Gene/Protein Disease Symptom Drug Enzyme Compound
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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 arising from direct trauma to, or compression injury of, peripheral nerves is a common clinical problem. It is characterized by the development of abnormal pain states (spontaneous pain, hyperalgesia, allodynia), which can persist long after the initial injury has resolved. The underlying mechanisms are poorly understood and, as a consequence, treatment is often unsatisfactory. Some of the main contributing factors are thought to be the morphological and phenotypic changes that occur centrally, including alterations in the expression of neurotransmitters and their associated receptors, both in the dorsal root ganglia and in the spinal dorsal horn. This article focuses on the functional role of the two structurally related peptides VIP and PACAP within the spinal cord, and their possible contribution to the altered transmission of sensory information in neuropathic conditions.
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PMID:VIP and PACAP: very important in pain? 1066 8

The postradical neck pain syndrome has been briefly described in the literature, but detailed characterization has not been reported. To further define this syndrome, 25 patients with persistent pain for at least 1 month following neck dissection were evaluated. The sample consisted of 13 men and 12 women with moderate to severe pain ranging from 1 month to 27 years in duration. All patients had at least one type of neuropathic pain: spontaneous, continuous burning pain (81%), shooting pain (69%), and/or allodynia (88%). Neuropathic pain sites were within the distribution of the superficial cervical plexus (SCP). Regional myofascial pain was also common (72%). Seventeen patients agreed to undergo diagnostic local anesthetic injections. Ten of these patients had both neuropathic and somatic (myofascial) pain. Local anesthetic injection of the SCP temporarily eliminated all neuropathic pain in the 17 patients who underwent the procedure. The 10 patients who also had myofascial pain reported temporary relief of their somatic pain following myofascial trigger point injections (TPI). Criteria for the postradical neck pain syndrome are proposed: (1) persistent, nonprogressive neuropathic pain involving one or more branches of the SCP, which may be accompanied by (2) regional nonprogressive somatic pain associated with myofascial pain trigger points in head and neck muscles.
J Pain Symptom Manage 1999 Aug
PMID:Characteristics of postradical neck pain syndrome: a report of 25 cases. 1048 56

Neuropathic pain resulting from peripheral nerve injury can often be relieved by administration of alpha-adrenergic receptor antagonists. Tonic activation of alpha-adrenergic receptors may therefore facilitate the hyperalgesia and allodynia associated with neuropathic pain. It is currently unclear whether alpha2A- or alpha2c-adrenergic receptor subtypes are involved in the pro-nociceptive actions of alpha-adrenergic receptors under neuropathic conditions. We therefore investigated the effects of peripheral nerve injury on the expression of these subtypes in rat spinal cord using immunohistochemical techniques. In addition, neuropeptide Y immunoreactivity was examined as an internal control because it has previously been shown to be up-regulated following nerve injury. We observed a decrease in alpha2A-adrenergic receptor immunoreactivity in the spinal cord ipsilateral to three models of neuropathic pain: complete sciatic nerve transection, chronic constriction injury of the sciatic nerve and L5/L6 spinal nerve ligation. The extent of this down-regulation was significantly correlated with the magnitude of injury-induced changes in mechanical sensitivity. In contrast, alpha2c-adrenergic receptor immunoreactivity was only increased in the spinal nerve ligation model; these increases did not correlate with changes in mechanical sensitivity. Neuropeptide Y immunoreactivity was up-regulated in all models examined. Increased expression of neuropeptide Y correlated with changes in mechanical sensitivity. The decrease in alpha2A-adrenergic receptor immunoreactivity and the lack of consistent changes in alpha2C-adrenergic receptor immunoreactivity suggest that neither of these receptor subtypes is likely to be responsible for the abnormal adrenergic sensitivity observed following nerve injury. On the contrary, the decrease in alpha2A-adrenergic receptor immunoreactivity following nerve injury may result in an attenuation of the influence of descending inhibitory noradrenergic input into the spinal cord resulting in increased excitatory transmitter release following peripheral stimuli.
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PMID:Effects of peripheral nerve injury on alpha-2A and alpha-2C adrenergic receptor immunoreactivity in the rat spinal cord. 1050 65

