Electromagnetic modulation method for improving the formation of glial scar layers around implanted electrodes

Abstract

This invention discloses an electromagnetic modulation method for improving the formation of glial scars around implanted electrodes. The method selects at least two electrode channels in an implanted brain-computer interface electrode array as stimulation channels and connects them to an external stimulation driving circuit. By outputting a charge-balanced low-frequency pulse stimulation current, it implements staged modulation of the local tissue around the electrodes at different stages after implantation. Simultaneously, it continuously monitors the electrode-tissue interface impedance and / or the signal-to-noise ratio of neural signals, and performs closed-loop switching between different stimulation parameters based on the monitoring results. This method is drug-free and can utilize bipolar or tripolar current-guided stimulation configurations to regulate the spatial distribution of the local electric field. Combined with the accompanying near-field electromagnetic effect, it provides electromagnetic parameter-dependent long-term modulation of the inflammatory response of microglia and astrocytes at the implantation interface, thereby improving the long-term electrical stability of the implantation interface and extending the lifespan of the implanted electrodes.

Description

Technical Field

[0001] This invention relates to an application technology of implantable electrodes, belonging to the fields of biomedical engineering and brain-computer interface technology, and particularly to an electromagnetic modulation method for improving the formation of glial scar layer around implantable electrodes. Background Technology

[0002] Currently, implantable neural electrodes are widely used in fields such as brain-computer interfaces (BCI) and deep brain stimulation (DBS). However, electrode implantation can trigger local tissue damage and immune inflammatory responses, manifested as: microglia activation and migration, astrocyte proliferation and formation of glial scar layers; simultaneously, the electrode-tissue interface impedance gradually increases, the quality of neural signal recording decreases, the stimulation threshold increases, and electrode function deteriorates or even fails with long-term use.

[0003] Existing technologies mainly alleviate the problem of gel scars through the following methods: 1. Improving electrode materials (flexible electrodes, conductive polymers, coatings); 2. Drug sustained release (anti-inflammatory drugs); 3. Optimizing surgical paths and implantation methods.

[0004] However, the above methods have the following shortcomings: material modification is difficult to adapt to individual differences, control is challenging, and glial scars that can still affect signal quality are generated; the duration of drug action is limited, and the safety of long-term use is restricted; optimization of surgical pathways and implantation methods cannot dynamically regulate the glial response in the long term after implantation. Therefore, there is an urgent need to develop a controllable, non-pharmacological, and long-term safe technology to improve the formation of glial scar layers around implanted electrodes, which has significant scientific and application value.

[0005] Chinese invention patent application CN117257317A, published on December 22, 2023, discloses a flexible brain-computer interface microdevice for closed-loop regulation of major brain diseases and its fabrication method. The flexible microdevice includes a base layer, an electrical shielding layer, an intermediate layer, a conductive layer, an insulating layer, and a biomaterial protective layer. The flexible base layer, intermediate layer, and insulating layer are flexible materials with low Young's modulus, which can be implanted at the front end in a needle-like shape with a trapezoidal hollow area. The conductive layer includes a detection site, a regulation site, an electrical shielding ring, wires, and pads. The shielding layer is a capsule-like structure and a ring-like structure placed below the orthographic projection of the regulation site and connected to the ground. The biomaterial protective layer is a biocompatible hydrogel material that encapsulates drugs and is attached to the surface of the device.

[0006] In application, this design forms a highly biocompatible hydrogel layer containing anti-inflammatory drugs outside the flexible insulating layer and flexible base layer. This not only inhibits protein adhesion but also reduces the immune rejection response generated in the brain after probe implantation, thereby reducing the occurrence of glial scars. However, it is essentially a drug sustained-release method and still has the drawbacks of limited drug action time and limited safety with long-term use.

[0007] The information disclosed in this background section is intended only to enhance understanding of the overall background of this application and should not be construed as an admission or in any way implying that the information constitutes prior art known to those skilled in the art. Summary of the Invention

[0008] The purpose of this invention is to overcome the defects and problems of existing technologies that cannot simultaneously possess controllable, non-drug, and long-term safe effects, and to provide an electromagnetic modulation method that can simultaneously possess controllable, non-drug, and long-term safe effects to improve the formation of gel scar layer around implanted electrodes.

