Restoring Sensation In Diabetic Patients
Statistics from the American Diabetes Association (ADA) reveal there were 86,000 amputations due to complications from diabetes mellitus in 2000. The ADA also points out that 50 to 70 percent of these patients will develop peripheral neuropathy sometime in the course of their disease.1
The most widely believed paradigm in mainstream medicine today is that loss of sensation in diabetic peripheral neuropathy is irreversible and the only treatment available is the achievement of euglycemic control and the ancillary use of medicines such as Elavil and Neurontin.2 Sadly, this belief is wrong. Even though this type of treatment may relieve some of the pain associated with diabetic peripheral neuropathy, this does nothing to re-establish sensation, which will prevent ulceration and potential amputation.
Examining The Pathophysiology Of Diabetic Peripheral Neuropathy
Jakobsen, in 1978, demonstrated the peripheral nerve in the diabetic rat increases in size by up to 50 percent and can become 50 percent heavier in cross-sectional volume when compared to a non-diabetic peripheral nerve.3 It was also shown that the diabetic peripheral nerve is more susceptible to injury than a non-diabetic nerve. It has also been well demonstrated that glycosylation of collagen, another of the systemic sequelae of diabetes, can predispose the diabetic patient to carpal tunnel syndrome.4 This is due to the fact that with the glycosylation of collagen, normal anatomical tunnels will become smaller and more constricted than in a non-diabetic situation. With a nerve that is anatomically larger in diameter and a smaller more constricted anatomical tunnel (i.e. the tarsal tunnel), this sets up an ideal situation for a chronic nerve entrapment.4
In summary, these are two metabolic changes in the peripheral nerves of the diabetic that render the nerve susceptible to chronic compression. There is increased water content within the nerve as the result of glucose being metabolized into sorbitol and there is a decrease in the slow anterograde component of axoplasmic transport.3,5
As we can see in the first photomicrograph (see top left photo), the ulnar nerve in a type 1 diabetic primate is stunningly normal. This section was taken from an area of no compression. While there is some mild “knuckling” of myelin, the axons appear with good myelination. There is a significant amount of endoneurial edema and sub-epineurial edema, but nothing in this section would indicate there would be difficulty with transmission of action potentials in these neurons. The second photomicrograph (see middle right photo) is the same ulnar nerve, taken under a higher power.
The third photo (see bottom left photo) was taken just several centimeters distal to the section in the first and second illustration from the area of a known site of entrapment—the cubital tunnel. It is hard to believe this photomicrograph is of the same peripheral nerve, as there is a significant axonopathy and destruction of myelin. These changes are due to a chronic nerve entrapment. The same metabolic process has affected both cross sections of ulnar nerve. Therefore, it would be impossible to attribute anything but a superimposed chronic entrapment as the etiology of this neural change.
Dellon, et. al., demonstrated this in rats in 1994.6 In this study, they took non-diabetic rats and made them diabetic by injecting them with streptozotocin, which, in effect, killed their islet cells in their pancreases with resultant blood sugars of 400 gm/dl. Walking track prints of these rats’ paws were made before and after they became diabetic. There was a significant splaying degradation of the paw print after the effects of diabetes, compared to the initial prints.
The researchers performed tarsal tunnel decompressions on similar weight-controlled rats. The rats were again rendered diabetic with blood sugars of 400 and researchers monitored their walking track patterns. There was no splaying or degernation of the paw print in contrast to those rats that were not decompressed.6