Does Surgical Decompression
for Symptomatic DPN Have a Place?

A number of evidence-based reviews for the treatment of diabetic neuropathies (DPN) have been published recently.1 Based on an all published material, the American Diabetes Association (ADA) has reviewed the evidence for treatment of autonomic neuropathy2 as well as somatic neuropathy3 and arrived at a position statement on recommendations for the treatment of diabetic neuropathies.4 The position statement supports an active pursuit of identifying patients with entrapment syndromes, and if proven, recommends medical or surgical therapy as deemed appropriate.

Surgical decompression of multiple nerves, however, is being used to treat common or garden-variety symptomatic DPN based on the hypothesis that diabetic nerves are more vulnerable to compressive injury and subject to a double crush. The first crush is metabolic, microvascular and autoimmune abnormalities and neurotrophin deficiency; the second is entrapment which occurs in confined compartments such as the tarsal tunnel. While this may be true, there are data to the contrary, ie that diabetic axons are really resistant to compression.5 Up to one-third of patients with diabetes have an entrapment syndrome, thus, it has become mandatory to distinguish entrapment from DPN, as well as its superimposition upon DPN.6 See related articles on pages 20 through 25.

Notwithstanding this difficulty in identifying appropriate patients for decompression, more than 240 surgeons in 41 states in the United States and 15 countries have been trained to perform decompression surgery. As recently reported (Chaudry et al Neurology, 2006, 66: 1805-1808), as of January 2006, 1,280, surgeries on 990 patients by 34 surgeons have been registered (www.neuropathyregistry.com). A literature search using Medline, EMBASE and PUBMED found 75 articles using the key words, diabetes mellitus, diabetic neuropathy and decompression and two more since this search. Only 11 articles dealt with decompressive surgery for DPN and only one that was prospective. In this study of 20 patients, 22% had nerve compression, 56% had DPN and 22% had DPN without nerve compression — the details of which were not provided. As indicated it can be difficult to discern but is mandatory if we are to pick those people who might be appropriate for surgical decompression.

Unfortunately, despite the contention that a positive Tinel’s sign identifies those people with entrapment superimposed upon DPN, there is a very high false positive and false negative rate. In a study of 1,528 hands diagnosed as having carpal tunnel syndrome, Nora et al7 reported that a Tinel’s sign was positive in only 34% and the Phalen’s sign in 56%. Much more distressing was the fact that there was a high false positive rate in patients with fibromyalgia and tendonitis. Thus, one would have to exercise extreme caution in using this sign as a determinant of candidates for surgical decompression.

Clearly the gold standard for diagnosis of nerve entrapment is nerve conduction demonstrating a block at the site which should be mandatory. In a study of 4,600 patients using the NC Stat system of measurement of nerve conduction at sites of possible entrapment it was extremely rare to find patients with entrapment of the tibial nerve that could be distinguished from DPN. In the reported results it has furthermore been impossible to determine if the improvements in nerve conduction have been in patients with DPN or those that actually have an entrapment. While the ADA strongly supports seeking out patients with entrapments who might benefit from decompression, it does not condone surgery in the absence of demonstrable entrapment.4

In the 10 nonblinded case series, eight of 10 studies reported pain relief by the operating surgeon 80% to 92% of the time even on the operating table recovering from the anesthetic. Patients have been evaluated pre and postoperatively for two-point discrimination using the Pressure-specified Sensory Device (Sensory Management Services, LLC, Baltimore) and reported an improvement in 67% to 89% of those studied who had the combined procedure of decompression of the posterior tibial, deep peroneal, common peroneal at the ankle and knee as well as the ulnar and median nerves. Studies on quantitative sensory perception in DPN have shown that there is >90% sensitivity and specificity (receiver operation characteristics) when using vibration detection threshold (VDT) and cold thermal perception (CDT). No such information is available, however, on two-point discrimination used by this cadre of surgeons. Furthermore, the variance of even CDT and VDT can be as high as 10% to 15%, making these measures unreliable as endpoints in clinical studies. Moreover, it has now been demonstrated that mechanical noise using stochastic resonance can improve detection thresholds for pressure and vibration8 or even tactile coactivation.9 If only symptoms are being reported, as has occurred in the 12 reported studies, this may be no better than magnet-field therapy,10 percutaneous electrical nerve stimulation11 or infrared therapy.12 all of which have been claimed to achieve improvement in symptoms at least on a short-term basis and are noninvasive. Additionally, the results of several large 6- to 12-month clinical trials of diabetic neuropathy have been besieged by the placebo effect (Vinik Medscape) in which there have been improvements not only in symptoms but in objective measures of neuropathy presumably related to better hygiene, cessation of smoking, the use of statins and ACE inhibitors among the possible variables that affect the symptom complex of neuropathy (Tesfaye ADA abstract). An extreme example of the placebo effect involved the Middlesex Hospital when 194 patients were placed on a waiting list for arthroscopy. Eighty seven (67 men) had waited >1 year with suspected meniscal tears, degenerative joint disease, ligamentous instability and sundry other complaints. At the end of a year 67% of patients who had not had surgery had recovered spontaneously!