[0009] To achieve the above objectives, the technical solution of the present invention is: an electromagnetic modulation method for improving the formation of glial scar layer around implanted electrodes, the electromagnetic modulation method comprising the following steps:

[0010] Step 1: First, select several electrode channels on the implantable brain-computer interface electrode array as stimulation channels, and then connect the selected electrode channels to the external stimulation driving circuit.

[0011] Step 2: Apply early low-frequency pulsed stimulation current to the electrode channel through the stimulation driving circuit to inhibit the release of pro-inflammatory factors by microglia until the acute inflammation at the implantation interface subsides.

[0012] The third step is to first adjust the early low-frequency pulse stimulation current to the mid-term low-frequency pulse stimulation current, which promotes the transformation of astrocytes into A2-type astrocytes and regulates the calcium signal in astrocytes, thereby forming a glial scar layer around the electrode. Then, when the impedance curve of the implantation interface completely enters the plateau phase and the signal-to-noise ratio of the nerve signal stops decaying, the glial scar layer is formed.

[0013] After the third step is completed, there is a fourth step;

[0014] Step 4: After the glial scar layer has been formed, the mid-term low-frequency pulse stimulation current is adjusted to the late-term low-frequency pulse stimulation current to control the release of anti-inflammatory cytokines by microglia and astrocytes and reduce the level of inflammatory mediators.

[0015] In the fourth step, the current parameters of the late-stage low-frequency pulse stimulation current include: current amplitude of 3.7-7.5μA, frequency of 15-40Hz, pulse width of 40-4000μs, and timing of 1-5 times per day, with each application lasting 1-5 hours.

[0016] In the second step, the resolution of acute inflammation at the implantation interface means that when the continuously monitored interface impedance value crosses the peak value and begins to fall back, and the daily average impedance change rate drops to below 5%-50% for 3 to 5 consecutive days, the resolution of acute inflammation at the interface can be determined.

[0017] In the second step, when the acute inflammation at the implantation interface subsides, the level of inflammatory markers is reduced by 20%–80% compared to the control group with the same implantation but without stimulation.

[0018] In the second step, the current parameters of the early low-frequency pulse stimulation include: current amplitude of 1.5-3.7μA, frequency of 40-60Hz, and timing of once a day, with each application lasting 15min-3h.

[0019] In the third step, promoting the transformation of astrocytes into A2-type astrocytes means that: a mid-term low-frequency pulsed stimulation current acts on the adenosine receptor-cyclic adenosine monophosphate signaling axis, which increases the concentration of cyclic adenosine monophosphate in astrocytes by upregulating the expression levels of A2A and A3 type adenosine receptors, thereby inhibiting the continuous activation of pro-inflammatory signaling pathways and ultimately promoting the transformation of astrocytes into A2-type astrocytes.

[0020] In the third step, the regulation of calcium signaling in astrocytes refers to the regulation of the dynamic changes of calcium ions in astrocytes by the electromagnetic field generated by the mid-term low-frequency pulse stimulation current, which affects the release of voltage-gated calcium channels and intracellular calcium stores.

[0021] In the third step, the current parameters of the mid-term low-frequency pulse stimulation include: current amplitude of 0.01-1.5μA, frequency of 60-75Hz, pulse width of 100-2000μs, and timing of 1-5 times per day, with each application lasting 1-24 hours.

[0022] In the first step, the electrode channel includes an inner electrode point, an outer electrode point, and a conductive trace between them, and the stimulation driving circuit is a constant current stimulation driving circuit.

[0023] The internal electrode point is in contact with the nerve tissue in the brain, and the external electrode point is connected to the constant current stimulation driving circuit through an external wire.

[0024] Compared with the prior art, the beneficial effects of the present invention are as follows:

[0025] 1. In the electromagnetic modulation method for improving the formation of glial scar layer around implanted electrodes, the present invention first selects several electrode channels on the implanted brain-computer interface electrode array as stimulation channels, then connects the selected electrode channels to an external stimulation driving circuit, and then applies an early low-frequency pulse stimulation current to inhibit the release of pro-inflammatory factors from microglia until the acute inflammation at the implantation interface subsides. Then, a mid-term low-frequency pulse stimulation current is applied to promote the transformation of astrocytes into A2-type astrocytes and regulate the calcium signal within astrocytes, thereby forming a glial scar layer around the electrodes. Subsequently, when the impedance curve at the implantation interface completely enters the plateau phase and the signal-to-noise ratio of the neural signal stops decaying, the glial scar layer is complete. The advantages of this design include:

