Paresis of the external rectus muscle of the left eye. Oculomotor nerve (n
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 lot of such paintings, they all have a number of common features.
These signs are as follows: 1) loss of corresponding eye movement, 2) strabismus, 3) secondary deviation of the healthy eye, 4) diplopia, 5) disorder of 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. Loss of one or another eye movement due to paralysis of any muscle is the simplest and most understandable symptom. For example, the external rectus muscle of the eye - m. rectus externus, - as is known, 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 the eyes to the side. Imagine that we are dealing with 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 in order. But when you ask to turn your eyes to the right, the left eye will perform this movement, but the right eye will not: the m rectus externus will not operate in it.
You will observe similar phenomena with paralysis of any muscle; only the direction in which the affected eye will not be able to move will change.
2. Strabismus, strabismus - this is essentially a passive contracture already known to you - only not on a limb, 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 true for the eye muscles.
If, for example, abducens nerve paralysis is observed, and therefore m. recti externi, then the antagonist of the last muscle, m. rectus
interims, pulls the eyeball inward and firmly fixes it in this position. This position of the eye is called strabismus.
Since the eye will be close to the midline, this type of strabismus is called convergent (strabismus convergens).
On the contrary, if m. is paralyzed. 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. Secondary deviation of a healthy eye will become clear to you if you remember that the movements of the eyeballs are associated and occur predominantly in one direction. If we voluntarily deviate the right eye to the right, then the left eye deviates in the same direction, i.e. to the right. This means what strength of impulse m receives. rectus extermis dexter, m. receives the same. rectus interims sinister. And the greater the impulse for the first muscle, the greater it is for the second.
Now imagine that you have right abducens palsy. The right eye, under the influence of a healthy antagonist, will move inward, i.e., it will take the position of converging strabismus.
As for the healthy left eye, at first glance it should not suffer any changes in the installation, since everything is fine 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 inward almost in the same way as the diseased right eye.
Convergent strabismus will occur on both sides, while one eye is paralyzed.
How to explain this phenomenon, strange at first glance? 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 a 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, that is, it will also become in the position of converging strabismus.
Thus, unilateral abducens nerve palsy will produce bilateral strabismus.
Now imagine paralysis of m. recti interni dextri. Under the influence of the antagonist, the right eye will move outward and assume the position of divergent strabismus. To bring the eye to its normal position, the patient will intensively innervate the paralyzed muscle. From this, the same amplified impulses will be sent to m. rectus externus sinister, since both of these muscles act cooperatively. But under this last condition, the left eye will be pulled outward, that is, it will also become in a position of divergent strabismus.
Thus, paralysis of one part of the recti interni gives bilateral divergent strabismus.
It is necessary to clearly understand that, despite the apparent similarity of the phenomena in both eyes, their nature is deeply different: in one eye the deviation is of paralytic origin, in the other, so to speak, 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, and 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 know one of the conditions necessary for this: 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 immediately disappears, and a person begins to see with each eye separately, i.e. doubly. With paralysis of the eye muscles, strabismus occurs, as you already know, i.e. deviation of the eyes from their normal alignment. In this case, the parallelism of the ocular axes is naturally disrupted, i.e., the main condition for the development of diplopia is provided.
It is necessary, however, to make a reservation that diplopia is not always accompanied by strabismus and loss of eyeball movements, noticeable during a normal test. Very often, during examination, the eyes 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 is only enough to cause 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, easily solves the problem if it is a matter of paresis of any one muscle. With combined paralysis of several muscles, the task becomes difficult or even completely impossible to solve.
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 in determining the distance plays a large role.
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” and reaches out his hand in the wrong place.
6. Doubling of objects and “false projection” cause dizziness in patients. We do not know how these phenomena follow from one another, what their internal mechanism is, but the very fact of this connection is beyond doubt. Patients themselves often notice it and fight the painful feeling of dizziness in such a way that they close or bandage the sore eye with a scarf. This protective technique results in monocular vision, 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 techniques, also, in essence, of a protective nature, but not entirely consciously invented. These are various peculiar postures that the head takes in such patients.
For example, with palsy of the right abducens nerve, the right eye cannot turn outward. The patient has difficulty seeing objects located to his right. To correct this defect, he turns his entire head to the right and, as it were, exposes the sore eye to visual impressions coming from the right side,
This defensive technique becomes permanent, with the result that a subject with abducens nerve palsy can be identified by the manner in which they hold their head in the direction of the paralysis.
With paralysis of m. recti interni dextri the right eye cannot move to the left, and the patient turns his entire head to the left in order to expose the diseased eye to the corresponding impressions. Hence the manner of holding the head turned to the side, i.e. essentially the same as in the previous case.
Due to the same mechanisms, patients with paralysis of m. recti superioris slightly tilt their head back, and with paralysis of the m. recti inferioris lower it downwards.
These are the common symptoms of paralysis of the external eye muscles. 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.
Among the particulars, paralysis of m. deserves special mention. levatoris palpebrae superioris - so-called ptosis. This is the result of damage to the oculomotor nerve; ptosis is expressed in the fact that the patient's upper eyelid remains drooping, and he cannot lift 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 palsy, the patient's eyes are positioned as if he were looking straight ahead, and there is no strabismus. But he has no lateral movement: 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 fasciculus (fasciculus longitudinalis posterior).
With vertical gaze palsy, lateral eye movements are not impaired, but there is no upward or downward movement, or, finally, both upward and downward.
This symptom is usually observed with lesions in the quadrigeminal region.
Another type of oculomotor disorder, somewhat similar to the previous one, is concomitant eye deviation. It is observed most often in 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 directed to the left. When asked to turn the eyes to the right, the patient performs this movement to a small extent and for a short time, after which they return to their previous position.
This symptom is observed with lesions in different parts of the brain. The eyes are usually squinted towards the hearth, less often in the opposite direction (ancient formulas: “the patient looks at his hearth,” “the patient turns away from his hearth”).
Another disorder of the oculomotor system, already with the character of hyperkinesis, is observed - nystagmus.
Motor neurons of the oculomotor nerves (n. oculomotorius, III pair of cranial nerves) are located on both sides of the midline in the rostral part of the midbrain. These nuclei of the oculomotor nerve innervate the five extrinsic muscles of the eyeball, including the levator palpebral muscle. The nuclei of the oculomotor nerve also contain parasympathetic neurons (Edinger-Westphal nucleus), which are involved in the processes of pupil constriction and accommodation.
There is a division of supranuclear groups of motor neurons for each individual eye muscle. The fibers of the oculomotor nerve innervating the medial rectus, inferior oblique and inferior rectus muscles of the eye are located on the side of the same name. The subnucleus of the oculomotor nerve for the superior rectus muscle is located on the contralateral side. The levator palpebrae superioris muscle is innervated by the central group of cells of the oculomotor nerve.
Trochlear nerve (n. trochlearis, IV pair of cranial nerves)
The motor neurons of the trochlear nerve (n. trochlearis, IV pair of cranial nerves) are closely adjacent to the main part of the complex of nuclei of the oculomotor nerve. The left nucleus of the trochlear nerve innervates the right superior oblique muscle of the eye, the right nucleus innervates the left superior oblique muscle of the eye.
Abducens nerve (n. abducens, VI pair of cranial nerves)
Motor neurons of the abducens nerve (n. abducens, VI pair of cranial nerves), innervating the lateral (external) rectus muscle of the eye on the side of the same name, are located in the nucleus of the abducens nerve in the caudal part of the pons. All three oculomotor nerves, leaving the brain stem, pass through the cavernous sinus and enter the orbit through the superior orbital fissure.
