Breach of the eye

All eye movements in humans are normally binocular and integrated with the visual system in order to ensure the perception of three-dimensional space. Both eyes function as a unit and move in such a way as to ensure a stable view of the moving object and to ensure the stabilization of the visual image on the retina. This requires a constant integration of afferent flows from visual, vestibular, proprioceptive, tonic cervical and (to a lesser extent) somatosensory stimuli. The oculomotor system is also influenced by hemispheric motor control systems, basal ganglia and the cerebellum. In addition, for the normal functioning of this system, the state of consciousness and wakefulness level is important.

Disorders of gaze movements depend on the localization, size, severity and type of damage. The hemispheric lesions can be manifested as irrational phenomena (tonic deviation of the eye, epileptic nystagmus), and paralytic (paralysis of friendly movements, that is, paralysis of the eye). The same can be said for lesions of the basal ganglia, which may be manifested by oculogic crises, on the one hand, and gaze pareses on the other (for example, in progressive supranuclear palsy). Damage to the mesencephalon can lead to violations of the vertical gaze (sight defect up, defect of the gaze down, a combination of both), the characteristic forms of nystagmus, violations of conjugate eye movements and crossed syndromes. Damage to the varioly bridge is characterized by defects of friendly movements, medial longitudinal beam syndromes and crossed syndromes. Processes in the medulla oblongata can manifest themselves in vzor phenomena only with nystagmus.

I. Friendly (conjugate) paralysis of the eyes.

A. Paralysis of the horizontal eye

1. Frontal lesions (vzorovye phenomena of irrigation and paralysis)

1. Stroke in the acute phase (and other diseases)
2. Epileptogenic damage (causing epileptic seizure)

2. Bridge (Pontine) Damage

1. Acute disorders of cerebral circulation
2. Paraneoplastic syndrome

B. Vertical Paralysis

I. Paralysis of the eye upward

1. Mammary Tumor
2. Hydrocephalus
3. Shunt dysfunction in hydrocephalus
4. Hemorrhagic or ischemic heart attack of thalamus or midbrain
5. Hypoxia
6. Multiple sclerosis
7. Craniocerebral injury
8. Lipidoses
9. Wilson-Konovalov's disease
10. Drug Intoxication
11. . Whipple's disease
12. Syphilis
13. Tuberculosis
14. Limiting the gaze up with Parkinson's disease
15. Restriction of the gaze upward and in case of vitamin B12 deficiency
16. Syndromes imitating the paresis of the gaze upward: Lambert-Eaton syndrome and Fisher syndrome

2. Paralysis of the gaze downward

1. Cerebral infarcts
2. Progressive supranuclear palsy
3. Nyman-Pick disease
4. Insufficiency of hexosaminidase-A in adults
5. OPCA
6. Ataxia-telangiectasia
7. Wilson Konovalov's disease
8. Houteon Huntington
9. Whipple's disease
10. Parkinson's disease (rare)
11. Gallervorden-Spartz disease
12. Disease of diffuse Levi bodies

II. Unfriendly (unconjugated) paralysis of the eye

A. Horizontal View

1. Syndrome of posterior longitudinal fascicle or syndrome of internuclear ophthalmoplegia:

One-sided internuclear ophthalmoplegia

1. Ischemic infarction of the brain stem
2. Encephalopathy Wernicke
3. Craniocerebral injury
4. Encephalitis
5. AIDS
6. Neurosyphilis
7. Tumor
8. Arnold-Chiari malformation
9. Hydrocephalus
10. Arterio-venous malformation
11. Metabolic disorders
12. Syringobulbia
13. Radiation encephalopathy
14. Progressive supranuclear palsy
15. Liver encephalopathy
16. Pernicious anemia
17. Drug Intoxication

Two-way internuclear ophthalmoplegia

1. Multiple sclerosis
2. Ischemic cerebral infarction
3. Paraneoplastic encephalomyelopathy

Syndromes capable of simulating internuclear ophthalmoplegia

1. Myasthenia gravis
2. Thyroid orbitopathy
3. Orbital pseudotumor
4. Partial paralysis of the oculomotor nerve
5. Miller Fisher Syndrome
6. Penicillin-induced pseudo-nuclear ophthalmoplegia
7. Surgical trauma of the medial rectus muscle of the eye
8. Myotonic dystrophy
9. Long-existing exotropy.

