Implants for regeneration of damaged neural tissue and use of implants

Abstract

The present application relates to medicine, and can be used in neurosurgery, traumatology, neurology, rehabilitation medicine. The present application aims to provide an implant suitable for regeneration of various damaged nerve tissues, which is used for regeneration in any period after severe damage of nerve tissues (especially spinal cord) and after just relief of life function disorder, so as to early and stably recover nerve conduction in acute period and prevent or reduce demyelination process. The implant is made of porous polytetrafluoroethylene (PTFE) and has potential to maintain enzymatic activity of neuron tissues and recover tissue structure of damaged nerve tissues; the implant at least comprises a flat cylinder with a height of 0.5 mm to 1.5 mm for being placed in a damaged nerve tissue region, and a bottom edge of the flat cylinder is in contact with an undamaged nerve tissue region; wherein the porous PTFE material has a three-dimensional structure comprising open through holes and blind holes, the blind holes are uniformly distributed on inner surfaces of the open through holes, and the open through holes and the blind holes are randomly distributed with a pore size in a range of 150-300 μm.

Description

[0001] This invention relates to medicine and can be used in neurosurgery, traumatology, neurology, and rehabilitation medicine.

[0002] A known treatment for the sequelae of traumatic spinal cord injury is to transplant intercostal nerves into the injured spinal cord [Yumashev GS, Ziablov VI, Korzh AA, et al. / / Orthopedist, Traumatol. - 1989 -1. P.71-74]. However, this approach has limited clinical effectiveness. Axons in the central nervous system (“CNS”) appear capable of regenerating within such implants, but not outside of them to restore connections with other CNS neurons; the regenerated neurons “stagnate” within the implant due to collagen scarring.

[0003] Another known method involves introducing small pieces of embryonic tissue between the central and peripheral ends of the damaged spinal cord [Russian Patent No. 2195941, published October 1, 2003]. This method cannot be considered sufficient because experimental studies have shown that when embryonic spinal cord fragments are transplanted, the superior axons grow outward to a maximum length of the implant, i.e., 1-1.5 cm. Recipient axons cannot grow to the more distal ends of the implant; they become trapped in collagen scar tissue.

[0004] Another known method for treating sequelae of spinal cord injury involves placing a container filled with Schwann's cells in a special gel between the two ends of the injured spinal cord. Schwann's cells, obtained from explants of human or rat nerves, are cultured and their numbers increase significantly. The cells are then placed in a matrix filling a semi-permeable tube, which is then placed between the severed ends of the spinal cord. In most cases, Schwann's cell transplants result in the regeneration of most CNS axons and their growth through the implant; however, the axons are unable to leave the microenvironment of the Schwann's cells to re-enter the spinal cord tissue and form new interneuronal connections [Chinese Patent No. 101653366, Publication Date: February 24, 2010].

[0005] Therefore, the aforementioned known methods cannot be used for effective restoration of spinal cord function because there is an insurmountable barrier in the axonal growth path: collagen (connective tissue) scarring. Axons cannot grow outside the implant to restore connections with other CNS neurons; the regenerated neurons are "stagnant" inside the implant.

[0006] Furthermore, the use of human tissue fragments as implants in the aforementioned methods may increase the risk of foreign body reactions and infection transmission.

[0007] The closest prior art document is [US Patent No. 7,147,647, published December 12, 2006], which describes an implant and a treatment method for spinal cord injury. The implant is described as a porous titanium tube with one or more porous layers on its inner and outer surfaces, with pore sizes of 1-3 μm and depths up to 0.5 μm. The tube diameter depends on the diameter of the nerve to be treated.

[0008] The treatment involves placing the damaged nerve inside a protective tube.

[0009] The drawback of this technical solution is that the axon growth region is only a porous layer on the inner surface of the tube, which determines that the number of restored neural connections is limited.

[0010] Furthermore, to place the damaged nerve in the described implant, it would require isolating the damaged nerve from the surrounding tissue, which is not feasible for all areas of human neural tissue. In particular, the described implant is not suitable for the spinal cord, nor for other areas immediately after the resolution of vital function disturbances at any stage of severe injury, which would otherwise help to restore nerve conduction early and steadily in the acute phase and prevent or mitigate the demyelination process.