In summary, tarsal tunnel release is being advocated as a procedure for common or garden DPN in the absence of entrapment even if there is no sign of recoverable nerve function!13 Unfortunately the studies reported have been of poor quality and design and it has not been possible to discern the differences in patients being treated who have only DPN from those who have an entrapment who might indeed have benefited. The standard testing of the individuals has not been blinded and only within subjects studies are reported which are notoriously unreliable. Standard testing of distal sensory loss of small and large fiber function, eg VDT and thermal perception, strength, reflexes and nerve conduction using validated instruments would be helpful. There is a need to grade severity of entrapment, use measures of sensory tests that have been validated, the presence of a Tinel’s sign, the presence of motor features and atrophy before considering surgery.14

We would recommend that before considering surgery the following caveats should be added:
• A conduction block must be present at the site proposed for decompression;
• There should not be such severe neuropathy as to preclude distinction from entrapment;
• Control sham operations should be compared with decompression for relief of symptoms if these are the only measure made; and

Objective standardized measures should be employed before and after the intervention to show bona fide improvement in nerve function.

As pointed out in a recent report from the American Academy of Neurology (Neurology. 2006,66:1805-1808) the utility of surgical decompression for symptomatic diabetic neuropathy would in their minds receive a Grade 1V rating, ie evidence from uncontrolled studies, case reports or expert opinion and assign the evidence a U grading which translates to unproven, the data being conflicting given the current knowledge and treatment not recommended at this point in time. Thus as I have previously concluded “there may be a place for surgical decompression of nerves in DPN but we have yet to find it”.

1. Vinik A, Ullal J, Parson H, Casellini C. Diabetic Neuropathies: clinical manifestations and current treatment options. Nature Clinical Practice Endocrinology & Metabolism. 2006; 5:269-281.
2. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic Autonomic Neuropathy. Diabetes Care. 2003;26:1553-1579.
3. Boulton A, Malik T, Arezzo JC, Sosenko J. Diabetic somatic neuropathies:technical review. Diabetes Care . 2004;27:1458-1486.
4. Boulton AJ, Vinik AI, Arezzo JC, Bril V, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care. 2005;28:956-962.
5. Tomlinson DR, Fernygough P.: Neurotrophism in diabetic neuropathy. In Frontiers in Animal Diabetes Research. Chronic complications in diabetes. 1st ed. Sima AAF, Ed. Amsterdam, Harwood, 1999, p. 167-182.
6. Vinik AI, Emley MS, Megerian JT, Gozani SN. Median and ulnar nerve conduction measurements in patients with symptoms of diabetic peripheral neuropathy using the NC-stat system. Diabetes TechnolTher. 2004;6:816-824.
7. Nora DB, Becker J, Ehlers JA, Gomes I: What symptoms are truly caused by median nerve compression in carpal tunnel syndrome? Clin Neurophysiol. 2005;116:275-283.
8. Khaodhiar L, Niemi JB, Earnest R, et al. Enhancing sensation in diabetic neuropathic foot with mechanical noise. Diabetes Care. 2003;26:3280-3283.
9. Dinse H, Kleibel N, Kalisch T, et al. Tactile coactiviation resets age-related decline of human tactile discrimination (Abstract). Ann Neurol. 2006.
10. Weintraub MI, Wolfe GI, Barohn RA, et al. Magnetic Research Group: Static magnetic field therapy for symptomatic diabetic neuropathy: a randomized, double-blind, placebo-controlled trial. Arch Phys Med Rehabil. 2003;84:736-746.
11. Hamza MA, White PF, Craig WF, et al. Percutaneous electrical nerve stimulation: a novel analgesic therapy for diabetic neuropathic pain. Diabetes Care. 2000;23:365-370.
12. Leonard DR, Farooqi MH, Myers S. Restoration of sensation, reduced pain, and improved balance in subjects with diabetic peripheral neuropathy: a double-blind, randomized, placebo-controlled study with monochromatic near-infrared treatment. Diabetes Care. 2004;27:168-172.
13. Vinik A, Mehrabyan A, Colen L Boulton A. Focal entrapment neuropathies in diabetes. Diabetes Care. 2004; 27:1783-1788.
14. Carneiro, R. Carpal tunnel syndrome: The cause dictates the treatment. Cleve Clin JMed. 1999; 66:159-164.
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