Relevant bibliographies by topics / Peripheral neuropathic pain

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Peripheral neuropathic pain'

Author: Grafiati
Published: 18 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Peripheral neuropathic pain"

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Di Stefano, Giulia, Andrea Di Lionardo, Giuseppe Di Pietro, and Andrea Truini. "Neuropathic Pain Related to Peripheral Neuropathies According to the IASP Grading System Criteria." Brain Sciences 11, no. 1 (December 22, 2020): 1. http://dx.doi.org/10.3390/brainsci11010001.

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Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system. Neuropathic pain represents a broad category of pain conditions, common complications of peripheral neuropathies, which are characterized by a combination of positive symptoms, including paresthesia and/or dysesthesia and sensory deficits in the painful area. In the present paper, we aimed to assess neuropathic pain frequency and clinical characteristics of peripheral neuropathies due to different aetiologies according to grading system criteria of the International Association for the Study of Pain for a definitive diagnosis of neuropathic pain. Epidemiological studies applying these criteria have been conducted in patients with diabetes, brachial plexus injury, and other traumatic nerve injuries. Neuropathic pain was diagnosed in 37–42% of patients with diabetic peripheral neuropathy, 56% of patients with brachial plexus injury, and 22% of patients with intercostobrachial neuropathy. The most frequent neuropathic pain type was ongoing pain (described as burning or pressing), followed by paroxysmal pain (electric shock-like sensations) and allodynia (pain evoked by brushing and pressure). By providing information on the frequency, clinical signs, and variables associated with neuropathic pain due to different aetiologies, these studies contribute to improving the clinical management of this condition.
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Lee, Ho Seong. "Treatment of peripheral neuropathy: a multidisciplinary approach is necessary." Journal of the Korean Medical Association 63, no. 8 (August 10, 2020): 432–34. http://dx.doi.org/10.5124/jkma.2020.63.8.432.

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The number of patients with peripheral neuropathy or neuropathic pain is increasing. The recommended treatment for peripheral neuropathy and neuropathic pain is proper medications, exercise, physical therapy, and support. Overly invasive interventions can be harmful rather than beneficial to patients. Many doctors do not understand the characteristics of peripheral neuropathy and neuropathic pain. Peripheral neuropathy is not a problem that is confined to a particular department. The most appropriate treatment is a combination of drug therapy, physical exercise, and psychological support. Thus, a multidisciplinary approach is necessary for the effective treatment of peripheral neuropathy and neuropathic pain.
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Jeong, Na Young, Youn Ho Shin, and Junyang Jung. "Neuropathic pain in hereditary peripheral neuropathy." Journal of Exercise Rehabilitation 9, no. 4 (August 31, 2013): 397–99. http://dx.doi.org/10.12965/jer.130057.

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Murphy, Douglas, Denise Lester, F. Clay Smither, and Ellie Balakhanlou. "Peripheral neuropathic pain." NeuroRehabilitation 47, no. 3 (November 13, 2020): 265–83. http://dx.doi.org/10.3233/nre-208002.

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Neuropathic pain (NP) can have either central nervous system causes or ones from the peripheral nervous system. This article will focus on the epidemiology, classifications, pathology, non-invasive treatments and invasive treatments as a general review of NP involving the peripheral nervous system. NP has characteristic symptomatology such as burning and electrical sensations. It occurs in up to 10% of the general population. Its frequency can be attributed to its occurrence in neck and back pain, diabetes and patients receiving chemotherapy. There are a wide range of pharmacologic options to control this type of pain and when such measures fail, numerous interventional methods can be employed such as nerve blocks and implanted stimulators. NP has a cost to the patient and society in terms of emotional consequences, quality of life, lost wages and the cost of assistance from the medical system and thus deserves serious consideration for prevention, treatment and control.
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Baron, Ralf, Christoph Maier, Nadine Attal, Andreas Binder, Didier Bouhassira, Giorgio Cruccu, Nanna B. Finnerup, et al. "Peripheral neuropathic pain." PAIN 158, no. 2 (February 2017): 261–72. http://dx.doi.org/10.1097/j.pain.0000000000000753.

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Castoro, Ryan, Megan Simmons, Vignesh Ravi, Derek Huang, Christopher Lee, John Sergent, Lan Zhou, and Jun Li. "SCN11A Arg225Cys mutation causes nociceptive pain without detectable peripheral nerve pathology." Neurology Genetics 4, no. 4 (July 20, 2018): e255. http://dx.doi.org/10.1212/nxg.0000000000000255.

