What is multiple sclerosis?

Causes and Symptoms

Multiple sclerosis (MS) is a chronic and disabling disease of the nervous system. Symptoms can be mild, such as limb numbness, or severe, such as paralysis and loss of vision. How the disease will progress and its severity in specific individuals are difficult to predict because it progresses differently in each of its victims.

Multiple sclerosis is caused by degeneration of the nervous system. A fatty substance called myelin surrounds and protects many nerve fibers of the brain and spinal cord. Myelin is important because it speeds up signals that move along the nerve fibers. In MS, the body undergoes an autoimmune reaction in which it attacks its own tissues, causing a breakdown in the myelin layer along the nerves. When any part of the myelin sheathing is destroyed, nerve impulses to and from the brain are slowed, distorted, or interrupted. The disease is called “multiple” because it affects many areas of the brain. Sclerosis refers to the hardening and scarring of tissue over the damaged areas of myelin.

The initial symptoms of MS may include tingling, numbness, slurred speech, blurred or double vision, loss of coordination, and muscle weakness. Later manifestations include unusual fatigue, muscle tightness, bowel and bladder control difficulties, sexual dysfunction, and paralysis. The most common cognitive functions influenced are short-term memory, abstract reasoning, verbal fluency, and speed of information processing. All the mental and physical symptoms listed may come or go in any combination. The symptoms may also vary in intensity from mild to severe throughout the course of the disease.

The symptoms of MS vary not only from person to person but also, on occasion, within the same person. This makes the prognosis of the disease difficult to foresee. Although the general course of the disease may be anticipated, the symptoms and their severity seem to be quite unpredictable in most individuals. In the “classic” course of MS, as time progresses, chronic problems gradually accumulate over many years, slowly worsening the sufferer’s quality of life. The total level of disability will vary from patient to patient.

The typical pattern of MS is marked by active periods of the disease during which the nerves are being ravaged by the immune system. These periods are called attacks, relapses, or exacerbations. The active periods of the disease are followed by calm periods called remissions. The cycle of attack and remission will differ from sufferer to sufferer. Some people have few attacks, and their MS disabilities slowly accumulate over time; in these cases, it takes decades for the sufferer to become truly debilitated. Most people with MS have what is known as the relapsing-remitting form of the disease. They suffer many attacks over time, and these attacks occur unpredictably; the attacks are then followed by complete remission, which may last months or years. Again, the injuries may take many years to accumulate to complete disability.

The most aggressive form of the disease is primary progressive MS. In this type of MS, the disease follows a rapid course that steadily worsens from its first onset. Although there are still attacks and partial remission, the attacks are quite severe and occur more regularly. Full paralysis may develop in primary progressive MS in three to five years. Secondary progressive MS occurs in patients who initially have the relapsing-remitting type and later develop the more aggressive form.

Both genetic and environmental factors have been implicated in inducing the onset of MS. While viral infection has been suggested as a cause, no single virus has ever been proved to be associated with MS, although Epstein-Barr virus and the human herpesvirus 6 (HHV-6) are considered likely candidates to be involved in some way. Infections such as influenza, the common cold, and gastroenteritis increase the risk of relapse, but flu vaccination is perfectly safe for patients with MS. Risk may be conferred by exposure to a specific environment during adolescence, but that environment and the genetic risk factors have not yet been characterized. Support for a genetic component comes from examining identical twins. The likelihood of MS in the second identical twin, when the first twin has MS, is 30 percent.

Researchers Sharon Lynch and John Rose suggested that certain racial and geographic populations are less susceptible than others to the disease. MS is uncommon in Japanese people and among American Indians. The disease is more common among northern European Caucasians and North Americans of higher latitudes. There is an additional sexual dimorphism in the epidemiology of MS; the disease is found more frequently in women, by a ratio of 2 to 1.

The disease usually begins its first manifestations in late adolescence (around age eighteen) to early middle age (around age thirty-five). It is not clear how the interaction between the genetics of the sufferer and the environment may trigger onset. The progressive type of MS is more common over the age of forty, so those with late-onset MS often have the quickest deterioration of motor function. The reason that an older age predisposes someone to primary chronic progressive MS is still not clear.

Studies by Swiss researcher Avinoam Safran have shown that occasionally MS manifests after the age of fifty. This condition has been named late-onset multiple sclerosis. Nearly 10 percent of MS patients demonstrate their first symptom after the age of fifty. This type of MS is often not recognized by physicians, who do not expect it in the aged.

Treatment and Therapy

Scientists have been encouraged by advancements in MS diagnosis using magnetic resonance imaging (MRI) brain scans. In 2002 it was announced that these scans appeared to detect damage around nerve fibers in patients with possible early signs of MS. This apparent damage helps doctors predict who will eventually develop MS and how severe one’s experience with the disease might be, which in turn allows the patient to begin a drug regimen earlier. In the past, doctors did not officially diagnose MS or start treatment until patients had two episodes of nerve problems in different areas of the body—recurrences that could come years apart while damage nonetheless continued silently. New research has found that putting patients on MS drugs at the first sign of nerve inflammation drastically slows the chances of developing MS within a few years, although most will eventually still develop the disease.

While there is no cure for MS, there are many effective treatments. In most cases, steroidal drugs are used to treat relapses or attacks of the disease. Adrenocorticotropic hormone (ACTH), or corticotropin, was the first steroidal immunosuppressant to be used widely in MS treatment. The primary effect of the drug is to shorten the duration of an attack, although it does not appear to reduce the attack's severity. While it is still used with patients who respond well to it, corticotropin has been supplanted by other drugs. Methylprednisolone is an immunosuppressant and steroid that has replaced corticotropin. It has been shown to control the inflammation that accompanies demyelination. These steroids seem to work by sealing leaking blood vessels in the brain and reducing the responsiveness of the white blood cells of the immune system so that they cannot attack the myelin as easily.

Several federally approved drugs can slow the rate of attacks. Avonex, Rebif, and Betaseron are preparations of interferon (proteins regulating the immune system), and Copaxone is a mixture of small peptides that protects myelin. Although these drugs do not stop MS entirely, they do limit the level of myelin destruction, as observed in MRI scans of the brain. Avonex slows down the rate of progression to disability, and all four slow down the natural course of MS. University of Western Ontario researcher George Ebers was the first to perform experimental treatments on MS patients with interferons. The myelin sheath is actually produced by a special nerve cell called an oligodendrocyte; presumably the oligodendrocytes are stimulated to protect themselves by exposure to interferons. Patients treated with human interferons demonstrated a 34 percent reduction in frequency of attacks that was sustained over five years of treatment. More impressive was the 80 percent reduction of MS activity detected in their brains. Steroid treatment was rarely required in these patients.

In 2002, researchers announced that preliminary studies using mice and a class of statin drugs used to lower cholesterol in heart patients showed an improvement and some reversal of the debilitating symptoms of MS. The animal data was encouraging: the statin drugs appeared to reprogram the immune cells that attack myelin so they instead protect nerve coatings. Also in 2002, a parallel study using MS patients and the drug sold as Zocor—part of the statin class—showed early positive signs of similar anti-inflammatory effects in humans. Another strategy using a monoclonal antibody, Natalizumab, was approved in 2006 for the treatment of the relapsing form of MS. In 2010, the US Food and Drug Administration (FDA) approved fingolimod, the first oral drug for MS treatment.

During the 1990s, in a study supported by the National Institutes of Health and conducted at the Mayo Clinic, plasma exchange, also called plasmapheresis, was proven to be an effective treatment for certain patients suffering from severe symptoms of multiple sclerosis who were not responsive to conventional methods of treatment. Plasma exchange involves removing the patient’s blood; eliminating the plasma-containing antibodies that target myelin; replacing the plasma with a fluid with similar properties, usually containing albumin; and returning the blood to the patient. This procedure has been used for treatment of other autoimmune diseases, such as myasthenia gravis and Guillain-Barré syndrome, in the past.

Investigators concluded that plasma exchange might contribute to recovery from an acute attack in people with MS who have not responded to standard steroid treatment. Therefore, they recommended that this treatment only be considered for individuals experiencing a severe, acute attack that is not responding to high-dose steroids. Since the vast majority (90 percent) of people experiencing acute attacks respond well to the standard steroid treatment, plasma exchange would be considered a treatment alternative only for the approximately 10 percent who do not. Because the exact reasons for the effectiveness of plasmapheresis are not known, researchers feel that further studies are warranted based on the idea that some people may have antibodies in their plasma that are instrumental in certain disease activities that allow disabilities to occur.

As additional therapy, patients with MS should participate in a regular exercise program. Exercise is vital to the maintenance of functional ability in MS sufferers. It strengthens muscles, benefits gait, and generally improves coordination. The best type of exercise is aquatic in nature. Sufferers are often heat intolerant, and participation in a regular aerobic program would be unpleasant. Also, aquatic exercise is a low-impact activity that puts less stress on chronically sore muscles. Exercise programs also encourage socialization of patients and engender peer support.

Perspective and Prospects

The first written report of MS was published in 1400 when the famed Dutch skater Lydwina of Schieden was diagnosed. It was recognized initially as a wasting disease of unknown origin. The disease was described clinically by Jean-Martin Charcot in 1877. Charcot initially characterized the clinical signs and symptoms of MS. He recognized that the disease affects the nervous system and tried many remedies, without success. In 1890, the cause of MS was thought to be suppression of sweat; the treatment was electrical stimulation and bed rest. At the time, life expectancy for a sufferer was five years after diagnosis. By 1910, MS was thought to be caused by toxins in the blood, and purgatives were alleged to be the best treatment. In the 1930s, poor circulation was believed to cause MS, and blood-thinning agents became the treatment of choice. From the 1950s through the 1970s, MS was thought to be caused by severe allergies; treatments included antihistamines. Not until the 1980s was the basis of MS understood and effective treatment developed.

