Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflex sympathetic dystrophy, posttraumatic dystrophy or complex regional pain syndrome is a particular type of chronic pain. Although the origin is unknown, some believe that wide-dynamic range neurons located in the dorsal horn of the spinal cord play an essential role. Others consider the role of psychogenic factors underestimated. Until now, controlled clinical trials mainly directed at modulation of the sympathetic system have not revealed clearly effective therapies. Tests with guanethidine, phenylephrine, phentolamine or lidocaine have essentially been negative. Use of low dose glucocorticoids, dimethylsulphoxide, biphosphonates and epidurally applied clonidine require confirmation in studies of larger size. There are indications that invasive electrical spinal cord stimulation may have some effect; randomized studies in patients with posttraumatic dystrophy are needed. So far, only application of physical therapy at an early stage has clearly shown effective pain relief and would also lead to cost reduction.
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PMID:[Treatment of posttraumatic dystrophy]. 1097 50

This article reviews the technique of thoracic (T)(2) and T(3) sympathetic ganglion block and neurolysis. Historic aspects of this technique are described. The concept of radiofrequency thermocoagulation (RFTC) of T(2) and T(3) is discussed and the technique is detailed. This procedure is useful for complex regional pain syndrome (CRPS), vascular compromise, and neuropathic pain syndromes of upper extremities. It is an alternative to stellate ganglion ablation and may be useful for patients with sympathetically maintained pain who have persistent pain after stellate ganglion procedures.
Curr Rev Pain 1999
PMID:Indications and Technique of Thoracic(2) and Thoracic(3 )Neurolysis. 1099 96

Chronic regional pain syndrome refers to a class of disorders thought to involve common neuropathic and clinical features. These disorders usually are caused by injury, and they manifest in pain and sensory changes that are disproportionate in intensity, distribution, and duration to the underlying pathology. The result of these injuries is significant impairment of motor function over time. This article is divided into two parts. Part I discusses background information such as pain, pathophysiology, diagnosis, clinical stages, and the most common treatment modality, sympathetic nerve blocks. Part II, discusses alternate treatment modalities, such as sympathectomy, physical therapy, stimulators, trigger point injections, acupuncture, tourniquet effects, placebo effects, and amputation.
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PMID:Chronic regional pain syndrome, type 1: Part I. 1100 61

The nomenclature, pathophysiology, and treatment modalities of complex regional pain syndrome (CRPS) are controversial. Thus far there are no specific, scientifically valid treatments for the management of CRPS. The numerous modalities of treatment range from sympathetic ganglion blocks, intravenous regional blocks, administration of a multitude of pharmacologic agents and behavioral interventions, to surgical sympathectomy. Minimally invasive radiofrequency lesioning for managing CRPS is a modality in its developmental stages. This article describes radiofrequency lesioning techniques in managing CRPS.
Curr Rev Pain 2000
PMID:The role of radiofrequency in the management of complex regional pain syndrome. 1106 May 89

There are reports that complex regional pain syndrome, type I (reflex sympathetic dystrophy; CRPS-I/RSD) can spread from the initial site of presentation, but there are no detailed descriptions of the pattern(s) of such spread. We describe a retrospective analysis of 27 CRPS-I/RSD patients who experienced a significant spread of pain. Three patterns of spread were identified. 'Contiguous spread (CS)' was noted in all 27 cases and was characterized by a gradual and significant enlargement of the area affected initially. 'Independent spread (IS)' was noted in 19 patients (70%) and was characterized by the appearance of CRPS-I in a location that was distant and non-contiguous with the initial site (e.g. CRPS-I/RSD appearing first in a foot, then in a hand). 'Mirror-image spread (MS)' was noted in four patients (15%) and was characterized by the appearance of symptoms on the opposite side in an area that closely matched in size and location the site of initial presentation. Only five patients (19%) suffered from CS alone; 70% also had IS, 11% also had MS, and one patient had all three kinds of spread. Our results suggest that CRPS-I/RSD spread may not be a unitary phenomenon. In some it may be due to a local spread of pathology (CS); in others it may be a consequence of a generalized susceptibility (IS). In the MS case, spread may be due to abnormal neural functioning spreading via commissural pathways. Alternatively, we discuss the possibility that all three kinds of spread may be due to aberrant CNS regulation of neurogenic inflammation.
Pain 2000 Dec 01
PMID:Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy). 1106 13

Chronic regional pain syndrome, type 1 (CRPS1) is a complex neurologic disease characterized by chronic, severe, burning pain; hyperesthesia; soft tissue swelling; dystrophy; hyperhidrosis; vasomotor and sudomotor instability; joint stiffness; and patchy osteoporosis. Five to six million people in the United States alone suffer from CRPS1. To date, CRPS1 is poorly understood and often is not recognized clinically. This syndrome requires early detection, pain control, and treatment in tandem with physical therapy to the affected area. Part I (published in September) discussed background information on CRPS1 and sympathetic nerve blocks. Part II focuses on the remaining treatment modalities (e.g., sympathectomy, physical therapy, stimulators, trigger point injections, acupuncture, tourniquet effects, placebo effects, amputation).
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PMID:Chronic regional pain syndrome, type 1: Part II. 1107 83