Clear binocular vision is ensured precisely by the joint activity of individual muscles of the eye (oculomotor muscles). Conjugate movements of the eyeballs are controlled by the supranuclear gaze centers and their connections. Functionally, there are five different supranuclear systems. These systems provide various types of eyeball movements. Among them there are centers that control:
- saccadic (rapid) eye movements
- purposeful eye movements
- convergent eye movements
- holding the gaze in a certain position
- vestibular centers
Saccadic (rapid) eye movements
Saccadic (fast) movements of the eyeball occur as a command in the opposite visual field of the cortex of the frontal region of the brain (field 8). The exception is rapid (saccadic) movements that occur when the central fovea of the retina is irritated, which originate from the occipital-parietal region of the brain. These frontal and occipital control centers in the brain have projections on both sides to the supranuclear brainstem centers. The activity of these supranuclear brain stem centers of vision is also influenced by the cerebellum and the vestibular nuclei complex. The paracentral sections of the reticular formation of the bridge are the stem center, providing friendly rapid (saccadic) movements of the eyeballs. Simultaneous innervation of the internal (medial) rectus and opposite external (lateral) rectus muscles when moving the eyeballs horizontally is provided by the medial longitudinal fasciculus. This medial longitudinal fasciculus connects the nucleus of the abducens nerve with the subnucleus of the complex of oculomotor nuclei, which are responsible for innervation of the opposite internal (medial) rectus muscle of the eye. To initiate vertical rapid (saccadic) eye movements, bilateral stimulation of the paracentral sections of the pontine reticular formation is required from the cortical structures of the brain. The paracentral sections of the pontine reticular formation transmit signals from the brain stem to the supranuclear centers that control the vertical movements of the eyeballs. This supranuclear eye movement center includes the rostral interstitial nucleus of the medial longitudinal fasciculus, located in the midbrain.
Purposeful eye movements
The cortical center for smooth targeted or tracking movements of the eyeballs is located in the occipital-parietal region of the brain. Control is carried out from the side of the same name, i.e. the right occipital-parietal region of the brain controls smooth, targeted eye movements to the right.
Convergent eye movements
The mechanisms of control of convergent movements are less understood, however, as is known, the neurons responsible for convergent eye movements are located in the reticular formation of the midbrain, surrounding the complex of oculomotor nerve nuclei. They give projections to the motor neurons of the internal (medial) rectus muscle of the eye.
Keeping your gaze in a certain position
Brainstem centers of eye movement, called neuronal integrators. They are responsible for holding the gaze in a certain position. These centers change incoming signals about the speed of movement of the eyeballs into information about their position. Neurons with this property are located in the pons below (caudal) the abducens nucleus.
Eye movement with changes in gravity and acceleration
Coordination of the movements of the eyeballs in response to changes in gravity and acceleration is carried out by the vestibular system (vestibular-ocular reflex). When the coordination of movements of both eyes is disturbed, double vision develops, since images are projected onto disparate (inappropriate) areas of the retina. In congenital strabismus, or strabismus, a muscle imbalance that causes the eyeballs to be misaligned (nonparalytic strabismus) may cause the brain to suppress one of the images. This decrease in visual acuity in the non-fixing eye is called amblyopia without anopia. In paralytic strabismus, double vision occurs as a result of paralysis of the muscles of the eyeball, usually due to damage to the oculomotor (III), trochlear (IV) or abducens (VI) cranial nerves.
Eyeball muscles and gaze palsies
There are three types of paralysis of the external muscles of the eyeball:
Paralysis of individual eye muscles
Characteristic clinical manifestations occur with isolated damage to the oculomotor (III), trochlear (IV) or abducens (VI) nerve.
Complete damage to the oculomotor (III) nerve leads to ptosis. Ptosis manifests itself in the form of weakening (paresis) of the muscle that lifts the upper eyelid and disruption of voluntary movements of the eyeball upward, downward and inward, as well as divergent strabismus due to the preservation of the functions of the lateral (lateral) rectus muscle. When the oculomotor (III) nerve is damaged, pupil dilation and lack of reaction to light (iridoplegia) and paralysis of accommodation (cycloplegia) also occur. Isolated paralysis of the muscles of the iris and ciliary body is called internal ophthalmoplegia.
Injuries to the trochlear (IV) nerve cause paralysis of the superior oblique muscle of the eye. Such damage to the trochlear (IV) nerve leads to outward deviation of the eyeball and difficulty moving (paresis) downward gaze. Paresis of downward gaze is most clearly manifested when turning the eyes inward. Diplopia (double vision) disappears when the head is tilted to the opposite shoulder, which causes a compensatory inward deviation of the intact eyeball.
Damage to the abducens (VI) nerve leads to paralysis of the muscles that abduct the eyeball to the side. When the abducens (VI) nerve is damaged, convergent strabismus develops due to the predominance of the influence of the tone of the normally working internal (medial) rectus muscle of the eye. With incomplete paralysis of the abducens (VI) nerve, the patient can turn his head towards the affected abductor muscle of the eye in order to eliminate the existing double vision using a compensatory effect on the weakened lateral rectus muscle of the eye.
The severity of the above symptoms in cases of damage to the oculomotor (III), trochlear (IV) or abducens (VI) nerve will depend on the severity of the lesion and its location in the patient.
Friendly gaze paralysis
Companionate gaze is the simultaneous movement of both eyes in the same direction. Acute damage to one of the frontal lobes, for example, during cerebral infarction (ischemic stroke), can lead to transient paralysis of voluntary conjugate movements of the eyeballs in the horizontal direction. At the same time, independent eye movements in all directions will be completely preserved. Paralysis of voluntary conjugate movements of the eyeballs in the horizontal direction is detected using the doll eye phenomenon when passively turning the head of a horizontally lying person or using caloric stimulation (infusion of cold water into the external auditory canal).
Unilateral damage to the inferiorly located paracentral part of the reticular formation of the pons at the level of the nucleus of the abducens nerve causes persistent gaze paralysis in the direction of the lesion and loss of the oculocephalic reflex. The oculocephalic reflex is a motor reaction of the eyes to irritation of the vestibular apparatus, as with the phenomenon of the head and eyes of a doll or caloric stimulation of the walls of the external auditory canal with cold water.
Damage to the rostral interstitial nucleus of the medial longitudinal fasciculus in the anterior midbrain and/or damage to the posterior commissure causes supranuclear upward gaze palsy. Added to this focal neurological symptom is the dissociated reaction of the patient’s pupils to light:
- sluggish pupil reaction to light
- rapid reaction of the pupils to accommodation (changing the focal length of the eye) and looking at nearby objects
In some cases, the patient also develops convergence paralysis (movement of the eyes towards each other, in which the gaze will focus on the bridge of the nose). This symptom complex is called Parinaud's syndrome. Parinaud's syndrome occurs with tumors in the pineal gland, in some cases with cerebral infarction (ischemic stroke), multiple sclerosis and hydrocephalus.
Isolated downward gaze palsy is rare in patients. When this occurs, the cause is most often blockage (occlusion) of the penetrating arteries in the midline and bilateral infarctions (ischemic strokes) of the midbrain. Some hereditary extrapyramidal diseases (Huntington's chorea, progressive supranuclear palsy) can cause restrictions in the movement of the eyeballs in all directions, especially upward.
