What are tics? |

Causes and Symptoms

Tics are small, inappropriate, involuntary, compulsive jerking or twitching movements that recur uncontrollably and appear to be nonrhythmic (erratic) in pattern. Tics are stereotyped movements of small portions of the body that last only briefly but may be repeated often. They are often set off by psychologically stressful events. In many cases, tics can be voluntary and temporarily suppressed, but often with the result that the same movements occur more forcefully afterward. The term “habit spasm” is often used for tics that occur among children. A tic is a symptom rather than a disease. Many tics are believed to be of psychogenic origin, and certain others seem to be related to epilepsy, encephalitis, or diseases of unknown origin.

Motor tics commonly involve coarse muscle movements of small magnitude, including movements of the face (such as eye blinks, grimaces, or sniffing movements), shrugging of the shoulders, jerks of the neck, or twitches of the body parts. Many motor tics (and also vocal tics) are easily imitated by others but are performed involuntarily and uncontrollably by the patient. Distracting the patient’s attention may stop certain tics. In most cases, the tic does not interfere with the patient’s use of the hands or feet, even in delicate movements. Several neurologists distinguish simple motor tics (eye winking, head twitching, shoulder shrugs, or facial grimaces) from complex motor tics using more muscles and requiring coordination. Complex motor tics may include touching oneself or other people, jumping, hitting, or throwing things.

Vocal or phonic tics include the making of sounds, which may include grunts, coughs, sniffs, clearings of the throat, animal noises (especially barking and yelping), or understandable words. The words may simply be repeated utterances of the patient’s own words (palilalia), repetition of words spoken to the patient (echolalia), or obscene and offensive words (coprolalia). Although coprolalia is one of the more striking symptoms of Tourette’s syndrome and has been vividly portrayed in many popular accounts of this disorder, it is usually a mild or transient symptom and appears in only a minority of cases.

Sensory tics are unusual sensations of pressure, cold, warmth, tickling, or other common sensations that are generally brief in duration. Some otherwise inexplicable movements may be interpreted as actions taken by the patient to alleviate these sensory tics. Sensory tics are reported to be present in about 40 percent of patients with Tourette’s syndrome.

Tic disorders can be classified into four types: tic douloureux, transient tic disorder of childhood, chronic tic disorder, and Tourette’s syndrome. One of the most common forms of tic is trigeminal neuralgia, also called tic douloureux, a disorder that affects about fifteen thousand individuals annually in the United States. Tic douloureux is a disorder of the trigeminal or fifth cranial nerve, the nerve that supplies motor stimulation to the jaw muscles and sensory innervation to much of the skin of the face. Tic douloureux usually begins with a very brief but very intense, sharp pain, often described as feeling like an electric shock or a stabbing, swiftly spreading in many cases along the course of the affected nerve. The pain is usually accompanied by uncontrolled spasms or paroxysms that last less than a second but continue to recur for several minutes. These episodes may be separated from one another by tic-free periods lasting from weeks to more than a year. The pain and twitching are generally confined to one side of the face, often to one of the three divisions of the trigeminal nerve, usually the maxillary or mandibular division, or, much less often, the ophthalmic division. In addition to the uncontrollable tics, patients suffering from tic douloureux
often wince visibly from the pain; this habit is responsible for the term “tic douloureux,” meaning “painful tic.”

The immediate event precipitating an attack of tic douloureux is usually a mild stimulation or irritation of a “trigger zone” on or about the face, lips, tongue, or gums. The trigger zone is often a small area that is constant for a particular patient; some patients can trigger an episode by stimulating the trigger zone themselves. The most common locations for the trigger zone are along the cheek or the attached parts of the lips; less common locations include the gums or the floor of the mouth beside the tongue. Some patients suffering an attack of tic douloureux will apply pressure to their faces, but the pain usually goes away by itself. Attacks generally occur during the day rather than at night, and they typically increase in intensity and become more frequent and exhausting to the patient until treatment is sought.

The stimulus that normally evokes an attack of tic douloureux may be an exposure to touch or pressure, to cold, to food in the mouth, or even to a puff of air. Because an attack can be precipitated by touching or otherwise stimulating the trigger zone, many victims of tic douloureux avoid touching the region in which the trigger zone is located. When the trigger zone is on the outside of the face, patients may become very fearful of touching the affected part, and men may avoid shaving. Some patients avoid brushing their teeth and remain unwashed for weeks or even months in the vicinity of their trigger area, with social consequences that often contribute to pessimistic feelings and even depression.

When tongue or cheek movements precipitate attacks, patients suffering from tic douloureux may develop the habit of holding the affected side of their face motionless, which sometimes restricts talking, eating, or similar everyday movements. In some cases, certain chewing movements or the presence of food in certain locations in the mouth may precipitate an attack; in these cases, patients are often very careful to avoid eating or chewing on the affected side, and in extreme cases they may so often avoid eating or drinking that they become dehydrated and emaciated. Some physicians advise such patients to modify their diet and drink only liquids, fortified with vitamins, that can be consumed without chewing. Malnutrition and physical inactivity are in many cases reinforced by the social consequences of facial uncleanliness and lack of hygiene, or by the fear of such consequences. The lack of social contact may result in pessimistic or negative feelings, feelings of inadequacy or lack of worth, preoccupation with loss and with past events, feelings of rejection or powerlessness, and other symptoms of clinical depression in many patients.

Dental disease or trauma may sometimes be associated with tic douloureux, but in most cases the tic has no apparent cause. Tic douloureux is more common after the age of forty and is slightly more common in women than in men. Some researchers believe that infection with a herpesvirus (especially herpes simplex) may be causally related to trigeminal neuralgia, but other researchers doubt this connection. Tumors of the trigeminal (Gasserian) ganglion, brain-stem tumors, multiple sclerosis, or localized damage to the brain stem tissue can sometimes give rise to conditions that closely resemble tic douloureux, but the majority of tics occur among patients having none of these conditions.

The remaining forms of tic disorder are considered by at least some researchers to be related to one another, or to form a spectrum of conditions from mild or imperceptible to severe. The mildest types are the tics or “habit spasms” of children. These tics are usually considered psychogenic in origin because they occur more often under conditions of stress or tension. Tics of this kind are more common in boys than in girls. Common types of childhood tics include eye blinks or other facial movements, as well as occasional vocal tics such as throat-clearing noises. In some children—perhaps many—tics of this kind may disappear (or be “outgrown”) spontaneously if no attention is drawn to them.

Chronic tics can be of either the motor or the vocal type. Chronic motor tics are uncommon tics in which three or more muscle groups are usually involved at the same time. Chronic vocal tics are also uncommon and consist of uncontrolled sounds that are more often animal sounds than words of articulate speech. Either kind of chronic tic can originate either in children or in adults, even beyond the age of forty. In either case, they usually last for the remainder of the patient’s life. The disorder is equally prevalent in both sexes. Some researchers think that these chronic tics, and possibly also the transient habit spasms of childhood, may result from the same (as yet unidentified) cause as Tourette’s syndrome, but in much milder form.

Tourette’s syndrome is a neurological disorder characterized by bizarre or unusual tics, compulsive swearing or cursing, strange facial gestures, and sudden barking or other animal-like sounds. The spectrum of these tics and other symptoms is broad, which has complicated earlier attempts to describe the disease or to find its cause. The disease usually first appears in children between five and ten years of age and continues throughout life.

The variability of symptoms is one of the characteristic features or highlights of Tourette’s syndrome. According to the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR (4th ed., 2000), among the diagnostic criteria for Tourette’s syndrome are that both motor and vocal tics must occur and that the number, frequency, complexity, severity, and anatomical location of these tics must change over time. The tics must occur many times a day, usually in bouts, and they must recur “nearly every day or intermittently throughout a period of more than one year.” The disease must appear before the age of twenty-one to be considered Tourette’s syndrome (although in many cases symptoms are so mild as to escape attention).

Associated with Tourette’s syndrome are a number of other conditions, including obsessive-compulsive behaviors,
attention-deficit disorder, hyperactivity, school phobias, test anxiety, conduct disorders, depression, dyslexia, poor socialization skills, and low self-esteem, though many of these symptoms can also appear by themselves. Several experts consider Tourette’s syndrome and attention-deficit disorder to be variable manifestations of a common underlying disorder that may relate to a chemical imbalance in the brain. About half of Tourette’s patients also show symptoms of attention-deficit disorder, such as frequent inattention, impulsiveness, and hyperactivity.

The association between Tourette’s syndrome and attention-deficit disorder should be regarded as provisional. The two disorders may have an underlying cause in common, such as a common genetic basis. In many cases, however, the motor and vocal tics are made worse by the administration of stimulants such as methylphenidate, which is commonly used for the treatment of the hyperactivity that so often accompanies attention-deficit disorder. Thus it is possible that the presence of Tourette’s syndrome in such cases may be attributable not to the attention-deficit disorder, but to the drugs used to treat the disorder. In certain cases, these drugs may have caused a transient or chronic tic disorder to progress to the more severe Tourette’s syndrome. Clearly, more research is needed to clarify the exact nature of the relationship between Tourette’s syndrome and attention-deficit disorder, both in the presence and in the absence of various drugs.

There are several other aspects of Tourette’s syndrome that are being examined. For example, a number of researchers now suspect that the factors that predispose a patient to develop Tourette’s syndrome may also predispose male patients to one form of alcoholism. Other researchers believe that the brain disorder responsible for Tourette’s syndrome is related to the endorphins, the brain’s natural opiates.

Some promising research involves the connection between this disorder and the neurotransmitter dopamine. Neurologists suspect that Tourette’s syndrome results from increased sensitivity of certain parts of the brain to dopamine. Some of the evidence for the hypersensitivity of dopamine receptors derives from the observation that drugs such as haloperidol, which is known to inhibit the dopamine receptors, are effective in reducing the symptoms of Tourette’s syndrome, while amphetamines and other drugs that enhance dopamine neurotransmission make the symptoms worse. Also, the cerebrospinal fluid of patients with Tourette’s syndrome contains reduced levels of homovanillic acid, a breakdown product of dopamine. The corpus striatum in the brain is considered to be the most likely location for the supersensitive dopamine receptors. One researcher has found a total absence of a brain peptide called dynorphin in fibers of the corpus striatum, where this peptide normally occurs. The fibers in question project to the globus pallidus at the base of the
cerebral hemispheres.