By the early twenty-first century, it was estimated that thousands of people had this disorder of the brain and spinal cord, which causes disruption in the smooth flow of electrical messages from brain and nerves to the body. The progress of the disease is slow and may take decades to achieve complete nerve degeneration and paralysis. Although often considered a disease of youth, MS has the potential to become an increasing problem in aging populations. More cases of late-onset MS have come to light in individuals over forty years of age, including such celebrities as comedian Richard Pryor, entertainer Annette Funicello, and talk-show host Montel Williams.

Several novel therapies that have been under investigation are sphingosine receptor modulator (fingolimod), vitamin D, inosine (Axosine), and antimicrobial agents. Various combinations of drugs are also being examined, including mitoxantrone (an immunosuppressant) and Copaxone. Ongoing clinical trials are likely to reveal treatment strategies that will further facilitate control of the symptoms and progression of MS.

Bibliography

Alan, Rick, and Rimas Lukas. "Multiple Sclerosis—Adult." Health Library. EBSCO, 25 Apr. 2014. Web. 26 Aug. 2014.

Alan, Rick, Rebecca J. Stahl, and Kari Kassir. "Multiple Sclerosis—Child." Health Library. EBSCO, 30 Sept. 2013. Web. 26 Aug. 2014.

Blackstone, Margaret. The First Year—Multiple Sclerosis: An Essential Guide for the Newly Diagnosed. 2nd ed. New York: Marlowe, 2007. Print.

“Brain and Nerves.” Mayo Clinic Family Health Book. Ed. Scott C. Litin. 4th ed. Des Moines: Time, 2009. 511–80. Print.

Halbreich, Uriel, ed. Multiple Sclerosis: A Neuropsychiatric Disorder. Washington: Amer. Psychiatric, 1993. Print.

Iams, Betty A. From MS to Wellness: My Personal Story of Overcoming Multiple Sclerosis. Chicago: Iams, 1998. Print.

Kalb, Rosalind C., ed. Multiple Sclerosis: The Questions You Have, the Answers You Need. 5th ed. New York: Demos, 2012. Print.

Matthews, Bryan, and Margaret Rice-Oxley. Multiple Sclerosis: The Facts. 4th ed. New York: Oxford UP, 2001. Print.

"Multiple Sclerosis." MedlinePlus. Natl. Lib. of Medicine, 6 Aug. 2014. Web. 26 Aug. 2014.

"Multiple Sclerosis: Hope through Research." National Institute of Neurological Disorders and Stroke. US Dept. of Health and Human Services, 21 May 2014. Web. 26 Aug. 2014.

Murray, T. Jock, Carol S. Saunders, and Nancy J. Holland. Multiple Sclerosis: A Guide for the Newly Diagnosed. 4th ed. New York: Demos, 2013. Print.

"NINDS Multiple Sclerosis Information Page." National Institute of Neurological Disorders and Stroke. US Dept. of Health and Human Services, 21 May 2014. Web. 26 Aug. 2014.

Polman, Chris H., et al. Multiple Sclerosis: The Guide to Treatment and Management. 6th ed. New York: Demos, 2006. Print.

Russell, Margot, ed. When the Road Turns: Inspirational Stories by and about People with MS. Deerfield Beach: Health Communications, 2001. Print.

Salter, Robert Bruce. Textbook of Disorders and Injuries of the Musculoskeletal System. 3rd ed. Baltimore: Lippincott, 1999. Print.

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Wood, Debra, and Rimas Lukas. "Conditions InDepth: Multiple Sclerosis (MS)." Health Library. EBSCO, 30 Sept. 2013. Web. 26 Aug. 2014.

What do swords represent in Romeo and Juliet?

In the very beginning of the play swords take on a sexual connotation. In Act I, Scene 1 the Capulet men, Gregory and Sampson, make a crude joke about raping the Montague women and use references to the male genitals. Sampson says,

Me they shall feel while I am able to stand,
and ’tis known I am a pretty piece of flesh.

On the heels of this conversation the Montague men approach and the two Capulets refer to their swords as "tools" and Sampson says,

My naked weapon is out. Quarrel, I will back
thee.

For Gregory and Sampson, then, swords are very much an extension of their manhood and they use them to intimidate their opponents. It's also interesting that when Lord Capulet goes for his sword, he calls it a "long sword", in contrast to the simple "swords" of his servants, suggesting that class distinction is an important element in the play.

In Act III, Scene 1 Mercutio refers to swords playfully. When he is joking about how Benvolio is a fighter (Shakespeare being ironic, since Mercutio is really the hothead) he says that Benvolio is likely to put his sword on the bar of a tavern and, after having a drink, use it on the bartender:

Thou art like one of these fellows that, when
he enters the confines of a tavern, claps me his
sword upon the table and says “God send me no
need of thee” and, by the operation of the second
cup, draws him on the drawer when indeed there is
no need.

A little later in the scene, while he is punning on the word "consort" (a group of people who associate with each other or a group of musicians) Mercutio grabs his sword and calls it his "fiddlestick", telling Tybalt,

Consort? What, dost thou make us minstrels?
An thou make minstrels of us, look to hear
nothing but discords. Here’s my fiddlestick; here’s
that shall make you dance. Zounds, consort!

Like everything else in the play swords become another vehicle for Shakespeare to display his keen ability to use figurative language. 

What message does Orwell convey in Animal Farm via the use of Benjamin?

Benjamin, a donkey, is the oldest animal on the farm. Orwell uses him to transmit the same message the Who so famously conveyed: "Meet the new boss, same as the old boss." Benjamin doesn't for a minute believe in the ideals of the revolution. As the narrator puts it:

He refused to believe either that food would become more plentiful or that the windmill would save work. Windmill or no windmill, he said, life would go on as it had always gone on—that is, badly.

Benjamin is proven right: except for a brief time of joy and solidarity right after the revolt, life does goes on as it had—badly, sometimes even worse than before.

Benjamin remains loyal to his friend Boxer throughout the book. He is the one who takes care of Boxer as much as he possibly can when Boxer is old and sick. 

Benjamin is also the animal who exposes the fact that the pigs are sending Boxer to the glue factory. He rouses the other animals, runs with them to the cart that is taking Boxer off and reads on the side of it:

 "'Alfred Simmonds, Horse Slaughterer and Glue Boiler, Willingdon. Dealer in Hides and Bone-Meal. Kennels Supplied.' Do you not understand what that means? They are taking Boxer to the knacker's!"

Benjamin is an intelligent animal who won't take sides in quarrels and steadily sticks to the routines he started before the Revolution. However, he does read to other animals the slogan that has replaced the Seven Commandments on the side of the barn:

ALL ANIMALS ARE EQUAL
BUT SOME ANIMALS ARE MORE EQUAL THAN OTHERS

Through Benjamin's steady, unchanging eyes, we see how the pigs have betrayed the revolution. Orwell uses Benjamin as an animal the reader can trust, because he has no agenda and no interest in politics.

What is Guillain-Barré syndrome?

Causes and Symptoms

Guillain-Barré syndrome (GBS) is an acute disease of the peripheral nerves, especially those that connect to muscles. It causes weakness, areflexia (loss of reflex), ataxia (difficulty in maintaining balance), and sometimes ophthalmoplegia (eye muscle paralysis). GBS demonstrates a variable, multifocal pattern of inflammation and demyelination of the spinal roots and the cranial nerves, although the brain itself is not obviously affected. By the 1990s and early 2000s, it was the most common cause of generalized
paralysis in the United States, averaging one to two cases per 100,000 people per year. The disease was first described in the early twentieth century by Georges Guillain and Jean-Alexander Barré, two French neurologists. Little was known of the cause of GBS or the mechanism for its symptoms, however, until the 1970s. Since then, symposia sponsored by the National Institute of Neurological and Communicative Disorders and Stroke have shed more light on this condition.

Most individuals with GBS have a rapidly progressing muscular weakness in more than one limb and also experience paresthesia (tingling) and
numbness in the hands and feet. These sensations have the effect of reducing fine muscle control, balance, and one’s awareness of limb location. The prevailing scientific opinion regarding GBS is that it is an autoimmune disorder involving white blood cells, which for some unknown reason attack nerves and/or produce antibodies against myelin, the insulating covering of nerves. The weakness is usually ascending in nature, beginning with numbness in the toes and fingers and progressing to total limb weakness. The demyelination is more prominent in the nerves of the trunk and occurs to a lesser extent in the more distal nerves. The brain and spinal cord are protected from GBS by the blood-brain barrier, although antibodies to myelin have been found in the cerebrospinal fluid of some patients.

With GBS, there is often a precipitating event such as surgery, pregnancy, upper respiratory infection, viral infection (such as cytomegalovirus), or vaccination. Preexisting debilitating illnesses such as systemic
lupus erythematosus (SLE) or Hodgkin’s disease also seem to predispose a person to GBS. GBS has been diagnosed in patients having heart transplants in spite of the fact that they are receiving immunosuppressive drugs. The increased risk with such surgery may be attributable to the stress associated with the procedure. Most patients who come down with GBS have had some prior condition that placed stress on the immune system prior to the appearance of GBS.

The patient with GBS is frequently incapable of communicating as a result of paralysis of the vocal cords. Typically, motor paralysis will worsen rapidly and then plateau after four weeks, with the patient bedridden and often in need of respiratory support. Autonomic nerves can also be affected, causing gastrointestinal disturbances, adynamic ileus (loss of function in the ileum of the small intestine), and indigestion. Other, less common symptoms include pupillary disturbances, pooling of blood in limbs, heart rhythm disturbances, and a decrease in the heart muscle’s strength. These patients are usually hypermetabolic because considerable caloric energy goes into an immune response that is self-destructive and into mechanisms that are attempting to repair the damage.

