Objective eye symptoms. Cantoplasty - changing the shape and width of the palpebral fissure See what "Superior orbital fissure syndrome" is in other dictionaries

Canthoplasty- an operation by which the shape and width of the palpebral fissure is changed. Technically, the intervention is performed by raising the corners of the eyes (Greek canthos - angle), it can have aesthetic and medical indications.

Some features of the structure of the skin of the eye zone

The skin surrounding the eye is somewhat different from that of other areas of the face. First of all, it is very thin and has increased sensitivity. In addition, large facial muscles and massive ligaments, which are a natural supporting frame in other areas, are not woven into it. These anatomical nuances explain the fact that the skin on the periphery of the eyes is the first to undergo age-related changes. The reason for this is the complex impact of external and internal factors, including:

• ultraviolet irradiation, causing the destruction of the collagen fibers of the dermis;
• weathering;
• intoxication (alcohol, toxic metabolic products in diseases of the liver and kidneys, industrial hazards);
• gravitational ptosis (displacement of tissues downwards under the influence of gravity);
• chronic local pathologies of the skin and mucous membranes (conjunctivitis and blepharitis);
• hereditarily conditioned reduced elasticity of the connective tissue.

With age, there is a general “sliding” of the skin of the face downwards, which in the eyelid area manifests itself in the form of drooping of the corners of the eyes, forming a “sad” and “tired” look. Sometimes such unpleasant transformations occur at a relatively young age. They can be corrected with canthoplasty, which is performed as an independent operation or in combination with blepharoplasty.

Quite often, a surgeon is contacted to correct the shape of the palpebral fissure, which does not suit the patient. There are three main types of eye section, which are determined by the position of the lines (axes) connecting their outer and inner corners:

• classic type (the corners of the eyes are at the same level when the axis passes along the lower edge of the pupil) - usually found in young people;
• Mongoloid (Eastern) type - the inner corner is lower than the outer one, the axis crosses the center of the pupil;
• anti-Mongoloid (European) type - the location of the outer corner is lower than the inner, the passage of the axis is below the pupil.

Among Eastern women, a very popular operation is to "correct" the Mongoloid incision to give the eyes a larger size and expressiveness, and the face - "Caucasian". On the contrary, among the inhabitants of the West there is a fashion for oriental color by forming a slight slanting or almond-shaped eyes. Some people want to lift naturally overly drooping outer corners to eliminate a “sad look” or overly round (“owl”) cut. There are also medical reasons for performing canthoplasty - congenital and acquired diseases of the eyelids and the eyeball.

Indications for surgery

• Age-related shift of the corners of the eyes down.
• The desire of the patient to change the shape of the palpebral fissure.
• Variants of myopia (nearsightedness), accompanied by exophthalmos (bulging eyes).
• Long-term inflammatory processes in the orbit (chronic and frequent acute conjunctivitis) to reduce the pressure of the eyelids on the eyeball.
• Partial fusion of the eyelids (congenital pathology or the consequences of injuries, burns or diseases).
• Narrowing and deformation of the palpebral fissure after suffering an adhesive process (blepharophimosis).

Contraindications

The most common contraindications to the operation:

• Decompensated form of diabetes mellitus and other severe endocrine problems.
• Serious pathologies of internal organs (liver, kidneys, heart, lungs).
• Blood coagulation disorders.
• oncological processes.
• Pregnancy and lactation.
• Glaucoma (increased pressure inside the eyeball).
• Dry eye syndrome.
• High myopia.
• Local infectious processes.

Preoperative preparation

It is mandatory to consult an ophthalmologist to identify contraindications. In their absence, the plastic surgeon, together with the patient, comes to a common vision of the desired result, the area of ​​future intervention is marked. A standardized examination is prescribed:

• Clinical blood tests.
• Biochemical research.
• Fluorography.
• Tests for infections (RW, HIV, hepatitis B and C).
• Consultation of a therapist (if indicated).
• Examination by an anesthesiologist (if general anesthesia is planned).

Operation technique

There are several types of operation. Usually lateral canthoplasty is performed in classic or modified form. The location of the outer corner of the eye is determined by the level of fixation of the canthal ligament to the periosteum of the orbit. The lateral (external) ligament, which is woven into the circular muscle of the eye, is crossed during the intervention and sutured in a higher position. To access it, an incision about 10 mm long is made, which passes through a natural skin fold. After moving and fixing the ligament, the wound is closed with a cosmetic suture. The duration of the operation can be from 1 to 2 hours, anesthesia is general or local. Others can be performed in parallel - for example, a lower eyelid lift (canthopexy), etc. A sterile dressing is applied to the orbital area. The effect obtained is persistent (about 10 years or more).

Recovery period

Usually, patients are concerned about irritation and dryness of the conjunctiva, swelling of the orbital area, which disappear on their own within a few days. To reduce discomfort, eye drops are prescribed, eye strain is limited (it is necessary to minimize watching TV, reading and working at a computer).

Possible Complications

The most common complications of canthoplasty are:

• Asymmetry of the cuts of the eyes.
• Overcorrection.
• Infection of the operating area.
• The appearance of a visible scar.

These problems may require additional intervention.

Canthoplasty- a surgical change in the shape of the eyes for aesthetic or medical reasons.

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Syndrome of the superior orbital fissure is a pathology that is characterized by complete paralysis of the internal and external muscles of the eye and loss of sensitivity of the upper eyelid, cornea, and part of the forehead. Symptoms may be caused by damage to the cranial nerves. Painful conditions arise as complications of tumors, meningitis and arachnoiditis. The syndrome is typical for elderly and middle-aged people; in a child, such a pathology is diagnosed infrequently.

Anatomy of the apex of the orbit

The orbit, or eye socket, is a paired bony recess in the skull, which is filled with the eyeball and its appendages. Contains structures such as ligaments, blood vessels, muscles, nerves, lacrimal glands. The apex of the cavity is its deep zone, bounded by the sphenoid bone, which occupies about a fifth of the entire orbit. The boundaries of the deep orbit are delineated by the wing of the sphenoid bone, as well as by the orbital process of the palatine plate, the infraorbital nerve, and the inferior orbital fissure.

Orbit structure

The orbit is represented by three zones, each of which is limited by nearby structures.

1. outdoor. It is formed by the zygomatic bone from below, the upper jaw (its frontal process), the frontal, lacrimal, nasal and ethmoid bones.
2. Inner zone. It originates from the anterior end of the infraorbital fissure.
3. Deep zone or apex of the orbit. It is limited to the so-called main bone.

Holes and slots

The apex of the orbit is associated with the following structures:

• wedge-frontal suture;
• external geniculate body;
• wedge-zygomatic suture;
• small and large wings of the main bone;
• wedge-shaped lattice seam;
• main bone;
• palatine bone;
• frontal process of the upper jaw.

The deep orbit has the following openings:

• visual aperture;
• lattice holes;
• round hole;
• infraorbital groove.

Deep orbit slots:

• lower orbital;
• superior orbital fissure.

Large nerves and blood vessels pass through the holes and through the cracks into the cavity of the orbit.

Causes of the syndrome

The syndrome of the upper orbital fissure can be caused by the following factors:

1. Mechanical damage, eye injury.
2. Tumors located in the brain.
3. Inflammation of the arachnoid membrane of the brain.
4. Meningitis.
5. Entry into the eye area of ​​a foreign body.

The occurrence of a symptom complex of the syndrome of the superior palpebral fissure is associated with damage to the nerves: oculomotor, abducent, block, ophthalmic.

Risk factors for the pathogenesis of the disease include living in environmentally polluted regions, eating foods containing carcinogens, and prolonged exposure to ultraviolet rays on the eyes.

Main features

The main manifestations and symptoms of pathology are:

• The drooping of the upper eyelid with the inability to lift it, resulting in a narrowing of the palpebral fissure of one eye. The cause of the anomaly is nerve damage.
• Paralysis of the internal and external eye muscles (ophthalmoplegia). The motor activity of the eyeball is lost.
• Loss of sensation in the skin of the eyelid.
• Inflammatory processes in the cornea.
• Pupil dilation.
• Anterior displacement of the eyeball (so-called bulging eyes).
• Retinal vein dilatation.

Some of the symptoms cause significant discomfort and are fixed by the patient, others are detected during examination by an ophthalmologist and further examination. The disease is characterized by a unilateral lesion with preservation of the functions of the second, healthy, eye.

The combination of several signs or some of them indicate a pathological syndrome, while the lower orbital fissure remains unchanged.

In the photo, patients show asymmetry of the eyes, ptosis of the affected organ.

Diagnostics

Diagnosis of the disease is complicated by the fact that other ophthalmic problems have similar symptoms. The syndrome manifests itself in the same way as the following conditions:

• myasthenic syndromes;
• aneurysm of the carotid artery;
• multiple sclerosis;
• periostitis;
• temporal arteritis;
• osteomyelitis;
• parasellar tumors;
• neoplasms in the pituitary gland;
• tumor formations in the orbit.

To differentiate the pathology from other diseases with similar manifestations, it is necessary to conduct diagnostic examinations in terms of ophthalmology and neurology:

• Collection of anamnesis with clarification of the nature of painful sensations and determination of the pathogenesis of the disease.
• Determination of visual fields and its acuity.
• Diaphanoscopy of the eye socket (illumination method).
• Ophthalmoscopy.
• Radioisotope scanning (to identify tumor formations).
• Ultrasound procedure.
• Biopsy (if a tumor is suspected).
• Computed tomography of the parts of the brain, disorders in which can provoke the symptom complex of the syndrome.
• Magnetic resonance imaging.
• Angiography (X-ray examination using a contrast agent).

After the discovery of the first manifestations of the syndrome, an urgent consultation of specialists is required: an ophthalmologist and a neurologist. Since the pathology is caused by damage to structures that are located near the orbital fissure, therapy involves acting on them in order to eliminate the root cause. Self-medication can lead to aggravation of the condition and the inability to provide effective medical care.

The fundamental method in the treatment of the syndrome is immunosuppressive therapy, which stops the protective response of the body in the case of an autoimmune nature of the disease. The low prevalence of pathology does not allow for large-scale studies, however, an analysis of the available data allows us to conclude that the use of corticosteroids is rational. The attending physician may appoint:

• "Prednisone"
• "Medrol",
• other analogues.

The drugs are administered intravenously or taken orally as tablets. The effect of such treatment appears already on the third or fourth day. If there is no improvement, there is a high probability that the disease was misdiagnosed.

Further monitoring of the patient's condition is important, since the steroids used also help to eliminate the symptoms of diseases and conditions such as carcinoma, lymphoma, aneurysm, chordoma, pachymeningitis.

In addition to immunosuppressive therapy, there is a treatment of the symptom complex, which is designed to alleviate the patient's condition. Analgesics are prescribed in the form of drops and tablets, anticonvulsants.

Vitamin complexes are shown as general strengthening agents. There is a reception of metabolic drugs for the regulation of metabolic processes in the affected structures of the eye.

Syndrome of the superior palpebral fissure has a symptomatic complex characteristic only of it. But in order to understand the cause of the appearance of this pathology, one should know the detailed structure of the eye orbit.

Description of the orbit of the eye and its structure

In the area between the outer and upper walls in the very depths of the orbit is the upper palpebral fissure - a slit-like space, the size of which is from 3 to 22 mm. It is limited to large and small wings of a wedge-shaped bone. It is intended to connect the middle cranial fossa and the cavity of the orbit itself. Usually the gap is tightened with a special film - connective tissue. She, in turn, passes through herself:

• superior and inferior veins;
• abducens nerve;
• block nerve;
• frontal, lacrimal and nasociliary branches of the optic nerve;
• oculomotor nerve.

Eye sockets having the shape of a tetrahedral pyramid with a truncated top of the recess in the skull, the bases converging outwards and in front.

