The remaining 10% is caused by physical trauma. Thus, it appears that the main precipitating factor for neuropathy is hypoxia and demineralization of the synaptic fluid, which creates shrinkage of the nerve cells, widening the gap between these cells, making it more difficult for normal sensations to propagate, and causing loss of electrical conductivity in the synaptic fluid itself. A temporary hypoxia of nerve tissue can be traced to most causes of neuropathy.The primary negative effects of this hypoxia are as follows:

• a defensive contraction of the nerve cell resulting in oversized synaptic junctions;
• a loss of electrical conductivity of the synaptic fluid between nerve cells; and
• 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 of accomplishing 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 (see Figure 2).This adds to the impairment of effective nerve transmission.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 electrical signals of the normal nerves across this gap.

As a result of hypoxic cellular atrophy, nerve signals must now try to jump a larger gap through a less conductive medium.This loss of nerve transmission is first perceived as tingling, then burning, and finally as pain when the demineralization and gap-widening process progresses. The initial perception associated with atrophied nerves and enlarged synaptic gaps is tingling as some of the normal signals are misdirected to nearby nerves. As the condition progresses, it happens more and more until more signals are misdirected then properly propagated, and the resulting sensation is one of pain. Finally, after the nerve signals can no longer be transmitted at all, numbness is the primary complaint.This secondary effect of neuropathy reduces the strength of the calf muscles, which, in turn, reduces the blood flow to the lower extremities. This condition often results in poor tissue perfusion, insecure gait, balance problems, and other mobility issues.