symptoms are combined with concomitant manifestations that cause disturbances in the functioning of friendly nerve fibers located nearby muscle groups and organs.
Diagnostics
Despite the presence of pronounced external signs, the following instrumental studies are prescribed;
Therapy consists in eliminating the causes of the disease, relieving pain and restoring, if possible, nervous and muscular activity.
Physiotherapy methods
Diagnosis of the type of disease and the causes that cause it is necessary for choosing a treatment method.
The disease is diagnosed by initial examination. It has pronounced external manifestations. To establish the nature of the disease and the causes, it is necessary to consult a neurologist and an ophthalmologist.
If neoplasms are detected, additional consultation with an oncologist may be needed.
After receiving all the necessary data about the disease and determining the causes, treatment is prescribed. It is aimed at eliminating the factors that resulted in ophthalmoplegia, pain relief and maximum restoration of nervous and muscular activity.
Timely formulation of an accurate diagnosis is half the success and the secret of a speedy recovery. The ophthalmologist determines the occurrence of defects by checking:
- position of the eyeball, possible deviation downward or outward;
- in what position the upper eyelid: the presence of ptosis;
- pupil reaction to light;
- the ability to focus, for this the doctor brings his finger to the patient's nose to see the reaction.
Based on the symptoms, the optometrist determines the approximate location where the failure occurred. Further, magnetic resonance imaging is prescribed for an X-ray examination of blood vessels to visualize the lesion and establish the nature of their origin.
Oculomotor palsy is not the only shutdown that causes muscle paresis. Research allows other reasons for rejection to be ruled out.
The newest research method is superposition electromagnetic scanning. With the help of it, the time to determine the causes of the disease is significantly reduced.
If there is a suspicion of a violation of the function of the oculomotor nerve, it is possible to confirm or deny this, as well as to identify the real cause of the deviation, only through high-quality professional diagnostics. Most often, this is done by an ophthalmologist, and only in some cases, if the diagnosis is in doubt, an additional consultation with a neurologist is prescribed.
Diagnostics and examination of the organs of vision are carried out using modern computer equipment, as well as by conducting a variety of specialized tests. As a result, after their complex implementation, the patient can be diagnosed.
Also, in addition to standard procedures carried out to check the condition of the fundus, determine the quality of vision, eye mobility, and identify the pupil's reactions to light, MRI and angiography are performed. If the etiology is not fully identified, and even if the lesion of the oculomotor nerve is confirmed, constant observation of the patient is mandatory, as well as repeated examinations.
The diagnosis is based on the patient's complaints, a detailed study of the disease, taking into account the past and existing diseases, examination and examination by an ophthalmologist. The specialist will determine the acuity and visual fields, carry out color testing and ophthalmoscopy, measure intraocular pressure. Ophthalmoscopy occupies a special place among all studies, it is with its help that the doctor can assess the condition of the optic nerve head and blood vessels in the fundus.
Features of the ophthalmoscopic picture:
- In primary atrophy, the disc has clear contours, is white with a bluish or gray tint, and the number of arteries feeding it decreases. Blanching of the disc depends on the severity of the process (at the beginning of the disease, the pallor is insignificant, at advanced stages it is completely white).
- Secondary pathology is characterized by: gray or dirty gray optic nerve disc with blurred contours, vascular funnel, which is filled with connective tissue.
- Glaucomatous atrophy presents with a pale disc with an excavation (depression) that can cover the entire disc.
If necessary, an additional examination may be prescribed: blood and urine tests, biochemistry and blood sugar, computed tomography, MRI of the brain, angiography of retinal vessels, electrophysiological examination. Differential diagnosis is carried out with cataracts, amblyopia.
Diagnostics and treatment
Recovery from paralysis occurs over a long period of time throughout the year. A known method of treatment consists in the use of physiotherapy - exposure to pulses of a low-frequency electromagnetic field, stimulation with electric current.
The method of treatment is analgesic, anti-inflammatory, sedative. The disadvantage is that recovery is very slow, and in some cases it does not come at all.
