Acute painful diabetic neuropathy induced by strict glycemic control (“insulin neuritis”): The old enigma is still unsolved

2009 ◽  
Vol 63 (4) ◽  
pp. 249-250 ◽  
Author(s):  
Franco Gemignani
2005 ◽  
Vol 31 (4) ◽  
pp. 523-540 ◽  
Author(s):  
Cynthia F. Corbett

Purpose Painful diabetic neuropathy (PDN) has a significant impact on patients’ quality of life, affecting sleep, mood, mobility, ability to work, interpersonal relationships, overall self-worth, and independence. The purpose of this article is to provide diabetes educators with current and essential tools for PDN assessment and management. Methods Medline and CINAHL database searches identified publications on the assessment and treatment of PDN. Identified research was evaluated, and information pertinent to diabetes educators was summarized. Results Recent advancements in assessment of neuropathic pain include identifying characteristics that distinguish between neuropathic and nonneuropathic pain. In the absence of treatment, research demonstrates that nerve damage may progress while pain diminishes. Many disease-modifying and symptom-management treatment options are available. Conclusion Good glycemic control is the first priority for both prevention and management of PDN. However, even with good glycemic control, up to 20% of patients will develop PDN. PDN recognition and assessment are critical to optimize management. Although several treatment modalities are available, few patients obtain complete pain relief. Recent advances in understanding the mechanisms underlying neuropathic pain should lead to better treatment and patient outcomes. Combination therapy, including nonpharmacologic modalities, may be required. Research evaluating the efficacy of combination therapy is needed.


Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1247
Author(s):  
Anne Worthington ◽  
Alise Kalteniece ◽  
Maryam Ferdousi ◽  
Luca Donofrio ◽  
Shaishav Dhage ◽  
...  

Impaired rate-dependent depression of the Hoffman reflex (HRDD) is a potential biomarker of impaired spinal inhibition in patients with painful diabetic neuropathy. However, the optimum stimulus-response parameters that identify patients with spinal disinhibition are currently unknown. We systematically compared HRDD, performed using trains of 10 stimuli at five stimulation frequencies (0.3, 0.5, 1, 2 and 3 Hz), in 42 subjects with painful and 62 subjects with painless diabetic neuropathy with comparable neuropathy severity, and 34 healthy controls. HRDD was calculated using individual and mean responses compared to the initial response. At stimulation frequencies of 1, 2 and 3 Hz, HRDD was significantly impaired in patients with painful diabetic neuropathy compared to patients with painless diabetic neuropathy for all parameters and for most parameters when compared to healthy controls. HRDD was significantly enhanced in patients with painless diabetic neuropathy compared to controls for responses towards the end of the 1 Hz stimulation train. Receiver operating characteristic curve analysis in patients with and without pain showed that the area under the curve was greatest for response averages of stimuli 2–4 and 2–5 at 1 Hz, AUC = 0.84 (95%CI 0.76–0.92). Trains of 5 stimuli delivered at 1 Hz can segregate patients with painful diabetic neuropathy and spinal disinhibition, whereas longer stimulus trains are required to segregate patients with painless diabetic neuropathy and enhanced spinal inhibition.


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