Complex Regional Pain Syndrome Research Update 12/12 | Part 1

Here are some recent papers looking at CRPS.

J Neuroimmune Pharmacol. 2012 Nov 29.

Inflaming the Brain: CRPS a Model Disease to Understand Neuroimmune Interactions in Chronic Pain.

Linnman C, Becerra L, Borsook D.


We review current concepts in CRPS from a neuroimaging perspective and point out topics and potential mechanisms that are suitable to be investigated in the next step towards understanding the pathophysiology of CRPS. We have outlined functional aspects of the syndrome, from initiating lesion via inflammatory mechanisms to CNS change and associated sickness behavior, with current evidence for up-regulation of immunological factors in CRPS, neuroimaging of systemic inflammation, and neuroimaging findings in CRPS. The initiation, maintenances and CNS targets implicated in CRPS and in the neuro-inflammatory reflex are discussed in terms of CRPS symptoms and recent preclinical studies. Potential avenues for investigating CRPS with PET and fMRI are described, along with roles of inflammation, treatment and behavior in CRPS. It is our hope that this outline will provoke discussion and promote further empirical studies on the interactions between central and peripheral inflammatory pathways manifest in CRPS. Link here


A possible role of the locus coeruleus in complex regional pain syndrome

Peter D. Drummond


Heightened sensitivity to painful stimulation commonly spreads from the affected limb to the ipsilateral forehead in patients with complex regional pain syndrome (CRPS). In addition, acoustic startle evokes greater auditory discomfort and increases in limb pain when presented on the affected than unaffected side. In contrast, limb pain ordinarily evokes analgesia in the ipsilateral forehead of healthy participants, and acoustic startle suppresses limb pain. Together, these findings suggest that hemilateral and generalized pain control mechanisms are disrupted in CRPS, and that multisensory integrative processes are compromised. Failure to inhibit nociceptive input from the CRPS-affected limb could sensitize spinal and supraspinal neurons that receive convergent nociceptive and auditory information from hemilateral body sites. Somatosensory, auditory, and emotional inputs may then aggravate pain by feeding into this sensitized nociceptive network. In particular, a disturbance in hemilateral pain processing that involves the locus coeruleus could exacerbate the symptoms of CRPS in some patients.

Full article here


Curr Pharm Des. 2012;18(29):4546-9.

Immunological aspects of the complex regional pain syndrome (CRPS).

Krämer HH.


Limb trauma can lead to the development of a complex regional pain syndrome (CRPS). CRPS is a descriptive term of a variety of different symptoms. According to the current IASP-approved criteria, human CRPS can be diagnosed if a combination of signs is present: continuing pain and hyperalgesia, disproportionate to the initial trauma, skin temperature and colour asymmetry, sweating asymmetry, edema, decreased range of motion, and trophic changes. The diagnosis and treatment of human CRPS can be demanding and the pathophysiology underlying the disease is still under investigation. Immunological aspects are considered to play an important role in the development of CRPS. The impact of elevated pro-inflammatory cytokines systemically as well as locally, increased neurogenic inflammation and auto-antibodies in the pathophysiological development of CRPS are discussed in this review

Link here


Can J Anaesth. 2012 Sep;59(9):875-81. doi: 10.1007/s12630-012-9748-y. Epub 2012 Jul 14.

Update on the pathogenesis of complex regional pain syndrome: role of oxidative stress.

Taha R, Blaise GA.



Complex regional pain syndrome (CRPS) is a chronic inflammatory pain syndrome that affects one or more extremities of the body. It is characterized by burning pain and abnormalities in the sensory, motor, and autonomic nervous systems. This review illustrates how oxidative stress and nuclear factor erythroid 2-related factor (Nrf2) activation might contribute to understanding the etiopathogenesis of CRPS.


The precise cause of CRPS remains unclear, and current treatments are not effective in many patients. The mechanism underlying CRPS may differ across patients and even within a single patient over time. Inflammatory and neuronal mechanisms have been suggested as key contributors to CRPS. Recent evidence demonstrates that oxidative stress is associated with clinical symptoms in patients with CRPS-I. Oxidative stress plays a key role in CRPS pathogenesis. The Nrf2 factor is a master regulator of the transcription of multiple antioxidants, which protects against oxidative stress and inflammation by inducing antioxidant and detoxifying genes through binding with an antioxidant response element. It has antinociceptive effects against inflammatory pain in an animal model.


This review summarises the effect of oxidative stress and mitochondrial dysfunction in the pathogenesis of CRPS. It also addresses the question of whether there is a potential role for Nrf2 (activated by pharmacological or nutritional activators) in alleviating the clinical features of CRPS or preventing its progression

Link here



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