Assessment of peripheral sympathetic nervous function for diagnosing early post-traumatic complex regional pain syndrome type I

Schürmann, Martin; Gradl, Georg; Andreß, H.-J.; Fürst, H.; Schildberg, F. W.

doi:10.1016/s0304-3959(98)00198-5

Cited by 109 publications

(75 citation statements)

References 47 publications

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“…CRPS patients also have increased vasoconstrictive responses to NE (Arnold et al, 1993;Birklein et al, 1997;Teasell & Arnold, 2004). Although early in the disease CRPS patients have reduced sympathetic function (Birklein et al, 1998;Wasner et al, 1999;Schurmann et al, 1999;, later in the disease CRPS patients have greater decreases in blood flow in response to sympathetic stimulation (Drummond et al, 2001;Wasner et al, 2001;Baron et al, 2002;Ackerman et al, 2005), and exhibit denervation supersensitivity of vasoconstrictive adrenoceptors (Kurvers et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Xanthos

Bennett

Coderre

2008

Pain

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Painful hypersensitivity to norepinephrine (NE) has been reported in various chronic pain conditions that exhibit sympathetically-maintained pain (SMP), particularly CRPS-I and II. We investigated the parallels between the nociceptive and vascular sensitivity to NE in rats with chronic post-ischemia pain (CPIP), an animal model of CRPS-I induced by hind paw ischemiareperfusion injury. Intradermal injections of NE to the affected hind paw induced dose-dependent nociceptive behaviours in CPIP rats, but not sham animals. These behaviours were blocked by α 1 -and α 2 -adrenergic receptor antagonists, or a nitric oxide (NO) donor. Using laser Doppler flowmetry, we detected vasoconstrictor hypersensitivity in the ipsilateral CPIP hind paw, as compared to responses in sham animals or the contralateral hind paw. The vasoconstrictor hypersensitivity was also attenuated by adrenergic antagonists. Intradermal injection of [Arg 8 ] vasopressin (AVP) or the endothelial NO synthase (eNOS) inhibitor, L-NIO, to the affected paw also induced nociceptive behaviours in CPIP rats, but not sham rats. These results suggest CPIP rats display abnormal nociceptive responses to adrenergic and non-adrenergic vasoconstrictive agents. Furthermore, the nociceptive responses to NE in CPIP rats are paralleled by enhanced vasoconstrictive responses to NE, and are relieved by α-adrenergic antagonists or a vasodilator. We conclude that persistent tissue ischemia and hypersensitivity to sympathetic vasoconstriction are important mechanisms for pain in CPIP rats, and that either reducing vasoconstriction or enhancing vasodilatation may be effective methods of relieving the pain of CRPS-I.

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Section: Discussionmentioning

confidence: 99%

Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Xanthos

Bennett

Coderre

2008

Pain

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show abstract

“…Impaired autonomic responses in both the affected and unaffected limbs have been found in CRPS (Schürmann et al 1999;Schürmann et al2000), with recovery of vasomotor function on resolution of the CRPS (Gradl & Schürmann, 2005;Wasner et al1999). However, the pattern of autonomic dysfunction in CRPS varies over time (Ide et al 1997;Wasner et al 1999) and its contribution to pain is unclear .…”

Section: Autonomic Disturbancesmentioning

confidence: 99%

Imaging and Clinical Evidence of Sensorimotor Problems in CRPS: Utilizing Novel Treatment Approaches

Bailey

Nelson

Lewis

et al. 2012

J Neuroimmune Pharmacol

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“…The complex cascade of CRPS is postulated to initiate after the sensitization of C-nociceptive fibers and release of neuropeptides, which are linked to vasodilatation and hypersensitization of nerve endings (Guo et al, 2004;Kurvers, 1998;Schurmann et al, 1999). Osteoclasts are also activated and this in turn leads to nociceptor stimulation and sensitization (Mach et al, 2002;Sevcik et al, 2004) leading to a vicious cycle.…”

Section: Pathomechanismmentioning

confidence: 99%

“…Other studies have shown that the immune and skeletal systems are closely related to maintain the homeostasis of the bone but when this www.intechopen.com interaction is disrupted in CRPS; the balance favors bone loss. This complex cascade is postulated to initiate after sensitization of C-nociceptive fibers and release of neuropeptides, which are linked to vasodilatation, hypersensitization of nerve endings (Guo et al, 2004;Kurvers et al, 1995;Schurmann et al, 1999), and osteoclasts activation, which increase bone resorption, lead to nociceptor stimulation and sensitization (Mach et al, 2002;Sevcik et al, 2004).…”

Section: Pathomechanismmentioning

confidence: 99%

Patchy Osteoporosis in Complex Regional Pain Syndrome

Park¹,

Im²,

Lim³

2012

Osteoporosis

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Assessment of peripheral sympathetic nervous function for diagnosing early post-traumatic complex regional pain syndrome type I

Cited by 109 publications

References 47 publications

Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Imaging and Clinical Evidence of Sensorimotor Problems in CRPS: Utilizing Novel Treatment Approaches

Patchy Osteoporosis in Complex Regional Pain Syndrome

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