Device for restraining too fast development of eye diopter

Abstract

The invention relates to a device for restraining too fast development of eye diopter, which comprises a multi-stage defocus compensation training lens and a sighting mark instrument for the multi-stage defocus compensation training lens to carry out adaptive training, and is characterized in that the multi-stage defocus compensation training lens is utilized to carry out trigger compensation training so as to form a stable restraining state; diopter development is controlled to be lower than a set threshold value, and the purposes of prevention and treatment are achieved.

Description

Technical Field

[0001] The invention relates to a device for restraining excessively rapid development of eye refraction, and belongs to the field of eye refraction identification and correction. Background Art

[0002] Humans use the refractive system inside the eye to focus the light emitted by objects outside the eye on the retina to form a light signal, which is then transmitted along the optic nerve to the cerebral cortex to form an image of the object. When the light focusing position of the eye's refractive system falls exactly on the fovea of ​​the retina, it is called focus. On the contrary, it is called defocus. When the defocus position is in front of the retina, it is called myopic defocus. When the defocus position is behind the retina, it is called hyperopic defocus.

[0003] The eye refractive system is mainly composed of refractive media such as the cornea, lens, and vitreous body. Refractive media have the ability to bend the propagation direction of light, and classical optical theory measures this ability in terms of refractive power. Therefore, refractive media such as the cornea, lens, and vitreous body have independent refractive powers. The image can be presented in the fovea of ​​the retina in a clear and focused manner, which is achieved by the optimal synergistic combination of corneal refractive power, lens refractive power, and vitreous refractive power, the aperture effect of the pupil, and the relaxation effect of the extraocular muscles (commonly known as the "three-linkage"). It must be emphasized that the quality of clear focus depends on the precise compensation of refractive power in the defocus state (referred to as "defocus compensation"), including the adjustment compensation of the lens with dynamically changing refractive power, and the convergence compensation of the extraocular muscles that can be dynamically relaxed. The focusing quality of the eye refractive system can be evaluated by testing the size of the eye's refractive power. For myopic eyes, the lower the test result of the eye's refractive power, the worse the focusing quality.

[0004] Vision is a high-level gift that distinguishes humans from other organisms in the process of biological evolution, because the formation of vision requires the participation of learning and thinking. Learning and thinking is a mechanism unique to humans. After the external object is imaged in the cerebral cortex, the human brain will refer to the tactile sensation formed by the contact between the limbs and skin and the object, and expand the image of the object in three dimensions, and finally form a three-dimensional vision. Learning and thinking is carried out precisely in the process of three-dimensional expansion. Ophthalmologists in the 16th century discovered that the image of the object transmitted to the cerebral cortex by the human retina is inverted, and people use the limbs to feel and test the size, distance, direction and position of the object, and learn and think in the centripetal conduction visual central system composed of "hand→brain→vision", and finally realize the flipping of the inverted visual image to form a positive three-dimensional world.

[0005] In addition, the human visual learning thinking mechanism is also manifested in the relearning and processing of new imaging signals. George Stratton wore a telescope that could produce inverted images (the telescope was invented by Kepler) to reverse the imaging of his visual central system and cause severe dizziness and brain swelling. With the help of support tools and the learning thinking mechanism, Stratton rebuilt the processing mechanism of the visual central system after a few weeks, thereby dispelling the dizziness and movement disorders. However, after taking off the telescope, Stratton returned to an extreme state of dizziness and movement disorders, and with the help of learning thinking again, he recovered his normal life ability after a few weeks. The Stratton Experiment showed that the brain's visual central system can form new processing results for new imaging signals through relearning thinking. This learning thinking is named visual psychology.

[0006] Visual psychology is widely used in daily life. For example, myopic patients who wear optical glasses for the first time will feel the tension of eye muscles or even dizziness. Optometrists will advise patients to adapt for one week before effective improvement. This is the process of visual central system activating visual psychology. The above visual learning thinking mechanism can be deeply applied in the work of restraining the rapid development of eye refraction.

