Paresis of the abducens optic nerve treatment. Causes and treatment of paresis of the oculomotor nerve

Ophthalmoplegia - paralysis of the eye muscle or several muscles, the nervous regulation of which is carried out by the lateral, abducens, oculomotor nerve trunks.

Human eyes move due to the work of six oculomotor muscles - two oblique, four straight. Disturbances in the motor function of the eyes occur due to damage at different stages of the visual process occurring in the body: at the level of the cerebral hemispheres, cranial nerves, and muscle fibers proper.

Concomitant eye dysfunction is a slightly different pathology, therefore, it is not considered in this article. Signs of ophthalmoplegia, or violations of the movement of the eyeball, are due to the location, size, nature of the damage.

The article describes in detail the acute conditions associated with paralysis of the oculomotor muscles.

Pathology can develop on one or both sides of the face. If the muscles located on the outside of the eye are paralyzed, then we are talking about external ophthalmoplegia. Accordingly, damage to the intraocular muscles is a sign of internal ophthalmoplegia.

Among all ophthalmoplegia, partial ones are more common, in which paralytic weakness of different muscles is expressed in different ways. In this case, the diagnosis may sound like "partial internal (or external) ophthalmoplegia."

Similarly, complete external (or internal) ophthalmoplegia may develop. If the patient has paralysis of both external and internal muscles, a diagnosis of "complete ophthalmoplegia" is made.

Causes of ophthalmoplegia

The causes of ophthalmoplegia are associated mainly with pathologies of the nervous tissue. Such diseases can be congenital, or they can be the result of nerve damage during life in the area of ​​the nuclei of the cranial nerve, large nerve trunks, branches and roots.

A congenital disease is a consequence of aplasia of the nuclei of the optic nerves, anomalies in the development of the fetus with the absence of any nerves or disorders of the muscle structure. In most cases, congenital ophthalmoplegia accompanies other malformations of the eye structure, and can also be included in the symptom complex of various syndromes and genomic anomalies. Often there is a hereditary condition of ophthalmoplegia.

Causes of ophthalmoplegia, or ophthalmoparesis:

1. Myasthenia.
2. Vascular aneurysm.
3. Sudden or traumatic carotid-cavernous fistula.
4. Disthyroid ophthalmopathy.
5. Diabetic ophthalmoplegia.
6. Tolosa-Hunt syndrome.
7. Tumor, pseudotumor of the orbit.
8. cerebral ischemia.
9. Temporal arteritis.
10. Tumors.
11. Metastases in the brain stem.
12. Meningitis of various etiologies.
13. Multiple sclerosis.
14. Encephalopathy Wernicke.
15. Migraine ophthalmoplegic.
16. Encephalitis.
17. Orbital damage.
18. Cranial neuropathies.
19. Thrombosis of the cavernous sinus.
20. Miller-Fisher syndrome.
21. The state of pregnancy.
22. Psychogenic disorders.

Acquired disease - the result of damage to the central nervous system by encephalitis, other infectious diseases including tuberculosis and syphilis. Ophthalmoplegia can develop against the background of tetanus, diphtheria, botulism, toxic poisoning, radiation damage to the body. The disease is registered against the background of tumor processes in the brain, vascular pathologies, TBI.

Ophthalmoplegia is often included in the complex of symptoms of ophthalmoplegic migraine. Such a disease is expressed in severe attacks of headache, which are accompanied by ophthalmoplegia, loss of areas from the field of view.

myasthenia gravis

The initial symptoms of this disease are often double objects, ptosis upper eyelid. Sometimes there is severe fatigue after physical work, but such a sign may be absent. The patient rarely pays attention to the fact that fatigue eventually appears already in the morning, and becomes more pronounced during the day.

It is possible to accurately detect this symptom by asking the patient to close and open his eyes often. Then fatigue sets in after a couple of minutes. Medical diagnosis is reduced to performing a test with proserin while monitoring EMG.

Vascular aneurysms

Most often, congenital aneurysms are located in the anterior part of the circle of Willis. The clinical picture is unilateral paresis or paralysis of the muscles outside the eye. As a rule, paralysis occurs in the third cranial nerve. The main way to diagnose an aneurysm is MRI.

