Eye movement disorders without axial divergence are known as concomitant palsies. They are always caused by damage to the supranuclear gaze centers in the brainstem or cortex. Nystagmus with gaze paresis is often accompanied by other disorders. Differentiation from progressive ocular muscular dystrophy(slowly progressive disease, often accompanied by ptosis, dysfunction of the pharyngeal muscles) with complete paralysis of all eye movements in parallel axes, is rarely difficult. The causes of concomitant paralysis may be:
Lesions of the stem center of gaze (“nucleus para-abducens”) in the caudal part of the pons. Damage to this area results in the inability to look at the affected side.
Causes: vascular (often in elderly patients, sudden onset, always accompanied by other disorders), tumors, multiple sclerosis, intoxication (for example, carbamazepine).
Damage to the frontal cortical center of gaze in field 8. When it irritates, there is a deviation of the eyes and head to the opposite side, which sometimes turns into an epileptic adversive attack. Damage to this area leads to deviation of the gaze and head to the side of the lesion, since the activity of the opposite field 8 (conjugal deviation) predominates; “The patient looks at the lesion.” A few days after the lesion appears, the patient is able to look straight ahead, but there is still restlessness of the eyeballs when trying to look in the opposite direction. Over time, even this function is restored. But the nystagmus observed with gaze paresis remains, with a fast component to the opposite side. Tracking eye movements are preserved.
Causes of damage to the frontal gaze center include strokes, tumors (often accompanied by symptoms of irritation, sometimes mental disorders frontal type); atrophic processes (in elderly patients, accompanied by dementia and other cortical disorders, in particular neuropsychological); trauma (indication in medical history, sometimes external injuries, skull fractures, subjective symptoms concussions, blood in the cerebrospinal fluid, rarely other neurological disorders).
Bilateral horizontal gaze palsy (a rare neurological phenomenon) has been described in multiple sclerosis, pontine infarction, pontine hemorrhage, metastases, cerebellar abscess and as a congenital disorder.
II. Paresis (paralysis) of upward gaze (as well as downward gaze)
Paresis of upward gaze (Parinaud's syndrome, when accompanied by convergence disorder), as well as downward gaze, indicates a lesion in the tegmental area of the rostral midbrain. However, it should be noted that many patients, especially older ones, in serious condition or stupor, experience restlessness of the eyeballs when looking up. True vertical gaze palsy can be recognized (and differentiated from peripheral paralysis of the external eye muscles) by the presence of the following signs:
Bell phenomenon. The examiner passively lifts the upper eyelid as the patient tries to forcefully close the eyes; reflex rotation is detected eyeball up. The phenomenon of “doll eyes”. When the patient's gaze is fixed on an object located directly in front of the eyes, the examiner bends the patient's head forward. In this case, the patient's gaze remains fixed on the object due to upward rotation of gaze (despite paresis of voluntary upward gaze).
The causes of progressive vertical ophthalmoplegia may be:
Brainstem tumor ( common reason, is also manifested by other oculomotor disorders, convergence paralysis, other neurological disorders, including symptoms of midbrain damage, headache, manifestations of increased intracranial pressure, with pinealoma also precocious puberty).
Non-communicating hydrocephalus (symptoms of increased intracranial pressure are noted; in children, an increase in the size of the head).
Progressive supranuclear palsy syndrome
Steele-Richardson-Olydevsky (observed in elderly patients, accompanied by akinetic parkinsonian syndrome, dementia, rarely total external ophthalmoplegia).
Whipple's disease (uveitis, dementia, gastrointestinal disorders).
Wilson-Konovalov disease.
Huntington's chorea.
Progressive multifocal leukoencephalopathy in malignant diseases.
B. Other visual disturbances
Other visual disturbances (which manifest themselves in part as reading difficulties) should also be briefly mentioned:
Ocular dysmetria, in which the eyes oscillate at a fixed object. This disorder is found in diseases of the cerebellum.
Congenital ocular apraxia or Cogan's syndrome. To shift the gaze to another object, the patient must turn his head further, beyond the object fixed by the gaze. When the eyes are again fixed on the object from the over-rotated position, the head is rotated back to the correct direction. This process leads to bizarre head movements (which must be differentiated from tics), as well as difficulties in reading and writing (which must be differentiated from congenital alexia).