[0007] like Figure 1As shown in the figure, the optical imaging path of the human eye and the principle of defocus compensation. In the long process of biological evolution, humans have evolved the eye into an extremely precise optical imaging device; whether it is to watch a grand scene in the distance or a subtle substance nearby, the light emitted by the target enters the eye refractive system through the cornea and pupil. Under the action of adjustment and convergence, the fovea of ​​the retina receives the imaging signal and transmits it to the brain. The brain grades the aberration of the imaging quality, and the grading results are fed back to the fovea of ​​the retina. After that, the retina activates the defocus compensation mechanism, sends chemical signals to the choroid adjacent to the retina, causes the choroid to undergo a structural phase change, and then causes the sclera closely attached to the choroid to undergo a structural phase change, promotes the physical position of the retina to change, and completes the compensation. Among them, the fovea of ​​the retina has densely distributed cones to receive light signals and form images, and secrete chemical factors to issue choroidal phase change commands. The choroid is mainly composed of three layers of blood vessels, including the large blood vessel layer (Haller Layer) close to the sclera, the capillary layer close to the retina, and the vascular interlayer (Satf l er Membrane) in the middle. The three layers of blood vessels in the choroid can change in thickness (thicken or thin) when receiving a phase change command. Choroidal thickening corresponds to myopic defocus compensation. Choroidal thinning corresponds to hyperopic defocus compensation. The sclera is composed of dense smooth collagen and elastic fibers, and can undergo elastic or plastic deformation under the driving force of the choroid. Elastic deformation is recoverable, while plastic deformation is irreversible. Myopic patients, especially those with rapid refractive power development, often experience choroidal thinning and scleral plastic deformation.

[0008] like Figure 2 The figure shows the compensation path when the human eye receives a sharp imaging signal; the so-called sharp imaging signal means that the imaging edge lines are thinner, the imaging contours are sharp, the lines are clear, and the details are bright. Figure 1 compared to, Figure 2The state represented is that the eye has an over-adjustment, that is, the eye has an overreaction to the light emitted by the object in front of the eyes, the amount of adjustment provided by the refractive system exceeds the required amount, the imaging signal transmitted to the fovea of ​​the retina is too sharp, the brain grades the image quality and feeds back high-order clear aberrations, and the retina issues a command to thicken the choroid in order to balance the over-adjustment of the eyes. The choroid increases its thickness through a series of actions such as increasing the surface area and osmotic activity of the proteoglycan complex to allow water to enter the vascular layer, increasing the number of osmotic active molecules by increasing the capillary fenestrations, draining fluid from the anterior chamber into the choroid, and the retinal fluid entering the choroid through the pigment epithelium. The thickened choroid will push the retina forward (i.e., toward the vitreous body), produce myopic defocus compensation, thereby eliminating over-adjustment and relaxing the refractive tension of the eyes. The movement of the retina toward the vitreous body will pull the scleral fibers to produce recoverable elastic compression, the sclera will not undergo plastic deformation, and the eye's refractive power will remain unchanged. This suggests that ophthalmologists can maintain the stability of the eye's refractive power by triggering the eye's myopic defocus compensation.

[0009] On the contrary, Figure 3 The figure shows the compensation path when the human eye receives a blurred imaging signal, and also shows the path of the rapid development of the human eye's refractive power due to blurred imaging; in contrast to sharp imaging, the image edge lines of blurred imaging are thicker, the image contour is deformed, and the lines and details are blurred. At this time, there is an adjustment lag in the eye, the adjustment amount provided by the refractive system is lower than the required amount, the brain feeds back high-order blur aberrations, and the retina issues a command to thin the choroid. The choroid reduces the blood flow in the vascular layer, releases water, reduces protein penetration, and causes its own thickness to thin. The retina then moves away from the vitreous body, producing hyperopic defocus compensation, thereby making up for the insufficient adjustment amount caused by the adjustment lag. The eye will activate the convergence compensation of the extraocular muscles to lengthen the eye axis and increase the distance the retina moves backward. The movement of the retina behind the vitreous body will tear the scleral fibers and produce irreversible plastic deformation, causing rapid development of the eye's refractive power. The greater the amount of adjustment lag, the greater the degree of thinning of the choroid and sclera, the longer the eye axis length, the faster the eye's refractive power develops, and the higher the degree of myopia. Obviously, the blurred imaging of the fovea is the key factor causing the rapid development of eye refractive power, while the hyperopic defocus compensation triggered by the accommodation lag causes the gradual deepening of myopia.

