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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 is often a difficult condition to treat. Clinical and laboratory studies using intravenously administered local anesthetics or antiarrhythmic agents support the use of these drugs for the treatment of neuropathic pain. The availability of the oral antiarrhythmic medication, mexiletine, has made it possible to study the effects of an orally administered medication on chronic neuropathic pain. The study used a double-blind placebo-controlled design to examine 11 subjects in whom treatment with conventional pain medications had been unsuccessful. Subjects had a history of peripheral nerve injury or dysfunction, and all complained of symptoms consistent with neuropathic pain. After baseline pain measurements, mexiletine or placebo was given in gradually increasing doses to a maximum daily dose of 750 mg mexiletine. After 1 month at steady state, the subject received the alternative medication. Mexiletine was found to produce a statistically significant reduction in reported pain when compared to baseline or placebo. Pain scores were rated on a scale from 0 (no pain) to 10 (unbearable pain). Median pain scores prior to mexiletine were 7, after placebo treatment 7, and while receiving mexiletine (750 mg/day) 4. Side effects were mild and well-tolerated. Mexiletine may be effective in reducing neuropathic pain for patients in whom alternative pain medications have been unsatisfactory.
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PMID:The use of oral mexiletine for the treatment of pain after peripheral nerve injury. 131 97

Neuropathic pain remains a major complication of various forms of injury to peripheral nerves in humans. Recently, 2 models of peripheral mononeuropathy in the rat have been described which closely resemble the human condition. Bennett and Xie3 described one model induced by the placement of 4 loose ligatures around the entire sciatic nerve; Seltzer et al. have described a second model produced by the placement of a tight ligature around one-third to one-half of the sciatic nerve. It is the purpose of this work to compare the effect of these injuries on the time course and magnitude of hyperalgesia as measured by paw withdrawal latency to a radiant heat stimulus. In addition, to evaluate the hypothesis that neuropathic pain develops as a result of injury-associated discharges, some injuries were induced following anesthesia of the sciatic nerve. Our results show that the partial constriction neuropathy (PCN) described by Bennett and Xie3 develops in a faster time frame than that produced by the tight ligature, or partial transection neuropathy (PTN), described by Seltzer and co-workers. In addition, the PCN shows a reduction in both the duration and magnitude of behavioral hyperalgesia obtained for those animals in which local anesthetic (lidocaine) was applied to the sciatic nerve, while the PTN does not show this sensitivity. The data suggest that injury-related discharge is one important factor contributing to the generation of hyperalgesia in the PCN model. The mechanism(s) responsible for the generation of hyperalgesia in the early stages of the PTN model are not lidocaine-sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential influence of local anesthetic upon two models of experimentally induced peripheral mononeuropathy in the rat. 131 90

Neuropathic pain, i.e., pain resulting from functional changes in peripheral and central pathways subsequent to injury to the peripheral nervous system, offers a most difficult challenge to therapy. To date, only the antidepressants and the anticonvulsants have shown any effectiveness, albeit incomplete and inconsistent, and many questions remain unanswered: What are the exact indications for the antidepressants? What component of neuropathic pain do they relieve, and through which mechanisms? Which type of antidepressants should be prescribed? A first-generation tricyclic? Or a new compound with a selective action on serotonin reuptake? What are the effective dosage and duration of the treatment? What is it mechanism of action? What other antalgic effects do carbamazepine and baclofen possess apart from their action on trigeminal neuralgia? The opiates are generally considered to be without effect, but recent clinical and experimental findings seem to point otherwise. In the meantime, following a few simple rules will optimize the benefit of drug treatment in neuropathic pain: treatment tailored to individual cases; adequate dosage and duration of treatment. However, it is from the near future that breakthroughs are being expected, dues to the multiplication of animal models and more accurate analysis; new clinical evaluation tools which help in distinguishing the different mechanisms underlying the various aspects of pain; the development of new substances, such as capsaicin, local anesthetics, anti-inflammatory agents (NSAIDs for example); and better defined methodological conditions for therapeutic trials.
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PMID:[Pharmacological treatment of neuropathic pain]. 133 88

From 1983-1989, 106 patients with breast cancer were treated in our pain management unit on 6767 treatment days. Pain was caused by bone metastasis in 73% of patients. Neuropathic pain was reported by 32% of the patients. In all but four of these patients, new tumour growth was diagnosed. Patients were treated according to WHO analgesic guidelines with non-opioids on 16% of the days, non-opioids in combination with weak opioids on 36% and with strong opioids on 38% (orally 90%, parenterally 4% of the days). Due to the prevalence of bone pain non-steroidal antiinflammatory drugs were given on 56% of the days. The high incidence of neuropathic pain led to frequent use of co-analgesics (antidepressants 17%, anticonvulsants 12%, steroids 12% of the days). Adjuvant therapy for symptoms other than pain was given on 86% of the days. Whilst 92% of patients reported more than moderate pain on admission, 45% obtained complete pain relief beginning from the first days of treatment. On 92% of the days, patients described their pain as moderate or less. Side effects were treated symptomatically and played a minor role in a reason to change therapy.
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PMID:[Therapy for symptomatic pain in advanced breast cancer]. 137 58