Mixed paralysis of gaze and individual muscles of the eyeball
The simultaneous combination of gaze paralysis and paralysis of individual muscles that move the eyeball in a patient is usually a sign of damage to the midbrain or pons. Damage to the lower parts of the pons with destruction of the abducens nerve nucleus located there can lead to paralysis of rapid (saccadic) horizontal movements of the eyeballs and paralysis of the lateral (external) rectus muscle of the eye (abducens nerve, VI) on the affected side.
With lesions of the medial longitudinal fasciculus, various gaze disturbances occur in the horizontal direction (internuclear ophthalmoplegia).
Unilateral damage to the medial longitudinal fasciculus caused by infarction (ischemic stroke) or demyelination leads to disruption of the inward adduction of the eyeball (to the bridge of the nose). This can manifest clinically as complete paralysis with the inability to move the eyeball inward from the midline, or as a moderate paresis, which will manifest itself as a decrease in the speed of adducting rapid (saccadic) eye movements to the bridge of the nose (adductive delay). On the side opposite to the lesion of the medial longitudinal fasciculus, as a rule, abduction nystagmus is observed: nystagmus that occurs when the eyeballs are abducted outward with a slow phase directed towards the midline and fast horizontal saccadic movements. An asymmetrical arrangement of the eyeballs relative to the vertical line often develops with unilateral internuclear ophthalmoplegia. On the affected side, the eye will be positioned higher (hypertropia).
Bilateral internuclear ophthalmoplegia occurs with demyelinating processes, tumors, infarction, or arteriovenous malformations. Bilateral internuclear ophthalmoplegia leads to a more complete syndrome of eyeball movement disorders, which are manifested by bilateral paresis of the muscles that lead the eyeball to the bridge of the nose, impaired vertical movements, purposeful tracking movements and movements caused by the influence of the vestibular system. There is a disturbance of gaze along a vertical line, upward nystagmus when looking up and downward nystagmus when looking down. Lesions of the medial longitudinal fasciculus in the overlying (rostral) parts of the midbrain are accompanied by a violation of convergence (convergent movement of the eyes towards each other, towards the bridge of the nose).
There are several classifications of paralysis, each type has its own characteristics.
The causes of the disease are primarily associated with pathologies of the nervous tissue; such pathologies can be congenital, or can arise as a result of damage to the nerves in the area of the cranial nerve nuclei, in the area of large nerve trunks, roots and branches.
Causes of acquired ophthalmoplegia;
Classification
In this case, the eye shifts to the zone of action of a healthy or less affected muscle. The patient has difficulty moving the eyes towards the paralyzed muscles, resulting in double vision.
With complete external ophthalmoplegia, the eyeball is constantly in a static position, which leads to the development of ptosis. Partial internal ophthalmoplegia occurs due to the dilation of a pupil that does not respond to light.
The symptoms of the disease are as follows:
When the first signs of the disease appear, it is recommended to immediately consult an ophthalmologist.
Diagnostics
Despite the presence of pronounced external signs, the following hardware tests are prescribed;
Therapy consists of eliminating the causes of the disease, alleviating pain and restoring, if possible, nervous and muscle activity.
Physiotherapeutic methods
Surgical intervention
Surgical treatment is prescribed if it is necessary to eliminate the tumor that caused the disease; the procedure allows you to restore the integrity of the nerve and restore muscle function.
Ophthalmoplegia
Ophthalmoplegia is a paralysis of the eye muscles that occurs when the oculomotor nerves are damaged.
Main causes of ophthalmoplegia
Ophthalmoplegia can occur with congenital or acquired lesions of the nervous system in the area of nerve roots or trunks, in the area of the cranial nerve nuclei. For example, congenital ophthalmoplegia occurs as a result of aplasia of the nuclei of the oculomotor nerves, and in some cases can be combined with changes in the eye muscles and aplasia of the nerve trunks. This pathology is often combined with malformations of the eyeball and can be observed in several members of the same family.
The causes of acquired ophthalmoplegia may be:
Ophthalmoplegia can also be a symptom of a rare condition called ophthalmoplegic migraine. It manifests itself as attacks of severe headaches, accompanied by unilateral ophthalmoplegia (complete or partial). Headaches can continue for a long time, while the function of the oculomotor nerves is gradually restored.
Types of ophthalmoplegia
Ophthalmoplegia can be unilateral or bilateral. External ophthalmoplegia occurs when the muscles that are located outside the eyeball are paralyzed, and when the intraocular muscles are paralyzed, internal ophthalmoplegia occurs. With varying degrees of muscle weakening during paralysis, partial internal or external ophthalmoplegia develops. If both the external and internal muscles of the eye are paralyzed at the same time, complete ophthalmoplegia occurs. Complete external and complete internal ophthalmoplegia may also occur.
The eyeball with external partial ophthalmoplegia will tilt towards the healthy or less paralyzed muscle, and its movements towards the action of the paralyzed muscles will be absent or significantly limited. In this case, doubling of objects will appear. With external complete ophthalmoplegia, the eyeball will become immobile and ptosis will develop. Internal partial ophthalmoplegia is characterized only by pupil dilation in the absence of reaction to light, decreased convergence and accommodation.
Ophthalmoplegia is the name given to a symptom of many neurological diseases in which the motor function of the eyeballs is limited due to decreased tone of the eye muscles. Simply - paralysis of the eye muscles due to disease of the optic nerves.
Reasons
Ophthalmoplegia can be congenital (due to congenital pathologies of the nervous system) or acquired. The causes of the disease may be:
In addition, ophthalmoplegia may be a symptom of the rare ophthalmoplegic migraine. After the attack ends, the eye slowly returns to normal.
Symptoms
The disease immobilizes the eyeball, and voluntary eye movements become impossible. Sometimes the eye is tilted to the side. A person begins to see double. Drooping of the upper eyelid (ptosis), headache and pain in the eyeball may appear. Or the mobility of the eyeball is preserved, but the pupil does not narrow in bright light. Convergence and accommodation are impaired - due to the incorrect position of the eyes and the impossibility of their synchronous work, the patient cannot focus his gaze on an object, regardless of its distance or approach. External signs also include bulging of the eyeball, redness of the eye and swelling around the orbit.
Ophthalmoplegia varies depending on which muscles and nerves of the eye are affected, to what extent, and what the nature of the damage is.
Diagnostics
Ophthalmoplegia has pronounced external signs. But to identify its causes, in addition to consultations with an ophthalmologist and neurologist, the patient is prescribed hardware tests:
Find out more about the symptom of blurred vision.
Treatment
Treatment of ophthalmoplegia consists of eliminating the causes of the disease, relieving pain and restoring, as far as possible, muscle and nervous activity.
- anti-inflammatory drugs;
- medications that prevent dehydration of the body during poisoning and intoxication;
- vitamins B6, B12, C, as a general tonic;
- vasodilators for vascular diseases of the brain;
- nootropic to improve nervous activity;
- anticholinesterase drugs that eliminate muscle weakness;
- corticosteroid hormones to normalize metabolism and restore muscle function.
The earlier the disease is detected, the more likely it is to successfully get rid of it. Do not ignore visits to the doctor and try to cure yourself.
Ophthalmoplegia is a disease accompanied by paralysis of individual or all eye muscles, which are driven by the abducens, trochlear and oculomotor nerves.
Congenital ophthalmoplegia is a consequence of aplasia of the nerve nuclei of the eye, anomalies in the intrauterine development of a child with no abnormalities in the structure of muscles or nerves.
