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  1. Home
  2. Books
  3. Neuropathic Pain
  • Cited by 10
  • Edited by Cory Toth, Department of Neurology, University of Calgary, Dwight E. Moulin, Department of Clinical Neurological Sciences, University of Western Ontario
Publisher:
Cambridge University Press
Online publication date:
December 2013
Print publication year:
2013
Online ISBN:
9781139152211
DOI:
https://doi.org/10.1017/CBO9781139152211
Subjects:
Anesthesia, Intensive Care, Pain Management, Neurology and Clinical Neuroscience, Medicine
Information

Book description

Central or peripheral neuropathic pain can be caused by a wide range of injuries, infections and diseases such as: spinal cord injury, multiple sclerosis, stroke, herpes zoster, diabetes and cancer. Many of these pain syndromes are difficult to treat, representing a challenge for many neurologists not routinely trained in pain management. Written by an international team of experts in the field, Neuropathic Pain: Causes, Management and Understanding gives readers an in-depth understanding of the multitude of conditions causing neuropathic pain. Epidemiology, clinical diagnosis, pathophysiology, outcome measurement and the best evidence-based management of individual and general neuropathic pain conditions are also described in depth. A unique chapter, written from a patient's viewpoint, gives new insight into how chronic neuropathic pain affects the lives of those patients with the condition. This book is essential reading for all pain specialists, neurologists, psychiatrists and anesthesiologists who wish to better understand their patients' neuropathic pain.

Reviews

“…Remarkable in its content and…clarity. The management is evidence based and to the point…the guidance is unambiguous and remarkably straightforward…very useful book for the treatment of patients suffering from neuropathic pain.”

- Doody's Review Service

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Contents

Page 1 of 2

Contents
  • Chapter 7 - Pathophysiology of neuropathic pain: inflammatory mediators
    pp 77-89
  • View abstract

    Summary

    This chapter summarizes a standard approach to identifying neuropathic pain for the clinician. For neuropathic pain, and for the condition of complex regional pain syndrome (CRPS) especially, the six Ss should be queried when obtaining details regarding the affected region. A useful tool to rapidly and accurately localize sources of chronic pain and assist in the diagnosis of causes of neuropathic pain is a pain diagram. The examination of a chronic pain patient should start with an appropriate and directed general examination including a neurological examination. Quantitative sensory testing (QST) provides indirect information used to evaluate underlying sensory function abnormalities using only small, portable tools and with less time requirement than protocols developed by the German Neuropathic Research Network. In the future, bedside QST is expected to continue to play a role in determining potential pain mechanisms to help direct further evaluation and treatment.
  • Chapter 9 - Diabetic and other peripheral neuropathies
    pp 101-119
  • View abstract

    Summary

    Diagnostic testing for determining the sources of neuropathic pain has evolved over time. Good clinical practice requires that the clinician takes a good history and performs an appropriate clinical examination to establish the diagnosis of neuropathic pain as possible or probable. Quantitative sensory testing (QST) is helpful in the early diagnosis and follow-up of peripheral neuropathy affecting small-fiber function. Peripheral nerve biopsy was performed in certain circumstances, such as when vasculitis, amyloid, or an unspecified inflammatory condition could be the etiology of peripheral neuropathy. Computerized tomography (CT) and magnetic resonance imaging (MRI) scans can facilitate diagnoses by identifying causes of central and peripheral nervous tissue ischemia, demyelination, compression, or infiltration. Functional MRI works on the principle that regional cerebral blood flow (rCBF) is related to regional cerebral activity. Autonomic function testing relies on indirectly accessing the function of unmyelinated postganglionic fibers, which cannot be tested directly by conventional neurophysiological techniques.
  • Chapter 10 - Post-herpetic neuralgia: the prevention of a scourge
    pp 120-129
  • View abstract

    Summary

    Epidemiology has long been a neglected aspect of clinical research related to neuropathic pain and until recently there was no reliable information regarding the general epidemiology of this type of pain, most notably its prevalence and incidence. Two large population-based postal surveys have been carried out to estimate the overall prevalence of chronic pain with neuropathic characteristics (NC) in the general population. The large epidemiological survey of the burden of illness due to chronic neuropathic pain was undertaken in the French general population. Assessment of quality of life in patients with or without pain was based on the Medical Outcome Short Form 12 scale (MOS-SF-12). The surveys have shown that all domains of quality of life, sleep duration, and quality and symptoms of depression and anxiety are consistently more impaired in subjects reporting chronic pain with NC than in subjects reporting chronic pain without NC.
  • Chapter 11 - Painful conditions affecting the nerve roots and plexus
    pp 130-144
  • View abstract

    Summary

    This chapter describes commonly used peripheral nerve injury models of neuropathic pain. It introduces the central, non-traumatic and orofacial models of neuropathic pain. Neuropathic pain of central origin is observed clinically after traumatic incidents, such as stroke or spinal cord injury (SCI). An important consideration is that the pain experience, in humans and animals, has both sensory and emotional dimensions. The focus on nociception in pain research has been associated with the clinical failure of several potential pain medicines. An understanding of both sensory and affective dimensions of pain may improve translational research. Further, interpretations made from animal nerve injury models should be considered in the context of gender, age, and species/strain studied. Finally, it appears that no animal nerve injury model is without limitations, therefore, behavioral, physiological, and biochemical studies can only speculate on the relevance of experimental findings to human neuropathic pain.
  • Chapter 13 - Central pain symptoms in multiple sclerosis
    pp 156-169
  • View abstract

