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

A variety of pharmacologic approaches to the management of pain due to nerve damage have been tried, with mixed results. Sympathetically maintained pain responds most commonly to sympathetic nerve blocks. Oral nifedipine may be a useful adjunct. Many-but not all-neuropathic pain patients experience relief from low-dose tricyclic antidepressants. When those drugs are not sufficient, the addition of an anticonvulsant, systemic local anesthetic, or both, to the antidepressant may be useful. Neuropathic pain with a major cutaneous component may respond well to topical therapy with the Substance P depletor capsaicin to reduce elevated prostaglandin levels. Topical therapy is most commonly used as an adjunct to systemic drugs. There is now good evidence that early treatment of acute herpes neuralgia with famciclovir may be effective in reducing postherpetic neuralgia. The role of opioids in chronic nerve pain is unclear. Most patients do not respond to these drugs, and should not receive them. Many patients with chronic neuropathic or sympathetically maintained pain need detoxification from opioids, sedative-hypnotics, and muscle relaxants. Some patients cannot carry out normal activities of daily living without opioids, however, and function well while taking low-dose, regularly scheduled opioids. The prognosis for successfully managing neuropathic and sympathetically maintained pain is greatly improved if appropriate therapy is initiated early in the course of the pain. When patients do not respond adequately to initial drug therapy, referral to an interdisciplinary pain management program for evaluation may be in order. Many neuropathic and SMP patients have complex pain syndromes which are most effectively managed through a coordinated, interdisciplinary approach. Careful attention to medical, pharmacologic, psychologic, and physical factors are the hallmarks of this type of treatment. The drugs now available provide marked relief to the majority of patients when therapy includes careful attention to the various dimensions of the pain syndrome. Although consistently effective drug therapy for all neuropathic and sympathetically maintained pain is not yet available, the probability of new NMDA antagonists being introduced in the next few years offers promise.
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PMID:Analgesic drugs for neuropathic and sympathetically maintained pain. 885 42

Neuropathic pain, a form of chronic pain caused by injury to or disease of the peripheral or central nervous system, is a formidable therapeutic challenge to clinicians because it does not respond well to traditional pain therapies. Our knowledge about the pathogenesis of neuropathic pain has grown significantly over last 2 decades. Basic research with animal and human models of neuropathic pain has shown that a number of pathophysiological and biochemical changes take place in the nervous system as a result of an insult. This property of the nervous system to adapt morphologically and functionally to external stimuli is known as neuroplasticity and plays a crucial role in the onset and maintenance of pain symptoms. Many similarities between the pathophysiological phenomena observed in some epilepsy models and in neuropathic pain models justify the rational for use of anticonvulsant drugs in the symptomatic management of neuropathic pain disorders. Carbamazepine, the first anticonvulsant studied in clinical trials, probably alleviates pain by decreasing conductance in Na+ channels and inhibiting ectopic discharges. Results from clinical trials have been positive in the treatment of trigeminal neuralgia, painful diabetic neuropathy and postherpetic neuralgia. The availability of newer anticonvulsants tested in higher quality clinical trials has marked a new era in the treatment of neuropathic pain. Gabapentin has the most clearly demonstrated analgesic effect for the treatment of neuropathic pain, specifically for treatment of painful diabetic neuropathy and postherpetic neuralgia. Based on the positive results of these studies and its favourable adverse effect profile, gabapentin should be considered the first choice of therapy for neuropathic pain. Evidence for the efficacy of phenytoin as an antinociceptive agent is, at best, weak to modest. Lamotrigine has good potential to modulate and control neuropathic pain, as shown in 2 controlled clinical trials, although another randomised trial showed no effect. There is potential for phenobarbital, clonazepam, valproic acid, topiramate, pregabalin and tiagabine to have antihyperalgesic and antinociceptive activities based on result in animal models of neuropathic pain, but the efficacy of these drugs in the treatment of human neuropathic pain has not yet been fully determined in clinical trials. The role of anticonvulsant drugs in the treatment of neuropathic pain is evolving and has been clearly demonstrated with gabapentin and carbamazepine. Further advances in our understanding of the mechanisms underlying neuropathic pain syndromes and well-designed clinical trials should further the opportunities to establish the role of anticonvulsants in the treatment of neuropathic pain.
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PMID:Anticonvulsants for neuropathic pain syndromes: mechanisms of action and place in therapy. 1112 21

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.
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PMID:Neuropathic orofacial pain part 1--prevalence and pathophysiology. 1135 93

