Examinando por Materia "Autonomic nervous system"

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  • Publicación
    Acceso abierto
    Fisiopatología y tratamiento del dolor de miembro fantasma
    (2013-12-12) Malavera Angarita, Mayra Alejandra; Carrillo Villa, Sandra; Gomezese Ribero, Omar Fernando; García, Ronald G.; Silva Sieger, Federico Arturo
    Introduction: Phantom limb pain may be present in up to 80% of patients subjected to amputation because oftrauma or peripheral vascular disease. Severalfactors have been associated with its occurrence, including pre-amputation pain, the etiology, and the amputation level. Objective: To review the current status of the pathophysiological mechanisms, treatment options and their efficacy for the management of phantom limb pain. Method: Non-systematic review ofthe literature in PubMed and Cochrane, of articles describing the pathophysiology and treatment of phantom limb pain. Results and conclusions: The proposed pathophysiological mechanisms are still in research and include peripheral, central and psychologicalfactors. Treatment options are still limited, and less than 10% of patients report long-term improvement.
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    Relationship between cardiac vagal activity and mood congruent memory bias in major depression
    (2016-01) García, Ronald G.; Valenza, Gaetano; Tomaz, Carlos A.; Barbieri, Riccardo
    Background Previous studies suggest that autonomic reactivity during encoding of emotional information could modulate the neural processes mediating mood-congruent memory. In this study, we use a point-process model to determine dynamic autonomic tone in response to negative emotions and its influence on long-term memory of major depressed subjects. Methods Forty-eight patients with major depression and 48 healthy controls were randomly assigned to either neutral or emotionally arousing audiovisual stimuli. An adaptive point-process algorithm was applied to compute instantaneous estimates of the spectral components of heart rate variability [Low frequency (LF), 0.04–0.15 Hz; High frequency (HF), 0.15–0.4 Hz]. Three days later subjects were submitted to a recall test. Results A significant increase in HF power was observed in depressed subjects in response to the emotionally arousing stimulus (p=0.03). The results of a multivariate analysis revealed that the HF power during the emotional segment of the stimulus was independently associated with the score of the recall test in depressed subjects, after adjusting for age, gender and educational level (Coef. 0.003, 95%CI, 0.0009–0.005, p=0.008). Limitations These results could only be interpreted as responses to elicitation of specific negative emotions, the relationship between HF changes and encoding/recall of positive stimuli should be further examined. Conclusions Alterations on parasympathetic response to emotion are involved in the mood-congruent cognitive bias observed in major depression. These findings are clinically relevant because it could constitute the mechanism by which depressed patients maintain maladaptive patterns of negative information processing that trigger and sustain depressed mood.
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    Acceso abierto
    Role of the autonomic nervous system in the endothelial dysfunction of the metabolic syndrome
    (2011) Lopez-Jaramillo, Patricio; Molina, Dora I.; Aguillon, Alba; Gómez Arbeláez, Diego; Sotomayor Rubio, Aristides; López López, Jose
    In the last decade there has been an accelerated growth in the prevalence of metabolic syndrome (MS), especially in Latin American countries, which has led an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (DM2). Recently has been raised the relationship between the autonomic nervous system (ANS), endothelial dysfunction (ED) and the appearance of MS. In the present article we review the evidence that support the proposal that abdominal obesity (AO) produce adypokines that result in insulin resistance and low degree inflammation, which increase the activity of ANS, causing vasoconstriction, hypertension, decreased peripheral glucose uptake, and decreased secretion of insulin, leading to hyperglycemia and increased lipolysis and hypertriglyceridemia. All these factors cause ED, explaining the higher risk of the patients with MS of developing DM2 and CVD.