Talk to your doctor and MS nurse if you have bladder or bowel control issues.
You may need some background knowledge to understand this post.
Green AL et al. Switching off micturition using deep brain stimulation at midbrain sites. Annals Neurol [Epub ahead of print]
Most of the time the bladder is locked in storage mode, switching to voiding (urination) only when it is judged safe and/or so socially appropriate to urinate. Here we show in humans and rodents, that deep brain stimulation in the periaqueductal grey (a centre in the brain that controls urination) can rapidly and reversibly manipulate switching within the micturation control circuitry, to defer voiding and maintain urinary continence, even when the bladder is full. Manipulation of neural continence pathways by Deep brain stimulation (DBS) may offer new avenues for the treatment of urinary incontinence of central origin. Deep brain stimulation was originally developed as a tool to probe brain function in animal models, has re-emerged as a powerful clinical neuromodulatory technique to normalise dysfunctional central sensory and motor control systems. Sensory input from the distended bladder activates a spino-midbrain-spinal nerve circuit (electrical circuit within the spinal cored and brain). Critical synapses in the pathway, located in the caudal ventrolateral periaqueductal grey matter (PAG), are normally subject to ongoing inhibitory GABAergic tone (GABA is a chemical the nerves use to speak to each other; a so called neurotransmitter) as revealed by microinjection of a GABA antagonist (A substance that blocks the action of GABA which is itself an inhibitor neurotransmitter and dampens down nerve excitation). During the act of voiding there is intense neuronal activation in the PAG accompanied by a decrease in the local extracellular GABA concentration. The reduction in ongoing inhibitory GABAergic tone permits the bladder control circuitry to switch from tonic storage mode to an acute period of phasic activity, which co-ordinates micturition. Here we demonstrate its potential to modulate autonomic function by showing in rodents and in humans that short periods of DBS at selected midbrain sites provide a rapid onset, reversible means of postponing micturition, by preventing the control circuitry switching from storage to voiding mode, thereby promoting continence, even when the bladder is full.
The micturation circuit
CoI: None
Most of the time the bladder is locked in storage mode, switching to voiding (urination) only when it is judged safe and/or so socially appropriate to urinate. Here we show in humans and rodents, that deep brain stimulation in the periaqueductal grey (a centre in the brain that controls urination) can rapidly and reversibly manipulate switching within the micturation control circuitry, to defer voiding and maintain urinary continence, even when the bladder is full. Manipulation of neural continence pathways by Deep brain stimulation (DBS) may offer new avenues for the treatment of urinary incontinence of central origin. Deep brain stimulation was originally developed as a tool to probe brain function in animal models, has re-emerged as a powerful clinical neuromodulatory technique to normalise dysfunctional central sensory and motor control systems. Sensory input from the distended bladder activates a spino-midbrain-spinal nerve circuit (electrical circuit within the spinal cored and brain). Critical synapses in the pathway, located in the caudal ventrolateral periaqueductal grey matter (PAG), are normally subject to ongoing inhibitory GABAergic tone (GABA is a chemical the nerves use to speak to each other; a so called neurotransmitter) as revealed by microinjection of a GABA antagonist (A substance that blocks the action of GABA which is itself an inhibitor neurotransmitter and dampens down nerve excitation). During the act of voiding there is intense neuronal activation in the PAG accompanied by a decrease in the local extracellular GABA concentration. The reduction in ongoing inhibitory GABAergic tone permits the bladder control circuitry to switch from tonic storage mode to an acute period of phasic activity, which co-ordinates micturition. Here we demonstrate its potential to modulate autonomic function by showing in rodents and in humans that short periods of DBS at selected midbrain sites provide a rapid onset, reversible means of postponing micturition, by preventing the control circuitry switching from storage to voiding mode, thereby promoting continence, even when the bladder is full.
The micturation circuit
CoI: None