To see the other types of publications on this topic, follow the link: Peripheral neuropathic pain.
Books on the topic 'Peripheral neuropathic pain'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 43 books for your research on the topic 'Peripheral neuropathic pain.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
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.
Full textAbstract:
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.
2
Khursheed, Faraz, and Marc O. Maybauer. Neuropathic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0012.
Full textAbstract:
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.
3
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.
Full textAbstract:
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.
4
Scadding, John. Neuropathic pain. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0386.
Full textAbstract:
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.
5
Cheng, Jianguo, ed. Neuropathic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190298357.001.0001.
Full textAbstract:
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.
6
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.
Full textAbstract:
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.
7
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.
Full textAbstract:
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.
8
1966-, Malmberg Annika B., and Chaplan Sandra R, eds. Mechanisms and mediators of neuropathic pain. Basel: Birkhäuser Verlag, 2002.
Find full text
9
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.
Full textAbstract:
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.
10
Cornblath, David R., and Richard A. C. Hughes. Peripheral neuropathy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0013.
Full textAbstract:
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.
11
Markman, John D. Diagnostic and Clinical Scales for Peripheral Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0120.
Full textAbstract:
Due to the absence of a definitive pathological finding, objective biomarker, or imaging correlate, neuropathic pain syndromes may be graded as possible or probable depending on the results of neurological assessment. It is important to acknowledge the diagnostic uncertainty inherent in such a grading system based on probability in a condition for which there is no “gold standard” upon which to base validation studies. Neuropathic pain is a multidimensional entity, and specific syndromes may have distinct sensory profiles (i.e. different combinations of sensory signs and symptoms). Clinical suspicion for an underlying neuropathic mechanism increases when pain is characterized by features such as numbness, paresthesias, and allodynia and when the symptoms are generally resistant to standard over-the-counter and prescribed analgesics. In this chapter a variety pain scales are reviewed.
12
Brown, Matthew. The chronic constriction injury model of neuropathic pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0067.
Full textAbstract:
The landmark paper discussed in this chapter is ‘A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man’, published by Bennett and Xie in 1988. This paper, in which the unilateral sciatic nerve chronic constriction injury (CCI) model was first presented, is one of the earliest and most comprehensive descriptions of a specific animal paradigm that was designed to model human neuropathic pain. The authors realized that human neuropathic pain rarely involves nerve transection but instead involves evoked changes in damaged and preserved nerve fibres. Furthermore, they systematically applied a barrage of sensory testing that demonstrated quantifiable hyperalgesia and cold allodynia reflecting some of the clinical observations of human neuropathic pain phenotype. CCI provided a high-quality template for the development of neuropathic pain models that impelled the subsequent development of other animal models striving to replicate the human condition faithfully and accurately.
13
Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.
Full textAbstract:
Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.
14
Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.
Full textAbstract:
Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
15
Chang, Victor T. Visceral pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0134.
Full textAbstract:
Visceral pain is pain that arises from, in, or around internal organs. Common examples include chest pain and functional abdominal pain. In palliative medicine, well-known visceral pain syndromes include pain from pancreatic cancer and bowel obstruction. Recent advances have increased our understanding of the diagnostic challenges and therapeutic possibilities for patients with visceral pain syndromes. Understanding the basis of referred pain is a key component of patient assessment. The complexity of visceral nociception and pain signalling is being unravelled through anatomical, immunohistochemical, and functional studies. On a molecular level, families of receptors and signalling proteins have now been described that will lead to a future with innovative therapies. This knowledge has developed within the paradigms of pain pathways, peripheral activation and peripheral and central sensitization, thereby linking and distinguishing visceral pain from somatic and neuropathic pain. Treatment options for visceral pain in palliative care encompass a wide variety of medical, interventional, and psychological approaches. With appropriate diagnostic measures and careful consideration of therapeutic options, most patients can achieve satisfactory relief.
16
Mauguière, François, and Luis Garcia-Larrea. Somatosensory and Pain Evoked Potentials. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0043.
