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Treatment of paresis of the abducens ophthalmic nerve. Abducens nerve palsy due to diagnostic and therapeutic interventions Optic nerve palsy symptoms and treatment

I. Congenital abducens nerve palsy (6 pairs of FMN):

1. A small percentage of healthy newborns have unilateral isolated sixth nerve palsy, presumably associated with birth trauma. It seems likely that many of these cases went undiagnosed, as complete spontaneous recovery is often observed within six weeks. The differential diagnosis of congenital sixth nerve palsy includes infantile esotronia with cross fixation. This condition is often not diagnosed until the baby is several months old.

2. Primary aplasia/hypoplasia of the abducens nerve nucleus. During the first year of a child's life, parents notice an imbalance in the alignment of the eyes. This variant of a congenital disorder of cranial innervation is considered a manifestation of Duane syndrome. The most characteristic form involves the inability to abduct both eyes with normal alignment of the eyes in the primary position or normal alignment when turning the head towards the affected side.
Most cases of unilateral Duane syndrome develop normal sensory binocularity and good motor fusion.

Duane syndrome can be unilateral or bilateral, sporadic or hereditary. Some cases develop secondary to teratogenic effects, such as thalidomide. Duane syndrome may be isolated or be a component of a larger cranial nerve disorder syndrome, such as Mobius syndrome or Poland syndrome and Goldenhar syndrome.

II. Acquired abducens nerve palsy (6 pairs of FMN). Young children rarely complain of diplopia. With sixth nerve palsy that develops in the first decade of life, parents usually notice that the child squints or closes one eye when concentrating visually. Or the child develops an adaptive turn of the head, which helps align the eyes. For older children, complaints of diplopia are more common, especially (with partial paralysis of the sixth nerve) diplopia when looking into the distance.

When collecting anamnesis, special attention should be paid to events that could explain the development of paralysis (trauma, recent infections, etc.) and to additional symptoms that could help localize the lesion or have diagnostic value. In many cases, the clinical context of symptoms may explain the cause of paralysis.

Pontine glioma.
(A) Axial T2-weighted tomography shows enlargement of the right colliculus facialis;
The child has bilateral paresis of the VI nerve and partial paresis of the VII nerve on the right.
(B) Clinical photograph.

A) Examination for abducens nerve palsy (6 pairs of FMN). To identify hidden esodeviation, cover and alternating cover tests for distance and long distance may be required. In older children, the use of the Hess screen helps to record the results of the study and assess the dynamics of the state. Signs to look for that can help localize lesions include muscle weakness or asymmetry, nystagmus, trigeminal sensory neuropathy, and Horner's syndrome. Myasthenia gravis may simulate any infranuclear (or inter-/supranuclear) oculomotor disorder; check for forced eye closure using the orbicularis oculi muscle.

Rule out spasm of the near reflex (convergence spasm) - evaluate the reactions of the pupils; dynamic retinoscopy may be informative. Examination of the optic disc is of great importance. Differential diagnosis includes:

1. Divergence palsy: that is, normal alignment at near, esotropia at distance, while maintaining full abduction. This condition can accompany various pathologies of the brain stem.

2. Supranuclear abduction paresis: unilateral or bilateral abduction paresis with slow abduction saccades +/- nystagmus of the adducted eye; the vestibulo-ocular reflex is unchanged. This “posterior internuclear abduction ophthalmoplegia” results from damage to the rostral pons/midbrain.

b) Important causes of abducens nerve palsy (6 pairs of FMN):

1. Tumor. Isolated, usually progressive, sixth nerve palsy may be the first sign of an intracranial tumor, usually a brain tumor, a pontine glioma, or another posterior fossa tumor such as an ependymoma or medulloblastoma. Chondroma of the clivus can manifest itself in the same way. Parasellar tumors, such as craniopharygneoma or pituitary tumor, can invade the cavernous sinus and cause sixth (or other oculomotor) nerve palsies.