[0026] Firstly, this invention does not completely inhibit glial scar formation. Instead, it uses the electrode channel as a stimulation channel and continuously modulates the electromagnetic parameters at different stages to change the electromagnetic field around the implanted electrode. This allows for long-term electromagnetic parameter-dependent regulation of the pro-inflammatory-repair phenotype transformation of microglia and astrocytes at the implantation interface, enabling glial scars to quickly complete tissue closure in the early and middle stages. This forms a thin and stable glial encapsulation interface around the implanted electrode as early as possible, preventing prolonged inflammation, reducing repeated inflammation activation, maintaining long-term electrical stability of the electrode-tissue interface, and extending the lifespan of the implanted electrode.

[0027] Secondly, this invention promotes the formation of glial scar layer by electromagnetically regulating microglia and astrocytes. The electromagnetic regulation is directly controlled by the external stimulation driving circuit, which has strong controllability.

[0028] Thirdly, this invention uses low-frequency pulsed stimulation currents with different parameters at different stages to perform different electromagnetic regulation on microglia and astrocytes, which can regulate glial responses in a long-term and dynamic manner. It is not only highly safe and reproducible, but also overcomes the defects of drug release in the prior art.

[0029] Fourthly, this invention first uses an early low-frequency pulsed stimulation current to gently modulate the tissue around the electrode to inhibit the overactivation of microglia and reduce the release of pro-inflammatory factors, thereby weakening the acute inflammatory response and reducing the microenvironmental signals that induce the generation of A1-type astrocytes from the source, creating an immune-permitted environment for subsequent repair responses. Then, through a mid-term low-frequency pulsed stimulation current, it simultaneously promotes the transformation of astrocytes into A2-type astrocytes and regulates calcium signals within astrocytes, thereby rapidly forming a glial scar layer around the electrode. This overall sequential design is consistent with the natural process of the human body's physiological rejection of foreign substances. The achievement of the first goal can promote the achievement of the second goal and is more conducive to the controllable formation of the glial scar layer.

[0030] Therefore, this invention can not only improve the formation of colloid scar layer through electromagnetic regulation, but also has the advantages of being controllable, non-drug-based, and having a long-term safe effect.

[0031] 2. In the electromagnetic modulation method for improving the formation of glial scar layer around implanted electrodes according to the present invention, after the glial scar layer has been formed, the mid-term low-frequency pulse stimulation current is preferably adjusted to the late-term low-frequency pulse stimulation current to control the release of anti-inflammatory cytokines by microglia and astrocytes and reduce the level of inflammatory mediators. This design can maintain a stable and low-intensity stimulation environment, continuously regulate local cell activity, construct a relatively low-inflammatory level immune tolerance microenvironment, maintain a stable thickness of glial scar layer and avoid abnormal proliferation, effectively limit the continuous thickening of glial scar in the late stage, forming a thin and stable interface structure, and further improve the long-term stability of implanted electrode-tissue interface impedance, nerve signal recording and stimulation, significantly extending the long-term service life of implanted electrodes. Therefore, the present invention can limit the continuous thickening of glial scar layer and improve the long-term impedance of implanted electrode-tissue interface. Attached Figure Description

[0032] Figure 1 This is a flowchart of the method of the present invention.

[0033] Figure 2 This is a diagram illustrating the mechanism of the present invention.

[0034] Figure 3 This is a schematic diagram of the system structure in Embodiment 5 of the present invention.

[0035] Figure 4 This is a schematic diagram of the connection when the stimulation channel in this invention is a bipolar current-guided stimulation configuration.

[0036] Figure 5 This is a schematic diagram of the connection when the stimulation channel in this invention is a tripolar current-guided stimulation configuration. Detailed Implementation

[0037] The present invention will be further described in detail below with reference to the accompanying drawings and specific embodiments.

[0038] See Figure 1 — Figure 5 An electromagnetic modulation method for improving the formation of glial scars around implanted electrodes, the electromagnetic modulation method comprising the following steps:

[0039] Step 1: First, select several electrode channels on the implantable brain-computer interface electrode array as stimulation channels, and then connect the selected electrode channels to the external stimulation driving circuit.

