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

This study describes suicidal behavior in a cross-sectional sample of chronic pain patients and evaluates factors associated with increased risk for suicidal ideation. One hundred-fifty-three adults with nonmalignant pain (42% back pain) who were consecutively referred to a tertiary care pain center completed a Structured Clinical Interview for Suicide History, the McGill Pain Questionnaire, and the Beck Depression Inventory. Nineteen-percent reported current passive suicidal ideation (PSI), 13% had active thoughts of committing suicide (ASI), 5% had a current suicide plan, and 5% reported a previous suicide attempt. Drug overdose was the most commonly reported plan and method of attempt (75%). Thirteen-percent reported a family history of suicide attempt/completion. Pain-specific and traditional suicide risk factors were evaluated as predictors of current PSI and ASI. Logistic regression analyses revealed that a family history of suicide attempts/completions was associated with a 7.5 fold increase in risk of PSI (P=0.001) and a 6.6 fold increase in ASI (P=0.003), after adjusting for significant covariates. Having abdominal pain was associated with an adjusted 5.5 fold increase in PSI (P=0.05) and a 4.2 fold increase in ASI (P=0.10). Neuropathic pain significantly reduced risk for both PSI (P=0.002) and ASI (P=0.01). Demographics, pain severity, and depression severity were not associated with suicidal ideation in multivariate analyses. These findings highlight the need for routine evaluation and monitoring of suicidal behavior in chronic pain, especially for patients with family histories of suicide, those taking potentially lethal medications, and patients with abdominal pain.
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PMID:Suicidal ideation, plans, and attempts in chronic pain patients: factors associated with increased risk. 1532 24

Patients with neuropathic pain present a clinical challenge. Neuropathic pain, when chronic, often leads to disability. Diagnosis can be difficult because both positive and negative sensory and motor signs and symptoms may be present, as well as a variety of comorbid conditions. In addition, there may be a high degree of interpatient variability. Currently, clinical evaluation, rather than diagnostic tests, is one of the best available tools for assessment and diagnosis. As with all chronic pain conditions, the key to a thorough assessment is a thorough history that includes medical, functional, and psychosocial evaluations. Currently available pain assessment tools, which are widely used in nursing practice, are still inadequate for use in patients with neuropathic pain. The physical and neurologic examination remains a critical element for patient evaluation. This includes an assessment of spontaneous pain (continuous or intermittent), pain evoked by daily activities (allodynia), and other abnormal sensations that are not necessarily painful (paresthesias, dysesthesias). Sensitivity to pinprick, touch, pressure, cold, heat, and vibration are measured, often confirming the suspected diagnosis. Patients may be confused by the unusual sensations they are experiencing and unable to effectively describe or communicate their symptoms. This communication barrier may contribute to an inadequate physical examination. With improved skills in patient assessment and through enhanced communication with patients, nurses can make an important contribution to treatment outcomes in patients with neuropathic pain.
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PMID:Neuropathic pain: a guide to comprehensive assessment. 1564 55

Neuropathic pain is defined as pain initiated or caused by a primary lesion or dysfunction in the nervous system. It is a devastating and difficult to manage consequence of peripheral nerve injury and has a variety of clinical symptoms. Neuropathic pain is a major health problem. It has been estimated that 70% of patients with advanced cancer and inflammatory pathologies are afflicted by chronic pain. About 95% of patients with spinal cord injuries have neuropathic pain problems. Chronic pain is debilitating and cause of depression and decreasing quality of life. Pharmacological treatment for the symptoms of painful neuropathy is difficult, because there has been limited understanding of the underlying causes and systemic levels that an effective dose can have on multiple side effects. The use of molecular methods, such as gene therapy, stem cell therapy and viral vector for delivery of biologic antinociceptive molecules, has led to a better understanding of the underlying mechanisms of the induction of intractable neuropathic pain.
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PMID:Neuropathic pain: is the end of suffering starting in the gene therapy? 1572 Feb 15

Neuropathic pain, a chronic disabling pain arising from nerve injury, develops a central component. In brain neurons, tumor necrosis factor-alpha (TNF) levels intensify and TNF-inhibition of norepinephrine (NE) release, dependent upon alpha(2)-adrenergic activation, amplifies during neuropathic pain onset. TNF-inhibition of NE release transforms to facilitation in the hippocampus of rats administered antidepressants (treat neuropathic pain), contemporaneous with decreased neuron TNF. Therefore, adrenergic drugs inhibit increased pain sensitivity (hyperalgesia) by decreasing TNF production, thereby inducing increased NE release. This study examined TNF- and alpha(2)-adrenergic-regulated NE release from hippocampal slices during both the onset and dissipation of hyperalgesia during sciatic nerve chronic constriction injury (CCI). The enhanced inhibition of NE release by TNF at peak hyperalgesia (day-8) transformed to facilitation of NE release at days 12, 14, 16, and 21 post-CCI, corresponding to dissipation of hyperalgesia. Chronic antidepressant drug administration alone to rats results in similar findings. Rats administered the antidepressant amitriptyline (10 mg/kg, i.p., 60 min) at day-8 post-CCI, no longer exhibited hyperalgesia. Interestingly, the presynaptic response to TNF transformed to facilitation of NE release. While TNF directs the development of hyperalgesia, it is also involved in the resolution of pain, a possible mechanism for management of chronic pain.
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PMID:The dissipation of neuropathic pain paradoxically involves the presence of tumor necrosis factor-alpha (TNF). 1572 Nov 77

Neuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.
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PMID:Understanding neuropathic pain. 1578 57

Neuropathic pain, a chronic pain state caused by injury to the nervous system, usually responds poorly to standard pain treatment. Antidepressants have been used to treat neuropathic pain, and animal and clinical studies have showed beneficial effects. However, the mechanisms underlying antidepressant antinociceptive effect in neuropathic pain are still unknown. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, can modulate synaptic plasticity and neurotransmitter release across multiple neurotransmitter systems. Recent animal and human studies have demonstrated that antidepressants can increase central as well as plasma BDNF levels. In addition: (1) BDNF is produced by a subset of primary sensory neurons that are located in the dorsal root ganglion; (2) BDNF levels change in animal models of neuropathic pain; (3) BDNF can indirectly depress sensory neuron transmission in the dorsal horn. From these findings, it is proposed that BDNF may play an important role in the antidepressant antinociceptive effect in neuropathic pain. The notion of BDNF mediating the therapeutic mechanisms of antidepressant in neuropathic pain may help to select the specific type and the optimal dose of antidepressants for the treatment of neuropathic pain. Exploration of this hypothesis could provide a new direction in the treatment of neuropathic pain, as well as other pain disorders.
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PMID:Possible involvement of brain-derived neurotrophic factor in the antinociceptive effect of antidepressants in neuropathic pain. 1590 42

A spinal cord injury (SCI) was produced in adult rats by complete spinal cord transection at L6-S1. Neuropathic pain behaviors similar to the chronic central pain (CCP) syndrome in human, such as thermal hyperalgesia, mechanical allodynia and autotomy, were present in these rats after spinal cord injury. Meanwhile, wide dynamic range (WDR) neurons recorded in the spinal dorsal horn rostral to the lesion responded as high frequency of spontaneous activities, long duration of after-discharges to noxious electrical stimuli and an augmented wind-up to 0.5 Hz stimuli. By using bupivacaine powder, a sodium channel blocker, at the locus of transection immediate after nerve injury, the chronic pain behaviors were prevented; the hyperexcitability of WDR neurons was also substantially reduced. It is suggested that spinal cord transection induces the CCP syndromes, which may be evoked and maintained by the hyperexcitability in WDR neurons rostrally. Reducing the neuronal activity at the site of lesion following injury may prevent the development of CCP after SCI.
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PMID:Spinal cord injury triggers sensitization of wide dynamic range dorsal horn neurons in segments rostral to the injury. 1608 64

Pain may be the most common reason patients seek treatment from physicians. When persistent and unrelieved, pain can frustrate both the person suffering with this condition and the physician trying to alleviate it. Relief from chronic pain may be particularly difficult to achieve and fraught with misconceptions. Treatment usually requires trials of physical, pharmacologic, and surgical interventions to achieve resolution. In cases that remain insoluble, patients must accept partial relief and seek adaptive strategies. The source of persistent pain may be nociceptive or neuropathic. Both utilize the same nervous system pathways for transmission, but significant physiologic differences exist in the mechanism through which the body processes and resolves these painful stimuli. Nociceptive pain that results from a known or obvious source (eg, trauma, cancer metastasis, ischemia, arthritis) is often easy to identify. Neuropathic pain, however, may occur in the absence of an identifiable precipitating cause. Physicians must remain alert to differences in presentation and course of neuropathic pain syndromes, some of which may be subtle or unusual.
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PMID:Management of neuropathic pain. 1627 20

Recent experimental research to treat spinal cord injury (SCI) pain has greatly increased our understanding of how such chronic pain might be modulated in the human population. Neuropathic pain is caused by the structural and biochemical changes associated with the peripheral and central nervous system damage associated with nervous system trauma, often leading to an imbalance in endogenous excitatory and inhibitory spinal systems that modulate sensory processing. But current pharmacological therapies are often ineffective over time for the greater number of patients. Although there are a variety of useful surgical and pharmacologic interventions (including electric stimulation, implantable mechanical pumps and a myriad of drugs for pain relief) cell and molecular technologies are a new frontier in pain medicine. These other potential therapeutic agents of pain are based on current and developing treatment strategies elucidated from recent research, especially concerning central spinal sensitization, and the spinal mechanisms that are thought to be the origin and ongoing cause of chronic pain, even when the injury is peripheral in location. Newly developing translational strategies such as molecular agents, viral-mediated gene transfer or cellular transplants to treat chronic pain are being evaluated in a variety of peripheral and central injury models. They seek to address both the causes of neuropathic pain, to interfere with its development and maintenance over time, and give the injured person with pain an improved quality-of-life that allows them to better deal with the larger tasks of daily life and the strenuous rehabilitation that might also improve motor function after SCI.
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PMID:Cell and molecular approaches to the attenuation of pain after spinal cord injury. 1662 36

Neuropathic pain is by definition a chronic pain condition that occurs and persists in a heterogeneous group of aetiologically different diseases characterised by a primary lesion or dysfunction of the peripheral or central nervous system. Neuropathic pain has an important prevalence in the general population, and a severe impact on quality of life and mood of affected patients. Therapy is based on tricyclic antidepressants and antiepileptic drugs, the most frequently studied drug classes. Opioids and analgesics are a second-line choice. Topical medications could be useful in several pain situations.
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PMID:Medications for neuropathic pain: current trends. 1668 27


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