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

Neuropathic pain can be triggered by non-painful stimuli (e.g., light touch), a sensory abnormality termed allodynia. The acute blockade of spinal glycine receptors with intrathecal strychnine induces a reversible allodynia-like state in the rat. We describe the application of in vivo differential normal pulse voltammetry with carbon fibre micro-electrodes for monitoring the catechol oxidation current (CAOC) of the locus coeruleus (LC) in the strychnine model of allodynia. In addition, we tested the effect of mexiletine, a drug useful in the management of clinical neuropathic pain in this model. Our results show that somatosensory processing in the spinal cord of urethane-anaesthetized rats is radically altered during glycine receptor blockade such that the normally innocuous stimulus of hair deflection causes the marked activation of the LC as determined using in vivo differential normal pulse voltammetry. Mexiletine suppressed the LC and cardiovascular responses of strychnine induced allodynia. Results of this study indicate that LC CAOC, an index of LC neuronal activity: (a) is a sensitive biochemical index of strychnine-allodynia; (b) is temporally correlated with the cardiovascular and motor responses evoked by hair deflection during glycine receptor blockade; and (c) can be used to quantitate allodynia in the strychnine model.
J Neurosci Methods 1997 Sep 05
PMID:Use of differential normal pulse voltammetry for the measurement of locus coeruleus catecholaminergic metabolism in an acute anaesthetized rodent model of allodynia: effect of mexiletine. 933 35

The degree of opioid responsiveness in patients with different pain syndromes associated with advanced head and neck cancer was studied with the aid of various indices that have proved to be easy to compare and capable of eliciting individual profiles of opioid responsiveness in cancer patients with pain. Thirty-seven patients requiring opioid therapy for more than 6 weeks were reviewed. The opioid escalation index (OEI) was lower in aged patients, albeit not significantly. Significant differences in OEI were found among patients belonging to the different categories of responses proposed. Although higher doses were needed than reported in the general population, pain was considered acceptable and most patients were classified as partially responsive. Neuropathic pain was associated with higher OEIs. The indices applied will be useful in clinical research to demonstrate individual profiles of opioid responsiveness, from cases of easy and immediate pain control to unresponsiveness to opioid treatment, which can be difficult to evaluate in the clinical setting.
Support Care Cancer 1998 Sep
PMID:Opioid responsiveness in patients with advanced head and neck cancer. 977 68

Neuropathic pain refers to syndromes that may be related to peripheral or central neural structure compression, infiltration, or damage. Cancer-related neuropathic pain results from compression or infiltration of nerves by the tumor, nerve trauma from operative procedures, or neuropathic pain related to cancer treatment. Management of neuropathic pain includes the use of opioids, antidepressants, anticonvulsants, local anesthetics, and other adjuvant medications. Intractable neuropathic pain may require the use of intraspinal delivery or anesthetic and neurosurgical procedures. The nurse practitioner plays an important role in the assessment and "trial and error" management of cancer-related neuropathic pain.
Nurse Pract Forum 1998 Sep
PMID:Cancer-related neuropathic pain. 978 99

Neuropathic pain has been suggested to be resistant to treatment with opiates. Such perceived lack of opioid responsiveness may be due to the dose-range over which specific opioid compounds have been studied as well as the efficacy of these compounds. Dihydroetorphine is a novel opiate that demonstrates significantly greater analgesic potency compared to morphine, and which also demonstrates diminished capacity for producing physical dependence in laboratory animals. The present study compared the intravenous (i.v.) efficacy, potency and duration of action of dihydroetorphine, fentanyl, heroin and morphine in producing anti-allodynic actions in a rat model of neuropathic pain (ligation of the L5/L6 nerve roots). All compounds produced significant anti-allodynic activity with dihydroetorphine being the most potent (A50 of 0.2 microg kg(-1), i.v.). Morphine was approximately 7440 times less potent than dihydroetorphine while heroin and fentanyl were approximately 163.5 and 6.9 times less potent in producing anti-allodynic actions. Dihydroetorphine also showed a maximal effect at 0.6 microg kg(-1) in all animals tested, while 100 microg kg(-1) was required for heroin to produce a maximal effect. Fentanyl and morphine did not elicit a maximum anti-allodynic response (74 and 76% maximum possible effect (%MPE), respectively). As expected, fentanyl showed a relatively brief duration of action (approximately 20 min at the highest tested dose), while dihydroetorphine and morphine demonstrated anti-allodynic actions for up to 45 min. Heroin had the longest duration of action, producing significant anti-allodynic effects for up to 90 min. These data show that dihydroetorphine and heroin produce potent and long-lasting anti-allodynic actions in this model. Additionally, in contrast to morphine and fentanyl, both dihydroetorphine and heroin were able to achieve a maximal response. The remarkable potency, maximal efficacy and duration of action of these compounds, particularly dihydroetorphine, suggests that these compounds may warrant further examination as potential therapeutic treatments for neuropathic pain states.
Eur J Pharmacol 1998 Sep 11
PMID:Anti-allodynic actions of intravenous opioids in the nerve injured rat: potential utility of heroin and dihydroetorphine against neuropathic pain. 978 70