Oculogyric crises are involuntary deviation of the eyes to one side, or more often upward. Previously observed in postencephalitic parkinsonism, being early symptom of this disease (indication in the anamnesis of a disease with high temperature, other extrapyramidal symptoms; which helps differentiate from hysteria). Currently, the most common cause is iatrogenic ( by-effect neuroleptics).
Psychogenic gaze deviations.
C. Concomitant strabismus
Concomitant strabismus has the following characteristics: It is observed from childhood.
Often accompanied by decreased visual acuity (amblyopia). When examining eye movements, strabismus is noted; one eye does not participate in certain directions of movement.
In a separate study of eye movements, when one eye is closed, the movements of the other eye are carried out in full.
The non-focusing eye (closed by the examiner) deviates to one side (concomitant divergent or convergent strabismus). This phenomenon may alternate in both eyes (concomitant alternating strabismus; eg, divergent strabismus), and can be detected by an eye-closing test. Also, strabismus is a consequence of a congenital or early acquired disorder of the balancing (equilibrium) of the eye muscles, usually accompanied by a decrease in visual acuity in one eye, and has no specific neurological significance.
D. Internuclear ophthalmoplegia
Internuclear ophthalmoplegia causes disruption of the ocular axes without double vision. Damage to the medial longitudinal fasciculi between the brainstem center of gaze and the nuclei of the oculomotor nerve interrupts impulses for lateral gaze traveling from the brainstem center and the homolateral nucleus of the abducens nerve to the orally located nuclei of the third nerve, which controls the internal rectus muscle of the opposite eye. The abducted eye moves laterally easily. The adducted eye does not cross the midline. However, convergence is preserved on both sides, since impulses going to both eyes from the rostral center of convergence (Perlia's nucleus) allow the “paretic” eye to move together with the “non-paretic” eye.
Complete internuclear ophthalmoplegia is rare, but many patients with partial internuclear ophthalmoplegia present with slow saccades in the adducted eye only.
The cause of internuclear ophthalmoplegia is usually a vascular lesion of the brainstem; multiple sclerosis or tumor. Very rarely, divergent eye movements without diplopia are the result of other causes - for example, as part of giant cell arteritis syndrome.
Diagnostic studies for internuclear ophthalmoplegia
- General and biochemical analysis blood,
- MRI or CT,
- Evoked potentials of different modalities
- Examination of cerebrospinal fluid, fundus, consultation with an ophthalmologist.
Global gaze palsy is the inability to voluntarily move the gaze in any direction (total ophthalmoplegia). Global gaze palsy is rare in isolation; it is usually accompanied by symptoms of involvement of adjacent structures.
Main reasons: oculomotor apraxia; Guillain-Barré syndrome; myasthenia gravis; thyroid ophthalmopathy (especially when combined with myasthenia gravis); syndromes of chronic progressive external ophthalmoplegia; Wilson-Konovalov disease; pituitary apoplexy; botulism; tetanus; progressive supranuclear palsy; intoxication with anticonvulsants; Wernicke's encephalopathy; acute bilateral injuries in the area of the pons or mesodiencephalon, abetalipoproteinemia, HIV encephalopathy, Alzheimer's disease, adrenoleukodystrophy, corticobasal degeneration, Fahr's disease, Gaucher's disease, Leigh's disease, neuroleptic malignant syndrome, neurosyphilis, paraneplastic syndrome, Whipple's disease
],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 joint activities 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 different kinds movements of the eyeballs. 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 fast (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 in 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. With congenital strabismus, or strabismus, an imbalance of muscles, leading to incorrect location eyeballs (non-paralytic 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 impairment voluntary movements of the eyeball upward, downward and inward, as well as to 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 section of the reticular formation of the pons at the level of the nucleus of the abducens nerve causes persistent paralysis of gaze 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. To this focal neurological symptom the dissociated reaction of the patient’s pupils to light is also added:
- 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 area 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, lead 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).