Neuropathic pain following nerve injury is thought to involve central nervous system Ca(2+)-mediated neuronal plastic changes. This study provides evidence that induction and/or maintenance of post-injury neuropathic pain behaviors in the rat is associated with increases in membrane-bound protein kinase C (PKC), a Ca(2+)-dependent process known to mediate central nervous system neuronal plasticity. In addition, spinal cord administration of GM1 ganglioside, an intracellular inhibitor of PKC translocation/activation, reverses both increased levels of membrane-bound PKC and pain-related behaviors. Thus, persistent post-injury neuropathic pain may be mediated by the initiation of excitatory neuropathological processes resulting from an increase in membrane-bound PKC.
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PMID:Pain-related increases in spinal cord membrane-bound protein kinase C following peripheral nerve injury. 139 64

Pain related to fibromyalgia may consist of a complex interaction of nociceptive, neuropathic, dysregulatory central nervous system and psychosomatic mechanisms. Nociceptor pain is based on the excitation of nervous sensors specialized to signal potentially harmful stimuli, i.e., the nociceptors. Metabolic deficiencies in muscle and neurogenic inflammation induced by the release of substance P and other neuropeptides from the peripheral nerve endings may result in chemical sensitization of nociceptors and an ensuing hyperalgesia particularly present in tender points. Neuropathic pain is due to pathological mechanisms within nerve cells and fibers in the peripheral and central nervous system. Pathophysiology may be related to compression (such as in the carpal tunnel syndrome or a vertebral disk herniation) or regeneration of nerves, resulting in ectopic impulse discharges and disturbances of axonal transport. The ensuing neuronal hyperexcitability and trophic changes induced by a disturbed axonal transport system may be major factors of pain in fibromyalgia. Dysregulatory pain denotes pain maintained by dysfunction of efferent control loops. Thus, if spinal motoneuron output results in excessive tension of postural muscle, nociceptors in muscles, tendons and joints might become more excited. Persistent abnormal spinal reflex transmission due to, e.g., peripheral trauma or inappropriate postural habits may result in a vicious circle between muscle hypertension and pain. Similarly, a defective sympathetic control may result in disturbed microcirculation and nociceptor excitation (e.g., in sympathetic algodystrophy). Many symptoms of pain in fibromyalgia (trigger points, pain referral, pain associated with muscle spasm or neurogenic joint immobilization) can be attributed to abnormal control mechanisms in a complex cybernetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin J Pain 1991
PMID:Pathophysiological mechanisms of fibromyalgia. 181 May 27

Neuropathic pain, originating in damaged nerve and not peripheral nociceptors, is often resistant to treatment by opiates given by the oral, parenteral or spinal routes. This failure to obtain satisfactory pain relief is generally ascribed to psychological factors or to individual peculiarities in drug metabolism or kinetics. Currently, psychotropic and antidepressant drugs are among the first choices in treating painful conditions due to partial nerve lesions. We present a 56-year-old man who suffered intractable pain confined to his left knee following emergency L2-3 vertebral decompression, after collapse due to metastatic disease. 12 mg of morphine and 10 of diazepam given together intravenously did not lessen pain. Acute, solitary spinal nerve root injury was hypothesized. 2 mg of haloperidol injected IV gave complete relief of pain without hypotension or deep sedation. There is no definite explanation for the resistance of neuropathic pain to opiates.
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PMID:[Neuropathic pain unrelieved by morphine, alleviated by haloperidol]. 235 28

Neuropathic pain is a major clinical problem and is often a source of persistent suffering and disability for patients with deafferenting injuries. In addition to the emotional burden of this persistent pain, patients' lives are frequently disrupted socially and financially. Understanding of the mechanisms that underlie neuropathic pain is poor, although there is evidence for widespread changes within the peripheral and central somatosensory nervous systems of such patients. In addition, treatment for neuropathic pain is often ineffective. Some degree of symptom control is often possible, however, through a multidisciplinary approach. This approach includes medications, physical treatments, and behavioral modifications. The limited understanding we have of the mechanisms of neuropathic pain is a strong reason to actively pursue further research into the pathophysiology of these conditions. Continued clinical and basic investigations into neuropathic pain also provide the best chance of finding treatments that are effective.
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PMID:Deafferentation pain syndromes. 265 78

Neuropathic pain is often a significant source of protracted suffering, seriously impairing efforts at functional rehabilitation of affected patients. The assessment and treatment of pain symptoms in patients with disease affecting peripheral and central somatosensory pathways is therefore an important problem in clinical management and rehabilitation of patients with neurologic disease.
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PMID:Clinical management of neuropathic pain. 282 5

Most children with cancer will experience pain during their illness, whether it may be cured or not. They may suffer from acute pain related to treatments or to invasive procedures, or from prolonged pain due to the evolution of cancer or sequellae of treatment. Pain must be considered as a major symptom and must be suspected, diagnosed and evaluated. Physicians have to analyse the different components, the physiopathologic data, and causes of pain. Treatments have to be prescribed, adjusted to each patient and monitored in conformity with rigorous guidelines in order to obtain the best analgesic efficacy and the lowest side effect levels. The use of opioids is frequent and their doses are higher as those used in adults. Neuropathic pain is frequent in children suffering from cancer and requires treatment by means of antidepressant drugs if clinical signs of neuropathic pain are predominant.
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PMID:[Strategy of treatment of cancer pain in children]. 748 Nov 61


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