What causes neuropathic pain and how is it diagnosed and treated? WebMD gives you an overview of the causes and treatment. Neuropathic pain is pain caused by damage or disease affecting the somatosensory nervous system. Neuropathic pain may be associated with abnormal. With neuropathic pain, the body sends pain signals to your brain unprompted. Here's what causes it and what you can do.
Central neuropathic pain syndromes appear to involve reorganization of central somatosensory processing; the main categories are deafferentation pain and sympathetically maintained pain. Both are complex and, although presumably related, differ substantially.
Deafferentation pain is due to partial or complete interruption of peripheral or central afferent neural activity. Phantom limb pain pain felt in the region of an amputated body part.
Mechanisms are unknown but may involve sensitization of central neurons, with lower activation thresholds and expansion of receptive fields. Sympathetically maintained pain depends on efferent sympathetic activity. Complex regional pain syndrome sometimes involves sympathetically maintained pain. Other types of neuropathic pain may have a sympathetically maintained component. Mechanisms probably involve abnormal sympathetic-somatic nerve connections ephapses , local inflammatory changes, and changes in the spinal cord.
Dysesthesias spontaneous or evoked burning pain, often with a superimposed lancinating component are typical, but pain may also be deep and aching. Other sensations—eg, hyperesthesia, hyperalgesia, allodynia pain due to a nonnoxious stimulus , and hyperpathia particularly unpleasant, exaggerated pain response —may also occur. Symptoms are long-lasting, typically persisting after resolution of the primary cause if one was present because the CNS has been sensitized and remodeled.
Neuropathic pain is suggested by its typical symptoms when nerve injury is known or suspected. The cause eg, amputation, diabetes may be readily apparent. If not, the diagnosis often can be assumed based on the description. Pain that is ameliorated by sympathetic nerve block is sympathetically maintained pain. Multimodal therapy eg, psychologic treatments, physical methods, antidepressants or anticonvulsants, sometimes surgery. Without concern for diagnosis, rehabilitation, and psychosocial issues, treatment of neuropathic pain has a limited chance of success.
For peripheral nerve lesions, mobilization is needed to prevent trophic changes, disuse atrophy, and joint ankylosis. Surgery may be needed to alleviate compression. Psychologic factors must be constantly considered from the start of treatment. Anxiety and depression must be treated appropriately. When dysfunction is entrenched, patients may benefit from the comprehensive approach provided by a pain clinic.
Several classes of drugs are moderately effective see table Drugs for Neuropathic Pain , but complete or near-complete relief is unlikely. Antidepressants and anticonvulsants are most commonly used. Evidence of efficacy is strong for several antidepressants and anticonvulsants 1. First-line treatment for trigeminal neuralgia. Considered as efficacious as carbamazepine for trigeminal neuralgia and useful for other paroxysmal neuropathic pain.
Unlike carbamazepine , no CBC or liver function monitoring necessary. The only US FDA-approved drugs for use with such devices are morphine and ziconotide an N-type calcium channel antagonist The most frequently reported adverse reactions associated with intrathecal ziconotide are dizziness, nausea, confusion, memory impairment, nystagmus uncontrolled movement of the eyes and an increase in the levels of serum creatine kinase.
Ziconotide is contraindicated in patients with a history of psychosis, and patients should be monitored for evidence of cognitive impairment, hallucinations or changes in mood and consciousness. No high-quality randomized trials have been conducted to assess the efficacy of ziconotide and morphine; hence, the recommendations are a consensus of experts based on clinical experience or case series.
For example, mirror therapy and motor imagery are effective in the treatment of pain and disability associated with complex regional pain syndrome type I and type II The quality of evidence supporting these interventions for neuropathic pain is weak and needs further investigation , People with chronic pain are not passive; they actively attempt to change the causes of pain and change their own behaviour in response to pain.