[0040] Step 2: Apply early low-frequency pulsed stimulation current to the electrode channel through the stimulation driving circuit to inhibit the release of pro-inflammatory factors by microglia until the acute inflammation at the implantation interface subsides.

[0041] The third step is to first adjust the early low-frequency pulse stimulation current to the mid-term low-frequency pulse stimulation current, which promotes the transformation of astrocytes into A2-type astrocytes and regulates the calcium signal in astrocytes, thereby forming a glial scar layer around the electrode. Then, when the impedance curve of the implantation interface completely enters the plateau phase and the signal-to-noise ratio of the nerve signal stops decaying, the glial scar layer is formed.

[0042] After the third step is completed, there is a fourth step;

[0043] Step 4: After the glial scar layer has been formed, the mid-term low-frequency pulse stimulation current is adjusted to the late-term low-frequency pulse stimulation current to control the release of anti-inflammatory cytokines by microglia and astrocytes and reduce the level of inflammatory mediators (such as prostaglandin E2).

[0044] In the fourth step, the current parameters of the late-stage low-frequency pulse stimulation current include: current amplitude of 3.7-7.5μA, frequency of 15-40Hz, pulse width of 40-4000μs, and timing of 1-5 times per day, with each application lasting 1-5 hours.

[0045] In the second step, the resolution of acute inflammation at the implantation interface means that when the continuously monitored interface impedance value crosses the peak value and begins to fall back, and the daily average impedance change rate drops to below 5%-50% for 3 to 5 consecutive days, the resolution of acute inflammation at the interface can be determined.

[0046] In the second step, when the acute inflammation at the implantation interface subsides, the level of inflammatory markers (including pro-inflammatory factors) is reduced by 20%–80% compared to the control group that was implanted but not stimulated.

[0047] In the second step, the current parameters of the early low-frequency pulse stimulation include: current amplitude of 1.5-3.7μA, frequency of 40-60Hz, and timing of once a day, with each application lasting 15min-3h.

[0048] In the third step, promoting the transformation of astrocytes into A2-type astrocytes means that: a mid-term low-frequency pulsed stimulation current acts on the adenosine receptor-cyclic adenosine monophosphate signaling axis, which increases the concentration of cyclic adenosine monophosphate in astrocytes by upregulating the expression levels of A2A and A3 type adenosine receptors, thereby inhibiting the continuous activation of pro-inflammatory signaling pathways and ultimately promoting the transformation of astrocytes into A2-type astrocytes.

[0049] In the third step, the regulation of calcium signaling in astrocytes refers to the regulation of the dynamic changes of calcium ions in astrocytes by the electromagnetic field generated by the mid-term low-frequency pulse stimulation current, which affects the release of voltage-gated calcium channels and intracellular calcium stores.

[0050] In the third step, the current parameters of the mid-term low-frequency pulse stimulation include: current amplitude of 0.01-1.5μA, frequency of 60-75Hz, pulse width of 100-2000μs, and timing of 1-5 times per day, with each application lasting 1-24 hours.

[0051] In the first step, the electrode channel includes an inner electrode point, an outer electrode point, and a conductive trace between them, and the stimulation driving circuit is a constant current stimulation driving circuit.

[0052] The internal electrode point is in contact with the nerve tissue in the brain, and the external electrode point is connected to the constant current stimulation driving circuit through an external wire.

[0053] The supplementary technical features of this invention are as follows:

[0054] In this invention, the implantation interface refers to the implantable electrode-tissue interface.

[0055] The connection between glial scar layers and inflammation involved in this invention is as follows: the presence of inflammation leads to the continuous thickening of glial scar layers. Both severe and persistent inflammation can cause excessive proliferation and thickening of glial scar layers, but a weak inflammatory response (such as an immunosuppressed state) will make it difficult for glial scars to form quickly. Therefore, this invention uses electromagnetic modulation to moderately control the degree of inflammation, which helps glial scars to form faster, become thinner, and have a more stable structure.