In addition to the loss of myelin, cell body damage to nerves may result and may be associated with permanent deficits. If the nerve cell itself is not severely damaged, regrowth and remyelination can occur. Antibodies to myelin proteins and to acidic glycolipids are seen in a majority of patients. Blood serum taken from patients with GBS has been shown to block calcium channels in muscle, and experiments in Germany have found that cerebrospinal fluid from GBS patients blocks sodium channels.

Like most autoimmune conditions, GBS is cyclic in nature; the patient will have good days and bad days because the immune system is sensitive to the levels of steroid hormones in the body, which are known to fluctuate. In addition to paralysis, there is significant pain with GBS. Many of the nerve fibers that register the pain response (nociceptors) are nonmyelinated and therefore are not interrupted in GBS. Pain management can be difficult, requiring the use of such drugs as fentanyl, codeine, morphine, and other narcotics. The course of the disease is variable and is a function of the level of reactivity of the patient’s immune system. The autoimmune attack is augmented in those patients experiencing activation of serum complement
protein induced by antibodies. Recovery usually takes months, and frequently the patient requires home health care. Complications can lead to death, but most patients recover fully, though some have residual weakness.

The physician must be careful to distinguish GBS from lead poisoning, chemical or toxin exposure, polio, botulism, and hysterical paralysis. Diagnosis can be confirmed using
cerebrospinal fluid (CSF) analysis. GBS patients have protein levels greater than 0.55 gram per deciliter of CSF. Macrophages are frequently found in the CSF, as well as some B cells. Nerve conduction velocity will be decreased in these patients to a value that is 50 percent of normal in those nerves that are still functioning. These changes can take several weeks to develop.

With GBS, macrophages and T cells have been shown to be in contact with nerves, as evidenced in electron micrographs. T-cell and macrophage activation in these individuals point to an immune response gone awry, possibly precipitated by a virus or exposure to an antigen that is foreign but similar in appearance to one of the proteins in myelin. T cells, upon encountering an unrecognizable antigen, will produce interleukin II, initiate attack, and recruit macrophages to participate. The use of an anti-T-cell drug theoretically should improve nerve function, but researchers at the University of Western Ontario failed to find any benefit from the infusion of an anti-T-cell monoclonal antibody. Unexpectedly, GBS has been found in patients testing positive for the human immunodeficiency virus (HIV) who are asymptomatic, in spite of the fact that their T cells are under attack from the HIV virus and are diminished in number. Although myelin proteins are thought to be the immunogens, other candidates include gangliosides in the myelin. Antiganglioside antibodies have been seen in a
majority of GBS patients. This trait may distinguish GBS from
amyotrophic lateral sclerosis (Lou Gehrig’s disease) and
multiple sclerosis, which seem to involve different myelin proteins as antigens.

In GBS, the white blood cells attack peripheral motor nerves more often than other types of nerves, implying a biochemical difference between motor and sensory nerves that has yet to be discovered. One possible cause of this disease is a similarity between a protein or glycolipid that is present normally in myelin and coincidentally on an infectious agent, such as a virus. The immune system responds to the agent, resulting in a sensitization of the macrophages and T cells to that component of myelin. B cells are then stimulated to produce antibodies against this antigen, and they unfortunately cross-react with components of the myelin protein. The severity of the disease will depend on the number of macrophages and lymphocytes activated and whether serum complement-binding antibodies are being produced. Serum complement proteins are activated by a particular class of antibodies, resulting in the activation of enzymes in the blood that potentiate tissue destruction and neurogenic atrophy. Serum complement levels can be determined by a serum complement fixation test.

In severe cases of GBS, intercostal muscles are more severely compromised and respiratory function needs to be monitored closely. The immune response will subside when T-suppressor cells have reached their peak levels. Halting the autoimmune response will not reverse the symptoms immediately, since it takes time for antibody levels to decrease and for the nerves to regrow and remyelinate, which occurs at the rate of 1 to 2 millimeters per day. Some nerves will undergo retrograde degeneration and be lost from the neuronal pool. Other nerves will have more closely spaced nodes and conduct impulses at a lower velocity. Nerve sprouting will also occur, which will result in one nerve’s being responsible for more muscle fibers or serving a larger sensory area and in decreased fine motor control.

Treatment and Therapy

In Guillain-Barré syndrome, the amount of muscle and nerve involvement can be assessed by performing an electromyogram, which can reveal the amount of motor nerve interruption and the conduction velocity of the nerves that continue to function. Based upon the assumption that an autoimmune response was in progress, corticosteroids such as prednisolone and methylprednisolone were once administered in high doses, but such drugs have been shown to have a deleterious effect on the disease and are no longer used.

More recently, a procedure known as plasmapheresis has been tried with better results, especially when performed in the first two weeks. This procedure involves removing 250 milliliters (a little more than a pint) of plasma from the blood every other day and replacing this volume with a solution containing albumin, glucose, and appropriate salts. Six treatments are typical and usually result in a faster recovery of muscle control than for those not receiving plasmapheresis. Because relapses may occur if the patient produces new antibodies to myelin, immunosuppressants are given to the patient after plasmapheresis. Another procedure, intravenous immunoglobulin therapy, is based on the strategy of blocking the binding of antibodies to nerves, which lessens the severity of the immune attack.

Cyclosporine, a T-cell inhibitor, is also being tried, with some promising results. Some researchers note, however, that transplant patients, who routinely take cyclosporine, have a higher-than-normal risk of developing GBS. Others emphasize that no one knows what their risk for GBS would be without the administration of cyclosporine. Because of the variability of the body’s immune response, the benefits of this drug will depend on whether, in a given individual, it is an antibody response or T-cell response. Cyclosporine will benefit those who have a strong T-cell response. T-cell reactivity can be tested with the mixed lymphocyte assay, and T-cell counts can be done.

Cerebrospinal fluid filtration is also being tried in order to remove antibodies. Serum so filtered loses its nerve-inhibiting effect, as evidenced by its application to in vitro nerve and muscle cells. GBS has been mimicked in animal models, which show antibody and T-cell reactivity to myelin protein. Guillain-Barré syndrome has many of the characteristics of an autoimmune disease and could serve as a model for an acquired autoimmune condition.

Not related to the neurology of this sudden-onset disease, but equally devastating, is the protracted psychological impact of simultaneously being able to think and have emotions while not being able to move limbs, fingers, toes, and facial and eye muscles. Even though most patients recover, progress is always torturously slow, as the myelin sheath gradually regenerates. Ongoing psychological support is an important element in treating these patients.

Perspective and Prospects

Guillain-Barré syndrome is an example of a delicate physiological balance gone awry. The immune system has the difficult task of distinguishing between self and enemy, and if it detects the latter it must either inactivate or eliminate the intruder. Mistakes in recognition or communication between immune cells can cause either an unintended attack or the failure to attack when appropriate. GBS probably represents an unnecessary self-attack on tissue, in this case myelin, and may be considered a form of hyperimmunity. Many diseases fall into this category. They include rheumatoid arthritis, juvenile diabetes, Crohn’s disease, ulcerative colitis, Graves’ disease, multiple sclerosis, amyotrophic lateral sclerosis, ankylosing spondylitis (inflammation of the joints between the vertebrae), and systemic lupus erythematosus. The other type of response, hypoimmune, is seen in cancer and immunodeficiency diseases such as Acquired immunodeficiency syndrome (AIDS).

Questions that arise with GBS are the same ones that arise in many other diseases. It must be determined why the immune system chose this time to initiate an attack against a self-antigen. The answer could be a mistake in recognition, an error in translating the deoxyribonucleic acid (DNA) code in the bone marrow cells, an alteration of the antigen by some environmental factor, or an alteration of an antigen-detector protein on a white blood cell. Researchers also try to discover if there is a genetic predisposition for GBS. Seeking answers about GBS may shed light on other conditions as well, and treatments beneficial to GBS patients have a high probability of benefiting patients with other immune disorders. GBS is a reminder that physiological stress can translate to immunological stress, and under stress the immune system can make mistakes.

Bibliography:

Abbas, Abul K., Andrew H. Lichtman, and Shiv Pillai. Basic Immunology: Functions and Disorders of the Immune System. 4th ed. Philadelphia: Saunders/Elsevier, 2012.

Adelman, Daniel C., et al., eds. Manual of Allergy and Immunology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2012.

Baron-Faust, Rita, and Jill P. Buyon. The Autoimmune Connection. Chicago: Contemporary Books, 2003.

"Guillain-Barré Syndrome." Genetics Home Reference, May 13, 2013.

"Guillain-Barré Syndrome." Medline Plus, May 21, 2012.

"Guillain-Barré Syndrome Fact Sheet." National Institute of Neurological Disorders and Stroke, August 19, 2011.

Kierman, John A., and Nagalingam Rajakumar.Barr’s The Human Nervous System: An Anatomical Viewpoint. 10th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2013.

Lechtenberg, Richard. Synopsis of Neurology. Philadelphia: Lea & Febiger, 1991.

Nicholls, John G., et al. From Neuron to Brain. 5th ed. Sunderland, Mass.: Sinauer, 2011.

Noback, Charles R., et al. The Human Nervous System: Structure and Function. 6th ed. Totowa, N.J.: Humana Press, 2005.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Guillain-Barré Syndrome. San Diego, Calif.: Icon Health, 2002.

Pearlman, Alan L., and Robert C. Collins. Neurobiology of Disease. New York: Oxford University Press, 1990.

Sticherling, Michael, and Enno Christophers, eds. Treatment of Autoimmune Disorders. New York: Springer, 2003.

In "The Kite Runner," if Hassan was the illegitimate son of Baba, then who was Ali?