• height at the entrance - 3.5 cm;
• length of the anteroposterior axis - 4.5 cm;
• depth - 5.5 cm;
• the width of the anteroposterior axis is 4 cm.

The orbits must contain:

The organs of vision themselves are in limbo, thanks to specific connective ligaments.

Four slanting walls perform special functions:

• lower - formed due to the upper jaw and the wall of the maxillary sinus;
• internal - the border in contact with the ethmoid bone. Between the lacrimal crests there is a recess, the so-called lacrimal fossa with a corresponding sac. The most fragile of borders;
• external - wedge-shaped due to the zygomatic and frontal bones. Protects from the temporal fossa and is the most durable;
• upper - exists due to the frontal bone, in which there is often also a sinus. Therefore, with inflammatory processes or tumor formations in this area, the disease also manifests itself in the orbit.

All walls have holes through which the control and nutrition of the organs of vision passes.

Pathogenesis

It is very difficult to describe the state of this disease. If you combine anesthesia of the upper eyelid, half of the forehead and cornea with full ophthalmology in one, you can correlate similar parameters.

This condition usually occurs when the ophthalmic, abducens, and oculomotor nerves are affected. This, in turn, occurs in various conditions - from a small number of pathologies to mechanical damage.

The main group of causes of this syndrome:

• a brain tumor located in the eye socket;
• deviations of the arachnoid membrane of the brain, which have an inflammatory nature - arachnoiditis;
• meningitis in the region of the upper palpebral fissure;
• eye injury.

The clinical picture, manifested in the syndrome of the upper palpebral fissure, is characteristic exclusively for this disease.

• ptosis of the upper eyelid;
• paralysis of the eye muscles caused by the pathology of the optic nerves - ophthalmoplegia;
• low tactile sensitivity in the cornea and eyelids;
• mydriasis - pupil dilation;
• dilated retinal veins;
• inflammation of the cornea of ​​a sluggish state.
• exophthalmos - exophthalmos.

Syndromes are not necessarily fully expressed, sometimes partially. During the diagnosis, this fact is always taken into account. If two or more signs coincide, you should immediately contact an ophthalmologist.

Treatment of the disease

In medical practice, there are cases of treatment of this syndrome. But the formation of this pathology is so rare that a novice ophthalmologist may be incompetent in this matter.

Doctors with rich many years of experience characterize the condition of a patient with this syndrome in this way:

• the eyeball is motionless;
• dilated pupil;
• drooping upper eyelid;
• completely absent skin sensitivity in the area of ​​the trigeminal nerve;
• expansion of veins in the fundus;
• exophthalmos;
• disturbed accommodation.

A similar condition is caused by diseases of the central nervous system, due to which the preliminary cause of the formation of the syndrome is revealed. Therefore, in order to prescribe the appropriate treatment, consultations will be needed not only with an ophthalmologist, but also with a neurosurgeon and a neuropathologist.

During treatment, the factor that provoked the onset of the syndrome is necessarily taken into account. Therefore, it is very important to consult a doctor on time. If you doubt something, you can first go to the therapist, and he will already direct you along the further path.

Eye diagnostics

Eyes can say a lot not only about the soul of a person, but also about the state of his health. In some diseases, the condition of the eyes and eyelids changes, which allows one to make an assumption about his health at one glance at a person.

Bags of floor eyes

This is the most common eyelid change. Bags under the eyes are evidence of kidney disease. Acute and chronic diseases of these organs cause edema, which manifests itself primarily on the face.

Also, the same bags can occur with anemia, after a coughing fit.

In addition, they can also appear in healthy people with overwork, a sleepless night, or for no apparent reason at all.

Dark coloration of the eyelids

Darkening of the eyelids can occur with thyrotoxicosis, Addison's disease (impaired function of the adrenal cortex).

Expansion of the palpebral fissure

This is possible with damage to the nerve responsible for the work of the upper eyelid. As a result, it is constantly raised: the eye is wide open, the person does not blink.

Well-marked bulging occurs with Graves' disease, caused by an increase in the amount of thyroid hormones in the body.

At the same time, the eyes are open so wide that a white strip is clearly visible between the iris and the upper eyelid. This strip becomes even more noticeable when a person looks up or down.

Narrowing of the palpebral fissure

Narrowing, as a rule, occurs due to edema. The cause of such edema is most often an insufficient amount of thyroid hormones in the body (with hypothyroidism, myxedema).

Lower eyelid prolapse

Constantly drooping lower eyelid is a sign of damage to the nervous system.

Sunken eyes

Sunken, as if pressed inward, eyes can be a sign of severe myopia.

In addition, this is one of the signs of peritonitis (inflammation of the peritoneum), and therefore, with the sudden appearance of such a symptom, especially in combination with severe pallor and cold sweat, you need to see a doctor as soon as possible.

Examination of the eye is the oldest diagnostic method. It is known that in India, Ayurvedic scientists used the examination and the characteristics of the iris obtained during it to determine heredity, constitution and disorders in the human body.

If there is retraction and narrowing of the eye, drooping of the upper or lower eyelid on one side, this indicates damage to the nerves or brain.

Strabismus

Such a violation can occur with paralysis of the mouse, moving the eyeballs. It also develops with lead poisoning, with botulism, syphilis. In addition, strabismus can develop with damage to the brain, such as meningitis (inflammation of the meninges), tuberculosis, or bleeding in the brain.

pupil changes

We cannot control the pupils, forcing them to expand or contract, everything here is controlled by the nervous system, regardless of our consciousness. That is why the pupils can determine brain damage, as well as some other conditions. In bright light, the pupils are constricted, in the dark - dilated. If a person moves from a dark room to a light one or vice versa, pupil size changes very quickly. However, in some diseases, the pupils stop responding to light.

Pupil constriction. This symptom is observed in the final stage of renal failure, when a large amount of harmful substances accumulate in the blood, with brain tumors and cerebral hemorrhage, as well as with drug poisoning (in particular, morphine). This symptom is also characteristic of diseases of the organ of vision itself (for example, inflammation of the iris, glaucoma, and some others).

Pupil dilation occurs in all comatose states, except for those that have developed due to renal failure or cerebral hemorrhage, as well as atropine poisoning.

Unequal pupils are a formidable sign that speaks of the defeat of one of the hemispheres of the brain.

Change in color of the sclera

The sclera is also called the white of the eye. In a healthy person, it is white. However, its color may change with some diseases.

Yellowish sclera. This color of the sclera is acquired with jaundice, which, in turn, can be caused by the simultaneous destruction of a large number of red blood cells and the release of bilirubin (for example, with large blood loss), impaired liver function and impaired bile outflow.

The red color of the sclera is acquired when the vessels of the eye rupture and hemorrhage into its mucous membrane.

Discharge from the eyes

Purulent discharge from the eyes is usually associated with inflammation of the mucous membrane of the eye - conjunctivitis. But conjunctivitis can be both an independent disease and a sign of other ailments in which the body's defenses are reduced.

Eye diagnostics received a rebirth in the middle of the 19th century: the Hungarian doctor Ignaz Pecceli developed the first diagram of projections of organs on the iris.

Redness of the mucous membrane of the eyes

Redness of the mucous membrane of the eyes, as a rule, is associated with its inflammation - conjunctivitis. In addition, it can occur when the eye is irritated by a stream of air, caustic substances, etc.

Syndrome of the superior orbital fissure

The superior orbital fissure is located on the border of the outer and upper walls in the depth of the orbit. It is a slit-like space (3 by 22 mm), bounded by the large and small wings of the sphenoid bone and connecting the middle cranial fossa with the cavity of the orbit. The superior orbital fissure is covered with a connective tissue film through which:

• inferior and superior vein;
• abducens nerve;
• three main branches of the optic nerve: frontal, lacrimal, and nasociliary;
• block nerve;
• oculomotor nerve.

Syndrome of the superior orbital fissure describes a specific symptomatic complex. In order to understand the causes, signs and treatment of this syndrome, it is necessary to consider the structure of the orbit in more detail.

The eye socket or orbit is a recess in the bones of the skull, the shape of which is similar to a tetrahedral pyramid. Its base is turned outward and forward. The height at the entrance area is 3.5 centimeters, and the length of the anteroposterior axis and the width are approximately 4.5 and 4 centimeters, respectively.

In the orbits there are vessels, fatty tissue, external muscles, nerves and eyeballs, which are in a suspended state, which is provided by special connective tissue ligaments. Also there are 4 bone walls: lower, outer, upper and inner. The lower wall of the orbit separates it from the maxillary sinus, and the inner wall borders on the ethmoid bone. From three sides, the orbit is in contact with the paranasal sinuses, therefore, in medical practice, there are often cases when various infectious and inflammatory processes spread from the sinuses to the eyes.

Causes and signs

This syndrome can be described as a combination of anesthesia of the upper eyelid, cornea and homolateral half of the forehead with complete ophthalmoplegia. As a rule, it is caused by damage to the ophthalmic, abducens, trochlear, and oculomotor nerves and occurs with many different conditions, from mechanical damage to diseases.

Let us consider in more detail the main causes of the syndrome of the superior orbital fissure:

1. brain tumors located in the eye socket;
2. arachnoiditis - inflammatory diseases of the arachnoid membrane of the brain;
3. meningitis in the area of ​​the upper orbital fissure;
4. traumatic injury to the orbit.

In the syndrome of the superior orbital fissure, a certain clinical picture is observed, which can be characterized by the following symptoms:

• Ptosis of the upper eyelid. The drooping of the upper eyelid up to the complete closure of the palpebral fissure occurs in both children and adults.
• Paralysis of the eye muscles due to the pathology of the oculomotor nerves - ophthalmoplegia. In most cases, this syndrome is manifested by immobility of the eyeball.
• Decreased tactile sensitivity of the skin of the eyelids and cornea.
• Pupil dilation - mydriasis. This condition can occur both in natural conditions, for example, when the level of illumination decreases, and when poisoned by certain chemicals.
• Retinal vein dilatation and other arterial changes.
• Slow inflammation of the cornea, which develops with damage to the trigeminal nerve - neuroparalytic keratitis.
• Bulging (protrusion) of the eyeball - exophthalmos.

If you experience 2 or more signs of this pathology, be sure to consult an ophthalmologist!

With this syndrome, the above symptoms may not be fully expressed, but partially. This fact should also be taken into account when diagnosing eye diseases.

Clinical picture

In medical practice, a case of examination and treatment of a patient with the above syndrome is described. From the records of the oculist ... “The eyeball is in a stationary state. The pupil is dilated. The upper eyelid is drooping. Skin sensitivity in the area of ​​branching of the endings of the branches of the trigeminal nerve and the cornea is absent. There is a slight expansion of the veins of the fundus and exophthalmos. Accommodation is disturbed, so the patient can neither read nor write at a normal distance. Such a condition is preceded by diseases of the central nervous system, which makes it possible to identify the preliminary cause of this pathology. Recommendations: consultations of a neurosurgeon and a neuropathologist will be required for the appointment of treatment.

Note! Accommodation is the ability of the eye to adapt to changes in distance when looking at objects.

The treatment regimen for this syndrome is determined taking into account the factor that provoked it, therefore it is very important to immediately contact an ophthalmologist and therapist when observing the symptoms of this condition. These medical specialists will refer you to a neurologist, etc. if necessary.

Treatment is based on the elimination of not only the cause of the disease, but also its accompanying conditions: ptosis, paralysis, dilated veins or pupil. Therefore, it takes time and effort.

