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The sensory signals that initiate vomiting originate mainly from the pharynx, esophagus, stomach, and upper portions of the small intestines. And the nerve impulses are transmitted, as shown in Figure 66-2, by both vagal and sympathetic afferent nerve fibers to multiple distributed nuclei in the brain stem that all together are called the “vomiting center.” From here, motor impulses that cause the actual vomiting are transmitted from the vomiting center by way of the 5th, 7th, 9th, 10th, and 12th cranial nerves to the upper gastrointestinal tract, through vagal and sympathetic nerves to the lower tract, and through spinal nerves to the diaphragm and abdominal muscles.
Antiperistalsis – the Prelude to Vomiting. In the early stages of excessive gastrointestinal irritation or overdistention, antiperistalsis begins to occur often many minutes before vomiting appears. Antiperistalsis means peristalsis up the digestive tract rather than downward. This may begin as far down in the intestinal tract as the ileum, and the antiperistaltic wave travels backward up the intestine at a rate of 2 to 3 cm/sec; this process can actually push a large share of the lower small intestine contents all the way back to the duodenum and stomach within 3 to 5 minutes. Then, as these upper portions of the gastrointestinal tract, especially the duodenum, become overly distended, this distention becomes the exciting factor that initiates the actual vomiting act. At the onset of vomiting, strong intrinsic contractions occur in both the duodenum and the stomach, along with partial relaxation of the esophageal-stomach sphincter, thus allowing vomitus to begin moving from the stomach into the esophagus. From here, a specific vomiting act involving the abdominal muscles takes over and expels the vomitus to the exterior, as explained in the next paragraph.
Vomiting Act. Once the vomiting center has been sufficiently stimulated and the vomiting act instituted, the first effects are (1) a deep breath, (2) raising of the hyoid bone and larynx to pull the upper esophageal sphincter open, (3) closing of the glottis to prevent vomitus flow into the lungs, and (4) lifting of the soft palate to close the posterior nares. Next comes a strong downward contraction of the diaphragm along with simultaneous contraction of all the abdominal wall muscles. This squeezes the stomach between the diaphragm and the abdominal muscles, building the intragastric pressure to a high level. Finally, the lower esophageal sphincter relaxes completely, allowing expulsion of the gastric contents upward through the esophagus.
Thus, the vomiting act results from a squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of the esophageal sphincters so that the gastric contents can be expelled.
“Chemoreceptor Trigger Zone” in the Brain Medulla for Initiation of Vomiting by Drugs or by Motion Sickness. Aside from the vomiting initiated by irritative stimuli in the gastrointestinal tract itself, vomiting can also be caused by nervous signals arising in areas of the brain. This is particularly true for a small area located bilaterally on the floor of the fourth ventricle called the chemoreceptor trigger zone for vomiting. Electrical stimulation of this area can initiate vomiting; but, more important, administration of certain drugs, including apomorphine, morphine, and some digitalis derivatives, can directly stimulate this chemoreceptor trigger zone and initiate vomiting. Destruction of this area blocks this type of vomiting but does not block vomiting resulting from irritative stimuli in the gastrointestinal tract itself.
Also, it is well known that rapidly changing direction or rhythm of motion of the body can cause certain people to vomit. The mechanism for this is the following: The motion stimulates receptors in the vestibular labyrinth of the inner ear, and from here impulses are transmitted mainly by way of the brain stem vestibular nuclei into the cerebellum, then to the chemoreceptor trigger zone, and finally to the vomiting center to cause vomiting.
2. Structure and function of intestine
Small intestine: The small intestine is a convoluted tube extending from the pyloric sphincter in the epigastric region to the ileocecal valve in the right iliac region where it joins the large intestine. It is the longest part of the alimentary tube, but is only about half the diameter of the large intestine, ranging from 2.5 – 4cm. It is 6-7m long in a cadaver but only about 2-4 m long during life because of muscle tone. The small intestine has 3 subdivisions: the duodenum, which is mostly retroperitoneal, and the jejunum and ileum, both intraperitoneal organs. The relatively immovable duodenum, which curves around the head of the pancreas is about 25cm long. Although it is the shortest intestinal subdivision, the duodenum has the most features of interest. The bile duct, delivering bile from the liver and the main pancreatic duct, carrying pancreatic juice from the pancreas, unite in the wall of the duodenum in a bulblike point called the hepatopancreatic ampulla. The ampulla opens into the duodenum via the volcano-shaped major duodenal papilla. The entry of bile and pancreatic juice is controlled by a muscular valve called the hepatopancreatic sphincter, or sphincter of Oddi. The jejunum, about 2.5m long, extends from the duodenum to the ileum. The ileum, approx. 3.6m in length, joins the large intestine at the ileocecal valve. The jejunum and ileum hang in sausage-like coils in the central and lower part of the abdominal cavity, suspended from the posterior abdominal wall by the fan-shaped mesentery. These more distal parts of the small intestine are encircled and framed by the large intestine.