One-and-a-half syndrome

1. Ischemic or hemorrhagic cerebral infarction
2. Multiple sclerosis
3. Brain tumor
4. Pseudo-spermic syndrome with myasthenia gravis

V. Vertical view

1. Monocular paresis of elevation
2. Vertical one and a half syndrome
3. Slanting deviation

III. Syndromes of spontaneous rhythmic vesory disorders

1. Oculogic crises
   • Encephalitis Economome
   • Craniocerebral injury
   • Neurosyphilis
   • Multiple sclerosis
   • Ataxia-telangiectasia
   • Rett syndrome
   • Stem encephalitis
   • Glioma of the third ventricle
   • Stryocapsular infarction
   • Drug Intoxication
2. Periodic alternating gaze
3. Ping-Pong visual syndrome
4. Periodic alternating deviation of the eye
5. Repeated divergence
6. Ocular Bobbing
7. Ocular Dipping
8. Prefective pseudobobbing
9. Vertical ocular myoclonus
10. Alternating slanting deviation
11. Psychogenic deviation of the eye.

IV. Congenital ophulomomotor apraxia.

I. Conjugate (friendly) paralysis of the eyes.

A. Paralysis of the horizontal gaze.

Localization of lesions responsible for horizontal paralysis of the gaze: frontal-bridge connections, mesencephalic reticular formation, reticular formation of the variolium bridge (and nucleus of the VI cranial nerve).

One-sided limitation of an arbitrary gaze to one side is usually due to contralateral frontal (but also contralateral parietal or occipital) or ipsilateral bridge damage. Weakness or paralysis of the contralateral friendly eye-out can be transient, lasting several hours (for example, in a postictal state) or can persist days and weeks, as in a stroke. Restriction of eye movements manifests itself in the horizontal plane and in the direction opposite to the side of the lesion.

Frontal lesions. (More often acute lesions with transient disturbances of eyesight): a tumor, a stroke, a traumatic brain injury or an infection. All of them can cause such an irrational phenomenon as a friendly deviation of the eyes in the direction opposite to the affected hemisphere (the patient looks from the hearth).

ONMK: in the acute phase, the patient "looks at the hearth" due to the preserved function of the opposite center of eye and head rotation to the side and, on the contrary, paralysis of eye and head rotation in the ipsilateral hemisphere (paretic phenomenon).

Epileptogenic frontal (as well as parietal, occipital and temporal) injuries are manifested by the transient deviation of the eyes and head into the contralateral side (the patient looks in the direction from the focus). Possible and ipsiversive deviations of the eyes and head. Paralysis or weakness of horizontal friendly eye movements of hemispheric origin is rarely found in the form of an isolated phenomenon. Almost always they are accompanied by other signs of hemispheric dysfunction (concomitant hemiparesis or hemiplegia).

Bridge (Pt) damage (patient "looks at hemiparesis"):

• ONMK is the most frequent reason for the above friendly eye deviation.
• Paraneoplastic syndrome (oppression of horizontal eye movements without hemiparesis) is a much more rare syndrome.

In patients over the age of 50, the most common cause of horizontal paralysis is cerebrovascular disease (ischemic or hemorrhagic). With subacute development of these eye disorders in patients under 50 years of age, multiple sclerosis should be excluded. Congenital syndrome is usually caused by Mobius syndrome. Other causes of acquired violations of the horizontal eye include systemic lupus erythematosus, syphilis, Wernicke's encephalopathy. Myasthenia gravis, as already mentioned, can simulate vazor disturbances. In the differential diagnosis of the causes of horizontal paralysis (paresis) of vision, MRI and cerebrospinal fluid are used.

