PERIPHERAL AND CENTRAL HYPEREXCITABILITY: DIFFERENTIAL SIGNS AND SYMPTOMS IN PERSISTENT PAIN |
|||||||||||||
|
Coderre, Terence J. and Katz, Joel (1997) PERIPHERAL AND CENTRAL HYPEREXCITABILITY: DIFFERENTIAL SIGNS AND SYMPTOMS IN PERSISTENT PAIN.
Short Abstract:In the present paper we will examine the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain. We will examine this evidence in four key areas of pain research: cutaneous hyperalgesia, referred pain, neuropathic pain and post-operative pain. In each of these cases there is a suggestion that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. We propose that in each case it is instructive to think of central sensitization of being comprised of both an initial central sensitization and an ongoing central sensitization that is driven by inputs from peripheral sources. We will develop an hypothesis whereby each of these factors, initial sensitization, ongoing central sensitization and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons, and thus influences the expression of persistent pain or hyperalgesia. We propose that since each of these factors, peripheral inputs and central sensitization (initial or ongoing) can contribute to both the initiation and maintenance of persistent pain, that therapies should be designed that target both peripheral and central sources of pathology. Long Abstract:In the present paper we will examine the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain. We will examine this evidence in four key areas of pain research: cutaneous hyperalgesia, referred pain, neuropathic pain and post-operative pain. In each of these cases there is a suggestion that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. We propose that in each case it is instructive to think of central sensitization of being comprised of both an initial central sensitization and an ongoing central sensitization that is driven by inputs from peripheral sources. We will develop an hypothesis whereby each of these factors, initial sensitization, ongoing central sensitization and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons, and thus influences the expression of persistent pain or hyperalgesia. We propose that since each of these factors, peripheral inputs and central sensitization (initial or ongoing) can contribute to both the initiation and maintenance of persistent pain, that therapies should be designed that target both peripheral and central sources of pathology.
Contact site administrator at: support@bbsonline.org |
||||||||||||