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