[0056] The glial scar layer involved in this invention is related to the electrode-tissue interface impedance. Specifically, the formation of the glial scar layer causes changes in the electrode-tissue interface impedance, which in turn affects the quality of neural signal recording. Furthermore, the interface impedance may also be affected by the electrode surface condition, the tissue fluid environment, and other interfacial factors. Therefore, interface impedance can serve as one of the indicators characterizing changes in the implantation interface state, and can be used to assist in judging the formation process of the glial scar layer and the degree of interface stability.

[0057] Example 1:

[0058] See Figure 1 — Figure 3 An electromagnetic modulation method for improving the formation of glial scars around implanted electrodes includes the following steps:

[0059] Step 1: First, select several electrode channels on the implantable brain-computer interface electrode array as stimulation channels, and then connect the selected electrode channels to the external stimulation driving circuit.

[0060] Step 2: Apply an early low-frequency pulsed stimulation current to the electrode channel via a stimulation driving circuit (preferred parameters for the early low-frequency pulsed stimulation include: current amplitude of 1.5–3.7 μA, frequency of 40–60 Hz, once daily, for 15 min–3 h each time) to inhibit the release of pro-inflammatory factors from microglia until acute inflammation at the implantation interface subsides; among which, preferred pro-inflammatory factors include interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and complement-related factors;

[0061] Step 3: First, adjust the early low-frequency pulse stimulation current to the mid-term low-frequency pulse stimulation current (preferred parameters for mid-term low-frequency pulse stimulation include: current amplitude of 0.01-1.5μA, frequency of 60-75Hz, pulse width of 100-2000μs, and timing of 1-5 times per day, with each application lasting 1-24 hours). This promotes the transformation of astrocytes into A2-type astrocytes and regulates the calcium signal within astrocytes (the operation aims to reduce the pathological hypertrophy response of astrocytes and optimize their migration and arrangement). This forms a glial scar layer around the electrode. Subsequently, when the impedance curve at the implantation interface completely enters the plateau phase (preferably, entering the plateau phase means no significant upward trend for 5-10 consecutive days) and the signal-to-noise ratio of the nerve signal stops decaying, the glial scar layer is complete.

[0062] Example 2:

[0063] The basic content is the same as in Example 1, except that:

[0064] After the third step is completed, there is a fourth step;

[0065] Step 4: After the formation of the glial scar layer, the mid-term low-frequency pulse stimulation current is adjusted to the late-term low-frequency pulse stimulation current (preferred parameters of the late-term low-frequency pulse stimulation current include: current amplitude of 3.7-7.5μA, frequency of 15-40Hz, pulse width of 40-4000μs, and timing of 1-5 times per day, with each application lasting 1-5 hours) to control the release of anti-inflammatory cytokines (preferably IL-10 or TGF-β) from microglia and astrocytes, and to reduce the level of inflammatory mediators (e.g., prostaglandin E2).

[0066] This design can maintain a stable and low-intensity stimulation environment, continuously regulate local cell activity, and construct an immune tolerance microenvironment with a relatively low level of inflammation. This helps to accelerate the local stability of the blood-brain barrier, reduce the secondary infiltration of peripheral immune cells, and thus construct a long-term stable immune tolerance microenvironment around the electrode, so that the glial scar layer maintains a stable thickness and avoids abnormal proliferation.

[0067] Example 3:

[0068] The basic content is the same as in Example 1, except that:

[0069] In the second step, the resolution of acute inflammation at the implantation interface means that when the continuously monitored interface impedance value crosses the peak value and begins to fall back, and the daily average impedance change rate drops to below 5%-50% for 3 to 5 consecutive days, the resolution of acute inflammation at the interface can be determined.

[0070] Meanwhile, when the acute inflammation at the implantation interface subsided, the levels of inflammatory markers decreased by 20%–80% compared to the control group with the same implantation but without stimulation.

[0071] Example 4:

[0072] The basic content is the same as in Example 1, except that:

[0073] In the third step, promoting the transformation of astrocytes into A2-type astrocytes refers to: mid-term low-frequency pulsed stimulation current acting on the adenosine receptor-cyclic adenosine monophosphate (cAMP) signaling axis, increasing the intracellular cAMP concentration by upregulating the expression levels of A2A and A3 adenosine receptors, thereby inhibiting the continuous activation of pro-inflammatory signaling pathways such as NF-κB, inducing astrocytes to transform into the A2-type phenotype with neuroprotective and tissue support functions, and then the A2-type astrocytes secrete a variety of neurotrophic factors and extracellular matrix regulatory molecules to form a structurally stable glial scar layer with a low level of inflammation around the electrode, thereby avoiding excessive proliferation and continuous interface remodeling in the chronic phase.