Nerve fibers serving the small intestine include parasympathetics from the vagus and sympathetics from the thoracic splanchnic nerves, both relayed through the superior mesenteric (and celiac) plexus. The arterial supply is primarily from the superior mesenteric artery. The veins parallel the arteries and typically drain into the superior mesenteric vein. From there, the nutrient-rich venous blood from the small intestine drains into the hepatic portal vein, which carries it to the liver.
The small intestine is highly adapted for nutrient absorption. Its length alone provides a huge surface area, and its wall has 3 structural modifications -plicae circulares, villi and microvilli- that amplify its absorptive surface enormously (> 600 times). Most absorption occurs in the proximal part of the small intestine, so these specializations decrease in number toward its distal end. The circular folds, or plicae circulars, are deep, permanent folds of the mucosa and submucosa. Nearly 1cm tall, these folds force chyme to spiral through the lumen, slowing its movement and allowing time for full nutrient absorption.
Villi are fingerlike projections of the mucosa, over 1mm high, that give it a velvety texture. The epithelial cells of the villi are chiefly absorptive columnar cells. In the core of each villus is a dense capillary bed and a wide lymph capillary called a lacteal. Digested foodstuffs are absorbed through the epithelial cells into both the capillary blood and the lacteal. The villi are large and leaflike in the duodenum (the intestinal site of most active absorption) and gradually narrow and shorten along the length of the small intestine. A “slip” of smooth muscle in the villus core allows it to alternately shorten and lengthen, pulsations that (1) increase the contact between the villus and the contents of the intestinal lumen, making absorption more efficient, and (2) “milk” lymph along through the lacteals.
- Absorption of the majority of nutrients takes place in the jejunum, with the following notable exceptions:
- Iron is absorbed in the duodenum.
- Vitamin B12 and bile salts are absorbed in the terminal ileum.
- Water and lipids are absorbed by passive diffusion throughout the small intestine.
- Sodium is absorbed by active transport and glucose and amino acid co-transport.
- Fructose is absorbed by facilitated diffusion.
The large intestine frames the small intestine on 3 sides and extends from the ileocecal valve to the anus. Its diameter (~7cm) is greater than that of the small intestine, but it is less than half as long (1.5m vs 6m). In terms of digestive system functioning, its major function is to absorb most of the remaining water from indigestible food residues (delivered to it in a fluid state), store the residues temporarily, and then eliminate them from the body as semisolid feces.
The large intestine exhibits 3 features not seen elsewhere – teniae coli, haustra and epiploic appendages. Except for its terminal end, the longitudinal muscle layer of its muscularis is reduced to 3 bands of smooth muscle called teniae coli. Their tone causes the wall of the large intestine to pucker into pocket-like sacs called haustra. Another obvious feature of the large intestine is its epiploic appendages, small fat-filled pouches of visceral peritoneum that hang from its surface. Their significance is not known.
The large intestine has the following subdivisions: cecum, appendix, colon, rectum, and anal canal. The saclike cecum which lies below the ileocecal valve in the right iliac fossa is the first part of the large intestine. Attached to its posteromedial surface is the blind, wormlike vermiform appendix. The appendix contains masses of lymphoid tissue, and as part of MALT, it plays an important role in body immunity. However, it has an important structural shortcoming-its twisted structure provides an ideal location for enteric bacteria to accumulate and multiply.
3. Regulation of body fluid and electrolytes
The relative constancy of the body fluids is remarkable because there is continuous exchange of fluid and solutes with the external environment as well as within the different compartments of the body. For example, there is a highly variable fluid intake that must be carefully matched by equal output from the body to prevent body fluid volumes from increasing or decreasing.
