Syndromes of impaired mobility of the eyeball in pathology of the central nervous system. Impaired movements of the eyeballs Causes of ophthalmoplegia, or ophthalmoparesis

PARALYSIS 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 palsies are observed mainly with hemorrhages and tumors in the nuclear area, with tabes, progressive paralysis, encephalitis, multiple sclerosis, and skull injuries. Brainstem 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 wounds.

Symptoms. With an isolated lesion of one of the muscles, the diseased eye deviates in the opposite direction (paralytic strabismus). The angle of strabismus increases as the gaze moves and the side of action of the affected muscle. When fixating an object with a paralyzed eye, the healthy eye deviates, and at a significantly larger angle compared to the one to which the diseased eye was deviated (the angle of secondary deviation is greater than the angle of primary deviation). Eye movements towards the affected muscle are absent or severely limited. There is double vision (usually with fresh lesions) and dizziness, which disappear when one eye is closed. The ability to correctly assess the location of an object viewed by the affected eye is often impaired (false monocular projection or localization). A forced position of the head may be observed - 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 drooping, the eye is deviated outward and slightly downward and can only move in these directions, the pupil is dilated, does not respond to light, and accommodation is paralyzed. If all three nerves are affected - oculomotor, trochlear and abducens, then complete ophthalmoplegia is observed: the eye is completely motionless. There is 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 is usually 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 is based on taking into account 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, a thorough neurological examination is necessary.

Treatment. Treatment of the underlying disease. Exercises to develop eye mobility. Electrical stimulation of the affected muscle. For persistent paralysis - surgery. To eliminate double vision, use glasses with prisms or an eye patch.

At the moment, stroke is increasingly affecting people, and if earlier this disease was considered senile, today many stroke patients are not even thirty years old.

This happens due to constant pollution, deteriorating living conditions, most young people are prone to bad habits, which also affects the failure of the nervous system.

The disease also has a number of negative consequences, which can then accompany the patient throughout his life.

Strabismus occurs during a stroke because the nervous system may be damaged, which contributes to the development of visual abnormalities. It is proposed to treat such strabismus in several ways at once in order to achieve the desired result as soon as possible.

Strabismus after stroke

Strabismus during stroke Source: GolovaLab.ru

In fact, partial or complete loss of vision after a stroke is quite common, occurring in about a third of patients affected by the disease. With small amounts of damage to areas of the brain, a gradual restoration of visual function is observed.

Volumetric necrotic phenomena lead to various problems with vision, up to its complete loss. In such cases, a combined course of therapy is required: taking medications and attending rehabilitation classes.

A stroke is an acute damage to the cerebral blood supply as a result of blockage or loss of integrity of blood vessels. The consequence of pathological disorders is the development of irreversible necrotic and atrophic phenomena, and as a result, the loss of certain functions.

If the pathology affects the areas of the brain responsible for vision, temporary or permanent blindness, strabismus or other abnormalities develop. Based on the symptoms, you can determine which part of the brain is affected, as well as the degree and volume of necrotic phenomena:

Loss of visual fields indicates a small volume of localized damage. This disorder is often called a “blind spot.” With relatively clear visibility, a small area appears that falls out of the field of view. In this case, as a rule, the eyes hurt. With a small amount of necrotic phenomena, vision after a stroke is restored independently, as the patient is rehabilitated. You may need to attend physical therapy and perform eye exercises.
Lack of peripheral vision - two lobes of the brain, right and left, are responsible for visual functions. The right-sided area receives visual information from the left side of the retina of both eyes. Similarly, information from the left side of the retina is processed by the right lobe of the brain. If peripheral vision disappears, it means that the brain tissue is seriously damaged. Restoring peripheral vision is possible thanks to intensive therapy and the ability of intact brain tissue to take over some of the lost functions.
Oculomotor nerve palsy - occurs due to atrophic phenomena affecting the fibers and muscles that control eye movement. As a result of the disturbances, the patient is unable to look straight. The eyes look in different directions, protrusion of the optic apple and squint are observed.

Most vision problems resulting from a stroke are reversible, provided that pathological changes are diagnosed promptly and adequate therapy is prescribed.

Pathogenesis of vision diseases

With strokes, tumors and other brain diseases, disturbances in conjugate eye movements, voluntary eye movements and strabismus occur. On the contrary, when nerves are damaged, usually only one eye is affected, and if both, then unequally.

Oculomotor disorders caused by central nervous system pathology include horizontal and vertical gaze paresis, vertical strabismus, eye dysmetria and various variants of nystagmus.

Conjugate eye movement disorders

Conjugate eye movements are provided by centers in the cerebral cortex, midbrain, pons and cerebellum and pathways. Therefore, oculomotor disorders with lesions of the central nervous system are common.

With unilateral damage to the pons involving the paramedian reticular formation or the nucleus of the abducens nerve, horizontal gaze paresis occurs in the direction of the lesion. With bilateral damage to these pontine structures, complete horizontal paresis of gaze occurs, in which eye movements are possible only in the vertical plane.

With a less severe lesion, incomplete horizontal paresis of gaze or installation horizontal nystagmus, the fast phase of which is directed towards the lesion, are possible. There are usually other neurological symptoms.

Lesions of the cerebral cortex and the upper part of the brain stem can also cause horizontal gaze paresis, usually transient - vestibulo-ocular reflexes are not impaired. Vertical eye movements are controlled by the midbrain.

When the roof of the midbrain is affected, paresis of upward gaze occurs, sometimes in combination with a weakened pupillary response to light, but a lively reaction to accommodation with convergence and converging nystagmus when attempting to look upward. In young people, these disorders are usually caused by pinealoma or hydrocephalus, in older people - by stroke.

Paresis of downward gaze is less common; it occurs with bilateral damage to the midbrain in the region of the red nucleus. Downgaze palsy can occur acutely, such as with a stroke, but usually develops gradually and is a manifestation of Parkinson's disease, progressive supranuclear palsy and other degenerative diseases of the central nervous system.

If the midbrain is damaged, there may be a violation of the parallelism of the visual axes in the vertical plane (vertical strabismus). At first glance, this pathology resembles trochlear nerve palsy, but there are still differences.

In addition, there are usually other central oculomotor abnormalities and focal neurological symptoms. Internuclear ophthalmoplegia is a common central oculomotor disorder caused by damage to the medial longitudinal fasciculus, which connects the oculomotor nuclei of the pons and midbrain.

This lesion results in paresis of the medial rectus muscle on the affected side, complete or partial impairment of adduction in that eye, and nystagmus in the other eye on lateral gaze. Internuclear ophthalmoplegia can be unilateral or bilateral and not accompanied by other neurological symptoms.