[0074] Meanwhile, the regulation of calcium signaling in astrocytes refers to the electromagnetic field generated by the mid-term low-frequency pulse stimulation current influencing the release of voltage-gated calcium channels and intracellular calcium stores to regulate the dynamic changes of calcium ions in astrocytes, reduce the pathological hypertrophic response of astrocytes, and optimize their migration and arrangement to promote the controllable formation of glial scar layers.

[0075] Example 5:

[0076] The basic content is the same as in Example 1, except that:

[0077] The electrode channel includes an inner electrode point, an outer electrode point, and conductive traces between them. The stimulation driving circuit is a constant current stimulation driving circuit. The inner electrode point is in contact with the nerve tissue in the brain, and the outer electrode point is connected to the constant current stimulation driving circuit through an external wire.

[0078] like Figure 3As shown, in some embodiments, the external electrode points are electrically connected to the constant current stimulation drive circuit via a multi-channel stimulation and recording interface module (including a channel selection switch matrix and a loop switch unit); the waveform / stimulation controller is electrically connected to the constant current stimulation drive circuit to provide stimulation control signals; and the impedance and signal monitoring module is electrically connected to the electrode array to acquire interface impedance and neural signals.

[0079] The implantable brain-computer interface electrode array is used to be implanted in the target brain region and form an electrical interface with the surrounding neural tissue. The electrode array contains multiple independent electrode channels, some of which are used for recording neural signals and some of which are used for outputting electrical stimulation signals. It can also be dynamically configured by the control system to switch between stimulation and recording functions.

[0080] The waveform / stimulation controller is used to generate a low-frequency pulse stimulation signal with preset parameters, and outputs it to the selected electrode channel through a constant current stimulation drive circuit.

[0081] The multi-channel stimulation and recording interface module includes a channel selection switch matrix and a return path switching unit, used to select the stimulation electrode and the return electrode to form a bipolar or multipolar stimulation structure. By changing the combination of electrode channels involved in stimulation and their spatial distribution, current steering can be achieved and the spatial distribution range of the local electric field around the electrode can be adjusted.

[0082] The constant current stimulation driving circuit preferably includes a charge balance circuit to ensure that the stimulation signal is a charge-balanced biphasic pulse, so as to avoid electrode polarization or tissue damage during long-term stimulation.

[0083] The impedance and signal monitoring module is used to monitor the electrical properties of the electrode-tissue interface in real time and adjust the stimulation parameters according to the monitoring results to achieve closed-loop control.

[0084] Through the above system structure, the present invention can generate a spatially controllable low-frequency electromagnetic stimulation environment in the tissue surrounding the implanted electrode, thereby enabling long-term regulation of neuroinflammatory responses and glial cell phenotypic transformation.

[0085] Example 6:

[0086] The basic content is the same as in Example 1, except that:

[0087] See Figure 4The figure shows a connection diagram of the bipolar current-guided stimulation configuration of the stimulation channel in this invention. In the bipolar working mode, two electrode channels are selected from the implantable brain-computer interface electrode array, which serve as the cathode (stimulation electrode) and anode (return electrode) respectively. A local current loop is formed between the two to form a stimulation loop, thereby forming an electric field, i.e., a stimulation channel, which then electromagnetically modulates the tissue around the electrode.

[0088] See Figure 5 The figure shows a connection diagram of the stimulation channel in this invention when it is a tripolar current-guided stimulation configuration. In the tripolar working mode, three electrode channels are selected from the implantable brain-computer interface electrode array to form a stimulation circuit. Generally, the middle electrode channel is used as the cathode (stimulation electrode), and there is an electrode channel on each side as the anode (return electrode), forming a symmetrical or asymmetrical electric field, i.e., the stimulation channel. This allows the electric field to be shaped in space, thereby electromagnetically modulating the tissue around the electrode and achieving precise control of the stimulation range.

[0089] The above description is only a preferred embodiment of the present invention. The scope of protection of the present invention is not limited to the above embodiments. Any equivalent modifications or changes made by those skilled in the art based on the content disclosed in the present invention should be included within the scope of protection set forth in the claims.