[0011] The closest prior art document is [WO2021 / 087281, published on May 6, 2021], which describes an implant made of porous material and in the form of an irregularly shaped insert or tube, into which the severed ends of a damaged nerve can be inserted from opposite ends of the insert or tube.

[0012] In practice, due to the fragile and non-rigid structure of neural tissue, it can be difficult to place and fix the distal and proximal ends of the damaged spinal cord in direct contact with irregularly shaped inserts. Inserting the ends of damaged nerves (especially the spinal cord) into known tubes is even more challenging. To enable insertion of these ends, the tube diameter must significantly exceed the diameter of the damaged nerve, and the neural tissue must be in direct contact with the porous material of the implant covering the injury area so that the neural tissue grows within the porous material rather than forming keloids; that is, the tube size should be as close as possible to the diameter of the damaged nerve.

[0013] The invention claimed in this application aims to provide an implant suitable for the regeneration of various types of damaged nerve tissue, enabling regeneration at any stage of severe nerve tissue (particularly the spinal cord) injury, immediately after the relief of vital function disorders, to restore nerve conduction early and stably during the acute phase, prevent or mitigate the demyelination process, and minimize scar formation and adhesions in the damaged nerve tissue area. The technical advantage of achieving this objective is ensuring sustainable tissue enzymatic activity of neurons and the restoration of the tissue structure of damaged nerve tissue.

[0014] The objective is achieved by an implant made of porous polytetrafluoroethylene (PTFE) for the regeneration of damaged nerve tissue. This implant has the potential to maintain the tissue enzymatic activity of neurons and restore the tissue structure of damaged nerve tissue. The implant comprises at least a flattened cylinder with a height of 0.5 mm to 1.5 mm for insertion into the damaged nerve tissue region. The bottom edge of the flattened cylinder contacts the undamaged nerve tissue region. The porous PTFE material has a three-dimensional structure comprising open pores and blind pores. The blind pores are uniformly distributed on the inner surface of the open pores and communicate with the inner surface of the open pores. The pore diameters of the open pores and the blind pores are randomly distributed in the range of 150 to 300 μm.

[0015] The implant is preferably equipped with a split connecting sleeve, with a flat cylinder as its integral component at the center, and the implant may also have a locking member above the split connecting sleeve, which is made to cover an additional elastic split connecting sleeve of at least 270°.

[0016] The flat cylinder can be placed at an angle of 30° to 90° relative to the central axis of the connecting sleeve.

[0017] The preferred nerve tissue is the auditory nerve or optic nerve, and the most preferred is spinal cord tissue.

[0018] The objective is further achieved by using a claimed implant to maintain the tissue enzymatic activity of neurons and restore the tissue structure of damaged neural tissue.

[0019] Compared to neurons located more cranially, neurons located caudally in the damaged nerve tissue may have lower activity of enzymes such as succinate dehydrogenase and acetylcholinesterase, while lactate dehydrogenase activity may be higher in these regions through compensation.

[0020] The present invention is illustrated by way of example in the following non-limiting drawings.

[0021] Figure 1 A schematic diagram of a first embodiment of the claimed implant is shown; Figure 2 Provided according to Figure 1 A side view of the implant requiring protection; Figure 3 It shows according to Figure 1 A schematic diagram of an additional embodiment of the implant; Figure 4 A schematic diagram of another embodiment of the claimed implant is shown; Figure 5 Provided according to Figure 4 A side view of the implant requiring protection; Figure 6A schematic diagram of a preferred embodiment of the claimed implant is shown; Figure 7 A schematic diagram of the locking mechanism of the implant for which protection is claimed is shown; Figure 8 A schematic diagram of a preferred embodiment of a protected implant assembled with a locking member is shown; Figure 9 A schematic diagram of yet another embodiment of the claimed implant is shown; Figure 10 Provided according to Figure 9 Cross-sectional view of the implant requiring protection; Figures 11 to 13 A spinal cord slice image representing Example 1; Figures 14 to 17 The image represents a spinal cord slice from Example 2.

[0022] Figure 18 The activity of glucose-energy metabolism enzymes in motor neurons is represented by succinate dehydrogenase (SDH) (A) and lactate dehydrogenase (LDH) (B), expressed in units of optical density. Figure 19 This represents the activity of acetylcholinesterase (AChE) in motor neurons, expressed in units of optical density.

