High acidity inactivates trypsin
the vagus nerve, which stimulates increased gastric acid secretion as well as promotes gastric emptying. However, the cause of dyspepsia may be multifactorial resulting from gastric hypersecretion (previously treated surgically with vagotomy and accompanied by pyloroplasty due to the vagotomy causing gastric stasis) or gastroparesis or delayed gastric emptying.
Improved autonomic balance: Vagal control of the heart is diminished in HF and dysfunctional ganglionic transmission may contribute to this abnormality.39 Defective ganglionic transmission has been reported to be prevented by repeated exposure with a nicotinic (N-) receptor agonist during the development of HF.40 Thus, VNS, by releasing acetylcholine, the natural N-receptor agonist, may prevent ganglionic malfunction in HF and improve autonomic control. Here, we have provided evidence that chronic VNS improved cardiac autonomic balance in HF as evidenced by increased HRV, baroreflex sensitivity, and reduced NE level in the VNS-treated dogs. Thus, improved autonomic balance is a likely contributor to the observed benefits.
VNS may inhibit the renin-angiotensin system: Vagal afferents from the cardiopulmonary region are reported to exert a tonic restraint on the release of renin.14 Vagal blockade significantly increased plasma renin activity in HF dogs.15 Our results show that VNS treatment reduced plasma Ang-II levels. Thus, inhibition of the renin-angiotensin system by VNS is an additional therapeutic pathway.
VNS has anti-inflammatory effects: VNS can suppress systemic inflammatory response through “the cholinergic anti-inflammatory pathway.”41,42 Our results clearly indicate that pacing induced HF promotes systemic inflammation, as evidenced by increased plasma CRP levels. VNS treatment markedly reduced CRP levels. VNS mediated inhibition of the inflammatory processes likely provide important benefits in HF treatment.43,44
Tenth Cranial Nerve - Vagus Nerve
The vagus nerve carries sensory afferent fibers from the larynx, trachea, esophagus, pharynx, and abdominal viscera. It also sends efferent motor fibers to the pharynx, tongue, thoracic and abdominal viscera, and the larynx. Testing of the vagus nerve is performed by the gag reflex and "ahh" test as described above.
A unilateral lesion affecting the vagus nerve can produce hoarseness and difficulty swallowing due to a loss of laryngeal function. Causes of unilateral lesions include trauma from surgical procedures of the neck, aortic aneurysm, and compression due to enlarged paratracheal lymph nodes caused by metastatic carcinoma.
Mult Scler. 2007 Nov;13(9):1200-2. Epub 2007 Jul 10.
Vagal nerve stimulation improves cerebellar tremor and dysphagia in multiple sclerosis.
Marrosu F, Maleci A, Cocco E, Puligheddu M, Barberini L, Marrosu MG.
Dipartimento di Scienze Neurologiche e Cardiovascolari, University of Cagliari, Italy.
Vagus nerve stimulation (VNS), an adjunctive approach for the treatment of epilepsy, was performed in three multiple sclerosis (MS) patients displaying postural cerebellar tremor (PCT) and dysphagia. Following VNS, improvement of PCT and dysphagia was manifested over a period of two and three months, respectively. In view of the involvement of the main brainstem visceral component of the vagus, the nucleus tractus solitarius (NTS), in modulating central pattern generators (CPGs) linked to both olive complex pathway and swallowing, improvement is likely to be VNS related. The results obtained suggest an additional therapeutic application for VNS and may represent a novel form of treatment in patients with severe MS.
There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. Other causes of trigeminal neuralgia in which demyelination is involved or implicated include multiple sclerosis and, probably, compressive space-occupying masses in the posterior fossa. Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. Similar foci of nerve root demyelination and juxtaposition of axons have been demonstrated in multiple sclerosis patients with trigeminal neuralgia. Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation. Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. The role of remyelination in initial symptomatic recovery after decompression is unclear. However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. In addition to causing symptomatic relief, vascular decompression leads to rapid recovery of nerve conduction across the indented root, a phenomenon that, we suggest, is likely to reflect the reversal of compression-induced conduction block in larger myelinated fibres outside the region of demyelination. Trigeminal neuralgia can occur in association with a range of other syndromes involving vascular compression and hyperactivity of cranial nerves. Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.
Vasovagal therapy is like supercharged CCSVI treatment. It is extreme pressure ballooning combined with external compression. The goal is delivery of maximal mechanical energy to the autonomic nerve fibers running along the vein.
Users browsing this forum: Robnl