Claims

1. An electromagnetic modulation method for improving the formation of gel scar layer around implanted electrodes, characterized in that: The electromagnetic control method includes the following steps: Step 1: First, select several electrode channels on the implantable brain-computer interface electrode array as stimulation channels, and then connect the selected electrode channels to the external stimulation driving circuit. Step 2: Apply early low-frequency pulsed stimulation current to the electrode channel through the stimulation driving circuit to inhibit the release of pro-inflammatory factors by microglia until the acute inflammation at the implantation interface subsides. The third step is to first adjust the early low-frequency pulse stimulation current to the mid-term low-frequency pulse stimulation current, which promotes the transformation of astrocytes into A2-type astrocytes and regulates the calcium signal in astrocytes, thereby forming a glial scar layer around the electrode. Then, when the impedance curve of the implantation interface completely enters the plateau phase and the signal-to-noise ratio of the nerve signal stops decaying, the glial scar layer is formed.

2. The electromagnetic modulation method for improving the formation of gel scar layer around implanted electrodes according to claim 1, characterized in that: After the third step is completed, there is a fourth step; Step 4: After the glial scar layer has been formed, the mid-term low-frequency pulse stimulation current is adjusted to the late-term low-frequency pulse stimulation current to control the release of anti-inflammatory cytokines by microglia and astrocytes and reduce the level of inflammatory mediators.

3. The electromagnetic modulation method for improving the formation of gel scar layer around implanted electrodes according to claim 2, characterized in that: In the fourth step, the current parameters of the late-stage low-frequency pulse stimulation current include: current amplitude of 3.7-7.5μA, frequency of 15-40Hz, pulse width of 40-4000μs, and timing of 1-5 times per day, with each application lasting 1-5 hours.

4. An electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2, or 3, characterized in that: In the second step, the resolution of acute inflammation at the implantation interface means that when the continuously monitored interface impedance value crosses the peak value and begins to fall back, and the daily average impedance change rate drops to below 5%-50% for 3 to 5 consecutive days, the resolution of acute inflammation at the interface can be determined.

5. An electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2, or 3, characterized in that: In the second step, when the acute inflammation at the implantation interface subsides, the level of inflammatory markers is reduced by 20%–80% compared to the control group with the same implantation but without stimulation.

6. The electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2 or 3, characterized in that: In the second step, the current parameters of the early low-frequency pulse stimulation include: current amplitude of 1.5-3.7μA, frequency of 40-60Hz, and timing of once a day, with each application lasting 15min-3h.

7. An electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2, or 3, characterized in that: In the third step, promoting the transformation of astrocytes into A2-type astrocytes means that: a mid-term low-frequency pulsed stimulation current acts on the adenosine receptor-cyclic adenosine monophosphate signaling axis, which increases the concentration of cyclic adenosine monophosphate in astrocytes by upregulating the expression levels of A2A and A3 type adenosine receptors, thereby inhibiting the continuous activation of pro-inflammatory signaling pathways and ultimately promoting the transformation of astrocytes into A2-type astrocytes.

8. An electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2 or 3, characterized in that: In the third step, the regulation of calcium signaling in astrocytes refers to the regulation of the dynamic changes of calcium ions in astrocytes by the electromagnetic field generated by the mid-term low-frequency pulse stimulation current, which affects the release of voltage-gated calcium channels and intracellular calcium stores.

9. An electromagnetic modulation method for improving the formation of gel scar layer around an implanted electrode according to claim 1, 2 or 3, characterized in that: In the third step, the current parameters of the mid-term low-frequency pulse stimulation include: current amplitude of 0.01-1.5μA, frequency of 60-75Hz, pulse width of 100-2000μs, and timing of 1-5 times per day, with each application lasting 1-24 hours.

10. An electromagnetic modulation method for improving the formation of colloid scar layer around an implanted electrode according to claim 1, 2 or 3, characterized in that: In the first step, the electrode channel includes an inner electrode point, an outer electrode point, and a conductive trace between them, and the stimulation driving circuit is a constant current stimulation driving circuit. The internal electrode point is in contact with the nerve tissue in the brain, and the external electrode point is connected to the constant current stimulation driving circuit through an external wire.

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