The distribution of fluid between intracellular and extracellular compartments, in contrast, is determined mainly by the osmotic effect of the smaller solutes-especially sodium, chloride, and other electrolytes-acting across the cell membrane. The reason for this is that the cell membranes are highly permeable to water but relatively impermeable to even small ions such as sodium and chloride. Therefore, water moves across the cell membrane rapidly, so that the intracellular fluid remains isotonic with the extracellular fluid.
Marieb: Electrolytes include salts, acids, and bases, but the term electrolyte balance usually refers to the salt balance in the body. Salts are important in controlling fluid movements and provide minerals essential for excitability, secretory activity, and membrane permeability. Although many electrolytes are crucial for cellular activity, here we will specifically examine the regulation of sodium, potassium, and calcium.
4. Structure and function of the kidney
The 2 kidneys lie outside the peritoneal cavity in close apposition to the posterior abdominal wall, 1 on each side of the vertebral column. Each of the 2 kidneys is a bean-shaped structure. The rounded, outer convex surface of each kidney faces the side of the body, and the indented surface, called the hilum, is medial. Each hilum is penetrated by a renal artery, renal vein, nerves, and a ureter, which carries urine out of the kidney to the bladder. Each ureter within the kidney is formed from major calyces, which, in turn, are formed from minor calyces. The calyces are funnel-shaped structures that fit over underlying cone-shaped renal tissue called pyramids. The tip of each pyramid is called a papilla and projects into a minor calyx. The calyces act as collecting cups for the urine formed by the renal tissue in the pyramids. The pyramids are arranged radially around the hilum, with the papillae pointing toward the hilum and the broad bases of the pyramids facing the outside, top, and bottom of the kidney (from the 12-o’clock to the 6-o’clock position). The pyramids constitute the medulla of the kidney. Overlying the medullary tissue is a cortex, and covering the cortical tissue on the very external surface of the kidney is a thin connective tissue capsule (Figure 1-1).
The working tissue mass of both the cortex and medulla is constructed primarily of tubules (nephrons and collecting tubules) and blood vessels (capillaries and capillary-like vessels). Tubules and blood vessels are intertwined or arranged in parallel arrays and, in either case, are always close to each other. Between the tubules and blood vessels lies an interstitium, which comprises less than 10% of the renal volume. The interstitium contains scattered interstitial cells (fibroblasts and others) that synthesize an extracellular matrix of collagen, proteoglycans, and glycoproteins.
1. Regulation of Water and Electrolyte Balance – The balance concept states that our bodies are in balance for any substance when the inputs and outputs of that substance are matched. Any difference between input and output leads to an increase or decrease in the amount of a substance within the body. Our input of water and electrolytes is enormously variable and is only sometimes driven in response to body needs. The kidneys respond by varying the output of water in the urine, thereby maintaining balance for water (ie, constant total body water content). Minerals like Na+, K+, Mg2+ etc are components of foods and generally present far in excess of body needs. As with water, the kidneys excrete minerals at a highly variable rate that, in the aggregate, matches input. Kidneys are able to regulate each of these minerals independently (ie, we can be on a high-sodium, low-potassium diet or low-sodium, high-potassium diet, and the kidneys will adjust excretion of each of these substances appropriately). When we have an unusually high or low level of a substance in our body relative to normal, this does not imply that we are perpetually out of balance. To raise the level of a substance in the body, we must be transiently in positive balance. However, once that level reaches a constant value with input and output again equal, we are back in balance.
2. Excretion of Metabolic Waste – Our bodies continuously form end products of metabolic processes. Usually, those end products serve no function and are harmful at high concentrations, including urea (from protein), uric acid (from nucleic acids), creatinine (from muscle creatine), the end products of hemoglobin breakdown (gives urine much of its color), the metabolites of various hormones etc.
3. Excretion of Bioactive Substances (Hormones and many foreign substances, specifically drugs) That Affect Body Function – Physicians have to be mindful of how fast the kidneys excrete drugs in order to prescribe a dose that achieves the appropriate body levels. Hormones in the blood are removed mostly in the liver, but a number of hormones are removed in parallel by renal processes.
4. Regulation of Arterial Blood Pressure – Blood pressure ultimately depends on blood volume, and the kidneys’ maintenance of sodium and water balance achieves regulation of blood volume. Thus, through volume control, the kidneys participate in blood pressure control. They also participate in regulation of blood pressure via the generation of vasoactive substances that regulate smooth muscle in the peripheral vasculature.