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.
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PMID:Neuropathic pain: Review of mechanisms and pharmacologic management. 1145 64

Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in damaged areas of the nervous system. In peripheral neuropathic pain, damaged nerve endings exhibit abnormal spontaneous and increased evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, although not explored in detail, the spontaneous pain and evoked allodynia are also best explained by a neuronal hyperexcitability. The peripheral hyperexcitability is due to a series of molecular changes at the level of the peripheral nociceptor, in dorsal root ganglia, in the dorsal horn of the spinal cord, and in the brain. These changes include abnormal expression of sodium channels, increased activity at glutamate receptor sites, changes in gamma-aminobutyric acid (GABA-ergic) inhibition, and an alteration of calcium influx into cells. The neuronal hyperexcitability and corresponding molecular changes in neuropathic pain have many features in common with the cellular changes in certain forms of epilepsy. This has led to the use of anticonvulsant drugs for the treatment of neuropathic pain. Carbamazepine and phenytoin were the first anticonvulsants to be used in controlled clinical trials. Studies have shown these agents to relieve painful diabetic neuropathy and paroxysmal attacks in trigeminal neuralgia. Subsequent studies have shown the anticonvulsant gabapentin to be effective in painful diabetic neuropathy, mixed neuropathies, and postherpetic neuralgia. Lamotrigine, a new anticonvulsant, is effective in trigeminal neuralgia, painful peripheral neuropathy, and post-stroke pain. Other anticonvulsants, both new and old, are currently undergoing controlled clinical testing. The most common adverse effects of anticonvulsants are sedation and cerebellar symptoms (nystagmus, tremor and incoordination). Less common side-effects include haematological changes and cardiac arrhythmia with phenytoin and carbamazepine. The introduction of a mechanism-based classification of neuropathic pain, together with new anticonvulsants with a more specific pharmacological action, may lead to more rational treatment for the individual patient with neuropathic pain.
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PMID:Anticonvulsants in neuropathic pain: rationale and clinical evidence. 1188 43

Pain caused by dysfunction or damage to the peripheral or central nervous system is typified by the symptoms described by patients with painful diabetic neuropathy, post-herpetic neuralgia and central poststroke pain. All these conditions are more common in the elderly. Neuropathic pain has long been recognised as one of the more difficult types of pain to treat; however, with the current emphasis on providing a multidisciplinary assessment and approach to management, more patients will be offered relief of their symptoms and an improved quality of life. Despite the use of combination drug therapy, adequate pain relief in the elderly is difficult to achieve without adverse effects. In an attempt to minimise these it is important to include non-drug treatment options in the management plan. Lifestyle changes and environmental modification, together with encouragement to adopt an appropriate exercise programme and an emphasis on maintaining mobility and independence should always be considered. Interventional therapy ranging from simple nerve blocks to intrathecal drug delivery can be of value. Drug treatment remains the mainstay of therapy. Tricyclic antidepressants such as amitriptyline, while having significant adverse effects in the elderly, have a number needed to treat (NNT) of 3.5 for 50% pain relief in diabetic neuropathy and 2.1 for 50% pain relief in postherpetic neuralgia. The newer antiepileptic drugs, such as gabapentin, appear to have a better adverse effect profile and provide similar efficacy with the NNT for treating painful diabetic neuropathy being 3.7 and 3.2 for treating pain in postherpetic neuralgia. As our understanding of the complexities of the pain processes increases, we are becoming more able to appropriately combine treatments to achieve not only improved pain relief but also improved function.
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PMID:Management strategies for the treatment of neuropathic pain in the elderly. 1249 68

Understanding the pathophysiology of a pain syndrome is helpful in selecting appropriate treatment strategies. Nociceptive pain is related to damage to tissues due to thermal, chemical, mechanical, or other types of irritants. Neuropathic pain results from injury to the peripheral or central nervous system. Common examples of neuropathic pain include postherpetic neuralgia, diabetic neuropathy, complex regional pain syndrome, and pain associated with spinal cord injuries. Nociceptive pain may have similar clinical characteristics to neuropathic pain. It is also possible for acute nociceptive pain to become neuropathic in nature, as with myofascial pain syndrome. A clear benefit of botulinum toxin therapy for treatment of neuropathic pain disorders is that it often relieves pain symptoms. Although the precise mechanism of pain relief is not completely understood, the injection of botulinum toxin may reduce various substances that sensitize nociceptors. As a result, botulinum toxin types A and B are now being actively studied in nociceptive and neuropathic pain disorders to better define their roles as analgesics.
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PMID:A focused review on the use of botulinum toxins for neuropathic pain. 1256 66

