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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.
Pain 2004 Sep
PMID:Suicidal ideation, plans, and attempts in chronic pain patients: factors associated with increased risk. 1532 24

This article presents the clinical characteristics, epidemiology, pathophysiology and treatment of 2 neuropathic conditions: trigeminal neuralgia and atypical odontalgia. A case report highlights the complexities involved in diagnosing neuropathic pain. Neuropathic pain is chronic, diverse in quality, difficult to localize and it occurs in the absence of obvious pathology. To avoid multiple, ineffective dental treatments, general practitioners must be familiar with the signs of nonodontogenic sources of tooth pain.
J Can Dent Assoc 2004 Sep
PMID:Diagnostic challenges of neuropathic tooth pain. 1536 15

Neuropathic pain involves co-regulation of many genes and their translational products in both peripheral and central nervous system. We used proteomics approaches to investigate expressional changes in cytosolic protein levels in rat brainstem tissues following ligation of lumbar 5 and 6 (L5, L6) spinal nerves, which generates a model of peripheral neuropathic pain (NP). Proteins from brainstem tissue homogenates of NP and SHAM animals were fractionated by two-dimensional (2-DE) gel electrophoresis to produce a high-resolution map of the brainstem soluble proteins. Proteins showing altered expression levels between NP and SHAM were selected. Isolated proteins were in-gel trypsin-digested and the resulting peptides were analyzed by matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry. Using the mass spectrometric data, we were able to identify 17 proteins of interest through searches of the Swiss-Prot and NCBi nonredundant protein sequence database. Several of the identified proteins, including fatty acid binding protein-brain (FABP-B), major histocompatibility complex (MHC) class 1, T-cell receptor (TCR) alpha chain, and interleukin-1 (IL-1), showed significantly higher levels in the NP rat brainstem. Proteomic analysis has identified several proteins with differential expression levels in NP as compared to SHAM. However, the function of the proteins identified is postulated; therefore, further experiments are required to determine the true role of each protein in NP.
Brain Res Mol Brain Res 2004 Sep 28
PMID:Proteomic identification of brainstem cytosolic proteins in a neuropathic pain model. 1536 94

There are many reports of neuropathic pain describing nerve injuries sustained by sticking or penetrating nerves by metal needles on venipuncture. However, there was no previous report of neuropathic pain caused by withdrawing a catheter from the vein as in this case. Neuropathic pain in this case was quickly cured by intravenous ketamine hydrochloride and stellate ganglion block. The neuropathic pain occurred when a medical student withdrew a catheter from the cephalic vein during clinical training. Clinical training of medical students is very important for medical education, but we must also recognize that this training involves many risks not only for patients but also for the students.
Masui 2004 Sep
PMID:[Case of radial nerve injury induced by withdrawing a catheter from the cephalic vein]. 1550 Jan 6

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.
Brain Res 2005 Sep 07
PMID:Spinal cord injury triggers sensitization of wide dynamic range dorsal horn neurons in segments rostral to the injury. 1608 64

Neuropathic pain is associated with numerous systemic illnesses, including HIV infection. The diagnosis and management of peripheral neuropathy presents diagnostic and therapeutic challenges. Among various forms of HIV-associated peripheral neuropathies, distal symmetrical polyneuropathy (DSP) is the most common. DSP may be caused or exacerbated by neurotoxic antiretrovirals, particularly the dideoxynucleoside analogues (d-drugs). Selection of appropriate pharmacologic intervention for peripheral neuropathy should be based on efficacy, safety, ease of administration, and cost. We review treatment options for painful HIV neuropathy, including experimental agents studied in recent and ongoing clinical trials.
Curr HIV/AIDS Rep 2004 Sep
PMID:Controlling neuropathic pain in HIV. 1609 Dec 34

Neuropathic pain is a neuropsychiatric condition in which pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Understanding the complexity of neuropathic pain becomes the cornerstone for appropriate diagnosis and management. Diagnosis must take into account comorbid conditions. Successful management depends on realistic patient and physician expectations and an individualized, multidisciplinary approach.
Psychiatr Clin North Am 2005 Sep
PMID:Chronic pain: physiological, diagnostic, and management considerations. 1612 76

