RU2257914C1 - Method for treating paralytic strabismus - Google Patents

Abstract

FIELD: medicine, ophthalmology.

SUBSTANCE: one should introduce Botulotoxin A-based Disport preparation into extra-ocular ipsilateral muscle being an antagonist of a paralyzed extra-ocular muscle at the dosage of 10-120 U to be injected into middle part of muscular bursa by leaving about 5 mm , not less against the site of its fixation to sclera. Moreover, additionally, one should inject the preparation suggested either into one or several muscles being contralateral synergists of paralyzed muscles, moreover, one should apply by 10% preparation less into those muscles which are ipsilateral antagonists in comparison with contralateral synergistic ones. The method provides stimulation of afferent nervous impulsation of paralyzed muscle that prevents its hypotrophy.

EFFECT: higher efficiency of therapy.

3 dwg, 3 ex, 12 tbl

Description

The invention relates to medicine, namely to ophthalmology, and can be used in the treatment of paralytic strabismus.

As you know, paralytic strabismus is a state of the oculomotor system in which one or more extraocular muscles completely or partially lose their function. Pathogenetic causes of this condition are pathological changes in the central or peripheral part of muscle innervation. With paralysis of the oculomotor muscles, an asymmetry of the position of the eyes occurs when fixing objects located in different directions of the gaze.

Symptoms of paralytic strabismus are: the absence of some arbitrary movements of the affected eye, the asymmetric position of the eyes, double vision.

Since the etiological causes of paralytic strabismus are neurological or neurosurgical pathology, active assistance in the early stages of rehabilitation (from the onset of the disease to 6-9 months) is carried out by specialists who deal with these problems, the ophthalmologist provides only symptomatic elimination of double vision by prescribing occlusion or certain optical correction .

After the early and late rehabilitation period (9-12 months from the moment of occurrence), surgical correction of paralytic strabismus is performed, the effectiveness of which is more dependent on the functional recovery of extraocular muscles involved in paralysis.

If we consider paralytic strabismus from the position of pathomorphological changes in the oculomotor muscles, then the following can be noted:

1. Partial or complete hypofunction of a paralyzed muscle will eventually lead to its hypotrophy.

2. The hyperfunction of its ipsilateral (localized in the same eye) muscle antagonist will lead to hypertrophy and contracture of the latter.

3. By the time of complete or partial restoration of the innervation of the paralyzed muscle, its morphological and, accordingly, functional imbalance with the antagonist will be more pronounced than at the time of the onset of the disease.

4. Accordingly, the etiological treatment of the causes of paralytic strabismus will not lead to a cure for the disease itself with all its symptom complex.

There are various methods of surgical treatment of paralytic strabismus, the essence of most of which is to perform resection of the paralyzed muscle, recession of its ipsilateral antagonist and (or) transposition of vertical intact muscles (or parts thereof) to the physiological site of attachment of the paralyzed extraocular paralyzed muscle.

A method for surgical treatment of paralytic strabismus is known, which consists in stitching the outer parts of the upper and lower rectus muscles to the upper and lower parts of the paralyzed external muscle in order to increase the amplitude of eye movement (Jensen CDF Trans. Pacific Coast Ophthalmol. Soc. 1964 , 45: 359). The known method allows you to restore some degree of mobility of the eye towards the paralyzed muscle, however, it has several disadvantages:

1. The terms for surgical correction of paralytic strabismus imply the patient’s exit from the acute and subacute period no earlier than 6–9 months after the onset of the disease. Therefore, the surgeon, trying to restore the mobility of the eye in the direction of the affected muscle, is passively content with the volume of functional rehabilitation and is faced with a contractural imbalance between the muscle involved in paralysis and its antagonist.

2. The volume of surgical intervention due to large tissue trauma and compression of the anterior ciliary arteries leads to significant edema of the conjunctiva and ischemia of the anterior segment of the eye.

3. Intervention on the vertical rectus muscles creates a risk of mild enophthalmos, narrowing of the palpebral fissure and the appearance of vertical strabismus.

