SLR - October 2019 - Elizabeth A. Ansert
Effects of Extracorporeal Shock Waves on Neuralgia in Diabetic Rats
Reference: Zhou, Yue, et al. Effects of Extracorporeal Shock Waves on Neuralgia in Diabetic Rats. Journal of pain research 12 (2019): 387.
Scientific Literature Review
Reviewed By: Elizabeth A. Ansert, DPM
Residency Program: St. Vincent Hospital – Worcester, MA
Podiatric Relevance: Neuropathy is one of the most common problems podiatrists face. Patients can experience pain, paresthesia, hyperalgesia and numbness. Not only will this cause a patient’s quality of life to diminish, but it causes an increased risk for ulceration, infection, loss of limb or loss of life.
Multiple theories have been put forth as to the cause of diabetic neuropathy. The majority of these theories attribute neuropathic complications of diabetes to chronic hyperglycemia. Specifically, inflammatory responses causing endothelial damage has been concluded to cause nerve injury. Tumor necrosis factor (TNF-α) is thought to be the most essential inflammatory factor. Sphk-1 is a mediator of TNF-α, making it a possible mechanism of extracorporeal shockwave therapy (ESWT).
While drug therapy is the majority of treatment for neuropathy, ESWT has become an experimental alternative modality. This therapy can be used in an office setting to attenuate or inhibit inflammatory responses. This leads to the idea that ESWT can be used for the treatment of this common diabetes mellitus complication. Recently, it has become increasingly important to explore non-invasive, safe, and effective treatment modalities of neuropathy due to the epidemic of diabetes and its complications.
Methods: Rats were divided into a control group, a diabetic neuralgia group and an ESWT treatment group. Each group had six rats. Rat models in the neuralgia and ESWT groups were injected streptozocin to create diabetic models, as determined by fasting blood glucose tests.
The right hind paws of the rat models were tested with mechanical withdrawal thresholds (MWT) and thermal withdrawal latencies (TWL) to determine the extent of clinical display of neuralgia. The sciatic nerve of each rat was examined under electron microscope for structural changes noted after completion of experimental treatments. Protein expressions of TNF-α and Sphk-1 were also traced in each model with Western blot and reverse transcription PCR techniques on the severed sciatic nerve.
Results: When compared to the control group and baseline threshold, the diabetic neuralgia and ESWT groups had significantly lower MWTs and TWLs. The ESWT group had increased MWTs and TWLs than the diabetic neuralgia group. TNF-α and Sphk-1 proteins were significantly increased in the neuralgia and ESWT groups, compared to the control. The neuralgia group also had significantly higher inflammatory proteins than the ESWT group.
Microscopic examination of the nerve showed looser and irregular myelin structure with numerous vacuoles for the diabetic neuralgia group. The ESWT group nerves showed neat, compact layers of myelin with occasional vacuoles. The ESWT group also had nerves with compressed individual axons without significantly swollen Schwann cells.
Conclusions: Authors concluded that ESWT can help alleviate diabetic neuralgia. TNF-α and Sphk-1 were significantly increased in experimental groups, indicating that inflammatory factors play a role in diabetic neuralgia. TNF-α and Sphk-1 decreased in ESWT group rats compared to untreated diabetic neuralgia rates, leading authors to believe that ESWT could help regulate the expression of TNF-α. Furthermore, Sphk-1 and TNF-α could lead to the development of diabetic neuralgia, and ESWT could improve pain symptoms by inhibiting the secretion of these inflammatory proteins.