scholarly journals Psychiatric Underpinnings of Chronic Diabetic Neuropathic Pain

2016 ◽  
Vol 30 (1&2) ◽  
pp. 37
Author(s):  
Syed H. Shabbir
Keyword(s):  
Neuropathic Pain ◽  
Diabetic Neuropathy ◽  
Psychiatric Illness ◽  
Treatment Options ◽  
Diabetic Polyneuropathy ◽  
Therapeutic Approaches ◽  
Diabetic Neuropathic Pain ◽  
Psychiatric Illnesses ◽  
Axis I

There is increasing evidence that psychosocial factors may be involved in the pathophysiology of chronic diabetic neuropathic pain. Individuals with diabetic polyneuropathy exhibit significantly higher rates of axis I psychiatric disorders, and worsening neuropathic symptoms correlate with worsened psychiatric illness. This association exists even when social-support and quality-of-life measures are controlled. Aberrant supraspinal structures and neuronal networks in diabetic neuropathy mimic those found in other psychiatric illnesses. Response to standard medications and therapeutic approaches remains unsatisfactory, and antidepressants continue to serve as first-line treatment for diabetic neuropathy. The exact interplay between neuropathic pain and psychiatric illness remains unclear and may have a common pathophysiological focus. This area of study needs to be revisited and psychological interventions must be explored as possible treatment options for diabetic neuropathy. 

Microglial Inhibition Influences XCL1/XCR1 Expression and Causes Analgesic Effects in a Mouse Model of Diabetic Neuropathy

2016 ◽  
Vol 125 (3) ◽  
pp. 573-589 ◽  
Author(s):  
Magdalena Zychowska ◽  
Ewelina Rojewska ◽  
Anna Piotrowska ◽  
Grzegorz Kreiner ◽  
Joanna Mika
Keyword(s):  
Neuropathic Pain ◽  
Diabetic Neuropathy ◽  
Cell Cultures ◽  
Neutralizing Antibody ◽  
Diabetic Neuropathic Pain ◽  
Nociceptive Transmission ◽  
Analgesic Effects ◽  
Primary Microglial Cell ◽  
Neuropathic Pain Model ◽  
Streptozotocin Induced Diabetes

Abstract Background Recent studies indicated the involvement of some chemokines in the development of diabetic neuropathy; however, participation of the chemokine-C-motif ligand (XCL) subfamily remains unknown. The goal of this study was to examine how microglial inhibition by minocycline hydrochloride (MC) influences chemokine-C-motif ligand 1 (XCL1)–chemokine-C-motif receptor 1 (XCR1)/G protein–coupled receptor 5 expression and the development of allodynia/hyperalgesia in streptozotocin-induced diabetic neuropathy. Methods The studies were performed on streptozotocin (200 mg/kg, intraperitoneally)-induced mouse diabetic neuropathic pain model and primary glial cell cultures. The MC (30 mg/kg, intraperitoneally) was injected two times daily until day 21. XCL1 and its neutralizing antibody were injected intrathecally, and behavior was evaluated with von Frey and cold plate tests. Quantitative analysis of protein expression of glial markers, XCL1, and/or XCR1 was performed by Western blot and visualized by immunofluorescence. Results MC treatment diminished allodynia (0.9 ± 0.1 g; n = 7 vs. 3.8 ± 0.7 g; n = 7) and hyperalgesia (6.5 ± 0.6 s; n = 7 vs. 16.5 ± 1 s; n = 7) in the streptozotocin-induced diabetes. Repeated MC administration prevented microglial activation and inhibited the up-regulation of the XCL1/XCR1 levels. XCL1 administration (10 to 500 ng/5 μl; n = 9) in naive mice enhanced nociceptive transmission, and injections of neutralizing XCL1 (4 to 8 μg/5 μl; n = 10) antibody into the mice with diabetic neuropathic pain diminished allodynia/hyperalgesia. Microglia activation evoked in primary microglial cell cultures resulted in enhanced XCL1 release and XCR1 expression. Additionally, double immunofluorescence indicated the widespread coexpression of XCR1-expressing cells with spinal neurons. Conclusions In diabetic neuropathy, declining levels of XCL1 evoked by microglia inhibition result in the cause of analgesia. The putative mechanism corroborating this finding can be related to lower spinal expression of XCR1 together with the lack of stimulation of these XCR1 receptors, which are localized on neurons.

