TY - JOUR
T1 - Nerve pathophysiology and mechanisms of pain in causalgia
AU - Devor, Marshall
PY - 1983
Y1 - 1983
N2 - In contrast to sensory endings in skin, muscle, etc., afferents in the mid-course of intact nerves are normally incapable of generating impulses upon slow or prolonged depolarization. However, after various types of nerve injury, including complete nerve section and local demyelination, an ectopic pacemaker capability develops. One peculiarity of such abnormally differentiated sites is chemosensitivity to α-adrenergic agonists and to sympathetic efferent discharge. Such ectopic chemosensitivity may well be involved in the etiology of paraesthesias and pain in reflex sympathetic dystrophies including causalgia. Specifically, it is proposed that the fundamental cause of these conditions is the development of abnormal electrogenic membrane properties in the region of demyelination and sprout outgrowth. These abnormal properties presumably include the appearance of excess inward current conductances and ectopic α-adrenergic receptors. Catecholamines released from sympathetic efferents in the area of injury locally depolarize damaged sensory fibers, and because of the abnormal electrogenic properties of these fibers, an abnormal afferent discharge is generated.
AB - In contrast to sensory endings in skin, muscle, etc., afferents in the mid-course of intact nerves are normally incapable of generating impulses upon slow or prolonged depolarization. However, after various types of nerve injury, including complete nerve section and local demyelination, an ectopic pacemaker capability develops. One peculiarity of such abnormally differentiated sites is chemosensitivity to α-adrenergic agonists and to sympathetic efferent discharge. Such ectopic chemosensitivity may well be involved in the etiology of paraesthesias and pain in reflex sympathetic dystrophies including causalgia. Specifically, it is proposed that the fundamental cause of these conditions is the development of abnormal electrogenic membrane properties in the region of demyelination and sprout outgrowth. These abnormal properties presumably include the appearance of excess inward current conductances and ectopic α-adrenergic receptors. Catecholamines released from sympathetic efferents in the area of injury locally depolarize damaged sensory fibers, and because of the abnormal electrogenic properties of these fibers, an abnormal afferent discharge is generated.
KW - causalgia
KW - nerve damage
KW - neuroma
KW - pain
KW - pathophysiology
UR - http://www.scopus.com/inward/record.url?scp=0020531852&partnerID=8YFLogxK
U2 - 10.1016/0165-1838(83)90090-5
DO - 10.1016/0165-1838(83)90090-5
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C2 - 6192166
AN - SCOPUS:0020531852
SN - 0165-1838
VL - 7
SP - 371
EP - 384
JO - Journal of the Autonomic Nervous System
JF - Journal of the Autonomic Nervous System
IS - 3-4
ER -