Nausea Nausea is an unpleasant sensation usually recognized as a feeling of imminent vomiting.

It is therefore a conscious recognition of subconscious excitation in an area of the brain associated with vomiting. It is caused by irritative impulses coming from the gastrointestinal tract, impulses that originate in the lower brain associated with motion sickness, or impulses from the cerebral cortex to initiate vomiting. Vomiting can occur without any forewarning sensation of nausea, highlighting that only certain parts of the brain involved in vomiting are associated with the sensation of nausea. [1] Vomitting Vomiting is the means by which the GI tract empties itself(by a means of forcefully ejecting through the mouth)of gastric or intestinal content when irritated, overdistended, or overexcitable. It is partially voluntary.[2] Vomiting is a complex process that requires central neurologic control. The sensory signals for vomiting are initiated mainly from the pharynx, oesophagus, stomach, and duodenum. These impulses are transmitted, via afferent pathways both vagal and sympathetic afferent nerve routes to multiple distributed nuclei in the medulla known collectively as the vomiting centre. This is where the neurological control of vomiting is provided from. From the vomiting centre, motor impulses leave to start the vomiting process. These efferent motor nerves transmit from the vomiting centre via the 5th, 7th, 9th, 10th, and 12th cranial nerves to the upper GI tract, through vagal and sympathetic nerves to the lower GI

tract, and through spinal nerves to the diaphragm and abdominal muscles. [1] Neurological control of vomiting The emetic /vomiting centre located in the medulla (to be specific, the dorsal portion of the lateral reticular formation in the vicinity of the fasciculus solitaries; keep note of this as I will ask a question about it). [2] Vomiting can also be activated outside stimuli in the GI tract from some areas of the brain directly. This area is known as the chemoreceptor trigger zone (CTZ) is located in the area postrema bilaterally on the floor of the fourth ventricle. Stimulation of this area can activate the vomiting centre; electrically or chemically through the administration of certain drugs such as opiods and digitalis derivatives. [1][2] The CTZ is outside, the blood-brain barrier and can therefore detect circulating endogenous and exogenous molecules that may induce vomiting. It is important to note: 1. Stimulation of the 5-hydroxytryptamine3 (5-HT3) serotonin receptor provokes release of dopamine, which in turn stimulates dopamine D2 receptors in the emetic center. This activates the vomiting reflex. This is exploited by antiemetic drug; 5-HT3 receptor inhibitor such as ondansetron, and dopamine D2 receptor antagonist such as metoclopramide which is effective in the treatment of chemotherapyinduced vomiting,[2] 2. Cannabinoid CB1 receptors in the dorsal vagal complex inhibit the vomiting reflex. Cannabinoid agonists also modulate 5-HT3 ion channels. Thus, the CB and 5-HT3 receptor systems co-localise and interact in the medulla. [2]

3. Neurokinin-1 (NK-1) receptors located in the area postrema and the solitary nucleus bind to substance P and are part of the terminal vomiting pathways. NK-1 antagonists reduce emesis induced by peripherally and centrally acting emetogens [2]

[3]
Process of Vomiting In the early stages of excessive GI irritation or overdistention, retrograde peristalsis begins to occur

before the act of vomiting occurs. This may begin as far down as the ileum, and the wave travels backward to push the intestinal contents to the duodenum and stomach. As the duodenum, become overly distended, this distension becomes the excitatory factor that initiates the vomiting process. When vomiting begins, strong contractions occur in both the duodenum and the stomach, along with some relaxation of the cardiac sphincter. This allows vomitus to move from the stomach to the oesophagus. The abdominal muscles take over and expel the vomitus to the mouth. These processes of vomiting are summarised below: 1. A deep breath. 2. Raising of the hyoid bone and larynx to pull the pharyngoesophageal sphincter open. 3. Closing of the glottis to prevent vomitus flow into the lungs, and lifting of the soft palate to close the posterior nares and prevent vomitus entering the nasopharynx. 4. A strong downward contraction of the diaphragm along with concurrent contraction of all the abdominal wall muscles. This squeezes the stomach between the diaphragm and the abdominal muscles, increasing the intragastric pressure. 5. At last, the lower oesophageal sphincter relaxes fully, allowing expulsion of the gastric contents upward through the oesophagus.

centre to cause vomiting. Histamine H1 and muscarinic M1 receptors are abundant in the vestibular nuclei and are therefore the favoured pharmacologic targets for preventing motion sickness, vestibular nausea, and pregnancy related vomiting.

References 1. Guyton and Hall. TEXTBOOK of Medical Physiology 11th edition. Copyright 2006 ELSEVIER. Unit XII Gastrointestinal Physiology. pp 823-824. 2. Feldman et al. Sleisenger and Fordtrans Gastrointestinal and Liver Disease. Chapter 14. Nausea and Vomiting by Juan-R. Malagelada and Carolina Malagelada. Copyright 2010 SAUNDERS. pp 197-199. 3. Figure 14-1. Feldman et al. Sleisenger and Fordtrans Gastrointestinal and Liver Disease. Copyright 2010 SAUNDERS. pp 198.

Motion sickness The motion stimulates receptors in the vestibular portion of the inner ear, and from here impulses are transmitted mainly by way of the medulla through the vestibular nuclei into the cerebellum, then to the chemoreceptor trigger zone, and finally to the vomiting