5. Regulation of Red Blood Cell Production – Erythropoietin is a peptide hormone that is involved in the control of erythrocyte (RBC) production by the bone marrow. Its major source is the kidneys although the liver also secretes small amounts. The renal cells that secrete it are a particular group of cells in the interstitium. The stimulus for its secretion is a reduction in the partial pressure of oxygen in the kidneys, as occurs, e.g., in anemia, arterial hypoxia, and inadequate renal blood flow. Erythropoietin stimulates the bone marrow to increase its production of erythrocytes. Renal disease may result in diminished erythropoietin secretion, and the ensuing decrease in bone marrow activity is one important causal factor of the anemia of chronic renal disease.
6. Regulation of Vitamin D Production – In vivo vitamin D synthesis involves a series of biochemical transformations. The last occurs in the kidneys. The active form of vitamin D (1,25-dihydroxyvitamin D3) is made in the kidneys, and its rate of synthesis is regulated by hormones that control calcium and phosphate balance.
7. Gluconeogenesis – Our CNS is an obligate user of blood glucose regardless of whether we have just eaten sugary doughnuts or gone without food for a week. Whenever the intake of carbohydrate is stopped for much more than half a day, our body begins to synthesize new glucose (the process of gluconeogenesis) from non-carbohydrate sources (amino acids from protein, glycerol from triglycerides). Most gluconeogenesis occurs in the liver, but a substantial fraction occurs in the kidneys, particularly during a prolonged fast.
Most of what the kidneys actually do to perform the functions just mentioned involves transporting water and solutes between the blood flowing through the kidneys and the lumina of tubules (nephrons and collecting tubules that comprise the working mass of the kidneys). The lumen of a nephron is topologically outside the body, and any substance in the lumen that is not transported back into the blood is eventually excreted in the urine.
5. Intestinal Motility (Different parts of guts move in different manner, movement of different parts – [Physiology]
Guyton and Hall:
Two types of movements occur in the gastrointestinal tract: (1) propulsive movements, which cause food to move forward along the tract at an appropriate rate to accommodate digestion and absorption, and (2) mixing movements, which keep the intestinal contents thoroughly mixed at all times.
The movements of the small intestine, like those elsewhere in the gastrointestinal tract, can be divided into mixing contractions and propulsive contractions. To a great extent, this separation is artificial because essentially all movements of the small intestine cause at least some degree of both mixing and propulsion. The usual classification of these processes is the following.
Mixing Contractions (Segmentation Contractions): When a portion of the small intestine becomes distended with chyme, stretching of the intestinal wall elicits localized concentric contractions spaced at intervals along the intestine and lasting a fraction of a minute. The contractions cause “segmentation” of the small intestine, as shown in Figure 63-3. That is, they divide the intestine into spaced segments that have the appearance of a chain of sausages. As one set of segmentation contractions relaxes, a new set often begins, but the contractions this time occur mainly at new points between the previous contractions. Therefore, the segmentation contractions “chop” the chyme two to three times per minute, in this way promoting progressive mixing of the food with secretions of the small intestine.
The maximum frequency of the segmentation contractions in the small intestine is determined by the frequency of electrical slow waves in the intestinal wall, which is the basic electrical rhythm described in Chapter 62. Because this frequency normally is not over 12 per minute in the duodenum and proximal jejunum, the maximum frequency of the segmentation contractions in these areas is also about 12 per minute, but this occurs only under extreme conditions of stimulation. In the terminal ileum, the maximum frequency is usually 8 to 9 contractions per minute.
The segmentation contractions become exceedingly weak when the excitatory activity of the enteric nervous system is blocked by the drug atropine. Therefore, even though it is the slow waves in the smooth muscle itself that cause the segmentation contractions, these contractions are not effective without background excitation mainly from the myenteric nerve plexus.
Peristalsis in the Small Intestine. Chyme is propelled through the small intestine by peristaltic waves. These can occur in any part of the small intestine, and they move toward the anus at a velocity of 0.5 to 2.0 cm/sec, faster in the proximal intestine and slower in the terminal intestine. They normally are very weak and usually die out after traveling only 3 to 5 centimeters, very rarely farther than 10 centimeters, so that forward movement of the chyme is very slow, so slow in fact that net movement along the small intestine normally averages only 1 cm/min. This means that 3 to 5 hours are required for passage of chyme from the pylorus to the ileocecal valve.