One theory that attempts to explain the relationship of the several symptoms in Tourette’s syndrome is that they all stem from a loss of the inhibition that normally controls involuntary movements. The obscene or offensive words, normally inhibited, are expressed more often than other types of words because the inhibition has been removed. This theory supposes that children who find that they have expressed “bad” words that should not have been said out loud become obsessed with these words and thus (in the absence of inhibitions) say them more often, making the problem worse.

Studies of the families of Tourette’s syndrome patients show that there are familial inheritance patterns, with many family members having at least some symptoms of tic disorders, attention-deficit disorders, or both. In many or most cases, the tic disorders of affected family members are so mild that they never caused any problems and were never mentioned to any physician. This finding leads many researchers to conclude that the underlying disorder is variable in the extent of its expression and that it is much more common than medical records show. One expert has even estimated that nearly 1 percent of the population has some form of tic disorder.

If all forms of tic disorder are included, it becomes clear that tics run in families and that Tourette’s syndrome is simply one end of a spectrum of variable expression. Studies on identical twins confirm that the trait has a genetic basis. Additional studies of family histories suggest that everyone with the gene experiences symptoms of the disorder. The penetrance of the gene is somewhat greater in males than in females, meaning that more males have symptoms while females are more often symptom-free. Among those family members who have symptoms, the expression of those symptoms is highly variable.

Mimicking some of the symptoms of Tourette’s syndrome are the so-called tardive tics that appear during adolescence or adult life. Tardive tics are considered by many researchers to be iatrogenic (drug-induced), arising from the prolonged use of neuroleptic drugs (tranquilizers) such as phenothiazines (Thorazine, Compazine, and Mellaril). Symptoms include isolated, short, quick, uncoordinated jerking movements. The mechanism by which tardive tics appear is unclear, but the same dopamine pathways may be involved as in genuine cases of Tourette’s syndrome.

Treatment and Therapy

Various treatments are available for tic douloureux, both medical and surgical. Partial relief may be afforded by medical treatments, which include carbamazepine (tegretol), trichloroethylene, anticonvulsants such as phenytoin or phenylhydatoin (Dilantin), vasodilators such as tolazoline (Priscoline), analgesic (pain-killing) drugs, vitamin B12, or the repeated injection of 95 percent ethyl alcohol directly into the trigeminal nerve ganglion.

None of these treatments is successful in all cases, however, and some, such as trichloroethylene, have toxic side effects. Surgical treatments include neurotomy (cutting of the affected branch of the trigeminal nerve), decompression of the posterior nerve root, or the cutting of one or more of the trigeminal tracts in the brain stem, either in the midbrain or in the medulla. The most frequently performed surgical procedures include destruction, or partial destruction, of the trigeminal ganglion, either by electrocoagulation, by radio frequency therapy, or by mechanical means. The facial paralysis or partial paralysis that follows nerve destruction often resembles Bell’s palsy except that the damage is usually permanent, with minimal possibility of recovery.

Treatment of childhood transient tic disorders usually consists of psychological intervention to control or reduce the level of stress. Many cases of transient or chronic tic disorder are so mild that they do not require any treatment.

For Tourette’s syndrome, haloperidol (Haldol) is most often prescribed, and it is said to be effective in 50 to 90 percent of the cases, depending on the authority consulted. Other drugs occasionally prescribed include clonidine, penfluridol, and pimozide. These drugs can reduce the severity and frequency of tics and may reduce impulsive or aggressive behavior. They also have side effects, however, causing sedation, depression, and weight gain in many patients.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. 4th ed. Arlington, Va.: Author, 2000.

Behrman, Richard E., Robert M. Kliegman, and Hal B. Jenson, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia: Saunders/Elsevier, 2007.

Bloom, Floyd E., M. Flint Beal, and David J. Kupfer, eds. The Dana Guide to Brain Health. New York: Dana Press, 2006.

Brill, Marlene Targ. Tourette Syndrome. Brookfield, Conn.: Millbrook Press, 2002.

Chipps, Esther M., Norma J. Clanin, and Victor G. Campbell. Neurologic Disorders. St. Louis, Mo.: Mosby Year Book, 1992.

Nicholls, John G., A. Robert Martin, and Bruce G. Wallace. From Neuron to Brain. 4th ed. Sunderland, Mass.: Sinauer, 2007.

Victor, Maurice, and Allan H. Ropper. Adams and Victor’s Principles of Neurology. 9th ed. New York: McGraw-Hill, 2009.

Waxman, Stephen G. Correlative Neuroanatomy. 25th ed. New York: Lange Medical Books/McGraw-Hill, 2002.

Woods, Douglas W., and Raymond G. Miltenberger, eds. Tic Disorders, Trichotillomania, and Other Repetitive Behavior Disorders: Behavioral Approaches to Analysis and Treatment. New York: Springer, 2006.

What is Gerson therapy? |

Cancers treated: All

Why performed: The theory behind Gerson therapy is that the body needs to be detoxified frequently in order to treat a disease’s underlying cause. It is theorized that people with cancer may contain levels of sodium in their bodies that are too high relative to the levels of potassium. Eating organic fruits and vegetables and taking supplements are believed to help restore a balance in the body.

Patient preparation: Patients with diabetes, brain metastases, kidney damage, and foreign bodies such as pacemakers and implants and those undergoing chemotherapy should consult a certified Gerson practitioner before beginning treatment.

Steps of the procedure: The therapy is based on maintaining a diet high in vitamins and minerals, which is achieved by consuming juices made from fresh, organic fruits and vegetables, as well as vegetarian meals. Medications are taken orally or injected.

In addition, in order to rid the body of toxins, enemas are administered. They are thought to increase bile flow, which facilitates the removal of toxins as well as the elimination of tumor and diseased tissue that is being broken down. Some items prohibited by the therapy include salt, oil, berries or nuts, coffee, drinking water, animal protein, and bottled, canned, preserved, or frozen food, as well as the use of aluminum utensils.

After the procedure: No special steps are taken following Gerson therapy.

Risks: The solutions used for enemas in Gerson therapy (such as coffee) can cause infections, dehydration, constipation, colitis, electrolyte imbalance, heart and lung problems, and even death. Some additional side effects that have been reported by those using Gerson therapy include dizziness or weakness, abdominal cramps, loss of appetite, diarrhea, aching, fever and sweating, and cold sores. The therapy can be especially problematic in women who are pregnant or breast-feeding.

Results: No conclusive scientific evidence has shown that this therapy is effective in preventing or treating cancer.

"Gerson Regimen." Memorial Sloan Kettering Cancer Center. Memorial Sloan Kettering Cancer Center, 5 Oct. 2012. Web. 6 Oct. 2014.

"Gerson Therapy." American Cancer Society. American Cancer Society, 11 Dec. 2012. Web. 6 Oct. 2014.

"The Gerson Therapy." Gerson Institute. Gerson Institute, 16 Sept. 2011. Web. 6 Oct. 2014.

"Gerson Therapy." National Cancer Institute. Natl. Institutes of Health, 10 Aug. 2012. Web. 6 Oct. 2014.

What is chikungunya? |

Definition

Chikungunya is a relatively rare form of viral infection caused by an alphavirus spread by mosquito bites. It is debilitating but generally nonfatal, with an estimated mortality rate of about one death per one thousand cases.

Causes

Chikungunya is transmitted primarily through two species of mosquito, Aedes aegypti and Aedes albopictus. The mosquitoes become infected when they feed on an infected person during the viraemic period (within five days of the onset of the mosquito bites and symptoms), then transmit the virus to other humans.

Risk Factors

The only known risk factor for chikungunya is an initial exposure to the virus through bites from infected mosquitoes. Before 2013, known outbreaks had occurred primarily in the Eastern Hemisphere, specifically in France, Italy, southern and southeastern Asia, the Arabian Peninsula, central and southern Africa, and various islands in the Indian and Pacific Oceans. In 2013, however, an outbreak of chikungunya in several Caribbean countries marked the first occurrence of the disease in the Americas. Since then, cases have been identified in the United States, Mexico, the Caribbean, Central America, and northern and central South America.

Symptoms

The clinical symptoms of the disease appear within two to twelve days after the initial infection. Symptoms include fever, debilitating joint pains, swelling and stiffness of joints, muscular pain, headache, fatigue, nausea, vomiting, and rash. Many of the clinical symptoms are short in duration, but joint pain can continue for as much as two years after initial infection, in some cases leading to chronic arthritis. Other nonspecific symptoms include conjunctivitis and slight photophobia. Infection with the virus, whether clinically symptomatic or silent, confers lifelong immunity.

Screening and Diagnosis

The common screening and diagnostic confirmation tests for chikungunya include detection of antigens or antibodies in the blood. The common laboratory tests are virus isolation, specific reverse transcription polymerase chain reaction (RT-PCR), and serological tests. The virus isolation test provides the most definitive diagnosis. This technique involves exposing specific cell lines to whole blood samples and identifying chikungunya-specific responses. The RT-PCR uses nested primer pairs to intensify several chikungunya-specific genes from whole blood, while the serological diagnosis uses an enzyme-linked immunoabsorbent assay to measure anti-chikungunya antibody levels of immunoglobulin M and immunoglobulin G.

Treatment and Therapy

There are no specific vaccines or antiviral treatments for chikungunya. Treatments include rest, fluids, and drugs to relieve the symptoms of fever and aching. Commonly used medications include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen. In cases of long-term joint pain, ribavirin or chloroquine may be used. The use of aspirin or corticosteroids is generally discouraged.

Prevention and Outcomes

The best way to prevent chikungunya is through effective control of the host-agent-environment (HAE) epidemiological triad factors to inhibit the spread of disease vectors—in this case, mosquitoes. HAE control consists of ridding the environment of mosquito breeding sites (such as stagnant water), avoiding mosquito bites, and using screens on windows and doors to keep mosquitoes out of the house. Other preventive measures include using insect repellants on exposed skin and wearing bite-proof long sleeves and trousers.