Spontaneous or traumatic carotid-cavernous fistula

All nerve endings innervating the extraocular oculomotor muscles are located in such a way that they cross the cavernous sinus. Therefore, any abnormal processes in this zone can cause paralysis of the external muscles of the eye, accompanied by diplopia. The appearance of a pathological opening - a fistula - is possible between the cavernous sinus and the carotid artery.

Often this pathology accompanies a serious head injury. Sometimes a fistula develops without visible reasons, but, as it turns out during the examination, due to the rupture of a small aneurysm. Against the background of such phenomena, the first branch undergoes changes trigeminal nerve, innervating the eyes and forehead.

The patient develops pain of characteristic localization. A preliminary diagnosis is made if clinical picture complemented by rhythmic noise in the head, which is synchronous with the beating of the heart. This noise reduces the intensity when squeezing carotid artery. The final diagnosis is made by angiography.

Diabetic ophthalmoplegia

This disease most often debuts acutely, violently and is expressed in paresis of the oculomotor nerve, pain in the head on one side. The disease belongs to diabetic neuropathies, and, as with other pathologies of the same group, sometimes occurs against the background of undiagnosed diabetes.

A characteristic feature of diabetic ophthalmoplegia is the preservation of functionality autonomic nerves directed towards the pupil. In this regard, the pupil does not expand abnormally, which is fundamentally different from paralysis of the third nerve against the background of an aneurysm.

Disthyroid ophthalmopathy

Pathology consists in an increase in the size of the external oculomotor muscles due to swelling, resulting in the development of paresis of these muscles, the phenomenon of diplopia. Dystheoid ophthalmopathy most often manifests itself in hyperthyroidism, but can also accompany hypothyroidism.

The method of diagnosing the disease is ultrasound of the orbit of the eye.

Tolosa-Hunt syndrome

This syndrome is also called painful ophthalmoplegia. It is reduced to nonspecific granulomatous inflammation in vascular wall, namely, in the cavernous sinus at the bifurcation point with the carotid artery. The disease is expressed in periorbital, retroorbital pain, which occurs due to damage to the third, fourth, fifth cranial nerve trunks, as well as one of the branches facial nerve.

As a rule, apart from local neurological signs, the patient is not bothered by anything. Pathology is successfully treated with glucocorticosteroids.

The diagnosis is made only after the exclusion of other pathologies, including severe systemic diseases (SLE, Crohn's disease), tumor neoplasms, etc.

Pseudotumor, orbital tumor

A tumor, or a pathological increase in volume of structures against the background of tumor processes, can exist in a slightly different form. The so-called "pseudotumor" develops due to inflammation of the external oculomotor muscles and their growth in size.

Swelling of tissues in the orbit can also occur with inflammation of the lacrimal glands, fatty tissue. Subjective signs are a small exophthalmos, conjunctival injection, pain behind the orbit, migraine-like pain, local pain in the head. The study is carried out with the help of ultrasound, CT of the orbit of the eye, the growth of the contents of the orbit is revealed.

Sometimes the same signs are fixed with disthyroid ophthalmopathy. In therapy, drugs of glucocorticosteroids are used.

The tumor of the orbit itself is also supplemented by compression of the second pair of nerves, which leads to a drop in vision, referred to as Bonnet's syndrome.

Temporal arteritis

The disease starts in old age. Most often, the patient is affected by the branches of the carotid artery, mainly the temporal artery. Temporal arteritis is characterized by an increase in the erythrocyte sedimentation rate, the development of pain in the muscles of the whole body. Blockage of the branch of the temporal artery in a quarter of all patients leads to loss of vision, both unilateral and bilateral.

Often accompanied by ischemia optic nerve. Ultimately, the disease can cause a lack of blood supply to the oculomotor nerves and the development of ophthalmoplegia. Often, against the background of temporal arteritis, a stroke suddenly occurs.

brain stem ischemia

Crashes in cerebral circulation in the zone of branches of the basilar artery cause damage to the third, fourth, fifth cranial nerves. The disease is characterized by the development of hemiparesis, a decrease in sensitivity in the innervated area. An acute development of a picture of a brain catastrophe is possible, which is often observed in individuals old age with a history of vascular pathologies.

Diagnosis is based on CT data, neurosonography.

Parasellar tumor

Tumor neoplasms in the pituitary gland, hypothalamus, as well as craniopharyngiomas lead to pathological disorders in the sella turcica. The clinical picture is reduced to changes in the fields of view, various hormonal disruptions, which is inherent in each type of tumor. Occasionally, the neoplasm can grow straight and outward.