However, for many patients, such change without therapeutic help is unachievable, and repeated misdirected attempts to solve the problem of pain drive them further into a cycle of pain, depression and disability At present, there is no evidence for identifying who is at risk of untreatable, difficult to manage neuropathic pain and who might benefit from psychological intervention, although research is underway on the former Psychological interventions are designed to promote the management of pain and to reduce its adverse consequences.
Treatments are often provided after pharmacological or physical interventions have failed, although they could be introduced earlier and in concert with non-psychological interventions.
Such treatments address mood typically anxiety and depression , function including disability and social engagement, as well as indirectly targeting analgesia.
Secondary outcomes are sometimes reported because they are deemed important to treatment delivery for example, therapeutic alliance and self-efficacy or because they are valued by one or more stakeholder for example, return to work and analgesic use.
A Cochrane systematic review of psychological interventions for chronic pain analysed data from 35 trials, which showed small-to-moderate effects of CBT over comparisons such as education, relaxation and treatment as usual In a companion review of 15 trials delivering treatment via the Internet, a similar broadly positive conclusion emerged, although the confidence in the estimates of effects was low Psychological treatments other than behavioural therapy and CBT were considered in this review, but none was of sufficient quality to include.
Another Cochrane review of trials specifically undertaken in patients with neuropathic pain found no evidence for or against the efficacy and safety of psychological interventions for chronic neuropathic pain , which is not surprising given the similar findings for non-psychological interventions An urgent need for studies of treatments that are designed specifically for patients with neuropathic pain exists, in particular, those with painful diabetic neuropathy, which is a growing problem Specifically, studies of CBT are needed with content that is specifically designed to meet the psychosocial needs of patients with neuropathy, in particular, with regard to the multiple sensory challenge, comorbidity and polypharmacy A recognition that neuropathic pain increases with age will also mean that an understanding of later-life accommodation to illness will be important In addition, a methodological focus on individual experience and trajectories of change is needed, either through single case experiments or through ecological momentary assessment Furthermore, communication technology, in particular, the use of mobile health innovation, is likely to play an important part in future solutions.
However, how to manage effective therapeutic relationships at a distance, and how technology can augment and improve face-to-face CBT remain to be clarified Technical psychological variables — such as catastrophic thinking, acceptance or readiness to change — should be relegated to process variables.
Conversely, a pragmatic focus on patient-reported outcomes will be essential to reduce pain, improve mood and reduce disability, which will ultimately improve quality of life. Neuropathic pain can substantially impair quality of life as it often associates with other problems, such as loss of function, anxiety, depression, disturbed sleep and impaired cognition.
Measures of health-related quality of life HRQOL that capture broad dimensions of health including physical, mental, emotional and social functioning are increasingly used when assessing the efficacy of different interventions to manage chronic neuropathic and non-neuropathic pain.
It is mainly useful when calculating quality-adjusted life years, which are necessary for cost-utility analyses. The most commonly used HRQOL instruments are general, whereas others have been designed specifically for those with neuropathic pain. The scores of all eight dimensions vitality, physical functioning, bodily pain, general health perceptions, physical role functioning, emotional role functioning, social role functioning and mental health in the SF were significantly lower in those with neuropathic pain than in the general population, which is in line with another study The onset of neuropathy in patients with diabetes mellitus has been shown to significantly decrease all aspects of quality of life If diabetic polyneuropathy is accompanied by pain, both physical and mental components of quality of life are further affected A recent study also showed that both EuroQol five dimensions EQ-5D and Short Form-6 dimension SF-6D questionnaires can discriminate between chronic pain with or without neuropathic pain Furthermore, the role of psychological factors in impairing quality of life in neuropathic pain has been analysed , showing, for example, that pain catastrophizing was associated with decreased HRQOL The SF and the EQ-5D have been the most commonly used instruments in clinical trials to assess the efficacy of treatments, such as gabapentin in postherpetic neuralgia , diabetic polyneuropathy and neuropathic pain due to peripheral nerve injury ; the efficacy of duloxetine in diabetic peripheral neuropathy ; and the efficacy of spinal cord stimulation in diabetic polyneuropathy Although nervous system mechanisms underlying chronic neuropathic pain have been uncovered through animal and human research, the development of novel interventions with improved efficacy and tolerability has been slow.