2. Injury. It has been established that the cause of sixth nerve palsy can be a closed head injury - sometimes very mild - without a skull fracture. When the base of the skull is fractured, it may be accompanied by paralysis of the ipsilateral facial nerve. Bilateral traumatic palsies of the VI nerve lead to enormous esotropia with cross fixation and abnormal position of the head, they can be observed with bitemporal compression of the head, which in children in most cases is also accompanied by palsy of the VII nerve and hearing loss.

3. Benign/post-viral/idiopathic/inflammatory. This condition is widely known, but it is a diagnosis of exclusion and is made in the absence of pathological changes in radiological examination, cerebrospinal fluid and blood tests. VI nerve palsy is usually complete, unilateral, and begins suddenly. It is assumed that the provoking factor is the most common infections, such as viral infections of the upper respiratory tract.

However, VI nerve palsies can develop with more severe neurotropic viral infections, such as chickenpox. The prognosis is good, recovery begins approximately six weeks after onset, full recovery occurs within 3-4 weeks.

Benign sixth nerve palsy of childhood may recur on the same side or in the contralateral eye. The localization and nature of the pathology remains unclear.

Focal demyelination affecting the VI pons nerve bundles can develop in acute disseminated encephalomyelitis and childhood-onset multiple sclerosis. Neurosarcoidosis can manifest itself as mononeuritis of the cranial nerve; most often, damage to the VII nerve develops, but damage to the VI nerve (or cranial polyneuritis) also occurs.

4. Intracranial hypertension. VI nerve palsy may develop due to intracranial hypertension. Paralysis may be the first sign of cerebrospinal fluid outflow tract obstruction by a tumor or idiopathic intracranial hypertension. In the latter case, children with the condition do not necessarily exhibit the habitus and BMI (body mass index) characteristic of this condition in adults.

5. Infection. It has been established that sixth nerve palsy can complicate the course of meningitis in newborns and in infancy/childhood, as well as tuberculous meningitis. Against the background of a middle ear infection complicated by petrous apicitis, Gradenigo syndrome may develop, which is characterized by palsy of the ipsilateral VI nerve, pain in the area of innervation of the V nerve, and ear pain/otorrhea. Middle ear infection can lead to thrombosis of the cerebral venous sinuses and secondary intracranial hypertension in combination with sixth nerve palsy.

Lemierre syndrome involves a peritonsillar abscess caused by Fusobacterium necrophorum (or other anaerobic infection) complicated by thrombosis of the internal jugular vein and septic thrombophlebitis. Ipsilateral palsy of the sixth or, rarely, fourth nerve may develop. Successful treatment of infection may not result in resolution of paralysis.

6. Vascular. Pontine vascular malformations, such as cavernoma, may present with or be complicated by ipsilateral sixth nerve palsy.

7. Other reasons. VI nerve palsy may develop after lumbar puncture due to intracranial hypotension. The paralysis is complete, develops suddenly and is accompanied by a hypotensive headache. Most cases resolve spontaneously. Idiopathic intracranial hypotension, rarely found in children, is accompanied by recurrent headaches and sometimes double vision due to sixth nerve palsy. MRI reveals characteristic signs.

V) Management and treatment of abducens nerve palsy (6 pairs of FMN). With acquired paralysis, treatment of the disease that caused it is of paramount importance. Once the condition has stabilized, patients should wait up to a year to allow spontaneous recovery before planning surgical treatment. In children with an immature visual analyzer, taping one eye plays an important role to prevent amblyopia.

In cases where spontaneous recovery does not occur, sixth nerve palsy with esotropia is not treatable using standard surgical techniques used in the treatment of strabismus. After temporary weakening of the internal rectus muscle by injection of botulinum toxin, temporal transposition of the entire superior and inferior rectus muscles to the insertion of the external rectus muscle is performed, usually in combination with reinforcing sutures. Subsequently, recession of the internal rectus muscle may be required.

a - Bilateral progressive sixth nerve palsy in a twelve-year-old patient.
Axial T2-weighted tomography shows a huge mass deep in the brainstem and left hemisphere of the cerebellum; aggressive pontine glioma.
b - Acute disseminated encephalomyelitis.
Axial T2-weighted tomography shows multifocal edema and cortical signal changes associated with gray matter lesions.
The patient had bilateral sixth nerve palsy.