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ObjectiveThe SCN11A gene encodes the NaV1.9 sodium channel found exclusively in peripheral nociceptive neurons.MethodsAll enrolled participants were evaluated clinically by electrophysiologic studies, DNA sequencing, and punch skin biopsies.ResultsAll affected family members are afflicted by episodes of pain. Pain was predominantly nociceptive, but not neuropathic in nature, which led a diagnosis of fibromyalgia in some patients. All patients had normal findings in nerve conduction studies for detecting large nerve fiber neuropathies and skin biopsies for detecting small nerve fiber pathology.ConclusionsUnlike those patients with missense mutations in SCN11A, small fiber sensory neuropathy, and neuropathic pain, the Arg225Cys SCN11A in the present study causes predominantly nociceptive pain with minimal features of neuropathic pain and undetectable pathophysiologic changes of peripheral neuropathy. This finding is consistent with dysfunction of nociceptive neurons. In addition, since nociceptive pain in patients has led to the diagnosis of fibromyalgia, this justifies a future search of mutations of SCN11A in patients with additional pain phenotypes such as fibromyalgia to expand the clinical spectrum beyond painful small fiber sensory neuropathy.
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Micu, Elena Claudia, and Laszlo Irsay. "The Rehabilitation of Oncological Patients Presenting Neuropathies." Medicine and Pharmacy Reports 87, no. 2 (June 30, 2014): 67–72. http://dx.doi.org/10.15386/cjmed-278.

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The International Association for the Study of Pain (IASP 2011) defines neuropathic pain as “the pain caused by an injury or disease of the somatosensory portion of the nervous system”. The central neuropathic pain is defined as “the pain caused by an injury or disease of the central somatosensory central nervous system”, whereas the peripheral neuropathic pain is defined as “the pain caused by an injury or disease of the peripheral somatosensory nervous system”. The peripheral neuropathy describes any affection of the peripheral nervous system. The etiology is vast, there being a number of over 100 possible causes, which causes the global morbidity rate to reach approximately 2.4%. The chronic nature of the pain superposes the everyday routine and leads to the high intake of medication for pain alleviation. The number of cases of neuroplasia has always increased today. This disturbing diagnosis which can potentiate the signs and symptoms of peripheral neuropathy as well as reduce and limit the treatment options associated with neuropathies. The treatment presupposes a multidisciplinary approach, while the solution to prevent complications involves the control of risk factors and pathophysiological treatment. Chemotherapy-induced peripheral neuropathy (CPIN) is a significant disabling symptom that is tightly connected to the administration of neurotoxic cytostatic agents used for the treatment of neoplasia. CPIN compromises the quality of life and produces pain or discomfort. I have sought to produce a presentation of the medicated and physical-kinetic treatment options that have proved their effectiveness during clinical studies or random trials and can be applied to cancer patients presenting with symptoms associated with peripheral neuropathy, namely with neuropathic pain, and support it with arguments
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Basu, Paramita, and Arpita Basu. "In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain." Molecules 25, no. 5 (March 5, 2020): 1171. http://dx.doi.org/10.3390/molecules25051171.

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Neuropathic pain is a common symptom and is associated with an impaired quality of life. It is caused by the lesion or disease of the somatosensory system. Neuropathic pain syndromes can be subdivided into two categories: central and peripheral neuropathic pain. The present review highlights the peripheral neuropathic models, including spared nerve injury, spinal nerve ligation, partial sciatic nerve injury, diabetes-induced neuropathy, chemotherapy-induced neuropathy, chronic constriction injury, and related conditions. The drugs which are currently used to attenuate peripheral neuropathy, such as antidepressants, anticonvulsants, baclofen, and clonidine, are associated with adverse side effects. These negative side effects necessitate the investigation of alternative therapeutics for treating neuropathic pain conditions. Flavonoids have been reported to alleviate neuropathic pain in murine models. The present review elucidates that several flavonoids attenuate different peripheral neuropathic pain conditions at behavioral, electrophysiological, biochemical and molecular biological levels in different murine models. Therefore, the flavonoids hold future promise and can be effectively used in treating or mitigating peripheral neuropathic conditions. Thus, future studies should focus on the structure-activity relationships among different categories of flavonoids and develop therapeutic products that enhance their antineuropathic effects.
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Falo, Clara P., Raquel Benitez, Marta Caro, Maria Morell, Irene Forte-Lago, Pedro Hernandez-Cortes, Clara Sanchez-Gonzalez, Francisco O’Valle, Mario Delgado, and Elena Gonzalez-Rey. "The Neuropeptide Cortistatin Alleviates Neuropathic Pain in Experimental Models of Peripheral Nerve Injury." Pharmaceutics 13, no. 7 (June 24, 2021): 947. http://dx.doi.org/10.3390/pharmaceutics13070947.