09.12.2011, 13:22
Good afternoon The child has paresis of the inferior oblique muscle of the right eye (something like this), noticed after a year, now 3.3 years old. The child, when looking up, goes into right side does not raise the pupil. Previously they thought that this was a feature, because it was not always observed that it would rise once. It would not rise once, when looking up at left side raises both pupils. Now somehow things seem to me to be worse. They checked my vision, everything seemed to be normal. Everything else was told to us by neurology, so we should consult a neurologist.
Tell me, is there no help at all from ophthalmology in this diagnosis, otherwise everyone is playing football? Maybe there are some physical procedures, although our child is still very afraid in terms of equipment, it doesn’t matter if it hurts or not, when he goes into the doctor’s office where there are some devices, he starts crying. We couldn’t even check the child’s visual acuity at the last appointment. And such a pathology will remain for life or with correct and proper treatment can it pass? Thank you in advance.
09.12.2011, 19:14
Pass... I don't know. But there is definitely no need for treatment. It can only cause harm.
12.12.2011, 08:05
Well, how can we fix it then? :(((Will this affect her vision? Well, for a girl, I don’t want to give up like that and leave everything as it is. While she’s little, can there still be some kind of treatment?
12.12.2011, 12:07
paresis of the inferior oblique muscle of the right eye (something like that)...
It will lift you once. It won’t lift you once...
I think...
Can you see the data from your full examination (if it took place, of course, taking into account your behavior)? And then a contradiction arose:
They checked my vision, everything seemed to be normal.
We couldn't even test visual acuity
12.12.2011, 13:58
Can you see the data from your full examination (if it took place, of course, taking into account your behavior)? And then a contradiction arose:
There is no statement in front of me, regarding vision, right eye +1.5, left eye +1.5, they couldn’t check the acuity, she doesn’t speak well with us, they didn’t show pictures, and they couldn’t check it on the device, because... cried. Otherwise, gaze palsy is OD (right eye inferior oblique).
He doesn’t look away from himself: when he raises his eyes up without raising his head, the right pupil remains below, closer to the bridge of the nose, the left one rises as expected.
12.12.2011, 14:01
They did an EEG, not for vision, of course; it did not reveal any areas of brain damage, there was only mild dysfunction of the interhemispheric spaces. The examination was carried out due to delayed speech development.
13.12.2011, 12:29
14.12.2011, 08:08
Here again is a contradiction - paresis and paralysis are different things.
To talk about specific steps, you need data that you apparently don’t have (visual acuity, deviation angle, refraction normally measured for a wide pupil, fundus examination...)
Doctors write this way, one writes OD gaze palsy, another writes OD gaze palsy. The acuity was not checked; they were checked for the presence of other pathologies, except for paresis of gaze; everything else is now normal. The deviation angle is 15 degrees (in this eye.) For a dilated pupil +1.5 diopters for each eye, the fundus is normal.
The first recommendations were given to Morozovskaya, the examination took place at Fedorov’s clinic, they don’t have what we need for physio, to stimulate this muscle using the physio and therapeutic exercises per muscle. If nothing changes, only then talk about surgical intervention, and then they do not recommend it, as they can worsen it.. For the rest, register with a neurologist, and he will prescribe medications. I generally doubt the neurologist, since we have already taken a bunch of all sorts of medications both for the type of eyes and for speech and all to no avail.
I would like to understand whether this will go away or will remain so, what is the cause of this pathology, how can it be determined? What examinations should I undergo to find the lesion. Ophthalmology, as I was told, corrects what is there. The rest goes to a neurologist. But our neurologists do not offer any examinations other than medications.
14.12.2011, 12:43
the rest is still normal for now.
Deviation angle 15 degrees (in this eye.)
This is not called “normal”, but at least paralytic strabismus. Which can lead to amblyopia and impairment binocular vision.
15.12.2011, 12:50
This is not called “normal”, but at least paralytic strabismus. Which can lead to amblyopia and impaired binocular vision.
The Morozov Hospital knows very well what to do with this. If you had a direction there, but you didn’t use it (as I understand from your words), then it was in vain. Get it from your eye doctor at the clinic again and don't delay.
