Peripheral Neuropathy Overview
Peripheral neuropathy is a condition that involves different types of common nerve disorders. These nerve disorders (generally involving the legs) are caused by inflammation or by vascular injury.
Peripheral Neuropathy Symptoms
Hypersensitive feet characterize symptoms of peripheral neuropathy. Patients will complain of numbness, “pins and needles” (paresthesias) and foot pain-especially burning type foot pain. Light touch can be ultrasensitive and very disagreeable. This touch may feel like a blowtorch across the skin (a condition called allodynia).
Some patients will complain that their feet “feel like wood” which is due to loss of sensation. Loss of proprioception (position sense) may lead to problems with balance during walking.
Most of these symptoms tend to be worse at night and some patients cannot tolerate the covers touching their feet (again hypersensitivity due to allodynia). The symptoms can progress over time and slowly extend up each leg. If these symptoms eventually rise up to the knees, the hands can become involved (called stocking and glove distribution).
Typically, all these symptoms are symmetrical (occur equally in each foot).
Patients with diabetes are more susceptible to peripheral neuropathy but many patients without diabetes can develop this disorder. In cases without a preexisting disease process, the disorder is called idiopathic peripheral neuropathy.
Are you suffering from symptoms of Peripheral Neuropathy?
There are two ways to consult with Dr. Corenman about your condition:
You can provide current X-rays and/or MRIs for a clinical case review.
You can schedule an office consultation that should be covered by your insurance.
(Please keep reading below for more information on this condition.)
Physiology (how the nerve cell works)
The reason these nerves become sick has to do to their length. Nerve cells are the longest cells in the body. The nerve cells in the leg can reach over three feet in length. Herein lies the problem.
The longer the length of the cell, the further away the cell nucleus is from the end of the nerve. The nucleus is both the “brain” of the cell and the manufacturing plant that makes certain protein-based machines (called organelles) to keep the nerve functioning. These little protein machines consist of tiny power plants (called mitochondria) and specialized pumps that attach to the nerve cell membrane to act as receptors and gates.
These organelles embedded in the cell membrane wear out over time and need to be replaced. New organelles have to be manufactured by the nucleus and transported down to the end of the nerve to maintain proper cell health.
The transportation system within the nerve is called the microtubule and there are many within the nerve cell. These tubules act as railroad tracks and allow substances to be transported to the end of the nerve. This pathway is called the axoplasmic flow. This flow can be interrupted by damage to the microtubules or loss of energy to the mechanism that transports these structures. This energy is derived from ATP from the mitochondria, which in turn requires adequate blood flow from the arteries on the nerve cell membrane.
Any interruption to this pathway can cause dysfunction at the end of the nerve. Obviously, longer nerves have a greater chance of interruption to this flow pattern.
The nerve cell, to function properly has to have an electrical charge across its membrane. The sodium/potassium pump is the mechanism that allows the nerve cell membrane to develop this electrical charge. These pumps (made out of the aforementioned protein machine/organelles embedded in the cell membrane) will pump in potassium and pump out sodium atoms through the cell membrane. The changes in concentration of sodium and potassium are responsible for the electrical change in the nerve membrane.
This pump mechanism requires a substance called ATP, the gasoline of the cell engine. The organelle that makes the ATP is the mitochondria- again made in the nucleus.
The raw material the mitochondrion needs to manufacture ATP derives from glucose and oxygen. Both of these essential substances are delivered by the blood stream through the vaso nervorum, the small network of blood vessels on the outside of the nerve membrane. Interruption of the blood supply to the nerve can starve the mitochondria and a loss of power to the cell is the result.
The further down the nerve, the more tenuous the blood supply is. The longer nerves have more problems with blood supply.
Keeping the nerve membrane polarized is somewhat like keeping up with a small leak in a boat. If you don’t use the bilge pump to pump out the water fast enough, the boat will eventually fill up with water and sink. The bilge pump needs lots of energy to keep it pumping.