Multiple sclerosis is a common cause of acute bilateral internuclear ophthalmoplegia in young people, especially women. Unilateral ophthalmoplegia in the elderly is usually caused by lacunar infarction and often occurs against the background of diabetes mellitus, vasculitis (for example, with SLE), cerebral aneurysms and other diseases.

With central lesions, both fast and slow eye movements may be selectively impaired. Violation of saccades leads to eye dysmetry: when looking from one object to another, the eyes either “do not reach” it or “skip” it.

In severe cases, opsoclonus is expressed to varying degrees: from short bouts of saccades in the horizontal plane (ocular myoclonus) to constant chaotic saccades. These disorders can occur when the cerebellum and brainstem are affected.

Opsoclonus occurs with neuroblastoma in children and paraneoplastic syndromes, such as oat cell lung cancer, in adults. Saccades are impaired in many degenerative diseases of the central nervous system, such as Wilson's disease, spinocerebellar degenerations, and progressive supranuclear palsy.

With congenital oculomotor apraxia, the patient is unable to direct his eyes in the desired direction. During the first 2 years of life, the patient develops compensatory saccadic head movements.

Such disorders can also be acquired; they occur with damage at the level of the cerebral hemispheres and the brain stem and lead to the impossibility of saccades or the occurrence of slow or hypometric saccades.

In some diseases of the central nervous system, the smoothness of slow tracking eye movements is lost and they become intermittent. This is not always a sign of pathology; such disturbances occur, for example, with fatigue, decreased attention, or taking medications.

If slow pursuit movements are impaired in only one eye, damage to the brainstem, cerebellum, or parieto-occipital cortex should be considered. Disturbance of vergence movements can be psychogenic, and distinguishing it from an organic lesion can be difficult.

Convergence may be impaired after stroke, traumatic brain injury, or demyelinating diseases. Patients complain of double vision when looking at close objects. Eye movements are intact except for convergence.

If these problems have been present for a long time and are combined with reading difficulty, it is possible that it is congenital convergence insufficiency, not associated with nerve damage.

In some patients, convergence persists even when looking into the distance; this may be due to a convergence spasm, which is combined with a spasm of accommodation and constriction of the pupils.

Spasm of accommodation causes blurred vision; it can be of an organic nature, for example, with neurosyphilis, traumatic brain injury, encephalitis, or psychogenic, for example, with emotional overload. Divergence disorders are less common.

It is manifested by sudden convergent strabismus and diplopia, while eye movements are preserved. If the disorder occurs acutely, after an illness, the prognosis is favorable and no treatment is required. Other causes include demyelinating diseases, neurosyphilis, encephalitis and trauma.

Precursors of stroke

Hemorrhagic stroke of the brain is more typical for people over 40 years of age and with a history of diseases that are accompanied by high blood pressure (hypertension) and/or a violation of the structure and strength of the vascular wall (amyloid angiopathy, atherosclerosis, aneurysms, vasculitis), blood diseases.

Symptoms of hemorrhagic stroke manifest themselves in the form of general cerebral disorders (due to problems with hemodynamics) and focal ones, which directly depend on the location of the hemorrhage (location of the lesion) and volume (amount of blood shed).

The disease usually begins acutely and suddenly; its occurrence is provoked by high blood pressure due to hypertension or due to severe anxiety, excessive physical exertion, stress and overwork. Typical cerebral manifestations of stroke:

sharp pain in the head, which intensifies when changing body position and persists in a lying position, accompanied by nausea and vomiting;
breathing quickens, becomes noisy and wheezing (stertorous);
the pulse is tense, rapid (tachycardia) with a transition to slow (bradycardia);
blood pressure is often elevated;
manifestations of hemiplegia (paralysis of the muscles of one side of the body) or hemiparesis (the possibility of voluntary movements of half the body is sharply weakened);
the patient’s speech is difficult, understanding the speech of others is impaired;
clarity of consciousness is impaired to a state of stupor, stupor or coma.

Focal symptoms appear in combination with general symptoms and often prevail in severity. Depending on the location and extent of brain damage and the functions for which this area is responsible, the prognosis of a hemorrhagic stroke for the patient is determined.

When hemorrhage is localized in the brain stem, disturbances in vital functions are observed - breathing and heart activity.

Symptoms of damage to the nuclei of the cranial nerves often manifest themselves in the form of strabismus, nystagmus (trembling of the eyes when moving), dilated pupils (mydriasis) or unequal pupil sizes in both eyes (anisocoria), “floating” eye movements, the swallowing process is impaired, pathological pyramidal reflexes are noted in both sides

When blood enters the thalamus, paresis of vertical gaze is detected - narrow pupils that do not respond to a beam of light, drooping eyelids (ptosis) and strabismus, as well as a pronounced decrease in sensitivity (hemisthesia) and unstable unilateral muscle paresis (hemiplegia).

Lesions of the pons of the brain are manifested by miosis (constriction of the pupil) and the presence of gaze paresis in the direction of the localization of the lesion.
Hemorrhage into the cerebellum is characterized by pain in the occipital region and neck, speech impairment (dysarthria), decreased (hypotonia) or absence (atonia) of muscle tone, uncoordinated movements of various muscles (ataxia).

Eye symptoms are detected in the form of nystagmus, strabismus, in which one eye is turned downward and inward (on the affected side), and the other upward and outward. General cerebral symptoms predominate with such localization of the lesion in the case of rapid hemorrhage.

The most complex course is typical for damage to the ventricles with their breakthrough. There is a sharp deterioration in the patient's condition, with bilateral muscle hypertonicity, impaired breathing, swallowing, the appearance of hyperthermia (high temperature) and convulsions, the presence of meningeal symptoms, deep and prolonged impairment of consciousness.

The effect of the disease on the visual organs

A stroke is an acute disruption of cerebral blood supply. It occurs as a result of spasm, blockage or disruption of the integrity of blood vessels in the brain. Subsequently, irreversible necrotic and atrophic processes of the medulla develop, which leads to the loss of certain functions.

Diagnosis of causes

In the case when the affected area is localized in the areas of the brain responsible for vision, permanent or temporary permanent blindness develops, as well as strabismus and other abnormalities. Doctors can determine the location of the pathological focus, its localization and the extent of necrotic phenomena by peripheral symptoms.

Thus, when visual fields are lost, we can talk about a small affected area. This violation is often called a “blind spot.” When visibility is relatively clear, patients experience vision loss in a small area. They usually complain of pain in the eyes.