a - Neurofibromatosis type 1. In a six-year-old girl, the disease manifests itself as intracranial hypertension, bilateral sixth nerve palsy, and papilledema.
An axial T1-weighted tomogram after gadolinium enhancement shows a huge right cerebellar cyst and an enhancing nodule, in association with obstructive hydrocephalus.
b - Apicitis of the pyramid of the temporal bone with painful paralysis of the right VI nerve in a six-year-old patient.
Axial T1-weighted (fat-suppressed, FS) tomography after gadolinium enhancement shows contrast enhancement at the petrous apex.

This 10-year-old patient first developed sixth nerve palsy and then right gaze palsy.
Axial T2-weighted tomography shows a pontine cavernoma.

The combination of neurological pathologies of the visual apparatus poses a great danger to humans, so it is important to monitor not only the state of vision, but also the health of the eye itself. One of the most serious diseases in this regard is paresis of the oculomotor nerve, which causes paralysis of the eyeball and other complications. In turn, the problem can only be a symptom of other diseases. It is difficult to treat and stop, so when you detect the first signs of a disorder, it is important to consult a doctor as soon as possible.

Description of the pathology, development mechanism

The oculomotor nerve is part of the third pair of cranial nerves and consists of viscemotor and somatomotor (motor) fibers. Its main function is to provide motor ability to the eyeball. The nerve controls the following systems:

Ciliary muscles;
Sphincter of the pupil (provides its ability to expand and contract depending on the lighting);
Optical-kinetic nystagmus (the ability to follow moving objects);
Muscles to regulate the movement of the upper eyelids;
Vestibulospectral reflex (the ability of the pupil to move when the head turns);
Accommodation (change in the curvature of the eye lens depending on surrounding objects and phenomena).

Thus, damage to the optic nerve always entails a limitation in the functionality of the visual apparatus. The movement of the eye and pupil is limited or lost. In turn, the lesion has its own reasons for occurrence or acts as a sign of another disease. Men and women of all ages are at risk, but statistics show that children are more likely to suffer from oculomotor nerve palsy.

Symptoms and signs of damage

In the early stages of oculomotor nerve paresis, there are practically no symptoms, which complicates its diagnosis and further treatment. With a longer course of the disease, the following symptoms gradually begin to appear:

Drooping of the upper eyelid (partial or complete);
Lack of reaction (constriction/dilation) of the pupil;
Diplopia (double vision due to loss of motor ability of the eye);
Divergent strabismus (occurs due to lack of resistance of the upper and lower muscles of the eyeball);
Loss of focusing and adaptation to changes in the distance between the eye and the object;
Loss of motor ability;

With extensive damage, immobility can become only part of the entire symptomatology of the disease if other cranial nerves are also damaged. In addition, oculomotor nerve palsy itself may be a symptom of a more serious systemic disease. Most often, the lesion affects only one eye.

Types of pathology

In medical practice, there are two main forms of the disease:

Congenital. Occurs as a result of intrauterine disorders of the development of muscles and nerves, as well as damage or damage to the facial and oculomotor nerves during development;
Acquired. May have neurological, mechanical (traumatic injuries, consequences of surgical operations), aponeurotic prerequisites.

Paresis also occurs as a result of the progression of systemic diseases. In such cases, therapy should be aimed not only at eliminating paralysis, but also at relieving its causes.

Causes, prerequisites and risk factors for damage

Systemic pathologies that can cause paresis and paralysis:

Diabetes mellitus;
Arterial hypertension, instability of blood pressure;
Benign tumors and oncology;
Cervical osteochondrosis and other diseases of the spine;
Aneurysm;
Long-term use of Amiodarone, anticancer drugs and medications for the treatment of cardiovascular diseases;
Hematomas;
Traumatic eye injuries, foreign body entry;
Inflammatory diseases of the brain (encephalitis, meningitis);

Ophthalmoplegic migraine;
Flu;
Diphtheria;
Syphilis;
Brain hemorrhage, stroke;
Vasculitis;
Myocardial infarction.