[0023] First embodiment of the claimed implant ( Figures 1 to 3 The material is made of porous polytetrafluoroethylene and is in the form of a flat cylinder 1 with a height (h) of 0.5 mm to 1.5 mm. The bottom dimension of the flat cylinder is not less than the diameter of the spinal cord to be operated on and does not exceed the diameter of the dura mater of the spinal cord to be operated on. The porous PTFE material has a three-dimensional structure including open pores and blind pores. The blind pores are uniformly distributed on the inner surface of the open pores and communicate with the inner surface of the open pores. The pore size is randomly distributed in the range of 150 to 300 μm.

[0024] Another embodiment of the claimed implant is made of porous polytetrafluoroethylene, in the form of a split connecting sleeve 2 and a centrally located flat cylinder 1. The split connecting sleeve 2 has two hollow cylinders 3, the size of which is not less than the diameter of the spinal cord to be operated on and does not exceed the diameter of the dura mater of the spinal cord to be operated on, integrally formed with the flat cylinder 1 such that the generatrix of the cylinder 3 coincides with the generatrix of the flat cylinder 1. Figure 4-5 Each hollow cylinder 3 has a cut along the generatrix, and half of the bottom circumference of each hollow cylinder 3 is separated from the flat cylinder 1 to form an elastic wing 4.

[0025] Another preferred embodiment of the claimed implant is made of porous polytetrafluoroethylene, in the form of a split connecting sleeve 5 and a centrally located flat cylinder 1. The connecting sleeve 5 has two hollow semi-cylinders 6, the size of which is not less than the diameter of the spinal cord to be operated on and does not exceed the diameter of the dura mater of the spinal cord to be operated on, integrally formed with the flat cylinder 1 such that the generatrix of the semi-cylinders 6 coincides with the generatrix of the flat cylinder 1. Figure 6 The implant in this embodiment is equipped with a locking member 7 (). Figure 7 The locking member is made into an additional resilient split-type connecting sleeve covering at least 270°, positioned above the split-type connecting sleeve 5. Figure 8 ).

[0026] Another embodiment of the claimed implant ( Figure 9 , 10 Made of porous polytetrafluoroethylene, it takes the form of a split connecting sleeve 2 and a flat cylinder 1 located at the center. The flat cylinder can be placed at an angle α relative to the central axis of the connecting sleeve, where α is 30° to 90°.

[0027] The claimed implant can be manufactured, for example, in the manner described in [Belarusian Patent No. 10325, published February 28, 2008]. The porous PTFE implant is made by mixing raw material particles with pore-forming agent (salt) particles, pressing the resulting mixture, washing away the salt from the resulting porous preform, and further sintering. In this case, the complex structure of the pores is created by the pulverized form of the pore-forming agent particles. The size of blind pores is determined by the size of the small-sized pore-forming agent particles, while the size of open pores is determined by the size of the large-sized pore-forming agent particles.

[0028] The implants requiring protection can be used for the surgical treatment of spinal cord injuries, as described below, for example.

[0029] Spinal cord NMR tomography was performed on patients with spinal cord injuries to determine the location and size of the spinal cord defect, the presence of cysts, and commissures. Based on this data, spinal cord implants of the target size and shape were selected from a pre-manufactured implant pool, then sterilized and stored in aseptic packaging. The porous structure of the implants could be impregnated with drugs or nerve tissue growth stimulants.

[0030] The patient was then placed in the lateral decubitus position for a routine laminectomy; the dura mater was opened. Then, a meningomyelolysis was performed under 3.5x magnification; the distal and proximal ends of the damaged spinal cord region were exposed. Existing collagen (connective tissue) scar tissue was removed.

[0031] The prepared flat cylinder 1 of the implant is inserted in such a way that it fills the space between the two ends of the patient's damaged spinal cord region.

[0032] In practice, due to the fragile and non-rigid structure of neural tissue, it may be difficult to place and fix the distal and proximal ends of the damaged spinal cord in direct contact with the bottom of the flat cylinder 1.

[0033] To overcome this difficulty, a system based on Figure 3 Implants, wherein the first embodiment ( Figure 1-2 The implant is provided with a fixation element 8 for attaching it to the dura mater to prevent displacement of the flat cylinder 1 that requires protection.