Thanks, no, we'll use it, it's just undergoing renovations right now.
18.12.2011, 17:27
Good afternoon We visited a neurologist today. They prescribed us Aminalon (both for the eyes and for the development of speech, we have a delay) and Glycine (as a sedative). Is there any point in taking these drugs? We have already taken so much (Cogitum, Encephabol, Cortexin injections) and nothing has helped us either for speech or for our eyes.
18.12.2011, 17:31
What can you see on an MRI? Is it worth doing it to a 3.3 year old child? I did an EEG, there is nothing on it, everything is according to age. Mild dysfunction of the interhemispheric spaces, but the doctor said that the brain is formed before the age of 18 and the EEG will never be ideal, everything is normal with you. But at the same time he still prescribes medications, why are they needed then?
26.01.2012, 14:12
Good afternoon We had a consultation at the Morozov clinic. The doctor said that at our age, the eye muscles are already formed, we don’t need surgery, we had to do any stimulating procedures until we are a year old. I only recommended eye exercises and annual examination vision.
In principle, I still don’t understand how it was possible to do something before a year, if we saw that the pupil does not rise upward only after a year...
Diagnosis of the doctor from Morozovskaya: OD-hypofunction of the inferior oblique muscle. OD-limitation (significant) of mobility to the top when looking inside the eyes deviates to the bottom. With vision, everything is still according to age. (01.5 per eye, sharpness 100%.
Now my question will remain the same for the rest of my life, neurologists, for their part, prescribe a bunch of medications, although they don’t work for us at all.
Thank you in advance.
26.01.2012, 18:37
it's just undergoing renovations right now
We've already drank so much and nothing has helped us.
The work of the eye clinic at Morozovka always continued even during renovations, just in a different building (on the territory of the hospital itself).
27.01.2012, 08:16
The work of the eye clinic at Morozovka always continued even during renovations, just in a different building (on the territory of the hospital itself).
Do I understand correctly that you never contacted them?
Contact us. I wrote their diagnosis just above and that she recommended only eye exercises and an annual vision test. She said nothing can be changed, well, at least everything is not as obvious as a feast of severe strabismus happens.
27.01.2012, 21:54
Contact us. I wrote a little higher
I apologize, the messages in the thread open somehow strangely. I just didn't see your previous message.
In this case, the really important thing is to undergo follow-up examinations with an ophthalmologist and follow the recommendations of a neurologist.
28.01.2012, 22:54
30.01.2012, 07:47
gaze paresis is a pathology of conjugate eye movements and has nothing to do with paresis of the actual muscles... paresis occurs in nerves, just like paralysis... in practice, this term refers to disorders of a supranuclear nature - gaze paresis with preservation of normal vestibulo-ocular reflexes and the absence of diplopia.. .and the discussion is about strabismus...question to the questioner: is there no strabismus when looking straight on? the problem only occurs when you try to look up and to the right? is there nystagmus?
strabismus and gaze paresis are generally different things and I am very confused by the spasmodic movement of the discussion with a shift towards muscle paresis...
Good afternoon The problem is only when looking up and to the right. Moreover, if you look straight up with both eyes equally, the pupil will move a little upward, and if up to the right, then the pupil will move a little to the lower corner. I'm talking about the right eye. Looks straight straight. In other directions the pupils are friendly. What is nystagmus? The doctor didn't say anything.
Do you need to post statements? The diagnoses are written there.
30.01.2012, 08:15
I have attached a file with eyes, normal condition of the eyes, i.e. there is nothing else. I’ll post the pathology a little later.
10.09.2014, 22:22
Good evening! The data from your examination is scant. I am interested in whether there is a forced position of the head, for example, tilting the head to the right, whether they checked the Bielschowsky test, whether there is hyperfunction of the superior oblique muscle on the right, and V-s-m or A-s-m, t Here, a differential diagnosis should be made between atypical strabismus (Brown's syndrome) or a true paralysis of the oblique muscle. With Brown's syndrome, surgery is performed in the case of a forced position of the head and vertical deviation of the affected eye.
Have you ever observed a lack of symmetry in the arrangement of eyelids in friends or yourself? If one eyelid droops too much, or both, this may indicate the presence of the following disease.