Full textAbstract:
This chapter discusses the use of somatosensory evoked potentials (SEPs) and pain evoked potentials for diagnostic purposes. The generators of SEPs following upper limb stimulation have been identified through intracranial recordings, permitting the analysis of somatosensory disorders caused by neurological diseases. Laser activation of fibers involved in thermal and pain sensation has extended the applications of evoked potentials to neuropathic pain disorders. Knowledge of the effects of motor programming, paired stimulations, and simultaneous stimulation of adjacent somatic territories has broadened SEP use in movement disorders. The recording of high-frequency cortical oscillations evoked by peripheral nerve stimulation gives access to the functioning of SI area neuronal circuitry. SEPs complement electro-neuro-myography in patients with neuropathies and radiculopathies, spinal cord and hemispheric lesions, and coma. Neuroimaging has overtaken SEPs in detecting and localizing central nervous system lesions, but SEPs still permit assessment of somatosensory and pain disorders that remain unexplained by anatomical investigations.
17
Desroches, Julie. Peripheral analgesia involves cannabinoid receptors. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0034.
Full textAbstract:
This landmark paper by Agarwal and colleagues was published in 2007, when the exact contribution of the activation of the cannabinoid type 1 receptor (CB1) receptors expressed on the peripheral terminals of nociceptors in pain modulation was still uncertain. At that time, while it was clearly demonstrated that the central nervous system (CNS) was involved in the antinociceptive effects induced by the activation of the CB1 receptor, many strains of mice in which the gene encoding the CB1 receptor was deleted by conditional mutagenesis were used to study the specific role of these receptors in pain. Creating an ingenious model of genetically modified mice with a conditional deletion of the CB1 receptor gene exclusively in the peripheral nociceptors, Agarwal and colleagues were the first to unequivocally demonstrate the major role of this receptor in the control of pain at the peripheral level. In fact, these mutant mice lacking CB1 receptors only in sensory neurons (those expressing the sodium channel Nav1.8) have been designed to highlight that CB1 receptors on nociceptors, and not those within the CNS, constitute an important target for mediating local or systemic (but not intrathecal) cannabinoid analgesia. Overall, they have clarified the anatomical locus of cannabinoid-induced analgesia, highlighted the potential significance of peripheral CB1-mediated cannabinoid analgesia, and revealed important insights into how the peripheral endocannabinoid system works in controlling both inflammatory pain and neuropathic pain.
18
Chong, Sam, and J. Ganesalingham. Acute pain in the neurological patient. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199234721.003.0016.
Full textAbstract:
Acute pain is a common presenting symptom in patients with neurological conditions. Acute onset headache may indicate a life-threatening underlying condition. Lumbosacral and cervical spine pain are commonly caused by degenerative disease but there are sometimes clues to indicate alternative pathologies. Acute pain arising from the peripheral nervous system and muscles are usually inflammatory in origin. A careful history and examination is crucial to assess patients with neurological pain. Opioids may be used in combination of an anti-epileptic or antidepressant drug in the treatment of acute neuropathic pain.
19
Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Neurology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0007.
Full textAbstract:
This chapter provides information on the ageing brain and nervous system, tremor, neuropathic pain/neuralgia, presentation of Parkinson’s disease, management of Parkinson’s disease, diseases masquerading as Parkinson’s disease, epilepsy and its drug treatment, neuroleptic malignant syndrome, motor neuron disease, peripheral neuropathies, subdural haematoma, sleep and insomnia, and other sleep disorders.
20
Gordon-Williams, Richard M., and Anthony H. Dickenson. Pathophysiology of pain in cancer and other terminal illnesses. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0092.
Full textAbstract:
Cancer pain involves a myriad of peripheral changes in the function of tissue and nerves, at the site of the tumour growth, as well as a number of consequent changes in the processing of pain messages at the spinal cord level with implications for the pain experience at higher centres. This chapter reviews the changes in peripheral pain signalling, notes the likely prevalence of both inflammatory and neuropathic components, and describes the altered events at spinal levels that can come some way towards explaining ongoing pain, hyperalgesia, and allodynias that patients with cancer and other terminal illnesses such as HIV/AIDs experience. Finally, changes induced by cancer at the level of the brain are discussed. The mechanisms of action of therapies, both existing and potential novel approaches, are included at peripheral and central levels.
