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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical research and practice have suffered because of lack of specificity when clinical diagnoses of pain are made. Distinction between neuropathic and inflammatory pain mechanisms is suggested, as well as the distinction between neuropathic pain from hypersensitivity pain disorders, previously termed neuropathic pain due to neurological dysfunction. Neuropathic pain is in this case defined as pain occurring in the ara of body affected by neurological disease or injury. This type of pain manifests not only with positive sensory phenomena such as pain, dysesthesia, and different types of hyperalgesia, but also with negative sensory phenomena and negative and positive motor and autonomic symptoms and signs.
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PMID:Defining neuropathic pain. 1293 71

Neuropathic pain impacts millions of people in the United States and around the world. Patients experience one of many symptoms, such as pain, paresthesia, dysesthesia, hyperalgesia, and allodynia, for many years because of unavailable or inadequate treatment. One of the major challenges in treating patients with neuropathic pain syndromes is a lack of consensus concerning the appropriate first-line treatment options for conditions associated with neuropathic pain, including postherpetic neuralgia, diabetic peripheral neuropathy, and trigeminal neuralgia. This review summarizes the published results of randomized trials involving treatment for neuropathic pain conditions. Anticonvulsants, such as gabapentin, carbamazepine, and lamotrigine, and tricyclic antidepressants, including amitriptyline and desipramine, have demonstrated efficacy in relieving pain associated with postherpetic neuralgia, diabetic peripheral neuropathy, and trigeminal neuralgia, in several studies. However, the lack of head-to-head comparison studies of these agents limits the conclusions that can be reached. Clinicians who must make decisions regarding the care of individual patients may find some guidance from the number of randomized trials with a positive outcome for each agent. Using quality-of-life study outcomes, treatment strategies must encompass the impact of therapeutic agents on the comorbid conditions of sleep disturbance and mood and anxiety disorders associated with neuropathic pain. Looking to the future, emerging therapies, such as pregabalin and newer N-methyl-D-aspartate-receptor blockers, may provide physicians and patients with new treatment options for more effective relief of pain.
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PMID:Pharmacologic management part 1: better-studied neuropathic pain diseases. 1499 28

Neuropathic pain is an increasingly common problem facing the cancer patient. Painful neuropathy can come from various sources and significantly impact quality of life. The most commonly observed scenario is paraesthesia and dysesthesia as a result of toxic effects of chemotherapies on the distal peripheral nerves. Neuropathic pain should be addressed ideally with the help of a neuro-oncologist, and it usually can be successfully treated with a variety of agents, including atypical analgesics such as antidepressants, newer drugs with analgesic benefit, and opioids for more refractory cases. Direct and indirect effects of the primary neoplasm need to be considered in the etiology of specific syndromes of mononeuropathies and plexopathies.
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PMID:Assessment of neuropathic pain in cancer patients. 1958 91

Neuropathic pain is a major health issue and is frequently accompanied by allodynia (painful sensations in response to normally non-painful stimulations), and unpleasant paresthesia/dysesthesia, pointing to alterations in sensory pathways normally dedicated to the processing of non-nociceptive information. Interestingly, mounting evidence indicate that central glial cells are key players in allodynia, partly due to changes in the astrocytic capacity to scavenge extracellular glutamate and gamma-aminobutyric acid (GABA), through changes in their respective transporters (EAAT and GAT). In the present study, we investigated the glial changes occurring in the dorsal column nuclei, the major target of normally innocuous sensory information, in the rat spared nerve injury (SNI) model of neuropathic pain. We report that together with a robust microglial and astrocytic reaction in the ipsilateral gracile nucleus, the GABA transporter GAT-1 is upregulated with no change in GAT-3 or glutamate transporters. Furthermore, [(3)H] GABA reuptake on crude synaptosome preparation shows that transporter activity is functionally increased ipsilaterally in SNI rats. This GAT-1 upregulation appears evenly distributed in the gracile nucleus and colocalizes with astrocytic activation. Neither glial activation nor GAT-1 modulation was detected in the cuneate nucleus. Together, the present results point to GABA transport in the gracile nucleus as a putative therapeutic target against abnormal sensory perceptions related to neuropathic pain.
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PMID:Upregulation of the GABA transporter GAT-1 in the gracile nucleus in the spared nerve injury model of neuropathic pain. 2054 84

