Autonomic neuroscience : basic & clinical
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Complex regional pain syndrome type I (CRPS I) is a frequent complication after injuries of the upper limbs. The pathophysiology of this disease remains unclear, although disturbances of the sympathetic nervous system have been detected in several clinical studies, and sympathetic blocks resolve the symptoms in many of the cases. To investigate the meaning of sympathetic dysfunction at the beginning of the disease, 27 patients with distal radial fracture were examined prospectively during the course of the disease with regard to their clinical symptoms and their peripheral sympathetic nervous function. ⋯ With regard to the unaffected contralateral hand, CRPS I patients also showed impaired sympathetic nervous function. The results of the present study suggest that the disturbances in the sympathetic nervous system in CRPS I patients are systemic and not limited to the affected limb. Their occurrence before the clinical breakout of the disease may serve as a marker that might be useful for early therapy and lead to further understanding of the pathophysiology of CRPS I.
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The results of neural tracing studies suggest that vagal afferent fibers in cervical and thoracic branches innervate the esophagus, lower airways, heart, aorta, and possibly the thymus, and via abdominal branches the entire gastrointestinal tract, liver, portal vein, billiary system, pancreas, but not the spleen. In addition, vagal afferents innervate numerous thoracic and abdominal paraganglia associated with the vagus nerves. Specific terminal structures such as flower basket terminals, intraganglionic laminar endings and intramuscular arrays have been identified in the various organs and organ compartments, suggesting functional specializations. ⋯ There is also good evidence for a role of vagal afferents in nociception, as manifested by affective-emotional responses such as increased blood pressure and tachycardia, typically associated with the perception of pain, and mediated via central reflex pathways involving the amygdala and other parts of the limbic system. The massive central projections are likely to be responsible for the antiepileptic properties of afferent vagal stimulation in humans. Furthermore, these functions are in line with a general defensive character ascribed to the vagal afferent, paraventricular system in lower vertebrates.
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Beyond the fundamental pathogenetic importance of Helicobacter Pylori a possible additional role of vagal innervation in favouring or modulating the clinical history of duodenal ulcer (DU) has been suggested by old studies employing invasive methodologies. Aim of this study was to assess whether vagal prevalence in autonomic modulation was present in healed DU patients (n=20) as compared to controls,(n=50), using a validated non-invasive methodology, based on spectral analysis of cardiovascular variability. This approach provides markers of the sympathetic and vagal modulations of the SA node, respectively by way of the normalized low frequency (LF(RR)) and high frequency (HF(RR)) components of RR interval variability; LF/HF ratio furnishes a marker of sympatho-vagal balance. ⋯ Conversely the LF component of SAP variability, a marker of sympathetic vasomotor modulations, and the index alpha, a measure of baroreflex control of the SA node, as well as respiratory patterns, were similar in the two groups. SAO/BAO ratio was significantly correlated with markers of autonomic control of the SA node (r = -0.67, P<0.0083 with HF(RR)). In conclusion results suggest an enhanced vagal modulation of heart period in DU patients at rest, that appears linked to indices of neurally mediated gastric acid secretion response.