Bibliography

“Chikungunya Virus.” Centers for Disease Control and Prevention. Dept. of Health and Human Services, 16 Nov. 2015. Web. 29 Dec. 2015.

Peters, Clarence J. “Infections Caused by Arthropod- and Rodent-Borne Viruses.” Harrison’s Principles of Internal Medicine. Ed. Dan L. Longo et al. 18th ed. Vol. 1. New York: McGraw, 2012. 1617–32. Print.

Simon, Fabrice, Elodie Vivier, and Philippe Parola. “Chikungunya: An Emerging Disease in Travelers.” Tropical Diseases in Travelers. Ed. Eli Schwartz. Hoboken: Wiley, 2009. 92–100. Print.

Tolle, Michael A. “Mosquito-Borne Diseases.” Current Problems in Pediatric and Adolescent Health Care 39.4 (2009): 97–140. Print.

Calculate the amount of 5.00 M HCl needed to make 50.0 mL of 1.00 M HCl.

Molarity is the ratio of moles of solute to the volume (in liters) of the solvent. Thus, a 1 molar (or 1 M) solution contains 1 mole of a solute dissolved in 1 liter of a solvent. 

Here, we are given 5 M HCl (hydrochloric acid) solution and we have to prepare 50 ml of 1 M solution from it. Since the given solution has a higher concentration (5 M), we can dilute it to...

Molarity is the ratio of moles of solute to the volume (in liters) of the solvent. Thus, a 1 molar (or 1 M) solution contains 1 mole of a solute dissolved in 1 liter of a solvent. 

Here, we are given 5 M HCl (hydrochloric acid) solution and we have to prepare 50 ml of 1 M solution from it. Since the given solution has a higher concentration (5 M), we can dilute it to get a lower concentration (1 M) solution. An easy way to do so is to calculate the number of moles of solute in both the solutions and use it to calculate the required volume.

Molarity = moles / volume

or, moles = molarity x volume = 1 M x 50 ml x 1 lt/1000 ml = 0.05 moles

Thus, 50 ml, 1 M HCl contains 0.05 moles of HCl.

The volume of 5 M HCl that contains the same number of moles of HCl is:

volume = moles/molarity = 0.05 / 5 = 0.01 liter x 1000 ml/liter = 10 ml.

Thus, 10 ml of 5 M HCl is used to prepare 50 ml 1 M solution. We need to mix 40 ml of water to 10 ml of 5 M HCl to get the required solution.

Hope this helps. 

Why are restriction enzymes referred to as scissors?

Restriction enzymes or restriction endonucleases are sometimes called scissors because they are able to cut through the sugar-phosphate backbone of double-stranded DNA. Each restriction endonuclease is able to scan a piece of DNA for a particular 4-6 base pair sequence. Every time this sequence is found, the enzyme cuts through both strands of the DNA.  This cut can be blunt or straight across both strands of DNA or it can be uneven leaving what are...

Restriction enzymes or restriction endonucleases are sometimes called scissors because they are able to cut through the sugar-phosphate backbone of double-stranded DNA. Each restriction endonuclease is able to scan a piece of DNA for a particular 4-6 base pair sequence. Every time this sequence is found, the enzyme cuts through both strands of the DNA.  This cut can be blunt or straight across both strands of DNA or it can be uneven leaving what are called sticky ends where dangling nucleotides are left on the strands.

Restriction endonucleases are important tools for producing recombinant DNA which is used frequently within the field of biotechnology. The endonucleases allow genes to be inserted into plasmids. The gene can be isolated and amplified using primers and a polymerase chain reaction and then a plasmid can be cut open using a restriction endonuclease and the gene can be inserted. Once it is inside of the plasmid, the plasmid can be put into competent bacterial cells so that they can express the gene inserted into the plasmid. Bacteria, especially E. coli, grow very rapidly to produce large populations so it is an efficient way of producing needed proteins like insulin.

What is fracture repair? |

Indications and Procedures

A fracture is a break in a bone, either partial or complete, resulting from an applied force that is greater than the bone’s internal strength. The most common causes of fractures are accidents and trauma.

Fractures are usually treated by reduction and immobilization. Reduction, which may be either closed or open, refers to the process of returning the fractured bones to their normal position. Closed reduction is accomplished without surgery by manipulating the broken bone through overlying skin and muscles. Open reduction requires surgical intervention. The broken pieces are exposed and returned to their normal positions. Orthopedic appliances may be used to hold the bones in the proper position (internal fixation); the most common appliances are stainless-steel pins and screws, but metal plates and wires may also be employed. These devices can be left in the body indefinitely or may be surgically removed after healing is complete. Local anesthesia is usually used with closed reductions; open reductions are performed in an operating room under sterile conditions, using general anesthesia.

After reduction, the broken bone and accompanying body part must be placed in an anatomically neutral position. Immobilization is generally accomplished by the use of a cast. Casts are usually made of plaster, but they may be constructed of inflatable plastic.

Individual ends of a single fractured bone are sometimes held in position by external pins and screws (external fixation). Holes are drilled through the bone, and pins are inserted as described above. The pins on opposite sides of the fracture site are then attached to each other with threaded rods and locked in position by nuts. This process allows a fractured bone to be immobilized without using a cast.

Traction, the external application of force to overcome muscular resistance and hold bones in a desired position, may also be used to immobilize a fracture. Commonly, holes are drilled through bones and pins are inserted; the ends of these pins extend through the surface of the skin. Part of the body is fixed in position through the use of a strap or weights. Wires are attached to the pins in the body part to be stretched. Force is applied to the wires via weights or tension until the broken bone parts are in the desired position. Traction is maintained until complete healing has occurred.

Uses and Complications

All broken bones must be held in position until healing takes place. The complications associated with repairing fractures include infection, which is rare, and loss of function. The potential for loss of function is minimized by placing the limb in an anatomically neutral position prior to the application of a cast.

The techniques of fracture repair have not changed radically in decades. New methods, however, are being tried. For example, electromagnetic fields are used with fractures that do not heal spontaneously. Such fields induce the growth of osteoblasts, which are bone-forming cells.

Bibliography

Browner, Bruce D., et al. Skeletal Trauma: Basic Science, Management, and Reconstruction. 4th ed. Philadelphia: Saunders/Elsevier, 2009.

Eiff, M. Patrice, and Robert L. Hatch. Fracture Management for Primary Care. 3d ed. Philadelphia: Saunders/Elsevier, 2012.

“Fractures.” MedlinePlus, May 15, 2013.

Gregg, Paul J., Jack Stevens, and Peter H. Worlock. Fractures and Dislocations: Principles of Management. Cambridge, Mass.: Blackwell Science, 1996.

Gustilo, Ramon B., Richard F. Kyle, and David C. Templeman, eds. Fractures and Dislocations. St. Louis, Mo.: Mosby, 1993.

“Helping Fractures Heal (Orthobiologics).” OrthoInfo, January 2010.

Hodgson, Stephen F., ed. Mayo Clinic on Osteoporosis: Keeping Bones Healthy and Strong and Reducing the Risk of Fractures. Rochester, Minn.: Mayo Clinic, 2003.

Magee, David J. Orthopedic Physical Assessment. 5th ed. St. Louis, Mo.: Saunders/Elsevier, 2008.

Ruiz, Ernest, and James J. Cicero, eds. Emergency Management of Skeletal Injuries. St. Louis, Mo.: Mosby, 1995.

Salter, Robert Bruce. Textbook of Disorders and Injuries of the Musculoskeletal System. 3d ed. Baltimore: Williams & Wilkins, 1999.

What are birth defects? |

Causes and Symptoms

As the human embryo develops, it undergoes many formative stages from the simple to the complex, most often culminating in a perfectly formed newborn infant. The formation of the embryo is controlled by genetic factors, external influences, and interactions between the various embryonic tissues. Because genes play a vital role as the blueprint for the developing embryo, they must be unaltered and the cellular mechanisms that allow the genes to be expressed must also work correctly. In addition, the chemical and physical communications between cells and tissues in the embryo must be clear and uninterrupted. The development of the human embryo into a newborn infant is infinitely more complex than the design and assembly of the most powerful supercomputer or the largest skyscraper. Because of this complexity and the fact that development progresses without supervision by human eye or hand, there are many opportunities for errors that can lead to malformations.

Errors in development can be caused by both genetic and environmental factors. Genetic factors include chromosomal abnormalities and gene mutations. Both can be inherited from the parents or can occur spontaneously during gamete formation, fertilization, and embryonic development. Environmental factors, called teratogens, include such things as drugs, disease organisms, and radiation.

Chromosomal abnormalities account for about 6 percent of human congenital malformations. They fall into two categories, numerical and structural. Numerical chromosomal abnormalities are most often the result of nondisjunction occurring in the germ cells that form sperm and eggs. During the cell division process in sperm and egg production, deoxyribonucleic acid (DNA) is duplicated so that each new cell receives a complete set of chromosomes. Occasionally, two chromosomes fail to separate (nondisjunction), such that one of the new cells receives two copies of that chromosome and the other cell none. Both of the resulting gametes (either sperm or eggs) will have an abnormal number of chromosomes. When a gamete with an abnormal number of chromosomes unites with a normal gamete, the result is an individual with an abnormal chromosome number. The missing or extra chromosome will cause confusion in the developmental process and result in certain structural and functional abnormalities. For
example, persons with an extra copy of chromosome number 21 suffer from Down syndrome, which often includes mental deficiency, heart defects, facial deformities, and other symptoms and can be caused by nondisjunction in one or more cells of the early embryo. Abnormal chromosome numbers may also result from an egg’s being fertilized by two sperm, or from failure of cell division during gamete formation.