Neuropathic pain is a disabling symptom frequently reported by patients with neuropathies. Pain-questionnaires are the best way to investigate it. Neuropathic Pain Symptom Inventory (NPSI) questionnaire specifically assesses the different symptoms of neuropathic pain. The objective of this study was to evaluate, through the NPSI, the different neuropathic painful symptoms in a population of neuropathic patients. 277 patients with different neuropathies were evaluated with the NPSI to investigate the prevalence of the different neuropathic symptoms. Neuropathic pain was reported by 94.4% of the patients, resulting to be common not only in diabetic and iatrogenic neuropathies, but also in hereditary, paraproteinemic, and idiopathic neuropathies. The majority of our patients (88.6%) presented paresthesia/dysesthesia. The results of our study point out the difference in the occurrence of the painful symptoms. A scale able to discriminate distinct types of neuropathic pain may provide clinicians with adequate therapeutic choices in the daily practice.
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PMID:Exploring neuropathic symptoms in a large cohort of Italian patients with different peripheral nervous system diseases. 2136 94

Neuropathic pain is difficult to diagnose and difficult to treat with certainty. So the aim of the study was to evaluate comparative clinical efficacy of pregabaline with amitriptyline and gabapentin in neuropathic cancer pain. A total of 120 patients with cancer having severe neuropathic cancer pain were enrolled in the study after taking approval from Institutional Ethics Committee and divided in to 4 groups: group AT-amitriptyline, group GB-gabapentin, group PG-pregabalin, and group PL-placebo. Oral morphine was used for rescue analgesic for continued pain. Pain score (Visual Analogue scale) and secondary outcome measures such as intensity of lancinating, dysesthesia, and burning on numerical rating scale, Global satisfaction score (GSS), Eastern Co-operative Oncology Group scoring (ECOG), and adverse effects were assessed. At the end of study there was significant decrease in pain score in group PG as compared to the other groups; group AT (P = .003), group GB (P = .042), and group PL (P = .024). Percentage of patients with lancinating pain and dysesthesia were significantly less in group PG as compared to groups GB and PL. All the patients in group PL needed rescue morphine. After 4 visits, maximum improvement in ECOG scoring and GSS scoring was observed in group PG patients. Our results suggested that all antineuropathic drugs are effective in relieving cancer-related neuropathic pain. There was statistically and clinically significant morphine sparing effect of pregabaline in relieving neuropathic cancer pain and neuropathic symptoms as compared to other antineuropathic drugs.
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PMID:A comparative efficacy of amitriptyline, gabapentin, and pregabalin in neuropathic cancer pain: a prospective randomized double-blind placebo-controlled study. 2174 32

Neuropathic pain is a chronic neurodegenerative disease. It is well characterized by spontaneous pain, hyperalgesia, hypothesia, dysesthesia and allodynia. The present study was designed to investigate the antinociceptive potential of Butea monosperma on vincristine-induced painful neuropathy in rats. Vincristine was administered for induction of neuropathic pain in experimental animals. Hot plate, acetone drop, paw pressure, Von Frey hair and tail immersion tests were performed to assess the degree of thermal hyperalgesia, cold chemical allodynia, mechanical hyperalgesia and allodynia in the hind paw and tail thermal hyperalgesia, respectively, as an index of peripheral and central pain sensation. Tissue thiobarbituric acid reactive substances (TBARSs), reduced glutathione (GSH) and total calcium levels were estimated to assess the biochemical changes in the sciatic nerve tissue. Microscopically, histopathological changes were also observed in the sciatic nerve tissue. Ethanolic extract of B. monosperma leaves and pregabalin were administered for 14 consecutive days. Vincristine administration resulted in significant reduction in behavioural (i.e. hyperalgesia and allodynic pain sensation) changes along with a rise in the levels of TBARS, total calcium and decrease in GSH levels when compared with the normal control group. Moreover, significant histological changes were also observed. Pretreatment with B. monosperma significantly attenuated vincristine-induced development of painful behavioural, biochemical and histological changes in a dose-dependent manner, which is similar to that of pregabalin-pretreated group. B. monosperma ameliorated vincristine-induced painful neuropathy. It may be due to its potential of antioxidative, neuroprotective and calcium channel inactivation.
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PMID:Antinociceptive effect of Butea monosperma on vincristine-induced neuropathic pain model in rats. 2228 18