Most often, congenital pathology is accompanied by other structural defects of the eye.
Other causes of congenital pathology:
Ophthalmoplegia can be unilateral and bilateral, external and internal. External develops as a result of paralysis of the muscles located outside the eye. Internal occurs due to paralysis of the intraocular muscles; with varying degrees of muscle damage, we can talk about partial ophthalmoplegia.
In medicine, a distinction is also made between complete external and internal ophthalmoplegia, in this case we are talking about simultaneous paralysis of the internal and external muscles.
As a result of complete internal oophthalmoplegia, the pupil dilates, it stops responding to light and convergence, and the ability to distinguish objects at different distances from the eye decreases.
Symptoms
Drug treatment
Depending on the causes of the disease, the following drugs may be prescribed:
In order to reduce pain, relieve spasms and strengthen muscles, acupuncture, electrophoresis and phonophoresis with medications are prescribed.
What is ophthalmoplegia, its types and treatment methods
Ophthalmoplegia is a disease that occurs as a result of damage to the optic nerves and is accompanied by paralysis of the eye muscles. This is a neurological pathology that limits the motor function of the eyeballs.
It can be due to many reasons: infectious diseases. head or eye injuries and poisoning.
Provoking pathologies
The key reasons for the development of ophthalmoplegia are pathologies of nerve tissue. The disease can be congenital or acquired.
The congenital form in most cases occurs with other pathologies in the structure of the eye and is part of a complex of symptoms of various genetic anomalies. There is a hereditary cause of the disease.
Acquired ophthalmoplegia develops as a result of the following reasons:
The disease can develop against the background of other infectious diseases - tuberculosis or syphilis, as well as tetanus, botulism and diphtheria.
Ophthalmoplegia can be an accompanying symptom of ophthalmoplegic migraine, a rare disease that causes severe headache attacks.
Clinical picture
Symptoms of the disease manifest themselves in different ways, the degree of their severity depends on the type of ophthalmoplegia. The main signs for diagnosing pathology are:
In severe forms of the disease, there may be a lack of activity and mobility of the eyeball, a deterioration in the reaction of the pupil to light and its immobility. If ophthalmoplegia develops against the background of other diseases, the clinical picture also includes additional symptoms.
Types of disease
Types of ophthalmoplegia are distinguished according to the following criteria:
Depending on the location of the damaged muscles, ophthalmoplegia is of two types:
Based on the degree of damage to the optic nerves, partial and complete ophthalmoplegia are distinguished. Partial can be external, in which the work of the extraocular muscle of the eyelid is disrupted, and internal, if only the nerve columns are affected by paralysis.
In the full form of the disorder, there is immobility of the eyeball and drooping of the upper eyelid, and the inability of the pupil to respond to light.
Depending on the nature of the lesions, ophthalmoplegia occurs:
Diagnosis and treatment
Diagnosis of the type of disease and the causes that cause it is necessary to select a treatment method.
The disease is diagnosed by initial examination. It has pronounced external manifestations. To establish the nature of the disease and its causes, consultation with a neurologist and ophthalmologist is necessary.
The following additional studies may be prescribed:
If neoplasms are detected, additional consultation with an oncologist may be required.
After receiving all the necessary data about the disease and determining the causes, treatment is prescribed. It is aimed at eliminating the factors that resulted in the development of ophthalmoplegia, relieving pain and maximizing the restoration of nervous and muscular activity.
There are three main types of treatment, which are prescribed depending on the severity of the disease and the nature of the damage:
- Drug treatment prescribed taking into account underlying diseases. Anti-inflammatory, vasodilating, and nootropic drugs may be prescribed. Part of the therapy is taking general strengthening agents: vitamins and minerals. Corticosteroid hormones are prescribed to normalize metabolism and regenerate muscle functions.
- Physiotherapeutic treatment consists of carrying out a series of procedures that strengthen muscles, relieve spasms and reduce pain. For this purpose, the patient is prescribed electrophoresis, phonophoresis and acupuncture.
- If the cause of the disease is neoplasms of different types, then it is prescribed surgical treatment to remove them. This type of treatment is also used to repair damaged muscles and remove aneurysms.
- avoid injury to the head and eyes;
- maintain the body’s immune strength by periodically taking vitamin complexes;
- if there are cases of ophthalmoplegia in your family, it is necessary to undergo preventive examinations by an ophthalmologist more often;
- treat infectious diseases in a timely manner and prevent the development of complications;
- do not abuse alcohol, minimize contact with substances that can cause intoxication of the body: lead, barbiturates;
- If you have any alarming symptoms, you should consult a doctor in order to promptly detect deviations from the norm;
- do not self-medicate.
The first two types of therapy are acceptable in the initial stages of the disease in the absence of serious concomitant diagnoses. With their help, you can get rid of ophthalmoplegia if you detect the disease in a timely manner and prevent the development of complications.
Preventive measures
There are no specific preventive measures to prevent ophthalmoplegia. The recommendations are general in nature, and following them helps protect the eyes not only from the development of this disorder, but also from other eye diseases. To reduce the risk of developing pathology, you must:
Ophthalmoplegia can develop against the background of other neurological diseases. A complete preventive examination should be completed 2 times a year in order to identify them in time and begin treatment.
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 muscle group 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.
20-02-2012, 20:51
Description
Dysfunction of extraocular muscles
Information on the frequency of oculomotor disorders in brain tumors is scarce. It is believed that they occur in 10-15% of cases [Tron E. Zh., 1966; Huber D., 1976]. Most often occur signs of impaired innervation of the abducens nerve, paresis and paralysis of the oculomotor nerve are rare, and lesions of the trochlear nerve are extremely rare.
Paralysis usually results to impaired binocular vision, especially if the superior rectus muscles are affected and vertical diplopia develops. In patients with severe paresis, especially horizontal paresis, binocular vision is absent in all parts of the visual field.
Paresis and paralysis of the III, IV, VI pairs of cranial nerves, arising as a result of increased intracranial pressure, do not have independent significance in the topical diagnosis of brain tumors.
Greatest vulnerability of the abducens nerve with increased intracranial pressure, it finds an explanation in its anatomical and topographic connections with individual structures of the brain, the vascular system and the bones of the base of the skull. The fact is that upon exiting the pons, the abducens nerve is located between the dura mater and the branches of the basilar artery. Sometimes for a short distance it lies between the branches of the basilar artery and the pons. In these cases, increased intracranial pressure can lead to pinching of the nerve between the pons and the posterior cerebellar artery. A partial disruption of the conduction of the abducens nerve develops and, as a result, a weakening of the external rectus muscle on the side of the same name develops. If the paresis is minor, clearly defined horizontal diplopia appears with extreme abduction of the eye towards the weakened muscle. Thus, diplopia is horizontal and homonymous in nature. There is information in the literature about the predominance of bilateral lesions of the abducens nerve in patients with brain tumors [Tron E. Zh., 1966; Kirkham T. et al., 1972].
Of interest are the daily fluctuations in severity abducens nerve palsy. In patients with brain tumors, daily variations in intracranial pressure were observed, and at the moment of its decrease, a sharp relaxation of paresis of the abducens nerve was noted. The latter is also observed during dehydration therapy.
Second section The abducens nerve has the least resistance to increased intracranial pressure where it passes over the upper edge of the pyramid of the temporal bone. A growing tumor and increased intracranial pressure can dislocate the brain, and the trunk of the abducens nerve is pressed against the sharp edge of the pyramid.