21
James, Nicholas D., and Elizabeth J. Bradbury. Autotomy. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0065.
Full textAbstract:
The landmark paper discussed in this chapter is ‘Autotomy following peripheral nerve lesions: Experimental anaesthesia dolorosa’, published by Wall et al. in 1979. This paper was the culmination of a series of studies in which Wall, together with a number of colleagues, investigated the underlying causes of neuropathic pain following peripheral nerve injury. In this paper, the authors used a variety of nerve injury models to show that the extent of resultant anaesthesia combined with ectopic firing from damaged axons in nerve-end neuromas correlated with the severity of self-mutilation (termed ‘autotomy’) observed in the affected hindlimb. The authors therefore suggested that these simple models might be suitable for studies of the prevention of irritations originating from chronic lesions of peripheral nerves. Indeed, this proved to be the case, sparking the development of numerous animal models of spontaneous pain following nerve injury and spawning a new field of neuropathic pain research.
22
Practicalities of using TENS for specific conditions and situations. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199673278.003.0007.
Full textAbstract:
Research studies have failed to evaluate different TENS techniques for specific conditions. Safe and appropriate TENS technique is based on the use of conventional TENS delivered at a strong, non-painful intensity at the site of pain in the first instance with patients selecting pulse pattern, frequency, and duration for reasons of comfort. In practice, it is necessary to adapt this approach for specific painful conditions. The purpose of this chapter is to demonstrate how the general principles of good practice are applied when using TENS to manage various painful conditions. The chapter discusses acute pain, including post-operative pain and labour pain, chronic musculoskeletal pain, including back pain and osteoarthritis, chronic neuropathic pain, including peripheral and central neuropathic pain, cancer pain, and TENS for children and the elderly.
23
Clinical research on the efficacy of TENS. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199673278.003.0008.
Full textAbstract:
The acceptance of a treatment into mainstream medicine is influenced by a wide variety of factors. Traditionally, practitioners rely on information gleaned from their experience of using treatments on their patients although this can be misleading. Clinical research uses experiments to determine whether therapeutic effects of a treatment are attributed to its active ingredient by removing biases that confound clinical observation. This helps to determine whether treatments are efficacious. The purpose of this chapter is to overview evidence from clinical research on the efficacy of TENS for the management of pain by covering evidence-based practice, clinical research on acute pain including post-operative pain and labour pain, chronic musculoskeletal pain, including back pain and osteoarthritis, chronic neuropathic pain, including peripheral and central neuropathic pain, and cancer pain. It also discusses challenges in TENS research.
24
Mason, Peggy. Somatosensation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0017.
Full textAbstract:
Under normal circumstances, the somatosensory system contributes more to shaping movements than to perception. Yet damage to the somatosensory system can result in spontaneous pain and other abnormal somatic perceptions. An exploration of the mechanisms and pathways involved in touch perception is slanted toward understanding the contribution of the dorsal column–medial lemniscus pathway to the generation of paresthesia and dysesthesia. Peripheral somatosensory afferents that contribute to the perception of sharp or aching pain, temperature, and itch are described. The properties of transient receptor potential (TRP) channels on nociceptors and thermoreceptors are described. Physiological and pharmacological mechanisms that lead to neurogenic inflammation are considered. How peripheral and central changes triggered by acute injury or disease can lead to long-lasting changes that support chronic pain is described. Persistent pain that occurs independently of any stimulus is termed neuropathic. Mechanisms of referred pain from deep structures including viscera are introduced.
25
Mechanism of action of TENS. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199673278.003.0009.
Full textAbstract:
There has been an abundance of research using animal, healthy human, and patients on the mechanism of action of TENS. Activity in peripheral nerves generated during TENS will influence physiological actions at peripheral, spinal, and supraspinal sites of the nervous system. Some of these physiological actions are mediated by alterations in the concentrations of neurochemicals dependent on the electrical characteristics of TENS. The purpose of this chapter is to discuss research evidence that has contributed to our knowledge about the physiological and pharmacological actions of TENS, including the mechanism of action of conventional TENS and AL-TENS, peripheral mechanisms of TENS, central mechanisms of TENS, findings from inflammatory and neuropathic models of pain, and the neuropharmacology of TENS hypoalgesia and TENS tolerance.