Ptosis (from the Greek word - fall) of the upper eyelid means its drooping. Normally healthy person the upper eyelid overlaps the iris by about 1.5 mm.
With ptosis, the upper eyelid droops by more than 2 mm. If ptosis is one-sided, then the difference between the eyes and eyelids is very noticeable.
Ptosis can occur in any person, regardless of gender and age.
Types of disease
The types of ptosis include:
- unilateral (appears in one eye) and bilateral (in both eyes);
- complete (the upper eyelid completely covers the eye) or incomplete (closes only partially);
- congenital and acquired (depending on the cause of occurrence).
The severity of ptosis is determined by how much the eyelid droops:
- 1st degree is determined when the upper eyelid covers the pupil from above by 1/3,
- 2nd degree - when the upper eyelid is lowered onto the pupil by 2/3,
- 3rd degree - when the upper eyelid almost completely hides the pupil.
The degree of visual impairment depends on the severity of ptosis: from a slight decrease in vision to its complete loss.
What can it be confused with?
The following pathologies of the visual organs can be mistakenly mistaken for ptosis:
- dermatochalasis, due to which excess skin of the upper eyelids is the cause of pseudoptosis or ordinary ptosis;
- ipsilateral hypotrophy, which is expressed in drooping of the upper eyelid following the eyeball. If a person fixes his gaze with the hypotrophied eye, while covering the healthy eye, pseudoptosis will disappear;
- the eyelids are poorly supported by the eyeball due to a decrease in the volume of the orbital contents, which is typical for patients with false eyes, microphthalmos, phthisis of the eyeball and enophthalmos;
- contralateral eyelid retraction, which can be determined by comparing the levels of the upper eyelids. It should be taken into account that covering the cornea with the upper eyelid by two millimeters is the norm;
- brow ptosis, caused by excess skin in the brow area, which can occur with facial nerve palsy. This pathology can be determined by raising the eyebrow using your fingers.
Causes of the disease
Let us examine in detail the reasons for which ptosis occurs.
Innate
Congenital ptosis occurs in children due to underdevelopment or even absence of the muscle that should be responsible for raising the eyelid. Congenital ptosis sometimes occurs together with strabismus.
When ptosis treatment is not treated for a long time, the child may develop amblyopia (lazy eye syndrome). Congenital ptosis is most often unilateral.
Acquired
Acquired ptosis develops for several reasons and is divided into:
- aponeurotic ptosis, which is due to the weakening or stretching of the aponeurosis of the muscle that should lift the upper eyelid. This type includes senile ptosis, which is one of the processes during natural aging of the body, ptosis that appears after eye surgery.
- neurogenic ptosis associated with damage to the nervous system after diseases (stroke, multiple sclerosis etc.) and injuries. Ptosis can appear with paralysis of the sympathetic cervical nerve, since it is the muscle that innervates the levator pallidum. Along with ptosis, constriction of the pupil (or miosis) and retraction of the eyeball (or enophthalmos) occur. A syndrome that combines these symptoms is called Horner's syndrome.
- with mechanical ptosis the cause is mechanical damage century foreign bodies. Athletes are at risk because eye injuries are quite common.
- false ptosis(apparent ptosis), which appears with excess skin folds on the upper eyelid, as well as hypotonia of the eyeball.
Establishing the cause of ptosis is an important task for the doctor, since surgery acquired and congenital ptosis are significantly different.
An interesting fragment from the program “Live Healthy” about ptosis of the upper eyelid
Symptoms of the disease
One of the main manifestations of ptosis is a directly drooping upper eyelid.
The following symptoms of ptosis are distinguished:
- inability to blink or close the eye completely,
- irritation of the eyes due to the fact that there is no way to close them,
- increased eye fatigue for the same reason
- possible double vision due to decreased vision,
- the action becomes habitual when a person sharply throws his head back or tenses his forehead and eyebrow muscles in order to open his eye as much as possible and lift the drooping upper eyelid,
- strabismus and amblyopia may occur if treatment is not started on time.
