Rethinking The Role Of The 5.07 Semmes-Weinstein Monofilament

Stephen Barrett DPM FACFAS

As a deputized epidermal protector, I was overcome by sadness as I read the report from Ferreira and colleagues.1 How could this be? I had always believed in this sacred agent, this bodyguard of all bodyguards. Surely, the report must be mistaken. Could this be a rogue report?

Agent 5.07’s reputation is legendary. Just ask anyone who deals with trying to prevent ulceration and potential amputation. Read any dossier and they all glowingly and unabashedly espouse that 5.07 will give patients with diabetes all the protection they need.2-5 Really, legend has it that agent 5.07 can rip up 007’s butt faster than “Q” can whip up a new exploding ballpoint pen.

Who is this agent 5.07 anyway? Well, he is a skinny nylon fellow whose ancestry traces back to the hair of a horse (the Von Frey filament). He has a family of 20 siblings of varying diameters but hardly anyone knows the other members of this “family.” The 5.07 is the filament with all the clout and up till now, there was never a doubt. Like all the other siblings, the 5.07 was the 1950s brainchild of Sidney Weinstein, MD, a neuropsychologist from New York. Weinstein apparently worked with this very adept neurophysiologist named Josephine Semmes, MD, and they started training their “agents” in trying to map out the cortical map of a monkey brain.6 Then, like needing another hole in their head, they started to study stereognosis in wounded soldiers from the Korean War with penetrating bullet injuries to their brains.

Ergo, the Semmes-Weinstein monofilament (SWM) is born.

Now I know what you are thinking. Why is Semmes’ name first? Why don’t we call it the Weinstein-Semmes? You would have to ask Weinstein himself but rumor has it that he respected Semmes’ work so much he wanted to pay tribute to her. If you read about him, his body of work is immense.

As we know from many examples of history, legend is legend and not necessarily fact. Agent 5.07 was never intended to be a solo agent. He just got the “rep” that has been widely and, to a probably very large extent, nearly completely misunderstood by even those using it as a prod every clinical day.

This family of agents starts with the little whisker: 1.65 (0.008 g of force) and ends with big brother coming in at 300 g of force being called the 6.65. Interestingly, the whole family is the same height: 38 mm. There are 18 others, the 5.07 being one of them in between.

So there is this huge misinterpretation out there that the 5.07, for example, measures about 5 g of force. Not so fast, my furious Meissner corpuscle evaluator. No sir, these markings are a representation of the logarithmic function to the base 10 in tenths of milligrams.7 So going from a 5.07 monofilament to a 6.1 takes that sensory end organ power punch from a 10 g hit to a 100 g hit.

Wow, now that is a big gap, isn’t it? How does that play in the real world? What if that “protected” foot got whacked with only a 2 g “love tap” by agent 4.31 and couldn’t feel it? Maybe treatment would start earlier and save that patient.

Well, we know from reading the “report” from Ferreira and colleagues that the 20 patients in their study all had an ulcer in one extremity and all could feel the 5.07.1 Twenty people with ulcers and all could feel agent 5.07 sneaking up on them. I would proffer that agent 5.07 isn't exactly a good protector.

Testing For Protective Sensation: What You Should Know

Here are some nerve facts that we need to pack into the noggin.

1. One-point discrimination is crude from a cortical perspective. Two-point discrimination is much more difficult for the cortex to determine and therefore may be more sensitive for assessment of protective sensation.

2. The big fibers (sensory A beta) are affected by compression first. The unmyelinated (A delta and C) fibers can withstand compression longer. Therefore, measurements of temperature and pain do not give us as early of a warning because those fibers are not affected early in compression.

3. The Semmes-Weinstein monofilaments (especially when using just one like the 5.07) do not make a quantifiable measurement. They only, if one uses a series, can give an estimate of range of sensitivity.

4. The monofilaments wear out. After 100 uses, they can have a 10 percent variability. This is not to mention that when they come out of the box, there is a given variability of at least 10 percent.7

5. If we were going to rely on one monofilament, why not pick a little brother down the line like the 4.31 (2.0 g of force)? My bet would be that there would be more protection from this agent and many fewer epidermal breaches.

