A Microchannel Neuroprosthesis for Bladder Control After Spinal Cord Injury in Rat

An electronic interface for recording and stimulating nerves that innervate the bladder helps to restore normal bladder function in rats with spinal cord injury. Getting to the Root of Bladder Control Injury to the spinal cord typically results in loss of conscious bladder emptying and the sensation of fullness. Currently, only limited treatment options are available, with most of the patients receiving catheterization. However, this is cumbersome and leads to urological complications including unsolicited episodes of bladder contraction, leading to inappropriate emptying. In a new study, Chew et al. design a “closed-loop” electronic device that can accurately record bladder filling from sensory nerves after spinal cord injury in rat. Using this information, bladder emptying can be artificially stimulated on demand by electrically modulating nerve firing. It is traditionally difficult to record robust neuronal activity from peripheral nerves in vivo. Typically, cuff electrodes are used to record from whole nerves, but produce poor signal quality and provide little indication of bladder filling. Through nerve microdissection, Chew et al. implanted fine-diameter nerves (“rootlets”) into insulated microchannels, recording action potential firing that accurately encoded bladder filling. The device had multiple microchannels for concurrent recording, greatly improving the resolution. Using this sensory information and by manipulating stimulation characteristics, the authors prevented the rat bladder from emptying inappropriately, and bladder contraction was initiated when desired. This work opens a new avenue for the design of a neuroprosthesis for bladder control after spinal cord injury. A severe complication of spinal cord injury is loss of bladder function (neurogenic bladder), which is characterized by loss of bladder sensation and voluntary control of micturition (urination), and spontaneous hyperreflexive voiding against a closed sphincter (detrusor-sphincter dyssynergia). A sacral anterior root stimulator at low frequency can drive volitional bladder voiding, but surgical rhizotomy of the lumbosacral dorsal roots is needed to prevent spontaneous voiding and dyssynergia. However, rhizotomy is irreversible and eliminates sexual function, and the stimulator gives no information on bladder fullness. We designed a closed-loop neuroprosthetic interface that measures bladder fullness and prevents spontaneous voiding episodes without the need for dorsal rhizotomy in a rat model. To obtain bladder sensory information, we implanted teased dorsal roots (rootlets) within the rat vertebral column into microchannel electrodes, which provided signal amplification and noise suppression. As long as they were attached to the spinal cord, these rootlets survived for up to 3 months and contained axons and blood vessels. Electrophysiological recordings showed that half of the rootlets propagated action potentials, with firing frequency correlated to bladder fullness. When the bladder became full enough to initiate spontaneous voiding, high-frequency/amplitude sensory activity was detected. Voiding was abolished using a high-frequency depolarizing block to the ventral roots. A ventral root stimulator initiated bladder emptying at low frequency and prevented unwanted contraction at high frequency. These data suggest that sensory information from the dorsal root together with a ventral root stimulator could form the basis for a closed-loop bladder neuroprosthetic.