Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. Accordingly, multiple endodontic procedures may be instigated to remove the likely anatomical source of the pain, yet the pain persists. There have been few studies and limited patient numbers investigating the condition. Two retrospective studies revealed the incidence of persistent pain following endodontic treatment to be 3-6% and 5% of patients; one author with wide experience in assessing the condition estimated its prevalence at 125,000 individuals in the USA alone. In one study, 50% of neuropathic orofacial pain patients reported persistent pain specifically following endodontic treatment. Patients predisposed to the condition may include those suffering from recurrent cluster or migraine headaches. Neuropathic pain states include postherpetic neuralgia (shingles) and phantom limb/stump pain. The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.
 ...
PMID:Neuropathic orofacial pain part 1--prevalence and pathophysiology. 1135 93

The effective treatment of patients suffering from a variety of difficult pain syndromes, including phantom pain and other neuropathic pains, remains a clinical challenge. Neuropathic pain has been shown to respond to drugs that block the N-methyl-D-aspartate (NMDA) receptor, such as ketamine and amantidine. A 44-year-old woman with a previous right-sided forequarter amputation presented to the Palliative Medicine Team complaining of neuropathic pain in her left arm, which was neurologically intact. The pain was treated with repeated infusions of intravenous ketamine. Twenty-one infusions were given over a period of four months. The pain intensity experienced by the patient lessened as the frequency of the ketamine infusions increased. This finding has not been described previously and supports the theory that there may be an optimum frequency of ketamine infusions to achieve adequate pain control.
 ...
PMID:An unusual case of chronic neuropathic pain responds to an optimum frequency of intravenous ketamine infusions. 1136 65

The effectiveness of intrathecal opioid therapy when applied to different pain mechanisms, in particular neuropathic and nociceptive pain conditions, was studied retrospectively in 43 patients suffering from cancer pain. On the basis of clinical and radiological data, the pain mechanisms were categorized as nociceptive (n = 23) and neuropathic (n = 20). The average duration of treatment of nociceptive pain was 5 months, of neuropathic pain only 2.5 months. The initial median reduction of pain with intrathecal opioid therapy was 77.8% for nociceptive and 61.1% for neuropathic pain. Long-term results with patients suffering nociceptive pain showed a continuing good median pain reduction of 66.7%. Patients suffering from neuropathic pain showed poor long-term results (11.1% median pain reduction). Neuropathic pain in the extremities reacted least to the application of intrathecal opioids. Optimal results were obtained for nociceptive pain in the trunk area of the body.
 ...
PMID:The significance of intrathecal opioid therapy for the treatment of neuropathic cancer pain conditions. 1141 61

Neuropathic pain is a challenge for clinicians because it is resistant to commonly prescribed analgesics, such as opioids and nonsteroidal antiinflammatory drugs. Fortunately, adjuvant analgesics, drugs not typically thought of as pain relievers, may be effective. It is helpful to classify adjuvant analgesics used to treat neuropathic pain into two broad categories: (1) membrane stabilizing agents, which inhibit ectopic discharges on damaged neural membranes, and (2) drugs that enhance dorsal horn inhibition, which may augment biogenic amine or GABAergic mechanisms in the dorsal horn of the spinal cord. Current evidence regarding efficacy generally does not support the use of one drug over another, and selection of a particular drug may depend on experience or expected side effects. The overall efficacy of tricyclic antidepressants for neuropathic pain is modest, and they may produce intolerable side effects. Based on current studies, gabapentin is a reasonable alternative to antidepressants, as initial monotherapy or add-on treatment, particularly for painful diabetic peripheral neuropathy and postherpetic neuralgia. From a practical standpoint, to optimize analgesia more than one drug may be necessary. Although polypharmacy is the result, this approach may improve therapy and minimize side effects. From a safety standpoint, medications generally should be started at low doses and titrated to effect. Although labor-intensive, this strategy can improve compliance and optimize patient care.
 ...
PMID:Neuropathic pain: Review of mechanisms and pharmacologic management. 1145 64

Neuropathic pain associated with abnormal tactile and thermal responses that are extraterritorial to the injured nerve is known to be difficult to diagnose and treat because of clinical observation of limited responsiveness to opioids and non-steroidal anti-inflammatory drugs. To reproduce the different pathological changes observed in neuropathic pain patients, several laboratory animal models have been proposed. Recent studies using such models suggest the involvement of neuronal plasticity in pain pathways through nociceptive neurons. Our new experimental model using specific pain-producing molecules that clearly distinguish three different nociceptive fibers from each other reproduces neuropathic pain-like hyperalgesia and less sensitivity to morphine. After nerve injury, the nociceptive responses through type I neurons, which are polymodal C-fibers and drive NK1-receptor mechanisms in spinal pain transmission, were completely lost, but without changes in type II ones, which are polymodal C-fibers and drive NMDA receptor-mechanisms, while type III ones, which are capsaicin-insensitive (possibly A-fibers) and drive NMDA-receptor mechanisms, were markedly enhanced. Such pain transmission switch mechanisms are clearly consistent with clinical effectiveness including less sensitivity to morphine and more sensitivity to NMDA-antagonists. This article also presents currently used methods for experimental neuropathic pain models.
 ...
PMID:[Animal models and peripheral nociception tests for the study of neuropathic pain]. 1153 Jun 84