[0010] Myopia is currently prevalent, with more than 600 million people suffering from myopia in China, and even affecting teenagers and preschoolers. The medical community calls for the establishment of a dynamic file of adolescent eye refraction, regular monitoring of adolescent eye refraction, and the adoption of measures to restrict rapidly developing refraction when necessary, limiting the proportion of low refraction below a given threshold, and ensuring excellent visual focus quality. Summary of the invention

[0011] The technical problem to be solved by the present invention is to provide a device for restraining the excessively rapid development of eye refraction, a multi-level defocus compensation training lens and a sight mark meter, wherein the multi-level defocus compensation training lens is obtained by the following method: step (1), using an optometry device to test the accommodation reserve and fusion reserve of the visual acuity to be tested, and obtaining the upper limit of the total amount of compensation trigger that can be implemented; the upper limit of the total amount of compensation trigger that can be implemented is 1 / 3 to 1 / 2 of the accommodation reserve and fusion reserve obtained by the optometry device.

[0012] Step (2), the total amount of compensation trigger that can be implemented is discretized into n-level arithmetic progressions, and a discrete function is proposed Acco is the total amount of compensation trigger that can be implemented. i Compensation trigger amount for each level, tolerance Obtain multi-level myopic defocus compensation training lenses, including obtaining 1 Lenses, acco 2 Lenses, acco 3 Lenses, acco 4 Lenses... acco n The lens is composed of a multi-level myopia defocus compensation training lens.

[0013] First stage compensation lens acco 1 Start with trigger compensation training. After obtaining clear images, start trigger compensation training of the compensation lens step by step. 1 The size of the relative adjustment can be obtained by implanting a positive spherical lens in front of the user's eyes through a comprehensive optometry table; the relative adjustment test process is to first obtain the tester's best near vision, then use the upper row of sight marks of the best near vision as the visual target, and add positive spherical lenses in front of the tester's eyes at intervals of +0.125DS until the tester can no longer see the sight marks clearly. At this time, the degree of the added spherical lens is the acco 1 The above n-level arithmetic series can be discretized according to acco 1 , tolerance, and total compensation are calculated and determined together.

[0014] The device for restraining the excessively rapid development of the eye's refractive power of the present invention is used to cause the user to wear multi-level defocus compensation training lenses, observe the sight mark on the sight mark instrument at a set distance, and carry out trigger compensation training. The eye's refractive power is converted into a stable restrained state, the parameter γ is reduced, and the refractive power development is controlled to be lower than a predetermined threshold, thereby achieving the purpose of prevention and treatment.

[0015] The present invention is a device for restricting excessively rapid refractive development as described above. Further, the sight mark instrument comprises a light box and a sight mark display screen, and the sight mark display screen has a sight mark filled with green light.

[0016] The present invention is a device for restricting excessively rapid refractive growth as described above, and further, the sight mark display screen has a sight mark filled with red light.

[0017] The present invention is a device for restraining excessively rapid development of refraction as described above. Further, the sight mark display screen is composed of an E-shaped sight mark in a triangular area, an E sight mark in an arc area, and a digital sight mark in a circle area.

[0018] The present invention is a device for restraining excessive development of refraction as described above. Further, the size of the E sight mark in the arc area is a 5-meter standard sight mark; the size of the digital sight mark in the circular area is designed according to the 30-centimeter near vision sight mark; the size of the E sight mark in the triangular area is set to a 3-meter, 4-meter, or 5-meter standard sight mark size according to the viewing distance.

[0019] The present invention proposes a method for identifying abnormal development of eye refractive power, obtaining a curve curvature parameter γ through sigmoidal function fitting, and then judging whether the refractive power development is normal or abnormal, and then intervening through a device for restraining excessive refractive power development, and based on the visual learning thinking mechanism, triggering the defocus compensation of the human eyeball through set conditions to achieve clear focus, restrain the excessive development of eye refractive power, and limit the eye refractive power development to below a predetermined threshold, thereby reducing the sigmoidal curve curvature parameter γ.