In the novel, Hassan was the result of Sanaubar (Ali's wife) and Baba's adulterous relationship. Since Sanaubar was already Ali's wife at the time Hassan was born, all the parties involved simply continued with their lives as if the affair never happened. This was presumably done to protect Baba's position in his Pashtun/Sunni Muslim community. After all, Sanaubar was a Hazara (like her husband, Ali), and Hazaras were Shia Muslims; it would have been unthinkable for a man of Baba's position to admit to an affair with Sanaubar, a member of a hated sect.

After Sanaubar left Ali, he continued to raise Hassan as his own son. In the middle of the novel, we learn Hassan's true paternal heritage from the conversation between Rahim Khan and Amir. Rahim Khan confessed to Amir that Ali had always been sterile and that Hassan was fathered by Baba. Amir's reaction was explosive:

"You  bastards,"  I  muttered.  Stood  up.  "You  goddamn  bastards!"  I   screamed.  "All  of  you,  you  bunch  of  lying  goddamn bastards!"

"How  could  you  hide  this  from  me?  From  him?"  I  bellowed.

"Please  think,  Amir  jan.  It  was  a  shameful  situation. People  would talk.  All  that  a  man  had  back  then,  all  that  he  was,  was  his  honor,  his  name,  and  if  people  talked...  We  couldn't  tell  anyone,  surely  you  can  see  that."  He  reached  for  me,  but  I  shed  his  hand.  Headed  for  the door.

After he learned the truth about Hassan's parentage, Amir felt even more beholden to Hassan. He realized that both he and his father betrayed Hassan in their own ways. This terrible knowledge led Amir to fight for Sohrab's freedom as a form of redemption.

What did Dexter Green's father do for a living?

At the beginning of Fitzgerald's short story "Winter Dreams," we learn that Dexter Green's father "owned the second-best grocery store in Black Bear," the small town where Dexter lives. Unlike other boys his age, who were "poor as sin," Dexter works as a caddie at the golf club to earn extra money; the other caddies must work to support themselves, but Dexter has the security of his father's store.

It is worth noting that Dexter's last name is important in connection with his father's solid middle-class background. Dexter is "green"—meaning he is inexperienced—but he is also the color of new money (dollar bills). Though Dexter makes a fortune when he is a young man, he cannot escape the "newness" of his money. He recognizes that Judy Jones, who is often described as golden (old money), represents the ease of old wealth he so desires.

How can a girl tell a boy that she loves him, too?

Telling someone your true feelings can be an intimidating situation, especially when it comes to romantic relationships!

First, I recommend you think about how you really feel about this person. It might be helpful to make a few notes to help organize your thoughts. What do you love about this boy? What kind of feelings come up when you are together or apart? The tricky part may be considering whether you are in love with or whether you feel love for someone. The difference can be hard to tell, and it is possible to have one but not the other. For example, it is possible to feel love for someone without desiring a romantic relationship with them. It is also possible to desire a romantic or intimate relationship with someone while not feeling love for them. 

If you've taken some notes, you might also wish to write down a few things you like doing with this person. What are some things that this boy does to make you feel love for him?

Next, consider how you would like to tell this person that you love him. How did he tell you? In person, or maybe through writing or text message? It is best to respond in the same way that he has professed love for you. This way, it does not set up a dynamic where one of you is trying to "one-up" the other by being more or less formal. 

When you tell this person that you love him, you could try to incorporate the notes you took (or thought of) earlier! While simply telling someone that you love them is sweet, it adds depth if you tell the person why you love them. Healthy relationships are built upon a foundation of the partners understanding what the other does and does not like. Telling this boy what you like about your friendship or budding romance can help lay a foundation for a healthy relationship.

Most importantly, be yourself and do what feels natural! Best of luck to you!

What are the characteristics of the major characters of Jerome K. Jerome's book Three Men in a Boat (To Say Nothing of the Dog)?

There are four major characters, as noted by the title of the book. All have some boating experience, but none could be considered seasoned seamen.

The narrator is referred to as J., but he should not be confused with the author of the book, Jerome K. Jerome. This is a work of fiction. J. tells the story as he sees and interprets it. We don’t know if he holds a “real” job, but he seems to have a journalistic bent, as well as a wry sense of humor. He can turn any random act into an interesting and detailed story.

William Samuel Harris is another gentleman in the story. He too may not hold much of a job, if any. He tends to make grand events out of small acts as well, much to the consternation and frustration of everyone around him. He believes he can do small tasks, but he really cannot. See Chapter VI for his recollection of getting lost in the Hampton Court maze, as well as his attempt to make scrambled eggs for breakfast in Chapter XI.

George works in a bank five and a half days a week. He seems to be a little better organized than his two friends are, but he can sometimes become clumsy or confused. See Chapter VI for the story about what he did one night when his watch stopped. George can also take charge and can get tasks done when they need to be finished.

Montmorency is the fox terrier. According to J., the dog looks like an adorable and angelic pup, but he has a habit of getting into fights with other dogs and also with cats. On the trip, he is stared down and scared by a cat on the street in Chapter XIII. He also tends to get under foot and interfere with some of the men's tasks.

What is vascular medicine?

Science and Profession

Vascular medicine, especially peripheral vascular
surgery, has become an important specialty of general surgery. In the past, general surgeons performed surgery on the arteries and veins, but technical advances have led to the creation of vascular surgery as a field of its own.

Western society has produced an older population because of its high level of primary care, but with this older population come the ravages of atherosclerosis. The modern lifestyle is ideally suited to the formation of atherosclerosis in many arteries as a result of cigarette smoking, stress and high blood pressure, a fatty diet, and a sedentary lifestyle. Peripheral vascular surgeons can contribute in a positive way and help many patients with these diseases. This help may come in the form of stroke prevention, the restoration of blood flow to a leg that might otherwise not be saved, or occasionally the saving of a life through repair of a ruptured aortic aneurysm.

One of the most common arteries affected by atherosclerosis is the carotid artery, in the neck. This artery branches high in the neck near the jawline. One branch continues up into the brain, supplying a large part of the area that controls motor and sensory function. Atherosclerosis tends to occur at areas of branching arteries, and the carotid bifurcation is no exception. The buildup of material in this location is especially hazardous, because small pieces of the material, called emboli, can break off the arterial wall, travel up the artery, and lodge in the brain.

When an embolus lodges in the small arteries of the brain, it blocks the flow of blood to the area of brain tissue supplied by those arteries. This results in ischemia, or restricted blood flow, and the body functions controlled by that part of the brain may be altered. If the ophthalmic artery is involved, then blindness can ensue. If the middle cerebral artery is involved, then symptoms of motor and sensory dysfunction, such as abnormal sensation, numbness, weakness, or paralysis of one side of the body, can occur. Fortunately, very small emboli often do not cause permanent loss of neurological function, and a complete recovery is possible. They are, however, warning signs that atherosclerotic debris resides in the carotid artery, and if treatment is not begun and the brain tissue is irreversibly damaged, a permanent stroke might occur. If this happens, the patient will lose some neurologic function and may be unable to see to his or her own daily needs. The patient also may need extensive and expensive rehabilitation. Strokes can be prevented if the warning signs are properly interpreted and acted upon.

Atherosclerosis also results in stenoses, or blockages, in other arteries. Depending on the location of these blockages, various symptoms can result. If the arteries to the intestines are involved, patients can feel abdominal pain that is very difficult to diagnose, given that there are many other causes of abdominal pain, such as ulcer disease, gallbladder problems, and colitis. Intestinal ischemia is somewhat rare and often is not thought of as a cause of abdominal pain. These patients may have to endure this pain for a long period of time and may experience severe eating problems, weight loss, and addictions to painkillers. If the problem is properly diagnosed, many patients can be helped with nonsurgical and surgical techniques, resulting in the cessation of pain, the regained ability to eat, and the maintenance of proper nourishment.

One form of atherosclerotic arterial disease is called
renovascular hypertension. In this syndrome, plaque builds up in the renal (kidney) arteries. Patients with renovascular hypertension exhibit a type of high blood pressure, or hypertension, that is somewhat different from the kind of high blood pressure that affects most patients. The majority of patients with hypertension have what is called essential hypertension, for which there is no known cause. For the minority of patients whose hypertension results from pathology in the renal arteries, the blood flow in these arteries is decreased because of atherosclerotic plaques in the arterial walls that severely limit the space through which blood can flow. When this happens, the kidney “senses” this decreased flow and releases a variety of chemical hormones that serve to increase the blood flow. These hormones indirectly raise the blood pressure by trying to preserve blood flow to the kidney.

Renovascular hypertension is often difficult to diagnose and treat. Many patients need to take up to five kinds of blood-pressure pills to keep their pressure under reasonable control; such patients should be screened for renovascular hypertension. A variety of treatments can be offered to these patients once a diagnosis is made, although the medicines they must take all have significant side effects.

The arteries that supply the muscles and nerves of the extremities also can be affected by atherosclerotic disease. Peculiarly, the upper extremities are usually spared of this disease, whereas the
lower extremities are not. The mildest form of lower-extremity disease manifests itself in the form of claudication, a term that describes the specific symptoms that develop in an ischemic limb. Most of the time, there are no symptoms when a patient is at rest, but when the patient undergoes the physical stress of walking or other exercise, pain develops in the limb in certain areas that correspond to the areas of muscle tissue supplied by the blocked artery. A characteristic pain syndrome develops after a certain amount of exercise and repeats itself regularly. The pain stops after exercise, and this cessation of pain also follows a pattern.

Claudication is the classic example of arterial occlusive disease. If the disease is severe enough, it may cause resting pain. Such patients have profound ischemia of their leg(s), which is limb threatening and requires intervention. People afflicted with ischemia of the leg have difficulty healing small scrapes and cuts on the feet, sometimes causing them to turn into large lesions that do not heal. If these lesions become secondarily infected, they can also become limb threatening and ultimately necessitate amputation. In many patients, however, amputation can be avoided by timely intervention with either surgery or other techniques.

