Neuromodulation therapies apply a therapeutic stimulus directly to the nervous system. Ideally, neuromodulation techniques should be noninvasive, biocompatible, and spatially and temporally controllable.
Examples of magneto-neuromodulation are Transcranial Magnetic Stimulation (TMS) and possibly Neuromagnetics.
As a magneto-neuromodulation therapy, Q Magnets tick all the boxes. Q Magnets stimulate and/or inhibit – or modulate – nerve activity through the application of a magnetic field.
From Science Magazine – A magnetic look into neuromodulation
“Neuromodulation therapy is a promising approach for a wide range of diseases and injuries, including chronic pain management. Here, the authors present an alternative neuromodulation technique using a magnetomechanical stimulus capable of remotely and noninvasively stimulating neuronal cells or other cells that express mechanosensitive ion channels.”
This recently published study (REF) describes a new method for using magnetic fields as the stimulus for neuromodulation; named magnetomechanical neuromodulation. It’s a process whereby tiny magnetic nanoparticles are bound to the cell membrane and manipulated by external magnetic field gradients to physically stretch the cell.
The magnetic nanoparticles are evenly distributed throughout what’s described as a 3D magnetic hydrogel. The mechanical forces applied to the cell membrane have been shown to modify the nerve cell’s Ca2+ channels via the mechanosensitive TRPV4 and PIEZO2 ion channels.
Since intracellular Ca2+ levels are known to affect cell signalling, this provides a mechanism to influence neural communication.
The PIEZO2 channel is understood to play a role in the sensitization process of chronic pain, for a recent paper see link here. Nerve cells such as dorsal root ganglions (DRG) adapt to external stimulus and may for instance, overexpress the production of PIEZO2 channels in people living with chronic pain.
From Pain News Network – Magnetic gel could someday treat chronic pain.
“Di Carlo and his colleagues used magnetic particles inside a gel to manage cell proteins that control the flow of calcium ions.The proteins are on the cell’s membrane and play a role in the sensations of touch and pain. When damaged by injury or disease, these “excitable” neuron cells continually send pain signals.
“Our results show that through exploiting ‘neural network homeostasis,’ which is the idea of returning a biological system to a stable state, it is possible to lessen the signals of pain through the nervous system,” said lead author Andy Kah Ping Tay, a recent UCLA doctoral graduate. “Ultimately, this could lead to new ways to provide therapeutic pain relief.””
Each nerve cell has within its membrane, thousands of these ion channels which allow the flow of specific ions such as Na+, Ca2+ and K+.
The channels open and/or closed to specific stimuli such as voltage, mechanical or chemical stimulus.
This process mediates most forms of electrical excitability throughout the nervous system.
For instance, analgesic drugs lidocaine and novocaine were created specifically to block Na+ channels. Of course it’s common with long term use of pharmaceuticals such as opioids, that the user becomes more sensitive to pain and may need to increase the dose for the same effect.
This is the process of compensatory adaptation, where the nervous system attempts to nullify the drug’s effects by expressing more and more ion channels and receptors within the cell’s membrane structure and thereby making it more “sensitive”.
This type of adaptation is thought to be based on homeostatic mechanisms, where cells attempt to maintain their equilibrium while exposed to a changing external environment. From the results of the study, the researchers believe that 3D magnetic hydrogel might reduce the expression of mechanosensitive PIEZO2 channels, thus potentially reducing pain sensitivity.
Q Magnets are thought to relieve pain through the direct application of an external magnetic field from a non-invasive wearable device. After 10 years of research including in-vitro cell studies and randomised controlled trials the group of neurologists at Vanderbilt Medical University lead by Dr Michael J. McLean, M.D., Ph.D., concluded that the evidence suggested that the most likely mechanism of action is that the steep field gradients generated by the quadrapolar magnetic field is altering nerve excitability as a result of changes in membrane permeability to Na+ and Ca2+ ions.
McLean (REF) describes the cell study where nerve fibres were exposed to the noxious stimuli capsaicin and after 5 minutes of exposure to the gradient of the Quadrapolar array, the action potential firing was totally blocked and fully recovered 10 minutes after the removal of the field.
Modelling has shown that the magnetic field gradients are thought to displace or rotate proteins that make up ion channels and hence change the cell’s membrane permeability to Na+ and Ca2+ ions.
So while magnetomechanical neuromodulation is based on a magnetic field indirectly inducing mechanical forces on the cell membrane.
Magneto neuromodulation with Q Magnets is based on an external magnetic field gradient acting directly on the protein structures of the ion channels.
Q Magnets don’t appear to cause the compensatory adaptation that’s common with therapeutic agents such as opioids. This is observed in practice, as once their effectiveness has been established, it seldom diminishes over time.
While the hydrogel is promising theoretically, the idea of introducing a foreign material into the body could trigger harmful reactions. This potential complication is completely avoided by applying an external static magnetic field such as Q Magnets.
See video below for news program, featuring interviews with the researchers who conducted the Magnetomechanical Neuromodulation study…
REFERENCES:
Tay A. (2018). A 3D Magnetic Hyaluronic Acid Hydrogel for Magnetomechanical Neuromodulation of Primary Dorsal Root Ganglion Neurons. Adv Mater. 2018 Jun 10 PMID: 29888402; doi
McLean, M., S. Engstrom, et al. (2001). “Static Magnetic Fields for the Treatment of Pain.” Epilepsy & Behavior. 2001, 2(3): S74-S80. doi