Control of Peristalsis by Nervous and Hormonal Signals. Peristaltic activity of the small intestine is greatly increased after a meal. This is caused partly by the beginning entry of chyme into the duodenum causing stretch of the duodenal wall, but also by a so-called gastroenteric reflex that is initiated by distention of the stomach and conducted principally through the myenteric plexus from the stomach down along the wall of the small intestine.
In addition to the nervous signals that may affect small intestinal peristalsis, several hormonal factors also affect peristalsis. They include gastrin, CCK, insulin, motilin, and serotonin, all of which enhance intestinal motility and are secreted during various phases of food processing. Conversely, secretinand glucagon inhibit small intestinal motility. The physiologic importance of each of these hormonal factors for controlling motility is still questionable.
The function of the peristaltic waves in the small intestine is not only to cause progression of chyme toward the ileocecal valve but also to spread out the chyme along the intestinal mucosa. As the chyme enters the intestines from the stomach and elicits peristalsis, this immediately spreads the chyme along the intestine; and this process intensifies as additional chyme enters the duodenum. On reaching the ileocecal valve, the chyme is sometimes blocked for several hours until the person eats another meal; at that time, a gastroileal reflex intensifies peristalsis in the ileum and forces the remaining chyme through the ileocecal valve into the cecum of the large intestine.
Propulsive Effect of the Segmentation Movements. The segmentation movements, although lasting for only a few seconds at a time, often also travel 1 centimeter or so in the anal direction and during that time help propel the food down the intestine. The difference between the segmentation and the peristaltic movements is not as great as might be implied by their separation into these two classifications.
Peristaltic Rush. Although peristalsis in the small intestine is normally weak, intense irritation of the intestinal mucosa, as occurs in some severe cases of infectious diarrhea, can cause both powerful and rapid peristalsis, called the peristaltic rush. This is initiated partly by nervous reflexes that involve the autonomic nervous system and brain stem and partly by intrinsic enhancement of the myenteric plexus reflexes within the gut wall itself. The powerful peristaltic contractions travel long distances in the small intestine within minutes, sweeping the contents of the intestine into the colon and thereby relieving the small intestine of irritative chyme and excessive distention.
Movements Caused by the Muscularis Mucosae and Muscle Fibers of the Villi. The muscularis mucosae can cause short folds to appear in the intestinal mucosa. In addition, individual fibers from this muscle extend into the intestinal villi and cause them to contract intermittently. The mucosal folds increase the surface area exposed to the chyme, thereby increasing absorption. Also, contractions of the villi-shortening, elongating, and shortening again-“milk” the villi, so that lymph flows freely from the central lacteals of the villi into the lymphatic system. These mucosal and villous contractions are initiated mainly by local nervous reflexes in the submucosal nerve plexus that occur in response to chyme in the small intestine.
Movements of the Colon:
The principal functions of the colon are (1) absorption of water and electrolytes from the chyme to form solid feces and (2) storage of fecal matter until it can be expelled. The proximal half of the colon, shown in Figure 63-5, is concerned principally with absorption, and the distal half with storage. Because intense colon wall movements are not required for these functions, the movements of the colon are normally very sluggish. Yet in a sluggish manner, the movements still have characteristics similar to those of the small intestine and can be divided once again into mixing movements and propulsive movements.
Mixing Movements-“Haustrations.” In the same manner that segmentation movements occur in the small intestine, large circular constrictions occur in the large intestine. At each of these constrictions, about 2.5 centimeters of the circular muscle contracts, sometimes constricting the lumen of the colon almost to occlusion. At the same time, the longitudinal muscle of the colon, which is aggregated into three longitudinal strips called the teniae coli, contracts. These combined contractions of the circular and longitudinal strips of muscle cause the unstimulated portion of the large intestine to bulge outward into baglike sacs called haustrations. Each haustration usually reaches peak intensity in about 30 seconds and then disappears during the next 60 seconds. They also at times move slowly toward the anus during contraction, especially in the cecum and ascending colon, and thereby provide a minor amount of forward propulsion of the colonic contents. After another few minutes, new haustral contractions occur in other areas nearby. Therefore, the fecal material in the large intestine is slowly dug into and rolled over in much the same manner that one spades the earth. In this way, all the fecal material is gradually exposed to the mucosal surface of the large intestine, and fluid and dissolved substances are progressively absorbed until only 80 to 200 milliliters of feces are expelled each day.