Diagnosis of the disease
When identifying a drooping eyelid, which is noticeable even with the naked eye, doctors need to determine the cause of the disease in order to prescribe treatment.
The ophthalmologist measures the height of the eyelid, studies the symmetry of the position of the eyes, eye movements, and the strength of the muscle that should raise the eyelid. When diagnosing, be sure to pay attention to the possible presence of amblyopia and strabismus.
In those patients who have acquired ptosis during life, the muscles that lift the eyelid are quite elastic and elastic, so they can completely close the eye when their gaze is lowered.
With congenital ptosis, the eye cannot close completely even with the gaze lowered to the maximum, and the upper eyelid makes movements of very small amplitude. This often helps diagnose the cause of the disease.
The importance of determining the cause of ptosis is that with congenital and acquired ptosis, different parts of the visual analyzer suffer (with congenital ptosis, the muscle that lifts the eyelid itself, and with acquired ptosis, its aponeurosis). Accordingly, the operation will be performed on different parts of the eyelid.
Treatment of the disease
Neither congenital nor acquired ptosis goes away on its own over time and always requires surgery. It is better to start treatment as early as possible to increase the chances of maintaining vision, because ptosis is not only an aesthetic and cosmetic defect.
The operation is performed by an ophthalmic surgeon under local anesthesia, with the exception of children, sometimes under general anesthesia. The operation takes from half an hour to 2 hours.
Until surgery is scheduled, you can hold the eyelid open during the day with an adhesive tape to prevent strabismus or amblyopia in children.
If acquired ptosis appears due to some disease, then in addition to the ptosis itself, it is necessary to simultaneously treat the provoking disease.
For example, with neurogenic ptosis, the underlying disease is treated, UHF procedures, galvanization are prescribed, and only if there is no result, surgical treatment is prescribed.
The operation to eliminate acquired ptosis is carried out as follows:
- remove a small strip of skin from the upper eyelid,
- then the orbital septum is cut,
- cut the aponeurosis of the muscle that should be responsible for raising the upper eyelid,
- the aponeurosis is shortened by removing part of it and sutured to the cartilage of the eyelid (or tarsal plate) just below,
- The wound is sutured with a cosmetic continuous suture.
During surgery to eliminate congenital ptosis, the surgeon’s actions are as follows:
- also remove a thin strip of skin from the eyelid,
- cut the orbital septum,
- isolate the muscle itself, which should be responsible for raising the eyelid,
- perform muscle plication, i.e. put several stitches on it to shorten it,
- The wound is sutured with a cosmetic continuous suture.
When congenital ptosis of the upper eyelid is severe, the levator palpebral muscle is attached to the frontalis muscle, thereby the eyelid will be controlled by tension of the frontalis muscles.
When the operation is completed, a bandage is applied to the operated eyelid, which can be removed after 2-4 hours.
There is usually no pain during or after surgery. Sutures are removed 4-6 days after surgery.
Bruising, swelling and other effects of surgery usually disappear within a week. The cosmetic effect of the treatment remains unchanged for life.
Surgery to treat ptosis can cause the following side effects:
- pain in the eyelid area and decreased sensitivity;
- incomplete closure of the eyelids;
- dry eyes;
These symptoms in most cases disappear on their own within a few weeks after surgery and do not require any treatment. Some patients may experience subtle asymmetry of the upper eyelids, inflammation and bleeding of the postoperative wound. The cost of surgery to treat ptosis in Russian clinics ranges from 15 to 30 thousand rubles.
Conclusion
Let us highlight the main points of the article:
- Ptosis is a disease of the upper eyelid in which it does not naturally droop.
- The disease can be congenital or acquired.
- Ptosis can negatively affect vision.
- Treatment is only possible through surgery.
Eyes can look into different sides due to disruption of the muscles responsible for the movement of the eyeballs. Medical language this pathological process called strabismus. Even if the right and left eyes are focused on the same object and see the same picture, this does not mean that the brain receives the same data from both sides. An eye that looks in a different direction is called amblyopic.
Due to the fact that the eyes are looking in different directions, the analyzer receives different images that it is not able to compare, which is why it is simply impossible to obtain a single holistic picture. In children, the pathological process, as a rule, is reversible, but you should act quickly. Otherwise, blindness may develop. So, why do the eyes cross?