If the volume of necrotic phenomena is small, then the vision of a patient who has suffered a stroke is restored independently, as he is rehabilitated. He needs physical therapy and eye exercises. After a stroke, patients may have no vision at all.

The fact is that both lobes of the brain, left and right, are responsible for visual function. The left lobe of the brain receives information from the right side of the retina of both eyeballs, and the right lobe receives information from the left side. With severe damage to brain tissue, lateral vision is lost.

It can be restored with intensive treatment methods. Restoring lateral vision is possible due to the ability of undamaged areas of the cerebral cortex to take over some lost functions.

With paralysis of the oculomotor nerve, atrophic processes occur in the muscle fibers, due to which movements of the eyeballs occur. As a result of such disorders, the patient loses the ability to look straight. His eyes “ran” in different directions.

With this pathology, exophthalmos (protrusion of the eyeball) and strabismus are also observed. If pathological changes are diagnosed in a timely manner and adequate treatment is carried out, then visual function can be completely restored over time.

Types of visual impairment

All types of visual impairment in post-stroke patients can be divided into the following types:

blurred vision in one or both eyes;
loss of vision;
visual hallucinations;
oculomotor disorders.

Visual disturbance may be transient or permanent. The first type is more common in the case of transient ischemic attack. Loss of vision can be complete or partial. The latter is characterized by loss of certain fields of vision or one-sided blindness.

Oculomotor disorders occur when the nuclei of the oculomotor nerves are damaged. The first place in the clinical picture is squint and complaints of double vision. The visual departments are very sensitive to lack of oxygen. Their defeat can be observed within one minute after the onset of hypoxia.

This explains the difficulties that patients and doctors face during the treatment process. The best results can only be achieved by following all medical recommendations as accurately as possible. Today, when vision deteriorates, three complementary treatment areas are used:

non-specific activities;
drug treatment;
gymnastics;
surgical intervention.

Symptoms of optic nerve damage

As a result of a stroke, which occurs due to blockage of brain capillaries or insufficient oxygen supply to the brain, some neurons die. Atrophy and necrosis of large areas of tissue occurs. Those areas that are damaged cease to perform the functions for which they were responsible.

If the parts responsible for visual function are affected, vision disappears and temporary blindness develops. If the damage was reversible, the foci of dysfunction are restored over time; with irreversible changes, disastrous consequences arise in the form of complete loss of vision.

Symptoms of visual impairment may indicate which parts of the brain were affected first and the extent of necrotic damage to neurons:

loss of visual fields - the lesion had a small localization. This type of pathology is called a “blind spot” because a separate area disappears from the field of view. The syndrome is accompanied by pain in the eye sockets. Minor brain damage leads to the fact that vision is restored independently during the rehabilitation period;
loss of peripheral vision - full visual function is provided by two brain lobes - left and right. Information from the retina of both eyes is processed by the opposite lobe (the left-side portion is responsible for the right side of the retina and vice versa). If peripheral (side) vision is lost, it means that the brain tissue has suffered extensive damage due to hemorrhage. Restoring lateral vision after a stroke is a difficult and lengthy process, requiring intensive drug and auxiliary therapy. Intact brain structures can take over some lost functions;
paralysis of the nerve responsible for the motor function of the eyes - such an atrophic disorder that occurs in the muscle fibers responsible for the movement of the eyeballs leads to protrusion of the eyes outward. Another consequence is squint.

Successful treatment and reversibility of visual impairment depends on timely diagnosis of stroke and immediate therapeutic assistance. Patients who have had a stroke may not be able to open their eyes due to damage to the oculomotor nerve.

As a result of ischemia or hemorrhage, a disruption of its structure occurs in the area located between two large cerebral arteries at the level of the superior colliculus of the midbrain. Pathological disorders lead to the following visual disturbances:

double vision;
nystagmus (quivering of the eyeballs);
exophthalmos (bulging eyes);
deterioration of visual acuity.

Diplopia, or double vision, occurs when it is impossible to control the direction of movements of the eyeballs. They turn in different directions, as a result of which visual perception is disrupted.

If atrophy of the oculomotor nerve occurs, patients experience impaired function of the levator palpebrae superioris muscle and experience trembling of the eyeballs, or nystagmus. Such severe visual impairments are in most cases irreversible.

If present, patients are assigned a visual disability. If the atrophic and necrotic processes are relatively minor, doctors are able to eliminate the consequences of a stroke and restore vision. Exophthalmos, or protrusion of the eyeballs, is another characteristic sign of oculomotor nerve atrophy.

As a result of a stroke, nerve paralysis occurs and the movements of the eye block are disrupted. Due to constant increased stress on the eyes, they begin to water, which indicates dryness of the cornea. To ensure that pathological changes do not become irreversible and vision does not drop to zero, it is necessary to take urgent measures.

In the case of hemorrhagic or ischemic stroke, temporary visual impairment develops. Timely treatment measures can prevent dangerous complications.

Diagnostics

Source: GolovaDOC.ru

With central oculomotor disorders, complaints are often vague and are of little help in diagnosis. The leading symptom is diplopia, blurred vision, difficulty looking to the side, difficulty reading (“merging” words), blurred vision in one direction of gaze, difficulty translating the gaze to close objects, a feeling of vibration of stationary objects (oscillopsia).

If there is any suspicion of CNS damage, the neurological status should be assessed. All oculomotor functions are examined: the range of eye movements in all directions, gaze fixation, saccades, slow pursuit movements, convergence are checked, and strabismus is detected using the eye-covering test.

The last thing to evaluate is oculomotor reflexes: a doll's eye test is performed and Bell's sign is checked (when you try to close the eye, it turns upward).

Vision treatment after stroke

The condition of a stroke is always characterized by acute circulatory disorders in one or another part of the brain, which is responsible for strictly defined vital functions of the body. Visual impairment after a stroke, fortunately, most often affects only part of the visual field.

For example, the patient may not see objects located to his right or left. In order to see the entire object, he has to turn his head. It is also possible to experience “squint,” a feeling of sand in the eyes, and double vision due to impaired movements of the eyeballs.

And today we will talk about how to restore normal vision after a stroke. Taking into account various factors, each ophthalmologist individually selects a vision restoration program for each patient, which may consist of drug treatment, surgery, a set of exercises and gymnastics.

One important note should be made right away: disturbances in focusing and accommodation, as a rule, are subject to complete recovery. Loss of visual fields often does not recover, but over time, patients stop noticing this, having become accustomed to looking with central vision.

Drug treatment involves taking a number of drugs aimed both at restoring brain cells in the area damaged by the stroke (cytoflavin, actovegin, etc.) and directly at the organs of vision (emoxipin, semax, capilar).

