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Neuropathic pain  [cached]
Giuseppe Re,Virgilio Ricci,Fabrizio Rasi
Emergency Care Journal , 2009, DOI: 10.4081/ecj.2009.1.17
Abstract: Neuropathic pain is the expression of a dysfunction or primary lesion of a nerve in the peripheral or central nervous system, or both, rather than the biological signal transmitted by the nerve following peripheral nociceptor activation. It represents about 20% of all painful syndromes, with an estimated prevalence of 1.5%, however is actual incidence is hard to pinpoint due to the difficulties encountered in distinguishing it from chronic pain, of which it represents a significant percentage, on account of the not infrequent concurrence of conditions. It is crucial to recognise the variety of symptoms with which it can present: these can be negative and positive and, in turn, motor, sensitive and autonomic. In public health terms, it is important to emphasise that the diagnosis of neuropathic pain does not in most cases require sophisticated procedures and does not therefore weigh on health expenditure. In clinical practice, a validated scale (the LANSS is mentioned) is useful for identifying patients presenting neuropathic pain symptoms. Therapy is based on three categories of medication: tricyclic antidepressants, anti-epileptics and opioids at high doses: neuropathic pain has a bad reputation for often resisting common therapeutic approaches and responding less well that nociceptor pain to monotherapy. Therapeutic strategies are all the more adequate the more they are based on symptoms and therefore on the pain generation mechanisms, although the recommendations are dictated more by expert opinions that double-blind randomised trials.
Neuropathic Pain: Mechanisms and Treatments  [PDF]
Long-Sun Ro,Kuo-Hsuan Chang
Chang Gung Medical Journal , 2005,
Abstract: Neuropathic pain is caused by functional abnormalities of structurallesions in the peripheral or central nervous system, and occurs withoutperipheral nociceptor stimulation. Many common diseases, such aspostherpetic neuralgia, trigeminal neuralgia, diabetic neuropathy, spinalcord injury, cancer, stroke, and degenerative neurological diseases mayproduce neuropathic pain. Recently, theories have been proposed thatstate there are specific cellular and molecular changes that affect membraneexcitability and induce new gene expression after nerve injury,thereby allowing for enhanced responses to future stimulation. In addition,the ectopic impulses of neuroma, changes of sodium and calciumchannels in injured nerves, sympathetic activation, and deficient centralinhibitory pathway contribute to the mechanisms of neuropathic pain.Currently, treatment of neuropathic pain is still a challenge.Pharmacotherapies (antidepressants, antiepileptics) remain the basis ofneuropathic pain management. However, patient satisfaction in theresults of the treatment of neuropathic pain is still disappointing. Sinceit has been established that intense noxious stimulation produces a sensitization of centralnervous neurons, it may be possible to direct treatments not only at the site of peripheralnerve injury, but also at the target of central changes. In order to provide better pain control,the mechanism-based approach in treating neuropathic pain should be familiar to physicians.In the future, it is hoped that a combination of new pharmacotherapeutic developments,careful clinical trials, and an increased understanding of the contribution and mechanisms ofneuroplasticity will lead to an improvement in the results of clinical treatments and preventionof neuropathic pain.
Contemporary treatment neuropathic pain  [PDF]
Cvijanovi? Milan,Simi? Svetlana,Bani?-Horvat Sofija,Jovin Zita
Medicinski Pregled , 2011, DOI: 10.2298/mpns1110443c
Abstract: Introduction. Neuropathic pain, or pain associated with disease or injury to the peripheral or central nervous system, is a common symptom of a heterogeneous group of conditions, including diabetic neuropathy, trigeminal neuralgia, postherpetic neuralgia and spinal cord injury. Chronic neuropathic pain should not be thought of as a symptom. It should truly be thought of as a disease with a very complicated pathophysiology. Pathophysiology. The mechanisms involved in neuropathic pain are complex and involve both peripheral and central pathophysiologic phenomenon. The underlying dysfunction may involve deafferentation within the peripheral nervous system (e.g. neuropathy), deafferentation within the central nervous system (e.g. post-thalamic stroke) or an imbalance between the two (e.g. phantom limb pain). Clinical characteristics. Neuropathic pain is non-nociceptive, in contrast to acute nociceptive pain, and it can be described as ”burning”, ”electric”, ”tingling”, and ”shooting” in nature. Treatment. Rational polypharmacy is often necessary and actually it is almost always the rule. It would be an exception if a patient was completely satisfied with his treatment. Treatment goals should include understanding that our patients may need to be titrated and managed with more than one agent and one type of treatment. There should be the balance of safety, efficacy, and tolerability. Conclusion. There are many new agents and new applications of the existing agents being currently studied which will most certainly lead to even more improved ways of managing this very complicated set of disorders.
