Point-Counterpoint: Nerve Decompression In Diabetic Patients: Should It Be Done?
Yes. This author discusses the etiology of diabetic peripheral neuropathy, cites reports of efficacy for peripheral nerve decompression in the literature and shares insights from his experience in performing the procedure. By Stephen L. Barrett, DPM Mainstream medical education is still teaching that the symptoms of diabetic peripheral neuropathy are progressive and irreversible. There is adequate and overwhelming basic and clinical medical science that contradicts this dogma.1-5 Indeed, one wonders how many additional outcome studies are needed in addition to those already reported before we achieve a better collective understanding of the etiology of symptoms in diabetic peripheral neuropathy. Additionally, we have also learned it is not safe to operate on patients with diabetes. However, that paradigm has recently shifted with the plethora of literature supporting Charcot reconstruction and other palliative procedures in patients with diabetes. It is interesting that we are still debating this issue when the basic medical science and clinical results have been available for many years. Prior to any discussion of this topic, it is imperative to stress that no one can surgically treat diabetic peripheral neuropathy. However, with proper selection criteria, peripheral nerve surgical decompression/neurolysis can be highly successful in patients who have superimposed chronic nerve entrapments that cause most of their symptoms of diabetic peripheral neuropathy.
What The Literature Reveals About The Etiology Of The Condition
Volumes have been written on the metabolic pathways that are involved in the development of diabetic peripheral neuropathy. In 1978, Jakobsen made rats diabetic with injections of streptozotocin. Their sciatic nerves developed endoneurial and subepineurial edema, resulting in a larger cross sectional area. The diabetic rats were heavier in comparison to the non-diabetic control group.6 The concept of “double crush” or multiple crush syndrome is well established in peripheral nerve physiology.7 Diabetes is known to act as the first “crush” of peripheral nerve entrapment. Chronic nerve compression studies have conclusively documented a cascade of histological events, beginning with the loss of the blood nerve barrier and ending with severe demyelination and axonal degeneration. It is well known that the peripheral nerve in patients with diabetes is more susceptible to chronic nerve compression due to endoneurial edema, decreased axoplasmic flow, which impairs neural repair, and glycosylation of collagen that makes the nerve stiffer. For those who are contemplating peripheral nerve decompression surgery, it is imperative to understand the etiological difference between neuropathic conditions. There is neuropathy that begins with axonal degeneration from the actual metabolic nature of whatever neural disease is present. Then there are neuropathies in which chronic nerve compression, due to an edematous “swelling” of the neve, ultimately ends up leading to axonal damage. When the neuropathic disease process directly affects the neuron, there is usually no role for peripheral nerve decompression surgery.8 Perhaps the most compelling argument from a basic medical science perspective comes from MacKinnon and Dellon’s Textbook of Peripheral Nerve Surgery.8 They clearly demonstrate astounding histological differences in a diabetic primate via photomicrographs of the ulnar nerve from two different anatomical sites. The authors compare a cross section of the ulnar nerve in the mid-upper arm, where there is no known site of anatomical compression, to a second photomicrograph of the same nerve (just several centimeters distal to the first photo) from the cubital tunnel, a known site of anatomical entrapment. The comparison of these photomicrographs reveal significant histological changes of nerve degeneration with loss of myelination.8 Clearly, if diabetic peripheral neuropathy were solely a disease of the axon as so many believe and are still teaching, then how could that explanation account for this tremendous histological difference in the same nerve only centimeters apart?