In addition, a scheme for restoring vision after a stroke includes introducing foods high in vitamin A into the diet and regular eye exercises.

Vision restoration

As you know, after a stroke or cerebral infarction, vision can deteriorate. As a result of insufficient cerebral blood supply or intracranial hemorrhage, atrophy of the optic or oculomotor nerve develops, which requires adequate drug treatment and rehabilitation measures.

Otherwise, the process of restoring visual functions will be lengthy and ineffective. If the oculomotor nerve is damaged, it is necessary to restore its function in three ways:

drug therapy;
oculomotor gymnastics;
surgical treatment.

In order to reduce the time it takes to restore vision, you can resort to unconventional methods of treating optic nerve pathology. To restore visual function, doctors prescribe medications depending on the clinical symptoms of a stroke.

Selection of treatment method

In case of dysfunction of brain tissue, therapy should be comprehensive, aimed at improving metabolic processes in nerve cells and blood supply to the brain.

In this case, there is no need to use any specific ophthalmic drugs, but moisturizing eye drops may be needed to maintain the functional activity of the visual organs.

For optic nerve atrophy, which manifests itself as blurred vision, neurologists and ophthalmologists prescribe medications to patients whose mechanism of action is aimed at restoring blood supply and normalizing metabolic processes in nerve cells.

Along with traditional methods of treatment for visual impairment in patients who have suffered a stroke, homeopathic medicines can be used. Their action is aimed at activating the body’s own reserves. The homeopathic approach to restoring visual functions is unique.

Unlike traditional pharmaceuticals, homeopathic medicines act on the root cause of the disease, rather than fighting its consequences. If it is not possible to restore visual functions using traditional and non-traditional methods, ophthalmic surgeons resort to surgical intervention.

Non-specific events

There are various rehabilitation measures that can help restore impaired vision after a stroke. These measures are aimed at significantly making the patient’s life easier and speeding up his recovery.

At first glance, it may seem that they have nothing to do with restoring the normal functioning of the visual analyzer, but in fact this is not the case.

Essentially, these simple steps force the patient to pay attention to the objects around him, constantly moving his gaze from object to object, which is a good addition to therapeutic exercises. So:

Use a variety of flooring materials. If the floor is covered, for example, with tiles in key areas of the home, lay small paths or rugs. They should differ significantly not only in texture, but also in color.
Make the stairs more convenient for movement. This means not only the installation of railings, but also the color scheme - contrasting steps that alternate will be very useful.
If possible, place bright accents - attracting the patient’s attention, they will not only help him orient himself, but will also play the role of a kind of eye simulator.

Drug treatment

Specific agents whose action is aimed at improving vision in patients after a stroke have not been developed to date. To help the patient recover faster, doctors use medications that serve the following purposes:

restoration of blood flow in the brain area;
normalization of rheological properties of blood;
correction of metabolic disorders of the brain;
reduction of the necrosis zone;
decreased sensitivity of neurons to lack of oxygen.

This approach will help minimize the number of dead nerve cells, and those located in the ischemic penumbra zone will be able to fully recover. Resuming blood flow in the affected area is the most effective method.

For this purpose, drugs are used that can dissolve blood clots formed in the vessels, after which the patient completely disappears all focal symptoms. A significant drawback of the method is its time limitation; it can only be used during the first three hours after a stroke.

Normalization of the rheological properties of blood is achieved by prescribing drugs that improve cerebral microcirculation and anticoagulants. From the first subgroup, pentoxifylline, trental, sermion are most often prescribed, from the second - heparin and its low molecular weight fractions.

The use of vasoactive drugs can reduce the area of necrosis - they improve blood flow in the ischemic penumbra zone and help neurons recover. The most popular of this group are Cavinton and aminophylline.

The sensitivity of brain tissue to hypoxia can be reduced with the help of antioxidants - vitamin E, and hypoxia protectors - Cerebrolysin, piracetam or nootropil.

Surgery

Considering the pathogenesis of visual impairment, surgical intervention on the eye muscles will not eliminate the existing problem. However, surgery can return the eye to its normal position and reduce the phenomenon of diplopia, that is, double vision.
Before consenting to such treatment, the patient must weigh all the nuances.

As a rule, the final decision is made jointly by the patient, the neurologist and the ophthalmologist. Restoring vision after a stroke is quite difficult. Not every patient can achieve success, even if they diligently follow all medical recommendations.

However, over time, his condition can improve significantly, since the loss of visual function is compensated by the increased work of other sensory analyzers. In addition, several months after the stroke, the patient develops new habits.

For example, when the lateral field of vision is lost, a person, without noticing it, begins to look to the side with central vision, as a result of which it seems to him that his peripheral vision has been restored. The defect can be identified during an instrumental examination of the patient.

Gymnastics

This is a very simple and affordable method of rehabilitation of patients after a stroke. It can easily be used at home. The only thing that is required from the patient is patience and careful implementation of the recommendations.

Light pressure with the fingers of both hands on the upper, lateral, and then lower edge of the eye sockets.
Slow and gentle pressure on the eyeballs.
Massage of the bridge of the nose.
Intense blinking of the eyes.
Movement of the eyes in horizontal and vertical directions.
Examination of an object located at different distances from the patient’s eyes.

Computer methods for restoring vision in patients after a stroke are of great interest.
Their task is to train brain neurons located in the vicinity of the affected ones. The program forces them to do the work that dead cells used to do.

Despite its effectiveness, it is not widely used. However, there are clinics that actively use the technique in their vision restoration programs.

Exercise No. 1. Cover your eyes with your palms and take several as deep breaths as possible. Next, you need to very delicately press your palms alternately on the upper and lower edges of the eye sockets. The exercise is initially repeated no more than 3-4 times, followed by an increase in the number of repetitions to 10-15 repetitions.
Exercise No. 2. Try to close your eyes as tightly as possible. Hold the position for 5 seconds and sharply relax the eye muscles.
Exercise No. 3. Hold the upper eyelid with your fingers, and in this position try to close your eye. Do the same with the lower eyelid. Do several approaches for each eye.
Exercise No. 4. Close your eyes and use gentle circular movements of your fingers to massage your eyeballs through your eyelids. The pressure on the eyelids should be barely noticeable.
Exercise No. 5. Take a pencil or any other small object in your hand and move it in front of your eyes in different directions, either moving it away or bringing it closer to your eyes. Try to follow the movements of the object without moving your head.

Eye exercises that you can do on your own are shown in the figure below. Daily practice is useful not only for restoring vision after a stroke, but also in general for people who, for various reasons, often have to strain their eyesight.