26
McDougall, Jason J., and Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.
Full textAbstract:
Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.
27
Donaghy, Michael. Focal peripheral neuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0487.
Full textAbstract:
Some causes of focal peripheral nerve damage are self-evident, such as involvement at sites of trauma, tissue necrosis, infiltration by tumour, or damage by radiotherapy. Focal compressive and entrapment neuropathies are particularly valuable to identify in civilian practice, since recovery may follow relief of the compression. Leprosy is a common global cause of focal neuropathy, which involves prominent loss of pain sensation with secondary acromutilation, and requires early antibiotic treatment. Mononeuritis multiplex due to vasculitis requires prompt diagnosis and immunosuppressive treatment to limit the severity and extent of peripheral nerve damage. Various other medical conditions, both inherited and acquired, can present with focal neuropathy rather than polyneuropathy, the most common of which are diabetes mellitus and hereditary liability to pressure palsies. A purely motor focal presentation should raise the question of multifocal motor neuropathy with conduction block, which usually responds well to high-dose intravenous immunoglobulin infusions.
28
Burke, Rebecca, and Akhila Reddy. Duloxetine for Chemotherapy-Induced Peripheral Neuropathy (DRAFT). Edited by Nathan A. Gray and Thomas W. LeBlanc. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190658618.003.0015.
Full textAbstract:
This chapter discusses the Smith et al. randomized, double-blind, placebo-controlled crossover trial determining the effectiveness of duloxetine compared to placebo in reducing painful chemotherapy-induced peripheral neuropathy. Patients were divided into the duloxetine-first or placebo-first group, then subsequently crossed over to the alternate group. The study particularly examined changes in pain severity, quality of life, interference with daily function, and adverse events. The study demonstrated that patients receiving duloxetine first reported a statistically significant decrease in pain, improvement in quality of life, and decreased pain interference with daily functioning. This chapter describes the basics of the study, including funding, year study began, year study was published, study location, who was studied, who was excluded, how many patients, study design, study intervention, follow-up, endpoints, results, and criticism and limitations. The chapter briefly reviews other relevant studies and information, gives a summary and discusses implications, and concludes with a relevant clinical case.
29
Peripheral Neuropathy Causes And Treatments Conditions Of Nerve Pain And Dysfunction. Createspace, 2011.
Find full text
30
Murinova, Natalia, and Daniel Krashin. Susceptibility of Peripheral Nerves in Diabetes to Compression and Implications in Pain Treatment. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0006.
Full textAbstract:
Diabetes affects a large and growing percentage of the population in most countries of the world. Diabetes causes many different health problems, but among the most severe and disabling is peripheral neuropathy. This progressive, often painful nerve condition causes suffering and disability and also predisposes patients to developing musculoskeletal deformities and foot ulcers that may threaten life and limb. This chapter reviews briefly the significance of this condition, the underlying pathophysiology, and surgical considerations. Surgical decompression is a possible treatment for this neuropathy and may help prevent disastrous complications of diabetic peripheral neuropathy. However, foot surgery in the setting of diabetic peripheral neuropathy also carries significant risks.
31
Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0338_update_001.
Full textAbstract:
Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide (Gb3), which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. Proteinuria and estimated glomerular filtration rate (eGFR) are strongly associated with risk of progression, but this may be reduced by treatment with angiotensin-converting enzyme inhibitors as well as by enzyme replacement therapy (ERT). ERT was approved in 2001; it improves pain and other neuropathic symptoms, and well-being, and has been proven to clear deposits of Gb3 from tissues, at variable speeds. There is limited randomized controlled trial data but protective effects have been proven for renal outcomes, death, and better outcomes in some other organ systems. Renal function may be protected if ERT is commenced before there is heavy proteinuria or substantial loss of GFR. It is recommended to start ERT as soon as the diagnosis is made in those with very low or absent enzyme. For those with intermediate levels it is recommended to commence treatment only when signs or symptoms appear. Proteinuria and eGFR give most information from a renal point of view, but renal biopsy is also useful for confirming the renal diagnosis and staging the disease as well as monitoring progress in selected cases. Management should include regular screening for complications including myocardial and neurological assessments. It is likely that registries will show progressive rises in median survival with this condition.
