Neuropathy and chronic pain results when nerve signal propagation is reduced between adjacent nerve cells due to insufficient oxygen being available to support nerve cell metabolism. This is responsible for 90% of all neuropathy and chronic pain cases. The remaining 10% is caused by physical trauma. Thus it appears that the main precipitating factor for neuropathy and chronic pain is hypoxia and demineralization of the synaptic fluid which creates shrinkage of the nerve cells which widens the gap between these cells making it more difficult for normal sensations to propagate, and loss of electrical conductivity in the synaptic fluid itself.
A temporary hypoxia of nerve tissue can be traced to most causes of neuropathy and chronic pain. The primary negative effects of this hypoxia are as follows:
- A defensive contraction of the nerve cell resulting in oversize synaptic junctions
- A loss of electrical conductivity of the synaptic fluid between nerve cells
- A defensive change in the electrical potentials of the cell membrane resulting in a higher resting state of the trigger level which effectively limits the sensitivity to incoming signals
For example, when the lumbar area experiences a muscle spasm, blood flow is restricted through that muscle resulting in reduced oxygen availability to the surrounding tissue, including nerve cells. Because muscles can use either oxygen or glucose metabolic pathways, they can recover quickly from a temporary reduction in the level of available oxygen. Nerve cells, on the other hand, are limited to the Krebs oxidative reductive metabolic system and must take immediate defensive steps to assure survival during this hypo oxygen state. One of the ways they accomplish this is to contract along their longitudinal axis like a rubber band, reducing their surface area and thus lowering their need for oxygen. (This also occurs when these cells are attacked by a harsh agent in the blood such as chemotherapeutic drugs, Agent Orange, environmental toxins, insecticides, etc.) The synaptic junctions between the axons of one nerve cell and the dendrites of the next nerve cell widen. Normal nerve transmission is now compromised because a nerve signal of normal intensity cannot jump this newly widened gap. The synaptic fluid between the nerve cells must be electrically conductive. Pure water does not conduct electricity, so this conductivity relies on minerals and specific neurotransmitters such as serotonin in the synaptic fluid to enable the propagation of the nerve signal. These minerals are delivered via the perfusion of adjacent tissues with fresh blood and kept in suspension by the periodic ionization of successfully transmitted nerve signals across the junction. When nerve signals are reduced because of these larger dimensions of the synaptic junction, necessary minerals are no longer held in place by electrical tension and are slowly leeched out. This adds to the impairment of effective nerve transmission.
Common short term remedies with prescription drugs only ameliorate the pain temporarily and do little or nothing to mitigate or cure the underlying condition. They may provide some level of temporary relief, but as the disease progresses, the effective dosage of the drug needed to continue suppressing the pain increases concurrently. The side effects of these types of drugs are difficult to deal with and add to the patient’s discomfort. When the increased drug dosage reaches a threshold level, the patient can become confused, ataxic, constipated, confined to a wheelchair or may become bedridden. Symptoms similar to Alzheimer’s may soon follow. When nerve signals can no longer jump the enlarged synaptic gap, the electrical tension that normally holds these minerals in place is absent, causing the synaptic fluid to leach out its mineral content. Electrical conductivity is reduced, thereby inhibiting the transmission of the normal nerves’ electrical signals across this gap.