Paresis of the abducens nerve is observed in patients with tumors subtentorial localization and their supratentorial location. Describing paresis of the abducens nerve with increased intracranial pressure, N. Cusching emphasized that this symptom in brain tumors should be regarded as a false localization sign. His opinion was confirmed in later works [Tron E. Zh., 1966; Gassel M., 1961; Nieber A., 1976].
The oculomotor nerve, departing from the cerebral peduncles, also passes between two vessels (posterior cerebral and superior cerebellar arteries). Therefore, increased intracranial pressure may cause nerve damage between vessels. In addition, the nerve may become pressed against Blumenbach's ring. Since the pupillary fibers running as part of the oculomotor nerve are more vulnerable, an early symptom may be unilateral mydriasis with complete areflexia.
In case of paresis and paralysis, to clarify the diagnosis, it is important to find out at what level the lesion occurred: 1) in the muscle, 2) in the nerve trunk, or 3) at the level of the nuclei or roots.
In recent years, topical diagnosis has become easier thanks to the use of electromyography .
Experience has shown that using this method it turned out to be possible to differentiate various types of myopathies (myositis, endocrine ophthalmopathies), myasthenia gravis, peripheral and central muscle paralysis.
Damage to the abducens nerve at the trunk level is characterized horizontal diplopia, especially with maximum eye abduction outward. If there is mild paresis, slight converging movements are possible. As mentioned above, the abducens nerve is most vulnerable when intracranial pressure increases. Assessment of only one brainstem palsy does not have independent diagnostic value. Its combination with other neurological symptoms (damage to III, IV, V, VII, VIII pairs of cranial nerves) is important.
Nuclear paralysis usually combined with gaze paralysis in the same direction, since the center of gaze for horizontal movements is located near the nucleus of the oculomotor nerve.
Fascicular palsy characterized by two syndromes. Millard-Gubler syndrome consists of the following features: paresis of the lateralis muscle, homolateral peripheral facial palsy, crossed hemiplegia. All signs of damage to the facial bundles of the VI and V pairs of cranial nerves can occur not only when the pathological process is localized in the pons, but also as a dislocation sign when the quadrigeminal or cerebellum is damaged.
Fauville syndrome characterized by paresis of the lateral rectus muscle, homolateral peripheral facial palsy, homolateral horizontal gaze palsy. Possible combination with Horner's syndrome.
Brainstem paralysis oculomotor nerve is characterized by dysfunction of all eye muscles innervated by this nerve. E. Zh. Tron (1966) notes that progressive truncal paralysis of the oculomotor nerve is characterized by the initial appearance of ptosis followed by damage to all other muscles.
Clinical picture of nuclear paralysis depends on the topography of the nuclei oculomotor nerve (Fig. 80).
Rice. 80. Scheme of the location of the nuclei innervating the eye muscles (according to Hubar A.) I - parvocellular medial nucleus (center of innervation of the ciliary muscle); II - small cell lateral nuclei (the center of innervation of the sphincter of the pupil); III - magnocellular lateral nuclei: 1 - levator nucleus, 2 - nucleus of the superior rectus muscle; 3 - nucleus of the medial rectus muscle; 4 - nucleus of the superior rectus muscle, 5 - nucleus of the inferior rectus muscle; IV - trochlear nerve nucleus; V - nucleus of the abducens nerve; 6 - cortical center of gaze.
They are represented by paired large-cell lateral nuclei that innervate the rectus oculi and levator muscles, paired small-celled Yakubovich-Westphal-Edinger nuclei that innervate the sphincter of the pupil, and a single nucleus of Perlia that sends fibers to the ciliary muscle. The large cell nuclei have a large extent under the bottom of the Sylvian aqueduct, as they are represented by five cellular formations that send a representative to each muscle. In this case, the superior rectus muscle and the levator receive fibers from the cellular formations of the same side, the inferior rectus muscle - from the cellular formations of the opposite side, and the fibers innervating the internal rectus and inferior oblique muscles have a bilateral representation. In this regard, nuclear palsies are characterized by dysfunction of single or several muscles in both eyes. There may be pupillary disorders (mydriasis, weakened pupillary reactions, accommodation paresis).
Fascicular palsies characterized by the possibility of the appearance of two syndromes.
Weber syndrome- unilateral complete paralysis of the oculomotor nerve with cross hemiplegia, cross paralysis of the face and tongue is possible.
Benedict's syndrome- unilateral paresis of the oculomotor nerve with crossed hemitremor. Sometimes it is combined with cross-hemianesthesia.
truncal trochlear nerve palsy has no independent diagnostic value for brain tumors. Isolated paralysis and paresis are extremely rare.
Nuclear palsies in combination with oculomotor nerve palsy and vertical gaze palsy, convergence spasm or its paralysis are characteristic of pineal tumors.
Paresis and paralysis of gaze with brain tumors, according to the literature, are extremely rare (about 1.5%). In contrast to paresis and paralysis of the extraocular muscles, paresis and gaze paralysis are characterized by an equal limitation of the mobility of both eyes. There is no strabismus or diplopia with them. The functions of the muscles concerned are only partially limited. They develop as a result of localization of the pathological process in supranuclear or nuclear centers. Gaze palsies can be vertical or horizontal.
Vertical gaze palsies observed when the center of gaze in the quadrigeminal region is turned off. Upward gaze paralysis is more common. With paresis of upward gaze, eye movements in this direction are not limited, but when trying to look upward, vertical nystagmus occurs. E. J. Tron (1966) emphasizes that in diseases of the quadrigeminal region, vertical nystagmus may precede the appearance of upward gaze paralysis.
Horizontal gaze palsies arise either as a result of turning off the cortical gaze center in the frontal gyrus, or when turning off the gaze center in the pons. There is a certain dependence of the nature of gaze paralysis on the level of the lesion.
Violation of the frontal center and frontopontine pathway leads to turning off voluntary eye movements, vestibular and optical eye movements are preserved.
Defeat in the center area in the pons leads to the absence of movements, both volitional, vestibular and optical, in the direction of gaze paralysis. Gaze paralysis is pronounced and stable. Friendly deviations of the eyes are rare and mild. R. Bing and R. Brückner (1959) believe that the loss of vestibular excitability of the extraocular muscles in gaze paralysis characterizes damage to the trunk. Lack of voluntary movements if the optical and vestibular ones are preserved, it indicates damage to the frontal center or frontopontine tract. A. Huber (1976) formulates the possibility of differentiation as follows: bilateral lesions of the frontopontine tract cause complete bilateral paralysis, often with the appearance of bilateral vertical paralysis. Bilateral lesions in the pons are usually accompanied by only paralysis, horizontal in both directions. At the same time, vertical movements are preserved.
Nystagmus- involuntary rhythmic movements of one or both eyes in a certain or any direction of gaze. Nystagmus may be pendulum-like, when eye movements in both directions are performed at the same speed and in the same volume; and jerk-like, in which there are two phases of the rhythm: in one direction the eye moves quickly (fast phase of nystagmus), in the opposite direction - slowly (slow phase of nystagmus). The direction of movement of nystagmus is determined by the direction of movement of its fast phase. Based on the direction of movement, horizontal, vertical, rotatory and mixed nystagmus are also distinguished. The latter is characterized by the presence of several components.
Based on the intensity of movements, they are distinguished three stages of nystagmus:
Stage I - nystagmus appears only when the eye is turned towards the fast phase, stage II - active nystagmus when the eye is turned towards the fast phase and when the gaze is directed straight ahead, and, finally, stage III - pronounced nystagmus when looking straight, expressed when the gaze is directed to the side fast phase and weak nystagmus when moving the eye towards the slow phase.
