When the pain transmission in sensitive nerves is impaired or interrupted by a partial or total organic deafferentation (DFT) the following main events occur: a) lowering of SP content into the ipsimetameric dorsal horn, [1,2]; b) an increase in SP receptor number in the same dorsal horn area ; c) a supersensitivity to locally-applied SP both in dorsal ipsilateral horn and in peripheral structures (vessels: permeabilization; iris: miosis; gland: secretion) innervated ipsimetamerically by the damaged nerve [3,4,5]; d) generation and rostral dissemination into the spinal cord and brainstem of “quasi epileptic foci” capable of emitting simil-epileptic firings of electrical signs, expression of start of “automatic pains”, then central in nature [6,7,8]; e) arising of phantom pain in amputated humans. Likely aches of the same nature are also responsible for the autotomy in animals, attributed to an attempt to get rid of the deafferentated leg, the apparent source of pain. The DFT, when complete, is characterized by chronic aches having the perverted characteristics of central pain, as well as ipsilateral vasomotor disorders and plasma extravasation (sterile inflammation) in the area where pain projects. In the DFT syndrome the SP empty neuron pathological unit could play a major role. SP secretion (even if in a meagre amount) is expected to provoke pain rostrally and inflammation caudally . The activity in neuraxis of SP in DFT syndrome could depend on: a) a secretion of residual SP in the damaged nerve and/or in some regenerated fibers; b) a secretion from intermetameric SP neurons having consistent compensatory plasticity.
Weitere Kapitel dieses Buchs durch Wischen aufrufen
- Substance P Empty Neuron: A Conceptualization of Organic and Functional Deafferentation Syndromes
M. G. Spillantini
- Springer New York
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