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.
 ...
PMID:[Pathogenesis of complex regional pain syndrome (CRPS)]. 1155 32

The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expressed only in nociceptive sensory neurons. This channel has been proposed to contribute significantly to the sensitization of primary sensory neurons after injury. We have studied the nociceptive behaviours of mice carrying a null mutation in the Nav 1.8 gene (Nav 1.8 -/-) in models of peripheral inflammation as well as a model of neuropathic pain. The results from the present studies reveal that Nav 1.8 is a necessary mediator of NGF-induced thermal hyperalgesia but is not essential for PGE2-evoked hypersensitivity. Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury.
 ...
PMID:A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain. 1156 40

Neuropathic pain is associated with changes in the electrophysiological and neurochemical properties of injured primary afferent neurons. A mRNA differential display study in rat L(4/5) dorsal root ganglia (DRGs) revealed upregulation of the calcium channel alpha2delta-1 subunit 2 weeks after partial sciatic nerve ligation (Seltzer model of neuropathic pain). The upregulated transcript appeared to represent previously unidentified sequence from the 3'-untranslated region of rat alpha2delta-1 mRNA. In situ hybridization using L(5) DRGs from sham operated rats showed that 73, 40 and 19% of small (<700 microm(2)), medium (700-1100 microm(2)) and large (>1100 microm(2)) neuronal profiles, respectively, expressed alpha2delta-1 mRNA. Two weeks following nerve injury there was a significant ipsilateral increase, both in the percentage of DRG neurons expressing alpha2delta-1 mRNA and in the intensity of the hybridization signal. Comparison of this ipsilateral expression with that in sham animals, revealed that for small, medium and large neurons, respectively, the proportion of neurons labelled increased by 1.2-, 1.8- and 2.7-fold, while the hybridization signal in alpha2delta-1-labelled neurons increased by 2.8-, 2.5- and 3.7-fold. The most intensely labelled neuronal profiles in ipsilateral, sham and contralateral DRGs, were generally those with small cross-sectional areas. The alpha2delta-1 auxiliary subunit is known to modulate calcium channel function in heterologous expression systems via its association with the pore-forming alpha1 calcium channel subunit. Therefore the increased levels of this subunit in the populations of primary afferents described may, via modulation of calcium-dependent processes such as neurotransmitter release and neuronal excitability, influence the processing of sensory information.
 ...
PMID:Dorsal root ganglion neurons show increased expression of the calcium channel alpha2delta-1 subunit following partial sciatic nerve injury. 1168 71

Neuropathic pain is a debilitating consequence of nerve damage. Existing treatment is largely ineffective. Current models of neuropathic pain recognise the importance of ectopic activity in primary sensory neurones impinging on a sensitised central nervous system. Neurotrophic factors have been shown to be neuroprotective for damaged sensory neurones, providing a rationale for testing their effects in neuropathic pain states. Recent data have demonstrated potent analgesic effects of one factor (glial cell line-derived neurotrophic factor) in animal models of neuropathy, and implicated changes in sodium channel alpha-subunits in the generation of afferent ectopic activity. The new findings provide a rational basis for the use of neurotrophic factors as a novel therapeutic treatment for neuropathic pain states.
 ...
PMID:Neurotrophic factors and neuropathic pain. 1171 38

Paclitaxel, an effective anti-neoplastic agent in the treatment of solid tumors, produces a dose-limiting painful peripheral neuropathy in a clinically significant number of cancer patients. Prior work has demonstrated paclitaxel-induced neurodegeneration and sensory loss in laboratory rodents. We describe here an experimental paclitaxel-induced painful peripheral neuropathy. Adult male rats were given four intraperitoneal injections on alternate days of vehicle or 0.5, 1.0, or 2.0 mg/kg of paclitaxel (Taxol). Behavioral tests for pain using mechanical and thermal stimuli applied to the tail and hind paws, and tests for motor performance, were taken before, during and after dosing for 22-35 days. All three doses of paclitaxel caused heat-hyperalgesia, mechano-allodynia, mechano-hyperalgesia, and cold-allodynia, but had no effect on motor performance. Neuropathic pain began within days and lasted for several weeks. We did not detect any dose-response relationship. Tests at the distal, mid, and proximal tail failed to show evidence of a length-dependent neuropathy. Vehicle control injections had no effect on any measure. No significant systemic toxicities were noted in the paclitaxel-treated animals. Light-microscopic inspection of the sciatic nerve (mid-thigh level), L4-L5 dorsal root ganglia, and dorsal and ventral roots, and the gray and white matter of the L4-L5 spinal cord, showed no structural abnormalities. Electron microscopic examination of the sciatic nerve (mid-thigh level) and the L4-L5 dorsal root ganglia and dorsal horns demonstrated no degeneration of myelinated and unmyelinated axons in the sciatic nerve and roots, but revealed endoneurial edema. This model may be useful in understanding a significant source of pain in cancer patients, and in finding ways to avoid the neurotoxicity that limits paclitaxel therapy.
 ...
PMID:A painful peripheral neuropathy in the rat produced by the chemotherapeutic drug, paclitaxel. 1173 Oct 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>