[0034] To overcome this difficulty, implants were designed in other embodiments. When used according to Figure 4 When implanting the device, after preparing the wound, bend the elastic wing 4 of the hollow cylinder 3 upwards. Figure 5 The lower part of the tube is placed below the undamaged spinal cord area, and the spinal cord is placed inside the hollow cylinder 3 by rotation, so that the flat cylinder 1 fills the space between the two ends of the damaged spinal cord segment. The elastic wing 4 is released, and both spinal cord segments are fixed inside the connecting sleeve 2.

[0035] When using according to Figure 6 When implanting the device, after preparing the wound, the semi-cylinder 6 of the connecting sleeve 5 is placed below the spinal cord segment, and the undamaged spinal cord segment is placed inside the semi-cylinder 6 by rotation, so that the flat cylinder 1 fills the space between the two ends of the damaged spinal cord segment. Then, the locking member 7 ( Figure 7 The edges of the locking member 7 are separated, and the locking member 7 is installed on the connecting sleeve 5. Due to the elasticity of the material, the locking member 7 wraps around the connecting sleeve 5 containing the internal spinal cord. Figure 9 ) and fix it.

[0036] The surgical wound was sutured tightly layer by layer.

[0037] Any implant designed for which protection is sought can be used for the surgical treatment of other major nerve injuries, such as the auditory or optic nerve.

[0038] Animal studies have been conducted, as described in the following examples, to verify the operability and effectiveness of the claimed invention.

[0039] Example 1

[0040] The experiment involved spinal cord injury in the T9-10 region. A complete transection was performed using a scalpel, and then a porous PTFE implant was placed in the injury area (first embodiment of the implant claimed in this invention). Figures 1 to 3 The results showed that the experimental animals' motor activity had fully recovered.

[0041] During examination of the laboratory animals, no skin damage was detected, the integrity of the visible mucous membranes remained intact, and no gross signs of inflammation were observed. Minipigs roamed freely in their cages. Feeding and watering were provided according to the animals' age and needs. No obvious signs of spinal cord injury were detected.

[0042] The degree of neurological deficit was assessed using the Garcia Scale (Garcia, JH Early reperfusion as a rationale from therapy in ischemic stroke. / JH Garcia / / Rev. Neurol. 1995. - Vol. 23, No. 123. - pp. 1067-1110). In the animals studied, almost no neurological deficit was found (17 out of 18 points were scored).

[0043]

[0044] Biological samples were obtained from an 80 kg male miniature pig six months after complete spinal cord transection and PTFE implant placement. Sampling was conducted in accordance with bioethical principles.

[0045] Histological sections of the damaged and implanted areas ( Figure 11 A - Contact area between granulation tissue (P) and spinal cord (CM); BD - Implant. Staining: Hematoxylin-eosin (A, B), Nissl stain (C, D). Magnification: ×40 (A), ×100 (B), ×400 (C, D), showing a mature gliomesodermal scar, mainly composed of connective tissue, interspersed with lymphocytes, and with identifiable myelinated nerve fibers. Figure 11 A). Connective tissue growth was detected in the implant pores. Figure 11 B), and microvascularization ( Figure 11 Nerve cells and microglia can be directly observed on the implant surface. Figure 11 D).

[0046] On the spinal cord cross section on the cranial side of the injury area ( Figure 12 Staining: Hematoxylin-eosin (A, B, D), Nissl stain (C). Magnification: ×40 (A), ×100 (B, D), ×400 (C), the characteristics of gray and white matter are clearly visible. Figure 12A, B). The gray matter has a distinctive symmetrical, butterfly-wing pattern, located in the center of the slice. The two stalks of the gray matter are connected by bridges composed of numerous unmyelinated fibers running within the gray matter, especially on the dorsal side of the central canal. The gray matter consists of nerve cell bodies, nerve fibers, and glial cells. The anterior horn contains a large number of morphologically intact motor neurons (A, B). Figure 12 C). The posterior horn contains clusters of nerve cells that are diffusely distributed and receive sensory impulses from nerve cells in the spinal ganglia. The posterior horn also contains motor nerve cells that transmit sensory impulses from the spinal ganglia to the anterior horn, as well as internal nerve cells from adjacent segments.

