Hiccup
Wesley C. Finegan, Angela McGurk, Wilma O’Donnell, Jan Pederson, Elizabeth Rogerson in Care of the Cancer Patient, 2018
This chapter describes the medical condition hiccup. Hiccups are caused by spasms of the diaphragm leading to a sudden intake of breath, which is cut off when the vocal cords close quickly, causing the characteristic sound which gives rise to their onomatopoeic name. Hiccups serve no known function, have no single reliable treatment and can be very exhausting for the patient, especially as they can persist for several days. Diaphragmatic spasm due to diaphragmatic irritation results in hiccups. The diaphragmatic irritation is often caused by gastric distension or liver enlargement, the diaphragmatic irritation being stimulated by involvement of two main nerve pathways, namely the vagus nerve and the phrenic nerve. Treatment of hiccup can be unsuccessful, and no single treatment can be guaranteed.
Chemosensation
Emily Crews Splane, Neil E. Rowland, Anaya Mitra in Psychology of Eating, 2019
This chapter focuses on the food-related signals that are received by the brain, the brain structures involved, and the types of integration of those signals that occurs to guide our feelings, thoughts, and behaviors. It reviews the conscious sensations of smell and taste, and the largely unconscious signals that arise internally from our digestive tract or gut. The brain areas that receive the action potentials arriving in thousands of axons from the mitral cells have to decode these signals. The simplest form of cell-to-cell signaling is via signal molecules that are secreted or released by one cell and are recognized by specific receptors for those molecules on the surface of or inside the recipient or target cell(s). The signals to the brain are of two main types: Action potentials in sensory afferents of the vagus nerve and specific hormones that are released into the blood stream as a result of specific enteroendocrine cell stimulation.
Henry Hallet Dale (1875–1968)
Andrew P. Wickens in Key Thinkers in Neuroscience, 2018
Henry Hallet Dale is widely regarded as the founder of biochemical pharmacology, and there are few who have made a colossal impact on their respective fields. Dale's most famous contribution to pharmacology, however, was his elucidation of the role of acetylcholine in autonomic and somatic nervous function. As Dale began to examine ergot, he realised it was a treasure trove of active pharmacological substances, many of which were isolated by his colleague George Barger. Dale showed that histamine is found in many other bodily regions and released in response to injury. Histamine then caused constriction of the arteries along with a general "leakage" of the capillaries – a reaction supporting the immune response. By the early 1930s, most pharmacologists accepted that the parasympathetic branch of the vagus nerve secreted acetylcholine. Dale soon realised that non adrenaline mimicked the effects of sympathetic nervous stimulation more faithfully than adrenaline itself.
Recent advances in devices for vagus nerve stimulation
Published in Expert Review of Medical Devices, 2018
Ann Mertens, Robrecht Raedt, Stefanie Gadeyne, Evelien Carrette, Paul Boon, Kristl Vonck
Introduction: Vagus nerve stimulation (VNS) has become a valuable treatment option for refractory epilepsy and depression. To improve clinical efficacy and minimize side effects, novel device technology for VNS is under development and investigation. Areas covered: For epilepsy, the AspireSR®, and SenTiva™ VNS therapy systems are the two most recently developed VNS devices. These novel devices have implemented a closed-loop approach and contain a cardiac based seizure detection algorithm. The mechanism of action of VNS remains to be further elucidated, but as preclinical research reveals VNS induced effects on brain plasticity, the autonomic nervous system and the inflammatory response, the indications of VNS are expanding. VNS devices are currently being investigated for stroke rehabilitation, treatment of chronic heart failure and rheumatoid arthritis. Recently devices to noninvasively affect vagus nerve functioning have been developed, with the aim of achieving similar effects without the drawbacks of a surgical procedure and continuous stimulation. Expert commentary: Several animal and human trials have shown promising results with minimal adverse events. However, further research needs to be conducted to validate the use of these devices and decide on optimal stimulation parameters.
Vagus nerve stimulation for the treatment of intractable epilepsy
Published in Expert Review of Neurotherapeutics, 2007
Vagus nerve stimulation is a safe and reliable treatment adjunct for patients with medically intractable epilepsy. It is both a preventive and abortive form of therapy, potentially effective against both partial and generalized seizures in adults and children. Vagus nerve stimulation also has a number of serendipitous effects on mood, memory and attention, and has been approved for the treatment of refractory depression. Owing to its pleiotropic effects, it also holds promise for several other diseases. Its principal limitations are its unknown mechanism of action, the low likelihood of complete cure and the inability to predict which patients will derive substantial benefit. This article reviews the theoretical rationale, practical background and clinical applications of vagus nerve stimulation therapy.
Vagus nerve stimulation reverses the extinction impairments in a model of PTSD with prolonged and repeated trauma
Published in Stress, 2019
Rimenez R. Souza, Nicole M. Robertson, David T. Pruitt, Phillip A. Gonzales, Seth A. Hays, Robert L. Rennaker, Michael P. Kilgard, Christa K. McIntyre
We have shown that vagus nerve stimulation (VNS) enhances extinction of conditioned fear and reduces anxiety in rat models of PTSD using moderate stress. However, it is still unclear if VNS can be effective in enhancing extinction of severe fear after prolonged and repeated trauma. Severe fear was induced in adult male rats by combining single prolonged stress (SPS) and protracted aversive conditioning (PAC). After SPS and PAC procedures, rats were implanted with stimulating cuff electrodes, exposed to five days of extinction training with or without VNS, and then tested for extinction retention, return of fear in a new context and reinstatement. The elevated plus maze, open field and startle were used to test anxiety. Sham rats showed no reduction of fear during extensive extinction training. VNS-paired with extinction training reduced freezing at the last extinction session by 70% compared to sham rats. VNS rats exhibited half as much fear as shams, as well as less fear renewal. Sham rats exhibited significantly more anxiety than naive controls, whereas VNS rats did not. These results demonstrate that VNS enhances extinction and reduces anxiety in a severe model of PTSD that combined SPS and a conditioning procedure that is 30 times more intense than the conditioning procedures in previous VNS studies. The broad utility of VNS in enhancing extinction learning in rats and the strong clinical safety record of VNS suggest that VNS holds promise as an adjuvant to exposure-based therapy in people with PTSD and other complex forms of this condition.
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