Of course, there are situations when a person who has suffered a stroke cannot perform such exercises on his own due to paresis or paralysis of the limbs. In this case, the exercises can be performed by an ophthalmologist or the patient’s relatives.

Traditional methods

Traditional healers recommend using medicinal herbs to restore impaired vision. They can be used as a supplement or at the end of a course of traditional therapy. Herbal medicines reduce the duration of the rehabilitation period and improve the patient’s well-being.

First of all, you need to change your diet. After a stroke, it is also recommended to use herbal tinctures and decoctions that improve blood supply to the brain. A good effect can be obtained from the use of mountain arnica.

It is believed that an infusion of this plant helps restore peripheral vision, which was impaired after a stroke. It can be taken both during illness and as a preventive measure. Decoctions, tinctures, decoctions and even jam are prepared from pine, spruce and cedar cones.

The cones contain a large amount of biologically active substances that clean blood vessels and improve blood flow to the atrophied area. In case of diplopia resulting from cerebrovascular accident, it is recommended to take lemon and garlic.

They contain ascorbic acid, or vitamin C. It restores the elasticity of blood vessels and eliminates their fragility, and also helps improve the quality of vision.

You need to know that it takes quite a long time to restore vision after a stroke, which resulted in atrophic and necrotic changes in the tissue of the brain or optic nerve. It may take several months to one year for it to stabilize.

The symptom develops in patients with multiple sclerosis and Redlich-Flatau disease.
The symptom is characterized by the absence of independent combined movements of the eyeballs. However, the ability to fix the gaze on a moving object and follow it is preserved. When fixating the gaze on an object, the turn of the head is accompanied by an involuntary rotation of the eyeballs in the opposite direction.

Bielschowsky's syndrome (A.) (syn. recurrent alternating ophthalmoplegia)
The etiology and pathogenesis of the disease are unclear. Currently, there are various theories of the origin of the pathological process - damage to the nuclei of the cranial nerves, allergic and viral processes.
The syndrome is characterized by the periodic appearance of paresis and paralysis of some, and sometimes all, external muscles of both eyes. The period of muscle dysfunction continues for several hours, then complete normalization of the activity of the extraocular muscles occurs. In some cases, symptoms of paralysis come and go more slowly.

Bilshovsky (A.)-Fisher-Kogan symptom (syn. incomplete internuclear ophthalmoplegia)
As a rule, it develops when the pathological focus is localized in the pons and occurs as a result of damage to the fibers connecting the nucleus of the oculomotor nerve with the nucleus of the abducens nerve of the opposite side.
With this syndrome, there is a lack of movement of the eyeball when looking in the direction of the action of the internal rectus muscle. However, the function of the internal rectus muscle during convergence is preserved.

Bilshovsky's symptom (M.)
Occurs when the midbrain is damaged. Disturbances in the movement of the eyeball are caused by an isolated lesion of the trochlear nerve, as a result of which paralytic strabismus and diplopia develop. It is characteristic that when the head is tilted back with a simultaneous turn in the direction of the nerve lesion, strabismus and diplopia intensify. On the contrary, when the head is slightly tilted forward and turned in the direction opposite to the nerve damage, diplopia disappears. To reduce diplopia, patients are forced to position their head. Symptoms of paralysis of the superior oblique muscle are combined with hemiparesis on the opposite side.

Gaze paralysis
This symptom is characterized by the impossibility of cooperative movement of the eyeballs in a certain direction. There are various options for disturbances in the movement of the eyeballs - vertical (up and down), horizontal (left and right), optical (convergence, installation and trail movements) and vestibular (observed when the apparatus of the vestibule sacs and semicircular canals of the inner ear is irritated when the head is tilted) reflex movements.
With this condition, the eyeballs may stand straight up. However, there is often a concomitant deviation of the eyes in the direction opposite to gaze palsy.
When the focus is localized in both hemispheres or in the pons, where both pontine centers of gaze are located close to each other, on both sides of the midline, so-called bilateral gaze paralysis develops, i.e. there is gaze paralysis both to the left and to the right.
It should be noted that when the process is located in the hemispheres, vertical gaze paralysis is also observed simultaneously with horizontal ones. The combination of vertical and horizontal paresis of gaze is called cycloplegia, or pseudoophthalmoplegia.
When the frontal center of gaze or the frontopontine pathway is affected on the side opposite to the direction of gaze paralysis, against the background of loss of the ability to voluntary movements, the preservation of optical and vestibular reflex movements of the eyeballs is characteristic.
The combination of impaired ability for voluntary movements and optical reflex movements of the eyeball with preservation of vestibular excitability of the eye muscles indicates preservation of the structure of the nuclei of the oculomotor, trochlear and abducens nerves and the posterior longitudinal fasciculus in the brain stem.
Isolated vertical gaze palsies are observed when the subcortical gaze center in the quadrigeminal region is affected.
With vertical gaze paralysis, as a rule, only volitional movements in the direction of paralysis are absent, while reflex movements, both optical and vestibular, in this direction are preserved. Since the nuclei of the oculomotor and trochlear nerves are located near the centers of gaze of vertical movements, a combination of vertical gaze palsies with convergence palsy (Parinaud's syndrome), pathology of pupillary reactions and paralysis or paresis of the extraocular muscles is possible. With mild vertical paresis of gaze, eye movements in the direction of the paresis are not limited, but when looking in this direction, vertical nystagmus occurs.

Symptom of hidden gaze paresis
Occurs with pyramidal insufficiency. Identification of this symptom helps in topical diagnosis of the affected side.
To identify the symptom, the patient is asked to close his eyelids tightly. Then, one by one, the palpebral fissure is forcibly opened. Normally, the eyeballs should be turned upward and outward. With hidden gaze paresis, a friendly rotation of the eyeballs is observed slightly upward and to one side of the localization of the lesion.

Spasm of gaze
With parkinsonism, epilepsy, acute cerebrovascular accident of the hemorrhagic type, patients may experience an involuntary paroxysmal spastic deviation of the eyeballs upward (less often to the sides) with holding them in this position for several minutes.

Hertwig-Magendie sign (syn. “swinging strobism”)
The causes of the symptom may be tumors located in the middle and posterior cranial fossae, as well as circulatory disorders in the area of the brain stem and cerebellum involving the posterior longitudinal fasciculus.
With this symptom, a characteristic type of strabismus occurs: there is a deviation of the eyeball on the side of the localization of the lesion in the brain downward and inward, and on the opposite side - upward and outward, that is, both eyes are deviated in the direction opposite to the lesion; the described position of the eyeballs is maintained when looking in any direction. In some cases, a turn of the head towards the lesion and rotatory nystagmus are observed. Diplopia is usually absent.