Ophthalmological examination

Complaints of patients: decreased visual acuity (neuritis and atrophy of the optic nerve), periodic short-term blurring of vision with increased intracranial pressure. Violation of the ability to recognize objects or their individual qualities (damage to the posterior parts of the parieto-occipital region). Loss of half or a quarter of the visual fields in both eyes (damage to the intracranial visual pathways). Pain in the eye area without signs of inflammation of the eyeball (migraine, trigeminal neuralgia). Doubling in the horizontal, vertical or oblique planes (damage to the oculomotor nerves III, IV, VI pairs or a pathological process in the orbit).

External eye examination

• a) The width of the palpebral fissures varies due to various reasons. The palpebral fissure is significantly narrowed when the upper eyelid is lowered - ptosis, which can be congenital or acquired. Acquired ptosis depends mostly on paralysis of the muscle that lifts the upper eyelid (III pair), on diseases of the muscles of the eye (myasthenia gravis, myopathy), paralysis of the sympathetic nerve (paralysis of the smooth muscle of the upper eyelid);
• b) Reflex spasm of the circular muscle of the eyelids (blepharospasm) is observed with lesions of the meninges, hysteria, initial manifestations of hemi- or paraspasm, and also often with extensive hemispheric lesions on the side of the focus;
• c) Expansion of the palpebral fissure is noted with paralysis of the facial nerve. The impossibility of closing the eyelids (lagophthalmos) is characteristic, as a result of which the eye is constantly open, watery;
• d) Protrusion of the eyeball from the orbit (exophthalmos) can be unilateral, bilateral, pulsating. Unilateral exophthalmos is observed in diseases of the orbit (retrobulbar tumor, inflammation of the Tenon's bag, etc.), brain tumors, and also with irritation of the cervical sympathetic nodes, when, along with exophthalmos, an expansion of the palpebral fissure and pupil is noted. With bilateral protrusion of the eyeballs, you need to think about endocrine edematous exophthalmos. Pulsating exophthalmos occurs when the internal carotid artery ruptures in the cavernous sinus; at the same time, along with the pulsation of the eyeball, a blowing noise is heard (through the eyeball), often felt by the patient himself;
• e) Retraction of the eyeball deep into the orbit (enophthalmos) in combination with narrowing of the palpebral fissure and pupil (miosis), which is called Horner's syndrome, indicates a loss of function of the cervical sympathetic nerve;
• f) The shape and size of the pupils are examined, as well as the reaction of the pupil to light (direct and friendly), with convergence and accommodation. Reflex immobility of the pupils, i.e., the absence of a direct and friendly reaction to light with preserved constriction during convergence (Argyll Robertson's symptom), in most cases is observed with tabes and progressive paralysis. Very often, uneven pupil width (anisocoria) is noted, as well as a change in the shape (elongated, angular) and edges (uneven) of the pupil. The pupils do not respond or respond very poorly to mydrietic and myopic agents. With Adie's syndrome, with convergence, a tonic reaction of the pupils is observed - for several seconds the pupil narrows, after the end of convergence it slowly expands (from 30-40 s to several minutes); anisocoria, a change in the size of the pupil during the day, its rapid narrowing under the influence of miotic agents and expansion from mydriatic ones are noted. As a rule, the process is one-sided;
• g) The deposition of a greenish-brown pigment on the periphery of the cornea in the form of a ring or a half ring (Kaiser-Fleischer's corneal ring) is pathognomonic for hepato-cerebral dystrophy;
• h) Violation of the mobility of the eyeball in the presence or absence of strabismus is observed in cases of damage to the oculomotor nerves (III, IV, VI).

Paralysis of the abducens nerve (VI) is accompanied by convergent strabismus (the eyeball is turned inwards), limitation of the mobility of the eyeball outward, increased doubling when looking outward. Isolated trochlear nerve palsy (IV) is extremely rare. At the same time, strabismus is observed, diverging in the vertical direction; the eyeball is turned up and inside, diplopia is noted only when looking down. Paralysis of the oculomotor nerve (III) may be complete or incomplete. With complete paralysis, the upper eyelid is drooping (ptosis); the eyeball is turned outward and slightly downward (divergent strabismus), diplopia, dilated pupil, blurred vision at close range (accommodation paralysis), the eye is somewhat protruding from the orbit (exophthalmos). With incomplete paralysis of the oculomotor nerve, individual muscles are affected. If complete paralysis of this nerve is accompanied by a lesion of the abducent and trochlear nerves, then complete ophthalmoplegia develops; if only the external muscles of the eye are affected, external ophthalmoplegia occurs, if only the internal muscles of the eye are affected, internal ophthalmoplegia occurs.

Associated disorders of the movement of the eyeballs to the sides, up and down with the possibility of isolated movement of one eye (gaze palsy) are observed when there is a violation of the connections between the nuclei of the optic nerves, mainly in the posterior longitudinal fasciculus, as well as in the quadrigemina and in the posterior frontal gyrus. Deviation of one eye upwards and outwards, and the other downwards and inwards from the midline (Hertwig-Magendie symptom) occurs when the brain stem is damaged. In this case, the lesion is localized on the side of the eye, deviated from top to bottom.

Ophthalmoscopic examination

Ophthalmoscopic examination reveals changes in the fundus in the pathology of the nervous system.

With the initial congestive disc, hyperemia, blurring of the boundaries, limited marginal edema, most often of the upper and lower edges of the optic nerve head, are observed. The caliber of the arteries is not changed, the veins are somewhat dilated, but not tortuous. Hemorrhages, as a rule, do not occur at this stage. A pronounced congestive disc is characterized by its more pronounced hyperemia, the spread of edema throughout the disc, a significant increase in its diameter and protrusion into the vitreous body, blurring of the boundaries. The arteries are narrowed, the veins are significantly dilated, plethoric and tortuous. Multiple hemorrhages and white foci are present not only on the surface of the disk, but also in the retina adjacent to it. With prolonged existence, the stagnant disc gradually turns into atrophy (atrophy after stagnation). A grayish tint of the disc appears, tissue swelling decreases, the veins become less full-blooded and dilated, hemorrhages resolve, the foci disappear.

A characteristic feature of the congestive disc is the long-term preservation of visual functions - visual acuity, visual field. Visual acuity may remain normal for several months, and sometimes for a longer time (one year). With the transition of the congestive disc to atrophy, there is a decrease in vision up to blindness and a narrowing of the boundaries of the visual field.

One of the earliest signs of congested discs (due to edema) is an increase in the blind spot, sometimes small, in other cases 3-4 times. An early sign of congestive discs is also an increase in pressure in the central retinal artery. This mainly concerns diastolic pressure, which rises to 60-80 mm Hg. Art. (norm - from 35 to 40 mm Hg. Art.).

With complicated congestive discs, along with the effect of increased intracranial pressure, there is also a direct effect of the pathological process on the visual pathway. This impact can be direct, either through the dilated ventricular system of the brain, or through dislocation of the brain. Complicated congestive discs are characterized by:

1. atypical changes in visual field;
2. high visual acuity with a sharply changed field of view;
3. a sharp difference in visual acuity of both eyes;
4. a sharp decrease in visual acuity with congestive discs without atrophic changes or with initial mild atrophy;
5. development of optic nerve atrophy in one eye with bilateral congestive discs.

Acute circulatory disturbance in the system of arteries feeding the optic nerve is observed in the cerebral form of hypertension and atherosclerosis. The disease begins acutely, with a sharp decrease in vision (up to several tenths or hundredths) in one eye. From the side of the fundus, there is a pronounced edema of the optic nerve head with a milky-white or yellowish color of the edematous tissue. The borders of the disc are blurred, its protrusion into the vitreous body is moderate. The retinal arteries are very narrow, inconspicuous, lost in the edematous tissue, the veins are not dilated. Hemorrhages on and around the disc. Edema of the optic disc lasts from several days to 2-3 weeks and turns into atrophy of the optic nerve. Visual functions are restored poorly.

Optic neuritis is an inflammatory process in this nerve. Occurs in acute inflammatory diseases of the nervous system (meningitis, encephalitis, encephalomyelitis). Of the chronic infectious diseases, neurosyphilis is of the greatest importance.

With a mild inflammatory process, the optic disc is slightly hyperemic, its boundaries are blurred, arteries and veins are slightly dilated. A pronounced neuritis is characterized by significant hyperemia and blurring of the boundaries of the optic nerve head. It merges with the surrounding background of the fundus and can be determined only at the exit point of large vessels. There are multiple hemorrhages and white foci of exudate on the surface of the disc and in the adjacent retina. Dramatically dilated arteries and veins are covered with cloudy disc tissue. In most cases, neuritis is characterized by the absence of protrusion of the optic nerve head above the level of the surrounding retina. With the transition of neuritis to atrophy, there is a decrease in hyperemia and the development of a barely noticeable disc blanching at first. Hemorrhages and foci of exudate gradually resolve, the vessels narrow (especially the arteries), the nipple becomes white and a picture of secondary atrophy of the optic nerves develops. Characterized by an early violation of visual functions, occurring simultaneously with the development of ophthalmoscopic changes. They manifest themselves in a decrease in visual acuity (from tenths to hundredths, in some cases to light perception), in changes in the visual field (concentric narrowing of the boundaries, central and paracentral scotomas), as well as in a disorder of color perception.

Retrobulbar optic neuritis is characterized by a diverse picture of the fundus. It is determined both by the localization of the process in the optic nerve and by the intensity of inflammatory changes. Along with the normal picture of the fundus, changes characteristic of both neuritis and congestive disc can be observed. It occurs mainly in multiple sclerosis, as well as opto-chiasmatic arachnoiditis, opto-myelitis, meningitis, encephalitis. A characteristic sign of retrobulbar neuritis is a discrepancy between ophthalmoscopic changes and the state of visual functions. With minor changes in the fundus, a rapid and sharp decrease in vision is observed: in some cases, within a few hours, vision drops to light perception, in others it drops to several hundredths. Along with this, pain behind the eyeball is noted, especially during its movements, and slight exophthalmos (due to swelling of the orbital tissue).

A sharp decrease in vision usually lasts from several days to several weeks, after which vision begins to recover, but recovery is not always complete. During this period, when examining the field of view, the central absolute or relative scotoma of white and other colors, characteristic of retrobulbar neuritis, is revealed. With retrobulbar neuritis, the papillomacular bundle is predominantly affected; as a result, blanching of the temporal half of the nipple is most often noted, which is almost pathognomonic for multiple sclerosis. However, sometimes simple atrophy develops with blanching of the entire optic disc.

Atrophy of the optic nerves is a consequence of a variety of processes. There is primary (simple) atrophy of the optic nerves and secondary. Primary develops with tabes, pituitary tumors, on the basis of trauma, with Leber's atrophy. From the side of the fundus, blanching of the optic nerve head with its clearly defined boundaries is noted. With severe atrophy, the optic disc is completely white, the vessels (especially the arteries) are sharply narrowed. Secondary atrophy develops after neuritis and stagnant discs. On the fundus, along with blanching of the optic nerve head, the blurring of its borders is revealed.

The combination of simple atrophy of the optic nerve in one eye with a congestive disc in the other (Foster-Kennedy syndrome) is observed most often in tumors, abscesses of the basal surface of the frontal lobe of the brain. In this case, atrophy of the optic nerve occurs on the side of the tumor or abscess, and congestive disc - on the opposite side.

With blockage of the internal carotid artery before the ophthalmic artery leaves, atrophy of the optic nerve on the side of the blocked artery is noted in combination with hemiplegia of the opposite side (cross-optic pyramidal syndrome).

Changes in the macula - in the childhood form of familial amaurotic idiocy, a round white focus is observed in the area of ​​the macula, 2-3 disc diameters in size with a cherry-red color in the center. Initially, the optic nerve head is not changed, later it becomes pale. With the juvenile form of this disease, a gradual deterioration of vision occurs up to blindness. On the fundus, pigmentary degeneration is noted in the central sections or on the periphery of the retina.