[0020] The method for obtaining the condition of refractive development by identifying abnormal refractive development of the eye comprises the following steps:

[0021] 1) Obtain multiple sets of corneal and axial parameters within the predetermined time of the second stage, and use the sigmoid function to convert the multiple sets of corneal and axial parameters into Simulate the growth and development of eye refraction,

[0022] Where, ref.(n) is the ocular refractive function, corresponding to the ocular refractive power at age n, and the metric unit is D;

[0023] δ is the eye refraction in the first stage, corresponding to the eye refraction at the age of 0 to 3 years old, and the metric unit is D. In the present invention, δ is the eye refraction in the first stage, preferably corresponding to the eye refraction at the age of 1 year old.

[0024] γ is the curvature parameter of the curve, dimensionless. The parameter γ is used to characterize the change slope of the curve in the second stage. The larger the parameter γ is, the higher the slope of the curve is; × represents the multiplication of the two;

[0025] Max is the ocular diopter of the third stage, corresponding to the ocular diopter after the age of 16, and the metric unit is D;

[0026] n is age, in metric units, years;

[0027] The first stage is the initial stage of 0 to 3 years old, the second stage is the development stage of 4 to 15 years old, and the third stage is the stable stage of 16 to 35 years old.

[0028] 2) The dynamic development value of the refraction represented by the corneal and axial parameters within the second stage is subjected to nonlinear fitting of the sigmoidal function to obtain the curve parameter γ. If the fitting parameter γ is greater than the parameter γ of the normal developing eyeball, std , it can be judged that the refractive power development is abnormal, otherwise, it can be judged that the development is normal.

[0029] The present invention proposes a mechanism of eye refractive power change during development, clarifies a method for identifying abnormal eye refractive power development, uses a sigmoidal function to obtain a fitting parameter γ, and compares the fitting parameter γ with the parameter γ of a normally developed eyeball. std Compare, if γ>γ std , it can be determined that the refractive power is abnormal; otherwise, it is determined to be normal; this method can dynamically monitor and determine the refractive power development, and control the refractive power development to be lower than a predetermined threshold. When determining the abnormal refractive power development, if it is determined to be normal, the prevention and treatment stage is entered, and the method of the present invention is used to control the refractive power development to be lower than a predetermined threshold, and the purpose of prevention and control is achieved through regular treatment. BRIEF DESCRIPTION OF THE DRAWINGS

[0030] Figure 1 This is a schematic diagram of the optical imaging path and defocus compensation principle of the human eye;

[0031] Figure 2 A compensation path diagram for when the human eye receives a sharp imaging signal;

[0032] Figure 3 It is a compensation path for the human eye when it receives a blurred imaging signal, and also shows a path diagram for the rapid development of the human eye's refractive power due to blurred imaging;

[0033] Figure 4 The device for restricting excessive diopter development of the present invention triggers a defocus compensation mechanism to restrict the path of excessive diopter development.

[0034] Figure 5 The curve characteristics and fitting results of the development of human eye refractive power with age under different refractive parameters are shown, including the refractive power development curves under normal or abnormal corneal refractive parameters and normal or abnormal axial length parameters.

[0035] Figure 6 The invention provides curves of eye refraction and age of normal individuals, myopic individuals and myopic individuals who have been treated with the device for restricting excessive refractive power development of the present invention and experimental results of effectiveness.

[0036] Figure 7This is a flow chart of interventional treatment for a method for identifying abnormal development of eye refractive power and a device for restraining excessively rapid development of refractive power according to an embodiment of the present invention.

[0037] Figure 8 Schematic diagram of the arrangement of sight marks in an optometry device for restraining excessively rapid development of refraction.

[0038] Fig. 9 for Figure 8 A magnified schematic diagram.