They also use the occipital method of administering a drug (neuromidin) to increase muscle contractility and affect connective muscle defects.
The method of using electrophoresis with a solution of 15% neuromidin has proven itself well. The duration of the sessions is 15 minutes daily for 15 days. After completing the procedure, it is recommended to lie down with your eyes closed for 10 minutes.
If improvement and restoration of the functioning of the abducent nerve is not observed after the treatment, and the lesion does not go away on its own, surgical intervention is used. The essence of the method is as follows: an injection of ultracain is made under the conjunctiva, an incision is made in half a circle.
The upper external and lower straight nerves are split into two bundles along and the lower ones are sutured with the upper fibers. This allows the eyeball to be rotated by more than 15–20 ° within a day after the operation, in some patients up to 25 °, binocular vision was restored in every fourth operated patient.
To alleviate the condition in violation of binocular vision, Fresnel prisms are used, which are attached to the glasses. The prisms have different angles and are individually selected. It is also possible to close one eye.
Most nerve diseases are associated with a violation of the central nervous system, so treatment is prescribed accordingly. After previous infections and successful treatment, the nerve abnormalities recover; in rare cases, when an inoperable tumor, serious trauma to the skull and the nerve itself, recovery may not occur.
In order to eliminate the problem with damage to the optic nerve, you need to carry out a comprehensive diagnosis. Based on the data obtained and after identifying the main cause of the pathology, it will be possible to prescribe the correct treatment procedures.
It should be borne in mind that nerve damage is not an independent disease. This problem always has an additional cause that must be eliminated. Otherwise, you should not count on an improvement in visual function.
Experts strongly recommend that at the first deterioration of vision, immediately undergo diagnostics and start treatment. This is the only opportunity not to miss the moment when you can solve the problem with a medication. Most often, medical therapy is aimed at relieving puffiness and reducing intracranial pressure.
Basically, to stimulate blood circulation in the brain and reduce edema, No-shpu, Papaverine, Eufilin or Halidol are prescribed. In addition, anticoagulants such as Tiklid and Heparin can be used. Vitamin complexes and biogenic stimulants have a positive effect.
However, if the lesion of the MN is caused by a traumatic brain injury, the patient may need an operation. It is impossible to get rid of a pinched nerve without surgery. Also, the problem cannot be solved without surgery if the damage to the MN is caused by pressure on the organs of vision by a tumor.
Any medications for damage to the optic nerve should be prescribed by a doctor only after a thorough examination of the patient. Self-medication for such a complex problem as visual impairment due to injury to the MN is categorically unacceptable. You need to be very careful with folk remedies. Taking them may not give the desired result, and the time that could have been spent on a full-fledged treatment will be lost.
Treatment for ophthalmoplegia consists of eliminating the causes of the disease, relieving pain and restoring, as much as possible, muscle and nervous activity.
- anti-inflammatory drugs;
- drugs that prevent dehydration of the body in case of poisoning and intoxication;
- vitamins B6, B12, C, as a general tonic;
- vasodilators for vascular diseases of the brain;
- nootropic to improve nervous activity;
- anticholinesterase drugs that eliminate muscle weakness;
- corticosteroid hormones to normalize metabolism and restore muscle function.
The sooner a disease is discovered, the more likely it is to get rid of it successfully. Do not ignore doctor visits and try to heal yourself.
After establishing an accurate diagnosis - paresis of the oculomotor nerve, the patient remains under the supervision of a specialist. In special cases, a re-examination is prescribed to exclude the possibility of error. In the overwhelming majority, treatment of paresis of the optic nerve gives a positive trend.
At the first suspicions, sometimes even before the final diagnosis is made, the doctor recommends performing special exercises to strengthen the muscles. The doctor has the right to prescribe taking vitamins and medicines, wearing bandages, glasses, viewing stereo pictures.
Such things have a healing effect, stimulating the affected eye to work actively, improving blood circulation and increasing the tone of the eye muscles. Within six months, there is a complete recovery of mobility. If there is no improvement, then an operation is performed: ptosis is surgically eliminated. But there is a high probability of exposure of the cornea of the eye.