Closest to the claimed method, the prototype, is a method for treating paralytic strabismus by administering a preparation containing Botulinum toxin-A as an active component in extraocular ipsilateral muscle antagonists (Scott A.B. Ophthalmol. 1985, 92: 676-683), which consists in the following. To inject Botox containing Botulinum toxin-A, use a 1.0 ml tuberculin syringe with a monopolar needle electrode with a diameter of 27. The needle tip is isolated so that the recorded signal is sent only from the tip of the needle. A monopolar needle electrode is inserted transoconjunctively into the extraocular muscle and connected to the electromyograph via an amplifier. The amplifier increases the electrical impulses and makes them audible through the speakers. Before injection, local anesthesia is performed by installing Propacaine or Amethocaine in the eye. The patient is asked to look away from the muscle into which the injection is supposed. After that, the surgeon inserts the needle into the extraocular muscle. Then the patient is asked to look towards the muscle into which the needle is inserted, this activates the motor fibers of the muscle. If the needle is inserted into the muscle, the electromyograph gives a sound signal of increased muscle activity until the needle reaches the largest part of the muscle. The sound signal helps the surgeon to be sure that the tip of the needle is correctly oriented in the muscle. Botox is injected into the muscle when the sound of the electromyograph reaches a peak. The dose of Botox administered is from 2.5 to 5 Units. The proposed method leads to a dosed relaxation of the ipsilateral antagonist muscle, which allows the paralyzed muscle to more fully restore its functions during the rehabilitation period and prevents the development of contracture between the antagonist muscles in the affected eye.

However, the proposed method of introducing the drug Botulinum toxin into the ipsilateral muscle antagonist transconjunctively under the control of the sound signal of the electromyograph has a number of significant drawbacks.

Firstly, the introduction of Botulinum toxin-A into the ipsilateral antagonist muscle partially eliminates the imbalance in the oculomotor system only on the affected eye. This does not take into account the imbalance between the eyes.

Secondly, there is a risk of perforation of the sclera needle.

Thirdly, there is a risk of perforation of the muscle bag and the release of Botulinum toxin-A into the supra- or infra-tenenone space and, thus, the effect on other extraocular muscles and the muscle that lifts the upper eyelid.

Fourth, the introduction of a needle under the control of the sound signal of an electromyograph is possible only with sufficient preservation (or restoration) of muscle function. In acute paralytic strabismus, this is possible only in the late stages of rehabilitation, which significantly reduces the effectiveness of Botulinum toxin-A. The sooner after the onset of paralysis, the drug is introduced into the muscle, which is a paralyzed antagonist, the greater the recovery effect.

Fifth, the impossibility of using this method of administering the drug to children and people who are afraid of the procedure.

Sixthly, in the presence of a state of contracture of the muscle antagonist of the affected muscle, when you try to look towards the latter, a jerky nystagmus appears in the extreme abduction of the gaze, which increases the risk of perforation of the sclera and muscle bag.

An object of the invention is to increase the effectiveness of treatment and reduce side effects.

The stated technical problem is achieved by the fact that the injection of the drug Dysport containing Botulinum toxin-A is produced in extraocular muscles, which are ipsilateral antagonists and contralateral synergists of paralyzed muscles.

After preparation of the surgical field and retrobulbar (or intravenous balanced multicomponent) anesthesia, access to the direct extraocular muscle, which is an antagonist of the muscle involved in paralysis, is released. A muscle is secreted without violating the integrity of the muscular bag. Further, departing at least 5 mm from the place of attachment of the muscle bag to the sclera, in its middle part, the drug Dysport is administered in a dose of 10-20 Units (Fig. 1). The surgical wound is sutured. In a similar way, surgical manipulations are performed on the extraocular muscle, which is the contralateral synergist of the paralyzed muscle (figure 2). If two or more extraocular muscles are involved in paralysis, then the drug is injected into the corresponding extraocular muscles - contralateral synergists (figure 3).

