Neuropathic pain is pain following a disease or injury to the nervous system, and can be categorized by the location of the causative injury. Chronic pain following injury of the peripheral nervous system, distal to the oligodendroglial cell – Schwann cell junction, can be termed deafferentation pain or peripheral neuropathic pain. Chronic pain “associated with lesions of the CNS” is termed central pain syndrome (Merskey, 1986; Bonica, 1991). There are many situations in which there is injury of both the peripheral and central nervous system, particularly with injuries of the conus medullaris. In this chapter we will consider primate neuropathic pain states, beginning with peripheral neuropathic or deafferentation syndromes, and concluding with central pain syndromes.

In general terms, both central and peripheral chronic pain syndromes have similar characteristics. These include evidence of sensory loss, ongoing pain and pain evoked by stimuli that are not normally painful (allodynia or hyperalgesia). The sensory loss and hypersensitivity are demonstrated by quantitative sensory testing (QST). In addition, a number of primate models have been developed which mimic the sensory abnormalities in patients with neuropathic pain.

Clinical characteristics of peripheral neuropathic pain

The cause of most neuropathies is based on the medical history, supported by laboratory investigations (Casey et al., 1996b). Diabetes is the most common cause of painful neuropathy. Generally, a progressive course suggests an inherited, metabolic or recurrent toxic etiology.