”How long does it take to work and how long will it last?”
The most common questions asked by patients with neuropathy are as follows.
Question 1: “Am I a good candidate for this procedure?” I often interpret this question as “Do I have a chance of success?”
Question 2, “How long will it take to recover from the surgery?” I would interpret this as “When will my pain go away and when will I be able to feel my foot again?”
Question 3, “How long will the results last?” I would interpret this as “If it works, will the pain and swelling come back?”
Now let’s answer them one by one.
Question 1: Probability of success
When evaluating a patient with neuropathy, I first try to determine if there is a nerve compression somewhere, and I tap along the area of the nerve where the compression is likely to occur. During tapping, if there is pain and tingling in the symptomatic area, this is considered a positive “Tinel’s sign”.
If the Tinel’s sign is positive, then the probability of success in relieving the symptoms by nerve decompression is at least 80%.
Question 2: How long does it take to get results?
Every patient with neuropathy can be examined by a pressure specific sensitometry (PSSD). It measures the sensitivity of the skin and relates it to clinical symptoms. In 1989, I developed a computer-assisted neurosensory test that can help measure peripheral nerve function in neuropathy by means of point touch pressure. The PSSD can provide better information than those fine nylon filaments known as Semmes-Weinstein monofilament diagnostics and vibration testers that can predict ulcers. These tests, shown in Figure 2-23, indicate the presence of neuropathy in the patient, and these tests also measure the degree of nerve damage. If you have moderate nerve damage, you will be able to recover 3 months after the Dalen triple decompression nerve procedure. If your injury is more severe and has damaged more nerve fibers, it will take up to 1 year to recover.
Question 3: How long does the surgical treatment last?
In 1982, I first treated patients with diabetic neuropathy who had nerve compression to relieve pain and restore sensation, and I have kept in touch with some patients for a long time since then. For example, Figure 2-4 shows a patient who had a triple nerve decompression surgery on her foot Dalen 15 years earlier, and she has regained sensation in her operated leg, completely avoiding ulcer formation and amputation.
”Why does diabetes cause so much nerve compression?” “Why did your surgery work?
I have been asked this question many times, and I have reported on this subject many times, but I still feel as if I am giving an answer that is too simplistic to be believable. Yet it is indeed the exact answer.
When the grape molecule provides energy to the nerve, which generates the nerve impulse and “uploads” the signal to the brain or “downlinks” it to the finger or toe, the glucose is converted into another sugar called sorbitol. We know that sugar is easily soluble in coffee and tea. Sorbitol in the nerve absorbs water and causes it to accumulate in the nerve, which swells. When nerve swelling occurs in a narrow area, such as when a nerve crosses the elbow, the side of the knee, into the wrist or ankle, the nerve becomes compressed. This compression can lead to slow blood flow to the nerve tissue, which can cause nerve hypoxia, resulting in numbness and tingling. Over time, the signal conduction velocity of the nerve fibers decreases, and nerve necrosis occurs with further time. Larger nerves are okay with adhesions to the nerve canal.
There are other factors that contribute to nerve compression in diabetic patients. One of these is the adhesion of glucose molecules to the connective tissue within the nerve fibers that hardens the nerve so that it does not glide smoothly, which is worse when the nerve is stretched. Likewise, this can narrow the nerve canal.
As a final point, we know that there are railroad-track-like structures in the nerve fibers that we call microtubulin, and that neurotrophic substances such as proteins are passed along this duct from the cytosol at the spinal cord to the fingers or toes. In diabetic patients, the conduction system is greatly diminished. Once the proteins cannot travel along the nerve to the site of compression, the nerve cannot repair properly.
These multiple metabolic processes combined are the underlying factors that make the nerves in diabetic patients susceptible to compression.
In my proposed approach, the metabolic processes are not altered, but the constricted areas of nerve compression are opened. Not all patients with diabetic neuropathy are candidates for surgery, and the Dalen triple neurological decompression procedure is only indicated to treat patients with significant nerve compression.