    Summary

    This chapter explores the cellular and genetic mechanisms important in the development of neuropathic pain and other forms of chronic pain related to the phenomenon of sensitization. Peripheral sensitization contributes to pain hypersensitivity found at the location of tissue damage and/or inflammation. The chapter reviews the events that underlie pain as well as the anatomical and pharmacological basis for nociceptive sensations and chronic pain. Nociceptor excitation via various transient receptor potential (TRP) channels can result from a number of contributing processes. Transduction of mechanical, thermal, and chemical stimuli begins with membrane depolarization, which, if sufficient, transforms into an action potential. There are three classes of cell surface proteins at the sensory neuron important for sensory transduction: ion channels, metabotropic G protein-coupled receptors (GPCRs), and receptors for neurotrophins or cytokines. An important concept in central modulation of pain is the central inhibitory pathways and networks.
  • Chapter 14 - Central post-stroke pain
    pp 170-176
  • View abstract

    Summary

    This chapter focuses on the voltage-gated sodium (Nav) channel and voltage-gated calcium channel (VGCC), since they are essential to pain transmission. The most basic structural plan of a eukaryotic voltage-gated ion channel consists of four sub-units surrounding a central pore, through which ions pass. Sodium channel inactivation is modulated by many factors, including toxins, disease states, mutations, and therapeutic drugs. In neurons, activation of VGCC in response to depolarized membrane potential leads to calcium entry, mediating calcium-dependent enzyme activation, gene expression, or release of neurotransmitters. Two main classes of VGCC have been reported, the T-type or low voltage activated (LVA) and the high voltage activated (HVA) channels. To manage different etiologies of neuropathic pain, a variety of therapeutic targets must be available. Drugs directed at specific targets, such as those channels expressed in nociceptors, or upregulated after injury, may give the best pain management while minimizing undesirable side effects.
  • Chapter 15 - The complex regional pain syndromes and post-traumatic neuralgias
    pp 177-190
  • View abstract

    Summary

    This chapter presents a detailed evidence of the involvement of algesic inflammatory mediators as well as anti-inflammatory mediators in neuropathic pain, including their structure, source, molecular targets, and effect on nociceptors, glia, and immune cells. It discusses some of the key inflammatory mediators implicated in neuropathic pain including kinins, purines, lipids, amines, and neurotrophic factors. Bradykinin contributes to ongoing inflammatory cascades by stimulating the release of pro-inflammatory cytokines and chemokines, as well as stimulating histamine release from mast cells. Cytokines, chemokines, and their receptors are widely expressed in the nervous system, and there is growing evidence they play a major role in the pathogenesis of neuropathic pain. Modulation of cytokine signaling by blocking pro-inflammatory cytokines and/or augmenting anti-inflammatory cytokines has shown considerable efficacy in models of neuropathy. Finally, the chapter discusses some of the key cytokines implicated in neuropathic pain.
  • Chapter 16 - The management of neuropathic pain in cancer patients
    pp 191-204
  • View abstract

    Summary

    This chapter reviews an important mediator and its associated factors, the Toll-like receptors (TLRs). It examines the possible role that TLRs serve in neuroimmune interactions within both the central and peripheral nervous systems. The chapter focuses on Toll-like receptor 4 (TLR4) as this TLR appears to contribute directly to neurological pathologies such as neuropathic pain and opioid-induced hyperalgesia, as well as epilepsy. Inflammation in the absence of infection contributes to both injury and disease processes in the nervous system. There are many similarities between the mediators and changes in synaptic connectivity between neuropathic pain and epilepsy. Epileptic seizure conditions are routinely characterized as a neurocentric disease due in large part to the abnormally excessive or synchronous neuronal activity in the brain. The opioid family of drugs, though potent analgesics, are known to be only partially effective in treating neuropathic pain due in large part to the myriad of side effects.
  • Chapter 17 - Fibromyalgia
    pp 205-216
  • View abstract

    Summary

    Diabetic sensorimotor polyneuropathy (DSP) is a condition that has escaped direct management at the present time. The diagnosis of painful DSP (PDSP) is based upon important historical and clinical examination aspects, with some diagnostic assistance provided by nerve conduction studies. There is great complexity in the pathophysiology of DSP. Hyperglycemia in both humans and in animal axonal models appears to drive several metabolic pathways contributing to initiation and progression in humans and to the presence of peripheral neuropathy in animal models. Pharmacological treatment is required in a majority of patients with PDSP. Most guidelines suggest that anticonvulsants and antidepressants be used first, prior to opioids due to the risk of dependency, tolerance, dose escalation, and diverse effects. Future treatments may include better methods to modulate loss of central inhibition, better topical applications, and directed therapy against neuroinflammatory changes of microgliosis and astrogliosis.

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