[1], [2], [3]

B. Paralysis of the vertical gaze.

One-sided hemispheric injuries do not in themselves cause paralysis of the sight in the vertical plane. If the latter is detected, it is usually due to latent additional or bilateral damage to the brainstem.

Extensive bilateral hemispheric lesions can cause paralysis of the eye in both horizontal and vertical directions. There are reports that bilateral hemispheric lesions can impair eye movements in all directions.

Rough damage to the oral sections of the tire covers the variola bridge causing pareses of both horizontal and vertical gaze. As a rule, these patients are in a coma.

Paralysis of the gaze upward. The syndrome is characteristic of pre-injuries involving the posterior commissure and is referred to as the Parino syndrome, the Sylvian water pipe syndrome, the prefectal syndrome, the dorsal midbrain syndrome and the Koerber-Salus-Elschnig syndrome. At the same time retraction of the upper eyelids can be observed. If the process spreads ventrally with the involvement of the nucleus of the third (oculomotor) nerve, then a bilateral ptosis joins. Sometimes "skew deviation" develops with a higher-positioned eye on the side of the lesion. In children with hydrocephalus, a sign of compression of the midbrain is the tonic deviation of the gaze downward with the retraction of the upper eyelid, the "setting sun" syndrome.

The main causes are: swelling (the most common cause, especially pituitary tumor and metastatic tumors); hydrocephalus (especially with the expansion of the third ventricle and the aqueduct, leading to deformation of the posterior commissure); dysfunction of the shunt in hydrocephalus; hemorrhagic or ischemic infarction of the thalamus or midbrain; hypoxia; multiple sclerosis; traumatic brain injury; neurosurgical (stereotactic) trauma; lipidases; Wilson-Konovalov's disease; drug intoxication (barbiturates, carbamazepine, antipsychotics); Whipple's disease; syphilis; tuberculosis; restriction of the gaze up in Parkinson's disease and (rarely) in case of vitamin B12 deficiency; encephalopathy Wernicke; syndromes that mimic the paresis of the gaze upward: Lambert-Eaton syndrome and Fisher syndrome.

Paralysis of the gaze downward. Isolated paresis of the gaze down is rare. If such a syndrome develops, it makes it difficult to read, eat and walk on an inclined surface. The syndrome is observed in bilateral lesions at the border of a mesencephal-diencephalic transition involving the area lying between the sylvic water pipe and the red core. There may be a pseudoptosis (relaxation of the m. Levator) when trying to move the gaze downward.

The main causes: heart attacks (in most cases, bilateral) in the basin of the paramedian thalamoesencephalic artery (branch of the posterior cerebral artery) is the most frequent cause of acute paralysis of the gaze downward.

Causes of progressive gaze-down restriction: progressive supranuclear palsy; Nyman-Pick disease; deficiency of hexosaminidase-A in adults; OPCA; ataxia-telangiectasia; Wilson-Konovalov's disease; Huntington's chorea; Whipple's disease; Parkinson's disease (rarely); Gallervoden-Spartz disease (rare); disease of diffuse Levi bodies.

Paralysis gaze down in addition significantly hamper walking and, therefore, contribute to the genesis of the dysbasia, which for almost all of the above diseases has a complex (polyfactorial) nature.

[4], [5], [6]

II. Unfriendly (unconjugated) paralysis of the eye

A. The horizontal look.

Syndrome of posterior longitudinal fascicle or syndrome of internuclear ophthalmoplegia.

Clinically, the syndrome is characterized by the weakness of the adduction (eye) muscle on the side of the lesion of the posterior longitudinal fascicle and the contralateral monocular nystagmus when the other eye is withdrawn. Convergence, however, is preserved. Sometimes patients complain of diplopia (due to oblique deviation) or oscilloscopy. In the absence of the latter, patients are usually not presented with complaints. Interocular ophthalmoplegia is often accompanied by oblique deviation with a higher located eye on the side of the lesion. It can also be combined with ipsilateral nystagmus directed downward and contralateral torsion nystagmus.