The presence of at least one of the listed diseases is a reason for a systematic medical examination with a mandatory examination by a neurologist and ophthalmologist.

Diagnosis of the disease

Treat oculomotor paresis
nerve is quite difficult. However, timely diagnosis and identification of the cause of the disorder will help simplify the process and increase the chances of recovery.

First of all, the examination should be performed by an ophthalmologist. During the diagnostic process, he must check:

The presence or absence of deviation in the position of the eyeball;
Absence or presence, strength of the pupil’s reaction to light exposure;
The presence or absence of ptosis (paralysis of the upper eyelid);
Eye focusing quality;
The reaction of the pupil and eyeball to the movement of an object in space.

Thus, the doctor determines the probable site of the lesion, which further magnetic resonance imaging, superposition electromagnetic scanning, and X-ray examination will help to accurately determine. It is also necessary to collect anamnesis and information from the medical history. Additional research:

Measuring intraocular pressure;
Examination of the condition of the fundus.

Often, additional consultations with specialists in other areas are required: endocrinologist, neurologist, surgeon, infectious disease specialist, etc. In turn, they can prescribe additional hardware and laboratory tests.

Therapeutic methods

One of the most important measures in the treatment of oculomotor nerve palsy is constant monitoring of the patient. In this case, a therapeutic effect on the root cause of paralysis is mandatory. If intervention is unavoidable, the doctor selects one of the more radical methods.

Computer program

The main task of the computer program is to strengthen the muscles of the eyeball while broadcasting special pictures. When viewing, patients experience increased nerve tension, due to which the body’s resources are mobilized and directed to improve their functioning. With systematic sessions, positive dynamics of treatment are observed.

Electrophoresis

Electrophoresis also gives good results of therapy. Before the session, electrodes are applied to the patient's closed eyes around the perimeter, as well as to the back of the head. The course of treatment consists of 15-20 sessions, the duration of which is no more than 20 minutes.

Surgery as a therapeutic method in the treatment of oculomotor nerve palsy is not always used. Typically, such a measure is required in two cases:

If conservative therapeutic measures are insufficiently effective;
With the progression of deterioration in the quality of vision, a decrease in acuity.

The operation is usually performed under local or general anesthesia (depending on the situation). After this, the patient must undergo a recovery period with a decrease in the load on the visual apparatus, as well as the introduction of a special regime of rest, sleep and physical activity. Additionally, the use of exercises and preventive medications is required.

Adjuvant therapy

Drug treatment in relieving paresis is ineffective. At the same time, to improve the patient’s condition, special eye drops that improve blood supply and tissue nutrition, physical therapy, and vitamin complexes can be used. Patients are also prescribed to wear bandages, sessions of viewing stereo images, proper rest and nutrition.

As a rule, eliminate
The pathology can be resolved within three to six months with timely and correct therapy. First of all, conservative methods are used for this. If no improvement is observed during the specified period, other therapeutic measures are also added. Congenital pathologies, as a rule, cannot be completely cured.

Abducens nerve - this is the sixth pair of cranial nerves, the root of the facial nerve forms a loop around the abducens nucleus. The abducens nerve innervates only the external rectus muscle, and its function is reduced to abducting the eyeball outward.

Pathology of the abducens nerve

There are two types of abducens nerve pathology - paresis and paralysis. Paresis of the abducens nerve is a restriction of outward movement of the eyeball. Abducens nerve palsy is a complete loss of outward movement of the eye. In this case, the norm of outward mobility of the eye is the possibility of the outer commissure of the eyelids touching the outer edge of the cornea. If this is not the case, then the pathology of the abducens nerve is obvious.

Clinical picture

The clinical picture of abducens nerve paresis is characterized by the following signs.

Limited mobility of the eyeball.
Secondary deviation of the eye.
Double vision.
The position of the head is involuntary-forced.
Orientation disorder.
Uneven, uncertain gait.

With a mild form of paresis, the symptoms are mild and practically do not cause concern to the patient. While with paralysis the same symptoms are severe and cause significant discomfort.