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Neuropathic pain is one of the most severe forms of chronic pain caused by the direct injury of the somatosensory system. The current drugs for treating neuropathies have limited efficacies or show important side effects, and the development of analgesics with novel modes of action is critical. The identification of endogenous anti-nociceptive factors has emerged as an attractive strategy for designing new pharmacological approaches to treat neuropathic pain. Cortistatin is a neuropeptide with potent anti-inflammatory activity, recently identified as a natural analgesic peptide in several models of pain evoked by inflammatory conditions. Here, we investigated the potential analgesic effect of cortistatin in neuropathic pain using a variety of experimental models of peripheral nerve injury caused by chronic constriction or partial transection of the sciatic nerve or by diabetic neuropathy. We found that the peripheral and central injection of cortistatin ameliorated hyperalgesia and allodynia, two of the dominant clinical manifestations of chronic neuropathic pain. Cortistatin-induced analgesia was multitargeted, as it regulated the nerve damage-induced hypersensitization of primary nociceptors, inhibited neuroinflammatory responses, and enhanced the production of neurotrophic factors both at the peripheral and central levels. We also demonstrated the neuroregenerative/protective capacity of cortistatin in a model of severe peripheral nerve transection. Interestingly, the nociceptive system responded to nerve injury by secreting cortistatin, and a deficiency in cortistatin exacerbated the neuropathic pain responses and peripheral nerve dysfunction. Therefore, cortistatin-based therapies emerge as attractive alternatives for treating chronic neuropathic pain of different etiologies.
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Giorgio, Cristina, Mara Zippoli, Pasquale Cocchiaro, Vanessa Castelli, Giustino Varrassi, Andrea Aramini, Marcello Allegretti, Laura Brandolini, and Maria Candida Cesta. "Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives." Biomedicines 9, no. 4 (April 7, 2021): 399. http://dx.doi.org/10.3390/biomedicines9040399.

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The complement system is a key component of innate immunity since it plays a critical role in inflammation and defense against common pathogens. However, an inappropriate activation of the complement system is involved in numerous disorders, including peripheral neuropathies. Current strategies for neuropathy-related pain fail to achieve adequate pain relief, and although several therapies are used to alleviate symptoms, approved disease-modifying treatments are unavailable. This urgent medical need is driving the development of therapeutic agents for this condition, and special emphasis is given to complement-targeting approaches. Recent evidence has underscored the importance of complement component C5a and its receptor C5aR1 in inflammatory and neuropathic pain, indicating that C5a/C5aR1 axis activation triggers a cascade of events involved in pathophysiology of peripheral neuropathy and painful neuro-inflammatory states. However, the underlying pathophysiological mechanisms of this signaling in peripheral neuropathy are not fully known. Here, we provide an overview of complement pathways and major components associated with dysregulated complement activation in peripheral neuropathy, and of drugs under development targeting the C5 system. C5/C5aR1 axis modulators could represent a new strategy to treat complement-related peripheral neuropathies. Specifically, we describe novel C5aR allosteric modulators, which may potentially become new tools in the therapeutic armory against neuropathic pain.
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Dissertations / Theses on the topic "Peripheral neuropathic pain"

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Taylor, Anna. "Peripheral mechanisms of trigeminal neuropathic pain." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97105.

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Trigeminal neuropathic pain is a unique type of neuropathic pain resulting from damage to primary afferents of the trigeminal nerve that innervates the head and neck region. It is characterized by intractable, unremitting pain in the absence of any overt tissue damage, and represents a significant clinical and societal burden. A thorough understanding of the mechanisms driving this condition is required to adequately treat, and ideally cure, this condition. The skin of the lower lip is innervated by several classes of primary afferents, including myelinated Aβ fibers, thinly myelinated Aδ fibers, and unmyelinated C fibers, which together are able to transduce the variety of innocuous and noxious stimuli encountered in the environment. Nociceptive stimuli are largely mediated by the unmyelinated C fibers, which have been further divided into 2 groups based on neurochemical and anatomical criteria, called the peptidergic and non-peptidergic C fibers. Given that nerve lesions initiating neuropathic pain conditions most often occur in the periphery, changes in the peripheral nervous system following nerve injury are particularly relevant in driving this aberrant pain condition. Therefore, the overall objective of this thesis is to explore the peripheral changes in an animal model of trigeminal neuropathic pain. The results of this thesis are presented in three chapters. The pattern of innervation of non-peptidergic C fibers in the skin of uninjured rats has been described, as well as how this fiber population changes following nerve injury. Concomitant ectopic autonomic fibers were observed in close apposition to the regenerating sensory fibers, and correlated with the behavioral phenotype of the animals. GDNF levels in the skin rapidly increased following nerve injury, and provided a possible mechanism for the ectopic parasympathetic fibers and regenerating non-peptidergic C fibers. Ablation of the non-peptidergic C fibers led to specific sprouting of parasympathetic fibers, but no change in behavior, however ablation of non-peptidergic fibers in neuropathic animals led to an exacerbated pain response. These results suggest an important role for non-peptidergic fibers and autonomic sprouting in neuropathic pain, and identifies GDNF as a potential factor for mediating these changes.
La douleur trigeminale neuropathique est une forme unique de douleur qui résulte d'un dommage aux afférents primaires du nerf trijumeau innervant la région de la tête et du coup. Cette douleur constante qui se manifeste en l'absence d'un dommage aux tissus périphériques représente un fardeau social et économique important. Une compréhension rigoureuse des mécanismes qui mènent à cette condition sera nécessaire pour mieux la traiter et préférablement la guérir.La peau de la lèvre inferieure est innervée par des afférents primaires appartenant à différentes classes, incluant les fibres myélinisées Aβ, les fibres légèrement myélinisées Aδ, ainsi que les fibres C non myélinisées. Ensemble, ces fibres peuvent transmettre une variété de stimuli nociceptifs ou inoffensifs tels que rencontrés dans l'environnement. Les stimuli nociceptifs sont majoritairement transmis par les fibres C non myélinisées, lesquelles peuvent être divisées en 2 catégories, peptidergiques ou non peptidergiques, selon des critères neurochimiques et anatomiques. Puisque les lésions nerveuses qui déclenchent la douleur neuropathique se produisent le plus souvent en périphérie, les changements au niveau du système nerveux périphérique sont centraux au développement de la condition douloureuse. Ceci étant dit, l'objectif général de cette thèse est d'explorer les changements périphériques qui se produisent dans un model animal de douleur trigeminale neuropathique.Les résultats de cette thèse sont présentés dans trois chapitres. L'innervation de la peau par les fibres C non peptidergiques chez le rat normal a d'abord été décrite. Ensuite, les changements subis par cette population suivant un dommage au nerf ont été documentés. Suite à un dommage nerveux périphérique, des fibres autonomiques ectopiques ont été observées en proximité des fibres sensorielles en régénération, et ce changement corrélait temporellement avec le phénotype comportemental des animaux. Les niveaux cutanés de GDNF ont rapidement augmenté après le dommage nerveux, fournissant un mécanisme potentiel permettant la régénération des fibres C non peptidergiques et la migration ectopique des fibres parasympathiques. L'ablation des fibres C non peptidergiques a déclenché la pousse des fibres parasympathiques sans changer le comportement des animaux. Par contre, l'ablation de ces fibres chez des animaux neuropathiques a exacerbé la réponse douloureuse de ceux-ci.Ces résultats suggèrent une participation importante des fibres C non peptidergiques et de la migration autonomique dans la douleur neuropathique. De plus, GDNF est rapporté comme étant un facteur pouvant produire ces changements.
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Wallace, Victoria C. J. "Peripheral nerve demyelination and neuropathic pain." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/27605.