scholarly journals Neuropathic pain is an independent predictor of worse quality of life in patients with diabetic neuropathy

2020 ◽  
pp. 17-17
Author(s):  
Zoran Vukojevic ◽  
Stojan Peric ◽  
Aleksandra Dominovic-Kovacevic ◽  
Ivo Bozovic ◽  
Sanja Grgic ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Neuropathic Pain ◽  
Diabetic Neuropathy ◽  
Independent Predictor

scholarly journals Therapeutic Approaches for Peripheral and Central Neuropathic Pain

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Délia Szok ◽  
János Tajti ◽  
Aliz Nyári ◽  
László Vécsei ◽  
Luigi Trojano
Keyword(s):  
Neuropathic Pain ◽  
Tricyclic Antidepressants ◽  
Treatment Options ◽  
Somatosensory System ◽  
Therapeutic Approaches ◽  
Chronic Neuropathic Pain ◽  
Central Neuropathic Pain ◽  
Psychological Therapies ◽  
First Choice ◽  
Pubmed Search

Neuropathic pain is a chronic secondary pain condition, which is a consequence of peripheral or central nervous (somatosensory) system lesions or diseases. It is a devastating condition, which affects around 7% of the general population. Numerous etiological factors contribute to the development of chronic neuropathic pain. It can originate from the peripheral part of the nervous system such as in the case of trigeminal or postherpetic neuralgia, peripheral nerve injury, painful polyneuropathies, or radiculopathies. Central chronic neuropathic pain can develop as a result of spinal cord or brain injury, stroke, or multiple sclerosis. As first-line pharmacological treatment options, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and gabapentinoids are recommended. In trigeminal neuralgia, carbamazepine and oxcarbazepine are the first-choice drugs. In drug-refractory cases, interventional, physical, and psychological therapies are available. This review was structured based on a PubMed search of papers published in the field from 2010 until May 2019.

A Review on Different Analytical Techniques for Determination of DNP Drugs and Their Metabolites in Pharmaceutical Formulations

2020 ◽  
Vol 16 ◽  
Author(s):  
Puja Bag ◽  
Bhupinder Kumar
Keyword(s):  
Mass Spectrometry ◽  
Neuropathic Pain ◽  
Liquid Chromatography ◽  
Diabetic Neuropathy ◽  
Analytical Methods ◽  
Pharmaceutical Formulations ◽  
Diabetic Patients ◽  
Liquid Chromatography Mass Spectrometry ◽  
Diabetic Neuropathic Pain ◽  
Drug Content

Background: Neuropathy is the most common perplexity of diabetes 1 and 2. About 50% diabetic patients develop Diabetic neuropathic pain (DNP). At the beginning of diabetic neuropathy; results loss of sense especially in the lower limb, pain, and difficulty in movement. Glucose regulation effectively prevents the development of diabetic neuropathy in type 1 diabetic patients but the consequences in type 2 diabetic patients are more drastic. Introduction: No single treatment exists to prevent or renovate the pain caused by diabetic neuropathy. The drugs used for the treatment of DNP come in various formulations and with different storage conditions. Till date, the number of analytical methodologies has been reported for analysis of DNP drugs. Few reports are published describing analytical methods of single DNP drugs. Method: The main objective of this review is to compile the different analytical methods developed at UV-Vis (Ultraviolet-visible) spectrophotometer, HPLC (High Performance Liquid Chromatography) and LC-MS (Liquid Chromatography-Mass spectrometry) to identify and quantify the drug content in various formulations which are used to treat or prevent the Diabetic neuropathic pain mainly focusing on γ-aminobutyric acid analogues, anti-depressants, serotonin noradrenaline reuptake inhibitors (SNRIs), aldose reductase inhibitors, opioids, and dietary supplements. Results and Discussion: We have compiled UV-Vis, HPLC and Liquid Chromatography-Mass spectrometry analytical methods developed to study the pharmacokinetic profile, quantify drug content and their metabolites in plasma as well as pharmaceutical formulations. The authors believe that the mentioned studies in the report will help audible readers to select a suitable method for analysis of these drugs and also help researchers to develop a more convenient, fast and sensitive method for these.