Causes of abducens nerve paresis

What causes abducens nerve paresis? As a rule, this occurs as a result of damage to the central nervous system due to infections and intoxications. Infections of this kind (which affect the oculomotor nerves) include diphtheria, epidemic encephalitis, syphilis, complications after influenza, and Heine-Medin disease. Intoxications that cause paresis of the abducens nerve include severe alcohol intoxication, lead poisoning (a compound of heavy metals), botulism, and carbon monoxide poisoning.

Damage locations

Based on the location of damage, paresis and paralysis of the abducens nerve are divided into cortical, nuclear, conductive, radicular and peripheral lesions.

Forecast

As already mentioned, paresis of the abducens nerve is a part. Therefore, both treatment and prognosis of the disease depend on the underlying disease and its etiology. After recovery from infectious diseases and intoxications, paresis of the abducens nerve is usually eliminated. Recovery does not occur only in cases of irreparable diseases - skull fractures, tumors, severe nerve injuries.

The movement of the eye is controlled by six motor muscles, which receive nerve impulses from three paired nerves of the skull:

the oculomotor nerve supplies the internal, superior nerves, penetrates the inferior rectus muscle and penetrates the inferior oblique muscle;
the trochlear nerve innervates the superior oblique muscle;
The abducens nerve penetrates with its fibers into the external rectus (lateral) muscle.

The abducens nerve “supports” the eye

A nerve called the abducens nerve plays a small regulatory role in eye motility by retracting it outward. These nerve fibers enter the oculomotor apparatus of the organ and, together with other nerves, control complex eye movements.

The eye can turn from side to side horizontally, make circular movements, and move in a vertical direction.

Abducens nerve function

The nerve originates in the nucleus, located in the middle part of the medulla. Its fibrous structure crosses the pons and the brain center, passing its surface, called the basal. Then the path of the fibers flows along a groove located in the medulla oblongata.

Next, the fibrous threads of the nerve cross the membrane of the brain region, pass close to the carotid artery, move to the upper part of the orbital fissure and end their path in the orbit, firmly attached to the eye.

Nerve fibers control the rectus externus (lateral) muscle, which moves the eye outward and makes it possible to move the eyes to the sides without turning the head. The muscle is the opposite of the internal muscle tissue that pulls the eye toward the center. They balance each other out.

If one of the two muscles is affected, it develops, since the other muscle pulls the eye organ towards itself, and the affected one cannot maintain balance. It is impossible to check the abducens nerve in isolation; it is examined together with the other two nerves.

Nerve pathology

Pathology of the abducens nerve

The fibers of the abducens nerve are located superficially, so during injuries they can easily be pressed to the base of the skull. Damage to the nerve is expressed in paresis - limited outward movement of the eye organ or complete paralysis.

With normal functionality of the abducens nerve, the edge of the cornea should touch the outer edge, the junction of the eyelids. If this is not observed, then there is nerve pathology. It has the following signs:

movement of the eye organ is limited;
objects inspected are split into two;
repeated deviation of the eye;
forced position of the head, which can be involuntary;
dizziness, disorientation in space, staggering gait.

Nerve damage can be caused by infections:

disease with encephalitis;
previous syphilis;
diphtheria disease;
influenza and its complications.

As a result of intoxication:

ethyl alcohol;
toxic metals;
combustion products;
a consequence of botulism.

Paralysis of the abducens nerve occurs for the following reasons:

previous meningitis;
presence of tumor inclusions;
the presence of hemorrhage, with pressure surges;
thrombosis;
purulent diseases of the nasal passages;
eye socket injuries;
temple bruises;
metabolic disorders;
multiple sclerosis;
stroke.

Nerve damage is distinguished by location:

Cortical and conductive – diseases are localized in the medulla and brainstem.
Nuclear defeat.
Radicular lesions are observed within the medulla. This lesion is called Fauville's palsy, when, on the one hand, there is damage to the abducens and facial nerves, and on the other hand, there is damage to the limbs.

Peripheral paralysis is divided into:

intradural is located inside the dura mater;
intracranial is localized in the cranial cavity;
orbital is located in a circle.