Changes in retinal vessels are observed most often in hypertension and atherosclerosis of cerebral vessels. There are three stages of fundus changes in hypertension.

1. Hypertensive angiopathy of the retina - at the bottom of the eye, there are changes only in the caliber of the vessels in the form of their narrowing, less often expansion, corkscrew-like tortuosity of venules in the macular region (Guist's symptom). At this stage, there are arterial spasms, slight swelling of the optic disc and the surrounding retina, small pinpoint hemorrhages in the retina are possible.
2. Hypertensive angiosclerosis of the retina - this stage is characterized by uneven caliber of the arteries, their tortuosity or, conversely, straightness; thickening of the arterial wall; the vascular reflex becomes yellowish (copper wire phenomenon). Later, the vessel becomes empty and turns into a thin white stripe (silver wire phenomenon). Sclerosis of the retinal arteries is often accompanied by the phenomenon of the Gunia-Salus arteriovenous chiasm: bending of the vein under pressure from the sclerosed artery lying on it.
3. Hypertensive retinopathy - further development of sclerotic phenomena in the retinal vessels leads to changes in the retinal tissue itself in the form of edema, degenerative foci and hemorrhages.

In the cerebral form of hypertension, changes are often observed in the optic disc and retina in the form of neuroretinopathy.

Angiomatosis of the retina is an independent disease or accompanies angiomatosis of the central nervous system (Tippel-Lindau disease). At the same time, on the periphery of the fundus there is a red spherical tumor with a diameter 2-4 times greater than the diameter of the disk, which includes two dilated and tortuous vessels - an artery and a vein coming from the optic nerve head. In the future, white exudates of various sizes appear. Tumor and exudates often lead to retinal detachment.

Neurology

Pupils and palpebral fissures

Pupil reactions and the width of the palpebral fissures depend not only on the function of the oculomotor nerve, these parameters are also determined by the state of the retina and optic nerve, which make up the afferent part of the reflex arc of the pupil's reaction to light, as well as sympathetic effects on the smooth muscles of the eye (see Fig. 6) . However, pupillary reactions are examined more often when assessing the condition of the third pair of cranial nerves.

Assess the size and shape of the pupils.

Normally, the pupils are round, equal in diameter. Under normal room lighting, the diameter of the pupils can vary from 2 to 6 mm. The difference in the size of the pupils (anisocoria), not exceeding 1 mm, is considered the norm.

We evaluate the direct reaction of the pupil to light: we ask the patient to look into the distance, then quickly turn on a flashlight and evaluate the degree and stability of the pupillary constriction of this eye. The included light bulb can be brought to the eye from the side of the temporal side in order to exclude the accommodative reaction of the pupil (its narrowing in response to the approach of the object).

Normally, when illuminated, the pupil narrows, this narrowing is stable, i.e. persists as long as the light source is near the eye. When the light source is removed, the pupil expands.

We evaluate the friendly reaction of the other pupil, which occurs in response to the illumination of the eye under study. Thus, it is necessary to illuminate the pupil of one eye twice: during the first illumination, we look at the reaction to light of the illuminated pupil, and at the second illumination, we observe the reaction of the pupil of the other eye. The pupil of the non-illuminated eye normally constricts exactly at the same rate and to the same extent as the pupil of the illuminated eye, i.e. Normally, both pupils react in the same way and at the same time.

We perform a test of alternating illumination of the pupils. This test allows you to identify damage to the afferent part of the reflex arc of the pupillary reaction to light. Illuminate one pupil and note its reaction to light, then quickly move the bulb to the second eye and now evaluate the reaction of its pupil. Normally, when the first eye is illuminated, the pupil of the second eye first constricts, but then, at the moment of transferring the light bulb, it expands slightly (reaction to the removal of illumination that is friendly with the first eye) and, finally, when a beam of light is directed at it, narrows again (direct reaction to light) . If at the second stage of this test, with direct illumination of the second eye, its pupil does not narrow, but continues to expand (paradoxical reaction), this indicates damage to the afferent pathway of the pupillary reflex of this eye, i.e. about the damage to his retina or optic nerve Read here, ways to increase the signal of a 3G modem at no cost. . In this case, direct illumination of the second pupil (pupil of the blind eye) does not cause its constriction. However, at the same time, it continues to expand friendly with the first pupil in response to the cessation of illumination of the latter.

We check the pupillary reflexes of both eyes for convergence and accommodation. Ask the patient to first look into the distance (for example, at the wall behind you), and then look at a nearby object (for example, at the tip of your finger, which you hold directly in front of the patient's nose). If the pupils are narrow, we darken the room where the patient is examined before the test.

Normally, setting the gaze on an object close to the eyes is accompanied by a slight constriction of the pupils of both eyes, combined with convergence of the eyeballs and an increase in the convexity of the lens (accommodative triad).

Thus, normally, pupil constriction occurs: in response to direct illumination (direct pupil reaction to light); in response to illumination of the other eye (friendly reaction to light with the other pupil); when focusing on a nearby object.

Sudden fright, fear, pain lead to the expansion of the pupils, except in those cases when the sympathetic fibers to the eye are interrupted.

Signs. Assessing the width of the palpebral fissures and the protrusion of the eyeballs, you can detect exophthalmos - this is a protrusion (protrusion) of the eyeball from the orbit and from under the eyelid. It is best identified by standing behind a seated patient and looking down at their eyeballs.

The causes of unilateral exophthalmos can be a tumor or pseudotumor of the orbit, thrombosis of the cavernous sinus, carotid-cavernous anastomosis. Bilateral exophthalmos is observed with thyrotoxicosis (unilateral exophthalmos occurs less frequently in this condition).

We evaluate the position of the eyelids in different directions of gaze. Normally, when viewed directly, the upper eyelid covers the upper edge of the cornea by 1-2 mm. Ptosis (drooping) of the upper eyelid is a common pathology, which is usually accompanied by a constant contraction of the frontalis muscle due to the involuntary attempt of the patient to keep the upper eyelid raised. If you've noticed the constant abbreviation m. frontalis on one side, look for ptosis on the same side.

In a patient with a drooping upper eyelid, the differential diagnosis is made mainly between the following conditions: damage to the oculomotor (III) nerve; congenital ptosis, which can be unilateral or bilateral and have varying degrees of severity; syndrome of sympathetic deinnervation of the eye of Bernard-Horner; myotonic dystrophy; myasthenia gravis; blepharospasm; eyelid edema due to injection, trauma, venous stasis; age-related tissue changes. Ptosis may be the first

a sign of damage to the oculomotor (III) nerve, developing due to weakness of the muscle that lifts the upper eyelid. Ptosis can be partial or complete. It is usually combined with other manifestations of impaired function of the third nerve: ipsilateral mydriasis (dilated pupil), lack of pupillary response to light, impaired movements of the eyeball up, down and inwards.

In Bernard-Horner syndrome, the narrowing of the palpebral fissure, ptosis of the upper and lower eyelids are caused by functional insufficiency of the smooth muscles of the lower and upper cartilage of the eyelids (tarsal muscles). Ptosis is usually partial, unilateral. It is combined with miosis (narrowing of the pupil), due to a lack of pupillary dilator function (due to a defect in sympathetic innervation). Miosis is most pronounced in the dark. Ptosis in myotonic dystrophy (dystrophic myotonia) is bilateral, symmetrical. The size of the pupils is not changed, their reaction to light is preserved. There are other signs of this disease. Ptosis without anisocoria often indicates its muscular origin. With myasthenia gravis, ptosis is usually partial, asymmetric, and its severity can vary significantly throughout the day. Pupillary reactions are not disturbed. Blepharospasm (involuntary contraction of the circular muscle of the eye) is accompanied by partial or complete closure of the palpebral fissure. Mild blepharospasm can be confused with ptosis, but with blepharospasm, the upper eyelid periodically rises actively and there is no contracture of the frontalis muscle.

Irregular attacks of expansion and contraction of the pupils, lasting for several seconds, are called hippus or undulation. This can be observed with metabolic encephalopathy, meningitis, multiple sclerosis. Mild anisocoria (small difference in pupil size), not accompanied by impaired pupillary reactions, is observed in many healthy individuals.

If the pupils differ significantly in size, the pathology can affect both one eye and both. Unilateral mydriasis (dilated pupil) in combination with ptosis and paresis of the external muscles is observed with damage to the oculomotor nerve.

Pupil dilation is often the first (anticipating other manifestations) sign of damage to the oculomotor nerve when the nerve trunk is compressed by an aneurysm and when the brain stem is dislocated.

On the contrary, with ischemic lesions of the III pair (for example, in diabetes mellitus), the efferent motor fibers leading to the pupil usually do not suffer, which is important to consider in the differential diagnosis. Unilateral mydriasis (dilated pupil), not combined with ptosis and paresis of the external muscles of the eyeball, is usually not characteristic of damage to the oculomotor nerve. Possible causes of such mydriasis: drug-induced paralytic mydriasis that occurs with the local application of a solution of atropine and other m-holinolytics in ophthalmic practice (in this case, the pupil ceases to narrow in response to the use of a 1% solution of pilocarpine); Adie's pupil; spastic mydriasis, caused by contraction of the dilator of the pupil during irritation of the sympathetic structures innervating it.

Adie's pupil, or pupillotonia, is usually seen on one side. It is characterized by pupil dilation on the affected side (anisocoria) and its abnormally slow and prolonged (myotonic) response to light and convergence with accommodation. Because the pupil does eventually respond to light, anisocoria gradually decreases during the neurological examination. There is denervation hypersensitivity of the pupil: instillation of a 0.1% solution of pilocarpine into the eye leads to its sharp narrowing to point sizes.

Pupillotonia is observed in a benign disease (Holmes-Eidy syndrome), which is often familial, occurs more often in women aged 20-30 years and, in addition to the "tonic pupil", may be accompanied by a decrease or absence of deep reflexes from the legs (less often from the hands) , segmental anhidrosis (local disturbance of sweating) and orthostatic hypotension.

Symptom Lrgile Robertson - when fixing the gaze near, the pupil narrows, retaining a reaction to accommodation, but does not react to light. Typically, Argyle Robertson's symptom is bilateral, associated with irregular pupils and anisocoria. During the day, the pupils have a constant size, do not respond to the instillation of atropine and other mydriatics. It is observed with lesions of the midbrain tegmentum, for example, with neurosyphilis, diabetes mellitus, multiple sclerosis, tumors of the epiphysis, severe traumatic brain injury, followed by expansion of the Sylvian aqueduct, etc.

A narrow pupil (due to paresis of the pupil dilator), combined with partial ptosis of the upper eyelid (paresis of the muscle of the upper cartilage of the eyelid), anophthalmos and impaired sweating on the same side of the face, indicates Bernard-Horner syndrome. This syndrome is caused by a violation of the sympathetic innervation of the eye. In the dark, the pupil does not dilate. Bernard-Horner syndrome is more often observed in the following pathological conditions: infarcts of the medulla oblongata (with Wallenberg-Zakharchenko syndrome) and the brain bridge, tumors of the brainstem (interruption of the central descending sympathetic pathways coming from the hypothalamus); Bernard-Horner syndrome occurs on the side of the infarction; damage to the spinal cord at the level of the ciliospinal center in the lateral horns of the gray matter of the Ex-O segments); complete transverse lesion of the spinal cord at the level of these segments (Bernard-Horner syndrome is bilateral, combined with signs of impaired sympathetic innervation of organs located below the level of the lesion, as well as conduction disorders of voluntary movements and sensitivity); diseases of the apex of the lung and pleura (Pankost's tumor, tuberculosis, etc.), lesions of the first thoracic spinal root, additional cervical ribs (interruption of fibers coming from the ciliospinal center to the upper cervical sympathetic node); Bernard-Horner syndrome is combined with damage to the lower trunk of the brachial plexus (weakness of the muscles of the arm); aneurysms of the internal carotid artery, tumors in the jugular foramen, cavernous sinus, tumors or inflammatory processes in the orbit (interruption of postganglionic fibers from the superior cervical sympathetic ganglion to the smooth muscles of the eye).

