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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.