This is the same condition with the nerve cell. The nerve membrane is leaky. This membrane has to continually pump out sodium and pump in potassium to keep the proper electrical charge across the nerve membrane. If this “bilge pump” (sodium/potassium pump) is not continuously going, the sodium will eventually leak back into the cell and cause the nerve to malfunction.
Keeping this sodium/potassium pump going requires much energy using ATP, making the nerve cell one of the hardest working cells in the body. In fact, 70% of the ATP manufactured in the nerve cell is used to power the sodium/potassium pump.
The ATP pump requires glucose and oxygen through the blood supply on the nerve root (the vasonervorum). Loss of this blood supply will cause the nerve to malfunction.
Myelin Sheaths (nerve insulation)
The larger nerves are insulated just like copper wires in a house. The insulation is not continuous but interrupted at small junctions. This insulation allows the nerve to conduct faster than if it was not insulated. The nerve will conduct slowly or not at all if the insulation is damaged. There are some peripheral neuropathy disorders that can injure the myelin sheath. This generally causes similar symptoms as the other neuropathy disorders.
Nerve Membrane or Blood Vessel Injury
So now you can see that there are four potential ways a long nerve cell can malfunction. One is the damage to the nerve cell membrane itself by white blood cells (an autoimmune mechanism). The second is damage to the insulators (the myelin sheath) again by a white blood cell attack. The third is the inability to transport the little protein machines down the railroad tracks (the microtubules). The last is the lack of fuel (oxygen and glucose) brought about by the damage to the blood supply.
Inflammation (due to any inflammatory condition like Lupus or Lyme disease) will cause white blood cells to migrate to the nerves and release chemical factors that actually attack the nerves. These factors can injure and sensitize the nerve. The result is either to block the message (numbness) or produce a discharge of the nerve membrane and send an aberrant signal. Either the nerve cell membrane itself (edema) or the myelin sheath that surrounds the nerve can be damaged. With either case, symptoms will occur.
The vasonevorum is the blood supply on the outside of the nerve (there is no blood vessel inside the nerve). Commonly, these blood vessels become injured (by increased sugar due to diabetes or an inflammatory disorder like Lupus) and the blood supply to the nerve diminishes.
Nerve cells work hard and require a substantial supply of fuel to keep functioning normally. Unfortunately, nerve cells do not have any fuel reserves and depend upon this abundant blood supply to continue the flow of fuel necessary for proper function.
Any interruption of this blood supply will cause the nerve to dysfunction. The simple experiment of resting your elbow on a hard surface and having your hand “fall asleep” is all the proof you need to understand how easy it is to interrupt this energy reserve.
Without this blood supply, the mitochondria cannot do its job making ATP. Without ATP, the nerve membrane sodium/potassium pump cannot do its job. Remember that the nerve membrane is somewhat leaky and will trigger a message if the sodium is not pumped out continuously. Also, transport of essential proteins may be hindered by the lack of a blood supply leading to dysfunction of the longest nerves. f
The symptoms noted depend upon the particular nerve that is triggered. If a nociceptive nerve is triggered, pain will result. If a proprioceptive nerve is triggered, “pins and needles” will be noted.
The opposite problem can also occur at the same time. If the nerve membrane is damaged by injury to the insulating sheath (the myelin sheath), the nerve signal can be blocked. Numbness and lack of position sense (position sense is knowing where the foot or leg is in space without looking) will result. Patients will complain that their feet “feel like a block of wood” or “I’m walking on stumps” and walking becomes difficult.
Treatment of Peripheral Neuropathy
There is no cure for peripheral neuropathy but there is treatment available. Treatment recommended by many physicians consists of medications such as membrane stabilizers (Lyrica and Neurontin/gabapentin), painkillers and anti-inflammatories.
Change in shoes to more comfortable, loose fitting shoes can be helpful. A rocker bottom sole can occasionally help as well.
Spinal cord stimulation can also be helpful for severe cases.
For additional resources on peripheral neuropathy, or to schedule a consultation with spine specialist and neck doctor Dr. Donald Corenman, please contact his Vail, Aspen, Denver and Grand Junction, Colorado office.