With irritation of the sympathetic fibers going to the eyeball, symptoms occur that are “reverse” to the Bernard-Horner syndrome: dilated pupil, dilated palpebral fissure and exophthalmos (Pourfure du Petit syndrome).

With unilateral loss of vision due to interruption of the anterior parts of the visual pathway (retina, optic nerve, chiasm), the direct reaction of the pupil of the blind eye to light disappears (since the afferent fibers of the pupillary reflex are interrupted), as well as the friendly reaction to light of the pupil of the second, healthy eye. However, in this case, the pupil of the blind eye is able to narrow when the pupil of the healthy eye is illuminated (i.e., the friendly reaction to light in the blind eye is preserved). Therefore, if the flashlight bulb is moved from a healthy eye to an affected one, one can note not a narrowing, but, on the contrary, an expansion of the pupil of the affected eye (as a friendly response to the elimination of illumination of the healthy eye) - a symptom of Marcus Gunn.

Occasionally, other phenomena of pupillary disorders can also occur: Bumke-Westphal syndrome (periodic spontaneous expansion of the pupils in the absence of their reaction to light, accommodation and convergence), Landolfi's sign (pulsating pupils - they narrow during heart systole and expand during diastole in cases of aortic valve insufficiency ); symptom of Somagi (expansion of the pupils with a deep breath and narrowing them when exhaling - in cases of severe vegetative lability); Squire's symptom (when breathing according to the Cheyne-Stokes type during breath holdings, the pupils are constricted and their reactions are absent, when the respiratory movements are resumed, the pupils gradually expand as the breathing deepens, and then narrow with a decrease in the amplitude of the breaths); abduction phenomenon (pupil constriction with intense eye aversion), pupillary Tournay reaction (pupil dilation on the side to which the maximum gaze aversion occurs, a physiological phenomenon); Meyer's phenomenon (with intense pressure on the iliac region, pupil dilation occurs with a decrease or even disappearance of their reactions to light, the cessation of pressure leads to the normalization of the diameter of the pupils and their reactions); Reder's symptom (narrowing of the pupils and palpebral fissures during an attack of cephalalgia, which occurs during hypertensive crises or migraine attacks); symptom of Varkovich (more pronounced than usual, the expansion of the pupils after instillation of a solution of atropine into the eyes, observed in pregnant women); vegetative symptom Leah (excessively prolonged and significant expansion of the pupil after the introduction of an adrenaline solution into the conjunctival sac is a sign of increased excitability of the sympathetic part of the nervous system); pupillary symptom of Gover-sa-Bekhterev (perversion of the pupil's reaction to light - expansion when it is illuminated, narrowing - when darkened, occurs in late neurosyphilis), Gudden's symptom (reduction or disappearance of the reaction of the pupils to light, often combined with pupillary constriction and anisocoria, observed with alcoholic delirium, severe alcoholic encephalopathy); pupillary symptom of Berger (deformation of the pupils of an ellipsoidal shape - with dorsal tabes and progressive paralysis); Roque's symptom (dilated pupil on the side of the tuberculous lesion of the apex of the lung). The expansion of the right pupil occurs with appendicitis, cholecystitis.

When examining the eye, it is necessary to pay attention to the color and uniformity of the color of the irises. Fuchs' symptom - on the side of the violation of the sympathetic innervation of the eye, the iris is lighter, it can be combined with other signs of the Bern-ra-Horner syndrome.

Hyaline degeneration of the pupillary edge of the iris with depigmentation occurs in the elderly, a manifestation of the involutionary process. Axenfeld's symptom is characterized by depigmentation of the iris without the accumulation of hyaline in it, occurs in disorders of sympathetic innervation and metabolism. With hepatocerebral dystrophy, copper is deposited along the outer edge of the iris, which is manifested by yellowish-green or greenish-brown pigmentation (Kaiser-Fleischer ring).

narrowing of the palpebral fissure

The shape and size of the palpebral fissure are subject to significant racial and individual fluctuations. In normal adults, the palpebral fissure is 22–30 mm long and 12–15 mm wide. In children, 1-2 mm of the sclera remain uncovered by the upper eyelid upward from the corneal limbus. In adolescence, the upper eyelid just reaches the limbus of the cornea, in adults it covers the cornea by 1-2 mm. The edge of the lower eyelid at all ages reaches almost to the lower limb of the cornea.

The expansion of the palpebral fissure may be due to mechanical or nervous factors. Mechanically, the palpebral fissure is expanded due to a decrease in the capacity of the orbit with tumors or inflammatory infiltrates, with high myopia due to an increase in the size of the eyeball, with cicatricial or senile eversion of the lower pitch. Of the nerve factors, the following lead to the expansion of the palpebral fissure: paralysis of the facial nerve, partially exophthalmos in Graves' disease, pathological regeneration in peripheral lesions of the oculomotor nerve, mental agitation (irritation of the sympathetic or increased flow of adrenaline in status postencephaliticus and tabes.

In both latter cases, the mechanism of palpebral fissure expansion is unclear.

Mechanical narrowing of the palpebral fissure develops with anophthalmos due to a decrease in orbital fiber. The following nerve factors lead to narrowing of the palpebral fissure: paresis of the striated muscle that lifts the upper eyelid (damage to the gas-motor nerve, Myasthenia gravis, congenital anomalies of the nucleus, nerve and muscle, leading to the development of ptosis), or paralysis of the sympathetic m. tarsals (Horner's syndrome). In addition, narrowing of the palpebral fissure is observed with prolonged squinting in case of refractive errors in order to obtain sharper images on the retina, when closing one eye to eliminate double vision in paralytic and occasionally in concomitant strabismus. All these are spastic phenomena, which are often mixed with paralytic ptosis.

Normal eyelid movements are due to the harmoniously coordinated activity of the facial and oculomotor nerves (contraction or reciprocal relaxation of the m. orbicularis oculi and levator palpebrae). In humans and mammals, the upper eyelid mainly participates in these movements, in reptiles and birds, on the contrary, the lower eyelid.

Connections between the trigeminal, facial, glossopharyngeal and vagus nerves (according to Harris - F. Harris, from Walsh)

Involuntary periodic blinking lasts 0.13-0.2 seconds, i.e., it occurs faster than the physiological sequential image lasts. Thanks to this, the continuity of the act of vision is not disturbed. The intervals between individual blinks are different, from 2 to 10 seconds. During a conversation, the blinking becomes more rare, when reading aloud it is less than when fixing. In patients with encephalitis, the average blinking frequency is clearly reduced, the same is observed with Graves' disease (Stellwag symptom).

Blind but otherwise healthy individuals have a normal blink rate. Blinding by bright light causes rapid blinking; this reaction comes to light after reaching the first year of life; it is absent in some hemiplegics. The frequency of the physiological act of blinking may be determined not only by afferent impulses coming from the cornea and conjunctiva (sensitive irritations due to drying). The existence of a special nictitating center in the basal ganglia was also assumed, from where periodic impulses could be delivered to the nucleus of the facial nerve.

The ability for asymmetric innervation of the nuclei of the facial nerve in humans (unlike most mammals) has been largely lost. Many healthy people have completely or almost completely lost the ability to close one eye; at the same time, the prevalence of one side is noted (possible confusion with paralysis of the facial nerve).

With active blinking, ligamentum canthi intern: stretches the lacrimal canaliculus and the top of the lacrimal sac. This suction mechanism seems to be necessary for normal tear drainage. In patients who have had encephalitis, who can look straight ahead for hours without blinking, the cornea does not dry out, apparently due to the delayed removal of tears. It is possible that small fluctuations in intraocular pressure caused by blinking are also important for fluid exchange in the eye cavity.

Of the physiological synkinesis, we will mention the following: concomitant lowering of the eyebrow downwards with forced closing of the palpebral fissure; wrinkling of the forehead (corrugator supercilii) with increased accommodation or squinting with refractive errors (due to the ongoing constant tension of the galea aponeurotica, this was considered as one of the causes of headaches), as well as when trying to close one eye; concomitant movements of the eyelids up or down when looking up or down. The concomitant movement of the upper eyelid when looking down also occurs with paralysis of the facial nerve and when lying on the back as opposed to gravity.

It is still debatable whether it is simply due to reciprocal relaxation of the striated levator palpebrae or whether it depends on other as yet unknown factors. In the same way, the genesis of the disorder of this concomitant movement is still unclear, namely, the lag or spasmodic movements of the upper eyelid with slow downward gaze (Graefe's symptom in Graves' exophthalmos and sometimes, in rare cases, after lethargic encephalitis). The retraction of the eyelids during movements of the eyeball in connection with the regeneration of the oculomotor nerve has already been discussed above (pseudosymptom Graefe). The composition of complex synkinesias includes, finally, the movements of the pitch during laughter, crying, yawning, in which the lacrimal gland is also involved, brought into excitation from various instances.

Formed by the body of the sphenoid bone and its wings, connects the orbit with the middle cranial fossa. Three main branches of the optic nerve pass into the orbit - the lacrimal, nasociliary and frontal nerves, as well as the trunks of the trochlear, abducens and oculomotor nerves. The superior ophthalmic vein leaves through the same gap.

With damage to this area, a characteristic symptom complex develops: complete ophthalmoplegia, i.e., immobility of the eyeball, drooping (ptosis) of the upper eyelid, mydriasis, decreased tactile sensitivity of the cornea and eyelid skin, dilated retinal veins and slight exophthalmos. However " superior orbital fissure syndrome" may not be fully expressed when not all are damaged, but only individual nerve trunks passing through this gap.

The concept of the norm of visual acuity, subjective and objective methods for determining visual acuity.

Visual acuity - the ability of the eye to distinguish two points separately with a minimum distance between them, which depends on the structural features of the optical system and the light-perceiving apparatus of the eye.

Central vision is provided by retinal cones occupying its central fovea with a diameter of 0.3 mm in the area of ​​the macula. As you move away from the center, visual acuity decreases sharply. This is due to a change in the density of the arrangement of neurons and the peculiarity of impulse transmission. The impulse from each cone of the fovea passes through individual nerve fibers through the weight divisions of the visual pathway, which ensures a clear perception of each point and small details of the object.

Determination of visual acuity (visometry). To study visual acuity, special tables are used containing letters, numbers or icons of various sizes, and for children - drawings (cup, herringbone, etc.). They are called optotypes.

Determination of visual acuity according to the Golovin-Sivtsev table placed in the Roth apparatus. The bottom edge of the table should be at a distance of 120 cm from the floor level. The patient sits at a distance of 5 m from the exposed table. First determine the visual acuity of the right, then the left eye. The other eye is closed with a flap.

The table has 12 rows of letters or signs, the size of which gradually decreases from the top row to the bottom. In the construction of the table, a decimal system was used: when reading each subsequent line, visual acuity increases by 0.1. To the right of each line, visual acuity is indicated, which corresponds to the recognition of letters in this row.

With visual acuity below 0.1, the subject should be brought closer to the table until he sees its first line. Visual acuity should be calculated according to the Snellen formula: V=d/D, where d is the distance from which the subject recognizes the optotype; D is the distance from which this ontotype is visible with normal visual acuity. For the first row, D is 50 m.

To determine visual acuity below 0.1, optotypes developed by B. L. Polyak are used in the form of bar tests or Landolt rings, intended for presentation at a certain close distance, indicating the corresponding visual acuity.

There is also an objective (not dependent on the patient's testimony) method for determining visual acuity, based on optokinetic nystagmus. With the help of special devices, the subject is shown moving objects in the form of stripes or a chessboard. The smallest value of the object that caused involuntary nystagmus (seen by the doctor) corresponds to the visual acuity of the examined eye.

