Today, “eye” symptoms as signs of brain damage include (A.V. Gorbunov, A.A. Bogomolova, K.V. Khavronina, 2014):

■ retinal hemorrhages;
■ the appearance of blood in the anterior chamber of the eye in the vitreous body (Terson's syndrome);
■ transient mononuclear blindness;
■ paresis of gaze due to damage to the cortical "center of gaze" (Prevost's symptom);
■ diplopia and strobism;
■ gaze paralysis to the side while maintaining consciousness;
■ strabismus, in which the eyeball on the side of the lesion is turned downward and inward, and the other - upward and outward (Hertwig-Magendie syndrome);
■ diplopia and oculomotor disorders;
■ Blindness in both eyes or bilateral hemianopia with possible preservation of central tubular vision.

EXPLANATION
Since the eye is part of the apparatus of the nervous system, circulatory disorders and subsequent cerebral hypoxia are risk factors for the onset and development of ocular ischemic syndrome. The ophthalmic artery is the first intracranial branch of the internal carotid artery (ICA), which largely determines its participation in the blood supply to the brain. Pathological changes in the extracranial and intracranial segments of the great vessels negatively affect not only the blood circulation parameters of the cerebral vessels, but also exacerbate violations of the blood circulation parameters of the eye vessels, which leads to the progression of ocular ischemic syndrome. W. Gowers in 1875 for the first time associated the appearance of right-sided hemiplegia and blindness in the left eye (optic-pyramidal syndrome) with unilateral occlusion of the ICA, which marked the beginning of the study of the problem of vascular lesions of the brain.

Pathology of the ICA can be accompanied by circulatory disorders not only in the basin of the ICA itself, but also in the basin of its branches involved in the blood supply to the structures of the eye. ICA stenosis can be manifested by a spectrum of “eye” symptoms, so patients with ICA pathology may seek medical help from an ophthalmologist for the first time. Detection of retinal hemorrhages in a patient with clinical signs of acute circulatory disorders (ACV) allows us to consider the process as a developed hemorrhagic stroke. With hemorrhage, along with hemorrhagic foci in the retina, blood may appear in the anterior chamber of the eye in the vitreous body (Terson's syndrome). Dynamic disturbance of blood flow in the ICA proximal to the origin of the ophthalmic artery is manifested by Petzl's vascular crisis. With it, on the side of the hemodynamic disorder, a short-term visual impairment occurs - transient mononuclear blindness, and on the opposite side - paresthesia. The formation of a lesion in the basin of the middle cerebral artery is accompanied by Prevost's symptom - gaze paresis due to damage to the cortical "center of gaze". In 1952, M. Fisher described patients with transient mononuclear blindness and subsequent contralateral hemiparesis (optopyramidal syndrome).

Clinical lesions of the vertebrobasilar system may have periodic episodes of diplopia and strobism (strabismus), in combination with other signs of damage to the brain stem or cerebellum, usually indicate the development of vascular crises in the patient by the type of transient ischemic attack in the basin of the vertebrobasilar system. Neuritis is characterized by a rapidly developing decrease in visual acuity with parallel changes in the fundus. The degree of reduction in visual acuity depends on the intensity of inflammation and the degree of damage to the papillomacular bundle. The more he is struck, the sharper the visual acuity is reduced. The change in visual fields in neuritis is characterized by concentric narrowing and the presence of positive central scotomas. The narrowing of the visual fields can be uniform and uneven, which is also affected by the localization and severity of inflammation. With neuritis, central scotomas are recorded less frequently than with retrobulbar neuritis. With retrobulbar neuritis, vision usually drops significantly and quickly - within a few hours. More often one eye suffers, pain in the eye may be disturbing, slight exophthalmos can be observed. With the development of an infarction focus at the base of the brainstem at the level of the pons, more often due to occlusion of the paramedial branches of the basilar artery (BA), it is possible to develop a "locked-in" syndrome, or ventral pontine syndrome or blocking syndrome - tetraplegia, pseudobulbar palsy and paralysis of gaze to the side with preserved conscious and normal electroencephalogram. Also, in violation of hemodynamics in the brain stem, Hertwig-Magendie syndrome is possible. This is a special form of strabismus, in which the eyeball on the side of the lesion is turned downward and inward, and the other is upward and outward. AD thrombosis is characterized by diplopia and oculomotor disorders, the nature of which is determined by the area of ​​formation of an ischemic focus in the brainstem, there is paralysis of gaze towards the ischemic focus that has arisen in the brain bridge. Occlusion of the BA bifurcation by an embolus or thrombus causes ischemia in the basin of both posterior cerebral arteries, this process is characterized by blindness in both eyes or bilateral hemianopsia with possible preservation of central tubular vision.

