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Vascular Symptoms (vascular + symptom)

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Medical Sciences100%

Selected Abstracts

Vibration exposure and disease in a shipyard: A 13-year revisit

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 6 2004
Martin Cherniack MD
Abstract Background In a 1988 study of shipyard workers, a progressive association was observed between cumulative exposure to vibration and the vascular and neurological symptoms of the hand-arm vibration syndrome (HAVS). In 2001, after a decade of exposure reduction and ageing of the workforce, a second study at the same site was initiated. Methods In 2001, 214 subjects were selected; they represented four current weekly vibration exposure time intervals,0 hr, >0,<,5 hr, ,5,<,20 hr, ,20 hr. The 1988 and 2000 cross-sectional populations were compared on the basis of exposure duration and current symptoms. Results In 2001, the study population was 9.6 years older than the 1988 group. Current weekly exposure hours were similar in the low and medium exposure groups 2001 and 1988, but exposure was reduced by an average of 9.7 hr per week in the highest exposure group (,20 hr) in 2001. Symptom severity was regressed polychotomously on estimated exposure (log cumulative hours); the OR was weaker in 2001 than in 1988 for sensorineural symptoms,1.44 [CI 1.04,1.98] versus 2.35 [CI 1.48,3.73]. This was also true for vascular symptoms,1.70 [CI 1.06,2.71] versus 3.99 [CI 2.27,7.01]. Vascular symptoms were more prevalent in the highest lifetime vibration exposure group in 1988 (68.7 vs. 43.2% in 2001); sensorineural symptoms were more prevalent in the least vibration exposed group in 2001 (52.6 vs. 20.7% in 1988). Conclusions The prevalence of vascular symptoms associated with cumulative vibratory exposure was significantly greater in 1988, but neurological symptoms were more common at lower exposure levels in 2001. The presumption that reducing exposure duration alone is sufficient, in the absence of change in vibration magnitude, is not supported by the results of this study. Am. J. Ind. Med. 45:500,512, 2004. © 2004 Wiley-Liss, Inc. [source]

What Does the Mechanism of Spinal Cord Stimulation Tell Us about Complex Regional Pain Syndrome?

PAIN MEDICINE, Issue 8 2010
Joshua P. Prager MD
Abstract Spinal cord stimulation (SCS) can have dramatic effects on painful, vascular, and motor symptoms of complex regional pain syndrome (CRPS), but its precise mechanism of action is unclear. Better understanding of the physiologic effects of SCS may improve understanding not only of this treatment modality but also of CRPS pathophysiology. Effects of SCS on pain perception are likely to occur through activation of inhibitory GABA-ergic and cholinergic spinal interneurons. Increased release of both neurotransmitters has been demonstrated following SCS in animal models of neuropathic pain, with accompanying reductions in pain behaviors. Effects of SCS on vascular symptoms of CRPS are thought to occur through two main mechanisms: antidromic activation of spinal afferent neurons and inhibition of sympathetic efferents. Cutaneous vasodilation following SCS in animal models has been shown to involve antidromic release of calcitonin gene-related peptide and possibly nitric oxide, from small-diameter sensory neurons expressing the transient receptor potential V1 (TRPV1) receptor. The involvement of sympathetic efferents in the effects of SCS has not been studied in animal models of neuropathic pain, but has been demonstrated in models of angina pectoris. In conclusion, SCS is of clinical benefit in CRPS, and although its mechanism of action merits further elucidation, what little we do know is informative and can partially explain some of the pathophysiology of CRPS. [source]

Vibration exposure and disease in a shipyard: A 13-year revisit

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 6 2004
Martin Cherniack MD
Abstract Background In a 1988 study of shipyard workers, a progressive association was observed between cumulative exposure to vibration and the vascular and neurological symptoms of the hand-arm vibration syndrome (HAVS). In 2001, after a decade of exposure reduction and ageing of the workforce, a second study at the same site was initiated. Methods In 2001, 214 subjects were selected; they represented four current weekly vibration exposure time intervals,0 hr, >0,<,5 hr, ,5,<,20 hr, ,20 hr. The 1988 and 2000 cross-sectional populations were compared on the basis of exposure duration and current symptoms. Results In 2001, the study population was 9.6 years older than the 1988 group. Current weekly exposure hours were similar in the low and medium exposure groups 2001 and 1988, but exposure was reduced by an average of 9.7 hr per week in the highest exposure group (,20 hr) in 2001. Symptom severity was regressed polychotomously on estimated exposure (log cumulative hours); the OR was weaker in 2001 than in 1988 for sensorineural symptoms,1.44 [CI 1.04,1.98] versus 2.35 [CI 1.48,3.73]. This was also true for vascular symptoms,1.70 [CI 1.06,2.71] versus 3.99 [CI 2.27,7.01]. Vascular symptoms were more prevalent in the highest lifetime vibration exposure group in 1988 (68.7 vs. 43.2% in 2001); sensorineural symptoms were more prevalent in the least vibration exposed group in 2001 (52.6 vs. 20.7% in 1988). Conclusions The prevalence of vascular symptoms associated with cumulative vibratory exposure was significantly greater in 1988, but neurological symptoms were more common at lower exposure levels in 2001. The presumption that reducing exposure duration alone is sufficient, in the absence of change in vibration magnitude, is not supported by the results of this study. Am. J. Ind. Med. 45:500,512, 2004. © 2004 Wiley-Liss, Inc. [source]

Increase in circulating endothelial precursors by atorvastatin in patients with systemic sclerosis

ARTHRITIS & RHEUMATISM, Issue 6 2006
Masataka Kuwana
Objective To evaluate whether atorvastatin can increase bone marrow,derived circulating endothelial precursors (CEPs) and improve the vascular symptoms in patients with systemic sclerosis (SSc; scleroderma). Methods The study was designed as an open-label, prospective study involving 14 patients with SSc who received 10 mg/day of atorvastatin for 12 weeks and were followed up for the subsequent 4 weeks. CEPs were quantified at weeks 0 (pretreatment), 4, 8, 12 (during treatment), and 16 (posttreatment) by cell sorting followed by 3-color flow cytometry. Raynaud's phenomenon variables, global measures, and psychological scales as well as circulating angiogenic factors and endothelial activation/injury markers were serially assessed. The potential of CEPs to differentiate into mature endothelial cells was examined in cultures with angiogenic stimuli. Results None of the patients experienced an adverse event, but 1 dropped out because of an excessive decrease in serum total cholesterol. Atorvastatin treatment resulted in a 1.7- to 8.0-fold increase in CEPs from baseline levels (P < 0.0001), but the numbers returned to within baseline levels at posttreatment. However, 8 patients (62%) experienced a gradual decrease in the number of CEPs, even while taking atorvastatin. Variables indicating the extent of Raynaud's phenomenon improved significantly, and up-regulated levels of angiogenic factors and vascular endothelial activation/injury markers decreased significantly during atorvastatin treatment. These variables returned to within baseline levels after discontinuation of the drug. In contrast, atorvastatin failed to improve the in vitro maturation potential of CEPs. Conclusion The results of this pilot study suggest that atorvastatin treatment can increase CEPs and may be effective in improving Raynaud's phenomenon, even in SSc patients who have CEP dysfunction intrinsically. [source]