The required amount of administration of the drug Dysport to achieve effective induced paresis of the extraocular muscle, which is an ipsilateral antagonist or contralateral synergist of a paralyzed muscle, depends on the degree of disturbance of the oculomotor function of the paralyzed muscle and on the period of occurrence of paralysis or paresis. Moreover, it is necessary to inject 10% less drug into the antagonist muscle than into the synergist muscle. This is dictated by the fact that as the muscle involved in paralysis leaves the acute period, its functionality will not be fully restored. And the increased impulse sent to this muscle to make the necessary excursion by the eye will cause hyperfunction of its contralateral synergist, which will entail a larger secondary strabismus angle and accordingly double vision, therefore it is necessary that the induced synergist paresis lasts longer.

Figure 1-3 schematically shows the topography of the administration of the drug Dysport, where

экстраокулярная мышца, вовлеченная в паралич;

extraocular muscle involved in paralysis;

экстраокулярная мышца - ипсилатеральный антагонист;

extraocular muscle - ipsilateral antagonist;

экстраокулярная мышца - контрлатеральный синергист.

extraocular muscle is a contralateral synergist.

A significant difference of the proposed method from the prototype is that the drug Dysport is administered not only in the ipsilateral muscle antagonists of the paralyzed extraocular muscle, but also in the extraocular synergists, which can not only significantly reduce the risk of hypotrophy of the paralyzed muscle and the development of its antagonist hypertrophy, leading to contractural state between these muscles, but also eliminate the likelihood of developing hyperfunction of the synergist contralateral muscle, as well as by creating its hyp function to stimulate the necessary afferent nerve impulse to more fully restore the performance of the paralyzed muscle. The intraoperative method of drug administration minimizes the risk of local complications and side effects.

The positive effect of the proposed method of administration of the drug Dysport is achieved by creating the following modulated biomechanical mechanisms:

- the creation of artificial muscle paresis, which is an antagonist of paralyzed extraocular muscle, balances their biomechanical capabilities, and therefore eliminates the likelihood of creating a contractural state between them;

- inducing paresis of the contralateral muscle, which is a synergist of a paralyzed muscle, reduces its secondary hyperfunction, and therefore reduces the secondary angle of strabismus and the magnitude of diplopia;

- the creation of a secondary hypofunction of the contralateral muscle, which plays a major role in the same direction of the gaze, leads to the induction of increased afferent impulse to the paralyzed extraocular muscle, which increases its functional recovery;

- the creation of induced paresis of extraocular muscles is reversible and coincides in timing with the end of the acute period of paralytic strabismus (4-6 months);

- the introduction of the drug under intraoperative control minimizes the likelihood of local complications and side effects.

The combination of these artificially created biomechanical conditions balances and potentiates the functionality of the paralyzed and counter- and synergistically working extraocular oculomotor muscles. Therefore, the rehabilitation period takes place not in a state of pronounced imbalance, but in conditions of favorable mutually regulated biomechanical stabilization.

A search by sources of scientific, technical and patent information did not reveal a method identical to the claimed one, in connection with which we can conclude that the claimed technical solution meets the criteria of "novelty" and "inventive step".

The invention is illustrated by the following examples of specific performance of the method.

Example 1

Patient G., 50 years old.

Diagnosis: Paralysis of n.oculomotorius of the left eye. Monolateral paralytic exoinfratropia of the left eye. Partial ptosis of the left eye.

On examination:

1. The magnitude of the strabismus angle:

Table 1 Gaze Right eye Left eye Seen to the right > -60 ° ↑ 10 ° > -60 ° ↓ 7 ° When looking directly > -60 ° ↑ 15 ° > -35 ° ↓ 10 ° When looking to the left > -10 ° ↑ 20 ° > -10 ° ↓ 12 °

2. Mobility:

table 2 Gaze Right eye Left eye Cast 45 ° 7 ° Bringing Up 40 ° 5 ° Up 40 ° 3 ° Lead up 45 ° 2 ° Abduction 55 ° 35 ° Lead down 40 ° 15 ° Way down 35 ° 5 ° Bringing Down 40 ° 3 °