[0039] In the accompanying drawings, the components represented by the reference numerals are listed as follows:

[0040] 1. E-shaped sight mark in the triangular area, 2. E-shaped sight mark in the arc area, 3. E-shaped sight mark, 4. Digital sight mark in the circle area. DETAILED DESCRIPTION

[0041] The principles and features of the present invention are described below in conjunction with the accompanying drawings. The examples given are only used to explain the present invention and are not used to limit the scope of the present invention.

[0042] Example 1

[0043] like Figure 5 As shown in the figure, the curve characteristics of the human eye refractive power under different refractive parameters as the age increases. This curve can be roughly divided into three stages according to age: the initial stage of 0 to 3 years old (the first stage), the development stage of 4 to 15 years old (the second stage), and the stable stage of 16 to 35 years old (the third stage).

[0044] The refractive power change characteristics corresponding to the first stage are universal, that is, the refractive power of most human eyes changes from +12.00DS to +3.00DS. The refractive power change characteristics corresponding to the third stage are that the rate of change is always small, and the refractive power development of the eye at this stage is basically stable. For all human eyes, the refractive power changes corresponding to the second stage are drastic and are affected to varying degrees by genetic and environmental factors.

[0045] The change in the curvature of the curve in the second stage directly determines the final refractive power of the human eye. Genetic factors determine the size of the corneal refractive power. It is generally believed that a corneal refractive power greater than 45.00D is called keratoconus; a corneal refractive power less than 41.00D is called flat cornea; and a normal human corneal refractive power is about 43.50D. Environmental factors affect the development of the axial length of the eye.

[0046] Based on the average of population statistics, ophthalmology has established a reference for normal standard axial length for each age group. Any axial length greater than this standard value is considered to be excessively long. The human eye is divided into four types according to the combination of corneal refractive power and axial length, including normal cornea + normal axial length (combination 1), normal cornea + excessively long axial length (combination 2), flat cornea + excessively long axial length (combination 3), and corneal cone + normal axial length (combination 4). Figure 5 It was found that compared with combination 1, the curvature changes of the second-stage eye refractive power curves in the other three combinations were larger, and combination 2 was the largest.

[0047] Table 1 shows the ocular refractive power development history of the above four combinations of corneal refractive power and axial length without interventional treatment, and records the test results at different stages from 1 to 30 years old.

[0048] Table 1 Refractive development history of eyes under four combinations of refractive parameters without interventional treatment

[0049]

[0050]

[0051] The method for identifying abnormal development of eye refractive power using the present invention comprises the following steps:

[0052] 1) Obtain multiple sets of corneal and axial parameters within the predetermined time of the second stage, and use the sigmoid function to convert the multiple sets of corneal and axial parameters into Simulate the growth and development of eye refraction,

[0053] Where, ref.(n) is the ocular refractive function, corresponding to the ocular refractive power at age n, and the metric unit is D;

[0054] δ is the eye refraction in the first stage, corresponding to the eye refraction at the age of 1, and the metric unit is D;

[0055] γ is the curvature parameter of the curve, dimensionless. The parameter γ is used to characterize the changing slope of the curve in the second stage. The larger the parameter γ is, the higher the slope of the curve is.

[0056] Max is the ocular diopter of the third stage, corresponding to the ocular diopter after the age of 16, and the metric unit is D;

[0057] n is age, in metric units, years;

[0058] The first stage is the initial stage of 0 to 3 years old, the second stage is the development stage of 4 to 15 years old, and the third stage is the stable stage of 16 to 35 years old.

[0059] 2) The dynamic development values ​​of the refractive power represented by the corneal and axial parameters within the predetermined time in the second stage were subjected to nonlinear fitting of the sigmoidal function to obtain the curve parameter γ, and the curve parameter γ under the four refractive parameter combinations was obtained, as shown in Table 2.

