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 |