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  • 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

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 2 of 2


  • Chapter 19 - Gabapentinoids and other anticonvulsants
    pp 225-239
  • View abstract

    Summary

    This chapter outlines the best current therapy of post-herpetic neuralgia (PHN) and herpes zoster (HZ) and the exciting promise of the zoster prevention vaccine. The clinical findings, on examining a patient with PHN, demonstrate three main features to the pain. There is a constant, steady burning pain, electric shock-like pains reminiscent of trigeminal neuralgia, and the skin is often very sensitive or painful to summating touch stimuli such as skin stroking. There are three possible approaches to managing PHN: the treatment of established PHN, the prevention of PHN by early and aggressive treatment of HZ, and the prevention of HZ and PHN by vaccination. Drugs such as Tricyclic antidepressants (TCAs), gabapentinoids, and opioids affect all features of the pain. An important question for clinicians is how satisfactory these drugs are for PHN patients in ordinary practice in terms of pain relief and disability, tolerability of side effects, and long-term benefit.
  • Chapter 20 - Opioids
    pp 240-248
  • View abstract

    Summary

    Nerve root compression can occur from osteophyte formation, disc herniation, or a combination. As only 1-2% of patients with back pain have a nerve root or spinal cord compression, an accurate diagnosis of the causes of painful radiculopathy relies on a thorough history and physical exam. It is important to note that many asymptomatic individuals have abnormalities such as disc herniations and foraminal stenosis on CT and MRI. Therefore, the imaging findings must be correlated with the history and examination findings. Surgery for spinal stenosis and neurogenic claudication is indicated if severe pain is present, and can provide sustained relief. Since the spinal cord terminates at the L1-2 vertebral level, lumbar pathology below this level may compress the distal nerve root, causing a cauda equina syndrome. A lesion affecting the lumbosacral plexus (LSP) can present with pain in the low back, hip or pelvis, or with sciatica pain.
  • Chapter 21 - Cannabinoids
    pp 249-266
  • View abstract

    Summary

    Neuropathic pain after spinal cord injury (SCI) is a type of central neuropathic pain and is a frequent complication of spinal injury which is often refractory. Studies in animal models describe a number of peripheral and central pathophysiological processes after nerve injury that would be the basis of underlying neuropathic pain mechanisms. A major inhibitory system related to pain is opioid receptor mediated analgesia. In neuropathic pain, N-methyl-d-aspartate (NMDA) receptor activation increases excitation in the pain transmitting systems. Recent advances in pain research indicate multiple mechanisms, including many components of peripheral and central sensitization mechanisms, underlying the initiation and maintenance of neuropathic pain. Neurosurgical interventions may be treatment options in patients with poor pain control despite pharmacotherapy. Besides the effectiveness of a treatment, the adverse event profiles of these analgesics have to be considered before starting therapy or combining different agents.
  • Chapter 23 - Spinal cord stimulation and other neuromodulation
    pp 273-289
  • View abstract

    Summary

    Multiple sclerosis (MS) can lead to numerous types of pain through the processes of inflammation and degeneration. The common types of pain seen in MS include dysesthetic/extremity pain, trigeminal neuralgia (TN), spasticity, L'hermitte's phenomenon, painful tonic spasms (PTS), musculoskeletal, headache, optic neuritis, and treatment related pain. This chapter focuses on the first five, with a particular focus on dysesthetic pain. The acute onset of dysesthetic pain in the setting of a relapse in a relapsing-remitting MS (RRMS) patient is clearly due to an inflammatory lesion. The inciting pathology of TN in MS is a lesion which affects the primary afferents of the trigeminal nerve after they enter the pons, distal to the trigeminal nuclear complex, in the root entry zone (REZ). Considering that people with MS are already predisposed to poor sleep, depression, and a poor quality of life, the presence of pain is particularly debilitating.
  • Chapter 24 - Drug synergy and therapeutic combinations
    pp 290-298
  • View abstract

    Summary

    This chapter discusses the epidemiology, sites of strokes, clinical presentation, pathophysiology, and treatment options for central post-stroke pain (CPSP). CPSP occurs after lesions at any level of the somatosensory pathways of the brain extending from the medulla to the thalamus to the somatosensory cortex. The diagnosis of CPSP is based on a history of stroke followed by pain within an area of the body corresponding to the presumed lesion of the central nervous system with confirmation of the lesion by imaging. The pharmacological and non-pharmacological management of CPSP is challenging and is complicated by comorbid depression, anxiety, and sleep disturbances which are common in this patient population. Tricyclic antidepressants and the anticonvulsant lamotrigine are first-line analgesics in the management of CPSP. Although the prevalence of CPSP is relatively low, the pain can be resistant to treatment and can have a major impact on quality of life.
  • Chapter 25 - The person with pain perspective and participation – an essential component of successfully managing chronic neuropathic pain
    pp 299-314
  • View abstract