Neuropathic pain is the focus of current clinical research, clinical identification, and treatment. It is unique from nociceptive pain and requires evaluation of the relevance and utility of common pain measures created for other painful conditions. This study evaluated the psychometric properties of a modified Brief Pain Inventory (BPI) for patients with painful diabetic peripheral neuropathy (BPI-DPN). Participants were patients with painful DPN (n = 255) enrolled in a DPN Burden of Illness survey referred through 17 outpatient settings (primary care physicians, endocrinologists, neurologists, and anesthesiologists). Patients completed the BPI-DPN and self-report measures of health-related quality of life, mood sleep, and health care use. Construct, criterion and discriminant validity, and internal consistency reliability were evaluated. Principal axis factoring with oblimin rotation revealed two interpretable factors (eigenvalues > 1.0), consistent with most published BPI validation studies: a severity scale comprising the four BPI Severity items and an interference scale comprising the seven Interference items, which satisfied criteria for interpretability and model fit. Cronbach's alpha was high (0.94) for both scales. Mean pain Severity was highly correlated with Bodily Pain from the Medical Outcomes Study Short Form-12, version 2 (r(s) = 0.63, P < .001), the Pain/Discomfort item in the Euro-QoL (r(s) = 0.58, P < .001), and a verbal rating scale measure of pain severity (r(s) = 0.74, P < .001). Individual BPI-DPN Interference domains were moderately correlated (r(s)'s > 0.5, P < .001) with analogous measures, and the Sleep Interference item had a high, significant association with the three primary Medical Outcome Study-Sleep scale subscales (r(s)'s = 0.66-71, P < .001). Worst Pain and Interference ratings were significantly associated with hospital use and outpatient visits because of DPN. These results replicate, in a pure peripheral neuropathic pain condition, the BPI psychometric characteristics documented in populations with nociceptive or mixed pain conditions. The BPI-DPN is a promising instrument in the evaluation of painful DPN.
J Vasc Nurs 2005 Sep
PMID:Validation of a modified version of the Brief Pain Inventory for painful diabetic peripheral neuropathy. 1612 33

Neuropathic pain is responsible for a significant amount of the morbidity associated with generalized and focal peripheral neuropathies. It is a consequence of alterations in neuronal function, chemistry, and structure that occur secondary to nerve injury. These manifestations of neuronal plasticity occur in the peripheral nerve, spinal cord, and brain. A variety of agents from diverse pharmacologic classes, the so-called adjuvant analgesics, have been used to treat neuropathic pain. These include antidepressants, first- and second-generation anticonvulsants, antiarrhythmic agents, topical agents, N-methyl-D-aspartate receptor antagonists, and opioid analgesics. The use of these adjuvant analgesics, either alone or in combination, should result in the alleviation of neuropathic pain in most patients. Recent advances in the understanding of pain mechanisms at multiple central nervous system levels should pave the way toward more effective treatment modalities.
CNS Spectr 2005 Sep
PMID:The treatment of neuropathic pain. 1726 75

Neuropathic pain from nerve injury by trauma, disease or surgery often causes prolonged suffering. To explore the molecular mechanisms that underlie neuropathic pain, we used mRNA from the L4--5 segments of the lumbar spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain, and differentially screened a cDNA library from the rat brain. A novel gene, termed RSEP1 (Rat Spinal cord Expression Protein 1), was identified. Northern blots revealed that RSEP1 was expressed mainly in the central nervous system including the cerebral cortex, hippocampus, brainstem and spinal cord, as well as in the kidney and ovary. In situ hybridization showed a high level of RSEP1 expression in the CA1, CA3 and dentate gyrus regions of the hippocampus and the small sensory neurons in the dorsal horn, as well as the large neurons in the ventral horn of the spinal cord. Intrathecal injection of RSEP1 antisense oligonucleotide into the spinal cord lumbar enlargement attenuated neuropathic pain behaviours in CCI rats, suggesting a functional involvement of RSEP1 in neuropathic pain.
Eur J Neurosci 2005 Sep
PMID:RSEP1 is a novel gene with functional involvement in neuropathic pain behaviour. 1617 50


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