A rather curious phenomenon occurs in some patients whereby there is a focal dilatation of a portion of an artery. The mechanism by which this occurs is largely unknown, but it may be related in some way to the atherosclerotic process. Instead of a buildup of debris in the arterial wall resulting in a blockage in the artery, aneurysms are characterized by a thinned-out wall. They enlarge over time and can cause problems. They may clot off entirely or become a source of emboli, giving rise to problems farther down the arterial tree. The most devastating complication of an aneurysm, however, is acute rupture. Laplace’s law of hemodynamics states that wall tension in a tube of fluid is related to the fourth power of the radius. Accordingly, as an aneurysm enlarges, the wall tension increases in exponential fashion. If rupture does occur, it can lead to rapid blood loss if expert medical and surgical care is not readily available.

Aneurysms can form anywhere in the body, but they most commonly occur in the aorta (the main artery coming out from the heart) directly beneath the umbilicus. Because this location is surgically accessible, repair of these aneurysms is a common operation. In this location, most aneurysms will not cause a problem until they measure approximately five centimeters in diameter, at which size the risk of rupture becomes significant. Smaller aneurysms are usually monitored with serial examinations over time, and if they do enlarge, then the appropriate therapy can be instituted. Other, less common areas of aneurysm formation include the splenic, renal, iliac, femoral, and popliteal arteries. Similar complications can ensue with these aneurysms.

The majority of peripheral vascular surgery practice deals with the diseases of the arteries, but venous disease is a very common problem that many physicians in many specialties must address. Patients with simple
phlebitis of the superficial
veins of the leg usually require no more than supportive care until they feel better, but if the clots are in or extend into the deep veins of the leg, much more aggressive treatment is necessary. A clot in this location has a chance of migrating into the lungs (pulmonary embolus) and can be fatal. Therefore, intensive treatment with intravenous and then oral blood thinners (anticoagulants) is mandatory. There are some patients who then have chronic venous problems because the clots in their legs can damage the valves in the veins. This results in severe pain, swelling, and even ulceration of the legs that can be very difficult to treat.

Diagnostic and Treatment Techniques

Many patients who suffer from vascular diseases are not treated with surgery right away. They may ultimately need an operation, but often long periods of time elapse before surgery is undertaken. Nonoperative therapy, such as quitting smoking, lowering serum cholesterol, or starting an exercise program, is often all that is needed to control certain aspects of the patient’s symptoms. Vascular surgeons provide guidelines for patients who need this sort of therapy.

Atherosclerosis may appear in many forms and affect patients differently. For example, a forty-five-year-old postal carrier complains of pain in his or her thighs in the same location whenever he or she walks more than a few hundred feet. This person may have been a heavy smoker for many years, his or her cholesterol levels may be elevated, and there may be many relatives in his or her family with hardening of the arteries. Such a person has a classic case of claudication resulting from atherosclerotic occlusive disease of the arteries that supply the thigh muscles. The patient has several options. Other causes of leg pain must be ruled out, such as nerve problems or back conditions, but when this is accomplished, the field of vascular surgery can help this patient maintain his or her lifestyle. If the patient would like to investigate options for intervention, an arteriogram is performed next. In this procedure, specially trained radiologists insert a small tube into the arteries and take pictures after dye has been injected. This allows an exact replica of the patient’s arterial anatomy to be projected in two dimensions. The arteriogram allows the surgeons and radiologists to determine the best course of action for this patient.

Some atherosclerotic plaques are in particular locations that may allow their treatment with balloon angioplasty rather than open surgery. In this procedure, again performed by trained radiologists or some vascular surgeons, a catheter with a balloon at its end is inserted into the artery, and the balloon is inflated in the area of the offending plaque in an effort to open the clogged artery. This procedure is often performed on the arteries of the heart, but it can also be performed on other arteries, such as those in the kidneys, intestines, or legs. A vascular surgeon usually oversees the care of the patient, as not all the balloon procedures are completely successful and open surgery is sometimes necessary. Open surgery might include a bypass graft with a woven or knitted prosthetic artery or a graft made with an expendable vein in the patient’s leg, using the same vein as for heart bypass surgery. The postal worker described above could be a candidate for either a balloon procedure or a surgical bypass graft, but in either case, he or she should be restored to almost normal walking capability and be able to return to work.

Another common scenario might involve a more serious situation. A person may have an open sore on his or her foot that has been there for more than six months and is getting bigger, perhaps infected. This person may also be a heavy smoker with cholesterol problems and severe diabetes mellitus. He or she has not walked more than a block in the past few years because this causes his or her feet to hurt. The problem may be related to poor blood flow to the legs and feet, and the diabetes certainly does not help. Before vascular surgery techniques became popular, this patient ultimately would have required an amputation of the leg, either below or above the knee. It is physically and emotionally difficult for patients to cope with such a loss, and the long, expensive period of rehabilitation includes learning to walk with a prosthetic extremity. This patient would be a good candidate for an arteriogram and would undoubtedly need some surgery. This would most likely be in the form of a bypass graft, which could stretch from the groin all the way to the foot, crossing the knee and the ankle. Ultimately, a successful outcome would be healing of the open sore and control of the infection; the patient would then be able to continue walking with his or her own leg.

Another situation that might involve vascular surgery is as follows. A patient has a history of deep vein clots following prior major surgery. Treatment consisted of long-term blood thinners, and the patient may have had no major problems since that time. The patient now needs a hip operation, however, and hip operations carry a high risk of blood-clot formation in the deep veins of the leg. Because deep-vein thrombosis carries risks of a pulmonary embolus as well as chronic problems in the leg, a vascular surgeon is called upon to help design a program that can prevent these complications from occurring. The usual methods of prophylaxis do not necessarily apply to this patient, and as the patient is labeled high risk, it might be most prudent to place a device in the body to catch any pulmonary emboli if they occur. The theory behind this management is that, in this high-risk patient, the formation of blood clots in the legs is almost unavoidable, and the majority of effort should be aimed at preventing the most serious, potentially fatal complication: the pulmonary embolus. In this case, vascular surgeons could place a filter device in the main vein that carries blood to the heart and lungs, which would effectively trap any free-floating emboli that could cause a problem.

Perspective and Prospects

Peripheral vascular surgery has assumed a paramount role in medical practice. By 1900, significant contributions had been made regarding the basic reconstructive techniques needed to sew arteries together. The work of Alexis Carrel in the early twentieth century is considered the most important contribution to the technical art of vascular surgery. His techniques for transplanting organs and sewing arteries together are still routinely performed. By the 1950s, synthetic materials were introduced as arterial replacements, which became acceptable treatment for many patients.

In addition to balloon angioplasty, nonsurgical or minimally invasive surgical techniques for opening blocked arteries and veins to improve blood flow include the use of a stent, or a small mesh tube, which can be expanded inside a blocked blood vessel to increase its diameter and then remain there to hold it open; an atherectomy, in which a thin tube is inserted into the vessel to cut away the plaque; and thrombolysis, which is the use of either traditional pharmaceuticals or biopharmaceuticals to break down blood clots. Although technically performing a bypass graft is feasible, the graft cannot approach the durability and performance of a native artery and typically does not last longer than fifteen years. Research involving the transplantation of human arteries may solve some of these problems and allow more patients to benefit from surgery.

Vascular surgery can benefit large numbers of people simply because of the nature of atherosclerosis. It may be a product of habits, the environment, or genetic makeup, but it is widely accepted that as the population ages, more and more people will suffer from diseases that can be helped by vascular surgery, allowing them to maintain lifestyles that are as productive as possible. Basic scientific research into the mechanisms of atherosclerosis may yield important answers and lead to new therapies for patients with vascular disease.

Bibliography

Ancowitz, Arthur. Strokes and Their Prevention: How to Avoid High Blood Pressure and Hardening of the Arteries. New York: Jove, 1980.

Cissarek, Thomas, et al., eds. Vascular Medicine: Therapy and Practice. New York: McGraw-Hill Medical, 2011.

Cronenwett, Jack L., and K. Wayne Johnston, eds. Rutherford's Vascular Surgery. 7th ed. Philadelphia: Saunders/Elsevier, 2010.

Ernst, Calvin B., and James C. Stanley, eds. Current Therapy in Vascular Surgery. 4th ed. St. Louis, Mo.: Mosby, 2001.

Jaff, Michael, and Corey Goldman. Handbook of Vascular Medicine for the Cardiologist: The Basics of Vascular Diagnosis and Therapy. Boston: Blackwell, 2003.

Marieb, Elaine N. Essentials of Human Anatomy and Physiology. 10th ed. San Francisco: Pearson/Benjamin Cummings, 2012.

Rooke, Thom W., Timothy M. Sullivan, and Michael R. Jaff, eds. Vascular Medicine and Endovascular Interventions. Columbia, Md.: Society for Vascular Medicine and Biology, 2007.

Society for Vascular Medicine. http://www.vascularmed.org

Tortora, Gerard J., and Bryan Derrickson. Principles of Anatomy and Physiology. 13th ed. Hoboken, N.J.: John Wiley & Sons, 2012.

"Vascular Diseases." MedlinePlus, September 3, 2013.

Melba Pattillo Beals wrote that some people called her a hero for participating in the integration of Central High School. Do you agree that Melba...