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Chronic neuropathic pain, characterised by allodynia (perception of innocuous stimuli as painful) and hyperalgesia (facilitated responses to painful stimuli), is poorly understood and is usually resistant to classical analgesics. Such abnormal pain phenomena can be associated with human demyelinating conditions such as Charcot-Marie-Tooth disease. Using mouse models of peripheral nerve demyelination, we have provided evidence for the consequent establishment of neuropathic pain and investigated possible underlying mechanisms. The first model investigated was the Prx-null mouse. The murine periaxin gene (Prx) is expressed in Schwann cells and encodes L- and S-periaxin, two abundant PDZ-domain proteins thought to have a role in stabilisation of myelin in the peripheral nervous system (PNS). Prx-null mice show progressive demyelination in peripheral nerves and electrophysiological investigations indicate the presence of spontaneous action potential discharge; abnormal activity thought to be critical for the development of persistent pain states. Consistent with the time course of demyelination, Rrx-null mice display an increased behavioural reflex sensitivity to cutaneous mechanical and noxious thermal stimulation. To further investigate the link between demyelination of peripheral nerves and neuropathic pain, we have also characterised a novel model of focal peripheral nerve demyelinating neuropathy. Focal demyelination of the sciatic or saphenous nerve was induced with lysolecithin (lysophosphatidylcholine) and resulted in an increased behavioural reflex sensitivity to both thermal and mechanical tests, peaking at 9-14 days following treatment. Nerve morphology was investigated using light and electron microscopy, which revealed 30-40% demyelination of the treated nerve, (without lysolecithin-treated axon loss) coinciding with peak behavioural changes. Changes in the excitability of saphenous nerves were revealed, with spontaneous action potential discharge of 2-3 impulses per second present at peak behavioural change. No associated change in peripheral activation thresholds or conduction velocity was observed. In both models, immunohistochemical investigations revealed no cell loss in the dorsal root ganglia (DRG) and no evidence for axonal damage. Similar methods revealed changes in the expression of neuropeptide Y, and the sodium channels Nav1.3 and Nav1.8 in DRG neurones. Such changes may account for increased nerve excitability and are known to occur in other models of nerve injury. However, these changes in the demyelinating models occur in a more restricted manner, specifically in the cells of formerly myelinated fibres. Intrathecal injections of the selective NMDA receptor antagonist, [R]-CPP, indicated that NMDA receptor-dependent changes are crucial for the development of a neuropathic pain-like state following peripheral nerve demyelination. Intrathecal administration of pharmacological agents indicated a role for the transcription factor NFkB in the production of the behavioural reflex sensitivity of lysolecithin-treated mice, as well as identifying the endogenous cannabinoid system as an effective inhibitory regulator and potential analgesic target. This study describes the first mouse models of peripheral nerve demyelination designed for the study of neuropathic pain and reveals phenotypic changes in DRG, which may contribute to the development of a neuropathic pain-like state. Therefore, these models may be useful for the evaluation of novel therapeutic targets for the treatment of demyelination-associated neuropathic pain.
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Liu, Xue Jun. "Peripheral regulation of inflammatory pain and neuropathic pain by adenosine." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66636.pdf.