In conclusion, it should be noted that visual acuity changes throughout life, reaching a maximum (normal values) by 5-15 years and then gradually decreasing after 40-50 years.

Ultraviolet ophthalmia (conditions of occurrence, diagnosis, methods of prevention).

Photophthalmia (electroophthalmia, snow blindness) is an acute lesion (burn) of the conjunctiva and cornea of ​​the eye by ultraviolet radiation.

6-8 hours after irradiation, a feeling of "sand behind the eyelids" appears in both eyes.

After another 1-2 hours, corneal syndrome develops: acute pain in the eyes, photophobia, blepharospasm, lacrimation

Moderate swelling and hyperemia of the eyelids (photodermatitis)

Conjunctival or mixed injection

Swelling of the conjunctiva

The cornea is in most cases transparent, shiny, although with high individual sensitivity to UV or long-term exposure, there may be edema, epithelium “poking”, single vesicles of raised epithelium or fluorescein-stained punctate erosions.

Diagnostics:

Visual acuity

External examination

Biomicroscopy with corneal staining with fluorescein

A solution of local anesthetic (dicaine 0.25% or trimecaine 3%) is instilled into the conjunctival sac - up to 4 times a day;

actovegin gel (solcoseryl) 20%,

eye ointment of tetracycline or erythromycin 1% is applied over the eyelids - all 3-4 times a day.

To reduce swelling of the eyelids, you can use cold lotions with water or a solution of baking soda or boric acid 2%.

Inside for 3-4 days, an antihistamine is prescribed (suprastin 0.025 g twice a day) and NSAIDs - diclofenac (ortofen) 0.025 g 3 times a day.

In most cases, all the symptoms of photophthalmia pass without a trace in 2-3 days;

if light photophobia persists, instillations of Vitasik or Actovegin should be continued for another 2-3 weeks,

wear glasses with filters

The prognosis is favorable - full recovery.

Prevention:

Wearing dark glasses made of a special compound that absorbs shortwave and ultraviolet rays.

Ticket 17

Tear-producing apparatus. Research methods. Dry eye syndrome

The intraocular fluid is produced by the ciliary body, enters the posterior chamber, through the pupil into the anterior chamber, then through the angle of the anterior chamber into the venous system.

The tear-producing apparatus of the human eye consists of the main lacrimal gland, the accessory lacrimal glands of Krause and Wolfring.

The lacrimal gland provides reflex tearing, which occurs in response to mechanical (for example, a foreign body) or other irritation of the reflexogenic zones, to provide a protective function. It is also stimulated by emotions, sometimes reaching 30 ml of tears in 1 minute in such cases.

Additional lacrimal glands of Krause and Wolfring provide basal (main) secretion, which is up to 2 ml per day, is necessary to maintain a constant moisture content of the cornea, conjunctiva of the eyeball and fornix, but constantly decreases with age.

Lacrimal ducts - lacrimal ducts, lacrimal sac, nasolacrimal duct.

Lacrimal tubules. They begin with lacrimal openings, they lead to the vertical part of the tubules, then their course changes to horizontal. Then, gradually approaching, they open into the lacrimal sac.

The lacrimal sac opens into the nasolacrimal duct. At the outlet duct, the mucous membrane forms a fold, which has the role of a closing valve.

A constant outflow of tear fluid is ensured by:

Blinking movements of the eyelids

Siphon effect with capillary flow of fluid filling the lacrimal ducts

Peristaltic changes in tubular diameter

Suction ability of the lacrimal sac

Negative pressure created in the nasal cavity during the aspiration of air.

Patency diagnostics:

Color nasal tear test - instill sodium fluroscein. After 5 minutes, blow your nose - there is fluroscein - test "+". After 15 minutes - there is a delayed test; after 20 minutes - no sample "-".

Polik's test (canalicular): drip collargol 3%. After 3 minutes, press on the lacrimal sac, if a drop of liquid appeared from the lacrimal punctum, then the test is +.

Washing: inject fluroscein solution into the canal.

Sounding.

X-ray contrast.

Tear-producing tests:

Stimulating test strips. Lay under the lower eyelid for 5 minutes. The Schirmer test is based on the properties of a strip of filter paper, placed at one end into the conjunctival cavity, to stimulate the production of tears and at the same time absorb liquid. Normally within 5 min. filter paper in the conjunctival cavity, it must be wetted for a length of at least 15 mm. And the smaller the size of the wetted strip, the less tears are produced, the more often and faster you can expect complaints and diseases of the cornea.

Study of basal tear production (Jackson, Schirmer-2 test)

Norn test. The patient is asked to look down and, pulling the lower eyelid with his finger, irrigate the limbus area at 12 o'clock with one drop of 0.1-0.2% sodium fluorescein solution. After that, the patient is seated at the slit lamp and before turning it on, they are asked to blink normally for the last time and then open their eyes wide. Through the eyepieces of the operating SC (a cobalt filter must first be introduced into its lighting system), the cornea is scanned in a horizontal direction. The time of formation in the colored tear film (SP) of the first rupture is noted.

Clinic: sensation of dryness in the eye, pain reaction to instillations into the conjunctival cavity of indifferent eye drops, photophobia, lacrimation

Chorioretinitis

Ticket 18

Conjunctiva (structure, functions, research methods).

The connective membrane of the eye, or conjunctiva, is the mucous membrane that lines the eyelids from the back and passes to the eyeball up to the cornea and, thus, connects the eyelid to the eyeball.

When the palpebral fissure is closed, the connective sheath forms a closed cavity - conjunctival sac, which is a narrow slit-like space between the eyelids and the eyeball.

The mucous membrane covering the back surface of the eyelids is the conjunctiva of the eyelids, and the covering sclera is the conjunctiva of the eyeball or sclera.

The part of the conjunctiva of the eyelids, which, forming the vaults, passes to the sclera, is called the conjunctiva of the transitional folds or vault. Accordingly, the upper and lower conjunctival arches are distinguished.

At the inner corner of the eye, in the region of the rudiment of the third eyelid, the conjunctiva forms a vertical semilunar fold and lacrimal caruncle.

The conjunctiva is divided into two layers - epithelial and subepithelial.

Eyelid conjunctiva tightly fused with the cartilaginous plate.

The epithelium is stratified, cylindrical, with a large number of goblet cells.

Smooth, shiny, pale pink, yellowish columns of meibomian glands passing through the thickness of the cartilage shine through.

Even in the normal state of the mucous membrane at the outer and inner corners of the eyelids, the conjunctiva covering them looks slightly hyperemic and velvety due to the presence of small papillae.

Conjunctiva transitional folds loosely connected to the underlying tissue and forms folds that allow the eyeball to move freely.

Conjunctiva fornix covered with stratified squamous epithelium with few goblet cells. The subepithelial layer is represented by loose connective tissue with inclusions of adenoid elements and clusters of lymphoid cells in the form of follicles.

The conjunctiva contains a large number of Krause's accessory lacrimal glands.

Scleral conjunctiva tender, loosely connected to the episcleral tissue. Multilayered flat epithet of the conjunctiva of the sclera smoothly passes to the cornea.

The conjunctiva is abundantly supplied with blood from the arterial branches of the eyelids, as well as from the anterior ciliary vessels.

Due to the dense network of nerve endings of the 1st and 2nd branches of the trigeminal nerve, the conjunctiva acts as an integumentary sensitive epithelium.

The main function of the conjunctiva is eye protection: when a foreign body enters, irritation of the eye appears, secretion of lacrimal fluid, blinking movements become more frequent, as a result of which the foreign body is mechanically removed from the conjunctival cavity.

The protective role is due to the abundance of lymphocytes, plasma cells, neutrophils, mast cells and the presence of Ig in it.

Research methods: Eversion of the upper and lower eyelids.

Non-penetrating wounds of the eyeball and emergency care tactics for them.

Classification: according to the localization of the wound (cornea, sclera, corneoscleral zone) and the absence or presence of one or more foreign bodies.

Non-penetrating wounds - irritation of the mucous membrane of the eye, lacrimation, photophobia, soreness, sometimes a significant decrease in vision when the process is localized in the optical zone.

The upper and lower eyelids are turned out to detect foreign bodies on the conjunctiva of the eyelids and in the vaults. A foreign body is removed from the cornea with a spear, chisel, bur in the emergency room. In cases of deep location of the fragment and its partial exit into the anterior chamber, it is better to perform the operation in stationary conditions, using appropriate surgical techniques.

Non-perforated wounds of the cornea can have a different shape, depth and localization, the question of the need for surgical treatment is decided individually.

To determine the depth of the wound, biomicroscopy is used, in addition, by pressing with a glass rod on the fibrous capsule of the eye near the site of the lesion, it is determined whether moisture filtration of the anterior chamber and divergence of the wound edges are observed. The most indicative is the test with fluorescein, based on the results of which one can confidently judge the presence or absence of a penetrating wound.

With a small wound of a linear shape with well adapted and closed edges, it is possible to refrain from suturing, however, in cases of extensive patchwork, deep scalped wounds, it is preferable to match their edges with sutures.

Treatment: gentamicin, levomycetin, tobrex, vitabact, zinc-boron drops in the form of installations, ointments (tetracycline, erythromycin, colbiocin, thiamine) and gels (solcoseryl, actovegin), which have antimicrobial and antiseptic effects, as well as repair stimulants.

The duration and frequency of the use of drugs depend on the dynamics of the course of the process, in some cases it is necessary to use AB and combined preparations in the form of subconjunctival injections, as well as mydriatics, depending on the severity of the inflammatory reaction of the eye.

Ticket 19

The optic nerve, its structure and functions. Ophthalmoscopic examination.

The optic nerve is formed by the axons of retinal ganglion cells and ends in the chiasm. In adults, its total length varies from 35 to 55 mm. A significant part of the nerve is the orbital segment (25-30 mm), which in the horizontal plane has an S-shaped bend, due to which it does not experience tension during movements of the eyeball.

papillomacular bundle

chiasma

Central artery and central retinal vein

4 departments: 1. intraocular (3 mm) 2. orbital (25-30 mm) 3. intratubular (5-7 mm) 4. intracranial (15 mm)

Blood supply: 2 main sources:

1.retinal (a.centr.retinae)

2. ciliary (a.a. ciliar. brev. post)

Plexus of Zinn-Haller

Other sources: Ophthalmic artery, pial vessels, choroidal, scleral vessels, anterior cerebral and anterior communicating arteries

Research methods: biomicroscopy.

Differential diagnosis of acute iridocyclitis, acute conjunctivitis and acute attack of glaucoma. Indications for the use of mydriatic and myotic remedies.

Acute iridocyclitis: intraocular pressure is normal, pain is localized mainly in the eye, pericorneal injection of vessels, the cornea is smooth, there are precipitates, the depth of the anterior chamber is normal, the iris is edematous, sluggish, the pattern is fuzzy, the pupil is narrow.

Acute conjunctivitis: intraocular pressure is normal, itching, burning, photophobia, pronounced conjunctival injection, mucopurulent discharge.

Acute attack of glaucoma: intraocular pressure is high, pain radiates to the temple and teeth, congestive injection of blood vessels, edematous cornea with a rough surface, no precipitates, shallow depth of the anterior chamber, the iris is not changed, the pupil is wide.

Long-acting mydriatics are used to achieve cycloplegia for exploration and refraction in children. In addition, they are used to treat semi-persistent and persistent accommodation spasms in children with refractive errors and in the complex therapy of inflammatory diseases of the anterior eye to prevent the development of posterior synechia.

Miotics - pilocarpine. Glaucoma.

Ticket 20

Ciliary (ciliary) body (structure, functions, research methods).

The middle part of the choroid, located behind the iris.