The patient was introduced Dysport of the claimed method. After retrobulbar anesthesia and treatment of the surgical field, an eyelid was introduced, exposing the eyeball as much as possible. Further, to provide access to the external rectus muscle of the left eye, the conjunctiva was taken with tweezers for 3 hours and the eyeball was brought. Conjunctival spring scissors performed one radial incision of the conjunctiva and tenon capsule 8 mm long along the meridian of 4 hours. The tenon capsule from the episclera was separated with scissors in the upper temporal quadrant. A muscle hook without a limiter was placed in the formed upper temporal space, the tip of the hook being directed away from the place of the proposed muscle attachment. Rotating the handle of the hook 180 ° (while the tip slides over the sclera), they grabbed the muscle at its attachment point. The hook was shifted 3-4 mm distal from the point of attachment along the muscle and raised 1.5-2 mm above the sclera. A spatula-mirror 4 mm wide was introduced under the muscle. The muscle hook was removed. The conjunctiva and tenon sheath were displaced to the edge of the muscle closed from the radial access zone with tweezers and brought over the edge of the spatula-mirror. Thus, the beginning of the muscle abdomen was isolated in the area of the conjunctival incision and raised above the sclera, while the muscle bag remained intact. After that, retreating 5 mm from the point of attachment of the muscle to the sclera distally along the muscle, a G 27 needle was injected into the middle of the muscle bag. The needle was displaced by 5 mm along the muscle in the distal direction, after which 10 Disport Units were introduced into the muscle bag. The needle was removed from the muscle bag in a reverse motion, having previously pressed the injection site with a cotton swab. After making sure that the injected drug did not leave the injection site, they removed the spatula-mirror from under the muscle. The edges of the cut conjunctival and tenon membrane closed. The wound was sutured with absorbable suture 7-0. In this case, a nodal suture was placed on the middle part of the radial section.

Under the conjunctiva, 0.3 ml of a 1% Dexazone solution was injected and dry Albucid was poured. The eyelid was removed and a sterile dressing was applied.

After that, they went on to perform surgery on the right eye according to the above technology on the contralateral synergistic muscles (m.rectus lateralis, m.rectus superior and m.rectus inferior). In this case, only the meridians of the radial sections were changed when accessing the operated extraocular muscles (Fig. 3) and the amount of the administered Dysport preparation was 12 units.

In the postoperative period, a 0.25% solution of Chloramphenicol 4 times a day for 7 days was installed in the conjunctival cavity of both eyes.

When examining the patient after 7 months, the following was revealed:

1. The magnitude of the strabismus angle:

Table 3 Gaze Right eye Left eye Seen to the right -17 ° ↓ 3 ° to -5 ° ↓ 3 ° -15 ° ↓ 3 ° to -5 ° ↓ 3 ° When looking directly -7 ° ↑ 15 ° to 0 ° -12 ° ↓ 5 ° to 0 ° When looking to the left -1 ° ↑ 2 ° to 0 ° -1 ° ↓ 2 ° to 0 °

2. Mobility:

Table 4 Gaze Right eye Left eye Cast 45 ° 7 ° Bringing Up 40 ° 22 ° Up 40 ° 10 ° Lead up 45 ° 7 ° Abduction 55 ° 40 ° Lead down 40 ° 20 ° Way down 35 ° 10 ° Bringing Down 40 ° 5 °

Thus, the magnitude of the primary and secondary strabismus has decreased significantly, while strabismus has shifted from the state of tropia to the state of horizontal phoria. The mobility of the eye increased, on which paralysis developed, and the reduction was restored to a greater extent.

Example 2

Patient B., 38 years old.

Diagnosis: Ophthalmoplegia of the left eye due to trauma. Monolateral paralytic exosupratropia of the left eye. Ptosis 3 degrees of the left eye. Left eye paralysis. Mydriasis of the left eye.

On examination:

1. The magnitude of the strabismus angle:

Table 5 Gaze Right eye Left eye Seen to the right > -90 ° > -45 ° When looking directly -90 ° - 5 ° ↑ 7 ° When looking to the left 7 ° ↑ 12 ° 5 ° ↑ 7 °

2. Mobility:

Table 6 Gaze Right eye Left eye Cast 45 ° -2 ° Up 45 ° 20 ° Abduction 60 ° 22 ° Way down 60 ° 15 °

In the patient during the acute course of the disease, the functions of vertical motors and m were restored at a fairly good pace. rectus lateralis, however, the reduction was completely absent without the planned positive dynamics. Therefore, in the acute period of development of ophthalmoplegia (2 months after the onset of the disease), the patient underwent rehabilitation treatment m. rectus medialis.

