SUMMARY |
A GENERAL THEORY ON PAIN AS AN INTEGRATED
THERMODYNAMIC MECHANISM |
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| A theory which postulates the occurrence of pain in the case of a relative deficit of the physiologic power balance of a cell. A dysfunction of the mitochondrial respiratory chain is defined as energy deficit. Through a resulting reduced activity of ATP-dependent ion channels occurs an extra-cellular ion shifting. This changes, according to the Hodgkin-Huxley model, the conditions of the neuronal membrane potential and its excitability pattern. |
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| Simplified Scheme on Pain Origin. Sequence of cell impairment (Noxis) with ion shifts and coupling with neuronal excitability due to changes (-/+∆) in the equilibrium of the physiologic power balance (Qo): Switch-over of a balance deficit into a relative ion product (∆IPo) in the interstitial space and subsequent change into an excitability product (∆Em) in the neuron. The energy deficit may be localised in the cell, in the neuron or in both. Depending from the location an anterograde or retrograde induction of ∆IPo, or a cross-over interaction, may be effected. In sum ∆IPo results from the inward/outward flux activities of ion channels, which are controlled by the actual ∆Qo. Vice versa ∆IPo dependent ion flux activities can also influence the actual status of ∆Qo. (modified excerpt from Med Hypotheses 2009, 73, 86) |
CONCLUSIONS |
- Pain is a centrally perceived neuronal signal which reflects a deficit in the physiologic power
balance of a cell. This relation can be formalised as P = f (-∆Qo).
- Pain results from ion shifts which couple a deficit of an intracellular power balance to a neuronal excitation.
- Pain is postulated as a closed-loop system, which also actively triggers central reactions in order
to repair the inducing power deficit.
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© 2010 Rainer K Liedtke |
