Mechanisms and Mediators of Neuropathic Pain

ISBN-13: 9783034894487 / Angielski / Miękka / 2012 / 260 str.

Annika B. Malmberg; Sandra R. Chaplan

Opis

Numerous improvements in our understanding of the mechanisms that underlie neuropathic pain states have come from the development of animal models, most of which involve partial peripheral nerve injury. The animal models have shown that nerve injury initiates a cascade of events resulting in altered neurochemistry and molecular biology of the peripheral neurons, the dorsal root ganglion cell, and changes in neurotransmitter and receptor expression in the dorsal horn of the spinal cord. Moreover, nerve injury produces anatomical changes with functional consequences.
This volume summarises the current understanding of the pathophysiological processes in the peripheral and central nervous system that contribute to the neuropathic pain. It provides a timely review of neuropathic pain mechanisms, written by experts in the field.

Spis treści

Peripheral consequences of nerve injury.- Electrophysiological characteristics of injured peripheral nerves.- Sodium channels and the molecular basis for pain.- Changes in DRG neurons after injury: possible involvement in the development and maintenance of neuropathic pain.- Neuroinflammation, cytokines and neuropathic pain.- Spinal cord plasticity following peripheral nerve injury.- Pharmacological plasticity associated with neuropathic pain states.- Sprouting and reorganization in the spinal cord after nerve injury.- Neuropathic pain: preclinical and clinical paradigms.- Pre-clinical nerve ligation models: behavior and electrophysiology.- Animal models of toxic and metabolic sensory neuropathies.- Role of adrenergic transmitters and receptors in nerve and tissue injury related pain.- Evaluation of neuropathic pain.- New treatment strategies for neuropathic pain.- Glutamate receptor antagonists and neuropathic pain.- Antiepileptic drugs for treatment of neuropathic pain.- Calcium channel antagonists for the treatment of pain.- Cholinergic, adenosinergic and a2 adrenergic mechanisms in chronic neuropathic pain.