Effect of Pentoxifylline on Diabetic Neuropathic Pain in Rats

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Raghda A.M Salama ◽  
Amany H Hasanin ◽  
May Hamza ◽  
Lobna A Saleh ◽  
Eman K Habib
Keyword(s):  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Diabetic Neuropathy ◽  
Atpase Activity ◽  
Diabetic Rats ◽  
Developmental Phase ◽  
Epidermal Thickness ◽  
Diabetic Neuropathic Pain ◽  
Late Treatment ◽  
Antiallodynic Effect

Abstract Background and Aim Diabetic neuropathy (DN) is the most common diabetic complication, which has a lifetime prevalence of about 50%. About 20 to 30% of patients with DN suffer from neuropathic pain. This study was designed to investigate the role of early and late treatment of pentoxifylline (PTX) in management of diabetic neuropathic pain (DNP). Method Diabetic rats were administered PTX (50 and 200 mg/kg/day, in drinking water) either one week after STZ injection and for 7 weeks or 6 weeks after STZ injection and for 2 weeks. Mechanical allodynia were assessed weekly, Iba-1 and GFAP immunorectivity, spinal NFκB & spinal sciatic TNF-α were estimated at the end of the study. Epidermal thickness of the food pad and Na+/K+-ATPase activity in sciatic nerve were measured as an outcome measure for predegenerative markers of DN. Results The results of the present study suggest that activated microglia and not astrocytes are involved in the development of experimental diabetic neuropathy. PTX inhibit neuroimmune activation of microglia, reduce the levels of proinflammatory cytokines and improve epidermal thickness of the food pad and Na+/K+-ATPase activity in sciatic nerve. Only PTX 200 mg/kg/day when administered early and late treatment in diabetic rats produced antiallodynic effect. Conclusion PTX is a fundamental drug whose antiallodynic effect depends on the pathogenetic mechanisms and has the ability to halt or inhibit the progression of the disease. The earlier the use of PTX in the developmental phase of mechanical hyperalgesia the more the antiallodynic effect of the drug.

scholarly journals Neuromidin Attenuates Neuropathic Pain in the Streptozocin-Induced Diabetes Model in Rats

2008 ◽  
Vol 62 (3) ◽  
pp. 85-90
Author(s):  
Vija Kluša ◽  
Juris Rumaks ◽  
Ñina Karajeva
Keyword(s):  
Neuropathic Pain ◽  
Diabetic Neuropathy ◽  
Diabetic Neuropathic Pain ◽  
Cholinergic Mechanism ◽  
Peripheral Neuropathic Pain ◽  
Pain Model ◽  
Diabetes Model ◽  
Neuropathic Pain Model ◽  
New Type ◽  
Anticholinesterase Drug

Neuromidin Attenuates Neuropathic Pain in the Streptozocin-Induced Diabetes Model in Rats Diabetic neuropathy, which affects all peripheral nerves and may cause dramatic pain, is one of the most severe pathologies associated with hyperglycaemia, damage in the blood vessels, and inflammation in nerves. Anticonvulsants and antidepressants are still the most commonly used options to manage diabetic neuropathy. However, to improve clinical benefit in the treatment of diabetic neuropathies, as well as to minimize side effects, search for a new type of drugs to protect/treat neuropathic pain is still important. The aim of this study was to investigate neuromidin (ipidacrine, amiridin, NIK-247), an anticholinesterase drug of tetrahydroaminoacridine series, in the streptozocin (STZ)-induced diabetic neuropathic pain model in rats. Neuromidin was administered per os at daily doses 0.3, 1.0 and 3.0 mg/kg for ten days. The dynamics in the development of hyperalgesia (pain threshold) was measured by algesimeter for five weeks. The data obtained show that neuromidin considerably protects the development of peripheral neuropathic pain caused by STZ. The most active dose was the lowest—0.3 mg/kg. Neuromidin did not affect STZ-hyperglycemia, nor the weight gain in animal groups. Neuromidin per se at the doses 0.3 and 1.0 mg/kg showed a short-term analgesic activity. The cholinergic mechanism of neuromidin may be considered as essential in attenuating of diabetic neuropathic pain; other mechanisms remain to be elucidated.

