scholarly journals Prevalence of Neuropathic Pain and the Need for Treatment

2006 ◽  
Vol 11 (suppl a) ◽  
pp. 5A-10A ◽  
Author(s):  
Pat Morley-Forster

Recent publications have suggested that more than two million adults in the United States suffer from neuropathic pain, but this number seems to be a significant underestimate. The prevalence of neuropathic pain from diabetes and postherpetic neuralgia alone, using the most conservative estimates of incidence, would equal two million Americans. Lesions of the nervous system responsible for pain genesis can occur either in the central or the peripheral nervous system. The most common causes of peripheral neuropathic pain syndromes worldwide are diabetes, HIV infection, cancer-related neuropathy (due to tumour invasion, surgical nerve damage, radiation or chemotherapy-induced nerve damage) and lumbar degenerative disc disease. Other less common, but significant, sources of suffering are postherpetic neuralgia, complex regional pain syndrome, phantom limb pain and postsurgical nerve trauma. Central neuropathic pain can be caused by stroke (infarct or hemorrhage), multiple sclerosis, spinal cord injury and syringomyelia. Certain pain syndromes such as trigeminal neuralgia and vulvodynia, although clearly neuropathic and a source of tremendous suffering, are not discussed in the present article due to space constraints. There is an unmet need for the treatment of neuropathic pain as evidenced by reports of pain despite the use of opioids and anticonvulsants, continuing psychological difficulties, lack of access to treatments and patients seeking access to complementary therapy.

2011 ◽  
Vol 64 (9-10) ◽  
pp. 443-447
Author(s):  
Milan Cvijanovic ◽  
Svetlana Simic ◽  
Sofija Banic-Horvat ◽  
Zita Jovin ◽  
Petar Slankamenac ◽  
...  

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.


2021 ◽  
Vol 64 (7) ◽  
pp. 461-467
Author(s):  
Bum Chun Suh

Background: Neuropathic pain is defined as pain arising as a direct consequence of a lesion or disease affecting the somatosensory system either at the peripheral or central level. In most cases, neuropathic pain is associated with poor general health and has a problem of suboptimal response to medical treatment. This review will discuss the neurologic and non-neurologic conditions that cause neuropathic pain and the results of epidemiologic studies on neuropathic pain.Current Concepts: Epidemiology would be a useful clinical tool for designing management and prevention strategies for various neuropathic pain syndromes. Validated neuropathic pain screening questionnaires are widely used as useful tools for the epidemiologic study of neuropathic pain. There are also validated Korean versions of these questionnaires. The overall prevalence of neuropathic pain was estimated at 6.9-10%. Common neuropathic pain syndromes include diabetic neuropathy, herpes zoster, and trigeminal neuralgia. In addition, neuropathic pain can also occur in central nervous system disorders such as spinal cord injury or stroke, and other conditions like cancerous diseases, intervertebral disc disease, and joint diseases.Discussion and Conclusion: Neuropathic pain does not respond well to medical treatment, which leaves both patients and physicians are less satisfied with such treatments. Therefore, physicians must identify the causes of the pain, explain them to the patient, and proceed with the treatment together with patients.


2016 ◽  
Author(s):  
James H. Diaz

Herpes zoster can plague anyone who has had varicella or has received the varicella or chickenpox vaccine. The incidence of herpes zoster increases with age and rises exponentially after 60 years of age. Postherpetic neuralgia (PHN) may occur after herpes zoster at any age but typically occurs after 50 years of age, with over 40% of persons over 60 years of age suffering from PHN after a shingles attack. Up to 1 million new cases of herpes zoster and 200,000 new cases of PHN may now be anticipated in the United States every year, with the incidence rate increasing as the population grows and ages with prolonged life expectancies. Although new antiviral medications will improve and shorten the course of herpes zoster, they do not guarantee the prevention of PHN. Given the high prevalence of PHN in an aging population and the availability of primary prevention by vaccination, the objectives of this review are to describe the epidemiology, pathophysiology, and clinical manifestations of zoster and PHN and to recommend a combination of strategies for the clinical management and prevention of PHN. This review contains 6 figures, 4 tables and 13 references Key words: evidence-based pain medicine, herpes zoster, neuropathic pain, postherpetic neuralgia


2009 ◽  
Vol 67 (3a) ◽  
pp. 741-749 ◽  
Author(s):  
Pedro Schestatsky ◽  
Osvaldo José M. Nascimento

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.


2015 ◽  
Vol 173 (1) ◽  
pp. 300-302 ◽  
Author(s):  
S. Hiom ◽  
G.K. Patel ◽  
R.G. Newcombe ◽  
S. Khot ◽  
C. Martin

2021 ◽  
pp. 097275312110463
Author(s):  
Gurwattan S. Miranpuri ◽  
Parul Bali ◽  
Justyn Nguyen ◽  
Jason J Kim ◽  
Shweta Modgil ◽  
...  

Spinal cord injuries incite varying degrees of symptoms in patients, ranging from weakness and incoordination to paralysis. Common amongst spinal cord injury (SCI) patients, neuropathic pain (NP) is a debilitating medical condition. Unfortunately, there remain many clinical impediments in treating NP because there is a lack of understanding regarding the mechanisms behind SCI-induced NP (SCINP). Given that more than 450,000 people in the United States alone suffer from SCI, it is unsatisfactory that current treatments yield poor results in alleviating and treating NP. In this review, we briefly discussed the models of SCINP along with the mechanisms of NP progression. Further, current treatment modalities are herein explored for SCINP involving pharmacological interventions targeting glia cells and astrocytes. The studies presented in this review provide insight for new directions regarding SCINP alleviation. Given the severity and incapacitating effects of SCINP, it is imperative to study the pathways involved and find new therapeutic targets in coordination with stem cell research, and to develop a new gold-standard in SCINP treatment.


