Healthy body, healthy bladder

It's established that epidural stimulation in SCI patients leads to changes in motor output. Basically, electrical stimulation (ES) primes the circuitry responsible for standing/walking to an extent that it becomes capable of responding appropriately to feedback from the sensory system; weight bearing leads to standing whereas introduction of locomotor activity (via a treadmill, for example) leads to the generation of patterned sensory signals coming from the legs that the cord responds to by trying to fire muscles in a coordinated extensor-flexor, left-right fashion. The work of Harkema and colleagues - a few years ago now - was published with much fanfare and interest remains high in the potential of electrical stimulation, particularly as it is so clinically feasible.

Anyway, one of the more intriguing observations from this seminal work was the anecdotal reports of improvements in bladder function in some of those earliest patients receiving epidural ES. What of this? The mechanism by which ES and locomotor training might couple to bladder function and other non-locomotor systems is less intuitive. Ward et al., recently showed that quadrupedal locomotor training in rats with SCI (contusion; T10) led to improved bladder function and that training led to changes in neurotrophin levels.

One question then is, does ES specifically engage with circuitry that contributes to improvements in bladder function or might it be the training "allowed" by ES that it key? L.R. Montgomery [#46.09] has added to the story. Montgomery presented data from a study that tested bladder function in three rodent groups; (i) injured, (ii) injured receiving quadrupedal training and, (iii) injured receiving forelimb locomotor training (basically, treadmill training with hind limbs hoisted off the ground, wheelbarrow fashion).

What she showed was that it didn't matter what training was received as both groups showed equivalent improvements in bladder function measures over injury alone, suggesting there are global and systemic mechanisms at play. There's a couple of more papers being presented this week relevant to this which might be worth looking at.

Elsewhere, a paper caught my eye on neuropathic pain. Tan presented [#66.01] a nice little poster on the correlation of dendritic spine (post-synaptic micron sized structures) distribution and morphology with the presentation of neuropathic pain. The correlation is tight such that neuropathic pain is always associated with remodelling of the dendritic spines. The group had already shown that if you acutely inhibited remodelling of the spines with Rac-1 inhibitor, neuropathic pain states did not develop. This poster looked at what happened if you inhibited remodelling after pain had been established. They found the pain state diminished and furthermore, when the drug is withdrawn remodelling is re-established and pain comes back.