Let's recall the main reasons for unilateral inter-nuclear ophthalmoplegia:

Ischemic infarction of the brain stem; encephalopathy Wernicke; craniocerebral trauma; encephalitis; AIDS; neurosyphilis; tumor; Arnold-Chiari malformation; hydrocephalus; arteriovenous malformation; metabolic disorders (eg, Fabry's disease, abelolipoproteinemia); syringobulbia; radiation encephalopathy; progressive supranuclear palsy; hepatic encephalopathy; pernicious anemia; drug intoxication (diphenin, amitriptyline, phenothiazines, tricyclic antidepressants, obzidan, lithium, drugs, barbiturates).

The main reasons are bilateral bilateral internuclear ophthalmoplegia: multiple sclerosis; ischemic cerebral infarction; paraneoplastic encephalomyelopathy.

Syndromes capable of simulating internuclear ophthalmoplegia (pseudo-ovarian ophthalmoplegia): myasthenia gravis; thyroid orbitopathy; orbital pseudotumor; other infiltrative lesions of external oculomotor muscles (tumor, amyloidosis, etc.); partial paralysis of the oculomotor nerve; Miller Fisher Syndrome (sometimes there is true internuclear ophthalmoplegia); Penicillin-induced pseudo-nuclear ophthalmoplegia; surgical traumomedial rectus muscle of the eye; myotonic dystrophy; neyromiotonia of the lateral rectus muscle of the eyeball.

Bilateral interocular ophthalmoplegia is usually observed with a direct gaze. Cases when internuclear ophthalmoplegia is combined with the removal of both eyes laterally are termed WEBINO-syndrome (wall-eyed bilateral internuclear ophthalmoplegia - internuclear ophthalmoplegia with strabismus). Convergence is often impossible. This syndrome is observed with damage to the midbrain with the involvement of both posterior longitudinal bundles. A similar syndrome and a one-sided (WEMINO-syndrome, wall-eyed monocular internuclear ophthalmoplegia), where also, as in bilateral syndrome, a divergence of the visual axes (exotrophy) is described.

The internuclear ophthalmoplegia of abduction is described. One-way or two-way internuclear ophthalmoplegia of the lead (the so-called posterior internuclear ophthalmoplegia) is sometimes accompanied by nystagmus when the contralateral eye is brought. This syndrome is described in ipsilateral lesions of the oral divisions of the variolium bridge or mesencephalon.

The one-and-a-half syndrome manifests itself as a friendly paralysis of the eye in one direction (one part of the syndrome) and weakness of the adductor muscle when viewed in the opposite direction (the "half" of the syndrome in comparison with the first part). Here, in the horizontal plane, only the retraction of one eye is retained, which manifests itself in addition to nystagmus during such withdrawal. Vertical movements and convergence are preserved. The syndrome is caused by unilateral damage to the lower part of the tire of the variolium bridge with ipsilateral involvement of the paramedian reticular formation of the bridge, the nucleus of the outgoing nerve and the adjacent fibers of the posterior longitudinal fascicle on this side (on the side of complete horizontal paralysis of the gaze).

The main causes: multiple sclerosis (the most common cause in people younger than 50 years); ischemic or hemorrhagic cerebral infarction (the most common cause in people older than 50 years); tumor of the lower parts of the variolium bridge; pseudoliveric syndrome in myasthenia gravis.

[7],

V. Vertical view

Monocular paresis of elevation ("double paralysis of the elevator") is characterized by the restriction of lifting one eye and can be observed with supranuclear pre-injury on the side of the contralateral or ipsilateral parietic eye, which interrupt the fibers from the posterior longitudinal fascicle to the m.superior rectus and m.oblique inferior. The double paralysis of the elevator can manifest as asymmetric gaze upward, which clinically manifests itself as a monocular paresis of the elevation on the side of the heavier-affected eye (thus there is no true monocular paralysis of the m. Elevator). Other causes: paresis of the external muscles of the eye; fibrositis or myositis of these muscles; myasthenia gravis; distearoid orbitopathy; muscle swelling; fracture of orbital bones.