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Caspani, Ombretta [Verfasser]. "Cold transduction mechanisms during peripheral neuropathic pain / Ombretta Caspani." Berlin : Freie Universität Berlin, 2008. http://d-nb.info/1023169932/34.

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Ramer, Matthew Stephen. "Sympathetic and sensory neuronal plasticity, peripheral substrates of neuropathic pain." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ31950.pdf.

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Bian, Di. "Peripheral and spinal mechanisms of neuropathic pain in the rat." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284087.

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The Chung peripheral nerve injury model shows consistent allodynia and thermal hyperalgesia, which represent the most common clinical neuropathic pain symptoms. Also clinically relevant, in the Chung model spinal morphine was inactive against tactile allodynia and diminished in potency in acute nociception without spinal/supraspinal antinociceptive synergy. Further, there are increased levels of dynorphin in multiple segmental regions of the spinal cord. This loss of spinal/supraspinal synergy and the spinal antiallodynic effect of morphine is restored by spinal MK-801 or antiserum to dynorphin. It is shown here that spinal transection blocks tactile allodynia, but not thermal hyperalgesia in Chung model rats, suggesting that thermal hyperalgesia involves both spinal and supraspinal circuits, whereas tactile allodynia depends on a supraspinal loop. The c-fiber specific neurotoxin resiniferatoxin before or after Chung surgery abolishes thermal nociception in Chung and sham-operated rats, but not allodynia in Chung model rats. These data suggest that tactile allodynia may be mediated by Aβ-fibers rather than c-fibers, offering a mechanistic basis for the observed insensitivity of allodynia to spinal morphine in Chung model rats. The data also show that PN3 sodium channel protein expression is increased in medium to large diameter neurons in the L4 ipsilateral DRG of Chung rats, and that selective knockdown of PN3 protein in the DRG with specific antisense prevents and reverses allodynia and hyperalgesia in Chung model rats without affecting normal nociceptive functions. Meanwhile, the increased dynorphin level in the spinal cord of Chung model rats returns to normal following spinal PN3 antisense. This suggests that increased PN3 protein in the DRG of Chung model rats may underlie an important mechanism for central sensitization and peripheral ectopic firing after nerve injury. Increased expression of PN3 is also found in the DRGs of diabetic and CFA model rats; knockdown of PN3 reverses allodynia and thermal hyperalgesia in these models. Together, these data suggest that relief from peripheral nerve injury, chronic inflammation, or diabetic neuropathy might be achieved by selective blockade of PN3. In light of the restricted distribution of PN3 to sensory neurons, such an approach might offer effective pain relief without a significant side-effect liability.
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McCormick, Barry. "Antioxidant protection in mitochondria in chemotherapy-induced neuropathic pain." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=229728.

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Neuropathic pain is a common and dose-limiting adverse effect of several cancer chemotherapeutic agents including paclitaxel. Current treatments for chemotherapy-induced peripheral neuropathy (CIPN) are largely ineffective and the pain can persist long after the cessation of the chemotherapy regimen. Whilst the specific underlying mechanisms are not fully understood, oxidative stress and mitochondrial damage are thought to be involved in the development of CIPN. Antioxidants which protect mitochondria may inhibit oxidative stress and protect mitochondrial function more effectively than antioxidants which do not specifically act within mitochondria, and may attenuate CIPN. The overall aim of the study was therefore to determine the effects of mitochondrial-targeted antioxidants on CIPN. This was addressed in two main parts. Firstly, in vitro studies aimed to determine the effects of paclitaxel alone and in combination with mitochondrial-targeted antioxidants melatonin and MitoVitE, and a non-targeted antioxidant, Trolox, on oxidative stress and mitochondrial function in cells. In vivo studies aimed to determine the effects of melatonin, MitoVitE and Trolox in a preclinical rat model of paclitaxel neuropathic pain. In vitro studies used a dorsal root ganglion (DRG) cell line (50B11). Cells were cultured with a range of concentrations of paclitaxel, with or without the addition of melatonin, MitoVitE or Trolox. Several measures of oxidative stress including free radical production, and glutathione levels, and measures of mitochondrial function, including mitochondrial metabolic rate, membrane potential, mitochondrial pore opening and ATP production were made. In vivo studies used a rat model of paclitaxel-CIPN, and assessed the effects of melatonin, MitoVitE and Trolox on behavioural measures of pain. In vitro studies showed that paclitaxel induced oxidative stress and caused mitochondrial damage in the DRG cell line. Compared to paclitaxel alone, cells co-treated with melatonin and MitoVitE had reduced oxidative stress and mitochondrial damage. Co-treatment of cells with paclitaxel and Trolox did not differ from conditions with paclitaxel only. In vivo studies demonstrated that melatonin and MitoVitE attenuated paclitaxel-induced mechanical hypersensitivity, whilst Trolox did not affect behavioural measures of CIPN. These studies suggest that mitochondrial-targeted antioxidants may be useful as a potential treatment strategy for CIPN.
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Erichsen, Helle Kirstein. "Characterisation of the spared nerve injury model of neuropathic pain /." Cph. : The Danish University of Pharmaceutical Scienes, Department of Pharmacology, NeuroSearch, Kongl. Carolinska Medico Chirurgiska Institutet, 2003. http://www.dfh.dk/phd/defences/Hellekirsteinerichsen.htm.