Structural chromosomal abnormalities result from chromosome breaks. Breaks occur in chromosomes during normal exchanges in material between chromosomes (crossing over). They also may occur accidentally at weak points on the chromosomes, called fragile sites, and can be induced by chemicals and radiation. Translocations occur when a broken-off piece of chromosome attaches to another chromosome. For example, an individual who has the two usual copies of chromosome 21 and, as the result of a translocation, carries another partial or complete copy of 21 riding piggyback on another chromosome will have the symptoms of Down syndrome. Deletions occur when a chromosome break causes the loss of part of a chromosome. The cri du chat syndrome is caused by the loss of a portion of chromosome number 5. Infants affected by this disorder have a catlike cry, are intellectually and developmentally disabled, and have cardiovascular defects. Other structural chromosomal abnormalities include inversions (in which segments of chromosomes are attached in reverse order), duplications (in which portions of a chromosome are present in multiple copies), and isochromosomes (in which
chromosomes separate improperly to produce the wrong configuration).

Gene mutations (defective genes) are responsible for about 8 percent of birth defects. Mutations in genes occur spontaneously because of copying errors or can be induced by environmental factors such as chemicals and radiation. The mutant genes are passed from parents to offspring; thus certain defects may be present in specific families and geographical locations. Two examples of mutation-caused defects are
polydactyly (the presence of extra fingers or toes) and microcephaly (an unusually small cranium and brain). Mutations can be either dominant or recessive. If one of the parents possesses a dominant mutation, there will be a 50 percent chance of this mutant gene being transmitted to the offspring. Brachydactyly, or abnormal shortening of the fingers, is a dominantly inherited trait. Normally, the parent with the dominant gene also has the disorder. Recessive mutations can remain hidden or unexpressed in both parents. When each parent possesses a single recessive gene, there is a 25 percent chance that any given pregnancy will result in a child with a defect. Examples of recessive defects are the metabolic disorders
sickle cell disease and hemophilia.

Environmental factors called
teratogens are responsible for about 7 percent of congenital malformations. Human embryos are most sensitive to the effects of teratogens during the period when most organs are forming (organogenetic period), that is, from about fifteen to sixty days after fertilization. Teratogens may interfere with development in a number of ways, usually by killing embryonic cells or interrupting their normal function. Cell movement, communication, recognition, differentiation, division, and adhesion are critical to development and can be easily disturbed by teratogens. Teratogens can also cause mutations and chromosomal abnormalities in embryonic cells. Even if the disturbance is only weak and transitory, it can have serious effects because the critical period for the development of certain structures is very short and well defined. For example, the critical period for arm development is from twenty-four to forty-four days after fertilization. A chemical that interferes with limb development, such as the drug thalidomide, if taken during this period, may cause missing arm parts, shortened arms, or complete absence of
arms. Many drugs and chemicals have been identified as teratogenic, including alcohol, aspirin, and certain antibiotics.

Other environmental factors that can cause congenital malformations include infectious organisms, radiation, and mechanical pressures exerted on the fetus within the uterus. Certain infectious agents or their products can pass from the mother through the placenta into the embryo. Infection of the embryo causes disturbances to development similar to those caused by chemical teratogens. For example, German measles (rubella virus) causes cataracts, deafness, and heart defects if the embryo is infected early in development. Exposure to large doses of radiation—such as those released by the accident at the Chernobyl nuclear power plant in 1986 or by the atomic bombs dropped on Hiroshima and Nagasaki, Japan, during World War II—can result in death and damage to embryonic cells. There was an increase of about 10 to 15 percent in birth defects in children born to pregnant women exposed to atomic bomb radiation in Japan. Diagnostic X-rays are not known to be a cause of birth
defects. Some defects such as hip dislocation may be caused by mechanical forces inside the uterus; this could happen if the amnion is damaged or the uterus is malformed, thus restricting the movement of the fetus. About 25 percent of congenital defects are caused by the interaction of genetic and environmental factors (multifactorial), and the causes of more than half (54 percent) of all defects are unknown.

Treatment and Therapy

Because many birth defects have well-defined genetic and environmental causes, they often can be prevented. Preventive measures need to be implemented if the risk of producing a child with a birth defect is higher than average. Genetic risk factors for such defects include the presence of a genetic defect in one of the parents, a family history of genetic defects, the existence of one or more children with defects, consanguineous (same-family) matings, and advanced maternal age. Prospective parents with one or more of these risk factors should seek
genetic counseling in order to assess their potential for producing a baby with such defects. Also, parents exposed to higher-than-normal levels of drugs, alcohol, chemicals, or radiation are at risk of producing gametes that may cause defects, and pregnant women exposed to the same agents place the developing embryo at risk. Again, medical counseling should be sought by such prospective parents. Pregnant women should maintain a well-balanced diet that is about 200 calories higher than normal to provide adequate
fetal nutrition. Women who become anemic during pregnancy may need an iron supplement, and the U.S. Public Health Service recommends that all women of childbearing age consume 0.4 milligram of folic acid (one of the B vitamins) per day to reduce the risk of spina bifida and other neural tube defects. Women at high risk for producing genetically defective offspring can undergo a screening technique whereby eggs taken from the ovary are screened in the laboratory to select the most normal appearing ones prior to in vitro fertilization and then returned to the uterus. Some couples may decide to use artificial insemination by donor if the prospective father is known to carry a defective gene.

The early detection of birth defects is crucial to the health of both the mother and the baby. Physicians commonly use three methods for monitoring fetal growth and development during pregnancy. The most common method is ultrasound scanning. High-frequency sound waves are directed at the uterus and then monitored for waves that bounce back from the fetus. The return waves allow a picture of the fetus to be formed on a television monitor, which can be used to detect defects and evaluate the growth of the fetus. In
amniocentesis, the doctor withdraws a small amount of amniotic fluid containing fetal cells; both the fluid and the cells can be tested for evidence of congenital defects by growing the cells in tissue culture and examining their chromosomes. Amniocentesis generally cannot be performed until the sixteenth week of pregnancy. Another method of obtaining embryonic cells is called
chorionic villus sampling and can be done as early as the fifth week of pregnancy. A tube is inserted into the uterus in order to retrieve a small sample of placental chorionic villus cells, identical genetically to the embryo. Again, these cells can be tested for evidence of congenital defects. The early discovery of fetal defects and other fetal-maternal irregularities allows the physician time to assess the problem and make recommendations to the parents regarding treatment. Many problems can be solved with therapy, medications, and even prenatal surgery. If severe defects are detected, the physician may recommend termination of the pregnancy.

Children born with defects often require highly specialized and intense medical treatment. For example, a child born with
spina bifida may have lower-body paralysis, clubfoot, hip dislocation, and gastrointestinal and genitourinary problems in addition to the spinal column deformity. Spina bifida occurs when the embryonic neural tube and vertebral column fail to close properly in the lower back, often resulting in a protruding sac containing parts of the spinal meninges and spinal cord. The malformation and displacement of these structures result in nerve damage to the lower body, causing paralysis and the loss of some neural function in the organs of this area. Diagnostic procedures including X-rays, computed tomography (CT) scans, and urinalysis are carried out to determine the extent of the disorder. If the sac is damaged and begins to leak cerebrospinal fluid, it needs to be closed immediately to reduce the risk of meningitis. In any case, surgery is done to close the opening in the lower spine, but it is not possible to
correct the damage done to the nerves. Urgent attention must also be given to the urinary system. The paralysis often causes loss of sphincter muscle control in the urinary bladder and rectum. With respect to the urinary system, this lack of control can lead to serious urinary tract infections and the loss of kidney function. Both infections and obstructions must be treated promptly to avoid serious complication. Orthopedic care needs to begin early to treat clubfoot, hip dislocation, scoliosis, muscle weakness, spasms, and other side effects of this disorder.

The medical treatment of birth defects requires a carefully orchestrated team approach involving physicians and specialists from various medical fields. When the abnormality is discovered (before birth, at birth, or after birth), the primary physician will gather as much information as possible from the family history, the medical history of the patient, a physical examination, and other diagnostic tests. This information is interpreted in consultation with other physicians in order to classify the disorder properly and to determine its possible origin and time of occurrence. This approach may lead to the discovery of other malformations, which will be classified as primary and secondary. When the physician arrives at a specific overall diagnosis, he or she will counsel the parents about the possible causes and development of the disorder, the recommended treatment and its possible outcomes, and the risk of recurrence in a subsequent pregnancy. Certain acute conditions may require immediate attention in order to save the life of the newborn.

In addition to treating the infant with the defect, the physician needs to counsel the parents in order to answer their questions. The counseling process will help them to understand and accept their child’s condition. To promote good parent-infant bonding, the parents are encouraged to maintain close contact with the infant and participate in its care. Children born with severe chronic disabilities and their families require special support. When parents are informed that their child has limiting congenital malformations, they may react negatively and express feelings of shock, grief, and guilt. Medical professionals can help the parents deal with their feelings and encourage them to develop a close and supportive relationship with their child. Physicians can provide a factual and honest appraisal of the infant’s condition and discuss treatments, possible outcomes, and the potential for the child to live a happy and fulfilling life. Parents are encouraged to learn more about their child’s disorder and to seek the guidance and help of professionals, support groups, family, and friends. With the proper care and home environment, the child can develop into an individual who is able to interact positively with family and community.

Perspective and Prospects

Birth defects have been recognized and recorded throughout human history. The writer of the Old Testament book of 2 Samuel (21:20) describes the defeat of a giant with six fingers and six toes. Defects were recorded in prehistoric art, and the cuneiform records of ancient Babylon considered birth defects to be omens of great significance. Aristotle described many common human birth defects such as polydactyly. Superstitions about birth defects abounded during the Middle Ages. People believed that events occurring during pregnancy could influence the form of the newborn; for example, deformed legs could be caused by contact with a cripple. Mothers of deformed children were accused of having sex with animals. In a book written about birth defects in 1573, Monstres et prodiges, Ambroise Paré describes many human anomalies and attempts to explain how they occur. Missing body parts such as fingers or toes were attributed to a low sperm count in the father, and certain characteristics such as abnormal skin
pigmentation, body hair, or facial features were said to be influenced by the mother’s thoughts and visions during and after conception.