[0047] White matter, located in the periphery of the spinal cord, is composed of longitudinally running, primarily myelinated nerve fibers, forming the posterior (ascending), anterior (descending), and lateral (ascending and descending) columns, as well as glial components. On the lesion side, microcysts were observed in numerous myelinated axons. Figure 12 D), and an increase in diffusely distributed glial cells was also found in the region.

[0048] At the tail end of the damaged area ( Figure 13 Staining: Hematoxylin-eosin (A, B, D), Nissl stain (C). Magnification: ×40 (A), ×100 (B, D), ×400 (C). Similar images were observed: spinal cord gray and white matter were clearly visible. Figure 13 A, B). The gray matter, exhibiting a symmetrical butterfly-wing pattern, is located in the center of the slice and consists of nerve cell bodies, nerve fibers, and glial tissue. Unaltered motor neurons were detected in the anterior horn. Figure 13 C). The posterior horn contains small nerve cells.

[0049] White matter, composed of myelinated nerve fibers and glial components, is located in the periphery of the spinal cord. Microcysts were observed in the myelinated axons on the injured side. Figure 13 D), and an increase in diffusely distributed glial cells was also found in the region. The number of microcysts and glial cells was slightly greater in the caudal region than in the region more cranial.

[0050] Significant preservation of spinal cord tissue structures was observed in the cranial and caudal regions of the injury. Connective tissue and glial components were found growing within the implant pores.

[0051] Therefore, when the implant was applied to spinal cord injury in pigs, significant restoration of the spinal cord structure in the injured area was observed, and glial-mesoderm scarring was formed.

[0052] Based on morphological measurements of the injured area, it was found that the spinal cord area was significantly reduced compared to sections closer to the cranial and caudal sides. Figure 1 5). Compared to white matter, the area of ​​gray matter in the sections was also significantly reduced. The ratio of gray matter to white matter was 0.30, while the ratios for the more cranial and more caudal regions were 0.42 and 0.35, respectively.

[0053] Example 2

[0054] The experiment involved spinal cord injury in the T9-10 region and was performed sequentially on two male miniature pigs. A complete transection was made using a scalpel, and a porous PTFE implant was then placed in the injury area (another embodiment of the implant claimed is available). Figure 4 , Figure 5 ) and preferred embodiments (according to Figures 6 to 8 )).

[0055] Dynamic observation showed that motor activity had fully recovered. Weight gain was dynamic and normal.

[0056] The degree of neurological deficit was assessed using the Garcia Scale (Garcia, JH Early reperfusion as a rationale from therapy in ischemic stroke. / JH Garcia / / Rev. Neurol. 1995. - Vol. 23, No. 123. - pp. 1067-1110). In the animals studied, almost no neurological deficit was found (18 out of 18 points were scored).

[0057]

[0058] Following dissection and sampling, the spinal cord remained intact despite the complete transection. No grossly significant deformities or pathological changes were found. No obvious signs of inflammatory process were recorded.

[0059] By referring to the microscopic images, the process of the spinal cord structure recovering its integrity was observed, accompanied by the activation of the body's defense system.

[0060] Histological sections of the damaged and implanted areas ( Figure 14 A - Contact area between the gelatinous-mesoderm scar and the implant; B - Granulation tissue growing within the implant pores. Staining: Nissl stain (A), hematoxylin-eosin (B). Magnification: ×400 (A), ×100 (B) shows a mature gelatinous-mesoderm scar, primarily composed of connective tissue. Figure 14 A). Significant connective tissue growth was detected in the implant pores. Figure 14 B), and form blood vessels of different sizes.

[0061] In a cross-section of the spinal cord on the cranial side of the injury area, the characteristics of gray and white matter are clearly visible. The gray matter has a distinctive symmetrical butterfly-wing pattern, located in the center of the slice. The gray matter is composed of neuronal cell bodies, nerve fibers, and glial tissue.

[0062] The anterior horn contains a large number of motor neurons. Figure 15 A). In a large number of unchanged motor neurons ( Figure 15 B), identifying nerve cells showing signs of chromatin dissolution ( Figure 15 C). The motor neurons in the anterior horn of the skull in the lesion area were smaller in size—averaging 471.82 μm. 2 .

[0063] The posterior horn contains clusters of nerve cells that are diffusely distributed and receive sensory impulses from nerve cells in the spinal ganglia. The posterior horn also contains motor nerve cells that transmit sensory impulses from the spinal ganglia to the anterior horn, as well as internal nerve cells from adjacent segments.