Vertical one and a half syndrome - vertical paralysis of the gaze and monocular paresis of the gaze downwards on the side of injury or contralateral damage - is described with thalamoesencephalic infarcts. The Bell phenomenon and all types of horizontal eye movements are preserved.

Skew Deviation. Although violations of vertical alignment of the eyes may be caused by damage to the motor nerves of the eye or muscles (for example, in myasthenia), the term "oblique deviation" is reserved for violations of the vertical symmetry of the eyes caused by supranuclear disorders. Unlike other variants of acquired vertical strabismus (for example, paralysis of m. Oblique superior, thyroid ophthalmopathy, myasthenia gravis), oblique deviation of the eye is usually not rotated. Slanting deviation develops when peripheral or central lesions cause an imbalance of otolith signals and can accompany pathological processes at different levels of the brainstem (from the mesencephalon to the medulla oblongata or cerebellum). Sometimes elevated intracranial pressure, Fisher's syndrome, or hepatic coma can cause oblique deviation.

If oblique deviation varies with different positions of the eye, this usually indicates a lesion of the medulla oblongata. The defeat of the peripheral vestibular organ can cause oblique deviation, with the contralateral eye located above the ipsilateral. Lateral pantomedullary lesions affecting the vestibular nucleus can lead to oblique deviation with a lowered eye on the side of the lesion. On the contrary, the eye on the side of the lesion of the posterior longitudinal fascicle is located higher.

III. Syndromes of spontaneous rhythmic vesory disorders

Oculogic crises.

Oculogic crises are episodic friendly deviation of the eyes (usually directed upwards and laterally, rarely - downwards or strictly laterally). These crises can be accompanied by other dystonic phenomena (blepharospasm, protrusion of the tongue, torticollis, etc.).

The main reasons: drug intoxication (neuroleptics, lithium, tetrabenazine, carbamazepine); Encephalitis Economome; craniocerebral trauma; neurosyphilis; multiple sclerosis; ataxia-telangiectasia; Rett syndrome; trunk encephalitis; glioma of the third ventricle; striatocapsular infarction.

Periodic alternating gaze.

Periodic alternating gaze (periodic alternating gaze deviation with dissociated head movements) is a complex cyclic three-phase syndrome:

1. friendly lateral deviation of the eyes, usually with a compensatory turn of the head in the opposite direction, lasting 1-2 minutes;
2. the switching phase to the home position (10-15 seconds) and
3. phase of friendly eye deviation to the other side with compensatory head rotation lasting from 1 to 2 minutes.

Practically all described cases are represented by processes in the posterior cranial fossa (spinal carbellar degeneration, cerebellar medulloblastoma, Arnold-Chiari malformation, cerebellar disgynia, etc.).

A sight-seeing syndrome of "ping-pong".

Ping-pong syndrome (in a patient in a coma) - periodic friendly eye deviation from one extreme position to another; the duration of each cycle is 2.5-8 seconds. The syndrome usually reflects a bilateral cerebral infarction with an intact brainstem, but is also described with hemorrhage in the posterior cranial fossa, basal ganglia infarction, hydrocephalus, overdose of the MAO inhibitor, in patients in a metabolic coma. Prognostic value does not matter.

Periodic alternating deviation of the eye. The periodic alternating deviation of the gaze differs from the visual syndrome of "ping-pong" and occurs not only in comatose, but also (more often) in awake patients: an alternating horizontal friendly deviation of the gaze lasting from 1 to 2 minutes in each direction is observed. It occurs in patients with structural lesions of the cerebellum and cerebral trunk (Arnold-Chiari malformation, medulloblastoma), but is also described in comatose patients with hepatic encephalopathy.

Repeated divergence.

Repeated divergence is a rare phenomenon in patients in a metabolic coma. In the rest phase, the eyes are in the middle position or slightly divergent. In the next phase, they slowly diverge, then a short period remains in the position of complete divergence and, finally, quickly return to the starting position before starting a new cycle. The movements are synchronous in both eyes.