The definition of a hero is someone who is admired for his or her courage or good deeds, so I think Melba Patillo Beals is a true hero. She had great courage to face the angry mobs that taunted her and the other African-American students who integrated Central High School in Little Rock, Arkansas, in 1957-1958. She faced these mobs and hostile students, some of whom threatened to hurt or kill her, every day during an entire school year. Someone even threw acid in her eyes, which she was able, with the help of the soldier guarding her, to quickly wipe out of her eyes. She never retaliated with violence, and though she was uncertain about whether she could go on, she returned to school day after day. Her actions showed great courage and perseverance. Her commitment to integration, to civil rights, and to her faith only grew in the face of the violence she faced, as she was dedicated to the cause and committed to making the world a fairer place. In order to advance the cause of civil rights, she sacrificed a year of her adolescence and later committed herself to continuing to fight for the cause. 

What was Mr. Lorry thinking on the evening of the third of September (Book 3 Chapter 4)? Were his thoughts proved right or wrong?

In Book the Third, Chapter 4, Doctor Manette has just returned from visiting Charles Darnay in prison, where he was unable to secure the release of his son-in-law, despite his stature as a former prisoner of the Bastille. As he sits in his chair, Mr. Lorry observes him closely. Doctor Manette is clearly upset at his failure, fearing for Charles’s future. Mr. Lorry is afraid that the doctor’s old troubles will return, reverting him back to the prisoner in 105 North Tower, wondering where the shoes are that he needs to repair. Instead, Doctor Manette seems strong. He decides that at last his suffering has brought him strength and power. He sees that Doctor Manette has a will of iron, that he will do whatever is necessary to release Charles. The years seem to have melted away, and Doctor Manette is once again the man of strong character of his youth. Yet, when Charles’s release is finally secured, it is only temporary. Charles is once again arrested and put in prison. When his true identity is revealed to all, Doctor Manette briefly struggles with keeping his grasp on reality.

What is hair?

Structure and Functions

Humans grow three kinds of hair. The downy hair that covers the fetus is lanugo. Soon after birth, it is replaced by vellus (or villus) hair. Vellus hair covers the entire skin surface except for the palms of the hands and the soles of the feet. It is fine, short, nearly colorless, and slow-growing.

The thick, pigmented hair on the head, eyebrows, and eyelids is terminal hair. Somewhere between 65 and 95 percent (by weight) of terminal hair is protein. Other components include water, fats (lipids), trace elements (minerals), and pigment. Because proteins twist into complex three-dimensional shapes held together by chemical bonds, hair is both rigid and flexible. Terminal hair replaces villus hair on the genitals at puberty. Called pubic hair, it is coarse and curly. Also at puberty, terminal hair begins to grow in the armpits and on the faces of males.

The shaft of a single hair has three layers. The outer casing is the cuticle, made of overlapping layers of proteinaceous material. Inside the cuticle lies the cortex, a column of cells containing keratin, the same protein that hardens tooth enamel and fingernails. The central core of the hair is the medulla. Also called the pith, it is made of small, hardened cells snared in a web of fine filaments.

Hair grows from a tiny pouch below the skin’s surface called a follicle. At the bottom of the follicle lies the papilla, an upward-growing finger of connective tissue. The papilla forms the root of the hair shaft. The actively growing part of the hair shaft is the hair bulb. The cells that generate the hair lie just above the hair bulb. As soon as hair cells are manufactured, they harden and die, forming the hair shaft.

Tiny blood vessels around each follicle supply nutrients. Sebaceous glands that open into the follicle produce the oily sebum that lubricates hair and skin. In the papilla of the follicle, melanocytes produce melanin, the same pigment that gives skin its color. There are two kinds of melanin: Eumelanin makes hair black or brown, while pheomelanin makes it red or blond. Melanin is deposited in the cortex of the hair shaft of terminal hair, giving it its color.

Hair helps insulate the body. Arrector pili muscles at the base of the follicle elevate hair in response to environmental stimuli, including cold. The high sulfur content of keratin gives it heat-retaining properties. Hair also retards water loss from the body. Body hair augments the sense of touch. Hair’s movement facilitates the detection of light touches and slight temperature changes.

Terminal hair cushions the head against blows and protects the scalp from sunburn. Eyelashes keep dirt, insects, and foreign objects out of the eyes. Eyebrows keep sweat from running down into the eyes. The hair inside the ears is coated with the waxy substance cerumen that traps dirt and prevents infections. Hair in the nose filters dust and bacteria from the air.

Hair growth and replacement occur in three stages. Anagen is the active growth stage. It lasts from two to six years. During catagen, lasting about two weeks, the lower segment of the hair follicle breaks down. A “club hair” separates from the papilla and falls out. Then, during telogen, the follicle “rests.” Telogen lasts several weeks or months. At any one time, about 80 to 90 percent of the hairs on the head are in anagen, 3 to 4 percent are in catagen, and the remainder are in telogen.

Disorders and Diseases

While a loss of fifty to one hundred scalp hairs per day is normal, alopecia, or noticeable hair loss, occurs in nearly one-third of women and two-thirds of men. Women typically notice a general thinning of the hair, while men usually experience male pattern baldness:
loss at the hairline and crown first, followed by loss at top of the head. The cause is neither a loss of follicles nor a cessation of hair growth. Instead, follicles gradually shrink and become less active, producing shorter, finer vellus hairs. Three interacting factors—heredity, hormones, and aging—cause the change in follicles. Genetic programming controls the age when hair loss begins and how fast it progresses. Male hormones (even in women) must be present for balding to occur.

No drug can reverse baldness in its later stages. However, minoxidil (trade name Rogaine) slows the rate of hair loss or promotes regrowth in about 25 percent of men and 20 percent of women. It received the approval of the Food and Drug Administration (FDA) in 1988 and became available without a prescription in 1996. Another drug, finasteride (trade name Propecia), was approved in 1997 for use in men only.

Surgical alternatives are available for those bothered by baldness. To transplant
or graft hair, surgeons remove segments of scalp from the sides and back of the head (where follicles are less sensitive to hormones) and transfer them to the top. To perform a scalp reduction, surgeons cut away a portion of hairless scalp, then stitch the remaining scalp together, reducing the total area of baldness. Another alternative is flap surgery. A flap of hair-bearing scalp is turned to cover the spot where bald scalp has been removed.

Alopecia areata is the loss of hair in round patches, usually on the scalp, beard, eyebrows, or pubic area. It is thought to be an autoimmune disease. The immune system “mistakes” the hair follicles for invading disease agents and attacks them, reducing their size and decreasing hair production. The disorder may result from fever, stress, surgery, allergies, crash diets, burns, scalds, and tumors. Other possible causes include radiation exposure, an overactive or underactive thyroid gland, liver or kidney disease, and illnesses ranging from influenza to scarlet fever. A deficiency of iron, zinc, or certain vitamins is the cause in some cases, as is chemotherapy for cancer. Hair loss is also a side effect of many drugs. Alopecia areata is seldom serious or permanent, but it can be disturbing. A doctor may prescribe drugs to combat it, but it generally resolves itself within a year.

Hirsutism, excessive hair growth on the face or body, can cause concern, especially for women. Although it can be triggered by tumors, diseases of the ovaries or adrenal glands, contraceptive pills, hormonal drugs, or anabolic steroids, the most common cause is the menopause. As production of the female hormone estrogen declines, the relative concentration of male hormones (produced naturally by the adrenal glands) rises, causing dark hairs to appear on the upper lip, chin, and cheeks. Shaving, tweezing, waxing, sugaring, or using depilatory creams and lotions removes hair temporarily. Electrolysis, in which a needle inserted into the follicle delivers a current that destroys the follicle, removes hair permanently. In severe cases, doctors may prescribe drugs that block the action of male hormones to treat hirsutism in women.

Perspective and Prospects

Since ancient times, people have sought to prevent or reverse the balding process. The Egyptians of the sixteenth century BCE prescribed a blend of iron, red lead, onions, and alabaster, along with prayers to the sun god. In 420 BCE, the Greek Hippocrates, often called the founder of modern medicine, recommended a mixture of opium, horseradish, pigeon droppings, beetroot, and spices.

The concept of surgical hair transplantation arose in the early nineteenth century, and in the twentieth century reliable techniques were developed. Japanese physicians pioneered hair transplantation and grafting in the late 1930s and early 1940s, but it was not until the 1980s that procedures yielding cosmetically acceptable results were achieved in the United States. Drug treatments for baldness were discovered by chance as side effects. Minoxidil originally treated hypertension; finasteride ameliorated prostate enlargement.

Attempts to remove unwanted hair have roots in prehistory. Sharpened rocks and shells used for hair removal have been found in archaeological sites dating back twenty thousand years. The ancient Sumerians invented tweezers, and the Egyptians buried razors and arsenic-based depilatories with their dead. Native American men tweezed facial hair with clamshells, and North American colonists in the seventeenth century used caustic lye to burn hair away. In 1903, the American inventor King Gillette marketed the first razor with a disposable blade. Jacob Schick introduced the electric shaver in 1931.

In the 1960s, lasers were first used to heat and disable hair follicles over large areas, and hair removal entered the arena of medical practice. Early lasers emitted a continuous wave that risked overheating and skin damage. The invention of a switching device allowed light energy to enter the follicle in controlled pulses. In 1995, the FDA approved the first laser device for hair removal. Most developed since that time use water or gel to cool the skin and laser light to target the melanin in the hair. Other strategies are being investigated, and studies of such variables as beam width, pulse duration, and delivery rate may result in laser hair removal treatments that are safe, effective, and permanent.

Basic research on the nature and action of the immune system may lead to treatments for autoimmune disorders, including alopecia areata. The cloning of individual, hair follicles may facilitate hair transplantation. Gene therapy could, in theory, be used to alter the genetic control of follicles, preventing inherited baldness entirely.

Bibliography

Anderson, Richard R. “Lasers in Dermatology: A Critical Update.” Journal of Dermatology 27, no. 11 (November, 2000): 700–705.