Sleep Disturbances in Patients With Psychiatric Illnesses

2006 ◽  
Vol 19 (6) ◽  
pp. 369-378 ◽  
Author(s):  
Angela Singh ◽  
Patty Ghazvini ◽  
Natalie Robertson ◽  
Angela J. Massey ◽  
Otis Kirksey ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Bipolar Disorder ◽  
Cognitive Function ◽  
Sleep Disturbances ◽  
Treatment Options ◽  
Well Being ◽  
Psychiatric Illnesses ◽  
Sleep Abnormalities ◽  
Mental Well Being

Sleep is essential not only for our physical well-being but also for our mental well-being. Researchers, however, have determined that specific alterations in sleep patterns do exist among patients with psychiatric illnesses. The causes of these abnormalities include both direct and indirect mechanisms. These abnormalities lead to declines in both cognitive function and quality of life. Management should include both nonpharmacological and pharmacological methods. This article will review the types of sleep abnormalities associated with schizophrenia, depression, bipolar disorder, and anxiety disorders and will additionally review treatment options available for each illness.

Synergistic Effects of Vitamin D and Mindfulness Training in Pain Severity, Pain-Related Disability and Neuropathy-Specific Quality of Life Dimensions in Painful Diabetic Neuropathy: A Randomized Clinical Trial with Placebo-controlled

2020 ◽  
Author(s):  
Roya taghadosi nia ◽  
mohammadreza davoudi ◽  
Seyyed Mojtaba Ahmadi ◽  
Amir Abbas Taheri
Keyword(s):  
Quality Of Life ◽  
Vitamin D ◽  
Neuropathic Pain ◽  
Diabetic Neuropathy ◽  
Mindfulness Training ◽  
Pain Severity ◽  
Oral Dosage ◽  
Life Questionnaire ◽  
Painful Diabetic Neuropathy

Abstract Background: This study aimed to examining Synergistic effect of Vitamin D (VD) Supplement and mindfulness on neuropathic pain severity, Pain-Related Disability and Neuropathy-Specific Quality of Life dimensions in painful diabetic neuropathy.Methods: In this randomized controlled trial, totally 225 patients with painful diabetic neuropathy were randomly allocated to five groups: (1) mindfulness and placebo, (2) placebo, (3) mindfulness, (4) VD, and (5) mindfulness and VD. Mindfulness training includes twelves sessions and VD patients received a daily four thousand IU oral dosage (four capsules) with 28,000 IU vitamin D weekly for 12 weeks. Laboratory analyses, Sun exposure time, Vitamin D intake, BMI and Physical activity measured in pre-test and posttest. Pain-Related Disability measured with The Pain Disability Index (PDI). For other outcome variables Neuropathy Specific Quality of Life questionnaire and Neuropathic pain severity scale was utilized.Results: In baseline, measures were not different among the groups. At the end-of-treatment, for outcome variables results showed improvement in all groups except the “placebo” group. About other groups, there was not any difference between VD and mindfulness groups (in and not combined with placebo). However, “VD + mindfulness” has a greater improvement rather than VD and mindfulness groups (P<0.05). Moreover, both protocols have no significant effects on, FBS, BMI and energy intakes (P>0.05).Conclusion: Combining VD and mindfulness can reduce pain severity and pain-related disability, so with these changes patients improve their quality of life.

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