The patient was administered the drug Dysport of the claimed method. The type of anesthesia, access to the target muscles, the technique of introducing the needle, suturing of the surgical wound and recommendations in the postoperative period corresponded to Example 1, with the only difference being that Dysport was introduced into the ipsilateral antagonist - m. rectus lateralis of the left eye in the amount of 12 Units and in the contralateral synergist - m. rectus lateralis of the right eye in the amount of 13.5 Units.

When examining the patient after 6 months, the following was revealed:

1. The magnitude of the strabismus angle:

Table 7 Gaze Right eye Left eye Seen to the right 0 ° 0 ° When looking directly 0 ° to 2 ° ↓ 2 ° 0 ° to 2 ° ↑ 2 ° When looking to the left -10 ° -7 °

2. Mobility:

Table 8 Gaze Right eye Left eye Cast 45 ° 25 ° Up 45 ° 22 ° Abduction 60 ° 45 ° Way down 60 ° 30 °

Thus, the primary and secondary deviation was eliminated when looking directly and to the right. Monocular mobility of the affected eye increased. The restored convergence allowed the patient to comfortably perform visual work near, and the restored binocular field of view provided a high level of social and professional adaptation of the patient.

Example 3

Patient P., 63 years old.

Diagnosis: Paralysis of n.abducens of the left eye of unknown origin. Monolateral paralytic intropy of the left eye.

The results of the initial examination 3 months after the onset of the disease (subacute period of paralysis):

1. The magnitude of the strabismus angle:

Table 9 Gaze Right eye Left eye Seen to the right 3 ° ↑ 2 ° 3 ° ↓ 2 ° When looking directly 20 ° 15 ° When looking to the left - 25 °

2. Mobility:

Table 10 Gaze Right eye Left eye Abduction 60 ° 0-3 °

Within 3 months after the onset of the disease, no positive dynamics were observed in the increase in the abduction of the left eye. Therefore, in the subacute period of development of paralysis of the VI pair of FMN (3.5 months after the onset of the disease) in order to create conditions for the restoration of functions m. rectus lateralis on the left eye of the patient was introduced Dysport of the claimed method.

The type of anesthesia, access to the target muscles, the technique of introducing the needle, suturing of the surgical wound and recommendations in the postoperative period corresponded to Example 1, with the only difference being that Dysport was introduced into the ipsilateral antagonist - m. rectus medialis of the left eye in the amount of 18 Units and in the contralateral synergist - m. rectus medialis of the right eye in the amount of 20 Units (figure 2).

When examining the patient 4 months after the administration of the drug Dysport, the following was revealed:

1. The magnitude of the strabismus angle:

Table 11 Gaze Right eye Left eye Seen to the right 0 ° 0 ° When looking directly 1 ° 1 ° When looking to the left 3 ° 2 °

2. Mobility:

Table 12 Gaze Right eye Left eye Abduction 60 ° 35 °

Thus, primary and secondary deviation in the first position of the gaze and when looking to the left, completely when moving the gaze to the right, is almost completely eliminated. The binocular field of view has been significantly restored.

Thus, the method allows to increase the effectiveness of treatment, to use a drug containing Botulinum toxin-A in the early periods of rehabilitation after acute paralysis of the oculomotor muscles, regardless of the age and psycho-emotional state of the patient and eliminates negative local side effects.

Claims (1)

A method of treating paralytic strabismus, including the introduction of a drug based on Botulinum toxin-A to the extraocular ipsilateral muscle - an antagonist of paralyzed extraocular muscle, characterized in that as a drug containing Botulinum toxin-A, use the drug Dysport in a dose of 10-20 Units, the introduction of which is carried out in the middle part of the muscle bag, deviating at least 5 mm from the place of its attachment to the sclera, while additionally administering the drug to one or more muscles that are contralateral synergists of paralyzed muscles, moreover, 10% less drug is injected into muscles that are ispilateral antagonists than in muscles that are contralateral synergists.

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