Consists of 5 layers:

Outer, muscular layer (muscles of Brücke, Muller, Ivanov)

Vascular layer (continuation of the choroid)

Basal lamina (continuation of Bruch's membrane)

2 layers of epithelium (pigmented and non-pigmented - continuation of the retina)

Inner limiting membrane

2 parts: inner - ciliary crown (corona ciliaris) and outer - ciliary ring (orbiculus ciliaris).

From the surface of the ciliary crown, ciliary processes (processus ciliares) extend towards the lens, to which the fibers of the ciliary girdle are attached. The main part of the ciliary body, with the exception of the processes, is formed by the ciliary, or ciliary, muscle (m. ciliaris), which plays an important role in the accommodation of the eye. It consists of bundles of smooth muscle cells located in three different directions.

The ciliary girdle is the junction of the lens with the ciliary body, acts as a ligament that suspends the lens.

Functions: production of intraocular fluid; fixation of the lens and changes in its curvature, participates in the act of accommodation. The contraction of the ciliary muscle leads to relaxation of the fibers of the circular ligament - the ciliary band of the lens, as a result of which the lens becomes convex and its refractive power increases.

Vascular network - long posterior ciliary arteries. Motor innervation - oculomotor and sympathetic nerves.

Research at lateral (focal) illumination, in the passing light, biomicroscopy, gonioscopy.

Concepts: "combined and associated damage to the organ of vision."

Combined: single-factor (mechanical, thermal, chemical, radiation, photo, biological), two-factor, multi-factor.

Combined: heads and faces, limbs, trunks, several areas of the body, the body as a whole (compression, contusion, poisoning)

Ticket 21

The optic tract and visual centers. Study of the visual field by the control method.

The retina is a layer of rods and cones (photoreceptors - I neuron), then a layer of bipolar (II neuron) and ganglion cells with their long axons (III neuron). Together they form peripheral part of the visual analyzer .

The pathways are represented by the optic nerves, chiasma, and optic tracts.

The latter terminate in the cells of the lateral geniculate body, which plays the role of the primary visual center. The fibers of the central neuron of the visual pathway originate from them, which reach the region of the occipital lobe of the brain, where the primary cortical center of the visual analyzer is localized.

optic nerve formed by the axons of retinal ganglion cells and ends in the chiasm. In adults, its total length varies from 35 to 55 mm. A significant part of the nerve is the orbital segment (25-30 mm), which in the horizontal plane has an S-shaped bend, due to which it does not experience tension during movements of the eyeball.

For a considerable length, the nerve has 3 sheaths: hard, arachnoid and soft. Together with them, its thickness is 4-4.5 mm, without them - 3-3.5 mm.

In the eyeball, the dura mater fuses with the sclera and Tenon's capsule, and in the optic canal, with the periosteum. The intracranial segment of the nerve and chiasm, located in the subarachnoid chiasmatic cistern, are dressed only in a soft shell.

All nerve fibers are grouped into 3 main bundles.

Axons of ganglion cells extending from the central (macular) region of the retina, make up papillomacular bundle, which enters the temporal half of the optic disc.

Fibers from the ganglion cells of the nasal half of the retina run along radial lines into the nasal half of the disc.

Similar fibers, but from the temporal half of the retina, on the way to the optic nerve head, “flow around” the papillomacular bundle from above and below.

The nerve is devoid of sensitive nerve endings.

In the cranial cavity, the optic nerves join over the sella turcica to form chiasma, which is covered with a pia mater and has the following dimensions: length 4-10 mm, width 9-11 mm, thickness 5 mm.

Chiasma from below borders on the diaphragm of the Turkish saddle, from above - on the bottom of the third ventricle of the brain, on the sides - on the internal carotid arteries, behind - on the funnel of the pituitary gland.

In the region of the chiasm, the fibers of the optic nerves partially cross due to portions associated with the nasal halves of the retinas.

Moving to the opposite side, they connect with fibers coming from the temporal halves of the retinas of the other eye, and form visual tracts . Here, the papillomacular bundles also partially intersect.

The optic tracts begin at the posterior surface of the chiasm and, having rounded the peduncles of the brain from the outside, end in outer geniculate body, the back of the thalamus and the anterior quadrigemina of the corresponding side.

Only the external geniculate bodies are the unconditional subcortical visual center.

Visual radiance(fibers of the central neuron) starts from the ganglion cells of the 5th and 6th layers of the lateral geniculate body. First, the axons of these cells form the so-called Wernicke's field, and then, passing through the posterior thigh of the internal capsule, fan-shaped diverge in the white matter of the occipital lobe of the brain. The central neuron terminates in the sulcus of the bird's spur.

This area represents sensory visual center - 17th cortical field according to Brodmann.

The field of view is examined using perimetry . The easiest way is a control (indicative) study according to Donders.

The subject and the doctor are facing each other at a distance of 50-60 cm, after which the doctor closes the right eye, and the subject - the left. In this case, the subject looks into the open left eye of the doctor with the open right eye and vice versa.

The field of view of the doctor's left eye serves as a control in determining the field of view of the subject. At the median distance between them, the doctor shows his fingers, moving them in the direction from the periphery to the center.

If the limits of detection of the fingers demonstrated by the doctor and the subject coincide, the field of view of the latter is considered unchanged.

If there is a mismatch, there is a narrowing of the field of view of the right eye of the subject in the direction of movement of the fingers (up, down, from the nasal or temporal side, as well as in the radii between them). After checking the field of view of the right eye, the field of view of the left eye of the subject is determined with the right closed, while the doctor's left eye is closed.

This method is considered indicative, since it does not allow obtaining a numerical expression for the degree of narrowing of the boundaries of the field of view. The method can be applied in cases where it is impossible to conduct a study on devices, including in bedridden patients.

The device for research of a field of vision - Foerster perimeter, which is a black arc (on a stand) that can be moved in different meridians.

Perimetry on the widely used universal projection perimeter(PPU) is also carried out monocularly. The correct alignment of the eye is controlled using an eyepiece. First, perimetry is carried out on white. When examining the visual field for different colors, a light filter is included: red (K), green (ZL), blue (S), yellow (Y). The object is moved from the periphery to the center manually or automatically after pressing the "Object movement" button on the control panel.

Modern perimeters on a computer basis. On a hemispherical or any other screen, white or colored marks move or flash in various meridians. The corresponding sensor fixes the parameters of the subject, indicating the boundaries of the field of view and areas of loss in it on a special form or in the form of a computer printout.

The widest borders have a field of view for blue and yellow, a slightly narrower field for red, and the narrowest for green.

The normal boundaries of the field of view for white color are considered upward 45-55 upward outward 65 outward 90, downward 60-70 °, downward inward 45 °, inward 55 °, upward inward 50 °. Changes in the boundaries of the visual field can occur with various lesions of the retina, choroid and visual pathways, with brain pathology.

Symmetrical dropouts in the visual fields of the right and left eyes- a symptom indicating the presence of a tumor, hemorrhage, or inflammation at the base of the brain, the pituitary gland, or the optic tracts.

Heteronymous bitemporal hemianopsia- this is a symmetrical half prolapse of the temporal parts of the visual fields of both eyes. It occurs when there is a lesion inside the chiasma of the crossing nerve fibers coming from the nasal halves of the retina of the right and left eyes.

Homonymous hemianopia- this is a half-named (right or left-sided) loss of visual fields in both eyes.

Atrial scotomas- these are short-term moving dropouts in the field of view that suddenly appear. Even when the patient closes his eyes, he sees bright, shimmering zigzag lines extending to the periphery.

Dystrophic pores of the conjunctiva of the cornea

Contusion of the eyeball (classification, diagnosis, tactics in case of detection of contusion changes in the fundus).

The strength of the blow that caused the concussion depends on the kinetic energy, which is made up of the mass and speed of the injuring object.

Concussion may be straight, i.e., occur when an object directly hits the eye, or indirect, i.e., be a consequence of the concussion of the torso and facial skeleton from the shock wave during explosions; a combination of these effects is also possible.

Damage to the sclera during a blunt impact goes from the inside outward, the inner layers of the sclera are torn earlier than the outer ones, with both complete ruptures and tears of the sclera occurring.

Ruptures of the membranes of the eye: more elastic membranes, such as the retina, are stretched, and less elastic ones (Bruch's membrane, pigment epithelium, vascular tissues, Descemet's membrane) are torn.

With high myopia, eye contusion can cause more severe traumatic changes than in healthy eyes.

Apart from pain in the craniofacial region on the side of the lesion, in most patients in the first days and hours after the injury, headache, dizziness, mild nausea a, difficulty in trying to read due to broken convergence.

In the first hours after injury mixed injection eyeball is expressed, as a rule, much weaker than in the following days. It increases within 1 day, remains at the same level for 3-4 days, and gradually begins to decrease by the end of the 1st - the beginning of the 2nd week.

Injuries are often associated with subconjunctival hemorrhages and scleral ruptures.

With contusions of the eyeball, hemorrhages often occur in different parts of the eye.

Hemorrhage into the anterior chamber (hyphema) is the most common symptom of eye contusion. The accumulation of a large amount of blood in the anterior chamber leads to a sharp decrease in vision due to imbibition of the cornea with blood.

If blood enters the vitreous body and it is completely permeated with blood, then this condition is called hemophthalmos.

Ultrasound scanning and CT diagnostics help to establish the correct diagnosis.

Hemorrhages under the choroid exfoliate the choroid and protrude it into the vitreous body in the form of a tubercle.

Corneal lesion. erosion of various sizes.

Iris damage. the pupil changes. It takes the form of an elongated oval, pear-shaped or polygonal shape due to tears or ruptures of the sphincter.

Paresis or paralysis of the sphincter causes paralytic mydriasis - a very sluggish or absent reaction to light remains, but the reaction to mydriatics remains. With an immobilized pupil, circular posterior synechiae are formed, pupillary block and secondary glaucoma occur.

Partial detachment (iridodialysis) of the iris root or its complete detachment, as a rule, is accompanied by hemorrhage into the eye cavity. In these cases, hemostatic therapy is prescribed. With large detachments that cover the pupil area, surgical reposition is performed.

Blunt trauma often develops cataract, occur lens displacement- dislocations and subluxations.

With a complete dislocation of the lens into the anterior or posterior chamber, its removal is indicated.

Choroid lesions- ruptures, always accompanied by hemorrhages.

To change ciliary body refers to its detachment - cyclodialysis, leading to free communication between the anterior chamber and the suprachoroidal space.

Pathology retina- Berlin opacity and retinal hemorrhage, which are detected in the first days after injury.

Treatment depends on clinical manifestations, as a rule, this is the complex use of drugs and surgical interventions.

Conservative therapy:

Antimicrobial agents for local and general use, including antibiotics and antiseptics;

Enzymes in the form of subconjunctival injections of gemase, fibrinolysin, lecozyme, lidase, chymotrypsin in the form of compresses, etc.;

Angioprotectors: dicynone (sodium etamsylate) - parabulbarno, intravenously or in tablets, ascorutin in tablets, aminocaproic acid intravenously;

Diuretics: oral diacarb, lasix intramuscularly or intravenously, oral glycerol, intravenous mannitol;

Antihistamines: suprastin, tavegil, claritin, diphenhydramine, diazolin in tablets or intramuscularly;

Detoxification agents: for infusions, isotonic solution of sodium chloride, gemodez, reopoliglyukin, glucose, polyphenam;

Analgesics and tranquilizers: tramal, relanium, phenazepam, etc. in the form of tablets or intramuscular injections.

Depending on the clinical manifestations of eye contusion, various surgical interventions are performed.

Ticket 22

Blood supply to the eyeball. Ophthalmoscopic picture of the fundus in case of circulatory disorders in the central artery and vein of the retina.