32
Yang, Lynda J.-S. Peripheral Nerve Neurosurgery. Edited by Thomas Wilson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.001.0001.
Full textAbstract:
This book presents cases in peripheral nerve surgery divided into four distinct areas of pathology: entrapment and inflammatory neuropathies, peripheral nerve pain syndromes, peripheral nerve tumors, and peripheral nerve trauma. Each chapter also presents pearls for the accurate diagnosis of, successful treatment of, and effective complication management for each clinical entity. The latter three focus areas will be especially helpful to neurosurgeons preparing to sit for the American Board of Neurological Surgery oral examination, which bases scoring on the three areas. Finally, each chapter contains a review of the medical evidence and expected outcomes, which is helpful for counseling patients and setting accurate expectations. Rather than exhaustive reference lists, the authors provide selected references recommended to deepen understanding.
33
Peripheral Neuropathy: When the Numbness, Weakness, and Pain Won't Stop (American Academy of Neurology). Demos Medical Publishing, 2006.
Find full text
34
Katirji, Bashar. Case 7. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0011.
Full textAbstract:
Diabetic amyotrophy is a relatively uncommon neurological complication of diabetes mellitus. However, the disorder is often not recognized by internists and neurologists and misdiagnosed as myopathy, radiculopathy, or peripheral polyneuropathy. The discussion starts by outlining the classification of the diabetic neuropathies. This case highlights the classical clinical presentation of diabetic amyotrophy, also referred to as diabetic polyradiculoplexopathy or subacute diabetic neuropathy, in a man with pain in the anterior thigh and knee followed by thigh and hip weakness. It also emphasizes the electrodiagnostic findings including the subacute needle electromyography changes and stresses the frequent coexistence of diabetic amyotrophy with the more common distal peripheral polyneuropathy in the majority of patients.
35
Coping With Peripheral Neuropathy: How to handle stress, disability, anxiety, fatigue, depression, pain, and relationships. iUniverse, Inc., 2007.
Find full text
36
Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 50-Year-Old Woman with Burning Feet. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0020.
Full textAbstract:
Small-fiber neuropathy typically presents with burning pain or with widespread brief stabbing pains, by atypical presentations including asymmetric sensory symptoms are common. Nerve conduction studies are usually normal, as this disorder test only interrogates large fiber function; in small-fiber neuropathy the pathology is restricted to smaller unmyelinated fibers. Autonomic neuropathy can accompany the painful peripheral neuropathy but can be difficult to recognize since the symptoms can be protean. In this chapter, clinical characteristics of small-fiber and autonomic neuropathy are discussed. Various diagnostic modalities are described, including the benefits and pitfalls of available options. The most common conditions causing small-fiber and autonomic neuropathy are reviewed. The controversy surrounding impaired glucose tolerance as an etiological factor is dicusssed. We discuss the available medications and outline a rational approach to treatment.
37
Elham, Bayat. Neurologic Manifestations of Hematological Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0193.
Full textAbstract:
A wide sprectum of hematologic disorders affect the central and peripheral nervous system. These disorders include porphyria, thrombotic thrombocytopenic purpura-hemolytic uremic syndromes, sickle cell disease, plasma cell dyscrasias, monoclonal gammopathy, primary systemic amyloidosis, primary systemic amyloidosis, Waldonstrom’s macroglobulinemia, myeloproliferative syndromes, cryoglobulinemia, and polycythemia vera. Some, like porphyria, cause both central and peripheral nervous system manifestations including sensory/motor peripheral neuropathy, dysautonomia, pain, seizures, and abdominal pain. Others such as sickle cell disease primarily affect the brain and cause both clinically apparent strokes associated with a vasculopathy of large intracranial blood vessels, as well as less obvious microstrokes that cause progressive cognitive decline if not treated.
38
Bodor, Marko, Sean Colio, and Christopher Bonzon. Hand and Wrist Injections: Ultrasound. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199908004.003.0045.