[0064] Caudal to the lesion area, the spinal cord structures were remarkably preserved: gray and white matter were clearly visible. The gray matter exhibited a distinctive symmetrical butterfly-wing pattern, located in the center of the slice, and consisted of neuronal cell bodies, nerve fibers, and glial tissue. Slices with a cross-sectional area larger than the lesion area and closer to the cranial side were found.

[0065] Unchanged motor neurons were detected in the anterior horn. Figure 16 Staining: Hematoxylin-eosin (A), Nissl stain (B). Magnification: ×100 (A), ×400 (B). Small neurons are present in the posterior horn. The size of the motor neurons varies slightly from the lesion area, averaging 751.63 μm. 2 Individual nerve cells with destructive changes were also identified. An increased number of diffusely distributed glial cells was also found.

[0066] Histochemical studies were conducted to determine the activities of sugar and energy metabolism enzymes (succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH)). Figure 17 Succinate dehydrogenase (A, B) and lactate dehydrogenase (C, D) in anterior horn neurons of the porcine spinal cord, located cranially (A, C) and caudally (B, D) in the lesion area. Method: Lloyd. Magnification: ×400; Figure 18 - The activity of sugar and energy metabolism enzymes in motor neurons: SDH(A) and LDH(B), expressed in units of optical density. -Statistically significant differences (p<0.05) were observed, as well as the activity of acetylcholinesterase (AChE), a marker of cholinergic neurons. Neuronal activity was studied in regions located in the cranial and caudal directions of the injury and implantation sites. Figure 19 - Acetylcholinesterase (AChE) activity in motor neurons, expressed in units of optical density. - The difference was statistically significant (p<0.05).

[0067] Following injury and implantation, compared to sections closer to the cranial side, the caudal region at the injury center showed reduced SDH activity in the anterior horn motor neurons of the spinal cord. Figure 17 A, B). Simultaneously, a compensatory increase in LDH activity was observed ( Figure 17 C, D) indicate the remodeling of the glycolytic pathway in neurons, which converts energy production to glucose oxidation.

[0068] Compared to the cranial region at the center of injury, AChE activity was significantly lower in the caudal region of the spinal cord.

[0069] Following implant placement in areas of complete spinal cord transection, miniature pig spinal cords showed significant restoration of tissue structure, with the formation of glial-mesoderm scars in the lesion area. Connective tissue and glial components were observed growing within the implant pores.

[0070] In the caudal region of the injury, although the tissue enzymatic activity of motor neurons was impaired compared to sections closer to the cranial side, significant preservation of spinal cord tissue structures was observed. In the cranial region of the injury, chromatin dissolution of some anterior horn neurons was observed in the gray matter, and microvesicles were found in the white matter. However, the tissue enzymatic activity of motor neurons remained high. This demonstrates the effectiveness of the unique method employed and the specific implant material, as such experimental results had not been previously reported.

[0071] No allergies, tumors or other pathologies were found.

[0072] Following potentially fatal spinal cord injury and implant placement, no significant pathological changes were detected in the morphological images of the porcine cerebral cortex and cerebellum. Data showed no significant changes due to transneuronal degeneration following peripheral axonal transection.

[0073] Six months later, the implantation of artificial materials allowed for the preservation of motor function, which was fully achieved under animal facility conditions. The dynamic recovery of the spinal cord after complete transection demonstrated the activation of the body's defense systems.

[0074] The characteristics of neural tissue remodeling suggest that six months is insufficient for complete recovery after a complete spinal cord transection in miniature pigs. However, no experimental studies have yet been able to achieve the results presented in this study.

[0075] The findings lead us to believe that the implantable material studied is safe and promising for use as a medical device.

[0076] The application of the claimed invention is permitted: 1. Implantation at any stage of severe spinal cord injury, immediately after the resolution of vital function disturbances, helps to restore nerve conduction early and steadily during the acute phase, preventing or mitigating the demyelination process. The restoration of spinal cord function eliminates the harmful consequences of prolonged inactivity, which is of great psychological, emotional, and socioeconomic importance to patients and their families.

[0077] 2. To mitigate the impact of disability caused by severe spinal cord injury.