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.
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PMID:Brain-derived TNFalpha mediates neuropathic pain. 1054 89

Neuropathic pain can seem enigmatic at first because it can last indefinitely and often a cause is not evident. However, heightened awareness of typical characteristics, such as the following, makes identification fairly easy: The presence of certain accompanying conditions (e.g., diabetes, HIV or herpes zoster infection, multiple sclerosis) Pain described as shooting, stabbing, lancinating, burning, or searing Pain worse at night Pain following anatomic nerve distribution Pain in a numb or insensate site The presence of allodynia Neuropathic pain responds poorly to standard pain therapies and usually requires specialized medications (e.g., anticonvulsants, tricyclic antidepressants, opioid analgesics) for optimal control. Successful pain control is enhanced with use of a systematic approach consisting of disease modification, local or regional measures, and systemic therapy.
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PMID:Following the clues to neuropathic pain. Distribution and other leads reveal the cause and the treatment approach. 1057 7

The aim of this study was to investigate a possible distinction in three categories of opioid response and to identify possible factors associated with a poor response. A prospective survey was carried out in 105 consecutive patients requiring morphine for at least 4 weeks before death. Mean pain intensity, opioid doses and symptom intensity at weekly intervals, pain syndromes, and the presence of psychological distress were assessed. Opioid escalation index (OEI%) was calculated from the parameters recorded. Three categories were considered, including (1) patients with slow increments of opioid dose and a mean analgesic 10-cm visual analogue scale (VAS) less than 4 (responders), (2) patients with an OEI% more than 5 but a mean VAS less than 4 (partial responders), and (3) patients with a mean VAS more than 4 (poor responders). Treating physicians were asked to make a judgment on the pain treatment difficulties on a numerical scale (0-10). Significant differences in opioid starting dose (OSD), opioid dose at--4 weeks, nausea and vomiting at--1 week, opioid maximum doses, mean VAS, and OEI were found in the three categories of response. Significant correlations with the physician judgment were found for opioid maximum dose, mean VAS, VAS at the different time intervals, the doses used at the different intervals, OEI, and confusion. Neuropathic pain was significantly associated with a judgment of poor pain outcome. The correlation between the physician judgment and the categories of opioid response was highly significant. Seven of the 12 patients in the third category (poor response) were considered as having a relevant psychological distress. The categorization of the opioid response used in this study could be used in clinical research and as an audit tool, and could be tested in other settings to compare different treatments.
J Pain Symptom Manage 1999 Nov
PMID:Investigation of an opioid response categorization in advanced cancer patients. 1058 58

The purpose of this study was to investigate strain-related differences in the onset and maintenance of thermal hyperalgesia following the induction of peripheral nerve injury in two inbred strains of rats (Fischer 344 and Lewis) and two outbred strains of rats (Sprague-Dawley and Wistar). Neuropathic pain was induced via unilateral ligation of the left sciatic nerve with chromic gut sutures. A plantar analgesia meter was used to measure paw-withdrawal latency from the ligated vs. unligated hind paws of inbred vs. outbred strains of rats to investigate strain-related differences in nerve injury-induced thermal hyperalgesia. The results demonstrated no significant effects of animal strain on presurgical paw-withdrawal latency values. Following the sciatic nerve ligation (SNL) surgery, a significant hyperalgesic response was elicited from the Sprague-Dawley and Wistar rats (outbred strains) for at least 28 days. Conversely, data analyses from the inbred strains failed to demonstrate significant hyperalgesic responses to peripheral nerve injury, with the exception of postsurgical day 10. These data emphasize the importance of considering the strain of the rat being investigated before extrapolating the results from animals experiments to treatment strategies for humans with chronic neuropathic pain.
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PMID:Strain differences in neuropathic hyperalgesia. 1063 47

