from Section 2 - Cancer Symptom Mechanisms and Models: Clinical and Basic Science
Published online by Cambridge University Press: 05 August 2011
The International Association for the Study of Pain (IASP) defines pain as “an unpleasant, sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” The pain that is commonly experienced by people with cancer may be caused by the disease itself or by cancer treatment. The three most common causes for cancer pain are: (1) tumors metastasizing to the bone; (2) tumors infiltrating the nerve and hollow viscus; and (3) cancer treatments such as chemotherapy, radiation, and surgery. Cancer pain thus involves multiple mechanisms, including inflammation and primary and secondary hyperalgesia after tissue or nerve injury.
In this chapter, we will describe the basic physiology of pain signal processing, including peripheral nociceptors that sense stimuli in multiple energy forms (eg, heat, mechanical, chemical) and central stations involved in coding pain sensibility. We will describe the mechanisms of primary and secondary hyperalgesia wherein normally innocuous stimuli become painful. Finally, we will discuss some of the alterations in the functions of neurons and nonneuronal cells when the nervous system itself is damaged.
Peripheral and central mechanisms of nociception
Peripheral nociceptors
Nociception – the ability to feel pain – is caused by activation of peripheral receptors known as nociceptors. Nociceptors respond selectively to a variety of noxious stimuli, such as heat, pinch, and chemicals, and provide information about the location and intensity of such stimuli. Nociceptors can be categorized into three classes according to their structural and functional properties.
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