By range of movements They distinguish small nystagmus, in which the amplitude of eye movements does not exceed 3°; average nystagmus, in which the amplitude of movements ranges from 5 to 10°, and rough nystagmus, in which the eye oscillates more than 15°.
Nystagmus may be physiological and pathological. The latter occurs with diseases of the labyrinth or with the action of a pathological process on the nuclei of the vestibular nerve or the paths extending from it to the nuclei of the nerves of the oculomotor apparatus. Vestibular nystagmus is almost always jerk-like, and in the direction of movement - horizontal, vertical or rotatory. Labyrinthine, or peripheral, nystagmus always has one direction in all directions of gaze and does not depend on body position. In addition, it is not particularly durable and tends to decrease as its duration increases. Often combined with dizziness and deafness.
Nuclear or central, nystagmus can change its direction with a change in gaze, which is never observed with peripheral nystagmus. It exists for a long time, months and even years, if the reason that caused it is not eliminated. Typically, central nystagmus is not accompanied by hearing loss and tends to increase as the period of its existence lengthens. Unlike peripheral nystagmus, it disappears when examining the patient in the dark (electronystagmography in the dark).
Central nystagmus usually occurs for tumors of subtentorial localization, especially in the area of the cerebellopontine angle. With tumors of the trunk, central pathological nystagmus is almost always a constant symptom. Vestibular central nystagmus is also possible with supratentorial tumors (tumors of the frontal, temporal lobes), but in these cases it is caused by displacement of the brain by the growing tumor.
In recent years, the attention of researchers has attracted state of saccadic eye movements for various diseases of the central nervous system. Micromovements of the eyes, or physiological nystagmus, are involuntary micromovements of the eyes that occur when fixing a fixed point. The function of saccadic eye movements is to move the image of objects to the area of the central fovea of the retina. By the nature of the movements that appear distinguish between drift, tremor and jumps.
Drift is called smooth, slow displacement of the eyes within 5-6 arcs. min. Oscillatory movements with an amplitude of 20-40 arc. min and with high frequency are called tremor. Microjumps, or microsaccades, are rapid eye movements ranging from 1 arc. min up to 50 arc. min. Normally, the saccades of both eyes are synchronous and have the same direction and amplitude.
S. A. Okhotsimskaya and V. A. Filin (1976, 1977) showed that saccadic eye movements with basal paresis and paralysis are directly dependent on the degree of damage to the oculomotor nerve. Thus, with mild paresis, microjumps practically do not differ from the norm. As the severity of paralysis increases, the interval between jumps increases and the number of jumps decreases. An increase in the degree of paralysis ultimately leads to a sharp decrease in the amplitude of all types of eye micromovements until their complete disappearance. These changes correspond to the side of the lesion and do not depend on which eye is the fixing one. The authors found that with paresis the drift amplitude increases, and with paralysis it decreases.
Brainstem lesion accompanied by a violation of the central mechanisms of control of fixation movements. The frequency, direction and amplitude of micromovements change, and pathological spontaneous nystagmus occurs. As noted earlier, spontaneous nystagmus often precedes paresis and paralysis of the oculomotor nerves. The close topographic relationships of the nuclei and supranuclear stem gaze centers in the brainstem lead, as a rule, to mixed lesions. Examining 15 patients with brainstem paralysis, S. A. Okhotsimskaya (1979) found that changes in saccadic eye movements can be detected in cases where clinical gaze paresis is still absent. Thus, these changes can be regarded as early symptom developing gaze paresis with intrastem lesions. A characteristic sign of unilateral nuclear palsy, according to S. A. Okhotsimskaya, can be considered an asymmetry in the distribution of “jumps, the loss of all types of jumps in the direction of the lesion for both eyes. This symptom was observed more clearly in patients with unilateral pontine tumors. With bilateral lesions of the trunk, there were no surges even in cases of incomplete ophthalmoplegia.
Disorders of pupillary reactions
The literature describes many syndromes associated with disorders of pupillary reactions in diseases of the central nervous system. Of practical importance are those pupillary disorders that occur with brain tumors. Of these, the most important is pupil reaction to light.
Before moving on to a description of changes in the shape of the pupils and their reaction in patients with brain tumors, it is advisable to dwell on the anatomical features pupillary reflex pathways(Fig. 81).
Fig 81. Diagram of the visual pathway and pupillary reflex. 1 - ciliary node; 2 - optical path; 3 - lateral geniculate body; 4 chiasmus; 5 - optical radiation (Graziole beam); 6 - visual cortex, Yakubovich-Westphal-Edinger nuclei; 8 - anterior quadrigeminal.
Afferent fibers of the pupillary reflex as they exit the optic cords form a synapse in the anterior quadrigeminal region (regio pretectalis), from where they are directed to the nuclei of the oculomotor nerve (Yakubovich-Westphal-Edinger nucleus), and some of the fibers are directed to the nucleus of the homolateral side, some of the fibers form a decussation in the posterior commissure, after which they reach the contralateral Yakubovich-Westphal nucleus. Edinger. Thus, each Yakubovich-Westphal-Edinger nucleus innervating the sphincter of the iris has a representation of fibers of the afferent pupillary arch of both the same and the opposite side. This explains the mechanism of direct and friendly pupillary reactions to light T.
With normal vision there is synkinetic constriction of the pupil with convergence of the eyeballs or contraction of the ciliary muscle during accommodation. There is no clear idea in the literature about mechanism of miosis in connection with convergence and accommodation. O. N. Sokolova (1963), referring to S. Duke Elder, describes this mechanism as follows: proprioceptive impulses arising from the contraction of the internal rectus muscles, through the oculomotor nerve, and possibly through the trigeminal nerve, reach the nuclei of the V nerve and the Yakubovich nuclei -Westphal-Edinger. Excitation of these nuclei leads to contraction of the sphincer of the pupil. Accommodation is stimulated by visual impulses arising in the retina and directed to the occipital lobe cortex, and from there to the Yakubovich-Westphal-Edinger nuclei. The efferent path for convergence and accommodation is common and it passes as part of the oculomotor nerve to the ciliary muscle and to the sphincter of the pupil.
The most subtle and delicate disorders of pupillary reactions were possible to identify only with the help of local pupillography method or local exposure to the subject being examined.
According to E. Zh. Tron (1966), impaired pupillary reactions are a very rare symptom in brain tumors (it occurs in no more than 1% of cases). Symptom of pupillary disorders appears, as a rule, with tumors of the quadrigeminal epiphysis, third ventricle and Sylvian aqueduct. Occlusion the latter is accompanied by the appearance of an early symptom of impaired pupillary reactions in response to local illumination of the macular area while maintaining the reaction to accommodation and convergence [Sokolova O. N., 1963]. The combination of pupillary disorders with a violation of the acts of accommodation and convergence is a later sign, indicating a significant spread of the tumor process, including the quadrigeminal area. Tumors of the quadrigeminal gland and pineal gland may also be accompanied by paresis and upward gaze paralysis.
Shape and size of pupils importance should also be given, since a change in the size of the pupils can sometimes be one of the symptoms of blindness that the patient is not aware of.