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Graefe's disease (syn. progressive external chronic ophthalmoplegia)
The disease occurs due to degenerative changes in the nuclei of the nerves innervating the extra- and intraocular muscles. The process appears to be hereditary.
At the onset of the disease, progressive bilateral ptosis occurs. Subsequently, ophthalmoplegia gradually intensifies - up to total immobility of the eyeballs, which are installed in a central position with a slight tendency to divergence. Moderate mydriasis and decreased pupillary response to light are observed. The peculiar facial expression that arises as a result of the immobility of the gaze is called “Hutchinson’s face.”
In some cases, other changes in the organ of vision occur - exophthalmos, swelling of the eyelids, chemosis, hyperemia of the conjunctiva. On average, 40% of patients develop retinal pigmentary degeneration and optic nerve atrophy. Headache and abnormal head position may occur.
Differential diagnosis is carried out with myasthenia gravis, pituitary tumor invading the cavernous sinus, disseminated encephalomyelitis, botulism, epidemic encephalitis.

Graefe myopathy (syn. ophthalmoplegic myopathy)
The disease is hereditary (inherited in an autosomal recessive manner). The disease is based on fatty degeneration of muscles, which is detected by biopsy.
Patients experience paresis, and sometimes paralysis of the facial muscles (“myopathic face”), larynx, pharynx, tongue, and shoulder girdle. Boulevard paralysis is possible. Ophthalmoplegia, ptosis, and lagophthalmos are characteristic.

Moebius syndrome (syn. congenital oculofacial palsy syndrome, Graefe syndrome)
The disease is associated with congenital underdevelopment of the nuclei of the III, VI, VII, IX, XII pairs of cranial nerves, which is caused by the damaging effect of the cerebrospinal fluid penetrating into the area where the nuclei are located from the IV ventricle. It cannot be ruled out that the cause of the lesion could be a woman suffering from rubella or influenza during 2-3 months of pregnancy, quinine poisoning, or injury.
Inheritance occurs most often in an autosomal dominant manner, but families with autosomal recessive inheritance have been described. There is a known variant of the syndrome with an isolated unilateral lesion of the nucleus of the facial nerve, transmitted by a dominant gene - possibly localized on the X chromosome.
Clinical signs and symptoms. Children develop an amicable, mask-like face. There is difficulty sucking and swallowing, and weakness of the masticatory muscles. Possible deformation of the auricles, micrognathia, stridor caused by a sharp narrowing of the lumen of the larynx, congenital heart defects, syndactyly, brachydactyly, clubfoot. Patients develop slurred speech due to impaired formation of labial sounds. Hearing loss and deafness often occur. Mental retardation occurs in approximately 10% of children.
Eye symptoms. Changes can be unilateral or bilateral. Lagophthalmos, lacrimation, rare blinking movements, ptosis, convergent strabismus, and weakness of convergence are observed. When all oculomotor nerves are involved in the process, complete ophthalmoplegia is possible. Hypertelorism, epicanthus, and microphthalmos may occur.

Mobius syndrome
The development of the syndrome is possibly associated with compression of the oculomotor nerve by the surrounding edematous tissue.
Patients experience severe headache, nausea, and vomiting, which is called ophthalmic migraine. Against the background of an attack of migraine pain, ptosis, impaired movements of the eyeball, mydriasis, and diplopia develop on the side of the headaches. Gradually all symptoms disappear. Mydriasis lasts the longest.

Diagnosis of paresis of the eye muscles by analysis of diplopia
One of the symptoms of damage to the extraocular muscles is the appearance of diplopia. In case of damage to only one muscle, it is possible to carry out topical diagnostics to analyze the nature of diplopia. This method for diagnosing paresis and double vision paralysis was proposed by Professor E.Zh. Throne. The method is simple, convenient, and, in addition, it eliminates errors associated with the simultaneous presence of heterophoria.
If the patient has damaged not one, but several muscles, this method cannot be used. In this case, you should examine the field of view.
The sequence of actions of the doctor when analyzing the nature of diplopia is as follows.
First, it is necessary to determine when the patient notices double vision: when looking with one or two eyes.
Monocular double vision occurs when the structures of the anterior segment of the eyeball are disrupted (corneal opacification, iris coloboma, astigmatism, lens opacification) or diseases of the retina of the corresponding eye (two lesions in the macular area, etc.). In these conditions, the image enters the retina and is perceived by two different parts of the retina.
Binocular double vision usually occurs due to paresis or paralysis of the extraocular muscles. This is a consequence of central paresis of the cranial nerves (III, IV, VI pair of cranial nerves) or damage to the external muscles of the eye in the orbit, which can occur due to its injury.
Next, it is necessary to identify the affected muscle and determine the tactics for further management of the patient.
If the eye occupies an incorrect position in the orbit (squints), its movement towards the affected muscle (opposite to the deviation) is absent or sharply limited, then, consequently, there is paresis or paralysis of the muscle (opposite to the deviation) of the squinting eye. It is necessary to clarify the details of the medical history, whether there was injury, infection, vascular accident, etc. and decide on appropriate treatment.
If the patient complains of double vision, but there are no obvious disturbances in the position of the eyeball in the orbit or disturbances in its movements, in this case the tactics are as follows.

1. It is necessary to compare the width of the palpebral fissure and the position of both eyes in the orbit. Next, the simultaneous movement of the two eyes is assessed, paying attention to the symmetry of eye movement, and each one separately. It should be remembered that with maximum inward rotation of the eye, the limbus should touch the semilunar fold, and with maximum abduction, the outer corner of the eye. With maximum upward gaze, the cornea is covered by the upper eyelid by 2 mm; with maximum downward gaze, the cornea is “hidden” by more than half behind the lower eyelid.
2. If there are no restrictions in the movement of one of the eyes, you should make sure that there is diplopia. To do this, from a distance of 1 to 5 meters, the doctor shows the patient any oblong object (pencil): first straight, then moves it left, right, up, down, up-out, up-in, down-out, down-whip -ri. The patient must follow the movement of the object with both eyes and answer whether there is double vision or not. If the patient does not notice double vision in any of the gaze positions, then it does not exist. And, conversely, if double vision is detected in at least one of the positions, the patient’s complaint is reliable.
3. The affected muscle and the affected eye should be identified. To do this, a red light filter is placed in front of one of the eyes (preferably the right one) and the patient is asked to look at the light source. Thanks to the color filter, it is easy to assess which eye belongs to each of the two images of the light source.