The process involves the third, fourth, fifth cranial nerves. There is a slow growth intracranial pressure but not in every case.

Metastases to the brain

Ophthalmoparesis can lead to metastases of tumors in the brain stem that affect the nuclei of the oculomotor nerves. This causes the slow development of various disorders of the movement of the eyeball, which occurs against the background of an increase in intracranial pressure.

Other signs of volumetric processes join, including gaze paralysis, neurological syndromes. If the patient is affected by the zone of the pons, as a rule, paralysis of the horizontal gaze develops. The vertical gaze is paralyzed when the mesencephalon, diencephalon is affected.

Meningitis

An infectious disease can have a different nature, including being caused by Mycobacterium tuberculosis, fungi, meningococci. Non-infectious meningitis is carcinomatous, lymphomatous, etc. The disease covers the lining of the brain and affects the oculomotor nerves. Some types of meningitis do not give a headache, while others have a very severe headache.

Diagnosis consists in the study of cerebrospinal fluid, MRI or CT, radioisotope scanning.

Multiple sclerosis

Multiple sclerosis often leads to doubling of objects in the patient, as well as to other disorders of the oculomotor muscles. Often there is internuclear ophthalmoplegia, as well as damage to individual nerves. During the diagnosis, it is necessary to identify two or more pathological foci, which will prove a recurrent nature and allow excluding other brain diseases. An MRI is required, the method of evoked potentials.

Wernicke's encephalopathy

The disease is associated with a lack of vitamin B12, develops in chronic alcoholics due to malabsorption or ischemia.

It is clinically manifested by an acute lesion of the brain stem, as well as the third cranial nerve. Among the symptoms are internuclear ophthalmoplegia, nystagmus, visual dysfunction, gaze paralysis, confusion, polyneuropathy, etc.

Ophthalmoplegic migraine

Such migraine develops infrequently, no more than 16 cases per 10 thousand patients with migraine. The condition occurs mainly in childhood up to 12 years old. Where there is ophthalmoplegia, the headache is much stronger. Sometimes pain appears several days earlier than oculomotor dysfunction.

Migraine can develop once a week, sometimes more often. Angiography and MRI are performed to exclude brain aneurysms.

Pathology is differentiated with glaucoma, brain tumors, pituitary apoplexy, and the consequences of diabetes mellitus.

Encephalitis

The disease can cover some parts of the brain stem, as is observed, for example, with Bickerstaff encephalitis. This pathology is associated with the development of paresis of the oculomotor muscles, as well as other ophthalmopathic manifestations.

Eye herpes

Ocular or ophthalmic herpes develops when the body is activated or first damaged by the herpes virus. It occurs quite often - up to 15% of cases among all patients. Symptoms - rashes in the area of ​​the first branch of the facial nerve, pain in the same area, damage to the cornea, mucous membrane of the eye.

Paresis or paralysis of the external oculomotor muscles, ptosis of the eyelid, mydriasis develops, and these signs indicate the coverage of 3,4,6 nerves by pathological processes and the defeat of the Gasser node.

Orbital trauma

Injury to the orbit and hemorrhage in the cavity of the orbit often causes disruption of the oculomotor muscles due to their direct damage.

Thrombosis of the cavernous sinus

This pathology leads to severe pain in the head, fever, confusion, fainting, chemosis, eye edema, exophthalmos. When examining the fundus, the doctor reveals its swelling. Often, vision suddenly drops due to damage to the branches of the facial nerve and some cranial nerves.

After a certain time, the phenomena develop already from two sides, since through the circular sinus the pathology spreads to the second cavernous sinus. The disease often occurs against the background of meningitis, empyema of the subdural space.

Cranial neuropathies

Such conditions can be observed in severe alcohol intoxication occurring with the involvement of the central nervous system. They often cause paresis, paralysis of the eye muscles. Cranial neuropathies, polyneuropathy sometimes accompany hyperthyroidism, and can also develop idiopathically or be genetically determined.

Miller Fisher Syndrome

Pathology is expressed in ophthalmoplegia without eyelid ptosis, accession cerebellar ataxia, the absence of some reflexes. These symptoms certainly accompany Miller Fisher syndrome. In addition, the cranial nerves may be affected, with associated symptoms. Among the very rare signs of the disease are confusion, nystagmus, tremor, pyramidal symptoms. The onset of the pathology is acute, later recovery follows.