[0060] Table 2 Sigmoid function fitting results of four refractive parameter combinations

[0061]

[0062] From the fitting results, we can see that the control parameter γ of the curvature change in the second stage of the four combined curves 1 <γ 4 <γ 3 <γ 2 The fitting conclusion perfectly matches the actual development status, that is, the combination of 2 parameters γ 2 The largest, indicating that the eye axis of combination 2 is too long and the eye refractive power develops most rapidly, while the parameter γ 1 The smallest, representing combination 1 is normal eye refractive power development and normal axial length. It can be seen that the curve parameter γ of the sigmoidal function is the core parameter for evaluating abnormal eye refractive power development. Although there are views that axial length can be used as a basis for judging excessive myopic refractive power, the axial length is a static parameter, and the curve parameter γ of the sigmoidal function is a dynamic parameter that characterizes the rate of change, which is more in line with the purpose of dynamic monitoring of adolescent refractive power.

[0063] Therefore, the present invention proposes the curve parameter γ of the sigmoidal function as the basis for identifying abnormal development of eye refraction, and the dynamic development value of adolescent refraction is subjected to nonlinear fitting of the sigmoidal function to obtain the curve parameter γ. If the fitting parameter γ is greater than the parameter γ of the normal development eyeball, std , it can be judged that the refractive power is abnormal. Otherwise, it is judged to be normal.

[0064] Example 2

[0065] like Figure 6 As shown, the curves of eye refractive power and age of normal individuals, myopic individuals (control group) and myopic individuals (experimental group) who were treated with the device for restraining excessively rapid development of eye refractive power (experimental group) are also experimental results representing the effectiveness of the device for restraining excessively rapid development of eye refractive power and interventional treatment (experimental group).

[0066] The development of refractive power of myopic patients is a geometric superposition of the influence of genetic factors and environmental factors, which exist and act simultaneously. Genetic factors are controlled by innate conditions and cannot be constrained by acquired factors. Therefore, the present invention only constrains the influence of environmental factors.

[0067] Table 3 shows Figure 6Refractive parameters under different refractive conditions. Through Sigma curve parameter fitting, it was found that the control group parameter γ was -0.17753, and the Sigma curve parameter γ representing the refractive power of the normally developed eye was -0.2309. The former was significantly greater than the latter, satisfying γ>γ sad , the control group was judged to have refractive abnormalities.

[0068] Table 3 Normal individuals, myopic individuals (control group) and myopic individuals undergoing interventional treatment

[0069]

[0070]

[0071] The experimental group and the control group were sampled in parallel. First, the experimental group was tested for the accommodative amplitude and the convergent amplitude using a comprehensive optometry table, and the total amount of compensation trigger was obtained as 1 / 2 of the accommodative amplitude and the convergent amplitude, that is, 13.2 / 2 = 6.10D. The compensation trigger was discretized into n = 21 arithmetic series (tolerance d = 0.25DS), 0.25 is a customary tolerance in optometry, and the acco 1 = +1.25DS, get acco 1 Lenses, set the distance to observe the sight mark on the sight mark instrument, carry out trigger compensation training for a predetermined number of days (such as two days), causing the patient's eye focus position to move forward to the retina, forming a sharp image 1 Then apply acco to the wearer. 2 Lenses, acco 2 = +1.50DS, conduct trigger compensation training, and obtain the second-level optical signal sharpen 2 , and gradually change in this way in the inner cycle, acco 3 , acco 4 ...acco 21 , and finally the total amount of optical signal sharpening is 6.25DS (the maximum is close to 6.1DS)

[0072] A tolerance of 0.125 can also be used, and finally 6.125DS can be accumulated. This is because the sharpening of the optical signal can eliminate the negative growth of the patient's eye refraction caused by environmental factors during the annual development period, and turn it into a stable constraint state.

[0073] The geometric superposition of the constraint state and genetic factors resulted in a step-by-step decrease in eye refraction year by year. Starting from the age of 4, the experimental group carried out year-by-year triggering compensation training and achieved the effect of refractive constraint. Compared with the control group, after entering the stable period at the age of 16, the final eye refraction of the experimental group decreased by 6.00D, and the myopia was controlled at a medium to lower level (-2.25DS), which greatly reduced the occurrence of high myopia and a series of retinal complications.