Treatment of paresis and abducens nerve palsy

Abducens nerve as a component of the nervous system

Recovery from paralysis occurs over a long period of time throughout the year. A well-known method of treatment is the use of physiotherapy - exposure to pulses of a low-frequency electromagnetic field, stimulation with electric current.

The treatment method has an analgesic, anti-inflammatory, calming effect. The disadvantage is that recovery is very slow, and in some cases does not occur at all.

The oculo-occipital method of administering the drug (neuromidin) is also used to increase muscle contractility and influence defects in the connective muscles.

The method of using electrophoresis with a solution of 15% neuromidine has proven itself well. The duration of the sessions is 15 minutes daily for 15 days. After completing the procedure, it is recommended to lie down with your eyes closed for 10 minutes.

If improvement and restoration of the functioning of the abducens nerve is not observed after treatment, and the lesion does not go away on its own, surgical intervention is used. The essence of the method is as follows: an injection of ultracaine is made under the conjunctiva, and a half-circle incision is made.

The superior external and inferior straight nerves are split into two bundles lengthwise and the lower fibers are sutured to the upper fibers. This allows you to rotate the eyeball by more than 15–20° within a day after surgery, in some patients up to 25°; binocular vision was restored in every fourth person operated on.

To alleviate the condition of impaired binocular vision, Fresnel prisms are used, which are attached to glasses. Prisms have different angles and are selected individually. Possibly also closing one eye.

Most nerve diseases are associated with a disorder of the central nervous system, so treatment is prescribed accordingly. After suffering infections and successful treatment, the nerve damage is restored.
In rare cases, when the tumor is inoperable, there is serious injury to the skull and the nerve itself, recovery may not occur.

Learn more about the abducens nerve in the video lecture:

Oculomotor nerve palsy usually manifests as sudden or progressive ptosis, combined with strabismus. The first step is to determine the cause of oculomotor nerve palsy, as in some cases the condition can be life-threatening. Treatment is difficult.

Epidemiology and etiology:
Age: any. It occurs rarely in children.
Gender: Equally common in men and women.

Etiology:
- ischemic capillary disease;
- compression (aneurysm, tumor);
- injury;
- ophthalmoplegic migraine (observed in children).

Anamnesis. Sudden onset of diplopia (when raising a drooping eyelid). May be accompanied by pain.

Appearance of oculomotor nerve palsy. Complete ptosis with fixation of the eye in a downward and outward position. Lack of upward, downward and inward eye movements. Mydriasis is possible. Aberrant oculomotor nerve regeneration needs to be assessed.

Special cases. In mydriasis, neuroimaging is necessary to exclude an aneurysm of the posterior communicating artery. In addition, it is performed for persistent or partial paralysis of the oculomotor nerve, as well as for any paresis of the oculomotor nerve with aberrant regeneration. Patients over 50 years of age undergo neuroimaging even if they do not have severe vascular disease. Paresis of the oculomotor nerve caused by vascular disorders resolves within 3 months.

Differential diagnosis:
Myasthenia gravis.
Chronic progressive external ophthalmoplegia.

Laboratory research. Magnetic resonance imaging (MRI) and magnetic resonance angiography or angiogram are performed in cases where pupillary symptoms are observed with oculomotor nerve palsy.

Pathophysiology. Disturbance in the conduction of nerve impulses along the oculomotor nerve can be caused by its compression or ischemia. With ischemia, the pupil does not dilate, and paresis resolves within 3 months.

Treatment of oculomotor nerve palsy. Before surgical correction, a sufficient amount of time must pass, since spontaneous restoration of mobility is possible. Before performing surgery to eliminate ptosis, it is necessary to correct strabismus. Suspension to the frontalis muscle using silicone suture is a safe surgical option for patients, but there is a risk of postoperative corneal exposure.

Forecast. Most oculomotor nerve palsies resolve spontaneously within 3-6 months. In cases where no change occurs during this time, it may be difficult to achieve a normal eyelid position without causing an unacceptable amount of corneal exposure. Often, after lifting the eyelid, patients have residual diplopia associated with limited mobility of the eyeball.