Preventing Foot Ulceration and Amputation by Decompressing Peripheral Nerves in Patients with Diabetic Neuropathy

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Author(s): 
A. Lee Dellon, MD

Susceptibility to Compression

Two metabolic changes in the peripheral nerves of the patient with diabetes render the nerve susceptible to chronic compression. The most critical metabolic change is the increased water content and subsequent increased volume within the nerve as a result of glucose being metabolized into sorbitol.1 The second metabolic change is a decrease in the slow anterograde component of axoplasmic flow.2 This component of axoplasmic flow transports the lipoproteins necessary to maintain and rebuild the nerve. The peripheral nerve, as it crosses known areas of anatomic narrowing (eg, carpal tunnel at the wrist, cubital tunnel at the elbow, fibular tunnel at the outside of the knee, and the tarsal tunnel at the ankle), passes through a region of increased external pressure. Because the peripheral nerve in the patient with diabetes has an increased volume, pressure on the nerve in each of these anatomic regions is increased.

This increased external pressure creates an increased intraneural pressure that decreases blood flow,3 resulting in a relative ischemic condition for the peripheral nerve. The neurophysiologic consequence of decreased blood flow in a peripheral nerve is the perception of paresthesias, interpreted centrally as numbness and tingling. The chronic pathophysiologic result of this area of increased pressure along a peripheral nerve is demyelination. The peripheral nerve with decreased axoplasmic flow, as in the person with diabetes, cannot transport sufficient protein structures to rebuild itself. Additionally, advanced glycosylation end (AGE) products reduce the normal gliding ability of the peripheral nerve. The nonenzymatic binding of glucose to the collagen within the nerve and in the epineurium are the basis for decreased elasticity. The combination of decreased peripheral nerve elasticity and its normal physiologic requirement to stretch as it glides across joints increases the stress and strain of the peripheral nerve within the areas of known anatomic narrowing. This increasing tension along the nerve further decreases blood flow within the nerve.4

The hypothesis that the peripheral nerve in the person with diabetes has an increased susceptibility to compression has been tested in the rat model.5 A group of rats was rendered diabetic by administering streptozotocin. Silicone bands were placed around the sciatic nerves of the diabetic rats and a control group of nondiabetic, age-matched rats. After 6 months of banding (a time interval demonstrated to be sufficient to develop electrophysiologic and histologic changes consistent with chronic nerve compression in this model6), electrophysiology was tested in both groups. The diabetic rats had a statistically significant lower conduction velocity and a statistically significant lower amplitude for the sciatic nerve measured across the region of compression than did the nondiabetic banded rats, confirming that the peripheral nerve has an increased susceptibility to chronic nerve compression in the diabetic rat.

References: 

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