New therapeutic approaches as well as improved clinical trial designs, specifically addressing genotypic and phenotypic profiles, have great promise to build on recent advances in basic and translational research.
The explanations for the slow progress in identifying treatments with improved efficacy that are receiving the greatest attention are inadequate clinical trial assay sensitivity and the need to target treatment to patients who are most likely to respond , Assay sensitivity refers to the ability of a clinical trial to distinguish an efficacious treatment from placebo or another comparator.
The possibility that recent neuropathic pain clinical trials suffer from limited assay sensitivity is consistent with the observation that a considerable number of recent trials in patients with neuropathic pain investigating medications with well-established efficacy have returned negative results 7 , For example, a recent analysis of neuropathic pain trials showed that assay sensitivity was compromised by including patients with highly variable baseline pain ratings , which suggests that trials might have greater assay sensitivity if highly variable baseline pain ratings were an exclusion criterion Several reasons could account for these results , , including high placebo responses, variability in the diagnostic criteria used for neuropathic pain in clinical trials and limited assay sensitivity.
Thus, it has been proposed that an alternative therapeutic approach to neuropathic pain should incorporate stratification of patients according to clinical phenotypes signs and symptoms 66 , 77 , , , whereas most trials have simply classified patients according to aetiology.
Several clinical trials provide support for the relevance of phenotypic subgrouping of patients, which has the potential to lead to a more personalized pain therapy in the future , , , In particular, two phenotypes — the presence of mechanical allodynia and preserved nociceptive function — are often combined and seem to predict the response to systemic and topical sodium channel blockers, botulinum toxin A and clonidine gel in recent clinical trials , , Indeed, any personalized pain treatments will rely on the ability to select patients who are likely to respond The strongest evidence showing that profiles of signs and symptoms can identify treatment responders stems from a trial in which patients who were defined as having an irritable nociceptor phenotype experienced a greater decrease in pain with oxcarbazepine versus placebo than those without this phenotype This is the only trial in which a pre-specified primary analysis demonstrated a difference in treatment versus placebo response in patient subgroups identified by phenotyping.
These results are very promising, but require replication as well as use of phenotyping measures that would be suitable for larger confirmatory trials and use in clinical practice Phenotyping could also be used to test whether certain patients have a more robust response to non-pharmacological treatments, for example, invasive, psychological and complementary interventions , as well as to identify which patients are most likely to respond to combinations of treatments.
Indeed, given the importance of expectations and psychological and social factors — including adaptive coping and catastrophizing — in the development and maintenance of chronic neuropathic pain, it would not be surprising if phenotyping has a great part to play in demonstrating the efficacy of psychological interventions as it does for medications.
To advance the design, execution, analysis and interpretation of clinical trials of pain treatments, several public-private partnerships have undertaken systematic efforts to increase assay sensitivity and provide validated approaches for phenotyping patients and identifying those who are most likely to respond to treatment.
Personalized medical care refers to the principle that patients can be stratified such that each patient receives the most effective and tolerable treatment for their individual needs. Patients can be stratified on several levels: Close consultation with the patient is required and this involves complex discussions around the uncertainties of genetic risk and the balance between efficacy and tolerability of potential treatments.
Human genetics studies have demonstrated that Na v 1. Loss-of-function mutations lead to congenital insensitivity to pain and gain-of-function mutations cause rare inherited pain disorders, including inherited erythromelalgia 31 , paroxysmal extreme pain disorder 32 and idiopathic small-fibre neuropathy which involves pain and small-fibre degeneration in the extremities Genetic information can, therefore, inform diagnostics; however, the interpretation of genetic results is complex and should be accompanied by functional analysis of mutant ion channels wherever possible For instance, in the context of small-fibre neuropathy, mutations might not be fully penetrant.