Arterial system of the organ of vision

The main role in the nutrition of the organ of vision is played by ophthalmic artery- from the internal carotid artery.

Through the optic canal, the ophthalmic artery enters the cavity of the orbit and, being first under the optic nerve, then rises from the outside upwards and crosses it, forming an arc. All the main branches of the ophthalmic artery depart from it.

Central retinal artery- a vessel of small diameter, coming from the initial part of the arc of the ophthalmic artery.

The central retinal artery emerges from the optic nerve stem, dichotomously divides up to the 3rd order arterioles, forming a vasculature that feeds the retinal medulla and the intraocular part of the optic nerve head. It is not uncommon to see an additional source of nutrition for the macular zone of the retina in the fundus of the eye during ophthalmoscopy.

Posterior short ciliary arteries- branches of the ophthalmic artery, which approach the sclera of the posterior pole of the eye and, perforating it around the optic nerve, form the intrascleral arterial Zinn-Haller circle.

They also form the choroid itself - the choroid. The latter, through its capillary plate, nourishes the neuroepithelial layer of the retina (from the layer of rods and cones to the outer plexiform inclusive).

Two posterior long ciliary arteries depart from the trunk of the ophthalmic artery - nourish the ciliary body. They anastomose with the anterior ciliary arteries, which are branches of the muscular arteries.

Muscular arteries are usually represented by two more or less large trunks - the upper one (for the muscle that lifts the upper eyelid, the upper straight and upper oblique muscles) and the lower one (for the rest of the oculomotor muscles).

At a distance of 3-4 mm from the limbus, the anterior ciliary arteries begin to divide into small branches.

medial arteries eyelids in the form of two branches (upper and lower) approach the skin of the eyelids in the area of ​​their internal ligament. Then, being located horizontally, they anastomose widely with the lateral arteries of the eyelids extending from the lacrimal artery. As a result, arterial arches of the eyelids are formed - upper and lower.

The supply of the conjunctiva of the eyeball is carried out by the anterior and posterior conjunctival arteries.

lacrimal artery departs from the initial part of the arc of the ophthalmic artery and is located between the external and superior rectus muscles, giving them and the lacrimal gland multiple branches.

supraorbital artery- nourishes the muscles and soft tissues of the upper eyelid.

Ethmoid arteries are also independent branches of the ophthalmic artery, but their role in the nutrition of the orbital tissues is insignificant.

Infraorbital artery, being a branch of the maxillary, penetrates into the orbit through the lower orbital fissure.

The facial artery is a fairly large vessel located in the medial part of the entrance to the orbit. In the upper section it gives off a large branch - the angular artery.

Venous visual system

The outflow of venous blood directly from the eyeball occurs mainly through the internal (retinal) and external (ciliary) vascular systems of the eye. The first is represented by the central retinal vein, the second - by four vorticose veins.

The fundus of the eye is the inner surface of the eyeball visible during ophthalmoscopy, including the optic disc, the retina with vessels and the choroid.

The fundus of the eye is normally red in ophthalmological examination with a conventional light source. The color intensity depends mainly on the amount of retinal (in the retina) and choroidal (in the choroid) pigment. On the red background of G., the optic disc, macula, and retinal vessels stand out. The optic disc is located medially from the central part of the retina and has the appearance of a clearly defined pale pink circle or oval with a diameter of about 1.5 mm. In the very center of the disc, at the exit point of the central vessels, there is almost always a depression - the so-called vascular funnel; in the temporal half of the disc, there is sometimes a cup-shaped depression (physiological excavation), which, unlike the pathological depression, occupies only part of the disc.

From the center of the optic disc or slightly medially from it, the central retinal artery (a branch of the ophthalmic artery) emerges, accompanied by the vein of the same name located outward from it. The artery and vein divide into two main branches, going up and down. Often, the division of the central retinal artery occurs even in the trunk of the optic nerve behind the eyeball, in which case its upper and lower branches appear separately on the head. The superior and inferior arteries and veins on or near the disc branch into smaller ones. The arterial and venous vessels of the retina differ from each other: the arterial vessels are thinner (the ratio of the caliber of arterioles and venules of the retina is 2:3) and lighter, less tortuous. Fluorescein angiography is an additional research method by which the condition of the fundus vessels is determined. When examining G., the area of ​​the yellow spot with the central fossa, located outward from the temporal border of the optic nerve head, is extremely important. The yellow spot is distinguished by a darker color and has the shape of a horizontally located oval. In the center of the yellow spot, a dark round spot is visible - a dimple.

Superficial keratitis (etiology, clinical forms, diagnosis, principles of treatment).

Bacterial keratitis usually appear as a creeping ulcer.

It causes pneumococcus, streptococcus and staphylococcus, the provoking factor is usually trauma - the introduction of a foreign body, accidental scratches with a tree branch, a sheet of paper, a dropped eyelash. Often small damages go unnoticed.

It begins acutely: lacrimation, photophobia appear, the patient cannot open his eye on his own, severe pain in the eye disturbs.

On examination, pericorneal injection of vessels, a yellowish infiltrate in the cornea are revealed. After its decay, an ulcer is formed, prone to spread.

A creeping ulcer is often accompanied by the formation of a hypopyon - a sediment of pus in the anterior chamber with a flat horizontal line.

The presence of fibrin in the moisture of the anterior chamber leads to gluing of the iris with the lens. The inflammatory process "creeps" not only on the surface, but also deep down to the Descemet's membrane, which resists the lytic action of microbial enzymes for the longest time.

A smear of the contents of the conjunctival cavity or scraping from the surface of a corneal ulcer in order to identify the causative agent of the disease and determine its sensitivity to antibacterial drugs, then prescribe treatment aimed at suppressing infection and inflammatory infiltration, improving corneal trophism.

To suppress the infection, AB is used: levomycetin, neomycin, kanamycin (drops and ointment), tsipromed, okatsin.

In order to prevent iridocyclitis, installations of mydriatics are prescribed. The frequency of their instillation is individual and depends on the severity of the inflammatory infiltration and the reaction of the pupil.

Steroid preparations are prescribed topically during the period of resorption of inflammatory infiltrates after the surface of the ulcer is epithelialized.

Bacterial keratitis most often ends with the formation of a more or less dense thorn in the cornea. With a central location of turbidity, restorative surgical treatment is carried out no earlier than a year after the inflammatory process subsides.

Marginal keratitis occur in inflammatory diseases of the eyelids, conjunctiva and meibomian glands.

Causes: microtrauma or destructive effect of conjunctival secretion toxins.

With prolonged conjunctivitis, barely noticeable gray dots first appear along the edge of the cornea, which quickly turn into nodules. With timely treatment, they quickly dissolve, leaving no trace. In other cases, the nodules merge into a continuous marginal semilunar infiltrate, prone to ulceration.

Marginal ulcers are characterized by abundant neovascularization from the vessels of the marginal looped network, but despite this, they do not heal for a long time. After scarring, rather coarse opacities sometimes remain, but they do not affect the function of the eye.

Treatment should be aimed at eliminating the cause of the disease, otherwise it is the same as for other corneal ulcers.

Fungal keratitis - rarely, they are caused by molds, radiant and yeast fungi.

Subjective symptoms and pericorneal vascular injection are mild in the presence of a fairly large lesion in the cornea. A white or yellowish color of the focus of inflammation, which has clear boundaries, is characteristic. Its surface is dry, the infiltration zone is similar to a saline inkrstat, sometimes it is bumpy or cheesy, as if it consists of grains and slightly protrudes above the surface of the cornea. The focus is usually surrounded by a restrictive roller of infiltration.

The clinical picture can be as if frozen for several days or even 1-2 weeks. However, the changes are gradually increasing. The infiltration roller around the focus begins to collapse, the corneal tissue becomes necrotic. At this time, the entire white, dry-looking lesion can separate on its own or can be easily removed with a scraper.

Under it, a recess opens, which slowly epithelializes, and is subsequently replaced by a walleye.

Fungal keratitis is characterized by the absence of neovascularization. Creeping ulcers of a fungal nature are usually combined with hypopyon.

In the treatment of fungal keratitis, oral itraconazole or ketoconazole, nystatin, or other drugs to which a particular type of fungus is sensitive is prescribed. Instillations of amphotericin, nystatin, sulfadimisin and actinolysate are used locally (for actinomycosis). Intraconazole is prescribed 200 mg orally once a day for 21 days.

Light eye damage

Blepharophimosis is a narrowing and shortening of the palpebral fissure, that is, a decrease in its horizontal and vertical dimensions. This is due to the formation of adhesions, fusion of the edges of the eyelids, more often from the outer edge.

The disease contributes to the formation of concomitant pathology, psychological problems may appear due to an external defect.

Causes

The disease can be congenital or acquired.

The main causes of the congenital form.

• A rare genetic disease with an autosomal dominant pattern of inheritance. Distant relatives can be sick, parents are usually outwardly healthy. Males are more commonly affected. It is combined with other anomalies of the eyes and disorders of the cardiac, skeletal, and reproductive systems.
• Exposure to negative factors during fetal development that disrupt the formation of the eyelids and palpebral fissure. Particularly important are the second month of pregnancy - the time of laying the eyelids, and the seventh, when they split into the upper and lower eyelids.

The acquired form is more common than the congenital form, it develops against the background of chronic inflammatory diseases of the organs of vision. With long-term blepharitis, conjunctivitis, trachoma, there may be the formation of adhesions in the area of ​​the outer canthus. A number of diseases of the endocrine, nervous, and muscular systems can contribute to the emergence of pathology.

Features of the congenital form

Congenital defects in this pathology:

• myogenic - eyelid dysplasia, including dystrophy of the circular muscle of the eye that lifts the upper eyelid;
• neurogenic - the formation of the oculomotor nerve is disturbed.

May manifest as an isolated external defect or as part of a systemic lesion when other developmental stigmas are present:

• microphthalmos;
• widely spaced eyes;
• microcephaly;
• syndactyly (fusion of fingers, the presence of a skin membrane between them);
• mental development disorders.

Classification of the congenital form of the disease:

• blepharophimosis and bilateral ptosis;
• telecanthus (wide-spaced eyes), ;
• telecanthus, ptosis, epicanthus.

Symptoms

There is a narrowing of the palpebral fissure due to the drooping of the upper eyelid. Shortening of the palpebral fissure from the side of the inner corner of the eye is formed due to the epicanthus (small semilunar skin fold); from the side of the outer corner of the eye - due to the fusion of the eyelids, which may be an acquired defect.

Characterized by low mobility of the upper eyelid, tension and incomplete closure of the eyelids due to adhesions in the corners of the palpebral fissure, eversion of the lower eyelids.

Diagnostics

The following medical activities are carried out:

• genealogical history (survey and examination of parents and relatives, especially in the male line);
• examination (mobility of the eyelids, the size of the palpebral fissure, the presence of scars or adhesions in the eyelids).

In order to see better with ptosis, a person strains the muscles of the forehead, tries to raise his eyebrows, throws back or tilts his head.

With a direct look, the eyelid is lowered; when looking down, it is located higher than the eyelid of a healthy eye.

Treatment

Only surgical correction will solve the problem. The formation of the muscles of the eye and eyelids ends at the age of three. After that, it is optimal to operate on the patient. Before surgery, parents are advised to lift the child's upper eyelid with a band-aid to avoid visual impairment.

The operation is carried out in two stages:

• palpebral fissure correction - canthoplasty;
• ptosis correction - the upper eyelid is sutured to the frontal muscles or the muscle that lifts the upper eyelid is shortened.

It is important to pay attention to the presence of blepharophimosis in time and consult an ophthalmologist, especially if there are similar cases among relatives. After all, it is necessary to make a surgical correction in time. So you can avoid the development of psychological problems in adolescence and serious complications from the organs of vision.