What One Study Reveals

Now turn to a very interesting article by Arad and colleagues.9 Their 2011 Diabetes Care study makes a couple of compelling statements. In my opinion, the following statement from the study is the most important.

“Indeed, although the graded SWM is widely used in practice to diagnose or screen for neuropathy, to document insensate feet, and to predict foot ulcers, repeated further testing with the SWM does not yield any useful information. Therefore, most patients with insensitive feet are referred for ‘preventative podiatry care’ and specialized shoes, but no attempt is made to target more aggressive prevention in those highest risk individuals.” (the bold emphasis is mine)

Final Notes

This is our professional calling folks. What more could these authors ask of our podiatric profession? We know that with lower extremity peripheral nerve decompression, we can change the history of the patient with diabetes and prevent the development of ulceration and potential amputation in this high-risk patient group.10-12

This is the biggest chance in the history of our podiatric profession to alter healthcare, positively impact the global economics of our nation, integrate and establish podiatric surgery to a higher and deservedly respected level, and most importantly help those many patients who are going week after week to the wound care centers.

I ask you to do two things. First, look at the way you are evaluating these high-risk patients with agent 5.07 and call in some of his co-operatives to get at least an estimate of range of sensibility—before the hole (ulcer) appears. Second, go to the Association of Extremity Nerve Surgeons website: (now an affiliate group of the American Podiatric Medical Association) and get involved. Let’s save some legs and be a hero for someone out there.


1. Ferreira MC, Vieira SAT, Carvalho VF. Comparative study of the sensitivity of diabetic lower extremities with and without ulcers using the PSSD. Acta Ortop Bras [online] 2011; 18(2):71-74.
2. 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(1):168-72.
3. Kochman AB, Carnegie DH, Burke TJ. Symptomatic reversal of peripheral neuropathy in patients with diabetes. J Am Podiatr Med Assoc. 2002; 92(3):125-30.
4. Modawal A, Fley J, Shukla R, et al. Use of monofilament in the detection of foot lesions in older adults. J Foot Ankle Surg. 2006; 45(2):76-81.
5. Jeng S, Michelson J, Mizel M. Sensory thresholds of normal human feet. Foot Ankle Int. 2000; 21(6):501-4.
6. Weinstein S. Fifty years of somatosensory research: from the Semmes-Weinstein monofilaments to the Weinstein Enhanced Sensory Test. J Hand Ther. 1993; 6(1):11-22; discussion 50.
7. Dellon AL, Mackinnon SE, Brandt KE. The markings of the Semmes-Weinstein nylon monofilaments. J Hand Surg Am. 1993; 18(4):756-757.
8. Yong R, Karas TJ, Smith KD, Petrov O. The durability of the Semmes-Weinstein 5.07 monofilament. J Foot Ankle Surg. 2000; 39(1):34-38.
9. Arad Y, Fonseca V, Peters A, Vinik A. Beyond the monofilament for the insensate diabetic foot: a systematic review of randomized trials to prevent the occurrence of plantar foot ulcers in patients with diabetes. Diabetes Care. 2011; 34(4):1041-1046.
10. Aszmann O, Tassler PL, Dellon AL. Changing the natural history of diabetic neuropathy: incidence of ulcer/amputation in the contralateral limb of patients with a unilateral nerve decompression procedure. Ann Plast Surg. 2004; 53(6):517-522.
11. Biddinger KR, Amend KJ. The role of surgical decompression for diabetic neuropathy. Foot Ankle Clin. 2004; 9(2):239-254.
12. Wood WA, Wood MA. Decompression of peripheral nerves for diabetic neuropathy in the lower extremity. J Foot Ankle Surg. 2003; 42(5):268-275.


I followed this topic with great interest several years ago when there seemed to be a boom in treating diabetic peripheral neuropathy with nerve decompression techniques in the OR. I did several and although it could have been my technique, the results were less than satisfactory for my patients and I.

If you do a Pubmed search, you will find that there are several studies that disprove the efficacy of this surgical technique with the desired result.

Also, I didn't notice if you discussed using a biothesiometer at all. It is an expensive device but I believe it to be the most accurate way to assess protective sensation. Is this correct?

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