Normal pupil width varies within a fairly wide range - from 3 to 8 mm. It should be taken into account that fluctuations in the diameter of the pupils are normally acceptable: anisocoria can reach. 0.9 mm [Samoilov A. Ya. et al., 1963]. Children's pupils are always wider than adults'. By pupil size The color of the iris also influences it. It has been noticed that blue-eyed and gray-eyed people have wider pupils than brown-eyed people. Ophthalmologists know the fact that pupils are dilated in nearsighted people, so the nature of refraction should be taken into account when assessing the pupils. Unilateral myopia can cause anisokeria. The latter is observed in diseases of the gallbladder and damage to the apexes of the lungs.
For brain tumors anisocoria occurs in approximately 11% of patients [Tron E. Zh., 1966]. Paralytic mydriasis, especially combined with paresis of accommodation- a typical sign of damage to the oculomotor nucleus in the midbrain. A. Huber (1966) describes unilateral mydriasis in tumors of the temporal lobe. In this case, anisocoria was combined with mild homolateral ptosis, which appeared earlier than mydriasis and was caused by compression of the peripheral part of the oculomotor nerve at the clivus by a displaced brain or a growing tumor. As the tumor process progresses, paralysis of the external rectus muscles of the eye may occur.
Orbital tumors, localized paraneurally and compressing the ciliary ganglion, sometimes cause mydriasis on the affected side with mild exophthalmos or even before its appearance [Brovkina A.F., 1974]. It should also be taken into account that after orbitotomy and tumor removal, unilateral mydriasis with the correct shape of the pupil, its lack of reaction to light and convergence as a result of a violation of the efferent pupillary soul. We observed in such patients paresis of accommodation and slight impairment of corneal sensitivity. Considering that postoperative mydriasis persists for 8-12 months, this symptom should be taken into account in the differential diagnosis of brain tumors.
Unilateral mydriasis in combination with paresis of the rectus muscles of the eye, it occurs when the pathological process is located at the apex of the orbit, in the area of the superior orbital fissure. Pituitary tumors, when they spread extrasellar to the temporal side, causing paresis of the oculomotor nerve, can also lead to the appearance of unilateral mydriasis and ptosis.
In 1909, S. Baer described unilateral mydriasis in patients with Tractus hemianopsia. A wide pupil and a noticeable widening of the palpebral fissure were found on the hemianopsia side. The syndrome described by S. Baer seems to facilitate the topical diagnosis of a tumor accompanied by hemianopia. However, E. Zh. Tron, analyzing cases of injury to the occipital lobe, found hemianopsia with anisocoria in 1/3 of cases. According to I. I. Merkulov (1971), this does not detract from the advantages of Baer syndrome in the topical diagnosis of tractus hemianopsia.
Changes in field of view
Brain tumors in almost half of cases are combined with changes in visual field. Often these changes make it possible to make a topical diagnosis of a tumor lesion.
It should be considered optimal to use kinetic and static perimetry, both suprathreshold and quantitative. In this case, the boundaries of the field of view from 1 to 3 isopters are examined. It should be noted, however, that in most cases in neurological patients it is extremely difficult to study isopters as well as performing profile static perimetry. This is due to the patient’s rapid fatigue, insufficient attention, and often to the lack of sufficient contact between the patient and the doctor. In such cases, it may be useful to study the central visual field (up to 25° from the point of fixation) with multiple objects on the so-called visual field analyzers [Astralenko G. G., 1978; Friedman, 1976]. When examining a visual field analyzer, the patient is presented with 2 to 4 suprathreshold objects simultaneously, a total of 50 to 100 objects. Examination of one eye takes 2-3 minutes.
In patients with low visual acuity or in the absence of proper attention, it is advisable to use a simple, so-called control method (confrontation test), in which the field of view of the subject is compared with the field of view of the examiner. The technique of the control method for studying the visual field is described in all manuals. Less known is the test proposed by A. Kestenbaum (1947). It is unjustifiably little used in control studies of neurological patients.
The essence of the Kestenbaum test or “contour” perimetry is that the field of view in the plane of the face approximately coincides with the outlines of the subject’s face. Therefore, the contours of the patient’s face can serve as a reference point. The test is carried out as follows. The patient looks straight ahead. The researcher, standing behind him, moves the object (finger or pencil) from the periphery to the center along 12 meridians in the plane of the patient’s face, but no further than 2 cm (!) from him. The patient must report when he begins to distinguish the object. Normally, the field of vision should coincide with the contours of the face: the nasal border runs along the line of the nose, the temporal border runs along the bony edge of the outer wall of the orbit. A. Kestenbaum believes that the error of the method in the hands of an experienced researcher does not exceed 10°.
Simplified methods for studying the visual field include the test reflex closure of the palpebral fissure. A hand is passed in front of the patient's eye on four sides, and the eyelids reflexively close. For hemianopsia in the zone of lack of vision, the eyelids will not close. This test can be recommended when examining patients with stupor, aphasia, or when visual acuity decreases before hand movements near the face.
Control study for relative hemianopsia carried out with both eyes of the patient open. The doctor moves both hands (or two fingers) symmetrically from the temple to the center along the four meridians. The main condition should be considered good lighting. The patient must say when he sees one or two hands or when he recognizes their contours (if visual acuity is poor). If there is a difference in perception on both sides, we can talk about relative hemianopsia, as opposed to absolute hemianopsia, which can only be detected with an isolated study of each eye. However, early topical diagnosis of lesions of the optic-nervous pathway requires qualified research using kinetic perimetry with a sufficient number of objects and campimetry.
A. Huber (1976) believes that at present there is no point in performing color perimetry. To detect scotoma in red, which is one of the early signs of developing atrophy of the optic nerve or tract, it is quite sufficient to conduct perimetry with a red object 5 mm from a distance of 33 cm (5/330).
At the core topical diagnostics damage to the optic nerve tract due to brain tumors lies a clear idea of the course of its fibers. A schematic representation of the visual pathway is shown in Fig. 82.
Rice. 82. Diagram of the location of nerve fibers in the chiasm. 1 - retina; 2 - optic nerve; 3 - chiasma; 4 - optical path; 5 - diagram of the cross section of the chiasm; 6 - pituitary gland; 7 - zone of passage and intersection of the papillomacular bundle.
We consider it advisable to stop on some features of the cross nerve fibers in the chiasm. Non-crossing nerve fibers, starting from the outer halves of the retina, pass in the outer part of the optic nerve. In the chiasm and optic tracts they also occupy a lateral position. The fibers from the nasal halves of the retina in the chiasm are decussated. The level of chiasm depends on the level of nerve fibers in the retina and optic nerve. Fibers starting from the inferior nasal sections of the retina are located in the lower sections of the optic nerve. In the chiasm they pass to the opposite side at its anterior edge closer to the lower surface. After crossing the chiasm, these fibers extend for some distance into the opposite optic nerve, where they form the anterior limb of the chiasm. Only after this they, located medially, pass into the optic tract. From the upper nasal parts of the retina, the nerve fibers, located in the upper half of the optic nerve, pass to the other side at the posterior edge of the chiasm closer to its upper surface. Before the chiasm, they enter the optic tract of the same side, where they form the posterior knee of the chiasm. The bulk of the crossed fibers are located in the medial parts of the chiasm. It should be remembered that the fibers of the papillo-macular bundle are also crossed.
Main types of visual field changes, occurring in brain tumors, are the following: 1) concentric narrowing of the visual field (symmetrical or eccentric); 2) unilateral sector-shaped visual field defects; 3) absolute or relative scotomas (central, paracentral, cecocentral); 4) heteronymous bitemporal and binasal hemianopsia; 5) homonymous hemianopsia. The listed visual field defects depending on the level of damage to the visual-nervous pathway are presented in Fig. 83.
