Syndrome of the superior orbital fissure includes. Syndrome of the superior orbital fissure: symptoms, diagnosis, treatment

sphenoidal fissure syndrome)

combination of complete ophthalmoplegia with corneal anesthesia, upper eyelid and the homolateral half of the forehead, due to damage to the oculomotor, trochlear, abducent and ophthalmic nerves; observed in tumors, arachnoiditis, meningitis in the region of the superior orbital fissure.

1. Small medical encyclopedia. - M.: Medical Encyclopedia. 1991-96 2. First health care. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

See what "Syndrome of the superior orbital fissure" is in other dictionaries:

- (syndromum fissurae orbitalis superioris; syn. sphenoidal fissure syndrome) a combination of complete ophthalmoplegia with anesthesia of the cornea, upper eyelid and homolateral half of the forehead, due to damage to the oculomotor, block, abductor and ... ... Big medical dictionary

- (syndromum fissurae sphenoidalis; Greek sphenoeides wedge-shaped) see Syndrome of the superior orbital fissure ... Big Medical Dictionary

Painful ophthalmoplegia syndrome Synonym: Toloz-Hunt syndrome. Ophthalmoplegia steroid sensitive. Aseptic inflammation (pachymeningitis) of the outer wall of the cavernous venous sinus or superior orbital fissure, manifested by sharp pains in the orbit in the zone of innervation of the first ...

Foix Syndrome (1)- Combined lesion III, IV, VI and the first branch of V cranial nerves. It is characterized by various variants of strabismus, inhibition of the corneal reflex and superficial sensitivity in the upper part of the face, and sometimes pain in the orbit. Sign ... ... Encyclopedic Dictionary of Psychology and Pedagogy

- (syndromum apicis orbitae) a combination of the syndrome of the superior orbital fissure with signs of damage optic nerve(atrophy of the optic disc, decreased visual acuity and narrowing of the boundaries of the visual field); observed in the localization of the inflammatory ... Big Medical Dictionary

Rolle's Orbital Apex Syndrome- A combination of signs of the syndrome of the superior orbital fissure, damage to the optic nerve, as well as exophthalmos, vasomotor and trophic disorders in the orbital zone. A likely sign of a tumor in the eye socket. Described by the French neurologist J. Rollet ... ... Encyclopedic Dictionary of Psychology and Pedagogy

- (J. S. Collier, 1870 1935, English neuropathologist) a combination of signs of unilateral damage to the oculomotor and ophthalmic nerves with periostitis in the region of the superior orbital fissure ... Big Medical Dictionary

- (nervi craniales; synonym for cranial nerves) nerves extending from the brain or entering it. There are 12 pairs of C. n., which innervate the skin, muscles, glands (lacrimal and salivary) and other organs of the head and neck, as well as a number of organs ... ... Medical Encyclopedia

Syndrome of the superior orbital fissure is a painful ophthalmic pathology, which is a fairly rare disease. The disease is accompanied not only by severe discomfort, but also by a number of neurological manifestations, in particular cranial nerve dysfunction. Let's look at what constitutes the syndrome of the superior orbital fissure. Photos will allow you to understand the overall picture of the pathology.

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What is the disease?

Syndrome of the superior orbital fissure consists in damage to the structure of tissues passing in the region of the ophthalmic veins and arteries. In some cases pathological changes may affect the trochlear, oculomotor, and abducens nerves. The combination of these manifestations is reflected in the formation of a stable pain syndrome in the region of the ophthalmic orbit. Ultimately, significant vision problems are observed.

Syndrome of the superior orbital fissure: causes

The mechanism of development of the syndrome is still not fully understood. It is only known for sure that it can be generated by:

neurological pathologies;
mechanical damage to the orbit of the eyes;
brain tumors that are located near the eye sockets;
inflammatory processes in the structure of the cerebral cortex;
meningitis that develops in the region of the orbital fissure.

The syndrome of the superior orbital fissure equally affects both the female and male part of the population. Especially often the pathology occurs in people in old age.

Syndrome of the superior orbital fissure: symptoms

Often, the manifestations of the disease occur rapidly, without prerequisites preceding it. You can determine the development of the disease by severe discomfort in the area behind eyeball. An additional symptom in this case is often aching pain in the superciliary, temporal or frontal zone.