Pregnancy

During pregnancy, the risk of developing various visual impairments against the background of damage to the oculomotor muscles is increased.

Psychogenic oculomotor disorders

Such disorders are expressed in the form of gaze disorders, including convulsions or gaze paralysis. In the overwhelming majority of cases, they occur in combination with other motor disorders, as well as various manifestations of a hysterical state. A thorough individual diagnosis of psychogenic disorders is required, which necessarily implies research to identify organic damage in the central nervous system.

Symptoms of ophthalmoplegia

Clinic of external partial ophthalmoplegia: visible deviation of the eye towards the healthy side. Where the eye muscles are paralyzed, the movement of the eyeball is limited or disappears altogether.

The patient may suffer from diplopia.

Complete external ophthalmoplegia is accompanied by ptosis and lack of eye activity. Partial internal pathology is manifested by pupil dilation, worsening of the reaction to lighting. If all the internal muscles of the eye are paralyzed, in addition to these symptoms, accommodation paralysis is observed. Complete ophthalmoplegia is expressed in exophthalmos and the final immobility of the eyeball and pupil. Treatment of all types of ophthalmoplegia is to eliminate their cause.

Weakness (paresis, paralysis) of the external rectus muscle of the eye due to dysfunction of the abducens nerve (n. abducens) is a rare reversible complication of diagnostic lumbar puncture, epidural, subarachnoid anesthesia, myelography, liquor shunting interventions for hydrocephalus (the incidence of paralysis n. abducens during epidural puncture space ranges from 1:300 to 1:8000). All of the above manipulations can cause a decrease in subarachnoid pressure (intracranial hypotension syndrome) due to leakage of cerebrospinal fluid (CSF) through a puncture defect in the dura mater. Against the background of intracranial hypotension, the brain shifts caudally, resulting in traction (tension) of the cranial nerves (in turn, tension leads to local ischemia and impaired nerve function). In this case, n.abducens most often suffers, since, compared with the rest of the cranial nerves, it passes the longest path in the subarachnoid space and passes anatomical structures that are most susceptible to compression by the caudally displaced brain (for example, pressing the abducens nerve against the clivus).

The development of paresis (paralysis) of the external rectus muscle of the eye due to dysfunction n. abducens are almost always preceded by an intense headache. In 75% of cases, nerve damage is unilateral. Characteristic symptoms, including diplopia, occur within 4 to 14 days after manipulation. Changes found on magnetic resonance imaging are typical of intracranial hypotension. This is, first of all, a decrease in the volume and asymmetry of the ventricles, a diffuse thickening of the meninges. Although about 2 ⁄3 of all episodes of paralysis n. abducens completely regress 7 to 10 days after diagnosis, and in approximately 25% of patients, symptoms may persist for a month or more. In 10% of cases, the duration of paralysis exceeds 3-6 months. Differential Diagnosis should be carried out with infiltrative and inflammatory changes, vascular formations and tumor lesions (diagnostic measures, especially in patients suffering from common forms of cancer, should include a consultation with a neurologist, an ophthalmologist, magnetic resonance imaging of the brain with intravenous contrast).

Should be remembered that after confirming the diagnosis, it is necessary to explain in detail to the patient in a form accessible to him about the cause of the incident, emphasizing the reversibility of the symptoms that have arisen.

Treatment. Therapy is aimed at restoring intracranial pressure (cerebrospinal fluid volume): bed rest, fluid therapy, caffeine [for more details, see "Post-Puncture Headache"]. A faster recovery of the abducens nerve is facilitated by the appointment of combined ones containing B vitamins, as well as anticholinesterase drugs (prozerin, neuromedin). In order to prevent this complication, when performing spinal anesthesia, Pencil Point needles of the smallest possible diameter should be used. When puncturing the epidural space, it is recommended to insert the Tuohy needle in such a way that the cut of its tip is parallel to the fibers of the dura mater, i.e. vertically. In this case, with an inadvertent puncture of the dura mater, the tip of the needle "spreads" the fibers, and does not cut them off with the formation of a defect, as with the horizontal position of the needle.

© Laesus De Liro

In the oculomotor nerve, which is mixed, the nuclei lie on the aqueduct of the brain, in the covering of the legs of the brain, at the level of the superior hillocks of the roof of the midbrain.