Finding a mutation in SCN9A may have immediate implications for treatment in choosing a drug with activity against voltage-gated sodium channels not normally first-line agents in the treatment of neuropathic pain , such as mexiletine, which is not recommended in the treatment of neuropathic pain but is used in inherited erythromelalgia, in which mexiletine has proven efficacy in normalizing abnormal channel properties in vitro and clinical efficacy in individual cases.
A further step has been taken in using structural modelling of Na v 1. Furthermore, the generation of nociceptors in vitro using patient-derived induced pluripotent stem cells is now possible. In rare Mendelian pain disorders such as inherited erythromelalgia , these nociceptors have been shown to be hyperexcitable Treatments targeting Na v 1.
Genetic stratification is more challenging in common acquired neuropathic pain states, such as painful diabetic neuropathy, because such conditions are polygenic and subject to considerable environmental interaction. Thus, the relevance of an individual target such as Na v 1.
Despite these limitations, the prospect of personalized medicine is a step forward towards promising pain management strategies. National Center for Biotechnology Information , U. Nat Rev Dis Primers. Author manuscript; available in PMC Mar Bennett , 13 Robert H.
Dworkin , 14 and Srinivasa N. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Nat Rev Dis Primers.
See other articles in PMC that cite the published article. Associated Data Supplementary Materials poster. Open in a separate window. Box 1 Key terms. Action potential An electrical event in which the membrane potential of a cell in the nervous system rapidly rises and falls to transmit electrical signals from cell to cell. Allodynia Pain caused by a normally non-painful stimulus.
C fibres Unmyelinated pain nerve fibres that respond to warmth and a range of painful stimuli by producing a long-lasting burning sensation due to a slow conduction speed 0. Chemoreceptors Receptors that transduce chemical signals.
Complex regional pain syndromes Also known as causalgia and reflex sympathetic dystrophy, complex regional pain syndromes are conditions that are characterized by the presence of chronic, intense pain often in one arm, leg, hand or foot that worsens over time and spreads in the affected area.
Conditioned pain modulation A reduction of a painful test stimulus under the influence of a conditioning stimulus. Dynamic mechanical allodynia A type of mechanical allodynia that occurs when pain is elicited by lightly stroking the skin. Expectancy-induced analgesia A reduction of pain experience due to anticipation, desire and belief of hypoalgesia or analgesia.
Hyperalgesia A heightened experience of pain caused by a noxious stimulus. Hypoalgesia A decreased perception of pain caused by a noxious stimulus. Mechanoreceptors A sensory receptor that transduces mechanical stimulations. Nociceptors A peripheral nervous system receptor that is responsible for transducing and encoding painful stimuli. Paradoxical heat sensation An experienced sensation of heat provoked by a cold stimulus.
Provoked pain Pain provoked by applying a stimulus. Pruriceptors Sensory receptors that transduce itchy sensations. Static pain Another kind of mechanical hyperalgesia in those with neuropathic pain when pain is provoked after gentle pressure is applied on the symptomatic area. Temporal summation The phenomenon in which progressive increases in pain intensity are experienced during the repetition of identical nociceptive stimuli. Thermoreceptors Sensory receptors that respond to changes in temperature.
Epidemiology The estimation of the incidence and prevalence of neuropathic pain has been difficult because of the lack of simple diagnostic criteria for large epidemiological surveys in the general population. Box 2 Validated screening tools for neuropathic pain.
Three clinical examination items touch hypoaesthesia reduced sense , pinprick hypoaesthesia and brush-evoked allodynia. Three items related to provoking factors overly sensitive to touch, touch-evoked pain and increased pain due to weather change.
Neuropathic Pain Symptom Inventory Ten descriptors burning, pressure, squeezing, electrical shocks, stubbing, pain evoked by brushing, pain evoked by pressure, pain evoked by cold stimuli, pins and needles, and tingling.