Brynie, Faith Hickman. 101 Questions About Your Skin That Got Under Your Skin . . . Until Now. Brookfield, Conn.: Twenty-first Century Books, 1999.

Burns, Tony, et al., eds. Rook’s Textbook of Dermatology. 7th ed. Malden, Mass.: Blackwell Science, 2004.

Dunn, Rob. "Hirsute Pursuits." New Scientist 214, no. 2869 (June 16, 2012): 44–47.

Freedberg, Irwin M., et al., eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. 2 vols. New York: McGraw-Hill, 2008.

Kuntzman, Gersh. Hair! Mankind’s Historic Quest to End Baldness. New York: AtRandom, 2001.

Unger, Walter P., Ronald Shapiro, Robin Unger, and Mark A. Unger, eds. Hair Transplantation. 5th ed. New York: Informa Healthcare, 2011.

Wood, Debra. "Alopecia." Health Library, October 31, 2012.

What is the fascia?

Structure and Functions

There are three layers of fascia: the superficial fascia, the deep fascia, and the visceral fascia. The superficial fascia, also known as the subcutaneous tissue, is a layer of adipose or fatty tissue that lies under the skin. The deep fascia is a layer of dense, fibrous tissue that lies under the superficial fascia, surrounding and penetrating the muscles, bones, nerves, body organs, and blood vessels. The deep fascia has extensions that stretch from the tendons that attach muscles to bone and lie in broad, flat sheets, called an aponeurosis. The deep fascia is so strong that it is rarely damaged, even in traumatic injuries. The visceral fascia surrounds the body organs, suspends them, and wraps them in a protective layer of connective tissue.

The superficial fascia has the capability of stretching to accommodate pregnancy and weight gain. Usually, it slowly reverts to its normal tension level after pregnancy or weight loss. The visceral fascia lacks the elastic properties of the superficial fascia, since its role is to protect the body organs. It provides for limited movement of the organs within their cavities, while not constricting the organs. The deep fascia contains many sensory receptors that are able to report pain and changes in body movement, in pressure and vibration within the body, in the chemicals produced by the body, and in body temperature.

The deep fascia contracts during the response to a threat, known as the “fight or flight” reflex. This increased tension increases the strength of it. The deep fascia relaxes at times when the body is stressed beyond what it can tolerate and when the body is put in a relaxing position. If the tension on the deep fascia persists, then it responds by adding collagen and other proteins, which bind to the existing proteins. While this increases the strength of the body, it can restrict the structures that it is supposed to protect. Hormones produced by the body can relax the deep fascia. For example, parasympathetic nervous system hormones can trigger its relaxation.

Disorders and Diseases

Due to the presence of fascia throughout the body, many conditions can be caused by its disorders. Some examples are adhesions, carpal tunnel syndrome, compartment syndrome, fibromyalgia, hernia, Marfan syndrome, meningitis, mixed connective tissue disease, myofascial pain syndrome, necrotizing fasciitis, pericardial effusion, plantar fasciitis, pleural effusion, polyarteritis nodosa, rheumatoid arthritis, scleroderma, and tendinitis.

Common conditions that affect the fascia are carpal tunnel syndrome, inguinal hernia, plantar fasciitis (heel spur), rheumatoid arthritis, and tendonitis. Carpal tunnel syndrome affects a small opening through the wrist into the hand. The median nerve and the carpal ligament pass through this opening. Narrowing of the opening pinches these structures and causes pain and numbness in the hand. The treatment includes physical therapy, wrist splints, and possibly surgery. An inguinal hernia is the protrusion of part of the bowel through an opening in the fascia. It protrudes through the openings in the abdominal aponeurosis for the two saphenous veins. Inguinal hernias are treated by surgery to support the aponeurosis in the area of these openings.

Plantar fasciitis is caused by chronic inflammation of the fascia that supports the arch of the foot, leading to calcification on the bottom of the heel. This condition is treated with orthotics or surgery. Rheumatoid arthritis is an autoimmune condition that affects symmetric joints in the body and causes chronic inflammation of the synovial membranes in the joints, leading to joint damage. Many medications are available to treat rheumatoid arthritis, but they suppress the immune response of the body and so have risks. Tendinitis is inflammation of a tendon, often as a result of injury or repetitive use, such as tennis elbow. This condition is treated with corticosteroid injections into the joint, the application of ice or heat, and rest.

Perspective and Prospects

The importance of the fascia has been embraced by practitioners other than doctors of traditional medicine. The fascia forms the basis for therapies such as Rolfing, massage, chiropractic, physical therapy, osteopathy, yoga, and Tai Chi Chuan. In the late 1800s, Sweden’s Pehr Henrik Ling, with his associates, wrote of the relationship of mind and body. His therapy was aimed at improving the mental status of a person by improving their ability to move their body. In 1984, Raymond Nimmo wrote of the importance of treating the fascia, as well as trigger points in the body.

Ida P. Rolf (1896–1979) was a notable pioneer in the understanding of the importance of the body fascia. Rolf felt that the fascia had been largely ignored by the medical community and developed a technique centered on structural integrity and the importance of gravity. Structural integrity deals with the property of the fascia that causes it to adapt to changes in the body, even when the change puts the body off balance, out of alignment, or causes pain. Rolf devoted much of her life to treating those disabled who had not responded to medical treatment. Her therapy is called Rolfing.

Medical doctors specializing in exercise physiology, neurology, and orthopedics are becoming more cognizant of the role of the fascia in the body. However, chiropractors continue to hold the primary role in dealing with problems of the fascia that do not respond to medical treatment. In 2007, the first International Fascia Research Congress was held in Boston, Massachusetts.

Bibliography

"Bones, Joints, and Muscles." MedlinePlus, December 5, 2011.

"Carpal Tunnel Syndrome." MedlinePlus, April 19, 2013.

Chwistek, Marcin. "Rheumatoid Arthritis." Health Library, September 30, 2012.

Leach, Robert E., and Teresa Briedwell. "Tendinopathy." Health Library, March 18, 2013.

Lindsay, Mark. Fascia: Clinical Applications for Health and Human Performance. Clifton Park, N.Y.: Delmar Cengage Learning, 2008.

Paoletti, Serge. The Fasciae: Anatomy, Dysfunction, and Treatment. Lisbon, Maine: Eastland Press, 2006.

Scholten, Amy, and Peter Lucas. "Groin Hernia—Adult." Health Library, March 18, 2013.

Schultz, R. Louis, and Rosemary Feltis. The Endless Web: Fascial Anatomy and Physical Reality. Berkeley, Calif.: North Atlantic Books, 1996.

Vorvick, Linda J., C. Benjamin Ma, and David Zieve. "Plantar Fasciitis." MedlinePlus, March 1, 2012.

In "The Scarlet Ibis," when the narrator says that Doodle is a "terrible liar," what does he really mean?

Doodle and his brother, who is never named, are the main characters in James Hurst's short story "The Scarlet Ibis." Almost everyone believes Doodle will die when he's a baby, but he survives and when he is five years old his brother teaches him to walk. They then spend much of their time out in nature, especially at Old Woman Swamp. It is during these excursions that the two tell wild tales. The brother, who is the narrator of the story, calls them lies, but they are really just imaginative stories, the kind children invent all the time. 

The brother says that his "lies were scary" but that Doodle's "were twice as crazy." Doodle's stories are fantastical with colorful birds and flying people. The stories are symbolic of two things. First, because Doodle is crippled, they reveal his wish for unrestricted freedom of movement. Instead of being just able to walk, he wants to fly. Second, the story of the peacock foreshadows Doodle's death. Every night the bird figuratively swallows up Peter in a reference to death with terms such as "go-to-sleep" and "burying." Hurst writes,

When Peter was ready to go to sleep, the peacock spread his magnificent tail, enfolding the boy gently like a closing go-to-sleep flower, burying him in the glorious iridescent, rustling vortex.

The stories reveal that Doodle is a sensitive boy and that he has an extremely vivid imagination. 

What is the relationship between birth defects and alcohol?

The Dangers of Drinking for Two

When a pregnant woman drinks alcoholic beverages, the alcohol in her blood crosses the placenta easily and enters the embryo or fetus through the umbilical cord. Children affected by prenatal exposure to alcohol may suffer lifelong consequences, including intellectual impairment, learning disabilities, and serious behavioral problems.

All drinks containing alcohol can hurt an unborn baby. A standard twelve-ounce can of beer has the same amount of alcohol as a four-ounce glass of wine or a one-ounce shot of straight liquor. In addition, some alcoholic drinks, such as malt beverages, wine coolers, and mixed drinks, often contain more alcohol than a twelve-ounce can of beer. Studies have not been done to establish a known safe amount of alcohol that a woman can drink while pregnant.

Any time a pregnant woman participates in regular drinking increases her chance of having a miscarriage and puts her unborn child at risk for growth deficiencies, learning disabilities, and behavioral problems. Birth defects associated with prenatal exposure to alcohol can occur in the first eight weeks of pregnancy, before a woman even knows that she is pregnant.

Between 2011 and 2013, one in ten pregnant women surveyed reported alcohol use, and one in thirty-three reported binge drinking within thirty days of the survey, according to the CDC.

Fetal Alcohol Syndrome

Fetal alcohol syndrome (FAS) is caused by alcohol consumption during pregnancy and is one of the leading known causes of mental disability and birth defects. It is characterized by abnormal facial features, including small head size, narrow eye slits, and abnormalities of the nose and lip areas; growth deficiencies; and problems with the central nervous system (CNS).

Children with FAS may have problems with learning, memory, attention span, problem solving, speech, and hearing. These problems often lead to difficulties in school and in getting along with others. FAS is an irreversible condition that affects every aspect of a child’s life and the lives of his or her family. FAS is preventable if a woman abstains from alcohol while she is pregnant.

