Introduction

Neuropathic pain occurs frequently in patients with cancer, both from direct tumor infiltration of neural structures and as a consequence of treatment of the neoplasm. Management of neuropathic pain presents a number of challenges. Such pain is often more resistant to conventional analgesic approaches than is nociceptive pain. Many of these patients will have mixed pain problems, where neuropathic pain is combined with elements of somatic or visceral nociceptive pain. Neuropathic pain also may signal progressive and often incurable disease, adding a significant suffering component to the pain problem.

Successful management of neuropathic cancer pain requires an understanding of the pathophysiologic processes that generate this type of pain and of the distinctive clinical features that identify it. In addition, a knowledge of the various clinical neuropathic pain syndromes that occur in the cancer patient and of the range of available treatments is essential.

Pathophysiology

Neuropathic pain occurs as a result of aberrant somatosensory processing in the nervous system, and as such may be sustained by peripheral mechanisms, central mechanisms, or both. Pain after peripheral nerve injury may occur through a variety of mechanisms. When a nerve is compressed or distended, nerve trunk pain may occur as a result of activation of the nervi nervorum, the normal nociceptive afferents that innervate the nerve sheaths themselves (1). Damage to primary nociceptive afferents may result in spontaneous ectopic activity, perhaps secondary to focal demyelination with exposure of sodium channels (2). Regenerating afferents may form neuromas, where sodium channels accumulate and spontaneous activity occurs (3). The dorsal root ganglion may represent an additional site of ectopic activity (3).