Author(s):  
Nanna Brix Finnerup ◽  
Nadine Attal

This article presents an update of the current classification, diagnosis, assessment, mechanisms, and treatment of neuropathic pain. Neuropathic pain, which is defined as pain associated with a lesion or disease of the somatosensory nervous system, may be caused by a variety of conditions, such as diabetic neuropathy, herpes zoster, surgical trauma, spinal cord injury, and stroke. The diagnostic criteria for neuropathic pain are a history of a nervous system disease or lesion and pain distribution and sensory signs in a neuroanatomically plausible distribution. The treatment of neuropathic pain is often multidisciplinary and involves specific drugs. Recent progress in the diagnosis, assessment, and understanding of its mechanisms offers the perspective of a more rational therapeutic management, which should result in better therapeutic outcome.


2019 ◽  
Vol 51 (6) ◽  
pp. 555-561 ◽  
Author(s):  
Anhui Wang ◽  
Changshui Xu

Abstract Neuropathic pain is caused by the damage or dysfunction of the nervous system. In many neuropathic pain models, there is an increase in the number of gap junction (GJ) channels, especially the upregulation of the expression of connexin43 (Cx43), leading to the secretion of various types of cytokines and involvement in the formation of neuropathic pain. GJs are widely distributed in mammalian organs and tissues, and Cx43 is the most abundant connexin (Cx) in mammals. Astrocytes are the most abundant glial cell type in the central nervous system (CNS), which mainly express Cx43. More importantly, GJs play an important role in regulating cell metabolism, signaling, and function. Many existing literatures showed that Cx43 plays an important role in the nervous system, especially in the CNS under normal and pathological conditions. However, many internal mechanisms have not yet been thoroughly explored. In this review, we summarized the current understanding of the role and association of Cx and pannexin channels in neuropathic pain, especially after spinal cord injury, as well as some of our own insights and thoughts which suggest that Cx43 may become an emerging therapeutic target for future neuropathic pain, bringing new hope to patients.


2017 ◽  
Vol 1 (21;1) ◽  
pp. E53-E63 ◽  
Author(s):  
Stephan A. Schug

Background: Patients with neuropathic pain (NeP) often receive combination therapy with multiple agents in the hopes of improving both pain and any comorbidities that may be present. While pregabalin is often recommended as a first-line treatment of NeP, few studies have examined the effects of concomitant medications on the efficacy of pregabalin. Objective: To examine the effects of concomitant medications on the efficacy and safety of pregabalin for the treatment of NeP. Study Design: Data were derived from 7 randomized placebo-controlled trials of pregabalin (150, 300, 600, and flexible 150 – 600 mg/d) for the treatment of postherpetic neuralgia (PHN) and 2 randomized placebo-controlled trials for the treatment of NeP due to spinal cord injury (SCINeP). On each day, patients rated the severity of their pain and pain-related sleep interference (PRSI) over the previous 24 hours on a scale from 0 to 10, with higher scores indicating greater severity. Patients were also continually monitored for the occurrence of adverse events. Setting: A pooled retrospective analyses of data from randomized clinical trials. Methods: Changes from baseline in mean weekly pain and PRSI scores were compared between patients who received concomitant NeP medications and patients who did not receive concomitant NeP medications. Results of these comparisons are presented separately for the PHN (through 4, 8, and 12 weeks) and SCI-NeP (through 12 weeks) cohorts. Common adverse events are also presented for each treatment group. Results: Pregabalin significantly improved both pain and PRSI scores relative to placebo at most dose levels and time points examined. Notably, little difference was observed in the extent of therapeutic response to pregabalin between patients who received concomitant NeP medications and patients who did not receive concomitant NeP medications. Additionally, the profile of treatment-emergent adverse events appeared to be largely unaffected by the use of concomitant NeP medications in the pooled patient population. Limitations: Our analysis is limited in that the original trials of pregabalin were not powered to examine the effects of concomitant NeP medications. Conclusions: The data presented here demonstrate that therapeutic response to pregabalin and the occurrence of adverse events in patients with NeP are generally unaffected by the concurrent use of other NeP medications. Trial Registration numbers: NCT00159666; NCT00301223; NCT00407745 Key words: Pregabalin, neuropathic pain, pain-related sleep interference, concomitant medications, postherpetic neuralgia, spinal cord injury, efficacy, safety


2021 ◽  
pp. 901-905
Author(s):  
James C. Watson

The International Association for the Study of Pain defines neuropathic pain as pain that is initiated or caused by a lesion or disease affecting the somatosensory system in either the peripheral nervous system or the central nervous system. Several well-recognized descriptors for neuropathic pain suggest a neuropathic rather than nociceptive pathophysiology (hot, burning, painful cold, freezing, prickling or tingling, pins and needles, electrical, shooting, stabbing, lancinating, and itching). However, whether the pain descriptors are used alone or incorporated into questionnaires to identify neuropathic pain, their sensitivity and specificity are limited (generally 70%-85%); therefore, verbal pain descriptors are insufficient for making the diagnosis of neuropathic pain.


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