[0078] 3. Improve the quality of life of patients with severe spinal cord injury.

[0079] Therefore, the present invention achieves large-volume regeneration of damaged nerve tissue, which in turn determines that the claimed implant is suitable for treating various types of nerve tissue injuries, at any time after severe nerve tissue injury (especially spinal cord injury), and is suitable for early and stable restoration of nerve conduction in the acute phase after the relief of vital function disorders, preventing or mitigating the demyelination process, and minimizing scar formation and adhesions in the area of ​​nerve tissue injury. Claims (as amended under Article 19 of the Treaty) 1. A porous material implant for regenerating damaged nerve tissue, the implant being made of porous polytetrafluoroethylene and in the form of a split connecting sleeve, characterized in that the central portion of the split connecting sleeve has a flat cylinder as an integral part thereof for placement in the region of damaged nerve tissue, the bottom edge of the flat cylinder contacting the region of undamaged nerve tissue, wherein the diameter of the split connecting sleeve is not less than the diameter of the tissue to be operated on, and the height of the flat cylinder is 0.5 mm to 1.5 mm. 2. The implant as claimed in claim 1, wherein the flat cylinder is positioned at an angle of 30° to 90° relative to the central axis of the connecting sleeve. 3. The implant as claimed in claim 1, characterized in that the split connecting sleeve is manufactured in the form of two hollow cylinders, the generatrix of the cylinders coincides with the generatrix of the flat cylinder located at the center of the connecting sleeve, each hollow cylinder has a cut along the generatrix, and half of the bottom circumference of each hollow cylinder is separated from the flat cylinder to form an elastic wing. 4. The implant as claimed in claim 1, wherein the split connecting sleeve is in the form of two hollow semi-cylinders, and the generatrix of the semi-cylinders coincides with the generatrix of the flat cylinder located at the center of the connecting sleeve. 5. The implant of claim 4, wherein the implant is provided with a locking member above the split connecting sleeve, the locking member being configured to cover an additional resilient split connecting sleeve of at least 270°. 6. The implant as claimed in claim 1, wherein the neural tissue is spinal cord tissue, auditory nerve, or optic nerve. 7. The implant of claim 1 is used to ensure the sustainable tissue enzymatic activity of neurons and to restore the tissue structure of damaged neural tissue. 8. The application as described in claim 7, characterized in that, compared with neurons located more cranially, neurons located caudally to the site of the damaged nerve tissue exhibit lower enzyme activities representing succinate dehydrogenase and acetylcholinesterase, while lactate dehydrogenase activity is compensatorily increased in these regions.

Claims

1. A porous material implant for regenerating damaged nerve tissue, characterized in that, The implant is made of porous polytetrafluoroethylene (PTFE) and has the ability to maintain the tissue enzymatic activity of neurons and restore the tissue structure of damaged nerve tissue. The implant includes at least a flat cylinder with a height of 0.5 mm to 1.5 mm for placement in the damaged nerve tissue region. The bottom edge of the flat cylinder contacts the undamaged nerve tissue region. The porous PTFE has a three-dimensional structure including open pores and blind pores. The blind pores are uniformly distributed on the inner surface of the open pores and connected to the inner surface of the open pores. The pore diameters of the open pores and the blind pores are randomly distributed in the range of 150 μm to 300 μm.

2. The implant as claimed in claim 1, characterized in that, The implant is equipped with a split connecting sleeve, with the flat cylinder as an integral part located at the center.

3. The implant as described in claim 2, characterized in that, The flat cylinder is positioned at an angle of 30° to 90° relative to the central axis of the connecting sleeve.

4. The implant as described in claim 2, characterized in that, The implant has a locking member above the split connector sleeve, the locking member being made to cover an additional elastic split connector sleeve of at least 270°.

5. The implant as claimed in claim 1, characterized in that, The neural tissue is spinal cord tissue, auditory nerve, or optic nerve.

6. The implant of claim 1 is used to ensure the sustainable tissue enzymatic activity of neurons and to restore the tissue structure of damaged neural tissue.

7. The application as described in claim 6, characterized in that, Compared to neurons located more cranially, neurons located caudally to the site of damage to the nerve tissue exhibit lower enzyme activities, representing succinate dehydrogenase and acetylcholinesterase, while lactate dehydrogenase activity is compensatorily increased in these regions.

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