What causes the disease?
The causes of strabismus can be either congenital or acquired. Let's take a closer look at the provoking factors:
- farsightedness or nearsightedness;
- astigmatism;
- abnormalities in the development of eye muscles;
- stressful situations;
- CNS disorders;
- paralysis or paresis;
- infectious diseases;
- chronic pathologies internal organs;
- mental trauma.
The hereditary factor plays great importance in the occurrence of strabismus
Associated symptoms
A healthy person has binocular vision, which means that the images received by the cerebral cortex from both eyes merge into a single picture. Thanks to this, we can see the distance between objects, perceive depth, as well as the integrity of the surrounding world. In case of strabismus, in order to avoid doubling of objects of the central nervous system, the image of amblyopic eye is excluded.
Varieties
Depending on the origin, experts divide strabismus into friendly and paralytic. Let's talk about them in more detail.
Friendly
This form is characterized by a violation of the coordinated work of the oculomotor muscles, in which not only the fixation of the eye is impaired, but also binocular vision. When distinguishing objects, there is no diplopia - double vision.
Most often, concomitant strabismus occurs in young children. The following reasons can lead to the development of a pathological process:
- farsightedness;
- myopia;
- significant difference in diopters of the right and left eyes;
- pathological processes in the cerebral cortex;
- eye injuries;
- illnesses optic nerve and retina;
- diseases of the central nervous system;
- paresis and paralysis of the oculomotor muscles;
- infectious processes;
- psycho-emotional disorders.
Concomitant strabismus can be convergent or divergent
Pathology can be congenital or acquired. The first type is associated with features anatomical structure eyes and central nervous system diseases. Congenital pathology often caused by myopia and farsightedness.
The acquired form is associated with a decrease in the visual functions of one of the organs of the visual apparatus. In turn, the acquired type can be convergent or divergent.
Convergent type
The cause of this condition may be overwork or overexcitement. In a calm, relaxed state, there is no disturbance. In this case, vision correction should be carried out before three years, otherwise the pathology will become permanent.
The sore eye with convergent strabismus is always directed towards the nose. If you need to focus your gaze on some object, then only one eye can do this.
Important! In some cases, both eyes may become squinting in turn.
Convergent strabismus is associated with the following complications:
- distortion of the overall picture;
- the brain turns off the amblyopic eye, otherwise double objects will occur;
- the retina of the squinting eye stops sending impulses;
- the functioning of the affected organ simply stops over time.
The convergent type is not characterized by progression. Sometimes it is even possible for the disease to disappear without the use of any methods. Still, you shouldn’t get your hopes up with thoughts of a cure. It is unknown how the pathology will behave with age, so contact a specialist for advice.
Concomitant strabismus is not prone to progression
Divergent type
Compared to the above form, it is quite rare. Complications of the divergent type appear less frequently. Weakening of the internal muscles of the visual apparatus is a common reason that the eyes diverge.
A feature of the divergent form is the absence of discrepancies when concentrating on objects that are close. Basically, the disease occurs against the background of severe myopia - myopia. The visual axis of a squinting eye can deviate upward or downward.
Treatment of concomitant strabismus includes the use of the following techniques:
- optical correction, including the prescription of contact lenses or glasses;
- hardware procedures to improve the quality of vision;
- orthoptic and diplotic treatment to improve binocular vision. A special “Synoptophore” apparatus is used, as well as interactive gaming programs. Diploptics involves reading through a grid.
Surgical intervention is prescribed in extreme cases when other methods are ineffective
Paralytic
The pathology is based on the deviation of the eye away from the central axis. Most often it occurs against the background of paresis or paralysis of the extraocular muscles. This can occur due to injury, infection and inflammatory processes, tumors, intoxication and more.
The patient develops the habit of turning towards the paralyzed muscle. Due to impaired binocular vision, objects become blurred. Most often, the eyeball does not move at all. Patients complain of sore eyes, headaches, tinnitus and dizziness. A split picture occurs when viewing the same object with both eyes. The patient tries to compensate for diplopia by tilting the head.