From the medulla, the oculomotor nerve enters the zones of the medial surface of the peduncle, in the interpeduncular fossa, at the base of the brain at the anterior edge of the bridge.

Next, the oculomotor nerve is placed between the posterior cerebral artery and the superior cerebellar artery, and through the dura and upper wall cavernous sinus enters through the superior orbital fissure orbital cavity outside of the internal carotid artery.

Before entering the orbit, the nerve divides into superior and lower branches.

This nerve activates four of the six oculomotor muscles, which ensures the movements of the eyeball - adduction, lowering, raising and turning.

Complete nerve damage has characteristic syndromes. For example, ptosis, or drooping of the eyelid, or divergent strabismus, in which there is a fixed position of the eye, and the pupil is directed outward and slightly downward, since the muscles that are innervated by the fourth and sixth pair of cranial muscles do not encounter resistance.

Double vision, or diplopia, is a subjective phenomenon that occurs when the patient looks with both eyes. This effect increases if you fix your gaze on a nearby object, or when you try to turn your gaze towards the internal rectus muscle of the eye, which is paralyzed. In this case, the focusable object in both eyes is located on non-corresponding areas of the retina.

Pupil dilation (mydriasis) and lack of pupillary response to light and accommodation is also one of the symptoms of the disease and is due to the fact that this nerve is part of the reflex arc of the pupillary reflex to light.

With accommodation paralysis, there is a deterioration in vision at close distances. Accommodation of the eye is a change in the power of refraction of the eye, necessary for the realization of the possibility of perceiving objects that are at different distances from it. Accommodation is due to the state of the curvature of the lens, also regulated by the internal muscle of the eye innervated by the oculomotor nerve. When this nerve is damaged, accommodation paralysis is observed.

There is also convergence paralysis, in which it is impossible to turn the eyeballs inward, as well as restrictions on the movement of the eyeball down, up and inward, as a result of paralysis of the muscles innervated by the oculomotor nerve.

by the most common causes lesions of both the nucleus and the passing fibers of the abducens nerve are tumors, infarction, hemorrhage, multiple vascular sclerosis and malformations.

Treatment of paresis of the oculomotor nerve

Treatment of paresis of the oculomotor nerve consists in eliminating the underlying cause, but it is often extremely difficult to find out this cause, even with a comprehensive examination. Most cases are still caused by microinfarcts, which are not uncommon in diabetes, or other diseases in which microcirculation disorders are observed. In some cases, the disease develops due to infection, in particular, this can occur after the flu.

Temporary use of prisms or bandaging can reduce diplopia until the paralysis resolves. If the necessary improvement is not observed, an operation is prescribed for, which in most cases restores its position, at least in the basic position. If nerve function cannot be restored, prescribe re-treatment to search for hidden causes, which may be chordomas, carotid-cavernous fistula, diffuse tumor infiltration of the meninges, myasthenia gravis.

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Anatomy

The actions of the external muscles of the eye are shown in Fig. 1. The superior oblique muscle of the eye is controlled by the trochlear cranial nerve, the external rectus muscle is controlled by the abducent. All other muscles are innervated by the oculomotor nerve, which also carries parasympathetic fibers to the pupillary sphincter and approaches the levator levator muscle. upper eyelid.

Rice. one. Motor effects and innervation of the external muscles of the eye (left eyeball)

Survey

Examination of a conscious patient includes an assessment of the tracking of an object (doctor's finger, hammer, pen) moving in vertical and horizontal directions. The subject should follow an H-shaped path (rather than a cruciform) in order to more accurately assess eyeball movements. This makes it possible to study the functions of the external muscles of the eye relatively independently of each other (Fig. 1).

eye tracking behind the object The best way detect existing violations, since normal tracking is ensured by the integrity of all pathways involved in friendly movements of the eyeballs. The elements of this complex system can be examined separately using other clinical methods:

• Saccades- fast eye movement achieved when the doctor asks the patient to quickly look to the right, left, up or down
• Convergence- the ability of the eyeballs to adapt to near vision by friendly inward convergence, while tracking and saccades use movement at a constant distance from the eyes
• Optokinetic movements observed during rotation of the cylinder with alternating white and black stripes in front of the patient's eyes. In the normal state, slow tracking is noticeable, alternating with fast corrective saccades ( optokinetic nystagmus). These movements are absent in the patient, with oppression of consciousness. The study of optokinetic nystagmus is valuable for identifying simulated disorders of consciousness.
• Vestibulo-ocular reflex. Unlike all the methods described above, which require a sustained level of wakefulness, this test can be used in a patient with depression of consciousness. Brainstem pathways, particularly those that connect the vestibular nuclei (receive signal from the vestibular apparatus in the inner ear; see below) to nerve nuclei III, IV, and VI, can be examined in the following ways:

Rice. 2. The study of the vestibulo-ocular reflex, a - intact trunk - turning the head causes a transient movement of the eyeballs in the opposite direction - the oculocephalic reflex, or a symptom of the doll's head. This reflex is also applicable to the vertical movements of the eyeballs during tilting and lowering the head. Caloric test - injection 50 ml cold water to the outer ear canal causes friendly abduction of the eyeballs in the direction of irritation; b - death brain stem: absence of oculocephalic and caloric reactions

These tests are important in diagnosing brainstem damage in an unconscious patient.

Eyeball and eyelid movement disorders

Symptoms

The patient may complain of drooping of the upper eyelid (partial or complete ptosis).

Diplopia, or doubling, in neurological practice occurs due to misalignment of the eyeballs, as a result of which light enters different parts of the two retinas and the brain cannot combine the two images. This is the case binocular diplopia that occurs with both open eyes, should be distinguished from monocular diplopia that occurs when looking with one eye. This disorder is not a symptom neurological disease and may be due to an ophthalmic disease (eg, clouding of the lens) or, more commonly, is a functional defect.

The cause of binocular diplopia is the imbalance in the work of the external muscles of the eye and the violation of their innervation. Diplopia is always clearly identified (or there is double vision, or it is not), but its severity can vary. The patient can tell in which direction the image splits - horizontal, vertical or oblique.

Defeat syndromes

The main disorders of the oculomotor innervation are quite easily detected in a conscious patient by identifying classic syndromes using a tracking test.

Paralysis of the oculomotor nerve (III nerve)

Ptosis in its full form is caused by paralysis of the muscle that lifts the upper eyelid. When the doctor lifts the eyelid of the patient, the eye is in a position lowered down and turned outward - the result of an action that does not meet with the resistance of the superior oblique and external rectus muscles. Paralysis of the oculomotor nerve can also include dysfunction of the parasympathetic fibers, as a result of which the pupil does not respond to changes in illumination and is dilated ( "surgical" paralysis of the third nerve) or pupillary reflexes are weakened ( "drug" paralysis). The reasons are given in table. one.

Table 1. Causes of damage to the oculomotor nerve

Palsy of the trochlear nerve (IV nerve)

Isolated unilateral anterior oblique palsy may result from mild head trauma. The patient usually experiences double vision when walking down stairs and tries to keep his head bowed to compensate for the diplopia. Paralysis of the superior oblique muscle is detected when an appropriate test is performed (see below).

Abducens nerve palsy (VI nerve)

The patient cannot abduct the affected eyeball outward due to the uncontrolled action of the medial rectus muscle, in extreme cases this leads to convergent strabismus. Diplopia appears when looking to the affected side with the occurrence of a horizontal bifurcation of the image. Isolated paralysis of the VI nerve is usually associated with a violation of the blood supply to the nerve (lesion vasa nervorum) due to diabetes or hypertension. Restoration of nerve functions after such microvascular disease occurs within a few months. Paralysis of the VI nerve can also be false sign of localization with increased intracranial pressure, since the nerve has a large length and a complex path of passage through the bones of the skull. As a result, there is a high risk of damage due to increased intracranial pressure or volume effects.

Horner's syndrome

Part of the muscles responsible for lifting the upper eyelid is innervated by sympathetic nerve fibers. As a result, damage to the oral sympathetic nervous system May present with partial ptosis miosis(constriction of the pupils as a result of paralysis of the sympathetic fibers that innervate the muscle that expands the pupil). Other signs of Horner's syndrome - deep standing of the eyeball in the orbit (enophthalmos), reduced or absent sweating on the affected side of the face (anhidrosis) - are less common. The source of sympathetic innervation of the pupil is the hypothalamus. Horner's syndrome may be caused by damage to the sympathetic fibers on the various levels(Fig. 3).

