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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 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

Neuropathic pain is a clinical entity designating the different types of pain associated with a lesion of the nervous system including a wide range of pathological conditions from painful peripheral lesions (for example diabetic neuropathy, post-zoster pain, trauma-induced nerve injury) and central pain (particularly stroke-induced pain, spinal lesions, and multiple sclerosis). Despite this wide range of etiologies, neuropathic pain has well characterized clinical features which generally allow distinction from other types of pain: continuous often burn-like pain, paroxysmal pain (electrical discharge, knife stab), evoked pain, highly invalidating pain (allodynia, hyperalgesia), and associated dysethesia and/or paresthesia. Over the last ten Years, very little work has been published on neuropathic pain, which is now becoming a very active domain of research in neurobiology. Advances to date have not been spectacular although better tolerated agents have been recently marketed. Future progress should enable an appropriate response to the therapeutic challenge of neuropathic pain.
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PMID:[Neuropathic pain: experimental advances and clinical applications]. 1503 77

Neuropathic pain and paroxysmal symptoms are common in multiple sclerosis (MS) patients, although no double-blind clinical trial has been conducted to support antiepileptic medications (AED) use in MS. The aim of the study was to evaluate the frequency of AED utilisation and reported adverse events, in a cohort of MS patients. For a period of 3 years the rationale for prescribing AED, adverse effects, treatment duration and reasons for discontinuation were recorded in a database. Carbamazepine (CBZ) was prescribed in 36 patients, with adverse effects reported in 20 cases, of which 12 mimicked a relapse. Gabapentin (GBP) was prescribed in 94 patients, with adverse effects reported in 16 cases and in one case mimicked a relapse. Lamotrigine (LMT) was prescribed in 22 patients, with adverse effects reported in 4 cases, none mimicking a relapse. The present study found a significantly higher incidence of adverse effects in patients treated with CBZ, with a high rate of discontinuation at low dosages and episodes of evident worsening of neurological functioning compared to GBP or LMT.
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PMID:Antiepileptic medications in multiple sclerosis: adverse effects in a three-year follow-up study. 1572 92

Neuropathic pain is underdiagnosed and, in consequence, not properly treated. Neuropathic pain is defined as pain initiated or caused by a primary lesion or dysfunction in the nervous system. The term dysfunction is not clearly defined and is suggested not used. The prevalence of neuropathic pain is unknown, but a few detailed studies show that neuropathic pain is more common than previously assumed. Some common causes of neuropathic pain are entrapment/injuries to peripheral nerves, painful neuropathies, infections in the nervous system (i.e. postherpetic neuralgia), spinal cord injuries, multiple sclerosis and cerebral infarcts. Evaluation of neuropathic pain is performed on the basis of a thorough clinical examination which includes detailed questioning of different types of pain. Both spontaneous (ongoing and paroxysmal) as well as evoked pain may occur. The ongoing pain may be described by a large number of adjectives such as burning, aching, throbbing, sore, cutting, but there is no pain descriptor which is diagnostic for neuropathic pain. Pain may usually be evoked by lightly touching the skin or by exposure to cold. A clinical neurological examination is necessary in the evaluation of the level of injury, possibly also electromyography/neurography in case of peripheral nerve lesions or CT/MR in case of central lesions. Neuropathic pain is almost always characterised by changes in sensibility, usually involving the thin-fibre system (peripheral nerve fibres or central projections). Special emphasis is put on the examination of sensory dysfunction.
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PMID:[Assessment of neuropathic pain]. 1621 13

Tissue damage, inflammation or injury of the nervous system may result in chronic neuropathic pain characterised by increased sensitivity to painful stimuli (hyperalgesia), the perception of innocuous stimuli as painful (allodynia) and spontaneous pain. Neuropathic pain has been described in about 1% of the US population, is often severely debilitating and largely resistant to treatment. Animal models of peripheral neuropathic pain are now available in which the mechanisms underlying hyperalgesia and allodynia due to nerve injury or nerve inflammation can be analysed. Recently, it has become clear that inflammatory and immune mechanisms both in the periphery and the central nervous system play an important role in neuropathic pain. Infiltration of inflammatory cells, as well as activation of resident immune cells in response to nervous system damage, leads to subsequent production and secretion of various inflammatory mediators. These mediators promote neuroimmune activation and can sensitise primary afferent neurones and contribute to pain hypersensitivity. Inflammatory cells such as mast cells, neutrophils, macrophages and T lymphocytes have all been implicated, as have immune-like glial cells such as microglia and astrocytes. In addition, the immune response plays an important role in demyelinating neuropathies such as multiple sclerosis (MS), in which pain is a common symptom, and an animal model of MS-related pain has recently been demonstrated. Here, we will briefly review some of the milestones in research that have led to an increased awareness of the contribution of immune and inflammatory systems to neuropathic pain and then review in more detail the role of immune cells and inflammatory mediators.
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PMID:Immune and inflammatory mechanisms in neuropathic pain. 1638 53