Ocular bobbing.

Ocular bobbing (syndrome of "float movements of the eyes") - periodic rapid friendly deviation of the eyes down from the middle position with the subsequent slow return to the initial middle position in patients in a coma. The syndrome is mainly characterized (but not pathognomonic) for damage to the variolium bridge (hemorrhage, tumor, infarction, central pontinous myelinolysis). It is also described in processes in the posterior cranial fossa (aneurysm rupture or cerebellar hemorrhage), diffuse encephalopathies. Possible monocular bobbing and, rarely, unfriendly bobbing then one, then the other.

Ocular Dipping.

Ocular dipping is the slow deviation of the eyes from the middle position downwards with the subsequent rapid return to the starting position. Described for anoxic coma and after prolonged epileptic status. Presumably, it reflects a diffuse brain dysfunction, and not some structural damage.

Prefect pseudobobbing.

Pretekal pseudobobbing in a coma is described in acute hydrocephalus and consists in arrhythmic repetitive movements of the eyes down and back in the form of a "V pattern."

Vertical ocular myoclonus. Vertical ocular myoclonus - pendulum

Isolated vertical eye movements with a frequency of 2 per second. In patients with the syndrome of "locked man" or in coma after the ONMK in the field of the varioly bridge. These movements are usually accompanied by myoclonus soft palate.

Alternating oblique deviation. An alternating oblique deviation in a coma is the intermittent descent of one eye and the ascent of the other. The phase of the change in the position of the eyeballs lasts from 10 to 30 seconds, and the phase of retention of the new position is from 30 to 60 seconds. The syndrome is typical for prefectural injuries, including acute hydrocephalus, tumor, ONMC, multiple sclerosis, craniocerebral trauma, lithium intoxication, Wernicke's encephalopathy, tentorial injection, spinocerebellar degeneration. Often reflects the severity of the process and in certain situations speaks of the need for urgent neurosurgical intervention.

Psychogenic deviation of the eye.

Psychogenic deviation of the eye (in any directions) is usually observed in the picture of a pseudo fit or psychogenic areactivity ("hysterical hibernation" - in old terminology) and is always combined with other demonstrative manifestations, the recognition of which helps correct diagnosis.

The tonic deviation of the gaze upwards (the forced upward view) refers to the rare phenomena observed in comatose patients and which should be distinguished from oculogic crises, seizures of petit mal and psychogenic coma. In patients who are in a coma, with a constant upward deviation of the eye, there is usually a diffuse hypoxic damage to the brain (hypotension, cardiac arrest, heat stroke) involving the cerebral hemispheres and the cerebellum with a relatively preserved brain stem. Some of these patients further develop myoclonic hyperkinesis and pronounced nystagmus "beating down". Rarely the tonic deviation of the gaze upwards can be psychogenic and in this case it is observed in the context of other motor conversion disorders.

Tonic deviation of the gaze downward (forced downward look) is observed in comatose patients after hemorrhage into the medial thalamus, with acute obstructive hydrocephalus, severe metabolic or hypoxic encephalopathy, or after massive subarachnoid hemorrhage. Thus eyes can be sometimes converged, as at a sight at the nose. A similar phenomenon can be observed in psychogenic coma (pseudocome).

IV. Congenital ocular motor apraxia

Congenital ocular motor apraxia or Cogan syndrome is characterized by an innate lack of ability for lateral gaze movements and is manifested by abnormal movements of the eyes and head when trying to arbitrarily change the position of the eyes during follow-up lateral movements.

This rare phenomenon is also described in ataxia-telangiectasia; agenesis of the corpus callosum; horee Huntington, Nyman-Pick disease.

There are no other syndromes of excessive rhythmic activity in the oculomotor muscles (opsoklonus, "nystagmus of the eyelids", alternating nystagmus and other unusual types of nystagmus, cyclic oculomotor paralysis with spasms, myoxia syndrome of the upper oblique muscle of the eye, ocular tilt reaction), since they do not refer to disturbances of the eye.