If the double images are located parallel to each other, it means that there is damage to the muscles of horizontal action - the internal or external rectus. If the muscles of vertical action (levators or depressors) are affected, double vision will be determined vertically.
Next, the diagnosis of the same name or cross diplopia is carried out. It is necessary to remember that diplopia of the same name causes damage to the external rectus muscles, and cross diplopia - to the internal ones. To do this, you need to identify where, according to the patient, the red candle is located (its image belongs to the right eye, since the red filter is located in front of the right eye) - to the left or to the right of the white one.
To determine which eye muscle is affected, you should remember the following pattern: double vision increases in the direction of the action of the affected muscle.
With horizontal double vision, the doctor moves the light source, located at arm's length from the patient, to the left or right, and the patient evaluates the distance between the double images. For example, if diplopia of the same name is detected, then the external rectus muscles suffer. Therefore, if diplopia increases when the light source shifts to the right (as the patient looks), then the external rectus muscle of the right eye is affected. Double vision when looking into the distance is sometimes caused by heterophoria (muscle imbalance). In this case, the distance between the double images remains constant.
With vertical double vision, the doctor moves the light source up and then down. The patient responds as the double vision increases. Here you need to remember the following: if double vision increases when the light source is shifted upward, then the lifters are affected; if the depressors are affected, diplopia increases as the light source moves downward. To identify the affected eye, it should be remembered that when the levators are affected, the eye whose image is higher is affected; When the lowerers are damaged, the eye whose image appears below is damaged.
It remains to determine which of the two muscles, elevating the eyes (superior rectus and inferior oblique) or depressing the eyes (inferior rectus and superior oblique), was affected. To do this, remember the following: the maximum lifting or lowering effect, therefore, the maximum double vision in the rectus muscles manifests itself during abduction, and in the oblique muscles during adduction. To identify it, you should make two movements with the light source, upward-outward and upward-inward, when damage to the levators is diagnosed. When damage to the descenders has already been identified, it is necessary to shift the light source downward-outward and downward-inward.

These syndromes are manifested by a violation of conjugate eye movements and are caused by damage to the central motor neurons that control the state of the nuclei of the III, IV and VI cranial nerves. These types of syndromes include:

paralysis of vertical and horizontal gaze;
vertical oblique deviation;
internuclear ophthalmoplegia;
one and a half syndrome;
dorsal midbrain syndrome.

Paresis of vertical gaze, vertical oblique deviation and retraction nystagmus are associated with damage to the stem mechanisms of vertical gaze. Horizontal gaze palsy and internuclear ophthalmoplegia have different mechanisms.

Vertical and horizontal gaze paralysis

Gaze paralysis is a violation of friendly unidirectional (conjugated) movements of the eyeballs during smooth tracking and on command in a situation where the oculocephalic (vestibulo-ocular) reflex is intact. Both eyeballs stop moving voluntarily in one direction or another (right, left, down or up), while the deficit of movements is the same in both eyes.

Gaze palsy occurs as a result of supranuclear disorders and not as a result of damage to the third, fourth, or sixth pairs of cranial nerves. With gaze paralysis, there are no disturbances in the movements of each eyeball individually, diplopia or strabismus (except for cases of spread of the pathological process to the nuclei of the III, IV or VI pairs of cranial nerves). Horizontal gaze palsy is diagnosed if the patient cannot look away to the right or left, vertical - if the patient cannot look up, and downward gaze palsy - if the patient cannot look down.

Horizontal gaze palsy occurs with extensive lesions of the frontal or parietal lobes or the pons.

Destruction of the cortical gaze center in the frontal lobe causes paralysis of voluntary gaze away from the lesion and lateral concomitant deviation of the eyes towards the lesion. Both eyeballs and the head are deviated towards the lesion (the patient “looks at the lesion” and “turns away from the paralyzed limbs”) due to the preserved function of the opposite center of rotation of the head and eyes to the side. This symptom is temporary and lasts only a few days as the gaze imbalance is soon corrected. The ability to reflexive tracking and the oculocephalic reflex (tested in a doll's eye test) may be preserved in frontal gaze palsy. Paralysis of horizontal gaze with damage to the frontal lobe is most often accompanied by hemiparesis or hemiplegia (Golubev V.L., Vein A.M., 2002).

A focal lesion of the Varoliev bridge can cause paralysis of voluntary gaze towards the lesion and lateral involuntary deviation of the eyes in the direction opposite to the lesion. The patient cannot fix his gaze on an object located laterally on the same side as the lesion (“turns away” from the stem lesion and “looks” at the paralyzed limbs). The mechanism of “pontine gaze paresis” is associated with the unilateral involvement in the pathological process of the initial sections of the medial longitudinal fasciculus together with the nucleus of the abducens nerve on the same side. This type of gaze paralysis usually lasts for a long time. May be accompanied by other symptoms of damage to the pons (for example, weakness of the facial muscles due to paralysis of the VII pair) and cannot be overcome with the help of the “doll's eye” maneuver.

Vertical gaze palsy up (less often down) in combination with convergence disorder and pupillary disorders is referred to as Parinaud's syndrome. It is observed in patients with ischemic stroke, brain tumor, multiple sclerosis and other pathologies when the lesion is localized at the level of the pretectal region (area pretectalis or preopercular area is the border area between the roof of the midbrain and the diencephalon), as well as the posterior commissure brain (commissura cerebri posterior). This syndrome also sometimes includes vertical or convergent nystagmus, hemiptosis of the eyelids, and impaired pupillary reactions. The upward gaze is most affected. Paresis of upward gaze can be distinguished from peripheral paralysis of the external muscles of the eye by signs of preservation of reflex eye movements, indicating the intactness of the oculomotor nerves and the muscles innervated by them. Such signs of preservation of brainstem reflex reactions are (Golubev V.L., Vein A.M., 2002):

Bell's phenomenon: when a patient tries to forcefully close his eyes, overcoming the resistance provided by the doctor, the eyeballs reflexively turn upward and outward, less often - upward and inward. This phenomenon is also observed in healthy individuals; it is explained by the connection between the innervation of the orbicularis oculi muscles and both inferior oblique muscles;
doll's eye phenomenon: if you ask the patient to continuously look at an object located directly in front of his eyes, and then passively tilt the patient's head forward, the eyeballs turn upward, and the patient's gaze remains fixed on the object. This eye deviation is also detected in healthy people if they correctly follow the doctor’s instructions and concentrate their gaze on a given object.

With paralysis of voluntary upward gaze, both the Bell phenomenon and the doll's eye phenomenon are preserved, except in cases where, along with pathology of the pretectal region, there is simultaneous damage to the oculomotor nerves (nuclei or trunks) with peripheral paralysis of the external muscles of the eye.