Neuropathic pain is typified by injuries to the peripheral and central nervous system and derives from such causes as cancer, diabetes, multiple sclerosis, post-herpetic neuralgia, physical trauma or surgery, and many others. Patients suffering neuropathic pain do not respond to conventional treatment with non-steroidal anti-inflammatory drugs and show a reduced sensitivity to opiates often associated with serious side effects. Recently, it has been demonstrated that botulinum neurotoxin serotype-A (BoNT/A) is able to induce analgesia in inflammatory pain conditions. The goal of this research was to test if BoNT/A was able to relieve also neuropathic pain symptoms. By using chronic constriction injury of the sciatic nerve, a mouse model of neuropathic pain, we observed that peripheral administration of BoNT/A strongly reduced the mechanical allodynia associated with this neuropathy. Remarkably, a single non-toxic dose of BoNT/A was sufficient to induce anti-allodynic effects, which lasted for at least 3 weeks. This result is particularly relevant since neuropathic pain is poorly treated by current drug therapies. This communication enlarges our knowledge on potentially new medical uses of BoNT/A in efforts to ameliorate human health conditions, with very important implications in the development of new pharmacotherapeutic approaches against neuropathic pain.
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PMID:Anti-allodynic efficacy of botulinum neurotoxin A in a model of neuropathic pain. 1721 63

Neuropathic pain is caused by functional abnormalities of structural lesions or dysfunction in the peripheral or central nervous system, and occurs without peripheral nociceptor stimulation. Neuropathic pain has a great impact on the quality of life. Majority of the patients are unable to maintain an independent lifestyle due to their moderate to severe chronic pain and often depression contributes to the illness. Many common diseases, such as stroke, multiple sclerosis and syringomyelia may produce neuropathic pain. Neuropathic pain is a complex disease, involving several molecular pathways. Neuropathic pain treatment is stil extremely difficult despite our knowledge about this difficult to diagnose and treat pain condition has improved a lot with the aid of recent experimental and clinical studies. This review summarizes the underlying mechanisms, diagnosis and treatment approaches based on different mechanisms of effect.
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PMID:[Neuropathic pain]. 1809 93

Neuropathic pain (NP) is defined as pain caused by lesion or dysfunction of the somatosensory system, as a result of abnormal activation of the nociceptive pathway (small fibers and spinothalamic tracts). The most common causes of this syndrome are the following: diabetes, post-herpetic neuralgia, trigeminal neuralgia, stroke, multiple sclerosis, spinal cord injury, HIV infection, cancer. In the last few years, the NP has been receiving special attention for two main reasons: (1) therapeutical refractoriness of a variety of pain syndromes with predominant neuropathic characteristics and (2) the development of diagnostic tools for neuropathic pain complaints. The present review article provides relevant information on the understanding and recognition of NP, as well as evidence-based therapeutic approaches.
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PMID:What do general neurologists need to know about neuropathic pain? 1972 68

Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB(1)/CB(2) agonists, CB(2) selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Delta(9)-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Delta(9)-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.
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PMID:Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside. 1978 75

Multiple sclerosis (MS) is an inflammatory, demyelinating, autoimmune disease of the CNS. There are currently a number of disease-modifying medications for MS that modulate or suppress the immune system; however, these medications do not directly relieve MS symptoms, which include visual deficits, gait problems, sensory deficits, weakness, tremor, spasticity and pain, among others. Pain is a common symptom in MS which has recently been estimated to be experienced by more than 40% of patients. Nociceptive pain occurs as an appropriate physiological response transmitted to a conscious level when nociceptors in bone, muscle or any body tissue are activated, warning the organism of tissue damage. Neuropathic pain is initiated as a direct consequence of a lesion or disease affecting the somatosensory system, with no physiological advantage. Nociceptive and neuropathic pain in MS may be present concurrently and at different stages of the disease, and may be associated with other symptoms. Central neuropathic pain has been reported to be among the most common pain syndromes in MS. It is described as constant, often spontaneous, burning occurring more frequently in the lower limbs. Treatment typically includes tricyclic antidepressants and antiepileptic medications, although studies have been conducted in relatively small samples and optimal dosing has not been confirmed. Cannabinoids have been among the few treatments studied in well designed, randomized, placebo-controlled trials for central neuropathic pain. In the largest of these trials, which included 630 subjects, a 15-week comparison between Delta9-tetrahydrocannabinol and placebo was performed. More patients receiving active treatment perceived an improvement in pain than those receiving placebo, although approximately 20% of subjects reported worsening of pain while on active treatment. Trigeminal neuralgia, while affecting less than 5% of patients with MS, is the most studied pain syndrome. The pain can be extreme and is typically treated with carbamazepine, although adverse effects can mimic an MS exacerbation. Painful topic spasms occur in approximately 11% of the MS population and are treated with antispasticity medications such as baclofen and benzodiazepines. Gabapentin has also demonstrated efficacy, but all studies have included small sample sizes. In general, evidence for treating pain in MS is limited. Many clinical features of pain are often unrecognized by clinicians and are difficult for patients to describe. Treatment is often based on anecdotal reports and clinical experience. We present a review of treatment options for pain in MS, which should serve to update current knowledge, highlight shortcomings in clinical research and provide indications towards achieving evidence-based treatment of pain in MS.
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PMID:Pharmacological management of pain in patients with multiple sclerosis. 2056 32


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