Abstract
Together with the nociceptive system, pain protects the body from tissue damage. For instance, when the RIII-reflex is evoked by sural nerve stimulation, nociceptive inputs activate flexor muscles and inhibit extensor muscles of the affected lower limb while producing the opposite effects on the contralateral muscles. But how do the spinal cord and brain integrate concurrent sensorimotor information originating from both limbs? This is critical for evoking coordinated responses to nociceptive stimuli, but has been overlooked. Here we show that the spinal cord integrates spinal inhibitory and descending facilitatory inputs during concurrent bilateral foot stimulation, resulting in facilitation of the RIII-reflex and bilateral flexion. In these conditions, high-gamma oscillation power was also increased in the dorsolateral prefrontal, anterior cingulate and sensorimotor cortex, in accordance with the involvement of these regions in cognitive, motor and pain regulation. We propose that the brain and spinal cord can fine-tune nociceptive and pain responses when nociceptive inputs arise from both lower limbs concurrently, in order to allow adaptable behavioural responses.
Highlights
Nociception and pain constitute an alarm system that detect actual or potential damage to body tissues, which evokes well characterized spinal[1,2] and cerebral[3,4,5,6] responses
As shown by Steffens & Schomburg[18], nociceptive afferents are constituents of the flexor reflex afferent (FRA) that add a nocifensive function to the FRA system, the later being dedicated to the control of movement and not to withdrawal and protection
We propose that the brain and spinal cord can fine-tune nociceptive and pain responses depending on the location of nociceptive input sources, in order to provide adaptable responses
Summary
Nociception and pain constitute an alarm system that detect actual or potential damage to body tissues, which evokes well characterized spinal[1,2] and cerebral[3,4,5,6] responses. The RIII-reflex was investigated by Hagbarth[23] and Hugon[24] and it was shown that nociceptive stimuli usually evoke ispilateral flexion, but extension may occur if the skin overlying flexor muscles is stimulated. This is why the more general term “withdrawal reflex” is sometimes used to refer to responses evoked by nociceptive stimulation of the limbs. The RIII-reflex produced by stimulation of the skin overlying the sural nerve in its retromalleolar pathway always consists in activation of the biceps femoris and flexion of the knee[1] This response relies on A-delta fibers and is strongly associated with pain perception[1,25,26]. This integration may be an essential neural process in response to pain perception in order to produce the most adapted behavioural responses
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