Introduction

In Chapter 5, we discussed the normal responses to a variety of noxious stimuli and their modulation by peripheral and central neural mechanisms. This review showed that noxious stimuli preferentially and most commonly activate a set of interconnected structures, namely the insula and secondary (SII) somatosensory cortices, anterior cingulate gyrus and thalamus. Several additional structures are also activated during normal acute pain although somewhat less frequently: the primary (SI) somatosensory cortex, components of the striatum, the cerebellum, premotor cortex, dorsolateral and orbitofrontal regions of the prefrontal cortex, and the medial midbrain in the region of the periaqueductal gray matter.

In this chapter we review the evidence that chronically painful conditions, whether of peripheral or central origin, may alter the nociceptive processing that normally follows the application of noxious or innocuous stimuli (see Chapter 7). In clinical practice and in the interpretation of the results of pain research, the assumption is often made that the perceptual abnormalities sometimes associated with chronic pain states are attributable only to changes occurring at the peripheral or spinal level. Although this assumption may be correct in most instances, functional imaging studies provide evidence to the contrary in some cases. We cannot assume that, in pathological or chronically painful conditions, information ascending through the spinothalamic tract will be processed by the same mechanisms used for acute pain; this has important clinical implications for the management of chronic pain.

The term “chronic pain” is seldom defined.