Neuropathic pain is a chronic pain state that develops a central component following acute nerve injury. However, the pathogenic mechanisms involved in the expression of this central component are not completely understood. We have investigated the role of brain-associated TNF in the evolution of hyperalgesia in the chronic constriction injury (CCI) model of neuropathic pain. Thermal nociceptive threshold has been assessed in rats (male, Sprague-Dawley) that have undergone loose, chromic gut ligature placement around the sciatic nerve. Total levels of TNF in regions of the brain, spinal cord and plasma have been assayed (WEHI-13VAR bioassay). Bioactive TNF levels are elevated in the hippocampus. During the period of injury, hippocampal noradrenergic neurotransmission demonstrates a decrease in stimulated norepinephrine (NE) release, concomitant with elevated hippocampal TNF levels. Continuous intracerebroventricular (i.c.v.) microinfusion of TNF-antibodies (Abs) starting at four days, but not six days, following ligature placement completely abolishes the hyperalgesic response characteristic of this model, as assessed by the 58 degrees C hot-plate test. Antibody infusion does not decrease spinal cord or plasma levels of TNF. Continuous i.c.v. microinfusion of rrTNF alpha exacerbates the hyperalgesic response by ligatured animals, and induces a hyperalgesic response in animals not receiving ligatures. Likewise, field-stimulated hippocampal adrenergic neurotransmission is decreased upon continuous i.c.v. microinfusion of TNF. These results indicate an important role of brain-derived TNF, both in the pathology of neuropathic pain, as well as in fundamental pain perception.
Brain Res 1999 Sep 11
PMID:Brain-derived TNFalpha mediates neuropathic pain. 1054 89

Neuropathic pain results from injury to neural structures within the peripheral or central nervous systems. Such injury promotes spontaneous and ectopic firing of nerves as well as reorganization of the nervous system. Neuropathic pain persists chronically. Patients who suffer from neuropathic pain exhibit persistent or paroxysmal pain without apparent immediate cause or pain hypersensitivity after tissue damage. This hypersensitivity is manifest as hyperalgesia and allodynia. Complex regional pain syndrome, CRPS is a category of neuropathic pain and is further divided into type I(reflex sympathetic dystrophy: RSD) and type II(causalgia). CRPS is characterized by localized autonomic dysregulation in the affected area with vasomotor and/or sudomotor changes, edema, colour difference, sweating abnormality, and atrophy.
Nihon Rinsho 2001 Sep
PMID:[Pathogenesis of complex regional pain syndrome (CRPS)]. 1155 32

Contemporary medicine is characterized by sophisticated specialization of the individual physician. The specialist in urological surgery may undertake one of the most important and primary medical tasks, the mitigation and therapy of pain. This review aims to provide an overview of the concepts of pain therapy in urology. Most patients benefit from basic concepts of analgesia, including measuring and documenting pain scores at the bedside by the nursing staff. Patients undergoing very painful operative procedures require more potent techniques of analgesia, e.g. intravenous patient-controlled analgesia and epidural analgesia. These techniques need adequate supervision by an acute pain service, but their implementation improves the outcome in some situations. Pain in acute renal obstruction varies in intensity and duration; hence, analgesic therapy has to be tailored to the individual patient. Pain syndromes from cancer can be more complex than those after surgery. Neuropathic pain is probably the most difficult to manage and requires consultation with a pain-management specialist. In the case of neuropathic pain, treatment only with opioids is of limited efficacy and combination with co-analgesics is necessary. In addition, invasive analgesic therapies should sometimes be considered.
BJU Int 2002 Sep
PMID:The treatment of pain in urology. 1217 84

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.
Anesth Analg 2003 Sep
PMID:Defining neuropathic pain. 1293 71

Neuropathic pain is a difficult clinical problem that is often refractory to medical management. Glial-derived neurotrophic factor (GDNF) administered intrathecally has been shown to prevent or reduce pain in an animal model of neuropathic pain, but cannot be delivered in the required doses to treat human pain. We have previously demonstrated that peripheral subcutaneous inoculation of a replication-incompetent herpes simplex virus (HSV)-based vector can be used to transduce neurons of the dorsal root ganglion. To examine whether HSV-mediated expression of GDNF could be used to ameliorate neuropathic pain, we constructed a replication-incompetent HSV vector expressing GDNF. Subcutaneous inoculation of the vector 1 week after spinal nerve ligation resulted in a continuous antiallodynic effect that was maintained for 3-4 weeks. Reinoculation of the vector reestablished the antiallodynic effect with a magnitude that was at least equivalent to the initial effect. Vector-mediated GDNF expression blocked the nonnoxious touch-induced increase in c-fos expression in dorsal horn characteristic of the painful state. Gene transfer to produce a trophic factor offers a novel approach to the treatment of neuropathic pain that may be appropriate for human therapy.
Mol Ther 2003 Sep
PMID:HSV-mediated gene transfer of the glial cell-derived neurotrophic factor provides an antiallodynic effect on neuropathic pain. 1294 9

Neuropathic pain and epileptic seizures bear several similarities, among them is the response to anticonvulsant drugs. It has therefore been hypothesized that epileptiform activity of nociceptive spinal dorsal horn neurons may contribute to paroxysmal forms of neuropathic pain. We used patch-clamp and field potential recordings from young rat spinal cord slices to test if nociceptive dorsal horn structures are indeed able to sustain epileptiform activity. Application of the convulsant 4-aminopyridine (100 microM) evoked epileptiform activity that was most pronounced in superficial dorsal horn and involved nociceptive lamina I neurons with a projection to the brain. The epileptiform activity was dependent on fast excitatory and inhibitory synaptic transmission through ionotropic glutamate receptors and GABA(A) receptors. During epileptiform activity, previously silent polysynaptic pathways from primary afferent C-fibers to superficial dorsal horn neurons were opened. Stimulation of primary afferents at Adelta- and C-fiber intensity interfered with the epileptiform rhythm, suggesting that both affect the same dorsal horn structures. Similar to neuropathic pain, spinal dorsal horn epileptiform activity was much less reduced by classical analgesics than by anticonvulsant agents.
Pain 2003 Sep
PMID:Epileptiform activity in rat spinal dorsal horn in vitro has common features with neuropathic pain. 1449 51


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