    Summary

    Over the past 150 years, regional post-traumatic pain has had various appellations, most recently complex regional pain syndrome (CRPS) and post-traumatic neuralgia (PTN). CPRS appears to be a complex endophenotype of PTN that involves neurogenic inflammation as well as pain. There is increasing evidence that peripheral and central inflammatory cascades triggered by nerve injuries contribute to CRPS and perhaps PTN as well. PTN and CRPS often spread beyond classic individual nerve territories, although when patients are asked to outline the epicenter, or most abnormal area, this frequently identifies a specific nerve injury. The most dramatic CRPS and PTN-associated movement abnormality is fixed distal dystonia. Nerve conduction studies and electromyography are useful in documenting and localizing peripheral nerve damage. Currently, four classes of medications are primary options for chronic CRPS/PTN: tricyclics and serotonin-noradrenaline reuptake inhibitors; opioids; gabapentinoids; and topical or systemic local anesthetics.
  • Chapter 27 - Impact of chronic pain upon anxiety, sleep, and mood dimensions
    pp 322-333
  • View abstract

    Summary

    Neuropathic pain is present in approximately 20-30% of cancer patients with pain. The pathological mechanisms responsible for neuropathic pain are multifactorial. Assessment of neuropathic pain is crucial to appropriate management. Several pain scales were developed for patients with cancer pain. A meticulous neurology examination is helpful to evaluate thoroughly cancer patients with neuropathic pain. The pharmacological management of neuropathic cancer pain has recently been reviewed. Tramadol, codeine, and dihydrocodeine are recommended for the treatment of mild-to-moderate cancer pain intensity. The use of an analgesic ladder should be individualized with appropriate application of supportive drugs (e.g. laxatives and antiemetics) for the prevention and treatment of opioid adverse effects. Non-pharmacological measures, such as radiotherapy and invasive procedures (nerve blockades and neurolytic blocks) should also be used as required. In patients with very severe neuropathic pain, a combination of opioids and N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. ketamine) are recommended.
  • Chapter 28 - Impact upon related conditions and quality of life
    pp 334-340
  • View abstract

    Summary

    Fibromyalgia is an illness seen mostly in women and characterized by widespread body pain with abnormality located in the nervous system. A diagnosis of fibromyalgia should be considered when a patient presents with widespread body pain lasting for longer than 3 months, with associated tenderness to palpation of soft tissues, as well as the possible presence of symptoms of sleep disturbance, fatigue, cognitive symptoms, and mood changes. Nervous system, genetic, and psychological mechanisms likely all play a part in the final expression of fibromyalgia, with evidence showing abnormalities at multiple levels. Ideal management includes both non-pharmacological and pharmacological treatments in a multimodal approach incorporating a strong patient-centered internal locus of control. Non-pharmacological treatments with emphasis on a regular exercise program, stress management, and coping skills should be an integral part of any treatment strategy for fibromyalgia. The traditional pharmacological treatment paradigm begins with simple analgesics and tricyclic antidepressant medications (TCAs).
  • Chapter 29 - The future: new concepts and potential therapies
    pp 341-356
  • View abstract

    Summary

    Tricyclic antidepressants (TCAs) and serotonin norepinephrine reuptake inhibitors (SNRIs) (venlafaxine, duloxetine) are recommended as the first-line agents for peripheral neuropathic pain, especially for painful polyneuropathy, the other first-line options being gabapentinoids and topical lidocaine. Tricyclic antidepressants became a mainstay in the management of neuropathic pain before their mechanisms were elucidated and before the advent of systematic ways to evaluate their efficacy. Venlafaxine and duloxetine should be used with caution in patients with a history of mania, seizures, or bleeding tendency. Due to risk of excessive serotoninergic effect, they should be used with caution in patients receiving concomitant selective serotonin reuptake inhibitor (SSRI) or tramadol treatment. When selecting the treatment for an individual patient, comorbid conditions and their medications need to be taken into account. More detailed information of the effects of pharmacological agents on various symptoms of neuropathic pain and sensory profiles may guide drug selection in the future.

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