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Klein, Johann, Sahr Sandi-Gahun, Gabriele Schackert, and Tareq A. Jratli. "Peripheral nerve field stimulation for trigeminal neuralgia, trigeminal neuropathic pain, and persistent idiopathic facial pain." Sage, 2015. https://tud.qucosa.de/id/qucosa%3A35439.

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Objective: Peripheral nerve field stimulation (PNFS) is a promising modality for treatment of intractable facial pain. However, evidence is sparse. We are therefore presenting our experience with this technique in a small patient cohort. Methods: Records of 10 patients (five men, five women) with intractable facial pain who underwent implantation of one or several subcutaneous electrodes for trigeminal nerve field stimulation were retrospectively analyzed. Patients’ data, including pain location, etiology, duration, previous treatments, long-term effects and complications, were evaluated. Results: Four patients suffered from recurrent classical trigeminal neuralgia, one had classical trigeminal neuralgia and was medically unfit for microvascular decompression. Two patients suffered from trigeminal neuropathy attributed to multiple sclerosis, one from post-herpetic neuropathy, one from trigeminal neuropathy following radiation therapy and one from persistent idiopathic facial pain. Average patient age was 74.2 years (range 57–87), and average symptom duration was 10.6 years (range 2–17). Eight patients proceeded to implantation after successful trial. Average follow-up after implantation was 11.3 months (range 5–28). Using the visual analog scale, average pain intensity was 9.3 (range 7–10) preoperatively and 0.75 (range 0–3) postoperatively. Six patients reported absence of pain with stimulation; two had only slight constant pain without attacks. Conclusion: PNFS may be an effective treatment for refractory facial pain and yields high patient satisfaction.
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Rode, Frederik. "Pharmacological testing in the spared nerve injury model of neuropathic pain /." Cph. : The Danish University of Pharmaceutical Sciences, Department of Pharmacology, 2005. http://www.dfuni.dk/index.php/Frederik_Rode/1938/0/.

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Books on the topic "Peripheral neuropathic pain"

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Donaldson, Katelyn, and Ahmet Höke. Animal Models of Peripheral Neuropathy and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0119.

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There are numerous types of peripheral neuropathies and conditions that cause neuropathic pain with varying symptoms and different mechanisms of pathogenesis. Therefore, it is not surprising that many different animal models of peripheral neuropathies and neuropathic pain have been developed with varying degrees of fidelity to recapitulate the human disease. Nevertheless, these models are useful in a deconstructive manner to examine role of specific molecular pathways in pathogenesis of different types of peripheral neuropathies and test potential new drugs.
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Khursheed, Faraz, and Marc O. Maybauer. Neuropathic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0012.

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Neuropathic pain is a common condition that arises from injury anywhere along the somatosensory axis. Although the presentation may vary based on mechanisms and locations of injury, most patients have characteristic burning, shocklike, lancinating pain, most often in the distribution of peripheral and spinal nerves or distal extremities. Various peripheral and central processes aggravate pain through abnormal impulse generation, modulation, and processing. Common conditions include complex regional pain syndrome, diabetic neuropathy, postherpetic neuralgia, spondylotic radiculopathy, and central pain syndromes. A detailed history and physical examination will aid in differentiating various neuropathic pain conditions. Neuropathic pain is best managed using a true multidisciplinary approach.
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Fowler, Ian M., Robert J. Hackworth, and Erik P. Voogd. Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0024.

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Neuropathic pain encompasses a vast number of clinical conditions that share the common characteristic of pain resulting from nerve injury or damage. Upon injury, pathophysiologic changes in the peripheral nervous system occur, including hyperexcitability and the spontaneous generation of impulses (ectopia). As a result of these peripheral changes, alterations in signal processing and intrinsic changes within the central nervous system occur. All of these changes contribute to the generation of neuropathic pain. This chapter attempts to capture the essence of the objectives and goals set forth by the International Association for the Study of Pain’s Core Curriculum for Professional Education in Pain for the topic of neuropathic pain. The questions cover topics including definitions, common clinical conditions, uncommon clinical conditions, therapeutic interventions, pathophysiological mechanisms, and current investigations.
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Scadding, John. Neuropathic pain. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0386.