We describe three patients with the limb pain of complex regional pain syndrome (CRPS) in childhood with autonomic nervous system function involvement. Their autonomic nerve abnormality was non-invasively examined by means of laser doppler flowmetry (LDF) and a sympathetic skin response (SSR) test. In one it was resolved with physiotherapy, but the others needed epidural anesthesia for pain control. Though CRPS used to be recognized as a refractory disorder in adults, childhood cases have been found in recent years, generally having a better prognosis than adult ones. However, even in the children, the prognosis or responses to the same therapy vary, and there are progressive and refractory cases. CRPS should be considered as a differential diagnosis of unexplained persistent limb pain even in childhood for early and appropriate management.
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PMID:Complex regional pain syndrome in childhood: report of three cases. 1110 30

The pediatric rheumatologist cares for children who may have a wide variety of causes of musculoskeletal pain. These include such diverse conditions as arthritis, low-back pain, hypermobility, metabolic bone pain, and amplified pain syndromes such as complex regional pain syndrome and fibromyalgia. This review examines the recent literature on these and other conditions causing musculoskeletal pain in children and adolescents. Overall, headway is being made, but differentiating soma from psyche remains a problem. This is perhaps due to the marked and unique effect pain brings to each of us. Children are different from adults in causes, presentations, and outcome. Vigilance in history, physical examination, and judicious use of laboratory investigations are usually sufficient in establishing a diagnosis, as well as an appreciation for the variety of presentations each condition can manifest.
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PMID:Pain syndromes in children. 1112 80

In order to find pieces of evidence for a central origin of autonomic failure in complex regional pain syndrome I (CRPS I), the pattern of autonomic symptoms in CRPS I patients was compared to patients a few days after stroke. Autonomic failure in the latter group is assumed to represent definite CNS origin. Seventeen stroke patients, 21 patients in the acute and late stage of CRPS I and a control group of 23 healthy subjects were investigated. Detailed neurological examination was performed, sweating was induced centrally (thermoregulatory sweating, TST) and peripherally by carbachol iontophoresis (QSART) and quantified by evaporation hygrometry. Skin temperature was assessed by infrared thermography. The incidence of motor-sensory dysfunction (without pain) and the incidence of edema was strikingly similar in stroke and CRPS patients. Furthermore, stroke patients had increased TST but not QSART responses on the contralesional limb (P < 0.05) and skin temperature was decreased (P < 0.001). The same pattern of autonomic failure was found in late CRPS (TST: P < 0.02, skin temperature: P < 0.01) whereas in acute CRPS additional, presumably peripheral mechanisms, contribute to sympathetic symptoms. In conclusion, our investigation suggests that many clinical symptoms and the main features of sympathetic dysfunction in CRPS could be explained by a CNS pathophysiology.
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PMID:Autonomic failure after stroke--is it indicative for pathophysiology of complex regional pain syndrome? 1115 85

Human TRKA (NTRK1) encodes the receptor tyrosine kinases (RTKs) for nerve growth factor (NGF) and is the gene responsible for congenital insensitivity to pain with anhidrosis (CIPA), an autosomal recessive disorder characterized by a lack of pain sensation and anhidrosis. We reported 11 putative missense mutations in 31 CIPA families from various ethnic groups. Here we have introduced the corresponding mutations into the TRKA cDNA and examined NGF-stimulated autophosphorylation. We find that wild-type TRKA precursor proteins in a neuronal and a non-neuronal cell line were differentially processed and phosphorylated in an NGF-dependent and -independent manner, respectively. Two mutants (L93P and L213P) in the extracellular domain were aberrantly processed and showed diminished autophosphorylation in neuronal cells. Five mutants (G516R, G571R, R643W, R648C and G708S) in the tyrosine kinase domain were processed as wild-type TRKA but showed significantly diminished autophosphorylation in both neuronal and non-neuronal cells. In contrast, R85S and (H598Y; G607V), detected previously as double and triple mutations, are probably polymorphisms in a particular ethnic background. The other putative mutant D668Y might be a rare polymorphism or might impair the function of TRKA without compromising autophosphorylation. Mutated residues in the tyrosine kinase domain are conserved in various RTKs and probably contribute to critical function of these proteins. Thus, naturally occurring TRKA missense mutations with loss of function provide considerable insight into the structure-function relationship in the RTK family. Our data may aid in developing a drug which targets the clinically devastating 'complex regional pain syndrome'.
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PMID:Congenital insensitivity to pain with anhidrosis (CIPA): effect of TRKA (NTRK1) missense mutations on autophosphorylation of the receptor tyrosine kinase for nerve growth factor. 1115 35


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