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Table 5 Summary

From: What is different about spinal pain?

Clinical Feature Mechanisms: Gillette, 2005 Mechanisms: Current report
Poorly localized pain (back, hip and leg; upper neck, TMJ, face) Spinal neuron “hyperconvergence” and large receptive fields Lower density of nociceptors in facet joints, discs (?)
Afferent branching
Referred pain from deep tissues Nociceptive input to low back neurons from deep tissues more powerful than skin input Multi-segmental DH input from spinal joints
Stronger bilateral DH projection from spinal afferents
Somatotopic organization of spinal vs limb neurons in DH
Weaker DH medio-lateral interneuronal modulation of pain
Lack of projection to Lamina II may result in weaker DH inter-laminar modulation of pain
Hyperconvergence of afferent inputs onto spinal neurons
Spontaneous, ongoing pain After-discharge in many spinal low back neurons after central sensitization (CS) / LTP Higher levels of ongoing discharge in spinal neurons
Referred hyperalgesia Increased responsiveness (of spinal low back neurons) to mechanical (noxious and non-noxious) input in the receptive field after CS / LTP Hyperconvergence
Radiation of pain Receptive field expansion following CS / LTP
Recruitment of additional low back neurons into activation by:
- Release and spread of excitatory substances from afferents
- “Unmasking” of latent excitatory synapses by noxious input
Persistent referred spinal pain Development of CS / LTP produces:
  - Sympathetically-mediated increases in noxious and non-noxious inputs
  - Lowered threshold to excitation by non-noxious inputs  
  - Loss of inhibitory controls  
  1. LTP = long-term potentiation.