With advances in science and medicine these superstitions were swept aside. Surgery for cleft palate was performed as early as 1562 by Jacques Honlier. William Harvey, a seventeenth-century English physician, recognized that some birth defects such as cleft lip are normal embryonic features that accidentally persist until the time of birth. The study of embryology, including experiments on bird and amphibian embryos, blossomed as a science during the nineteenth century, leading to a better understanding of how defects arise. At the same time, physicians were developing improved ways to treat birth defects. By 1816, Karl von Graefe had developed the first modern comprehensive surgical method for repairing cleft palate. The modern technique for repairing congenital pyloric stenosis (narrowing of the junction between the stomach and small intestine) was developed by Conrad Ramstedt in 1912. The principles of genetic inheritance developed by Gregor Mendel in the mid-nineteenth century were rediscovered by biologists at the beginning of the twentieth century and soon were applied to the study of human heredity, including
the inheritance of birth defects. Geneticists realized that defects such as hemophilia and Down syndrome are inherited diseases. Beginning in the 1930s, other scientists began to show that congenital defects could be induced in experimental animals by such factors as dietary deficiencies, hormone imbalances, chemicals, and radiation. In some cases, a lack of complete testing of environmental factors such as drugs has led to tragedies but also a better understanding of the nature of birth defects. The tranquilizer
thalidomide caused limb malformations in more than seven thousand children in Europe before it was withdrawn from the market in 1961. Pregnant women treated for cervical cancer in the 1960s with large doses of radiation bore children with defects and developmental disabilities.

Indeed, much of the medical and environmental health research today centers on the effects of drugs, toxic chemicals, radiation, and other factors on human health and development. Genetic counseling and testing of parents at risk for inherited defects has become an accepted part of medical practice. In addition, there have been many advances in the treatment of congenital defects since the 1950s. Modern orthopedic and plastic surgery is used to correct such problems as clubfoot and cleft palate. Transplants are used to correct deficiencies of the liver, kidneys, and other organs. Biomedical engineers have developed improved prosthetic devices to replace lost limbs and to aid in hearing, speaking, and seeing. An understanding of metabolic disorders such as phenylketonuria (PKU) has led to better treatment that utilizes special diets and medications. Because it is difficult to undo the damage of congenital defects fully, the most promise seems to be in the areas of prevention and protection. Prospective parents and their medical care providers need to be alert to potential hereditary problems, as well as to exposure to hazardous
environmental agents. Pregnant women need to maintain a healthy diet and check with their physicians before taking any drugs. With advances in preventive medicine, diagnosis, and treatment, the future is much brighter for reducing the health toll of congenital malformations.

Bibliography:

"Birth Defects." MedlinePlus, May 2, 2013.

"Birth Defects: Overview." National Institute of Child Health and Human Development, Apr. 3, 2013.

"Birth Defects: What They Are and How They Happen." March of Dimes, 2013.

"Facts about Birth Defects." Centers for Disease Control and Prevention, Feb. 24, 2011.

Heyman, Bob, and Mette Henriksen. Risk, Age, and Pregnancy: A Case Study of Prenatal Genetic Screening and Testing. New York: Palgrave, 2001.

Moore, Keith L., and T. V. N. Persaud. The Developing Human. 8th ed. Philadelphia: Saunders/Elsevier, 2008.

Nixon, Harold, and Barry O’Donnell. The Essentials of Pediatric Surgery. 4th ed. Boston: Butterworth Heinemann, 1992.

Sadler, T. W. Langman’s Medical Embryology. 12th ed. Philadelphia: Lippincott Williams & Wilkins, 2012.

Sherwood, Lauralee. Human Physiology: From Cells to Systems. 8th ed. Pacific Grove, Calif.: Brooks/Cole/Cengage Learning, 2013.

Stray-Gundersen, Karen, ed. Babies with Down Syndrome. Rev. ed. Kensington, Md.: Woodbine House, 1995.

What are bedsores? |

Causes and Symptoms

Bedsores are caused by sustained pressure on the skin, blocking blood flow. Impaired circulation causes the skin tissue to die and tear.

Persons at risk for bedsores include the bedridden, wheelchair-bound, immobile, or unconscious. Paraplegics and others with spinal cord disease or neuromuscular injuries are at risk because of their inability to sense pain in affected limbs or because of sitting in a wheelchair. Bed-bound persons who lie in one position for extended lengths of time may develop bedsores. The malnourished may experience bedsores as a result of little padding over bony areas. The elderly prove more vulnerable to bedsores because of thin skin, decreased circulation, and restricted mobility. Chronic diseases such as diabetes, urinary incontinence, or vascular disease can increase the risk of bedsores.

Bedsores typically occur in the skin over bony areas such as the elbows, heels, ankles, back, lower spine or tailbone, hips, shoulders, and back of the head. In the early stage, the skin becomes red, soft, and warm to the touch. If pressure is relieved by changing body position, then the skin will heal. If the pressure continues, however, then the skin may blister and then break down, leaving an open wound. Without intervention, the bedsore can progress to skin cell death, with damage to deeper levels of skin or muscle. An advanced bedsore smells odorous and becomes infected without proper treatment. Unattended, the bedsore can result in infection leading to fever, confusion, and death.

Treatment and Therapy

Certain measures can prevent or minimize the development of bedsores in persons at risk. Relief from pressure on the skin by frequently changing body position is critical. Other approaches include keeping the skin clean and dry, minimizing friction against the skin, and maintaining healthy nutrition.

Treatment for bedsores includes monitoring the skin for redness and taking immediate measures to minimize further breakdown. The bedsore should be cleansed and covered with a dressing as prescribed by the health-care provider. Dead tissue can be removed to prevent infection and encourage healing through surgical debridement or mechanical debridement by gentle scrubbing or wound irrigation. Enzyme preparations are available to dissolve dead tissue. Antibiotic solutions can be applied to the bedsore and oral antibiotics can be taken to decrease the risk of secondary infections.

Bibliography

Brown, Pamela. Quick Reference to Wound Care. Sudbury, Mass.: Jones and Bartlett, 2009.

MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); [updated 2005 Aug 12]. Pressure Sores; updated 2013 Aug. 26; reviewed 2013 June 5; cited 2013 Aug. 29; about 2 p.

Ousey, Karen. Pressure Area Care. Malden, Mass.: Blackwell, 2005.

Pieper, Barbara. Pressure Ulcers: Prevalence, Incidence, and Implications for the Future. Washington, D.C.: National Pressure Ulcer Advisory Panel, 2012.

Webster, J. G. Prevention of Pressure Sores: Engineering and Clinical Aspects. New York: Taylor & Francis, 1991.

What are nausea and vomiting?

Causes and Symptoms

Nausea is defined as a subjectively unpleasant sensation associated with awareness of the urge to vomit. It is usually felt in the back of the throat and epigastrium and is accompanied by the loss of gastric tone, duodenal contractions, and reflux of the intestinal contents into the stomach. Retching is defined as labored, spasmodic, rhythmic contractions of the respiratory muscles (including the diaphragm, chest wall, and abdominal wall muscles) without the expulsion of gastric contents. Vomiting, or emesis, is the forceful expulsion of gastric contents from the mouth and is brought about by the powerful sustained contraction of the abdominal muscles, the descent of the diaphragm, and the opening of the gastric cardia (the cardiac orifice of the stomach).

Nausea and vomiting are important defense mechanisms against the ingestion of toxins. The act of emesis involves a sequence of events that can be divided into three phases: preejection, ejection, and postejection. The preejection phase includes the symptoms of nausea, along with salivation, swallowing, pallor, and tachycardia (an abnormally fast heartbeat). The ejection phase comprises retching and vomiting. Retching is characterized by rhythmic, synchronous, inspiratory movements of the diaphragm and the abdominal and external intercostal muscles, while the mouth and the glottis are kept closed. As the antral (cavity) portion of the stomach contracts, the proximal (nearest the center) portion relaxes, and the gastric contents oscillate between the stomach and the esophagus. During retching, the hiatal portion of the diaphragm does not relax, and intra-abdominal pressure increases are associated with a decrease in intrathoracic pressure.

In contrast, relaxation of the hiatal portion of the diaphragm (near the esophagus) permits a transfer of intra-abdominal pressure to the thorax during the act of vomiting. Contraction of the muscles of the anterior abdominal wall, relaxation of the esophageal sphincter, an increase in intrathoracic and intragastric pressure, reverse peristalsis (movement of the contents of the alimentary canal), and an open glottis and mouth result in the expulsion of gastric contents. The postejection phase consists of autonomic and visceral responses that return the body to a quiescent phase, with or without residual nausea.

The complex act of vomiting, involving coordination of the respiratory, gastrointestinal, and abdominal musculature, is controlled by what researchers label the emetic center. This center in the brain stem has access to the motor pathways responsible for the visceral and somatic output involved in vomiting, and stimuli from several areas within the central nervous system can affect this center. These include afferent (inward-directed) nerves from the pharynx and gastrointestinal tract, as well as afferents from the higher cortical centers (including the visual center) and the chemoreceptor trigger zone (CTZ) in the area postrema (a highly vascularized area of the brain stem). The CTZ can be activated by chemical stimuli received through the blood or the cerebrospinal fluid. Direct electrical stimulation of the CTZ, however, does not result in emesis.

Clinical assessment of nausea and vomiting usually focuses on the occurrence of vomiting, namely the frequency and number of episodes. Nausea, however, is a subjective phenomenon unobservable by another. Few data-collection instruments that measure separately the patient’s experience of nausea and vomiting and his or her symptom of distress have been reported in the literature. In fact, the Rhodes Index of Nausea and Vomiting (INV) Form 2 is the only available tool that measures the individual components of nausea, vomiting, and retching. This index measures the patient’s perception of the duration, frequency, and distress from nausea; the frequency, amount, and distress from vomiting; and the frequency, amount, and distress from retching (dry heaves). The INV score provides a measurement of the total symptom experience of the patient.

While the causes of nausea and vomiting are numerous, including gastrointestinal diseases, infections, intracranial disease, toxins, radiation sickness, psychological trauma, migraines, and circulatory syncope, three of the most common causes are motion sickness (air, sea, land, or space), pregnancy, and anesthesia administered during operative procedures.