With hemodynamic disorders in the hypothalamic-mesencephalic region, Lermitt's peduncular hallucinosis sometimes occurs: peculiar visual hallucinations of the hypnotic type. Visual hallucinations in cerebrovascular pathology can also occur with a stroke in the basin of the branches of the posterior cerebral arteries. With high intracranial pressure, as a result of compression of the cavernous or sigmoid sinus, a violation of the outflow from the venous sinus of the orbit is possible, which leads to the development of exophthalmos and other oculomotor disorders. During epilepsy, with a simple absence, the patient freezes in the same position with a frozen gaze, sometimes there are rhythmic twitches of the eyeballs or eyelids, dilated pupils, visual seizures are characterized by false perceptions, in some cases there is a paroxysmal appearance of scotoma.

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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 sphincter of the pupil and approaches the muscle that lifts the upper eyelid.

Rice. 1. Motor effects and innervation of the external muscles of the eye (left eyeball)

Survey

Examination of a conscious patient includes an assessment of tracking 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 following an object is the best way to detect existing disturbances, 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, in particular 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 - the introduction of 50 ml of cold water into the external auditory canal causes a friendly abduction of the eyeballs in the direction of irritation; b — death of the 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 eyes open, it must be distinguished from monocular diplopia that occurs when looking with one eye. This disorder is not a symptom of a 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 may also involve dysfunction of the parasympathetic fibers, causing the pupil to become unresponsive to changes in illumination and dilated ( "surgical" paralysis of the third nerve) or pupillary reflexes are weakened ( "drug" paralysis). The reasons are given in table. 1.

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 the appearance of 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, the defeat of the oral part of the sympathetic nervous system can be manifested by partial ptosis along with 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 can be caused by damage to sympathetic fibers at various levels (Fig. 3).

Rice. 3. Causes of Horner's syndrome, classified according to 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 of the inner ear (labyrinth) (see below), brain stem or cerebellum, and may also occur as a side effect of drugs (eg, 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 that connect the nuclei of the abducens pontine nerves with the contralateral nuclei that provide innervation to 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 outwards are preserved, with the impossibility of movements of 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 found 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 in a patient with gaze paralysis, when examining the oculocephalic reflex, the movements of the eyeballs are preserved, there is most likely a supranuclear lesion. Extensive damage to the brainstem 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. 4. Friendly gaze palsy. The direction of 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 region 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 the cortical center of gaze, heading to the nuclei of the pons varolii 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 is bifurcated - 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 maximum when looking to the right, while the image splits 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 general practitioners. L. Ginsberg

When any of the external muscles of the eyes is paralyzed, a special clinical picture develops with its own special symptoms. Although there are quite a few such paintings, they all have a number of common features.

These signs are as follows: 1) loss of the corresponding eye movement, 2) strabismus, 3) secondary deviation of the healthy eye, 4) diplopia, 5) disorder in the perception of spatial relationships ("false projection"), 6) dizziness and 7) change in head position.

Let's take a closer look at each of these symptoms.

1. You drop this or that eye movement with paralysis of some muscle is the most simple and understandable symptom. For example, the external rectus muscle of the eye - m. rectus externus, - as you know, turns the eye outward. If, depending on the damage to the abducens nerve, it turns out to be paralyzed, then the patient will not be able to perform the test that I spoke about, that is, turn his eyes to the side. Imagine that the case is about paralysis of the right abducens nerve. The patient will fulfill your request to turn his eyes to the left well, since the corresponding mechanism is all right. But when you ask to turn the eyes to the right, the left eye will perform this movement, but the right will not: m rectus externus will not act in it.