[0074] The experimental group was subjected to nonlinear fitting of the sigmoidal function, and the second-stage curve change rate parameter γ=-0.1912 was obtained. Compared with the control group γ=-0.17753, the interventional treatment proposed by the present invention mainly improved the second-stage curve change rate parameter γ of the sigmoidal function. To be precise, the parameter γ was reduced, and the rate of diopter development was reduced. Therefore, the key implementation age group of the present invention corresponds to the development of diopter during the process of 4 to 15 years old in the second stage of the sigmoidal function curve.

[0075] like Figure 7 As shown, a schematic diagram of the process of the method for identifying abnormal development of eye refractive power and the device for restraining rapid development of refractive power of the present invention for triggering compensation training.

[0076] like Figure 8 , 9 As shown, the sight mark display screen in the device for restricting the rapid overdevelopment of diopter of the present invention includes an E sight mark in the triangular area, an E sight mark in the arc area, and a digital sight mark in the circle area. The size of the E sight mark in the arc area is a 5-meter standard sight mark; the size of the digital sight mark in the circular area is designed according to the 30-centimeter near vision sight mark; the size of the E sight mark in the triangular area is set to the standard sight mark size of 3 meters, 4 meters, and 5 meters according to the viewing distance.

[0077] In order to enhance the therapeutic effect of the sight mark in this area, the E-shaped sight mark in the triangular area can be filled with green or red. Filling green can make the sight mark emit green light, and filling red can make the sight mark emit red light. Green light and red light have different wavelengths. Using the principle of chromatic aberration of the human eye's refractive system, green light focusing in front of the retina can trigger myopic defocus, and red light focusing behind the retina can trigger hyperopic defocus.

[0078] Therefore, in the treatment process of myopic patients, the use of green light can enhance the treatment effect. In addition, the size of the E sight mark in the arc area is a 5-meter standard sight mark, which is convenient for patients to test and judge the quality of their vision. When the vision test results are stable, it can be indirectly inferred that the refractive power development is stable; and when the vision test results decrease, it can be indirectly inferred that the refractive power development is faster. For the size of the digital sight mark in the circular area, it is designed according to the 30-centimeter myopia sight mark, which can be used to treat the refractive power constraint of patients with delayed accommodation.

[0079] The above description is only a preferred embodiment of the present invention and is not intended to limit the present invention. Any modifications, equivalent substitutions, improvements, etc. made within the spirit and principle of the present invention should be included in the protection scope of the present invention.

Claims

1. A device for restricting the rapid development of eye refractive power, characterized in that, a multi-stage defocus compensation training lens and a visual acuity chart instrument, and the multi-stage defocus compensation training lens is obtained by the following method: Step (1), using an optometry device to test the accommodation reserve and fusional reserve of the vision to be tested, and obtaining the upper limit of the total amount of compensable triggers that can be implemented, and the upper limit of the total amount of compensable triggers that can be implemented is 1 / 3 to 1 / 2 of the accommodation reserve and fusional reserve obtained by the optometry device; Step (2), the total implementable compensation trigger amount is discretized into an n - level arithmetic progression, and a discrete function is proposed where Acco is the total implementable compensation trigger amount, and acco i is the compensation trigger amount for each level, and the common difference To obtain multi - level myopic defocus compensation training lenses.

2. The device for restricting the rapid development of refractive power according to claim 1, characterized in that, the visual acuity chart instrument includes a light box and a visual acuity chart display screen, and the visual acuity chart display screen has visual acuity charts filled with green light.

3. The device for restricting the rapid development of refractive power according to claim 2, characterized in that, the visual acuity chart display screen has visual acuity charts filled with red light.

4. The device for restricting the rapid development of refractive power according to claim 2, characterized in that, it is composed of the E visual acuity chart in the triangular area, the E visual acuity chart in the arc area, and the digital visual acuity chart in the circular area of the visual acuity chart display screen.

5. The device for restricting the rapid development of refractive power according to claim 4, characterized in that, the size of the E visual acuity chart in the arc area is the standard visual acuity chart at 5 meters; the size of the digital visual acuity chart in the circular area is designed according to the near visual acuity chart at 30 cm; the size of the E visual acuity chart in the triangular area is set to the standard visual acuity chart sizes of 3 meters, 4 meters, and 5 meters according to the viewing distance.

Images