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The nociceptive flexion reflex can be used as a tool to investigate modulation of nociceptive transmission at spinal level.
In primary headaches, such as migraine and cluster headache, an abnormal processing of pain stimuli at trigeminal, as well as at spinal level, has been demonstrated.
Some studies with animal models have demonstrated that prostaglandins play pivotal roles in central sensitization at spinal level, resulting in induction of hyperalgesia and CA (touch-evoked pain) [10].
These data suggest that the antinociceptive response to S--ketoprofen involves serotoninergic mechanisms via both supraspinal 5-HT1/5-HT2/5-HT7 receptors and 5-HT3 receptors located at spinal level.
In cluster headache (CH) during the active period we described a facilitated temporal summation (TS) of nociceptive signals at spinal level linked to a defective suprapinal control of pain and followed by a normalization of the values during the remission period[1].
Thus, the comparison between the two studies indicates that spinal DTI is a reliable and very sensitive method for detecting anatomical tract defects at spinal level.
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The meninges have also been recently implicated in pain processing even at spinal levels [22].
Whereas TSSP-M of heat induced pain is well-characterized in human subjects at spinal cord levels related to the upper body, TSSP-M at spinal levels related to the lower body has not been previously studied.
All CT scans were interpreted for each parameter at spinal levels L2-L3, L4-L5, L5-S1, and L5-S1.
It has been demonstrated that a compression injury inflicted at the T8-9 level can lead to oligodendrocyte apoptosis at spinal levels as far away as T1-L2 [ 68].
ACh is an important modulator of motor and sensory processing, especially at the spinal level, at which point pain-related nociceptive stimuli enter the CNS, which integrates the stimuli and relays them to the brain.
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