Neuropathic Pain - Current Concepts
HP Meyer
South African Family Practice , 2008,
Abstract: Neuropathic pain (NP) represents a common and diverse group of disorders with peripheral and/or central nervous system damage or dysfunction. Many patients report intractable and severe pain that is resistant to simple analgesics. The diagnosis of NP is primarily based on clinical evaluation rather than diagnostic tests. Distinct pain qualities in the patient's history and findings on clinical examination, such as hyperalgesia and other sensory findings in an area correlating with the patient's pain pattern are important in diagnosis. Various screening tools may assist in the diagnosis of NP. A number of pathophysiological mechanisms have been identified in NP, including sodium- and calcium-channel upregulation and spinal cord hyperexcitability (central sensitisation).Appropriate management includes evaluation of the functional impact of NP, patient education and reassurance. A multi-model biopsychosocial approach that includes various nonpharmacological modalities is recommended. Appropriate pharmacological management is based on evidence-based recommendations that provide guidance for selecting first-, second- and third-line medications, alone or in combination. It is hoped that future treatment advances will improve the care of patients who live with NP. South African Family Practice Vol. 50 (3) 2008: pp. 40-49
Neuronal mechanism for neuropathic pain
Min Zhuo
Molecular Pain , 2007, DOI: 10.1186/1744-8069-3-14
Abstract: Pleasure and pain are two major emotions of animals and humans. While the pleasure from different activities is what animals and human are seeking daily, both animals and humans avoid pain. Pain is divided into two major groups: physiological pain and pathological pain. Physiological pain is an important physiological function for survival. Depending on pain experience, animals and humans gain knowledge of potential dangerous stimuli in the environment, and pain-related unpleasantness help to form long-term avoidance memory in order to protect themselves. Although animals have the capability to enhance their sensitivity as well as motor responses to subsequent noxious stimuli, animals' ability to distinguish pain from other sensation is intact, at least not permanently altered.Unlike physiological pain, pathological pain only happen after injury (e.g., tissue or nerve injury), and is not the result of repetitive application of physiological pain. Long-term changes are likely to occur after injury, both peripherally and centrally. Consequently, the injury and injury-related areas undergo long-term plastic changes, and pain sensation is significantly enhanced (hyperalgesia) or non-noxious stimuli cause pain (allodynia). It should be pointed out that allodynia is one of the major problems in pathological pain. Because it is induced by non-noxious stimuli, it is mostly likely that central plastic changes play important roles.Thus, pathological pain is likely a result of long-term plastic changes along somatosensory pathways, from the periphery to cortex. Due to long-term plastic changes in central regions, pain specificity is lost at the first synapses of the somatosensory pathway, at least from areas where allodynia was reported. Here I will review recent progress related to neuronal mechanism for neuropathic pain, a form of persistent pain resistant to conventional treatment. I will focus on central plasticity, in particular the forebrain areas that are critical for t
Translational investigation and treatment of neuropathic pain
Bo Xu, Giannina Descalzi, Hai-Rong Ye, Min Zhuo, Ying-Wei Wang
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-15
Abstract: Neuropathic pain develops from a lesion or disease affecting the somatosensory system [1]. Triggers for neuropathic pain are numerous and diverse. It can be caused by direct and indirect injury to nerve systems. The classification of neuropathic pain is often based on the anatomical location of neurologic involvement (central or peripheral). Major forms of clinical neuropathic pain are given in Table 1. It is estimated that neuropathic pain afflicts millions of people worldwide [2]. Neuropathic pain reduces the patients' overall health-related quality of life (sleep, mood, work, social and recreational capacities), and generates health-care costs several times higher than in control groups [3]. However, the management of patients with chronic neuropathic pain is of utmost difficulty, and the response to existing treatments is often inadequate. Therapy for neuropathic pain includes the use of both pharmacological and non-pharmacological (psychological, physical, and surgical treatment) methods. The objectives of this review are to outline the underlying mechanisms and current therapies, and to discuss the recent advances that should be useful to guide the treatment of neuropathic pain in the future.According to the new definition by IASP, neuropathic pain is a type of chronic pain caused by a lesion or disease of the somatosensory nervous system. Lesion means the directly damage to somatosensory system, while disease refers to indirectly injury by metabolic stress, autoimmune conditions or inflammatory and so on [1]. Such damage or lesion can take place not only somatosensory nerves, but also those innervating visceral organs. Hence, neuropathic pain is an aberrant somatosensory processing that contrasts with the normal plasticity of somatosensory system in nociceptive pain. According to the location of injury sites, neuropathic pain can be further divided into central neuropathic pain and peripheral neuropathic pain. Central neuropathic pain is pain caused by a lesi
Nischal Tyagi, Vineeta Tripathi, Preeti Vishwakarama, Radha Goel*
International Journal of Bioassays , 2013,
Abstract: Neuropathic pain is a chronic pain that worsens the quality of life of the patient occurring as a result of peripheral or central nerve injury. It is characterized by spontaneous ongoing and evoked increased pain sensation upon contact with noxious or non-noxious stimuli. The management of neuropathic pain involves interdisciplinary approach and mainly focuses on pharmacological treatment. The drugs found effective in management of neuropathic pain are antiepileptics, antidepressants, opioid analgesics, NSAID’S (Non-Steroidal Anti Inflammatory Drugs), local anesthetics. Combination therapy is generally required in patients with severe neuropathic pain.