Fetal Alcohol Effects

In the past, the term fetal alcohol effects (FAE) was generally used to describe children who did not have all of the clinical signs of FAS, but who had various problems, including growth deficiency, behavioral problems, or problems with motor and speech skills. FAE has also been used to describe children who have all of the diagnostic features of FAS, but at mild levels. Because experts in the field were unable to agree on a single definition for FAE, the Institute of Medicine (IOM) proposed the terms alcohol-related neurodevelopment disorder (ARND) and alcohol-related birth defects (ARBD). ARND describes the functional or mental impairments linked to prenatal alcohol exposure, such as behavioral or cognitive abnormalities. These include learning difficulties, poor school performance, poor impulse control, and problems with mathematical skills, memory, attention, and judgment. ARBD describes malformations of the skeletal system and major organ systems. Such malformations may include defects of the heart, kidneys, bones, and auditory system.

Treatment and Prevention

There is no cure for either fetal alcohol syndrome or fetal alcohol effects. They are irreversible, lifelong conditions that affect every aspect of a child’s development. With early identification and diagnosis, a child with FAS can receive services that can help to maximize his or her potential.

The easiest way to prevent FAS is to abstain from alcohol use during pregnancy. Any amount of alcohol consumed during pregnancy is potentially dangerous to an unborn baby. If a pregnant woman is drinking during pregnancy, it is never too late for her to stop. The sooner a woman quits drinking, the better it will be for both her and her baby. If a woman is not able to quit drinking, she should contact her local social service agency or health plan for alcohol abuse treatment, if needed. If a woman is not yet pregnant, she should use an effective form of birth control until her drinking is under control.

Mothers are not the only ones who can help prevent FAS, however. Significant others, family members, schools, social organizations, and communities alike can help to prevent FAS through education and intervention. Also, emerging research suggests that long-term alcohol abuse among men may alter sperm cells in ways that introduce defects to the fetus at conception. Continued research will help to clarify this link and improve prevention efforts.

Bibliography

Chaudhuri, J. D. “Alcohol and the Developing Fetus—A Review.” Medical Science Monitor 6.5 (2000): 1031–41. Print.

“Drinking Alcohol During Pregnancy.” March of Dimes. March of Dimes Foundation, Nov. 2008. Web. 29 Mar. 2012.

“Drinking and Your Pregnancy.” NIAAA. Natl. Inst. on Alcohol Abuse and Alcoholism, May 2010. Web. 29 Mar. 2012.

"Fetal Alcohol Spectrum Disorders (FASDs): Data and Statistics." Centers for Disease Control and Prevention. CDC, 24 Sept. 2015. Web. 28 Oct. 2015

Nayak, Raghavendra B., and Pratima Murthy. “Fetal Alcohol Spectrum Disorder.” Indian Pediatrics 45.12 (2008): 977–83. Print.

“Prenatal Exposure to Alcohol.” Alcohol Research & Health 24.1 (2000): 32–41. Print.

Thackray, Helen M., and Cynthia Tifft. “Fetal Alcohol Syndrome.” Pediatrics in Review 22 (2001): 47–55. Print.

“Treating Individuals Affected with FASD.” NOFAS. Natl. Org. on Fetal Alcohol Syndrome, 2004. Web. 29 Mar. 2012.

What do the lyrics of the song have to do with signing the petition?

Lyddie's roommate, Betsy, becomes more and more dissatisfied with the work at the factory as the novel progresses. She complains that she can no longer handle the speed of the equipment and the greater demands being placed on her as a worker. She says to Amelia, "We're all working like black slaves, is what." She then says she is ready to sign the petition for working ten-hour instead of thirteen-hour days. Over Amelia's objections, she resolves to sign the petition, explaining to Lyddie, "Our real wages have gone down more often than they've gone up. Merciful heaven! Why waste our time on a paper petition? Why not a good old-fashioned turnout?"

By this she means that the workers should participate in a rally protesting the poor working conditions. She then sings the song, "I cannot be a slave." She learned the song when she was only ten, working as a doffer. This indicates that Betsy has been working many years in the factory already. The line that says "Isn't it a pity that such a pretty girl as I should be sent to the factory to pine away and die" actually foreshadows Betsy's fate. She becomes very ill and ends up using all her savings to pay for the doctor and the hospital. She was saving money so she could go to college and have a chance to do what she wanted to do with her life. However, she ends up almost dying and then having no "liberty" to do what she really wants to do despite having slaved away for all those years.

What is pediatric surgery?

Science and Profession

A pediatric
surgeon is a general surgeon who has received additional training in operating on infants and children. The full course of training includes four years of medical school, followed by five years of general surgery
residency and two years of pediatric surgery residency. Pediatric surgeons generally practice in large referral hospitals or children’s hospitals. The relatively small number of American training programs in this specialty are all located at major teaching hospitals.

Children are not simply small adults. They experience some different surgical disorders than adults, especially congenital defects. Their ability to withstand the stress of surgery is less than that of an older person. Also, many of their surgical problems require years of follow-up care by a surgeon who understands child growth and development.

In the first half of the twentieth century, when pediatric surgery was developing as a specialty, the pediatric surgeon was trained to operate on all parts of the child’s body. As the specialty matured, however, the pediatric surgeon came to perform only general surgical procedures on infants and children. This trend was made possible by the development of pediatric subspecialties in the other surgical fields, such as neurosurgery and cardiac surgery. In addition, pediatric surgeons work closely with pediatricians. As a team, they share in evaluating the patient and in providing preoperative and postoperative care.

To a degree, pediatric surgeons differ from general surgeons in their point of view. Infants and children change constantly as they grow, and common surgical diagnoses also change with the age of the patient. Additionally, the ability of a child’s body to cope with disease and with surgery alters with age. It is therefore necessary for the pediatric surgeon to understand child growth and development.

Although a disorder may be surgically corrected in infancy, the child may continue to have postoperative difficulty for many years. An example is the removal of a large amount of intestines, which must sometimes be done with premature infants. It takes considerable patience and expertise to follow this sort of patient for years, adjusting the child’s diet and treatment to achieve as nearly normal growth as possible. The pediatric surgeon is specially trained to provide this care.

The organs and tissues of an infant or child are much smaller than those of an adult. The pediatric surgeon must develop expert skills to perform surgery on these small structures. Also, the pediatric surgeon is trained to work rapidly when performing surgery. It is important to complete procedures quickly to minimize stress on the pediatric patient.

Congenital defects are, fortunately, relatively uncommon. The pediatric surgeon treats relatively more of these conditions than a general surgeon would and therefore has greater experience in caring for them. Examples of congenital defects treated by pediatric surgeons include defects of the abdominal wall and diaphragm and the obstruction or absence of a part of the intestinal tract.

Because the patient is a child, the pediatric surgeon must also deal with the patient’s family. This specialist is trained to build a supportive relationship with parents and to teach them about their child’s disorder so that they can be informed participants in decisions regarding the patient’s care. Especially with chronic diseases, the parents must be kept aware of their child’s progress and changing needs so that they can participate fully in the child’s recovery.

Diagnostic and Treatment Techniques

The pediatric surgeon’s day is split between the operating room and the clinic. This specialist spends relatively more time in the clinic than does a general surgeon. Surgical correction is only one step in pediatric surgery: careful evaluation and planning must precede any procedure. Afterward, extended follow-up care is often necessary, sometimes for years. This type of care requires patience and an interest in long-range planning on the surgeon’s part.

The pediatric surgeon relies heavily on history taking and physical examination of the patient. This information, plus knowledge of the incidence of specific disorders at different ages, leads the surgeon to the most likely diagnosis. Specific laboratory and radiographic tests are ordered to aid in the diagnostic process.

The pediatric surgeon works very closely with the anesthesiologist, the physician responsible for keeping the patient anesthetized and his or her vital functions stable during surgery. The needs of a child are different from those of an adult during surgery. Many hospitals with pediatric surgeons are also staffed with pediatric anesthesiologists.

Like other surgeons, the pediatric surgeon also performs minor surgery on children, often in the clinic. Examples of minor procedures are the suturing of lacerations, the drainage of small abscesses, and the excision of small benign growths under the skin.

Perspective and Prospects

Pediatric surgery began as an offshoot of general surgery in the first half of the twentieth century. For decades, the specialty met resistance from general surgeons. The American Academy of Pediatrics was the first medical group in the United States to recognize the value of pediatric surgeons and, following a meeting by the academy in 1948, established a surgical section. C. Everett Koop, the surgeon general under President Ronald Reagan, was a vigorous advocate of pediatric surgical education and a developer of new surgical techniques for children from 1946 through the 1990s. He was an important proponent in the eventual recognition of pediatric surgery as a surgical specialty. It was not until 1973, however, that the US Board of Pediatric Surgery certified the first specialists in the field. The number of training programs for pediatric surgeons has grown since then, although their limited number of graduates, in comparison to other specialities, means that pediatric surgeons will continue to be in great demand.

Bibliography

American Pediatric Surgical Association, 2013.

Azarow, Kenneth S., and Robert A. Cusick. Pediatric Surgery. Philadelphia: Saunders, 2012.

Cockburn, Forrester, et al. Children’s Medicine and Surgery. New York: Oxford University Press, 1996.

Coran, Arnold G., et al. Pediatric Surgery. 7th ed. Philadelphia: Elsevier Mosby, 2012.

Glick, Philip L., et al. Pediatric Surgery Secrets. New York: Hanley & Belfus, 2001.

Koop, C. Everett. “Pediatric Surgery: The Long Road to Recognition.” Pediatrics 92 (October, 1993): 618–21.

O’Neill, Jr., James A., et al., eds. Principles of Pediatric Surgery. 2d ed. St. Louis, Mo.: Mosby, 2004.