Five clinically relevant dimensions evoked pain, paroxysmal pain, abnormal sensations, superficial and deep components of spontaneous ongoing pain. Neuroanatomical distribution of pain symptoms and sensory signs in neuropathic pain conditions Distribution of pain and sensory signs in common peripheral and central neuropathic pain conditions. Box 3 Neuropathic pain and diabetes mellitus. Pain signalling changes Peripheral neuropathy alters the electrical properties of sensory nerves, which then leads to imbalances between central excitatory and inhibitory signalling such that inhibitory interneurons and descending control systems are impaired.
Box 4 Challenges in translating animal studies to therapeutic pharmacological targets in humans. Ion channel alterations Neuropathy causes alterations in ion channels sodium, calcium and potassium within the affected nerves, which can include all types of afferent fibres that then affect spinal and brain sensory signalling. Inhibitory modulation changes In addition to changes in pain transmission neurons, inhibitory interneurons and descending modulatory control systems are dysfunctional in patients with neuropathic pain.
Schematic representation of the conditioned pain modulation The conditioned pain modulation CPM paradigm is used in the research setting to assess the change of perceived pain by a test stimulus under the influence of a conditioning stimulus Pain modulation mechanisms Some patients with neuropathic pain are moderately affected, whereas others experience debilitating pain.
Diagnosis, screening and prevention A system was proposed to determine the level of certainty with which the pain in question is neuropathic as opposed, for example, to nociceptive pain 5 FIG. Diagnosing neuropathic pain, a The flowchart summarizes the clinical steps in diagnosing neuropathic pain, which involves taking the patient history, examining the patient and following up with confirmatory tests.
Confirmatory tests for nerve damage Different psychophysical and objective diagnostic tests are available to investigate somatosensory pathway function, including bedside evaluation and assessment of sensory signs as well as neurophysiological techniques, skin biopsy and corneal confocal microscopy FIG.
Bedside sensory assessment of sensory signs Neuropathic pain presents as a combination of different symptoms and signs Quantitative sensory testing Quantitative sensory tests use standardized mechanical and thermal stimuli to test the afferent nociceptive and non-nociceptive systems in the periphery and the CNS.
Neurophysiological techniques Laser-evoked potentials LEPs are widely considered the most reliable neurophysiological tool to assess nociceptive functions 67 , Skin biopsy Skin biopsy to assess epidermal innervation is regarded as the most sensitive tool for diagnosing small-fibre neuropathies Prevention Given that the available treatments for neuropathic pain have meaningful but modest benefits see Management , interventions that prevent neuropathic pain can have a substantial effect on public health.
Management The management of neuropathic pain generally focuses on treating symptoms because the cause of the pain can be rarely treated; furthermore, the management of aetiological conditions, such as diabetes mellitus, is typically insufficient to relieve neuropathic pain. Medical intervention Numerous therapeutic recommendations, with different classes of drug, for neuropathic pain have been proposed 95 — Table 1 Available pharmacotherapy for neuropathic pain.
First-line treatments Antidepressants and antiepileptics have been the most studied drugs in neuropathic pain. Second-line treatments Lidocaine is thought to act on ectopic neuronal discharges through its sodium channel-blocking properties. Third-line treatments Botulinum toxin A is a potent neurotoxin commonly used for the treatment of focal muscle hyperactivity and has shown efficacy of repeated administrations over 6 months, with enhanced effects of the second injection Emerging treatments A few drugs targeting novel mechanisms of action are under clinical development for the treatment of peripheral neuropathic pain.
