OBJECTIVES: Despite evidence that the activation of visceral afferents modulates spinal motoneurone activity in humans the responsible circuits remain unclear. We investigated changes in spinal motoneurone excitability during bladder filling in 8 healthy subjects and in 8 patients with spinal cord lesions and 5 patients with multi-infarct encephalopathy. METHODS: Spinal motoneurone excitability was studied by analysing changes in H-reflex, F-wave and motor-evoked potential (MEP) size recorded from the calf muscles under different bladder filling conditions. RESULT: In normal subjects, maximal bladder filling significantly suppressed the H-reflex, F-wave and MEPs; after bladder voiding these responses returned to normal. In patients with encephalopathy maximal bladder filling strongly reduced H-reflex size; similarly to normal subjects H-reflex returned to control value after bladder voiding. In patients with spinal cord lesions, activation of bladder afferents left the H-reflex unchanged. CONCLUSIONS: These findings indicate that bladder distension induces post-synaptic inhibition of spinal motoneurones through a suprasegmental pathway, which is interrupted by rostral spinal cord lesions. This vesical-induced inhibition is probably mediated by the propriospinal system rather than by the diffuse noxious inhibitory control circuit.
OBJECTIVES: Despite evidence that the activation of visceral afferents modulates spinal motoneurone activity in humans the responsible circuits remain unclear. We investigated changes in spinal motoneurone excitability during bladder filling in 8 healthy subjects and in 8 patients with spinal cord lesions and 5 patients with multi-infarct encephalopathy. METHODS: Spinal motoneurone excitability was studied by analysing changes in H-reflex, F-wave and motor-evoked potential (MEP) size recorded from the calf muscles under different bladder filling conditions. RESULT: In normal subjects, maximal bladder filling significantly suppressed the H-reflex, F-wave and MEPs; after bladder voiding these responses returned to normal. In patients with encephalopathy maximal bladder filling strongly reduced H-reflex size; similarly to normal subjects H-reflex returned to control value after bladder voiding. In patients with spinal cord lesions, activation of bladder afferents left the H-reflex unchanged. CONCLUSIONS: These findings indicate that bladder distension induces post-synaptic inhibition of spinal motoneurones through a suprasegmental pathway, which is interrupted by rostral spinal cord lesions. This vesical-induced inhibition is probably mediated by the propriospinal system rather than by the diffuse noxious inhibitory control circuit.