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There are three broad types of neuropathy associated with diabetes: sensory, autonomic and motor: Sensory or peripheral neuropathy (usually referred to as neuropathy) affects the nerves that carry information to the brain about sensations from various parts of the body – how hot or cold something is, what the texture of something feels like, the pain caused by a sharp object or heat, etc. This is the most common form of diabetic neuropathy.

Autonomic neuropathy affects the nerves that control involuntary activities of the body, such as the action of the stomach, intestine, bladder and even the heart. Motor neuropathy affects the nerves that carry signals to muscles to allow motions like walking and moving fingers. This form of neuropathy is very rare in diabetes. Sensory neuropathy can lead to pain, numbness or tingling in the extremities and, ultimately, an inability to feel heat, cold, pain or any other sensation in affected areas. Autonomic neuropathy can lead to impotence in men, bladder neuropathy (which means the bladder is unable to empty completely), diabetic diarrhea, or bloated stomach. Motor neuropathy can lead to muscle weakness.


Peripheral neuropathy is a general term for diseases that cause damage to the nerves outside of the brain and spinal cord. While diabetes is a frequent cause of neuropathy, it is not the only cause. Nutritional deficiencies (B-12 and folate), chemical exposures, pressure on nerves, or medications (such as some of those used for chemotherapy or to treat AIDS), can also cause neuropathy. Theories abound as to why exactly neuropathy occurs in people with diabetes. In general, diabetic neuropathy is thought to be a result of chronic nerve damage caused by high blood sugars. Nerves are surrounded by a covering of cells, just like an electric wire is surrounded by insulation, called Schwann cells. One theory suggests that excess sugar circulating throughout the body interacts with an enzyme in the Schwann cells, called aldose reductase. Aldose reductase transforms the sugar into sorbitol, which in turn draws water into the Schwann cells, causing them to swell. This in turn pinches the nerves themselves, causing damage and in many cases pain. Unless the process is stopped and reversed, both the Schwann cells and the nerves they surround die.

The application of photobiostimulation to these cells prevents or reverses these biochemical processes that cause this damage. The resulting increased circulation removes excess fluid from the Schwann cells, thereby removing any possible pressure necrosis to the rest of the nerve cell, and provides a vehicle to remove cellular waste such as sorbitol. Another theory is that certain intracellular metabolites, such as myoinositol, become depleted, leading to nerve damage. Other theories hold that pathways such as the protein kinase C pathway are triggered by chronic high blood sugars, resulting in several diabetes complications, including neuropathy.

Laser therapy applied to these nerve cells stimulates the mitochondria within the nerve cell and increases the respiratory rate of these individual cells. Therefore, intracellular metabolites do not have a chance to become depleted and the production of any destructive protein kinases is halted Pain relief is also accomplished in the diabetic patient through the following mechanisms:

  • Increased nerve cell action potentials
  • Ion channel normalization
  • Blocked depolarization of C-fiber afferent nerves

Healthy nerve cells tend to operate at about -70 mV, and fire at about -20 mV. Compromised cell membranes have a lowered threshold as their resting potentials average around this -20 mV range. That means that normal non- noxious activities, such as touching, produce pain. Laser therapy can help restore the action potential closer to the normal -70 mV range.

This is accomplished by ion channel normalization. Photobiostimulation promotes normalization in Ca++, Na+ and K+ concentrations across the cell membrane, resulting in pain reduction as a result of these ion concentration shifts.

The pain blocking effect of photobiostimulation can be pronounced, particularly in low velocity neural pathways, such as non-myelinated afferent axons from nociceptors. Laser irradiation suppresses the excitation of these fibers in the afferent sensory pathway.