Interventional therapies Interventional treatments, such as nerve blocks or surgical procedures that deliver drugs to targeted areas, or modulation of specific neural structures, provide alternative treatment strategies in selected patients with refractory neuropathic pain , FIG. Example interventional treatments for neuropathic pain. Neural blockade and steroid injections A perineural injection of steroids provides transient relief 1—3 months for trauma-related and compression-related peripheral neuropathic pain Dorsal root ganglion, peripheral nerve and peripheral nerve field stimulation Neurostimulation of afferent fibres outside the spinal cord for example, the dorsal root ganglion, which contains the cell bodies of sensory neurons, and peripheral nerves and subcutaneous peripheral nerve field stimulation have been reported to provide pain relief in various chronic neuropathic pain states, including occipital neuralgia and postherpetic neuralgia , Epidural and transcranial cortical neurostimulation Epidural motor cortex stimulation ECMS , repetitive transcranial magnetic stimulation rTMS and transcranial direct current stimulation tDCS of the pre-central motor cortex at levels below the motor threshold have been proposed as treatment options for patients with refractory chronic neuropathic pain , Deep brain stimulation The use of long-term intracranial stimulation for neuropathic pain remains controversial.
Intrathecal therapies Intrathecal therapies have been developed to deliver drugs to targeted nerves through an implanted and refillable pump in patients with severe and chronic pain that is refractory to conservative treatments, including psychological, physical, pharmacological and neuromodulation therapies , Psychological therapies People with chronic pain are not passive; they actively attempt to change the causes of pain and change their own behaviour in response to pain.
Quality of life Neuropathic pain can substantially impair quality of life as it often associates with other problems, such as loss of function, anxiety, depression, disturbed sleep and impaired cognition. Outlook Although nervous system mechanisms underlying chronic neuropathic pain have been uncovered through animal and human research, the development of novel interventions with improved efficacy and tolerability has been slow.
Clinical trial design The explanations for the slow progress in identifying treatments with improved efficacy that are receiving the greatest attention are inadequate clinical trial assay sensitivity and the need to target treatment to patients who are most likely to respond , Phenotyping Several clinical trials provide support for the relevance of phenotypic subgrouping of patients, which has the potential to lead to a more personalized pain therapy in the future , , , Personalized pain medicine Personalized medical care refers to the principle that patients can be stratified such that each patient receives the most effective and tolerable treatment for their individual needs.
Supplementary Material poster Click here to view. Footnotes Author contributions Introduction L. Prevalence and characteristics of painful diabetic neuropathy in a large community-based diabetic population in the U. This review presents differences and commonalities among distinct chronic pain states. The specific disease burden of neuropathic pain: The epidemiology of chronic pain of predominantly neuropathic origin. Results from a general population survey.
Finnerup NB, et al. This is an updated grading system to guide clinical diagnosis of neuropathic pain by illustrating the significance of confirmatory tests, the role of screening tools and potential uncertainties about anatomical pain distributions.
Fluctuating baseline pain implicated in failure of clinical trials. Tuttle AH, et al. Increasing placebo responses over time in U. This study explores factors explaining why novel analgesics that were designed to treat neuropathic pain failed.
Neuropathic pain in the general population: This is one of the first attempts to review epidemiological studies of neuropathic pain in the general population; however, the heterogeneity of the studies precluded meta-analysis, indicating a need for standardized tools and diagnostic approaches.
Bouhassira D, et al. Patient perspective on herpes zoster and its complications: Prevalence of postherpetic neuralgia after a first episode of herpes zoster: Daousi C, et al. Chronic painful peripheral neuropathy in an urban community: The prevalence, severity, and impact of painful diabetic peripheral neuropathy in type 2 diabetes.
Chronic pain with neuropathic characteristics in diabetic patients: The impact of neuropathic pain on health-related quality of life: Solaro C, et al. The prevalence of pain in multiple sclerosis: Central pain in multiple sclerosis — prevalence and clinical characteristics. Rayment C, et al. Bennett MI, et al.
Prevalence and aetiology of neuropathic pain in cancer patients: Bouhassira D, Attal N. Diagnosis and assessment of neuropathic pain: This review describes the main clinical tools that are used for the screening and measurement of neuropathic pain, focusing on the potential value and limitation of each tool. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire DN4 Pain.
