Complex Regional Pain Syndrome of the Upper and Lower Extremity

Author(s):  
Agnes Stogicza ◽  
Bartha Peter Tohotom ◽  
Edit Racz ◽  
Andrea Trescot ◽  
Alan Berkman

Complex regional pain syndrome (CRPS) is a chronic debilitating pain condition of the extremities; it can affect, less commonly, other areas of the body (face, pelvis, abdomen). Its early presentation—pain disproportionate to the injury, skin temperature changes, hyperalgesia, allodynia—is often not recognized, delaying treatment. In later phases, with sympathetic nervous system involvement, it presents with skin and muscle atrophy, hair loss, allodynia, loss of function, and decreased range of motion. In severe cases, it can spread from one area to the other. Imaging findings (X-ray, MRI, bone scintigraphy) are nonspecific. They are used to support the diagnosis, and to exclude conditions that can present similarly. Treatment is challenging and includes physical therapy, psychologic support, medication management, and minimally invasive interventions to decrease pain, to positively influence the sympathetic nervous system, and to preserve function. A multidisciplinary approach is likely to be the most beneficial.

2004 ◽  
Vol 9 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Robert W Teasell ◽  
J Malcolm O Arnold

The pathophysiology of the pain associated with complex regional pain syndrome, spinal cord injury and diabetic peripheral neuropathy is not known. The pain of complex regional pain syndrome has often been attributed to abnormal sympathetic nervous system activity based on the presence of vasomotor instability and a frequently reported positive response, albeit a temporary response, to sympathetic blockade. In contrast, the pain below the level of spinal cord injury and diabetic peripheral neuropathy are generally seen as deafferentation phenomena. Each of these pain states has been associated with abnormal sympathetic nervous system function and increased peripheral alpha-1 adrenoceptor activity. This increased responsiveness may be a consequence of alpha-1 adrenoceptor postsynaptic hypersensitivity, or alpha-2 adrenoceptor presynaptic dysfunction with diminished noradrenaline reuptake, increased concentrations of noradrenaline in the synaptic cleft and increased stimulation of otherwise normal alpha-1 adrenoceptors. Plausible mechanisms based on animal research by which alpha-1 adrenoceptor hyperresponsiveness can lead to chronic neuropathic-like pain have been reported. This raises the intriguing possibility that sympathetic nervous system dysfunction may be an important factor in the generation of pain in many neuropathic pain states. Although results to date have been mixed, there may be a greater role for new drugs which target peripheral alpha-2 adrenoceptors (agonists) or alpha-1 adrenoceptors (antagonists).


2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Alessandra Castaldi ◽  
Tania Zaglia ◽  
Vittoria Di Mauro ◽  
Pierluigi Carullo ◽  
Giacomo Viggiani ◽  
...  

Rationale: The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, over-activation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors (βARs) in cardiomyocytes (CMs) and lead to increased heart rate and cardiac contractility. However, chronic stimulation of βARs leads to impaired cardiac function and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MiR-133 is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of mRNA translation/stability. Objective: To determine whether miR-133 affects βAR signaling during progression to heart failure. Methods and Results: Based on bioinformatic analysis, β1AR and other components of the β1AR signal transduction cascade, including adenylate cyclase VI and the catalytic subunit of the cAMP-dependent protein kinase A (PKA), were predicted as direct targets of miR-133 and subsequently validated by experimental studies. Consistently, cAMP accumulation and activation of downstream targets were repressed by miR-133 overexpression in both neonatal and adult CMs following selective β1AR stimulation. Furthermore, gain- and loss-of-function studies of miR-133 revealed its role in counteracting the deleterious apoptotic effects caused by chronic β1AR stimulation. This was confirmed in vivo using a novel cardiacspecific TetON-miR-133 inducible transgenic mouse model (Tg133). When subjected to transaortic constriction, Tg133 mice maintained cardiac performance and showed attenuated apoptosis and reduced fibrosis compared to control mice. Conclusions: MiR-133 controls multiple components of the β1AR transduction cascade and is cardioprotective during heart failure.


Cephalalgia ◽  
2003 ◽  
Vol 23 (1_suppl) ◽  
pp. 43-48 ◽  
Author(s):  
W Jänig

Involvement of the (efferent) autonomic nervous system in the generation of pain is ongoing matter of debate. Based on clinical and experimental observations, there are good arguments that the sympathetic nervous system may be involved in pain following trauma, with and without nerve lesion, at an extremity, such as in complex regional pain syndrome type I and II. However, the mechanisms involved are in many cases still unclear. In various types of headache there is no convicing evidence that the sympathetic nervous system is involved in the generation of pain, although these pains may be accompanied by considerable autonomic reactions which are dependent on activity in sympatheitc neurons. Migraine and headaches with autonomic symptoms are accompanied by autonomic reactions which are dependent on activity in cranial parasympathetic neurons. Whether parasympathetic neurons innervating cranial blood vessels are involved in activation or sensitization of trigemino-vascular afferents is discussed and needs experimental verification.


The Distribution of the Chromaffine System in the Annelid Kingdom . The possession of a chromaffine system, consisting of cells which take a yellow stain with chrome salts, is a common property of almost all the members of the vertebrate kingdom. The presence of this reaction is coincident with, and probably dependent upon, the secretion by these cells of the substance adrenalin. The investigations of Lewandowski (30), Langley (29), Elliott (11), and others have established that the physiological actions of this latter substance are the same as those which result from the stimulation of the sympathetic nervous system. The latest researches of Elliott (12), Von Anrep (43) and others, have shown in addition that the adjuvant action of adrenalin is essential for the efficient performance of the functions of the sympathetic nervous system. This is supported by pathological considerations, for it has long been recognised that many of the symptoms of Addison’s disease, in which the chief lesion is the destruction of the medullary chromaffine tissue of the suprarenal glands, are those of failure of the sympathetic nervous system. From a physiological standpoint, it is, therefore, necessary that the two systems should co-exist, and a close morphological relationship between them is rendered probable. The researches of Kohn (26) on the embryological origin of the chromaffine system in the mammalia have established that the ganglion cells of the sympathetic system and the cells of the chromaffine system, which are in the embryo widely distributed through the body, arise from a common group of mother cells; Kohn therefore names the chromaffine system the Paraganglion system. These researches are in agreement with the original statement of Balfour (2) that the paired suprarenal bodies of Elasmobranchs, which consist of chromaffine cells, are developed in the sympathetic ganglion masses; Kohn has also made similar investigations in these fishes and confirmed the observations of Balfour.


1997 ◽  
Vol 87 (10) ◽  
pp. 473-477 ◽  
Author(s):  
CK Harvey

The author has developed a technique of dilute anesthetic ankle block that appears, on the basis of these preliminary observations, to relieve pathologic pain that may be maintained by the sympathetic nervous system. Symptomatic relief following the use of this injection confirms that the patient's problem is not somatic and that further evaluation and treatment of sympathetically maintained pain syndrome may be indicated.


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