Articles: neuropathic-pain.
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J Pain Palliat Care Pharmacother · Sep 2019
Case ReportsKetamine: When Delirium and Desperation Call for a Hero.
The use of ketamine in palliative care is becoming more common for challenging symptom management, namely cancer related pain and psychiatric conditions. However, there is much that remains unstudied and uncertain about ketamine's clinical utility. ⋯ Despite concerns regarding baseline delirium we successfully used ketamine to better manage neuropathic pain, decrease overall opioid need, without exacerbating the preexisting delirium. Our case highlights the benefits of ketamine for neuropathic pain control in the face of delirium.
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The specific impact of neuropathic pain and recommended neuropathic pain treatments on the hormonal and immune status of patients has been so far poorly explored. This study aimed at studying, in real life, the hypothalamic-pituitary-adrenal axis and the cytokine profile of patients with neuropathic pain. It also explored their links with cognition, emotion, quality of life, and drug treatment. ⋯ An impairment of the hormonal status and of the immune system was observed in patients. It identified testosterone as a potential pivotal mediator between antidepressants/antiepileptics and quality of life. Further studies must address the exact impact of different types of drugs on central effects, of gender differences, and of the immune system of neuropathic pain.
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To measure and compare the total and normalised tibial nerve movements during forward bending in patients with and without failed back surgery syndrome (FBSS) and persistent leg pain following anatomically successful lumbar decompression surgery and demonstrated no psychological stress. Nerve pathomechanics may contribute to FBSS with persistent leg pain following anatomically successful lumbar decompression surgery. ⋯ This was the first study to quantify the decreased total and normalised tibial nerve mobility in FBSS patients with persistent leg pain when compared with non-FBSS patients following anatomically successful lumbar decompression surgery. Further research could investigate the efficacy of intervention, such as nerve mobilisation in this particular group of patients with failed back surgery syndrome and limited nerve mobility. These slides can be retrieved under Electronic Supplementary Material.
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Neurochemical research · Sep 2019
N-methyl-D-aspartate Receptors in the Prelimbic Cortex are Critical for the Maintenance of Neuropathic Pain.
The mechanisms underlying chronic and neuropathic pain pathology involve peripheral and central sensitisation. The medial prefrontal cortex (mPFC) seems to participate in pain chronification, and glutamatergic neurotransmission may be involved in this process. Thus, the aim of the present work was to investigate the participation of the prelimbic (PrL) area of the mPFC in neuropathic pain as well as the role of N-methyl D-aspartate (NMDA) glutamate receptors in neuropathic pain induced by a modified sciatic nerve chronic constriction injury (CCI) protocol in Wistar rats. ⋯ Mechanism of neuropathic pain. The infusion of CoCl2, a synapse activity blocker, into the prelimbic (PrL) division of the medial prefrontal cortex (mPFC) decreased the severity of mechanical allodynia, showing the late participation of the limbic cortex. The glutamatergic system potentiates chronic neuropathic pain via NMDA receptor activation in the PrL cortex.
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Vincristine (VCR) is a well-known anticancer drug which frequently induced painful neuropathy and impairs the quality of life of patients. The present study was designed to investigate the alleviative potential of a novel cyclohexenone derivative (CHD), i.e., ethyl 6-(4-methoxyphenyl)-2-oxo-4-phenylcyclohexe-3-enecarboxylate, against VCR-induced neuropathic pain in mice model. VCR was administered intraperitoneally for 10 days in two cycles to induce neuropathic pain. ⋯ CHD significantly augmented the paw withdrawal duration (PWD) in paw cold allodynia, while the same compound only increased the paw elevation and paw licking in the delayed phase of formalin nociception. Moreover, CHD significantly inhibited the DPPH free radical scavenging action (IC50 = 56), butylated hydroxytoluene (BHT) (IC50 = 39), and ascorbic acid (IC50 = 2.93). In conclusion, CHD exhibited a profile of potential attenuative effect against the VCR-induced neuropathic pain which might be attributed to its possible antinociceptive and antioxidant effect.