The sequence of symptoms and signs that constitute motion sickness is fairly characteristic. Premonitory symptoms often include yawning or sighing, lethargy, somnolence, and a loss of enthusiasm and concern for the task at hand. Increasing malaise is directed toward the epigastrium, a sensation best described as “stomach awareness,” which progresses to nausea. Diversion of the blood flow from the skin toward the muscles results in pallor. A feeling of warmth and a desire for cool air is often accompanied by sweating. Frontal headache and a sensation of disorientation, dizziness, or light-headedness may also occur. Vomiting occurs early in the sequence of symptoms for some; in others, malaise is severe and prolonged, and vomiting is delayed. After vomiting, there is often a temporary improvement in well-being; however, with continued provocative motion, symptoms build again and vomiting recurs. The symptoms may last for minutes, hours, or even days.

The most coherent explanation for the development of motion sickness is provided by sensory conflict theory. Motion sickness is generally thought to occur as the result of a “sensory conflict” between information arising from the semicircular canals and organs of the vestibular system, visual and other sensory input, and the input that is expected on the basis of past experience or exposure history. It is argued that conflicts between current sensory inputs are by themselves insufficient to produce motion sickness, since adaptation occurs even though the conflicting inputs continue to be present. Visual input alone, however, can produce symptoms of motion sickness, such as watching motion pictures shot from a moving vehicle or looking out of the side window (as opposed to the front window) of a moving vehicle.

Nausea and vomiting in the early morning during pregnancy, so-called morning sickness, is so common that it is accepted as a symptom of normal pregnancy. Occurring soon after waking, it more often takes the form of retching rather than actual vomiting and usually does not disturb the woman’s health or her pregnancy. The symptoms nearly always cease before the fourteenth week of pregnancy. In a very small number of cases—approximately 0.3 percent to 2 percent of pregnancies—the vomiting becomes more serious and persistent, occurring throughout the day and even during the night. The term “hyperemesis gravidarum” is given to this serious form of vomiting. Theories on the etiology of morning sickness have tended to be grouped under four main areas: endocrine (caused by estrogen and progesterone levels), psychosomatic (a conscious or unconscious wish not to be pregnant), allergic (a histamine reaction), and metabolic (a lack of potassium).

Nausea and vomiting occur frequently as unpleasant side effects of the administration of anesthesia in many clinical procedures. Most postoperative vomiting is mild, and only in a few cases will the problem persist so as to cause electrolyte disturbances and dehydration. The factors affecting postoperative nausea and vomiting (PONV) may be divided into two categories: the type of patient and surgery, and the anesthetic and preoperative and postoperative medications used. Patients with a history of motion sickness have a predisposition to PONV. An article published in OR Nurse 2012 reported that approximately 30 percent of surgical patients experience PONV within the first twenty-four hours after surgery, while patients with a history of either PONV or motion sickness are two to three times more likely to experience PONV in the future. The length of the surgical procedure is also a factor; a procedure lasting 30 minutes or less carries a 28 percent risk of PONV, while a procedure lasting between 151 and 180 minutes carries a 46.2 percent risk.

No direct association between vomiting and age has been found. That vomiting may be hormonally related, however, is suggested by the higher incidence of nausea and vomiting in women, particularly women in the latter half of their menstrual cycles. Other factors that may affect nausea and vomiting associated with anesthesia include patient weight (female obese patients being particularly more vulnerable), degree of hydration, metabolic status, and psychological state. With regard to the type of surgery performed, the highest incidences of nausea and vomiting appear to be associated with abdominal surgery and ear, nose, and throat surgery, with middle-ear surgery being the major category.

Most of the causes of vomiting associated with general anesthesia are expected to be eliminated with regional or spinal anesthesia. The type of anesthesia used also has an effect on nausea and vomiting. Research indicates that cyclopropane, ether, and nitrous oxide are potent emetics.

Treatment and Therapy

Since the generation of sensory conflict underlies all motion environments that give rise to motion sickness, practical measures that reduce conflict are likely to reduce the incidence. Motion sickness can be minimized if the subject has the widest possible view of a visual reference in which the earth is stable. Passengers aboard ships are less likely to be seasick if they remain on deck at midship, where vertical motion is minimized, and view the horizon. In a car or bus, individuals should be in a position to see the road directly ahead, since the movement of this visual scene will correlate with the changes in the direction of the vehicle. While head movements in a rotating environment are known to precipitate motion sickness, there is no clear experimental evidence that they elicit nausea in mild linear oscillation. Thus, some nonpharmacologic remedies for motion sickness include restricting head movements, lying in a supine position, and closing one's eyes. In addition, the use of acupressure wrist bands has proven effective in combating motion sickness.

Pharmacologically, the drug hyoscine hydrobromide (also called hyoscine or scopolamine) emerged as a valuable prophylactic drug following extensive research during World War II into the problems of motion sickness in troops transported in aircraft, ships, and landing craft. It remains one of the most effective drugs for short-duration exposures to provocative motion. Doses in excess of 0.6 milligram, however, are very likely to lead to drowsiness, and there is much experimental evidence that the drug impairs short-term memory. Hyoscine can be absorbed transdermally, and in order to extend the duration of action, a controlled-release patch was developed to deliver 1.2 milligrams on application and 0.01 milligram hourly thereafter. There is substantial evidence of its sustained effectiveness, but, perhaps as a result of variable absorption rates, there is an increased risk of blurred vision after more than twenty-four hours of use.

Amphetamines, ephedrine, and a number of antihistamines (such as dimenhydrinate) have been found to be clinically useful in motion sickness. Following oral administration, these drugs are generally slower than hyoscine in reaching their peak efficacy, but they have a longer duration of action.

For most susceptible subjects whose exposure to motion-sickness-inducing stimuli is infrequent, prophylactic drugs offer the only useful treatment. When exposure to provocative stimuli is more frequent, as in the case of professional aircraft pilots, spontaneous adaption typically occurs during training, and an initially high incidence of motion sickness decreases with time.

In medical conditions in which the cause is relatively unknown, it is usual to find a wide variety of suggested therapies, and morning sickness and hyperemesis gravidarum are no exception. Suggested therapy is mainly drugs of the antiemetic variety; however, since the thalidomide tragedy, in which severe deformities occurred in the children of women who took thalidomide while pregnant, there has been a reluctance to use drugs of any kind during early pregnancy. Probably the only value of drug therapy is at the stage of morning sickness, when antiemetics or mild sedatives may counter the feeling of nausea and prevent women from experiencing excessive vomiting and entering the vicious cycle of dehydration, starvation, and electrolyte imbalance. Once the patient has reached the stage of hyperemesis gravidarum, much more basic therapy is required, including correction of dehydration, carbohydrate deficiency, and ionic deficiencies. This program is best managed by intravenous therapy, with or without the addition of vitamin supplements and sedative agents.

Nonpharmacologic self-care actions for morning sickness fall into the three broad categories: manipulating diet, adjusting behavior, and seeking emotional support. Some of the most effective self-care actions are getting rest, eating several small meals rather than three large ones, avoiding bad smells, avoiding greasy or fried foods, avoiding cooking, and receiving extra attention and support.

In terms of PONV caused by anesthesia, it has been found that routine antiemetic prophylaxis of patients undergoing elective surgical procedures is not indicated. Of those who develop these symptoms, many have transient nausea or only one or two bouts of emesis and do not require antiemetic therapy. In addition, commonly used antiemetic drugs can produce significant side effects, such as sedation. Nevertheless, antiemetic prophylaxis may be justified in those patients who are at greater risk for developing PONV. Such therapy is often given to patients with a history of motion sickness, as well as those undergoing gynecologic procedures, inner-ear procedures, oral surgery (in which the jaws are occluded by wires, causing a high risk of breathing in vomitus), operations on the ear or eye, and plastic surgery (in order to avoid disruption of delicate surgical work).

Many different antiemetic drugs are available for the treatment of PONV. Researchers have found it difficult to interpret the results of antiemetic drug studies because the severity of PONV and the response to therapeutic agents can be influenced by many other variables. Even when the same drugs are used in a homogeneous population undergoing the same procedure, the severity of emesis varies from individual to individual.

Because antiemetic drugs have differing sites of action, better results can be obtained by using a multidrug approach. If a combination of drugs with similar sites of action is used, however, the incidence of side effects may be increased. There is little data regarding combination antiemetic prophylaxis or therapy for PONV. Drug combinations have been avoided in postsurgical patients because of concerns about additive central nervous system toxicity. One exception is the combination of low-dose droperidol and metoclopramide, which appears to be more effective than droperidol alone for outpatient gynecologic procedures.

Although a full stomach is best avoided before any operative procedure, in certain situations, such as emergencies, where danger from vomiting is acute, a rapid sequence of administering anesthesia (induction) and clearing the air passage (intubation) remains the method of choice to avoid nausea and vomiting in patients with a full stomach. After the procedure, it is recommended that the patient minimize movement in order to avoid nausea and vomiting. It has been found that avoiding solid food for at least eight hours after a surgical procedure is helpful in preventing postoperative nausea and vomiting.

Perspective and Prospects

Though it has existed for as long as there have been human beings, the symptom of nausea has never received much attention in health care practice or research. In fact, until the early 1970s, the sensation was frequently dismissed as merely a passing phenomenon. The rationale for this dismissal was most likely the knowledge that nausea is self-limiting (it always passes with time); is never life-threatening in itself; is probably psychogenic in nature, at least to some degree; and, being subjective, is very difficult to measure. In addition, in the past, the most predictable nausea was related to pregnancy, which may also explain the lack of attention.

Until the late 1980s, there was still little research being conducted on nausea associated with pregnancy, although it is a common symptom. The historical lack of interest in nausea and vomiting during pregnancy may be traced to the fact that because the symptoms generally persist only through the first trimester, health-care professionals have viewed the problem as relatively insignificant. As more pregnant women work outside the home in demanding positions, however, they have exhibited less tolerance for illness. Demands on the health-care industry and on personal physicians for more research and effective treatment have become more widespread.

While it is surprising that nausea has received scant attention in the history of clinical research, it is even more astonishing that vomiting, an observable behavior, has received so little attention as well. Although vomiting is a primitive neurologic process that has remained almost unchanged in the evolution of animals, the mechanisms that regulate the behavior remain virtually unknown.

