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Brain-Computer Interfaces Could Eliminate Lower Back Pain


If your lower back hurts, you’re in good company. Back pain inflicts itself on almost everyone during their lives. But there are some unlucky folk who get injured, or have a degenerative disorder or neuropathic condition that leaves them in chronic pain. And for people who have pain doctors can’t explain or really treat, things can start looking pretty bleak. Pain for the rest of my life, that I can’t alter or relieve. Grand.

So it may come as a bit of welcome news that there are scientists working on brain-computer interfaces capable of intercepting noise and cross-talk between neurons — with the net result that people who have just been slogging through under the burden of invisible, intractable pain may be able to catch a glimpse of light. And it’s a glimmer from the end of the tunnel, not the headlight of an oncoming train.

Back pain can be classified in a few broad categories. There are disorders like a slipped or “burst” disc, which can result in runaway local inflammation that makes things worse over time. There are the class of disorders that come from pinched or otherwise damaged nerves, such as sciatica and other neuropathic pain. Then there are musculoskeletal disorders that are brought on or made worse by an injury to the muscles, tendons, and ligaments, or the bones of the spine itself.

But in all these cases, there’s this unpleasant inversion of a law of the body that makes things more fragile and friable and inflamed, rather than sound and whole. We’re often told that nerves can’t regrow after they’re damaged. But that’s not completely true. And it’s a big part of the problem here.

Schematic_Examples_of_CNS_Structural_Changes_in_chronic_pain

Long-term chronic pain causes changes in the CNS. Schematic Examples of CNS Structural Changes. Red circles signify decreased gray matter density relative to controls. A. Subjects with chronic back pain show decreases in gray matter density in bilateral dorsolateral prefrontal cortex (DLPFC) and right anterior thalamus (adapted from [25]). B. Patients with fibromyalgia show decreases in cingulate cortex (CC), medial prefrontal cortex (Med. PFC), parahippocampal gyrus (PHG) and insula (adapted from [27]). 3-D surface renderings were created using Freesurfer. Image and caption from 2007 chronic pain report by Borsook D, Moulton EA, Schmidt KF, Becerra LR.

It’s true that we don’t yet know how to reliably induce the proper growth and integration of neurons in the brain and spine — neurons of the central nervous system. As far as we know, neurons aren’t fungible, because of their unique synaptic connections. But we can exert a little influence over the regrowth and development of peripheral neurons, the ones we feel and sense with.

For example, your sense of touch is intimately related to your sense of itch. Individual neuronal fibers carrying data about different stimuli — pressure, itch, vibration, temperature, and even pH or electrical current — all get bundled into the same physiological nerve sheath, that acts like conduit carrying a bunch of cat5 cables. Each fiber carries different sensations, or different data. But once they’re all inside the nerve sheath, we call the whole shebang a “nerve.” Some people get full sensation back in the affected region after an injury that damages the nerves, while some others don’t. With the right kind of physical therapy and rehab, though, it’s surprising how well peripheral nerves can resume most of their function after terrible injuries.

But even with these successes, there are often problems with the way peripheral nerves reintegrate themselves into the body’s nervous system. After a back injury, a person can develop a thing called a glial scar that can cause chronic pain with no known treatment other than pain-relieving medications or even a rhizotomy, where they literally sever a spinal nerve so it can’t beam back pain signals.

And even with all our casual jokes about “I hope they gave you the good stuff” after surgery, the kind of pain relievers it takes to get even temporary relief from disabling pain are nothing to laugh at. They have their own deeply unpleasant side effects. Fentanyl, which is manna from heaven delivered intravenously before things like dental surgery or bone grafts, is a common enough contaminant in heroin that it’s causing a nationwide epidemic of overdose fatalities. And even after all these things, there are people who suffer from intolerable pain or itching or muscle cramping — in a phantom limb after amputation.

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It would be nice if we could do something that wasn’t drugs to relieve the kind of pain that nothing else helps. Brain-computer interfaces might not be the first thing that springs to mind when you’re thinking of ways to make your back stop hurting, but they’re starting to have something to say in this discussion. In January of this year, ClinicalTrials.gov approved a feasibility study on the use of implantable BCIs that could learn a patient’s brainwaves, deduce what they were feeling, and convey that information to an external resource so the patient could use it in a super-spiffy version of biofeedback therapy.

Similarly, IEEE published a report of an implantable BCI that could deduce what motion a patient was planning to make, interface with damaged neurons, and then convey that information to other neurons associated with the implant. Patients who engaged in this study were able to mentally manipulate things like a prosthetic, work an impaired limb distal to the damaged site, or even to finally work with a phantom limb.

And then there’s the report from just this spring, claiming to have developed “a completely new technological approach toward BCIs aimed at reversing the maladaptive plasticity induced by musculoskeletal pain.” Basically they argue that nerves can become conditioned to transmit pain signals, and that BCIs can help reverse this change. In summary, the authors said, “we have developed a neurofeedback system for musculoskeletal pain that is capable of providing rapid, accurate and reliable neurofeedback in dynamic conditions, allowing the users to train their brain to reduce the pain.” This amounts to interacting with the central pain relief pathways currently used by endorphins and opiates.

BCIs even have value in treating neuropathic pain — the idiosyncratic, infuriating, diffuse pain that many nerve injuries can leave behind.

All of these techniques rely on the concept of neuronal plasticity, the idea that nerves can rewire themselves and restore their connections after injury. It’s clear that much more work needs to be done in the field. But with all these advances, it won’t be long before these devices start popping up out of startups and making their way into consumer hands…or brains.



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