Features of treatment tactics
What to do? Treatment of paralytic strabismus is a long process. Binocular vision may take several years to develop. The following factors influence the forecast:
- time of onset of the disease;
- variety;
- initial visual acuity indicators;
- deflection angle;
- general condition of the patient;
- time when treatment was started.
First of all, it is necessary to eliminate the root cause of strabismus. In case of vascular disorders, the patient should visit a neurologist. Brain tumors are examined by a neurosurgeon.
Often patients do not attach importance to preventive measures, and then run around hospitals trying to fix it. Don't forget about simple visual exercises. Place two fingers in front of your nose and fix your gaze on them, and then slowly move them apart and try to linger on these objects with your eyes for as long as possible. With your eyes closed, draw a circle, figure eight, rectangle. It is also useful to focus your gaze on close and distant objects.
Strabismus impairs visual ability, which may cause difficulties in choosing a profession in the future.
Different types of strabismus require different approaches to the choice of treatment. To develop coordination of eye movements, increase visual acuity and improve binocular vision, hardware treatment is prescribed: software-computer treatment, Franel lenses, Synoptophore, Amblyocor, Mirage.
If hardware techniques are unsuccessful, surgical intervention may be required. Many parents put off the decision to undergo surgery, but it is worth remembering that if the operation is not performed on time, it can permanently impair the visual ability to perceive the image in a coordinated manner. And in the future, all attempts to change the situation will not bring any results.
Strabismus is one of those diseases that parents can identify on their own without the help of a specialist. Treatment begins at six months of age, and its essence lies in the use of special exercises.
The pathological process in a newborn is associated with weakness of the extraocular muscles. In infancy, the child does not yet know how to control the movement of the eyeballs, which is why from time to time the eyes may look in different directions. Also, the brain does not yet know how to control the functioning of the eye muscles. That is why in the first month of life this should not worry parents, since the eye muscles are still strengthening.
It is also worth taking into account the fact that infants are characterized by only horizontal vision, and vertical vision is mastered only with time. If by six months the situation has not returned to normal, parents should contact a pediatric ophthalmologist.
Children are born unprepared for a new environment. Already from the first minutes of life, adaptation of vital organs and systems, including the visual apparatus, begins.
Strabismus in a newborn may be normal
Let us highlight the main reasons why an ophthalmological defect may develop:
- brain injuries and infections;
- myopia or farsightedness;
- congenital diseases;
- birth injuries;
- improper care of the baby. This may include placing toys too close in front of your eyes;
- hereditary factor.
Parents may want to note the following:
- the child is not able to simultaneously direct both eyes to one point;
- one eye squints or closes in the sun;
- in order to look at an object, the child turns or tilts his head;
- The child often bumps into objects. This is due to a violation of the perception of spatial depth.
In some cases, treatment can last two to three years. Let us highlight the main methods of the treatment process:
- occlusion - a shutter is placed over the healthy eye. In this way, the vision of the squinting eye is stimulated;
- a special set of exercises;
- orthoptic treatment affecting the brain;
- diploptic treatment restores binocular and stereoscopic vision;
- computer techniques help weak eye focus correctly on the subject;
- in the absence of positive dynamics of treatment, surgery may be required, which is performed no earlier than three years of age.
Explain to your child the importance of doing eye exercises. It is best to spend it during the day, when he is not yet so tired. Gymnastics should be performed systematically:
- looking away from a close object to a distant one;
- drawing eyes closed eight, square, dial;
- squinting and wide opening of eyes;
- look to the left as much as possible, then to the right, as well as up and down.
Conclusion
So, strabismus is a pathological process that can occur in both adults and children. The disease can be congenital or acquired. Experts distinguish between concomitant and paralytic strabismus. Friendly, in turn, is divided into convergent and divergent.
Treatment largely depends on the form of the ophthalmological disorder. Timely diagnosis will help get rid of pathology. In newborn children, a squinting eye may be a consequence of insufficiently strengthened eye muscles. In this case, the problem goes away on its own within six months. Do not self-medicate, follow all doctor’s recommendations and do not forget about prevention.