Full textAbstract:
Two basic ultrasound-guided approaches are used for procedures to diagnose and treat chronic pain in the upper extremity. The short-axis approach is best for injections of superficial, vertically oriented joints, whereas the long-axis approach is best for relatively deep injections and more open joints or whenever it is necessary for the needle to be seen at all times. Ultrasound can guide injections for nerve compressions. Carpal tunnel syndrome is the most common peripheral nerve entrapment syndrome. Ulnar tunnel syndrome occurs in the setting of space-occupying lesions. Ultrasonography can identify a space-occupying lesion, while electrodiagnostic studies can help differentiate ulnar neuropathy at the wrist from ulnar neuropathy at the elbow. Ultrasound can also guide injections at joints such as the basilar join of the thumb, phalangeal joints, and wrist joints. Ultrasound-guided injections are also useful for tendon dysfunctions including de Quervain’s Tenosynovitis, trigger finger, intersection syndrome, and tendon impingement.
39
Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0020.
Full textAbstract:
Muscle stiffness is a nonspecific term meaning limited muscle mobility that is not due to weakness. It is opposite to flexibility. Muscle and joint pain may be described as stiffness. Painful sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy), while resting and nocturnal cramps are neurogenic (neuropathy, motor neuron disease, etc). Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome. Upper motor neuron lesions are associated with spasticity and stiffness (HSP, PLS, myelopathies, etc.). Painful cramps and fasciculations are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
40
Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.
Full textAbstract:
Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
41
Stoneley, Sarah, and Simon Rinald. Sensory loss. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0047.
Full textAbstract:
Sensory disturbance can either be a complete loss (anaesthesia) or a reduction (hypoaesthesia) in the ability to perceive the sensory input. Dysaesthesia is an abnormal increase in the perception of normal sensory stimuli. Hyperalgesia is an increased sensitivity to normally painful stimuli, and allodynia is the perception of usually innocuous stimuli as painful. A complete loss of sensation is likely to be due to a central nervous system problem, while a tingling/paraesthesia (large fibre) or burning/temperature (small fibre) sensation is likely due to an acquired peripheral nervous system problem. Shooting, electric-shock-like pains suggest radicular pathology, a tight-band spinal cord dysfunction. Positive sensory symptoms are usually absent in inherited neuropathies, even in the context of significant deficits on examination. This chapter describes the clinical approach to patients with sensory symptoms. Common patterns of sensory loss and their causes are described.
42
Katirji, Bashar. Electromyography in Clinical Practice. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.001.0001.
Full textAbstract:
Clinical Electromyography in Clinical Practice provides case-based learning of clinical Electromyography (EMG) with a main mission of reducing the gap between theory and practice in the field of electrodiagnostic medicine. The book format includes four introductory chapters that acquaint the discipline and scope of the EMG Examination to the beginners. This include chapters on nerve conduction studies, needle EMG, and specialized testing including late responses, repetitive nerve stimulation and single fiber EMG. Discussion on the electrodiagnostic and clinical EMG findings in the numerous neuromuscular disorders including anterior horn cell disorders, peripheral neuropathies, neuromuscular junction disorders and myopathies. The second part of the book includes comprehensive presentations of 27 cases that encompass the most common disorders encountered in the EMG laboratory and are presented in a similar layout. These are subdivided into (1) focal disorders of the lower extremity, (2) focal disorders of the upper extremity, and (3) generalized neuromuscular disorders. The book focuses on problem solving through analysis of the data obtained on nerve conduction studies and needle EMG. This is meant to be a bedside analysis of data, similar to what occurs in the EMG laboratory on a daily basis. The exact values obtained on nerve conduction studies are examined and the details of the findings on needle EMG are studied. A final diagnosis is then made. This is followed by a detailed discussion of the clinical and electrodiagnostic findings of the disorder. Clinical Electromyography in Clinical Practice is an ideal book for physicians interested in learning and mastering the clinical practice of clinical EMG. This includes specialists in the field of neurology, physical medicine and rehabilitation, orthopedics, hand surgery, neurosurgery, spine, rheumatology and pain management.
43
Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.
Full textAbstract:
Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.