Propulsive Movements -“Mass Movements.” Much of the propulsion in the cecum and ascending colon results from the slow but persistent haustral contractions, requiring as many as 8 to 15 hours to move the chyme from the ileocecal valve through the colon, while the chyme itself becomes fecal in quality, a semisolid slush instead of semifluid.
From the cecum to the sigmoid, mass movements can, for many minutes at a time, take over the propulsive role. These movements usually occur only one to three times each day, in many people especially for about 15 minutes during the first hour after eating breakfast.
A mass movement is a modified type of peristalsis characterized by the following sequence of events: First, a constrictive ring occurs in response to a distended or irritated point in the colon, usually in the transverse colon. Then, rapidly, the 20 or more centimeters of colon distal to the constrictive ring lose their haustrations and instead contract as a unit, propelling the fecal material in this segment en masse further down the colon. The contraction develops progressively more force for about 30 seconds, and relaxation occurs during the next 2 to 3 minutes. Then, another mass movement occurs, this time perhaps farther along the colon.
A series of mass movements usually persists for 10 to 30 minutes. Then they cease but return perhaps a half day later. When they have forced a mass of feces into the rectum, the desire for defecation is felt.
Initiation of Mass Movements by Gastrocolic and Duodenocolic Reflexes. Appearance of mass movements after meals is facilitated by gastrocolic and duodenocolic reflexes. These reflexes result from distention of the stomach and duodenum. They occur either not at all or hardly at all when the extrinsic autonomic nerves to the colon have been removed; therefore, the reflexes almost certainly are transmitted by way of the autonomic nervous system.
Irritation in the colon can also initiate intense mass movements. For instance, a person who has an ulcerated condition of the colon mucosa (ulcerative colitis) frequently has mass movements that persist almost all the time.
6. Food hygiene (What the government does, public health etc.)
The five key principles of food hygiene, according to WHO, are:
- Prevent contaminating food with pathogens spreading from people, pets, and pests.
- Separate raw and cooked foods to prevent contaminating the cooked foods.
- Cook foods for the appropriate length of time and at the appropriate temperature to kill pathogens.
- Store food at the proper temperature.
- Use safe water and raw materials
7. Taste aversion
Taste aversion-learning to avoid a food that makes you sick-is an intriguing form of classical conditioning. The signal or CS (conditioned stimulus) is the taste of a food. The reflex that follows it is sickness. Organisms quickly learn to associate taste with sickness. Taste aversion can occur even though a person knows that an illness occurred because of a virus, not because of food. It does not matter; the body jumps to the conclusion that the food was bad, and the food becomes repulsive to us. This illustrates how classical conditioning involves automatic, involuntary, primitive processes in the human brain. The tendency to blame food for illness, even if the food had nothing to do with the illness, is called the Garcia Effect.
A conditioned taste aversion can occur when eating a substance is followed by illness. E.g. if you ate a taco for lunch and then became ill, you might avoid eating tacos in the future, even if the food you ate had no relationship to your illness. Conditioned taste aversions can develop even when there is a long delay between the conditioned stimulus (eating the food) and the unconditioned stimulus (feeling sick). In classical conditioning, conditioned food aversions are examples of single-trial learning. It requires only one pairing of the conditioned stimulus and the unconditioned stimulus to establish and automatic response.
The type of counterconditioning most widely used for therapeutic purposes is systematic desensitization, which is employed to reduce or eliminate fear of a particular object, situation, or activity. An early example of systematic desensitization was an experiment that is also the first recorded use of behavior therapy with a child. In a paper published in 1924, Mary Cover Jones, a student of the pioneering American behaviorist John Watson, described her treatment of a 3-year-old with a fear of rabbits. Jones countered the child’s negative response to rabbits with a positive one by exposing him to a caged rabbit while he sat some distance away, eating one of his favorite foods. The boy slowly became more comfortable with the rabbit as the cage was gradually moved closer, until he was finally able to pet it and play with it without experiencing any fear.
In the 1950s South African psychiatrist Joseph Wolpe (1915- ) pioneered a prototype for systematic desensitization as it is generally practiced today. Like Cover’s experiment, Wolpe’s technique involved gradually increasing the intensity of exposure to a feared experience. However, instead of countering the fear with a pleasurable stimulus such as food, Wolpe countered it with deliberately induced feelings of relaxation. He had the client imagine a variety of frightening experiences and then rank them in order of intensity. The c
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