Neuropathic pain impacts millions of people in the United States and around the world. Patients experience one of many symptoms, such as pain, paresthesia, dysesthesia, hyperalgesia, and allodynia, for many years because of unavailable or inadequate treatment. One of the major challenges in treating patients with neuropathic pain syndromes is a lack of consensus concerning the appropriate first-line treatment options for conditions associated with neuropathic pain, including postherpetic neuralgia, diabetic peripheral neuropathy, and trigeminal neuralgia. This review summarizes the published results of randomized trials involving treatment for neuropathic pain conditions. Anticonvulsants, such as gabapentin, carbamazepine, and lamotrigine, and tricyclic antidepressants, including amitriptyline and desipramine, have demonstrated efficacy in relieving pain associated with postherpetic neuralgia, diabetic peripheral neuropathy, and trigeminal neuralgia, in several studies. However, the lack of head-to-head comparison studies of these agents limits the conclusions that can be reached. Clinicians who must make decisions regarding the care of individual patients may find some guidance from the number of randomized trials with a positive outcome for each agent. Using quality-of-life study outcomes, treatment strategies must encompass the impact of therapeutic agents on the comorbid conditions of sleep disturbance and mood and anxiety disorders associated with neuropathic pain. Looking to the future, emerging therapies, such as pregabalin and newer N-methyl-D-aspartate-receptor blockers, may provide physicians and patients with new treatment options for more effective relief of pain.
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PMID:Pharmacologic management part 1: better-studied neuropathic pain diseases. 1499 28

Neuropathic pain is often resistant to opioids, so other medication classes, such as tricyclic antidepressants, anticonvulsants, and local anesthetics, are often used. Central sensitization, or pain 'wind-up', may perpetuate chronic neuropathic pain even when ongoing peripheral sensory input is absent. Wind-up is thought to cause allodynia, hyperalgesia, and hyperpathia. Receptors such as NMDA, AMPA, and M-glu have recently been identified for their role in central sensitization or pain 'wind-up'. Ketamine has been proposed recently for neuropathic pain secondary to its NMDA receptor activity. The current application as a topical gel stems from the theory that ketamine has peripheral action at both opioid and Na+-K+ channels. This case study involved 5 patients from 25 to 70 years old (3 RSD, 1 lumbar radiculopathy, 1 post-herpetic neuralgia). Dose used was determined by site and surface area of involvement and ranged from 0.093 mg/kg to 9.33 mg/kg. All five patients reported significant pain relief at initial application and wished to continue treatment. The average numerical analogue scale (NAS) score preapplication was 8.8. The average 15 minutes post application NAS was 1.6. Patients reported alterations in temperature sensation, feelings of relaxation and decreased tension in the area of application, and pain relief. Reduction in numerical pain scores postapplication of ketamine gel ranged from 53-100% using a 1-10 numerical pain intensity scale. No significant side effects were reported. Ketamine Gel may provide clinicians with a new option in the battle against chronic neuropathic pain. Until further information is available and larger trials can be conducted, we can only recommend this type of therapy for refractory cases in which all primary and secondary options have been exhausted.
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PMID:Topical ketamine gel: possible role in treating neuropathic pain. 1510 68

Neuropathic pain (NP), caused by a primary lesion or dysfunction in the nervous system, affects approximately 4 million people in the United States each year. It is associated with many diseases, including diabetic peripheral neuropathy, postherpetic neuralgia, human immunodeficiency virus-related disorders, and chronic radiculopathy. Major pathophysiological mechanisms include peripheral sensitization, sympathetic activation, disinhibition, and central sensitization. Unlike most acute pain conditions, NP is extremely difficult to treat successfully with conventional analgesics. This article introduces a contemporary management approach, that is, one that incorporates nonpharmacological, pharmacological, and interventional strategies. Some nonpharmacological management strategies include patient education, physical rehabilitation, psychological techniques, and complementary medicine. Pharmacological strategies include the use of first-line agents that have been supported by randomized controlled trials. Finally, referral to a pain specialist may be indicated for additional assessment, interventional techniques, and rehabilitation. Integrating a comprehensive approach to NP gives the primary care physician and patient the greatest chance for success.
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PMID:Contemporary management of neuropathic pain for the primary care physician. 1559 38


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