One reason for the paucity of information on the subject of nausea in particular stems from the lack of a reliable animal model. This fact has hampered research aimed at establishing the etiological basis for nausea and its relationship to vomiting. While some species of lower animals, such as rats, cannot vomit, it is not known whether they experience the phenomenon of nausea. Thus, no effective means of measuring nausea in lower animals has been devised.

Since the early 1970s, there has been a noticeable increase in research on nausea as a drug side effect because it is so frequently seen in chemotherapy treatment for cancer. As more powerful chemotherapy agents and aggressive combinations were clinically investigated, patients began to experience severe, potentially life-threatening nausea and vomiting. Older drugs such as antihistamines, phenothiazines, and benzodiazepines are still used for their antiemetic characteristics, but they are augmented by newer agents such as benzamides, neurokinin-1-receptor antagonists, and serotonin antagonists.

Another interesting branch of scientific investigation has begun exploring alternative ways of managing these symptoms. Behavioral interventions, such as progressive muscle relaxation, biofeedback, imagery, and music therapy, have been used to alleviate postchemotherapy anxiety. These methods may also be used to treat other patients suffering from the symptoms of nausea and vomiting, such as pregnant women.

Another noninvasive, nonpharmacologic measure that has been considered in the relief of nausea and vomiting is transcutaneous electrical nerve stimulation (TENS). Several research studies indicate that TENS may be useful in alleviating chemotherapy-related nausea and vomiting, including delayed nausea and vomiting. Side effects from using TENS units are negligible, and with further study they may prove to be an acceptable, helpful relief measure.

Bibliography

Blum, Richard H., and W. LeRoy Heinrichs. Nausea and Vomiting: Overview, Challenges, Practical Treatments, and New Perspectives. Philadelphia: Whurr, 2000. Print.

Casey, Georgina. "Treating Nausea and Vomiting." Kai Tiaki Nursing New Zealand 18.11 (2012): 20–24. Print.

Edmundowicz, Steven A., ed. Twenty Common Problems in Gastroenterology. New York: McGraw, 2002. Print.

Funk, Sandra G., et al., eds. Key Aspects of Comfort: Management of Pain, Fatigue, and Nausea. New York: Springer, 1989. Print.

Hesketh, Paul J., ed. Management of Nausea and Vomiting in Cancer and Cancer Treatment. Sudbury: Jones, 2005. Print.

Kucharczyk, John, David J. Stewart, and Alan D. Miller, eds. Nausea and Vomiting: Recent Research and Clinical Advances. Boca Raton: CRC, 1991. Print.

Litin, Scott C., ed. Mayo Clinic Family Health Book. 4th ed. New York: Harper, 2009. Print.

Palatty, Princy Lous, et al. "Ginger in the Prevention of Nausea and Vomiting." Critical Reviews in Food Science and Nutrition 53.7 (2013): 659–69. Print.

Rao, Kamakshi V., and Aimee Faso. "Chemotherapy-Induced Nausea and Vomiting: Optimizing Prevention and Management." American Health & Drug Benefits 5.4 (2012): 232–40. Print.

Sleisenger, Marvin H., ed. The Handbook of Nausea and Vomiting. New York: Caduceus, 1993. Print.

Tinsley, Mary H., and Claudia P. Barone. "Preventing Postoperative Nausea and Vomiting." OR Nurse 2012 6.3 (2012): 18–25. Print.

What is the Career Occupational Preference System (COPS)?

Introduction

The Career Occupational Preference System (COPS), an interest inventory, presents 168 job-related items that can be grouped into fourteen job-determinant areas: science, professional; science, skilled; technology, professional; technology, skilled; consumer economics; outdoor; business, professional; business, skilled; clerical; communication; arts, professional; arts, skilled; service, professional; and service, skilled. The descriptor professional can be best characterized as referring to those job choices that require at least four years of college education and lead to a career, as opposed to those that do not.

The person completing the inventory is asked to rate the 168 job-related items, noting whether these are things they like very much, like moderately, dislike moderately, or dislike very much. The person completing the inventory uses the scale to state preferences concerning a number of different job activities.

The COPS was first developed in the late 1960s and has undergone several editions and revisions. Editions in foreign languages are available. Although the test is untimed, most individuals who take the test finish in less than one hour. The scores recorded by the COPS can be used to enter most occupational information systems. Both professionals and nonprofessionals can benefit from information received from the COPS. However, like most reference or interest systems, the COPS should be used to guide exploration and not judge respondents. Given the reading level of the inventory and the types of information solicited, it would be appropriate for the COPS to be used in junior high schools, senior high schools, community colleges, and four-year colleges and universities.

Technical Aspects

The COPS has been developed and interpreted through the statistical procedure of multiple-factor analysis. The purpose of this type of analysis is to understand which sets of variables match up or correlate best with one another. For example, are the “professional” and “skilled” items the same or different? If the cluster of items is the same, reporting and interpreting the scores would be influenced one way; however, if the cluster of items is different, the way the scores are reported and interpreted would be very different. With that in mind, it is possible to suggest that all fourteen clusters present as “different” when using this statistical procedure.

In addition to the statistical procedure of multiple-factor analysis of the variables in the cluster, it is equally important to understand whether the items themselves are relevant to the world of work. Additionally, the specific descriptions used in the clusters should match up, specifically, to the world of work. For example, descriptions of skills used in the clerical cluster should generally deal with clerical duties and specifically detail expected clerical duties. Without this type of matching, much of the usefulness of the COPS would be compromised. The 168 items used in the COPS match both the general and the specific nature of clusters. This provides further evidence that individual scores do match what might be expected during the accomplishment of the fourteen general clusters.

Of equal importance is whether the COPS can be considered statistically reliable, whether it is internally consistent (demonstrated by correlation studies), and whether it can be relied on to give the same results over time (demonstrated by time-sequential statistical correlation studies). It is difficult to place much confidence in a survey that does not hold together or that does not give the same results over time; therefore, these factors are extremely important to the usefulness of the COPS as an assessment.

The COPS does well on both counts of reliability considerations. Reports of internal consistency, parallel forms (different items for the same clusters from completely different, independent tests), and tests given after time periods ranging from one week to one year all point to the usefulness of the COPS. In fact, COPS scores do seem to point to a similarity between attained scores and choices of college major, actual job location, and actual job title.

Critique

For individuals to enter an appropriate career, they must begin to identify specific interests and examine the relative importance of those interests. Some individuals will need little guidance in making career choices, while others will need the guidance of a survey instrument such as the COPS interest inventory when beginning the process of career selection. In the decades since the introduction of the first interest inventory, millions of people have received important information to use in decision making. Caution is always expressed by the authors of these inventories that no decision should be made on the basis of the results determined by one inventory. The COPS interest inventory is only one of many inventories in use within the broad field of career and personnel testing.

Bibliography

Bauernfeind, R. H. “COPSystem Interest Inventory.” Test Critiques. Vol. 5. Austin: Pro-Ed, 1992. Print.

Brown, Steven D., and Robert W. Lent, eds. Career Development and Counseling: Putting Theory and Research to Work. Hoboken: Wiley, 2013. Print.

Capuzzi, David, and Mark D. Stauffer, eds. Career Counseling: Foundations, Perspectives, and Applications. New York: Routledge, 2012. Print.

Murphy, L. L., and J. C. Conoley, eds. Tests in Print IV. Vol. 1. Lincoln: Buros Institute of Mental Measurements, 1994. Print.

Quinn, Barbara. Snap, Crackle, or Stop: Change Your Career and Shape Your Own Destiny. New York: Basic, 2003. Print.

Swanson, Jane L., and Nadya A. Fouad. Career Theory and Practice: Learning through Case Studies. Los Angeles: Sage, 2010. Print.

What are sexual behavior patterns?

Introduction

Sexual behavior patterns represent one of the most important aspects of an organism’s life. These patterns not only provide for the successful perpetuation of the species but also allow the individual to contribute genetically to future generations. Sexual behavior is unlike other physical motives, such as feeding and drinking, which are required for the individual’s survival and which are initiated to some extent by measurable changes in blood sugar and cellular hydration. Engaging in sexual behavior is neither necessary to live nor stimulated by the depletion of a bodily fluid or chemical substance.

Two types of questions, relating to ultimate and proximate causality, must be addressed when sexual behavior patterns are examined. The first question asks why the pattern developed; the second asks how it occurs. For example, many species breed only during particular seasons, and the onset of these periods is often associated with changes in plumage or coloration, or the growth of anatomical structures such as antlers. Why do these changes take place? This question of ultimate causality is really asking about purpose or function; in these examples, one answer could be that the alteration makes the animal more attractive to a potential mate.

The second question, concerning proximate causation, asks how these changes come about or what the more immediate cause is. In this case, the answer could be related to a change in the animal’s hormonal secretions. Thus, the sexual behavior pattern of a given species is determined by many factors, each with ultimate and proximate causes.

Sexual Selection and Mating Systems

One of these factors is sexual selection, a concept originated by Charles Darwin in
The Descent of Man and Selection in Relation to Sex
(1871) and related to the example mentioned above. There are two kinds of selection, intersexual and intrasexual. In the first, one sex’s ability to secure a mate is related to its anatomical and behavioral traits. Examples that pertain to males include antlers, the peacock’s feathers (and the way the male displays the fully fanned-out feathers for the female), and the songs of some bird species used to “advertise” the male’s availability for mating as well as the fact that he has obtained a territory relatively free of intruders.

Intrasexual selection involves those anatomical and behavioral traits that are used to compete with members of the same sex for access to a member of the other sex. The battle between males to establish dominance that for the winner often leads to the opportunity to mate is a common example. A well-known phenomenon in mice, the Bruce effect, provides a different sort of intrasexual selection example. The presence of an unknown male during the early stages of pregnancy can cause a female to abort, which results in her becoming sexually receptive and hence a potential mate for the strange male. In this case, the ultimate cause is that this enables the male to sire more offspring, while the proximate cause is that his odor alters the female’s hormone secretions in such a way as to terminate pregnancy.