A few weeks after the activation of the above clinical manifestations a feeling of double vision is added, the inability to control one of the eyeballs. All this eventually develops into strabismus on the side where discomfort is most pronounced.

Quite often, the syndrome of the superior orbital fissure is expressed by lesions of various optic nerves in separate combinations. For this reason, some patients may experience prolonged conjunctivitis, while others may experience exophthalmos.

Usually, the pain syndrome persists until the full manifestation of the clinical picture of the disease, which takes about two months. In some cases, the symptoms are supplemented by sharp jumps in body temperature, inexplicable changes in indicators during sequential blood tests.

Diagnostics

Studies aimed at identifying the syndrome of the superior orbital fissure are multifaceted. At the first suspicion of the development of the disease, an ophthalmologist is consulted. The specialist performs diagnostics of visual acuity and visual fields. Next, the patient is sent to a neurologist, who collects an anamnesis and conducts a comprehensive examination.

Subsequent diagnosis is performed using neuroimaging methods. Here they resort to MRI and CT of the brain, echography and angiography of the orbits of the eyeballs. According to the requirements that apply to the final diagnosis, it is possible to judge the presence of the syndrome of the superior orbital fissure only if granulomatous inflammation of the cavernous sinuses is detected by magnetic resonance imaging.

Treatment

To date, the only productive method of therapy for the development of the syndrome of the superior orbital fissure is the use of steroids. Positive results with such drug treatment observed on the first day.

With the development of this pathology, doctors who study the problem note a fairly high efficiency of corticosteroids. Usually, the patient is prescribed prednisolone tablets or its analogues.

In general, it is rather difficult for specialists to conduct controlled studies using placebo on a sample of experimental subjects, which would allow to distinguish truly effective drugs. The reason for this is the relative rarity of the disease.

Eventually

Therapy aimed at eliminating the syndrome involves, first of all, the identification of factors that provoke the manifestation of pathology. Therefore, when identifying the first symptoms of the disease and their accompanying conditions, it is extremely important to immediately seek help from an ophthalmologist for a set of diagnostic procedures.

If a negative impact occurs on the upper region of the orbital fissure, which connects the middle cranial fossa with the orbit, the syndrome of the superior orbital fissure may appear. As a result of this process, III, IV, VI nerves of the skull, the first branch of the V nerve are affected.

There is complete ophthalmoplegia and anesthesia of various parts of the eye - the cornea, upper eyelid, homolateral half of the frontal part.

Causes of the syndrome

The occurrence of the syndrome is due to a number of lesions of the nerves around the eye. From the negative impact suffer:

oculomotor;
block;
diverting;
ophthalmic nerve.

The syndrome can occur as a result of mechanical damage to the eye, and also become a consequence of various diseases in the human body:

The most common cause of the syndrome is the appearance of tumors in the brain. If they are close to the eye, they can cause nerve damage.
The syndrome has been observed arachnoid. In this case, it is caused by inflammation of the arachnoid membrane in the brain.
At meningitis in the area of the upper fissure of the eye, a complication may occur.
If a the orbit of the eye was injured, then damage can lead to the onset of the syndrome.
Sometimes the syndrome is caused hit foreign body in the eye area. As a result of this, compression of the nerve endings and veins in the upper region of the orbit can occur.

Symptoms of the disease

For the syndrome of the superior orbital fissure, the following symptoms are characteristic:

When the upper eyelid droops, ptosis. The palpebral fissure may be completely or partially closed.
As a result of development pathological condition oculomotor nerves, the occurrence of eye muscle paralysis. This state is called ophthalmoplegia. In a sick person, there is a lack of motor activity of the eyeball.
The skin of the eyelids and cornea becomes less sensitive with tactile contact.
After the lesion, the pupil may dilate ( mydriasis). This condition is caused by a decrease in the amount of light, as well as poisoning with chemicals.
With the syndrome dilated retinal veins, as well as changes in the arteries.
As a result of defeat trigeminal nerve the cornea becomes inflamed. The process is called neuroparalytic keratitis and proceeds sluggishly.
Sometimes there is the occurrence of bulging - exophthalmos, at which the protrusion of the eyeball occurs.