You will observe similar phenomena with paralysis of any muscle, only the direction in which the sore eye cannot move will change.

2. Strabismus, strabismus (strabismus) - this is in essence a passive contracture already known to you - only not on the limbs, but on the eye. You remember that when a muscle is paralyzed, its antagonists bring the limb into a special forced position called contracture.

This law, common to most voluntary muscles, is also justified in the eye muscles.

If, for example, paralysis of the abducens nerve is observed, and therefore, m. recti externi, then the antagonist of the last muscle, m. rectus

interims, will pull the eyeball inward and firmly fix it in this position. This position of the eye is called strabismus.

Since in this case the eye will be close to the midline, this type of strabismus is called converging (strabismus convergens).

On the contrary, if m. rectus interims, its antagonist will pull the eye outward and fix it in this position. This type of strabismus is called divergent (strabisnms divergens).

3. The secondary deviation of a healthy eye will become clear to you if you remember that the movements of the eyeballs are associated and are performed mainly in one direction. If we arbitrarily deviate the right eye to the right, then the left eye deviates in the same direction, i.e., to the right. This means that what strength the impulse receives m. rectus extermis dexter, m. rectus interim sinister. And the greater the impulse for the first muscle, the greater it is for the second.

Now imagine that you have right abducens nerve palsy. The right eye, under the influence of a healthy antagonist, will move inwards, i.e., it will take the position of converging strabismus.

As for the healthy left eye, at first glance it would not have to undergo any changes in the installation, since everything is healthy in it. However, the clinic will show you that this is not the case: with paralysis of the right abducens nerve, the obviously healthy left eye will deviate inwards in almost the same way as the diseased right.

Converging strabismus will occur on both sides, while one eye is paralyzed.

How can we explain this seemingly strange phenomenon? When, from the moment of paralysis of the right abducens nerve, the right eye moves inward, the patient will constantly innervate the diseased muscle in order to put the eye in its normal position.

But, as I already told you, under this condition, n m will receive amplified impulses. rectus internus sinister. And from this, the left eye will be brought to the midline, i.e., it will also become in the position of converging strabismus.

So unilateral abducens nerve palsy will give bilateral strabismus.

Now imagine paralysis m. recti interni dextri. Under the action of the antagonist, the right eye will move outward, take the position of divergent strabismus. To bring the eye to its normal position, the patient will intensely innervate the paralyzed muscle. From this, the same amplified pulses will be sent to m. rectus externus sinister, since both of these muscles act in concert. But under this last condition, the left eye will be pulled outward, i.e., it will also become in a position of divergent strabismus.

So paralysis of one t. recti interni gives a bilateral divergent strabismus.

It must be clearly understood that, despite the apparent similarity of the phenomena in both eyes, their nature is profoundly different: in one eye, the deviation is of paralytic origin, in the other, if I may say so, spastic.

4. Diplopia, or double vision, is a condition when a patient, looking at one object, sees it twice. To understand its origin, you must remember the physiology of visual acts.

When we look at an object, each eye perceives it separately, but we still see one object, not two. Somewhere in the cortex there is a process of merging two perceptions into one. We do not know the mechanism of this fusion, but we do know one of the conditions necessary for this: the parallelism of the visual axes. As long as the installation of the eyeballs is such that the visual axes are parallel, we see one object with both eyes; but as soon as this parallelism disappears, the fusion disappears immediately, and the person begins to see with each eye separately, i.e. doubly. With paralysis of the eye muscles, as you already know, strabismus occurs, that is, deviation of the eyes from the normal setting. In this case, of course, the parallelism of the eye axes is violated, i.e., the main condition for the development of diplopia is given.

It is necessary, however, to make a reservation that diplopia is not always accompanied by strabismus and loss of eyeball movements, which are noticeable during a normal test. Very often, the eyes during the study perform all movements, and strabismus is not visible, but the patient still complains of diplopia. This means that the paresis of some muscle is very insignificant and it is enough only for a slight violation of the parallelism of the visual axes. To find out which muscle has paresis, they use a special research method using colored glasses. This method, the technique of which should be known to you from the course of eye diseases, solves the problem without much difficulty if it is a question of paresis of any one muscle. With combined paralysis of several muscles, the task becomes already difficult or even completely unsolvable.