Supranuclear palsy - impairment of eye movements on command and smooth tracking with preservation of the vestibulo-ocular reflex - can occur with some degenerative diseases of the brain, primarily with progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome). The latter disease is characterized by vertical, and later horizontal paresis of gaze, disturbances in smooth pursuit eye movements, progressive hypokinesia, rigidity of the muscles of the limbs, increased tone of the extensor muscles of the trunk, a tendency to frequent falls and dementia.

"Global gaze palsy"(total ophthalmoplegia) is manifested by the inability of a person to voluntarily move his gaze in any direction. Usually combined with other neurological symptoms. The main causes are Guillain-Barré syndrome, myasthenia gravis, thyroid ophthalmopathy, progressive supranuclear palsy, Wernicke encephalopathy, intoxication with anticonvulsants (Golubev V.L., Vein A.M., 2002).

Impairment of eye movements alone on command(voluntary saccades), while maintaining pursuit eye movements, can be observed in cases of damage to the frontal lobe cortex.

Isolated violation of smooth tracking alone may occur with a lesion in the occipital-parietal region, regardless of the presence or absence of hemianopia. Reflex slow tracking movements of the eyes towards the lesion are limited or impossible, but voluntary movements and movements on command are preserved. In other words, the patient can make voluntary eye movements in any direction, but cannot follow an object moving towards the lesion.

Combination of gaze paralysis and eye muscles indicates damage to the structures of the Varoliev bridge or midbrain.

To determine the level lesions with such eye deviation The following considerations are mainly relevant. A larger number of supranuclear frontopoitin fibers ending in the pontine center of vision are crossed and come from the opposite hemisphere of the cerebrum. Only a small part of the fibers comes from the hemisphere of the same side.

Crossed supranuclear tract for horizontal viewing directions, it crosses the midline at the level of the front edge of the bridge. If this path is interrupted by a pathological process located proximal to the intersection, then when the lesion is located on the right, it becomes impossible to look to the left. If the right-sided focus is located in the bridge, i.e., distal from the point of crossover, then the gaze to the right falls out. Due to the predominance of continuous antagonistic innervation, eye deviation occurs: in the first case to the right and in the second to the left.

When, therefore, when turning off supranuclear innervation Deviation conjuguee develops, first described by the Genevan physiologist Prevost, then when the focus is localized above the bridge, the patient looks towards the focus. If there is a break in the bridge, then the patient, in contrast, looks in the direction opposite to the focus.

Deviation conjuguee, however, is not a persistent symptom. For the innervation of the lateral directions of gaze, the hemisphere of the opposite side is of predominant importance. Along with this, the relationships that we have outlined in relation to the bilateral cortical innervation of the eye muscles are also important. Thus, with cerebral hemorrhage (the most common cause of Deviation conjuguee), the patient only looks towards the source of the disease during the first quarter of an hour or the first hours after a stroke. This is an excellent criterion for establishing on which side there is hemiplegia even at the stage of general muscle relaxation.

Then this one phenomenon, which is often combined with a long turn of the head of the same name, disappears. The latter is due to the fact that instead of the switched off conductors, the corticonuclear connections of the other hemisphere are switched on.

Thus, temporary Deviation conjuguee indicates that the lesion is located “somewhere” between the cortex and the pons. For more accurate localization, it is necessary to take into account other, including non-ocular, symptoms. Clinical experience shows that in cases where Deviation conjuguee turns into divergence of the eyeballs, death quickly occurs. Deviation conjuguee due to a supranuclear lesion in the pons itself is rarely observed.

“Deviation conjuguee” of the head and eyes together with a spasm of the left facial nerve at the beginning of a Jackeon’s seizure with a right-sided brain tumor (according to Bing)

Diagnostic rules for supranuclear (supranuclear) eye palsies

Supranuclear disorders eye movements are characterized by the fact that their combination is preserved (internuclear palsy). Persistent gross gaze paralysis in diseases of the cerebrum - even with lesions of both hemispheres - is relatively rare. Most often they are still observed in meningitis, spreading to the entire convex surface of the brain.

If sick still looks straight ahead, then a positive puppet phenomenon or a slow deviation of the eyes after introducing cold water into the external auditory canal indicates an iptactic brain stem, i.e., a supranuclear lesion (cerebral cortex - white matter or corticobulbar tracts).

If at persistent gaze paralysis If it is possible to identify a true abducens nerve palsy on the same side (recognized by the fact that the internal rectus muscle of the other eye functions normally during convergence), this indicates that the lesion is localized at the caudal end of the pons. Because the facial nerve genu forms a loop around the abducens nerve nucleus, longitudinal gaze palsy is usually associated with a facial palsy (peripheral type) on the same side. Vertical eye movement disorders are almost always caused by lesions of the quadrigeminal region (bilateral oculomotor nerve palsies may simulate gaze palsies; see also aqueduct of Sylvius syndrome).

If Jacksonian seizure begins with convulsions of the gaze, this indicates a lesion in the cortex of the frontal lobe of the opposite side. The patient looks in the direction opposite to the lesion. Occasional isolated convulsions of the gaze without spreading the convulsions to other muscle groups, regardless of whether the eyes deviate in the vertical or horizontal direction, in contrast, indicate damage to the brain stem due to Encephalitis lethargica. As an exception, they are also observed with skull trauma and tumors.

The same applies to disorders- both paralysis and spasms - symmetrical movements of the eye, namely during convergence for near and the necessary divergence when moving from close to distance viewing. In this case, we should not forget about possible ocular causes (weakness of convergence in myopia, excessive convergence up to spasm in hypermetropia, hidden strabismus or insufficient binocular vision due to refractive errors or unilateral amblyopia), as well as convulsions due to hysteria or insufficient attention of patients. Sometimes the observed phenomenon of so-called predominant gaze movements seems to indicate damage to the brain stem due to trauma. So, for example, when asked to look down, there is first a short look up, followed by a look down.

Research experience only eye movement disorders protects against errors to some extent. In particular, one should beware of haste in diagnosing gaze paralysis in patients with clouded consciousness and in patients who have not sufficiently understood what is required of them. On the other hand, it should be noted that in patients with multiple focal arteriosclerotic changes (miliary foci of softening and hemorrhages in the capsula interna, thalamus opticus and corpus striatum), in whom paralysis of bilaterally innervated muscles that provide speech, swallowing and chewing also indicate clinical picture of pseudobulbar palsy, however, only in exceptional cases is it possible to identify the presence of gaze paralysis.