Involving traditional methods in treatment will not be superfluous, the main thing is to consult a doctor for contraindications and possible individual intolerance. In the reviews, they write a lot about herbal decoctions: garden marjoram, chamomile, wild rose, black elderberry, tannic sumac, evading peony.
Alternative medicine should not be given the main role in the treatment of neuritis. It is here only as an auxiliary element, more suitable for the prevention of disease.
This is very important, because the timely detection of the further progression of the disease, as well as constant monitoring of the treatment prescribed by the doctor, are of great importance for the entire state of the eye and all further human life. So, for example, neuritis of the oculomotor nerve in most cases has a positive trend if the patient observes all the prescriptions, however, treatment is carried out only with the constant supervision of specialists.
Science does not stand still, and recently one of the innovative diagnostic methods is superposition electromagnetic scanning of the oculomotor muscles to assess their functional activity. Thanks to this method, the time allotted to identify the cause of the violation is significantly reduced, and it becomes possible to begin treatment much faster and achieve positive results.
As soon as there is a suspicion of a possible dysfunction of the oculomotor nerve, the patient is immediately advised to do exercises to strengthen the muscle responsible for the movement of the organs of vision. Of course, trying to strengthen it as much as possible is not bad at all, and not only when problems have arisen, but even for prevention, but this is suitable only at the very beginning of the occurrence of a violation. If a rather large part is already affected, these exercises will not help cure, although they are still an integral part of the treatment.
The next most common recommendation is to take appropriate vitamins and medications, which also work to strengthen the eye muscle and restore its function. It can be special vitamins, eye drops, glasses, bandages that make the sore eye work more actively.
Special computer programs are very popular today. These are mainly so-called stereo pictures.
It has been proven that when viewing such pictures, the eye muscles are trained, and, accordingly, blood circulation in them improves. At this time, the nerves responsible for the normal functioning of the eye are in an increased tense state, and all the body's reserves are aimed at controlling them, because most of the other organs at the time of viewing are in a relaxed state and do not require such attention.
Stereo pictures really have a very positive result on vision, but they can be used only after consulting a doctor. Indeed, in some cases they are just a panacea, while in others they are capable of causing irreparable harm.
If, after several complementary diagnostics, it is confirmed that the oculomotor nerve is affected, treatment should be started without delay. One of those that have proven themselves on the positive side and have been used in practical ophthalmology for several years now is treatment with electropharesis of the affected areas with 1.5% neuromidin.
It is carried out by imposing three round electrodes of different area between each other, two smaller of which are placed on the skin of the orbital region and upper eyelids with closed eyes. They are connected with a bifurcated wire with an electrode of a larger area, which is located in the cervico-occipital region of the patient's head.
The duration of this procedure with a course of treatment up to 15 sessions carried out daily is 15-20 minutes. The method allows you to locally and purposefully affect the defective neuromuscular synapses of the eyeball, as well as the nuclear structures of the oculomotor nerves.
Therapy of optic nerve atrophy directly depends on the cause that caused it. It should begin as early as possible, when it is still possible to stop the process, since the changes during atrophy are irreversible. If the cause can be eliminated, then the chances of maintaining vision are increased. When a nerve is compressed, treatment is primarily surgical.
Physiotherapy methods
- Open eye ultrasound;
- ultraphonophoresis on the eye area with proteolytic enzymes;
- magnetotherapy;
- electrical stimulation of the optic nerves;
- drug endonasal electrophoresis with vasodilators (nicotinic acid, drotaverine);
- medicinal electrophoresis on the eye through a bath with potassium iodide, lidase, chymotrypsin;
- laser therapy.
Exposure to physical factors increases the effectiveness of the therapy, stimulates the optic nerves, increases the likelihood of restoration of visual function, provided that treatment is started on time.
Preventive measures
Ophthalmoplegia can develop against the background of other neurological diseases. A full preventive examination must be carried out 2 times a year in order to identify them in time and begin treatment.
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