Signs of the syndrome may not be fully revealed. It depends on the degree and amount of nerve damage. If the patient feels two or more alarming signs, it is necessary to urgently visit a doctor for examination.

Diagnosis of the syndrome

Diagnosis of the syndrome is difficult due to the similarity of its symptoms to other diseases. The occurrence of symptoms observed in the syndrome may be due to manifestations:

parasellar and tumors of the middle fossa of the skull, pterygoid bone, pituitary gland;
retrobulbar volumetric processes;
aneurysms of the carotid artery;
periostitis;
osteomyelitis, etc.

Also, the symptoms are characteristic of myasthenic disorders, diseases thyroid gland, temporal arteritis, meningitis, multiple sclerosis, migraine with aura. All diseases can become a source of ophthalmoplegia as a result of dysfunction of the nerves of the cranial region.

Therefore, when contacting a medical institution, the patient must undergo a diagnosis. At the first stage, an examination by an ophthalmologist is shown. He examines the field and visual acuity, the condition of the fundus.

After examining the eyes, a neurologist is connected to work. The doctor interviews the patient during the history taking. A detailed inspection is also shown.

Among the methods instrumental diagnostics allocate:

CT (computed tomography) brain and Turkish saddle;
MRI(magnetic resonance imaging) of the brain and the Turkish saddle.
also held angiography and echography.

If granulomatous inflammation of the outer wall of the cavernous sinus is detected during the diagnosis during an MRI study, then Tholos-Hunt syndrome is diagnosed.

A biopsy is performed to confirm the result. In the absence of a granuloma, a diagnosis of "syndrome of the superior orbital fissure" is made.

Methods of therapy and prevention

The syndrome is treated with immunosuppressive therapy. In studies conducted in the choice of therapy for this disease, corticosteroids showed the highest efficiency.

When diagnosing the syndrome, the patient may be prescribed Prednisolone, as well as a drug with a similar effect, Medrol. When taking tablets, a dosage of 1 to 1.5 mg is observed, depending on the patient's body weight (the indicated dosage is multiplied by the number of kg). Also, the drug is administered intravenously. A daily dose of 500 to 1000 mg is indicated.

The result after the use of steroids is evaluated after 3 days. If the diagnosis is correct, then the symptoms should disappear. However, the drug helps to reduce the symptoms that also appear when:

pachymeningitis;
chordome;
lymphoma;
aneurysm;
carcinoma.

Therefore, it is important to correctly diagnose so that treatment is carried out in the direction of its elimination. Also during symptomatic therapy, analgesics and anticonvulsants are used to reduce pain. The intake of general metabolic agents and vitamins is shown to strengthen all body systems.

Preventive measures are applied depending on the disease that provoked the syndrome of the superior orbital fissure. If the syndrome is the result of trauma, then further damage to the eye should be avoided. This can lead to irreversible consequences.

The main rule after the onset of the syndrome is an emergency consultation of an ophthalmologist and a neurologist. They will help to diagnose the disease in time and prevent complications by prescribing therapy.

The superior orbital fissure is located on the border of the outer and upper wall deep in the eye. 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.

There are blood vessels in the eye sockets adipose tissue, external muscles, nerves and eyeballs, which are in limbo, 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. On three sides, the orbit is in contact with paranasal sinuses nose, therefore, in medical practice, there are often cases when various infectious and inflammatory processes 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 multiple different states: from mechanical damage to diseases.

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

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

In the syndrome of the superior orbital fissure, there is a certain clinical picture 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 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. Upper eyelid omitted. 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. This condition is preceded by diseases of the central nervous system, which allows 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 if necessary, they will redirect you to a neurologist, etc.

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.

Video with exercises for the eyes:

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 yellow spot. 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

The solution is instilled into the conjunctival sac local anesthetic(dikain 0.25% or trimekain 3%) - 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 appoint antihistamine(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 change in the diameter of the tubules

- Suction ability of the lacrimal sac

- Negative pressure created in the nasal cavity during aspiration air movement.

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: enter into channel rr fluroscein.

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.

Protective role - due to the abundance of lymphocytes, plasma cells, neutrophils, mast cells and the presence of Ig.

Research methods: Eversion of the upper and lower eyelids.

