4. Painful diabetic polyneuropathy.

Saved in:
Bibliographic Details
Title: 4. Painful diabetic polyneuropathy.
Authors: Zuidema, Xander, de Galan, Bastiaan, Brouwer, Brigitte, Cohen, Steven P., Eldabe, Sam, Argoff, Charles E., Huygen, Frank, Van Zundert, Jan
Source: Pain Practice. Feb2024, Vol. 24 Issue 2, p308-320. 13p.
Subjects: Diagnosis of diabetic neuropathies, Blood sugar analysis, Treatment of diabetic neuropathies, Spinal cord, Diabetic neuropathies, Glycemic control, Radio frequency therapy, Evidence-based medicine, Catheter ablation, Polyneuropathies, Electric stimulation, Pain management, Neural stimulation
Abstract: Introduction: Pain as a symptom of diabetic polyneuropathy (DPN) significantly lowers quality of life, increases mortality and is the main reason for patients with diabetes to seek medical attention. The number of people suffering from painful diabetic polyneuropathy (PDPN) has increased significantly over the past decades. Methods: The literature on the diagnosis and treatment of diabetic polyneuropathy was retrieved and summarized. Results: The etiology of PDPN is complex, with primary damage to peripheral nociceptors and altered spinal and supra‐spinal modulation. To achieve better patient outcomes, the mode of diagnosis and treatment of PDPN evolves toward more precise pain‐phenotyping and genotyping based on patient‐specific characteristics, new diagnostic tools, and prior response to pharmacological treatments. According to the Toronto Diabetic Neuropathy Expert Group, a presumptive diagnosis of "probable PDPN" is sufficient to initiate treatment. Proper control of plasma glucose levels, and prevention of risk factors are essential in the treatment of PDPN. Mechanism‐based pharmacological treatment should be initiated as early as possible. If symptomatic pharmacologic treatment fails, spinal cord stimulation (SCS) should be considered. In isolated cases, where symptomatic pharmacologic treatment and SCS are unsuccessful or cannot be used, sympathetic lumbar chain neurolysis and/or radiofrequency ablation (SLCN/SLCRF), dorsal root ganglion stimulation (DRGs) or posterior tibial nerve stimulation (PTNS) may be considered. However, it is recommended that these treatments be applied only in a study setting in a center of expertise. Conclusions: The diagnosis of PDPN evolves toward pheno‐and genotyping and treatment should be mechanism‐based. [ABSTRACT FROM AUTHOR]
Copyright of Pain Practice is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
Full text is not displayed to guests.
Description
Abstract:Introduction: Pain as a symptom of diabetic polyneuropathy (DPN) significantly lowers quality of life, increases mortality and is the main reason for patients with diabetes to seek medical attention. The number of people suffering from painful diabetic polyneuropathy (PDPN) has increased significantly over the past decades. Methods: The literature on the diagnosis and treatment of diabetic polyneuropathy was retrieved and summarized. Results: The etiology of PDPN is complex, with primary damage to peripheral nociceptors and altered spinal and supra‐spinal modulation. To achieve better patient outcomes, the mode of diagnosis and treatment of PDPN evolves toward more precise pain‐phenotyping and genotyping based on patient‐specific characteristics, new diagnostic tools, and prior response to pharmacological treatments. According to the Toronto Diabetic Neuropathy Expert Group, a presumptive diagnosis of "probable PDPN" is sufficient to initiate treatment. Proper control of plasma glucose levels, and prevention of risk factors are essential in the treatment of PDPN. Mechanism‐based pharmacological treatment should be initiated as early as possible. If symptomatic pharmacologic treatment fails, spinal cord stimulation (SCS) should be considered. In isolated cases, where symptomatic pharmacologic treatment and SCS are unsuccessful or cannot be used, sympathetic lumbar chain neurolysis and/or radiofrequency ablation (SLCN/SLCRF), dorsal root ganglion stimulation (DRGs) or posterior tibial nerve stimulation (PTNS) may be considered. However, it is recommended that these treatments be applied only in a study setting in a center of expertise. Conclusions: The diagnosis of PDPN evolves toward pheno‐and genotyping and treatment should be mechanism‐based. [ABSTRACT FROM AUTHOR]
ISSN:15307085
DOI:10.1111/papr.13308