Various mating systems have evolved that also determine the type of sexual behavior pattern. Monogamy
represents a sexual relationship between one female and one male, sometimes for life. One advantage is that it precludes the effort necessary to search for a mate during each breeding cycle or season. It may, however, sometimes be more advantageous for a female to enter a good territory already inhabited by a male and one or more other females than to form a monogamous relationship with a male who lives in a dangerous territory or one with fewer resources. These systems are called polygynous, as opposed to those that are polyandrous, in which one female has a sexual relationship with more than one male. Although polyandrous systems are uncommon, polyandry does occur in situations in which the female can lay many eggs in various nests while the different males do most or all of the incubating.

Unlike some species, such as humans, who reproduce throughout the year, most species breed only during one or more restricted times of the year. The ultimate cause could be that hatching or birth occurs at a time when the environmental features are more optimal in terms of temperature, predators, or food availability. Proximate factors have been well studied, and it is known that changes in the amount of light per day or temperature can cause an animal’s endocrine system to become reproductively active. In female mammals, these periods are called estrous cycles; it is only during these cycles that pregnancy can occur. Animals kept in laboratories and maintained with constant and optimal amounts of light and other environmental factors will breed all year long.

The changes in hormonal secretions that precede the onset of a breeding period are critical for several reasons. Physiological processes such as maturation of the egg or ovum, the formation of the hard shell of the egg in birds and reptiles, ovulation, preparation of the uterus for implantation of the ovum in mammals, and development of sperm depend on particular hormones.
Hormones are also important because they act directly on regions of the brain to increase an organism’s motivation to reproduce. In addition, by affecting sensory processes, hormones directly or indirectly enable an animal to communicate its reproductive readiness over distances. Examples include pheromones, which are odors that are emitted by many species to attract a sexual partner, some types of singing in birds and croaking in frogs, and the increased swelling and reddening of the genital region in monkeys.

Sexual Behavior in Doves

Sexual behavior patterns are extremely varied; only by studying them in detail have scientists uncovered some general principles that apply to various groupings of species. Appreciating the differences between even closely related species prevents making oversimplified generalizations from one species to another.

Many species of birds have relatively prolonged and intricate courtship and mating patterns. The ring dove was extensively studied in the laboratory by Daniel Lehrman and his colleagues in the 1950s and 1960s and by a number of other scientists since then. Although the dove has breeding cycles in nature, it reproduces almost the entire year if kept in the laboratory under constant conditions of fourteen hours of light and ten hours of dark per day, at a temperature of 22 degrees Celsius.

The male dove’s courtship begins with cooing sounds while in a bowing posture. This continues for a period of time until he selects a nest site and then coos from that location. When sufficiently aroused, the female also “nest coos,” which tells the male that it is time to gather material for the nest. Eventually the female ovulates, and the birds mate. She lays two eggs; both parents incubate the eggs, and both participate in feeding the young squabs by regurgitation.

Experiments have shown that androgens, the male sex hormones secreted from the testes, stimulate the male dove’s courtship behavior, which in turn stimulates the female’s ovaries to release the female sex hormones estrogen and progesterone. Hearing her own nest coos affects the female’s physiology by playing a major role in the development of the follicles, the ovarian structures that contain her gametes, or eggs, which will be fertilized by the sperm. These hormones are important for ovulation and for mating behavior. Behavioral participation in the building of the nest produces further hormonal changes, which increase each partner’s motivation to sit on the eggs. Visual and tactile sensory input from the eggs stimulates prolactin from the pituitary gland in both sexes, which functions to keep the parents incubating until the eggs hatch; it also causes the production of crop milk, the partially digested food that is regurgitated for the hatchlings. These behavioral-hormonal interrelationships have been shown to exist in other species, and they point out the importance of particular sexual behavior patterns for successful reproduction.

Sexual Behavior in Rats

Another example of the role of behavior patterns in the survival of the species comes from experiments on rats by Norman Adler. A female rat comes into “heat” or estrus on only one day during the latter portion of her four-day estrous cycle. Her period of heat begins several hours before ovulation and ends several hours afterward. It is only during this time that she will mate and can become pregnant. During the first few days of the estrous cycle, the female secretes hormones that cause growth of the follicles, ovulation, and sexual behavior. If her eggs or ova are fertilized, her estrous cycling stops until after delivery of the litter. As in the case of the dove, a female rat will continue to have estrous cycles all year long under constant environmental conditions in the laboratory, unless she becomes pregnant.

Under those constant conditions, the male continues to secrete androgens and is almost always ready to mate. Placing a sexually receptive female and sexually active male together in a cage results in a predictable sequence of behaviors. The male will investigate the female and, on the basis of certain odors attributable to her estrogen and progesterone, will find her “attractive.” In response to the male’s interest in her and her attraction to him, she engages in proceptive behaviors—sexually stimulating activities that maintain the pair’s interaction. In the rat, these behaviors include a “hopping and darting” form of locomotion and ear quivering. The male will mount the female, and if sufficiently motivated, she will show receptivity by adopting the lordosis posture (characterized by immobility, arched back, and raised genital region). On many of these mounts, the male will be able to intromit his penis into her vagina; after an average of ten to fifteen intromissions, he will ejaculate. A number of minutes will elapse and the sequence will begin again; it will be repeated several times in a single sexual session.

In one experiment, males were allowed to intromit a varying number of times with a first female; then, before ejaculating, they were each placed with a second female. In this way, various females received different numbers of intromissions prior to an ejaculation. The significant finding was that the female needs a number of intromissions plus an ejaculation to become pregnant. If she receives only one or two intromissions prior to an ejaculation, her likelihood of becoming pregnant is greatly reduced. The stimulation she receives from these intromissions is necessary to alter her hormonal secretions in preparation for pregnancy. Additionally, males who intromit fewer than six times prior to an ejaculation release fewer sperm, hence reducing the probability that their partners will become pregnant. This result is related to the fact that subdominant male rats have fewer intromissions and reduced fertility, but only when a more dominant male is nearby.

Sexual Behavior in Primates

Scientists study primate species both because they are interesting in their own right and because the researchers wish to gain some understanding of human behavior. The rhesus monkey, a commonly studied primate, is polygynous and native to India; it has a breeding season that begins in the fall and lasts about five months. Instead of an estrous cycle, it has a menstrual cycle that is almost identical to that of human females.

Mating behavior is not controlled as exclusively by hormones as it is in lower species, but the frequency of copulation is greatest around the time of ovulation. Attractivity of the female is enhanced by estrogen, but unlike in the rat, it is reduced by progesterone, the hormone that is at its highest level after ovulation in the second half of the menstrual cycle. Experiments have shown that for optimal mating behavior to occur, androgen is necessary for the male, and both estrogen and androgen are required in the female. Female monkeys, like female humans, normally secrete androgen, although at much lower levels than males do (just as male monkeys and humans secrete female sex hormones). Studies on human females have shown that levels of androgen during the menstrual cycle correlate with increased sexual motivation and gratification.

From Evolution to Ethology

Darwin was influential in convincing scientists and nonscientists alike that humans and other animals are products of evolution and that they share common ancestors. Further, Darwin and his successors have argued that behavior, like anatomy, has changed as a result of natural selection, the process whereby traits that allow an organism to produce more offspring will be inherited by subsequent generations.

In part because of Darwin’s emphasis on the similarity between animals and humans, William James in the late nineteenth century and William McDougall in the early twentieth century proposed the instinct theory, that much of human behavior is based on instincts. Instincts are behaviors that are characterized by their lack of dependence on learning, fairly rigid performance, and presence in all members of at least one sex of a species.

The question of instincts is a key issue in the long-standing controversy in psychology between “nature” and “nurture,” or the relative role of inborn versus environmental or learned factors in behavior. Over the years, some behaviors that were thought to be pure instincts have been shown to be affected by learning or experience, and other behaviors have been shown to be more inborn than originally thought. Advances in the field of genetics has enabled further study into which behaviors, including sexual behaviors, may be more inborn than others. Furthermore, simply calling a behavior an instinct does little to shed light on either its ultimate or its proximate causes.

Partly as a result of the debate over instincts, the study of animal and human behavior has taken two somewhat separate paths. On one side are primarily psychologists, psychobiologists, and neuroscientists who investigate the more proximate causes of sexual behavior patterns in the laboratory under controlled conditions. Their progress has helped to gather information on the nervous system, the endocrine system, the interaction between the two, and their relationship to environmental factors such as light, temperature, and the presence of potential mates.

Evolutionary biologists, animal behaviorists, sociobiologists, and ethologists tend to study sexual and other behaviors under natural conditions. Ethologists Konrad Lorenz and Nikolaas Tinbergen focused on more instinctive, species-specific behaviors emphasizing ultimate causation.

It is often difficult for a laboratory scientist to devote much attention to evolutionary concerns, and it is equally difficult for the animal behaviorist to focus on the nervous and endocrine systems. Information from one approach often complements the other, however, and a complete understanding of the effect of all relevant factors is necessary for the study of sexual behavior patterns.

Bibliography

Crews, David, ed. Psychobiology of Reproductive Behavior: An Evolutionary Perspective. Englewood Cliffs: Prentice, 1987. Print.

Dixson, A. F. Primate Sexuality: Comparative Studies of the Prosimians, Monkeys, Apes and Human Beings. Oxford: Oxford UP, 2012. Print.

Gray, Peter B., and Justin R. Garcia. Evolution and Human Sexual Behavior. Cambridge: Harvard UP, 2013. Print.

Hutchison, John Bower, ed. Biological Determinants of Sexual Behaviour. New York: Wiley, 1979. Print.

Komisaruk, Barry R., et al., eds. Reproduction: A Behavioral and Neuroendocrine Perspective. New York: New York Acad. of Sciences, 1986. Print.

Lehrman, Daniel S. “The Reproductive Behavior of Ring Doves.” Scientific American Nov. 1964: 48–54. Print.

Levay, Simon, and Janice Baldwin. Human Sexuality. 4th ed. Sunderland: Sinauer, 2011. Print.

Pincott, Jena. Do Gentlemen Really Prefer Blondes? Bodies, Behavior, and Brains—The Science behind Sex, Love, and Attraction. New York: Delacorte, 2008. Print.

Yasukawa, Ken. Animal Behavior. Vol. 2. Santa Barbara: ABC-CLIO, 2014. Print.