Sukhvir kaur1
International Journal of Pharmacy and Biological Sciences , 2011,
Abstract: Neuropathic pain (NP) is a wide term, associated with damage to peripheral nerves, spinal nerves and to the central nervous system (CNS). It is a leading cause of morbidity and mortality and its prevalence is continuously increasing in industrialised nations. It is characterised by allodynia, hyperalgesia and hyperpathia leading to sympathetic dysfunction and dystrophic changes. Number of synthetic drugs are used in the management of neuropathic pain but are of no use as they elicit several adverse effects. Hence the present review delineated with the management of neuropathic pain by the aid of herbal drugs and few newer synthetic drugs that are efficacious and potent.
Assessment of Neuropathic Pain and Clinical Evaluation of Patients with Suspected Neuropathic Pain  [PDF]
Zita Jovin,Milan Cvijanovic,Miroslav Ilin,Aleksandar Kopitovic
Aktuelnosti iz Neurologije, Psihijatrije i Grani?nih Podru?ja , 2010,
Abstract: Pain is an unpleasant sensory and emotional experience associated with existing or potential damage to the tissue or that is experienced as such. According to the current defi nition, the term neuropathic pain refers to pain that occurs as a direct consequence of a lesion or disease aff ecting the somatosensory system. Neuropathic pain is particularly problematic for its severity, chronicity and resistance to common analgesics. It aff ects around 2-3% of the general population, although the estimates vary widely. Evaluation of neuropathic pain includes neurophysiological tests, skin biopsy, quantitative sensory testing, physical examination and pain assessment. Neuropathic pain causes positive and negative symptoms and can occur spontaneously or following a provoking stimulus. A detailed medical history and thorough clinical evaluation aid localizing the damage to the neuraxis. Precise determination of localization, intensity, quality and pattern of pain are of the utmost importance.
TNF-α and neuropathic pain - a review
Lawrence Leung, Catherine M Cahill
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-27
Abstract: Despite intense research over the last 30 years, debate is still ongoing regarding the nature of neuropathic pain, including controversy as to whether such pain is peripheral or central in origin, and as to whether its etiology is inflammatory or non-inflammatory. Increasing evidence has provided better understanding of the roles of both immune and pro-inflammatory mediators (e.g., the interleukins, TNF-α, complement components, ATP and the chemokines) in the mechanisms of both peripheral and central neuropathic pain [1-4]. This review will concentrate on current knowledge and experimental models regarding the role of TNF-α, among other cytokines, in neuropathic pain; with an appraisal of available potential therapeutic targets related to TNF-α and directions for future developments in this area.Neuropathic pain is characterized by disproportionate hypersensitivity to stimuli (hyperalgesia), abnormal pins-and-needles or electric-shock-like sensations (hyperpathia) and, finally, nociceptive responses to non-noxious stimuli (allodynia). It is a pathological type of pain that persists despite resolution of the inciting damage to the nerve and the surrounding tissues. From a behavioral standpoint, nociception is an adaptive tool for better survival, while neuropathic pain is considered maladaptive. The prevalence of neuropathic pain ranges from 1% in UK [5] to 1.5% in the US [6] to 17.9% in Canada [7]. Weir Mitchell [8] is often credited with the first descriptive account of neuropathic pain from nerve injuries seen in the US Civil War, using terms that range from "burning", "mustard red hot", "red-hot file rasping the skin" to "with intensity ranging from most trivial burning to a state of torture". Clinically, the top three most common types of neuropathic pain are post-herpetic neuralgia, trigeminal neuralgia and diabetic neuropathy [9]. Neuropathic pain is among the most difficult types of chronic pain to treat, which not only significantly impairs patients' quality
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