Rice. 83. Scheme of typical changes in visual fields depending on the level of localization of the pathological focus (according to Duke-Elder S.).
1 - unilateral amaurosis with monolateral damage to the optic nerve; 2- unilateral amaurosis and contralateral temporal hemianopsia with damage to the intracranial portion of the optic nerve near the chiasm; 3 - bitemporal hemianopsia with damage to the medial part of the chiasm; 4 - incongruent homonymous hemianopsia with damage to the optic tract; 5 - homonymous hemianopsia without preservation of the macular zone with damage to the posterior part of the optical tract or the anterior part of the optical radiation; 6 - incongruent superior homonymous quadrantopsia with damage to the anterior part of the optical radiation (temporal lobe); 7 - weakly expressed incongruent homonymous inferior quadrantopsia with damage to the internal part of the optical radiation (parietal lobe); 8 - incongruent homonymous hemianopsia without preservation of the macular zone with damage to the middle part of the optical radiation; 9 - congruent homonymous hemianopsia with preservation of the macular zone with damage to the posterior part of the optical radiation; 10 - congruent homonymous hemianoptic central scotoma with damage to the occipital lobe.
Of primary importance for the topical diagnosis of damage to the visual-nervous pathway are hemianopic visual field defects[Troy E. Zh., 1968]. They can be unilateral or bilateral, complete, partial, quadrant (quadrantopia) and, finally, can be presented as hemianopic scotomas (central or paracentral).
Unilateral hemianopic changes develop with lesions intracranial portion of the optic nerve. Bilateral hemianopic defects occur when nerve fibers in the chiasm, optic tract, or central optic neuron are damaged. They can be heteronymous when opposite sides of the visual fields fall out (binasal or bitemporal, Fig. 84)
Rice. 87. Incomplete homonymous incongruent left-sided hemianopsia (lesion at the level of the anterior parts of the right optical radiation).
The nervous type of hemianopsia occurs with lesions in the posterior part of the radiatio optica or in the cerebral cortex. The second type of hemianopsia is detected in patients with damage to the optic tracts.
Concentric narrowing of the visual field in patients with a brain tumor is usually due to developing secondary post-congestive optic atrophy. Bilateral tubular narrowing of the visual field is sometimes the result of bilateral homonymous hemianopsia with preservation of the macular region in patients with a tumor localized in the calcarine sulcus. Unilateral concentric narrowing visual field is observed in cases where the intracranial part of the optic nerve between the optic foramen and the chiasm is involved in the pathological process. This can be observed with tumors of the optic nerve itself, meningiomas of the tubercle of the sella turcica, crest of the sphenoid bone or olfactory fossa. The described changes in the visual field were also observed in craniopharyngiomas and pituitary adenomas with extrasellar distribution.
Without dwelling on other causes that cause unilateral concentric narrowing of the visual field (diseases of the retina, orbital portion of the optic nerve), we consider it necessary to emphasize difficulty in differential diagnosis its reasons. In some cases, the true genesis of optic nerve atrophy and perimetric symptoms can be established only by analyzing a whole range of additional research methods, and perhaps by dynamic observation over a period of time.
Unilateral visual field defects are more common in combination with scotomas. A. Huber (1976) observed quadrant unilateral defects visual fields merging with the blind spot area when the optic nerve is compressed by a tumor. We observed similar changes [Brovkina A.F., 1974] in the case of eccentric growth of meningioma of the orbital part of the optic nerve. With a sufficiently high visual acuity (0.5 on the affected side), an inferotemporal visual field defect was detected in the visual field, merging with the area of the blind spot (Fig. 88).
Rice. 88. Unilateral inferotemporal quadrantopsia in a patient with a tumor of the right optic nerve.
Of great importance in the early diagnosis of tumor lesions of the visual-nervous tract is the identification absolute or relative scotomas. At the onset of the disease, they can only be determined when examining colored objects or when examining small objects for white color (no more than 1 mm on the Förster perimeter or 0.25 mm on hemispherical perimeters). Based on their location, these scotomas are classified into central, paracentral, cecocentral and peripheral.
Unilateral central or paracentral scotomas s arise when the optic nerve is involved in the pathological process in its orbital (Brovkina A. F., 1974] or intracranial part [Tron E. Zh., 1968; Huber A., 1976].
Scotomas with chiasmal tumors can be unilateral or bilateral, forming typical temporal hemianopic defects.
Homonymous hemianopic central scotomas develop only in cases of damage to the papillo-macular bundle above the chiasm. The anatomical basis for the appearance of these symptoms is the isolated position of the papillo-macular bundle and its partial decussation in the chiasm. However, homonymous hemianopic scotomas rarely occur with tumors involving the optic tract. More often they are associated with damage to the radiatio optica and are negative in nature, that is, they are not felt by the patient. These scotomas should be regarded as a sign of slow progressive damage to the optic nerve tract in the postchiasmatic region.
Heteronymous bitemporal defects visual fields are almost pathognomonic for lesions of the central part of the chiasm.
It is known that chiasma from above it borders with the bottom of the third ventricle, below - with the diaphragm of the sella turcica, behind the chiasm is adjacent the infundibulum, descending from the gray tubercle to the pituitary gland. In front, the chiasm is sometimes closely adjacent to the main bone in the area of the chiasmal groove. The chiasma is surrounded on the sides by the arteries of the circle of Willis. Thus, tumors growing in the chiasm area are capable of cause fiber damage in any part of the chiasm, but mainly in its central section. Thus, for example, tumors of the sella turcica region lead to the appearance of typical bitemporal hemianopsia or hemiapopic bitemporal defects in the visual field. Symmetrical bitemporal quadrantopsia or hemianopsia are most common in pituitary tumors, while asymmetrical bitemporal hemianopsia or quadrantopsia are more common in parasellar or suprasellar tumors (Fig. 89).
Rice. 89. Hemianopic bitemporal visual field defects due to compression of the chiasm from above.
Often tumors have asymmetrical growth pattern. In such cases, one of the optic nerves (if the tumor grows anteriorly) or the optic tract (if the tumor grows posteriorly) may be directly involved in the tumor process. As a result, typical symptoms develop, shown in Fig. 82.
Homonymous hemianopic visual field defects indicate damage to the optic tract or the central neuron of the visual pathway on the opposite side. Homonymous hemianopic defects in the form of quadrantopsia indicate an incomplete interruption of the optical path or optical radiation. With classic homonymous hemianopsia, there is no doubt about damage to the visual-nervous pathway in some area along the entire diameter. It is possible to differentiate tractus hemianopsia from hemianopsia caused by damage to the radiatio optica and higher by the signs of congruence. An incongruent onset with a progressive change in the visual fields passing through the point of fixation (without preserving the macular area), blanching of the temporal half of the optic nerve head is characteristic of damage to the optic tract (tumors of the temporal lobe, middle fossa, thalamus, quadrigeminal). Temporal lobe tumors often accompanied by the appearance of upper quadrant hemianopia; on the contrary, lower quadrant hemianopsia occurs in patients with tumors of the parietal region. With tumors of the occipital lobe, complete homonymous hemianopia develops. Congruent homonymous hemianopsia without preservation of the macular area, according to A. Huber, most often indicates complete damage to the radiatio optica.
Continued in the next article: Changes in the organ of vision in diseases of the central nervous system | Part 3.
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