5. The correct assessment of spatial relationships depends, among other things, on the state of the muscular apparatus of the eye. No matter how psychologists look at this issue, for us doctors, there can be no doubt that the degree of effort that the eye muscles make at the same time plays a big role in determining the distance.

When a muscle is paralyzed, the patient makes unusually great efforts to put the eye in its normal position. This excessive innervation corresponds to an incorrect assessment of the distance between objects and their relative position - the so-called "false projection". As a result of this, the patient, wanting, for example, to take a knife, fork, etc., from the table, constantly “misses”, stretches out his hand in the wrong direction.

6. Doubling of objects and "false projection" cause dizziness in patients. We do not know how these phenomena follow one from the other, what is their internal mechanism, but the very fact of this connection is beyond doubt. Patients themselves often notice it and struggle with the painful feeling of dizziness in such a way that they close or tie a handkerchief to the sore eye. From such a protective technique, monocular vision is obtained, in which there can no longer be either diplopia or false projection. And then the dizziness stops.

7. Blindfolding is a conscious protective technique by which the patient is saved from the consequences of paralysis of the eye muscles. There are other methods, also, in essence, of a protective nature, but not quite consciously invented. These are various peculiar postures that the head takes in such patients.

For example, with paralysis of the right abducens nerve, the right eye cannot turn outward. The patient is hard to see objects located to the right of him. To correct this defect, he turns his whole head to the right and, as it were, exposes the sore eye to the visual impressions coming from the right side,

This defensive technique becomes permanent, with the result that a subject with abducens nerve palsy can be recognized by the manner in which the head is turned in the direction of the palsy.

With paralysis m. recti interni dextri the right eye cannot move to the left, and the patient turns his whole head to the left in order to expose the affected eye to the corresponding impressions. Hence the manner of keeping the head turned to the side, i.e. essentially the same as in the previous case.

Due to the same mechanisms, patients with paralysis m. recti superioris tilt their head back a little, and with paralysis m. recti inferioris lower it down.

These are the general symptoms of paralysis of the external muscles of the eye. Knowing them, as well as the anatomy and physiology of each muscle separately, it is possible to theoretically construct a specific clinical picture of paralysis of each muscle separately, and these theoretical constructions, generally speaking, are justified in practice.

Of the particulars, the paralysis of m. levatoris palpebrae superioris - the so-called ptosis (ptosis). This is the result of damage to the oculomotor nerve; ptosis is expressed in the fact that the patient's upper eyelid remains lowered, and he cannot raise it, cannot open his eyes.

In addition to paralysis of individual muscles, there is another type of paralysis in this area - the so-called associated paralysis, or gaze paralysis. They are horizontal and vertical.

With horizontal gaze paralysis, the patient's eyes are set as if he were looking straight ahead, and there is no strabismus. But he has no movements to the sides: both eyes cannot cross the midline. Interestingly, convergence can sometimes persist.

This disorder is usually observed with lesions in the pons; apparently it is associated with damage to the posterior longitudinal bundle (fasciculus longitudinalis posterior).

With vertical gaze paralysis, the lateral movements of the eyes are not disturbed, but there are no movements up or down, or, finally, both up and down.

This symptom is usually observed with lesions in the quadrigemina.

Another type of oculomotor disorders, somewhat reminiscent of the previous one, is a friendly deviation of the eyes. It is observed most often the first time after a cerebral stroke. As a rule, it is combined with the same deviation of the head. The disorder consists in the fact that the patient's head is turned to the side, for example to the left, and the eyes are also turned to the left. When asked to turn the eyes to the right, the patient performs this movement in a small volume and for a short time, after which they again return to their previous position.

This symptom is observed with foci in different parts of the brain. The eyes are usually slanted in the direction of the hearth, less often in the opposite direction (old formulas: “the patient looks at his hearth”, “the patient turns away from his hearth”).

Another disorder of the oculomotor apparatus, already with the nature of hyperkinesis, is observed - this is nystagmus.

PARASES AND PARESIS OF THE EYE MUSCLES. Etiology and pathogenesis. They occur when the nuclei or trunks of the oculomotor, trochlear and abducent 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 occur 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 deviated 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 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.