Complex regional pain syndrome type I (RSD)

Abstract

In chronic RSD, efferent nerve fibers were histologically unaffected; from afferent fibers, only C-fibers showed histopathologic abnormalities. Skeletal muscle showed a variety of histopathologic findings, which are similar to the histologic abnormalities found in muscles of patients with diabetes.

Role of NFκB in an Animal Model of Complex Regional Pain Syndrome–type I (CRPS-I)

“…A major issue of concern is that human CRPS is most commonly preceded by a fracture or sprain and not by an evident ischemic injury. However, ischemia is actually relevant in at least part of the cases of human CRPS, as is demonstrated by findings consistent with oxidative stress in CRPS-affected limbs, 29,53 and by the beneficial effect of treatment with free radical scavengers. 43 Like IR injury, fracture or sprain can cause an acute inflammatory response, which may induce sensitization leading to allodynia and microvascular changes that may result in prolonged ischemia.…”

“…Some of these rely on direct nerve injury and are therefore more representative for CRPS type II and not for CRPS type I. 28,30 Animal models that claim to mimic CRPS-I involve tibia fracture and casting, 19 local infusion of a free radical donor, 53 interarterial infusion of SP, 18 and IR injury (CPIP model). 14 The IR injury or CPIP model that was used in the present study resembles human CRPS-I in several aspects.…”

“…54 A previously described automated analysis of literature has revealed that the transcription factor nuclear factor kappa B (NFkB) is involved in all these disease mechanisms. 21 For example, affected limbs of human CRPS patients show signs of chronic ischemia, 29,53 which can induce NFkB activation, mediated by the formation of reactive oxygen species (ROS) and peroxinitrite. 16,20 Inflammatory mediators, including tumor necrosis factor alpha (TNFa), interleukin-1 (IL-1), and IL-6 have been demonstrated in blister 23 and spinal cord fluid1 of CRPS patients, and can activate or are activated themselves by NFkB.…”

Complex Regional Pain Syndrome: What's in a Name?

“…Thus, muscle tissue from an amputated CRPS limb was found to exhibit lipofuscin pigment, atrophic fibers, and severely thickened basal membrane layers of the capillaries. 90 Although amputated tissue may represent extreme cases of CRPS, this conclusion is also supported by functional observations of increased density of perfused vessels, lower capillary filtration capacity, arteriovenous shunting, and ischemia of peripheral subcutaneous tissue in intact CRPS limbs. 57,78 It has also been reported that CRPS limbs have high arterial flow, but low oxygen consumption, as well as high lactate flux-indicative of tissue ischemia, despite increased flow in large vessels.…”

“…Importantly, arterial venous shunting and collapsed capillaries have been observed in the limbs of patients with CRPS. 57,90 Furthermore, IR injuries initially produce enhanced vascular permeability that contributes to the damage causing vasospasms, but as vasospasms progress to no-reflow, plasma extravasation is diminished, as there is reduced blood flow within the microvasculature. 59 This shift from initial high plasma extravasation to later capillary no-reflow, could explain why many CRPS patients start out with significant edema, but then progress to a state with less edema and more ischemia.…”