Injured afferent neurons produce spontaneous activity that is generated away from the normal impulse generation site. Since this activity, referred to as ectopic discharges, may play a significant role in neuropathic pain, it is important to systematically analyze the activity in various pain states. The present study used the segmental spinal nerve injury model of neuropathic pain to quantify the ectopic discharges from injured afferents in the neuropathic rat under various conditions. All aspects of measured ectopic discharges declined as postoperative time lengthened. Neuropathic pain behaviors declined in a similar fashion over the same time period. Surgical sympathectomy on neuropathic animals lowered the level of ectopic discharges along with neuropathic pain behaviors. The data indicate that the level of ectopic discharges is well correlated with that of pain behaviors in a rat neuropathic pain model, and this reinforces the supposition that ectopic discharges are important to the maintenance of neuropathic pain behaviors. The data suggest that there are two components of ectopic discharge generator mechanisms: sympathetically dependent and sympathetically independent components.
Pain 2000 Feb
PMID:Characteristics of ectopic discharges in a rat neuropathic pain model. 1066 30

The usefulness of sensory symptoms in the assessment of diabetic polyneuropathy is unclear. In the present study, we studied the hypothesis that pain is associated with small nerve fibre function, and that sensory alteration is associated with large nerve fibre function. In addition, we assessed the reproducibility and the ability to detect changes in clinical status over time of the nerve function tests currently used in clinical trials. Patients (78) with stable diabetic polyneuropathy were examined on three separate occasions with a test-retest interval of 17 and 52 weeks. Small nerve fibre function was measured using temperature discrimination thresholds for warmth (TDTwarmth) and cold (TDTcold). Large nerve fibre function was measured by testing sensory and motor nerve conduction velocities (SNCV and MNCV) and vibration perception thresholds (VPT). Neuropathic pain was only significantly associated with TDTcold, and with the MNCV of the tibial nerve. Sensory alteration was associated with almost all nerve function tests except the SNCV and MNCV of the ulnar nerve. The measurements of symptom severity and the nerve function tests all proved to be sufficiently reproducible. The standardized smallest detectable difference on group level (SDD) of the measurement of sensory alteration and neuropathic pain were almost the same (9% and 12%, respectively). Among the nerve function tests, the SNCV and MNCV had the smallest SDD (3-4%), and were, therefore, potentially the most responsive instruments. The SDD of the TDT was greater than the VPT (9-14% vs 21-28%, respectively). In conclusion, neuropathic pain was not associated with small nerve fibre function, and sensory alteration was associated with both large and small fibre function. In addition, the standardized measurement of symptom severity, the SNCV and MNCV tests, and the VPT test appear to be useful for monitoring the course of polyneuropathy in clinical trials.
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PMID:Methods for assessing diabetic polyneuropathy: validity and reproducibility of the measurement of sensory symptom severity and nerve function tests. 1067 Sep 7

Neuropathic pain may respond poorly to morphine and is often difficult to relieve. Recent attention has been drawn to the role of the N-methyl-D-aspartate (NMDA) receptor in the potentiation of neuropathic pain. Magnesium is known to block the NMDA receptor. It reduces the neuropathic pain response in animals, and attenuates postoperative pain and migraine in humans. We have examined the safety, tolerability, and efficacy of two intravenous doses of magnesium sulfate in 12 patients with neuropathic pain due to malignant infiltration of the brachial or lumbosacral plexus. The first six patients received 500 mg, the remainder 1 g. Apart from a mild feeling of warmth at the time of the injection, both doses were well tolerated. After receiving 500 mg, three patients experienced complete pain relief and two experienced partial pain relief for up to 4 hours duration; pain was unchanged in one patient. After receiving 1 g, one patient experienced complete relief and four experienced partial pain relief of similar duration; pain was unchanged in one patient. Intravenous magnesium sulfate in these doses appears to be safe and well tolerated. A useful analgesic effect may be obtained in some patients and further evaluation is warranted.
J Pain Symptom Manage 2000 Jan
PMID:The safety and efficacy of a single dose (500 mg or 1 g) of intravenous magnesium sulfate in neuropathic pain poorly responsive to strong opioid analgesics in patients with cancer. 1101 12


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