Articles: vagus-nerve-physiopathology.
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C(2) spinal hemisection (C2HS) interrupts ipsilateral bulbospinal pathways and induces compensatory increases in contralateral spinal and possibly supraspinal respiratory output. Our first purpose was to test the hypothesis that after C2HS contralateral respiratory motor outputs become resistant to vagal inhibitory inputs associated with lung inflation. Bilateral phrenic and contralateral hypoglossal (XII) neurograms were recorded in anesthetized and ventilated rats. ⋯ Bilateral vagotomy greatly enhanced ipsilateral phrenic bursting, which was either weak or absent in vagal-intact rats at both 2 and 8 wk post-C2HS. We conclude that 1) compensatory increases in contralateral phrenic and XII output after C2HS blunt the inhibitory influence of vagal afferents during lung inflation and 2) vagal afferents robustly inhibit ipsilateral phrenic bursting. These vagotomy data appear to explain the variability in the literature regarding the onset of the spontaneous crossed phrenic phenomenon in spontaneously breathing (vagal intact) vs. ventilated (vagotomized) preparations.
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Psychother Psychosom · Jan 2010
Age-specific associations between cardiac vagal activity and functional somatic symptoms: a population-based study.
Functional somatic symptoms (FSS) are symptoms not explained by underlying organic pathology. It has frequently been suggested that dysfunction of the autonomic nervous system (ANS) contributes to the development of FSS. We hypothesized that decreased cardiac vagal activity is cross-sectionally and prospectively associated with the number of FSS in the general population. ⋯ Decreased cardiac vagal activity is associated with a higher number of FSS in adults aged
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New epidemiologic evidence suggests that referred craniofacial pain in coronary heart disease is more common than previously believed. Current medical reports suggest that in addition to coronary disease, thoracic disorders such as aortic dissection, pericarditis, and lung cancer can cause referred craniofacial pain. Recent physiologic evidence from animals and humans suggests that the vagus nerve mediates this referral of cardiac pain to the maxillofacial region. This article discusses the critical role of the dentist in patient education and recognition of referred head and neck pain in thoracic disease, in relation to the need for prompt medical treatment for these life-threatening conditions.
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To verify whether vagal dysfunction is associated with chronic pain, we evaluated the effects of subdiaphragmatic vagotomy (vgx) on the sensitivity toward noxious stimuli in rats. Vgx rats showed sustained hyperalgesia in the gastrocnemius muscle without tissue damage (no increase in vgx-induced plasma creatine phosphokinase or lactose dehydrogenase levels) accompanied by hypersensitivity to colonic distension. We found a dramatic increase in the levels of metabotropic glutamate receptor 5, protein kinase C (PKC) gamma and phosphorylated-PKCgamma within the spinal cord dorsal horn in vgx rats, which suggests that vgx may evoke sensory nerve plasticity. ⋯ Muscle hyperalgesia in vgx rats was also attenuated by gabapentin and amitriptyline, but was not affected by diclofenac, dexamethasone or diazepam. These findings indicate that subdiaphragmatic vagal dysfunction caused chronic muscle hyperalgesia accompanied by visceral pain and both gabapentin and amitriptyline were effective for subdiaphragmatic vagotomy-induced pain, which are partially similar to fibromyalgia syndrome. Furthermore, this chronic muscle pain may result from nociceptive neuroplasticity of the spinal cord dorsal horn.
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Postoperative cognitive dysfunction (POCD) is a decline in cognitive function for weeks or months after surgery. It may affect the patients' length of hospital stay, quality of life, the rehabilitation process, and work performance. Prolonged POCD occurs frequently after cardiac surgery, and the risk of POCD increases with age. ⋯ However, emerging evidences indicate that various inflammatory mediators are involved in the pathophysiology of POCD and inflammatory response may a potential pathogenic factor. The vagus nerve stimulation has been shown to decrease production and release of pro-inflammatory cytokines through the cholinergic anti-inflammatory pathway (CAP) in both animal model and human. Considering that the inflammation plays a definite role in the pathogenesis of POCD and the vagus nerve can mediate inflammation via CAP, we hypothesize that the transcutaneous vagus nerve stimulation may attenuate POCD by decreasing inflammatory response in elderly patients.