Prevalence of chronic pain with neuropathic characteristics in the general population. Freynhagen R, et al. Screening of neuropathic pain components in patients with chronic back pain associated with nerve root compression: Neurological diseases and pain.
Watson JC, Sandroni P. Central neuropathic pain syndromes. Stavros K, Simpson DM. Understanding the etiology and management of HIV-associated peripheral neuropathy. Acute and chronic pain associated with leprosy. Not all neuropathy in diabetes is of diabetic etiology: This article discusses common disorders in the differential diagnosis of peripheral neuropathy. Yang Y, et al. Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia.
Fertleman CR, et al. SCN9A mutations in paroxysmal extreme pain disorder: Faber CG, et al. Gain of function Nav1. Haroutounian S, et al. Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy. Vaso A, et al. Peripheral nervous system origin of phantom limb pain. Serra J, et al. Microneurographic identification of spontaneous activity in C-nociceptors in neuropathic pain states in humans and rats.
Kleggetveit IP, et al. High spontaneous activity of C-nociceptors in painful polyneuropathy. Mechanisms and management of diabetic painful distal symmetrical polyneuropathy. Peripheral input and its importance for central sensitization. Patel R, Dickenson AH. Neuronal hyperexcitability in the ventral posterior thalamus of neuropathic rats: A special focus on allodynic pain mechanisms.
Gagnon M, et al. Chloride extrusion enhancers as novel therapeutics for neurological diseases. Microglia and intractable chronic pain. Brain circuits encoding reward from pain relief.
Bannister K, Dickenson AH. What the brain tells the spinal cord. Role of endogenous pain modulation in chronic pain mechanisms and treatment. Conditioned pain modulation in populations with chronic pain: Conditioned pain modulation predicts duloxetine efficacy in painful diabetic neuropathy.
This article presents a new perspective of predicting drug responses in patients with painful diabetic neuropathy based on CPM mechanisms. Patients with chronic pain after abdominal surgery show less preoperative endogenous pain inhibition and more postoperative hyperalgesia: J Pain Palliat Care Pharmacother. Preoperative pain mechanisms assessed by cuff algometry are associated with chronic postoperative pain relief after total knee replacement.
Kosek E, Ordeberg G. Lack of pressure pain modulation by heterotopic noxious conditioning stimulation in patients with painful osteoarthritis before, but not following, surgical pain relief. Normalization of widespread hyperesthesia and facilitated spatial summation of deep-tissue pain in knee osteoarthritis patients after knee replacement.
Colloca L, Miller FG. Role of expectations in health. Hall KT, et al. Conscientiousness is modified by genetic variation in catechol- O -methyltransferase to reduce symptom complaints in IBS patients. Kaptchuk TJ, et al. Components of placebo effect: The contributions of suggestion, desire, and expectation to placebo effects in irritable bowel syndrome patients. Placebo, nocebo, and neuropathic pain. Petersen GL, et al.
Placebo manipulations reduce hyperalgesia in neuropathic pain. There are many ways of managing neuropathic pain, and drug treatment is just one aspect of that. As well as talking to your doctor about drug treatments that could help, it is important to talk to your doctor about what you can do to help yourself feel better.
When the cause of the neuropathy cannot be determined, it is called idiopathic neuropathy. About 30 to 40 percent of neuropathy cases are idiopathic. Another 30 percent are the result of diabetes. Discover more information about each of these topics, along with tools and resources that may help:. Prevention or Disease Remission You can prevent some causes of nerve damage. Drink alcohol in moderation.
Neuropathic pain results from damage to or dysfunction of the peripheral or central nervous system, rather than stimulation of pain receptors. Diagnosis is. Neuropathic pain (also called neuropathy, neuralgia, or nerve pain) occurs in about 7 - 10% of adults over age 'Neuropathy affects people. Neuropathic pain can be contrasted to nociceptive pain, which is the type of pain which occurs when someone experiences an acute injury, such as smashing a.