Rice. 3. Causes of Horner's syndrome, classified depending on the level of damage to the sympathetic nervous system - from the hypothalamus to the eyeball

nystagmus

Nystagmus is an involuntary rhythmic swaying movement of the eyeballs that occurs when you try to fix your gaze in the extreme vertical or horizontal directions, less often observed when looking in front of you. Nystagmus can occur with the same speed of movement of the eyeballs in both directions ( pendulum nystagmus), but more often the slow phase (return to the original position from the direction of gaze) alternates with a corrective fast phase - movement in the opposite direction ( jerky nystagmus). Such nystagmus is defined as a push in accordance with the direction of the fast phase, although these are almost normal saccades, the purpose of which is to compensate for the pathological process represented by the slow component.

Classification of jerky nystagmus:

1. Appears only when looking towards the fast component.
2. Appears in the normal direction of gaze (gaze is directed straight ahead).
3. Appears when looking towards the slow component.

Nystagmus may be congenital, in which case it is usually pendular. Acquired nystagmus may be a sign of disease inner ear(labyrinth) (see below), brainstem or cerebellum, and may also occur as a consequence side effects medicines(for example, anticonvulsants). Rotational (rotary) nystagmus is observed when either the peripheral (labyrinth) or central (brain stem) parts of the vestibular analyzer are damaged. Vertical non-drug-related nystagmus usually indicates brainstem involvement and is of some value for topical diagnosis of the lesion (at the foramen magnum) if the fast phase of the nystagmus is downward when looking down. Usually patients do not feel nystagmus, although it may be associated with systemic dizziness (vertigo) (see below). Sometimes the rhythmic movements of the eyeballs with nystagmus are perceived subjectively ( oscillopsia), especially common in vertical nystagmus. At the same time, the patient is aware that the world around him moves up and down unpleasantly.

Internuclear ophthalmoplegia

A normal friendly look with both eyes to the right or left is due to the coordinated action of the external rectus muscle of one eyeball, together with the reverse action of the internal rectus muscle of the other. The anatomical basis of friendly movements of the eyeballs is medial longitudinal bundle- a strip of fast-conducting myelinated nerve fibers connecting the nuclei of the abducens nerves of the bridge with the contralateral nuclei that provide innervation of the internal rectus muscles. Due to the defeat of this conduction path, the possibility of friendly movements of the eyeballs is lost - the conditions for normal abduction of one eye outward are preserved when it is impossible to move the other eye inwards. It is also possible the appearance of nystagmus when looking to the side, more pronounced in the outwardly retracting eye. This combination of symptoms is known as internuclear ophthalmoplegia and is commonly seen in multiple sclerosis. Damage to the medial longitudinal fasciculus can also cause different vertical position eyeballs, in which one eyeball is higher than the other in all positions.

Complete or partial loss of the ability of both eyeballs to move in a certain direction is caused by supranuclear lesion pathways responsible for the movement of the eyeballs ( supranuclear gaze palsy). At the same time, the connections of the nuclei of the III, IV and VI nerves with the overlying structures suffer. As a rule, there is no diplopia, since the optical axes can remain aligned with each other.

The lesion may be due to both compression and destruction of the relevant structures (for example, hemorrhage or infarction). Supranuclear gaze palsy can be chronic and progressive, such as in extrapyramidal disorders. If the movements of the eyeballs are preserved in a patient with gaze paralysis during the study of the oculocephalic reflex, there is most likely a supranuclear lesion. Extensive damage to the brain stem or cerebral hemispheres significantly affects the level of consciousness, as well as the state of the systems responsible for the movement of the eyeballs, and may be the cause converging gaze paresis(Fig. 4). The center that controls eye movements in the horizontal direction is located in the pons (higher centers in the cerebral hemispheres); centers of vertical vision are not as well understood, but are presumably located in the upper parts of the midbrain.

Rice. four. Friendly gaze palsy. The direction of the deviation is diagnostically valuable in determining the lesion in patients with hemiparesis and impaired consciousness, a - partial epilepsy with a focus of pathological activity in one frontal lobe; eyeballs deviate towards the affected limbs, which does not correspond to the hemisphere in which the epileptic focus is located; b - destruction of one of the frontal lobes; eyeballs deviate from paralyzed limbs, since the centers that control eye movements (frontal gaze center) in the unaffected hemisphere do not send signals to resist; c — unilateral lesion of the brainstem (in the area of ​​the Parolian pons); eyeballs deviate to the affected side. The lesion is located above the intersection of the pyramids, so hemiparesis is detected on the side opposite to the lesion. However, the focus is located below the intersection of fibers from cortical center gaze directed to the nuclei of the pons and controlling the horizontal movements of the eyeballs. In this situation, an action that does not meet the resistance of the oculomotor center of the unaffected half of the bridge leads to the deviation of the eyeballs in the same direction.

