Diabetic Neuropathy
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Diabetic neuropathy is a disease process associated with diabetes. It affects sensory axons, autonomic axons, and later, to a less extent, motor axons. How diabetes affects neurons/axons remains debated. Progressive diabetic neuropathy involves retraction and dying back of terminal sensory axons in the periphery. Data suggest that dysfunction of key plasticity molecules promotes abnormal protein processing, oxidative damage, and mitochondrial dysfunction, leading to the loss of peripheral nerve function. Diabetes is associated with a wide range of neuropathies, including mononeuritis multiplex, compression and entrapment mononeuropathies, cranial neuropathies, and autonomic neuropathies. It can also cause amyotrophy and dysautonomia. When diabetic neuropathy is severe, it can lead to ulcerations, infections, and eventual amputations of the affected areas of the body. Differential diagnosis is difficult because not all sensorimotor neuropathies are caused by diabetes. The classifications of the various types of diabetic neuropathy are shown in Figure 4.1.
Herbal and Supplement Use in Pain Management
Sahar Swidan, Matthew Bennett in Advanced Therapeutics in Pain Medicine, 2020
Dosing: Diabetic neuropathy: Cyanocobalamin 0.25 mg three times daily for 9 weeks, methylcobalamin 1500 mcg daily for 3–4 months.133Postherpetic neuralgia: methylcobalamin 100 mcg SC six times weekly for 4 weeks.134Peripheral neuropathy: preliminary clinical research shows that taking a specific product containing 3 mcg vitamin B12, folic acid 400 mcg, and uridine monophosphate 50 mg (Keltican) daily for 60 days reduced pain by 44% and decreased concomitant analgesic requirements by over 75% compared to baseline in patients with peripheral neuropathy, including those with lumbar/lumbosacral radiculopathy, sciatic pain, and cervical radiculopathy.135
Diabetic Neuropathy
Jack L. Leahy, Nathaniel G. Clark, William T. Cefalu in Medical Management of Diabetes Mellitus, 2000
Rarely are simple analgesics, such as aspirin or acetaminophen, helpful for long-term treatment of neuropathic pain. Surprisingly, an occasional patient will report good pain relief when taking ibuprofen 400-600 mg (18). Most patients referred to neurologists require treatment with long-term agents. Helpful medications for the treatment of diabetic neuropathy include tricyclic antidepressants, antiepileptic drugs, selective serotonin-reuptake inhibitors, antipsychotics, and benzodiazepines. Narcotics may occasionally be necessary for breakthrough pain, but should be avoided as the primary analgesic because of their propensity to induce taxiphylaxis and dependency.
Mechanisms behind diffuse idiopathic peripheral neuropathy in humans – a systematic review
Published in Scandinavian Journal of Gastroenterology, 2023
Hanna Tufvesson, Viktor Hamrefors, Bodil Ohlsson
If we are familiar with mechanisms behind neuropathy, this complication may be prevented or postponed. Identification of etiology may be of importance to provide targeted treatments, instead of symptomatic treatments often given to reduce the symptoms [3,10]. The most important step to prevent diabetic neuropathy is to optimize the metabolic control [21]. Even though painful diabetic neuropathy originally stems from the peripheral nervous system, the changes of increased pain sensitivity become imprinted in the central nervous system [19]. It is believed that microglia, which are immune cells of the central nervous system, become activated due to a persistent noxious stimulus in the peripheral tissues. Moreover, hyperglycemia may have a direct effect on the microglia. The persistent activation of the microglia is creating a neuroinflammatory response that activates the sympathetic nervous system and hypothalamic-pituitary complex. This leads to an increased sensation to pain also in the central nervous system, a phenomenon known as central sensitization. In diabetic neuropathy, especially spinal microglia have been of particular interest [19].
The time to develop treatments for diabetic neuropathy
Published in Expert Opinion on Investigational Drugs, 2021
2.1 CLINICAL MEASURES. Clinical research to develop pharmacologic agents to improve neuronal function in diabetic neuropathy has been unrewarding. Diabetic neuropathy is a clinical condition that is defined by a spectrum of symptoms and signs of nerve impairment. Design of a protocol to measure the various aspects of this complexity has proven a formidable challenge. Several scales have been developed to quantitate symptoms and loss of sensation [29–39] (Table 3). There is considerable variability in assessment of clinical signs and symptoms among investigators [40]. Despite attempts to standardize clinical techniques, that variability persists [41,42].
Effects of adipose derived stromal vascular fraction on diabetic neuropathy: an experimental study
Published in Journal of Plastic Surgery and Hand Surgery, 2019
Berrak Karatan, Ersin Akşam, Esra Erden, Mustafa Erol Demirseren
There are several experimental and clinical studies on the etiology and treatment of diabetic neuropathy. Rats, which became diabetic through streptozotocin administration, have been presented as an appropriate model for studies on diabetic neuropathy in the literature [3]. Antioxidants have been utilized to treat diabetic neuropathy, and have been shown to improve walking function, and reduce pain related to neuropathy in a rat model of diabetic neuropathy [3]. Besides the antioxidants, it has been shown that both stem cells derived from the bone marrow and growth factors have been shown to improve the structure of nerve fibers in diabetic neuropathic rats [4].
Related Knowledge Centers
- Diabetes
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- Proximal Diabetic Neuropathy