Implants that read and decipher our brain activity have allowed people to control computers, robotic limbs or even remote-controlled helicopters, just by thinking about it. These devices are called BMIs, short for brain-machine interfaces.
But our cyborg future isn’t limited to machines that hook up to our brains. At the University of Cambridge, James Fawcett has created a BMI where the B stands for bladder. The implanted machine senses when a bladder is full, and automatically sends signals that stop the organ from emptying itself.
So far, it works in rats. It will take a lot of work to translate the technique into humans, but it could give bladder control back to people who have lost it through spinal injuries.
As the bladder fills up, its walls start to stretch. Neurons in the bladder wall detect these changes and send signals to the dorsal root, a structure at the back of the spinal cord. If left to themselves, these signals trigger a reflex that empties the bladder. That doesn’t usually happen because of neurons that travel in the opposite direction, descending from the ventral root at the front of the spine into the bladder. These counteract the emptying reflex and allow us to void the bladder when we actually want.
Spinal injuries often rob people of that control, by damaging the ventral neurons. “Take those away and you dribble all over your clothes every half hour,” says Fawcett.
There are two fixes. The first was developed by an eccentric British neuroscientist called Giles Brindley in the 1970s. Brindley is infamous for a lecture in which he demonstrated the effectiveness of a treatment for erectile dysfunction, by dropping his trousers and showing his erect penis to the audience. But his real claim to fame is an implant that stimulates the ventral root directly, allowing people with spinal injuries to urinate on demand.
There’s a catch—it only works if surgeons cut the neurons in the dorsal root so the bladder can’t spontaneously empty itself. This has severe side effects: men can’t get erections, women have dry vaginas, and both sexes end up with weak pelvic muscles.
The only other alternative is to paralyse the bladder with botox. Now, it can’t contract at all, and people have to empty it by sticking a catheter down their urethra. That’s expensive, difficult, unpleasant, and comes with a high risk of infection.
Fawcett’s team, led by Daniel Chew and Lan Zhu, have developed a better way.
First, they hack into the bladder’s communication lines. Rather than cutting through the dorsal root, they tease out fine strands of neurons called dorsal rootlets, and thread them into tiny sheaths called microchannels. The channels record the signals going from the bladder to the spine, revealing what the organ is up to.
When the bladder is ready to empty itself, the channels detect a big spike in activity. They react by sending signals to a stimulator that’s hooked up to the nerves leading into the bladder’s muscles. The stimulator hits these nerves with a high-frequency electric pulse that stops them from firing naturally. The bladder’s muscles don’t contract, and no unwanted urine is spilled. When the user actually wants to wee, they just push a button and the stimulator delivers a low-frequency pulse instead. Only then does the bladder contract.
This device does everything that a normal bladder does, but uses electronics to stand in for damaged nerves. It works on a closed loop, so users should be able to go about their day to day lives without worrying about incontinence. And it doesn’t sever the dorsal root, so it carries none of the side effects of the Brindley method.
“That would be a major advance,” says Kenneth Gustafson, a biomedical engineer from Case Western Reserve University. “Restoration of bladder control is one of the most important problems of individuals with spinal cord injuries.”
“The quality of the neural recordings that they’re showing with their channel electrodes is really very impressive and convincing,” says Robert Gaunt from the University of Pittsburgh, who has also worked on neural prosthetics for the bladder.
The team have successfully tested their device in rats, and they’re working on scaling it up to humans. “We haven’t actually trying dissecting human dorsal roots into rootlets but the anatomy’s quite similar,” says Fawcett.
“It’s good to see this has come to fruition,” says Clare Fowler from University College London, who studies ways of solving incontinence in people with neurological problems. “There have been a lot of very clever developments to get this working, and they are to be congratulated.” However, she adds that the device is “many years away from translation into human usefulness.”
Gaunt adds that the nerves that control the bladder muscles are near to those that control its sphincter. If you shut down the former with high-frequency pulses, you might risk accidentally shutting down the sphincter too—it would then relax, and the bladder might empty.
But the main problem is longevity. The device needs to be turned into something like a pacemaker, which can be implanted reliably for long periods of time. Currently, that’s impossible because the rootlets can only survive for 18 months in the microchannels before they build up fatal amounts of scar tissue. “That’s not long enough to be useful,” says Fawcett, who is working on ways of extending their lifespan.
Fawcett adds that his work isn’t just about the bladder. His microchannels offer a new way of effectively recording signals from nerves outside the brain—a goal that has historically been very difficult. Tap into the right nerves, and the device could potentially be used to control everything from prosthetic limbs to immune reactions to the digestive system.
Again, that’s a far-off goal. “We’re not sure that outside the dorsal root, we can tease the peripheral nerves into rootlets,” says Fawcett. “They weave around a lot more, so you’d risk damaging them. We’re looking into that currently.”
Reference: Chew, Zhu, Delivopoulos, Minev, Musick, Mosse, Craggs, Donaldson, Lacour, McMahon & Fawcett. 2013. A Microchannel Neuroprosthesis for Bladder Control After Spinal Cord Injury in Rat. Vol 5 Issue 210 210ra155