Complex oculomotor disorders

Combinations of palsies of several nerves that supply the eyeballs may be different (for example, damage to the III, IV and VI nerves caused by a pathological process in the cavernous sinus or a fracture of the upper edge of the orbit), the causes of which are not established (for example, damage to the brain stem is unclear nature). It should be borne in mind the curable cause of the disease - myasthenia gravis or damage to the muscles of the eyeball due to thyroid disease.

Diplopia

In many patients with binocular diplopia, its mechanism is revealed by observing eye movements, when weakness of certain muscles is detected. In some cases, the defect is not so pronounced and the movements of the eyeballs seem normal on examination, although the patient still notes doubling. In such cases, it is necessary to determine the direction in which the diplopia is most pronounced, and also to establish in which direction the image splits - horizontal, oblique or vertical. The eyes are closed in turn and note which of the images disappears. Usually false image(for the affected eye) more distant from the center. So, in the case of assessing diplopia with one covered eyeball in a patient with mild paralysis of the right external rectus muscle, diplopia is maximal when looking to the right, while the image bifurcates horizontally. When the right eyeball is closed, the image far from the center disappears, while when the left eyeball is closed, the near one disappears.

Neurology for doctors general practice. L. Ginsberg

PARALLIES AND PARESIS OF THE EYE MUSCLES. Etiology and pathogenesis. They occur when the nuclei or trunks of the oculomotor, trochlear and abducens nerves are damaged, as well as as a result of damage to these nerves in the muscles or the muscles themselves. Nuclear paralysis is observed mainly with hemorrhages and tumors in the nuclear region, with tabes, progressive paralysis, encephalitis, multiple sclerosis, and skull trauma. Stem or basal paralysis develops as a result of meningitis, toxic and infectious neuritis, fractures of the base of the skull, mechanical compression of the nerves (for example, by a tumor), and vascular diseases at the base of the brain. Orbital or muscle lesions are found in diseases of the orbit (tumors, periostitis, subperiosteal abscesses), trichinosis, myositis, after injuries.

Symptoms. With an isolated lesion of one of the muscles, the deviation of the diseased eye in the opposite direction (paralytic strabismus). The angle of strabismus increases as the gaze moves and the direction of action of the affected muscle. When fixing any object with a paralyzed eye, the healthy eye deviates, and at a much larger angle compared to that at which the diseased eye was deviated (the angle of the secondary deviation is greater than the angle of the primary deviation). Eye movements in the direction of the affected muscle are absent or severely limited. There is double vision (usually with fresh lesions) and dizziness that disappears when one eye is closed. The ability to correctly assess the location of an object viewed by a sore eye is often impaired (false monocular projection or localization). There may be a forced position of the head - turning or tilting it in one direction or another.

Diverse and complex clinical picture occurs in cases of simultaneous damage to several muscles in one or both eyes. With paralysis of the oculomotor nerve, the upper eyelid is lowered, the eye is tilted outward and somewhat downward and can only move in these directions, the pupil is dilated, does not respond to light, accommodation is paralyzed. If all three nerves are affected - the oculomotor, block and abducent, then complete ophthalmoplegia is observed: the eye is completely motionless. There are also incomplete external ophthalmoplegia, in which the external muscles of the eye are paralyzed, but the sphincter of the pupil and the ciliary muscle are not affected, and internal ophthalmoplegia, when only these last two muscles are affected.

Flow depends on the underlying disease, but, as a rule, long-term. Sometimes the process remains persistent even after the cause has been eliminated. In some patients, double vision disappears over time due to active suppression (inhibition) of the visual impressions of the deviated eye.

Diagnosis based on accounting characteristic symptoms. It is important to establish which muscle or group of muscles is affected, for which they resort mainly to the study of double images. To clarify the etiology of the process requires a thorough neurological examination.

Treatment. Treatment of the underlying disease. Exercises for the development of eye mobility. Electrical stimulation of the affected muscle. With persistent paralysis - surgery. To eliminate double vision, glasses with prisms or a bandage over one eye are used.