Neuropathic pain is experienced as a result of disease or physical injury affecting the somatosensory system. It can be associated with abnormal sensations (dysesthesia) or evoked by normally nonpainful stimuli. Glia has emerged as key regulators of neuropathic pain perception and potential targets for drug development. Glia are activated upon peripheral nerve damage and secrete a number of proinflammatory factors. This process involves many mechanisms including neuroinflammation, ion channel activation, and ligand-receptor interactions. This review describes recent advances in the understanding of neuropathic pain, including the role of glia and their targeting by current treatment approaches.
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PMID:Role of glia in neuropathic pain. 2438 24

Neuropathic pain, defined as pain caused by a lesion or disease of the somatosensory nervous system, is characterized by dysesthesia, hyperalgesia, and allodynia. The number of patients with this type of pain has increased rapidly in recent years. Yet, available neuropathic pain medicines have undesired side effects, such as tolerance and physical dependence, and do not fully alleviate the pain. The mechanisms of neuropathic pain are still not fully understood. Injury causes inflammation and immune responses and changed expression and activity of receptors and ion channels in peripheral nerve terminals. Additionally, neuroinflammation is a known factor in the development and maintenance of neuropathic pain. During neuropathic pain development, the C-C motif chemokine receptor 2 (CCR2) acts as an important signaling mediator. Traditional plant treatments have been used throughout the world for treating diseases. We and others have identified food-derived compounds that alleviate neuropathic pain. Here, we review the natural compounds for neuropathic pain relief, their mechanisms of action, and the potential benefits of natural compounds with antagonistic effects on GPCRs, especially those containing CCR2, for neuropathic pain treatment.
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PMID:Food-Derived Natural Compounds for Pain Relief in Neuropathic Pain. 2789 21

Fahr disease is an idiopathic disorder characterized with deposition of calcium and a few other minerals in basal ganglia, cerebellum and subcortical brain area. A 51 years old female with the complaints of pain, numbness, tingling and weakness in both upper extremities for six months was referred to our electromyography laboratory with a suspicion of carpal tunnel syndrome. She got the diagnosis of Fahr disease upon the investigations for the convulsions that she experienced ten years ago. Beside, she had a generalized anxiety disoder. Neurological examination revealed mild to moderate weakness in flexion and extension of forearm, and extension of hand on both sides. She described dysesthesia on C6 & C7 dermatomes, bilaterally. Symmetric calsifications on both cerebellar hemispheres and basala ganglia were present on cranial CT. Median and ulnar nerve conduction studies were normal on both sides. Concentric needle electromyography revealed chronic neurogenic changes on the morphology of motor unit potentials recorded from the muscles of C6 & C7, bilaterally. Cervical magnetic resonance imaging revealed discopathies on C4-5, C5-6 and C6-7 levels causing myelomalacia. Neuropathic pain, paresthesia or muscle weakness on upper extremities are rare in Fahr disease. Presented case got the diagnosis of cervical discopathies in late as those findings were supposed to be related with Fahr disease. Therefore, clinicians should be aware of common findings occured during the course of this disease, and consider the possible coincidental pathologies when the atypical neurological deficits are observed in these patients.
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PMID:[Late diagnosed cervical myelomalesia in a case of Fahr disease experiencing a neuropathic pain]. 3040 77


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