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Pain signalled by a normal sensory system, nociceptive pain, serves a vital protective function. The peripheral and central nervous somatosensory systems permit rapid localization and identification of the nature of painful stimuli, prior to appropriate action to minimize or avoid potentially tissue damaging events. A reduction or absence of pain resulting from neurological disease emphasizes the importance of this normal protective function of pain. For example, tissue destruction occurs frequently in peripheral nerve diseases which cause severe sensory loss such as leprosy, and in central disorders such as syringomyelia. Neuropathic pain results from damage to somatosensory pathways and serves no protective function. This chapter provides an overview of neuropathic pain, considering its context, clinical features, pathophysiology, and treatment.In the peripheral nervous system, neuropathic pain is caused by conditions affecting small nerve fibres, and in the central nervous system by lesions of the spinothalamic tract and thalamus, and rarely by subcortical and cortical lesions. The clinical feature common to virtually all conditions leading to the development of neuropathic pain is the perception of pain in an area of sensory impairment, an apparently paradoxical situation. The exception is trigeminal neuralgia.Neuropathic pain is heterogeneous clinically, aetiologically, and pathophysiologically. Within a given diagnostic category, whether defined clinically or aetiologically, there are wide variations in reports of pain by patients. This heterogeneity poses one of the greatest challenges in understanding the mechanisms of neuropathic pain. Knowledge of the pathophysiology is an obvious pre-requisite to the development of effective treatments. The goal of a pathophysiologically based understanding of the symptoms and signs of neuropathic pain is, of course, just such a rational and specific approach to treatment. While this is not yet achievable, clinical-pathophysiological correlations have led to some recent advances in treatment.
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Cheng, Jianguo, ed. Neuropathic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190298357.001.0001.

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Neuropathic pain is a category of chronic pain disorders that are most common, debilitating, costly, and difficult to treat. It is a significant challenge to individuals suffering from it, healthcare providers, and society at large. This book is written by expert clinicians and investigators from multiple disciplines to provide the most comprehensive and updated information on neuropathic pain disorders that are commonly encountered in clinical practice. It strives to reflect the current understanding of the concepts, classification, mechanisms, assessment, diagnosis, and treatment of neuropathic pain. Following chapters addressing these topics in general terms are chapters devoted to specific neuropathic pain disorders consequent to lesions or diseases of the central and peripheral nervous systems. These chapters take a case-based format to stimulate situation-guided thinking, predicting, and learning. The textbook serves to inform best practices and stimulate innovative investigations to advance patient care, as well as the science behind it.
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Wong, Stacy N., and Line G. Jacques. Neuropathic Groin Pain. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0017.

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Chronic neuropathic groin pain may be iatrogenic or posttraumatic and can be disabling or even crippling in some individuals. Patients may have significant sleep disturbances and may experience psychosocial effects along with significant physical limitations. A combination of pharmacologic treatments with physical therapy and local infiltrations may be useful. Neurostimulation techniques, including spinal cord stimulation, peripheral nerve stimulation, and dorsal root ganglion stimulation, have shown promising results in the treatment of chronic neuropathic pain. In certain cases, surgical approaches, including selective neurectomy, can be effective; in other cases, the pain will remain chronic and intractable despite all interventional measures. In summary, patients with neuropathic groin pain can be treated after a thorough pretreatment investigation. Dorsal root ganglion stimulation is a viable option and should be considered when treating this challenging patient population.
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Keltner, John R., Cherine Akkari, and Ronald J. Ellis. Neurological Complications of HIV in The Peripheral Nervous System. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0027.

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HIV sensory neuropathy affects approximately 50% of persons diagnosed with HIV and, in 40%, results in disabling symptoms including paresthesia and/or pain. This chapter focuses on providing guidance to psychiatrists in the clinical management of pain in persons with HIV and sensory neuropathy. The differential diagnostic evaluation of HIV sensory neuropathy, other peripheral neuropathies, and spinal cord mimics and management of HIV sensory neuropathy are reviewed, as well as management of HIV distal neuropathic pain. The differential diagnostic evaluation of peripheral neuropathies is simplified using a graphical decision tree. The chapter also reviews the pathophysiology of HIV sensory neuropathy and warning signs of advanced disease. Procedures to diagnose HIV sensory neuropathy, including nerve conduction studies and electromyography, quantitative sensory testing, skin biopsy, and the autonomic sweat test are discussed, as are clinical aspects of HIV distal neuropathic pain. The chapter addresses the impact of HIV distal neuropathic pain on quality of life and depression and concludes with a discussion of treatments for HIV distal neuropathic pain.
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1966-, Malmberg Annika B., and Chaplan Sandra R, eds. Mechanisms and mediators of neuropathic pain. Basel: Birkhäuser Verlag, 2002.

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Ghazi, Arif H., and Obi Agu. Acute pain in peripheral vascular disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199234721.003.0018.

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Pain in vascular disease is often severe. Atherosclerosis is the commonest cause of ischaemic pain. Angioplasty, stents, and surgical revascularization should be attempted to treat the underlying cause. Pain relief is also aimed at neuropathic and sympathetic components of pain. In end stage ischaemic disease, amputation may be necessary often leading to long-term pain.
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Cornblath, David R., and Richard A. C. Hughes. Peripheral neuropathy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0013.

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Disorders of peripheral nerves are one of the most common neurological problems today and include the increasing number of people with diabetes worldwide and those with inherited neuropathy, toxic neuropathy, carpal tunnel syndrome, inflammatory neuropathy, radiculopathies, and, increasingly, traumatic nerve injuries. Neuropathic pain is a growing problem without solution. In this chapter, ten landmark papers in peripheral nerve disorders have been selected, covering Bell’s palsy, Charcot-Marie-Tooth disease, carpal tunnel syndrome, paraneoplastic neuropathy, neurophysiology, familial amyloid polyneuropathy, chronic inflammatory demyelinating polyradiculoneuropathy, toxic neuropathy, diabetic neuropathy, and Guillain–Barré syndrome. These important papers set the stage for many subsequent advances in the field but may be forgotten now, so they are brought to the reader’s attention.
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Book chapters on the topic "Peripheral neuropathic pain"

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Devor, Marshall. "Peripheral Neuropathic Pain." In Encyclopedia of Pain, 2838–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_3279.