Non-penetrating wounds of the eyeball and tactics of rendering emergency care with 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 corneal wounds may have 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 drug use depend on the dynamics 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 spasms of accommodation of a semi-persistent and persistent nature in children with refractive errors and in complex therapy inflammatory diseases anterior section eyes to prevent the development of posterior synechiae.

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 - with 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 posterior thigh 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.

Device for the study of the field of view - 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 color. 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 colors, a slightly narrower field in red and the narrowest field in 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 chiasm of intersecting 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.

Bleeding into the anterior chamber (hyphema) is the most common symptom eye contusion. Cluster a large number 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 - there is a very sluggish or no reaction to light, but there is a reaction to mydriatics. 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 topical and general use, including AB 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 sodium solution chloride, hemodez, 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 soft tissues 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 is the inner surface of the eyeball visible during ophthalmoscopy, including the optic disc, retina with vessels and 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 this case the upper and lower branches it is shown on G. separately. 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. Additional method a study by which the state of the vessels of the fundus is determined is fluorescein angiography. Extremely importance when examining G., the village has an area of yellow spot with a central fossa, located outward from the temporal border of the optic nerve head. 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 eyes on his own, disturb severe pain in the eye.

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 into 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 the corneal ulcer to identify the causative agent of the disease and determine its sensitivity to antibacterial drugs followed by treatment aimed at suppressing the infection and inflammatory infiltration, improvement of 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, a restorative surgery not earlier than a year after the subsidence of the inflammatory process.

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. At 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

There is complete ophthalmoplegia and anesthesia of various parts of the eye - the cornea, upper eyelid, homolateral half of the frontal part.

Causes of the syndrome

The occurrence of the syndrome is due to a number of lesions of the nerves around the eye. From the negative impact suffer:

oculomotor;
block;
diverting;
ophthalmic nerve.

The syndrome can occur as a result of mechanical damage to the eye, and also become a consequence of various diseases in the human body:

Symptoms of the disease

For the syndrome of the superior orbital fissure, the following symptoms are characteristic:

Diagnosis of the syndrome

Diagnosis of the syndrome is difficult due to the similarity of its symptoms to other diseases. The occurrence of symptoms observed in the syndrome may be due to manifestations:

parasellar and tumors of the middle fossa of the skull, pterygoid bone, pituitary gland;
retrobulbar volumetric processes;
aneurysms of the carotid artery;
periostitis;
osteomyelitis, etc.

Also, the symptoms are characteristic of, thyroid diseases, temporal arteritis, meningitis,. All diseases can become a source of ophthalmoplegia as a result of dysfunction of the nerves of the cranial region.

After examining the eyes, a neurologist is connected to work. The doctor interviews the patient during the history taking. A detailed inspection is also shown.

Among the methods of instrumental diagnostics are:

(computed tomography) of the brain and sella turcica;
(magnetic resonance imaging) of the brain and the Turkish saddle.
also held angiography and echography.

If granulomatous inflammation of the outer wall of the cavernous sinus is detected during the diagnosis during an MRI study, then Tholos-Hunt syndrome is diagnosed.

A biopsy is performed to confirm the result. In the absence of a granuloma, a diagnosis of "syndrome of the superior orbital fissure" is made.

Methods of therapy and prevention

The syndrome is treated with immunosuppressive therapy. In studies conducted when choosing therapy for this disease, corticosteroids showed the highest efficiency.

The result after the use of steroids is evaluated after 3 days. If the diagnosis is correct, then the symptoms should disappear. However, the drug helps to reduce the symptoms that also appear when:

pachymeningitis;
chordome;
lymphoma;
aneurysm;
carcinoma.

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.

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:

brain tumors located in the eye socket;
arachnoiditis - inflammatory diseases of the arachnoid membrane of the brain;
meningitis in the area of the upper orbital fissure;
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.

Video with exercises for the eyes:

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.

outdoor. It is formed by the zygomatic bone from below, the upper jaw (its frontal process), the frontal, lacrimal, nasal and ethmoid bones.
Inner zone. It originates from the anterior end of the infraorbital fissure.
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:

Mechanical damage, eye injury.
Tumors located in the brain.
Inflammation of the arachnoid membrane of the brain.
Meningitis.
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.

A combination of several signs or individual of them indicate 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.