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Shetter, A. G. "Peripheral Nerve Stimulation for Neuropathic Pain." In Textbook of Stereotactic and Functional Neurosurgery, 2349–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-69960-6_139.

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Machelska, Halina. "Peripheral Neuroimmune Interactions and Neuropathic Pain." In Neuroinflammation and Neurodegeneration, 105–16. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1071-7_6.

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Bhadra, Narendra. "Peripheral Nerve Interface Applications: Neuropathic Pain." In Encyclopedia of Computational Neuroscience, 1–4. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_203-1.

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Bhadra, Narendra. "Peripheral Nerve Interface Applications, Neuropathic Pain." In Encyclopedia of Computational Neuroscience, 2281–84. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_203.

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Michaelis, Martin. "Electrophysiological characteristics of injured peripheral nerves." In Mechanisms and Mediators of Neuropathic Pain, 3–22. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8129-6_1.

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Zhang, Ji. "Peripheral and Central Immune Mechanisms in Neuropathic Pain." In Neuroinflammation, 107–21. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118732748.ch7.

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Gybels, J., R. Kupers, and B. Nuttin. "What Can the Neurosurgeon Offer in Peripheral Neuropathic Pain?" In Advances in Stereotactic and Functional Neurosurgery 10, 136–40. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9297-9_31.

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Woolf, Clifford J. "The Pathophysiology of Peripheral Neuropathic Pain—Abnormal Peripheral Input and Abnormal Central Processing." In Advances in Stereotactic and Functional Neurosurgery 10, 125–30. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9297-9_29.

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Gok Metin, Zehra. "Common Meanings of Living with Diabetic Peripheral Neuropathic Pain from the Perspective of Patients." In Meanings of Pain, 209–31. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24154-4_11.

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Conference papers on the topic "Peripheral neuropathic pain"

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Carozzi, Valentina Alda, Cynthia Renn, Rhee Peter, Danisha Gallop, Paola Marmiroli, Guido Cavaletti, and Susan Dorsey. "Abstract 934: Electrophysiological, behavioural and molecular characterization of the neuropathic pain in bortezomib-induced peripheral neuropathy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-934.

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Pettersen, Pernille Steen, Tuhina Neogi, Marthe Gløersen, Karin Magnusson, Hilde Berner Hammer, Tore K. Kvien, Till Uhlig, and Ida Kristin Haugen. "THU0418 NEUROPATHIC-LIKE PAIN IN PERSONS WITH HAND OSTEOARTHRITIS AND ASSOCIATIONS WITH PERIPHERAL AND CENTRAL SENSITIZATION." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4060.

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Koehler-McNicholas, Sara R., Lori Danzl, and Lars Oddsson. "The Effect of a Lower-Limb Sensory Prosthesis on Balance and Gait in People With Peripheral Neuropathy." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3466.

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Peripheral neuropathy (PN), commonly caused by diabetes mellitus, is a debilitating condition that currently affects approximately 20 million Americans. Chronic symptoms of PN often involve pain and weakness of the lower limbs, with eventual sensation loss on the plantar surfaces of the feet. According to epidemiological studies, reduced foot sole sensation has been linked to decreased standing stability [1] and an increased risk of falling [2]. Consequently, cost-effective interventions are needed to improve balance and mobility in this population. A growing body of research suggests that vibrotactile cues delivered to sensate areas of the lower limb may be an effective way to provide information about foot sole pressure to PN patients who experience poor balance control. Indeed, sensory substitution devices that provide vibrotactile feedback have been shown to aid in balance and improve postural control in various patient populations [3–7]. However, none of these technologies have been based on measurements of foot pressure nor have they been used as a balance prosthesis. The goal of this study was to investigate the effect of a new external lower-limb sensory prosthesis, the Walkasins™, on the balance and gait of individuals with PN who experience balance problems [8]. Walkasins™ consist of two parts: a leg unit and a foot pad (Figure 1). The leg unit wraps around the lower leg of the user and contains electronics for reading foot pad pressure signals, a microprocessor, and four vibrating motors that provide gentle tactile sensory cues to the front, back, medial, and lateral surfaces of the user’s leg. These cues reflect real-time foot pressure information at a location above the ankle where skin sensation is still present. The leg unit has a power button, two status LEDs, and a reset button (not shown in Figure 1). Power is supplied by a rechargeable internal battery. The foot pad is a thin consumable sole insert that can be cut to size and fit into a regular shoe. The foot pad connects to the leg unit through a physical cable. In this study, subjects performed gait and balance assessments with and without the Walkasins™ turned on in order to determine its short-term effects.
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