What is digeorge syndrome? |

Causes and Symptoms

Chromosomes possess two parts. The upper arms are called “p” arms and the lower arms are called “q” arms. Patients with DiGeorge syndrome are missing a tiny interstitial piece inside the long arm of chromosome 22. The specific region inside the long “q” arm is labeled 11.2. Thus, DiGeorge syndrome is also referred to as 22q11.2 deletion syndrome or chromosome 22 interstitial deletion.

Most microdeletions such as these cannot be observed under a microscope because they are so tiny. A molecular cytogenetic test known as fluorescence in situ hybridization (FISH) is used. It includes the use of deoxyribonucleic acid (DNA) probes made from the DiGeorge chromosomal region (DGCR). A green fluorescent probe is used to identify chromosome 22, while a red probe is specific to the DGCR. In DiGeorge syndrome, one of the chromosomes will lack the red fluorescence.

About 93 percent of patients have a spontaneous (de novo) deletion of a 22q11.2, and 7 percent have inherited the deletion from a parent. The very high de novo rate indicates that the deletion recurs with a high frequency as a result of new mutations occurring in the population. This deletion is inherited in an autosomal dominant manner. The offspring of persons with the deletion have a 50 percent chance of inheriting it. This interstitial deletion encompasses about three million base pairs of DNA in the majority of patients. About 90 percent of patients have the same three million base pair deletion, while 10 percent have a 1.5 million base pair deletion. Therefore, the deletion is large enough to contain nearly one hundred genes.

DiGeorge syndrome is initiated by defective embryonic development of the third and fourth pharyngeal pouches during the fifth week of development. These pouches normally become the thymus and the parathyroid glands. In the absence of a thymus, T lymphocyte maturation is stopped at the precell stage. DiGeorge syndrome is one of the most severe forms of deficient T cell immunity. Children with DiGeorge syndrome develop recurrent viral infections and have abnormal cellular immunity, as characterized by severely reduced or absent T lymphocytes. They also have defects in T cell–dependent antibody production. A spectrum of abnormal phenotypes may develop. These defects arise from the absence of key genes that are not available for normal development when a 22q microdeletion is present. Infants with this disease may suffer from congenital heart disease of various types, palatal abnormalities (such as cleft palate), and learning difficulties.

Treatment and Therapy

Children with a 22q11.2 deletion may exhibit a wide spectrum of problems and much variation in the severity of symptoms. A patient with DiGeorge syndrome may have several organs or systems affected. DiGeorge syndrome may result in problems in different body systems, such as the heart or palate, and in cognition, such as learning style. Consequently, a multidisciplinary approach is needed for management of a specific patient.

In the neonatal period, the following clinical and laboratory studies are pursued. The serum is tested for calcium; a low concentration points to the need for supplementation. The lymphocytes are measured; a low absolute count means referral to an immunologist, who will look at T and B cell subsets. A renal ultrasound examination should be performed because of the high incidence of structural renal abnormalities. A chest X-ray is needed to identify thoracic vertebral anomalies. A cardiac evaluation is recommended for all patients with DiGeorge syndrome because possible malformations may include tetralogy of Fallot, ventricular septal defect, interrupted aortic arch, or truncus arteriosus. Pediatric cardiologists are necessary for the treatment and therapy that is needed. An endocrinologist could follow up possible growth hormone deficiencies. Since there is a high incidence of speech and language delay, speech therapy and early educational intervention are highly recommended. All children with the 22q deletion should be seen by a cleft palate team to diagnose problems and schedule surgery if necessary.

Other medical needs of children are met through evaluation by a feeding specialist, especially in the newborn period; a neurologist, for possible seizure disorders or problems with balance; a urologist, for possible kidney problems; and an otorhinolaryngologist (ear, nose, and throat doctor) for problems in this region.

Perspective and Prospects

DiGeorge syndrome is relatively frequent, occurring with a frequency of one in four thousand live births. Therefore, this disorder is a significant health concern in the general population. Since the phenotype associated with it is broad and variable, many types of clinical and laboratory specialists are needed. The medical geneticist is the most likely person to have an overview of the diagnosis. A yearly genetics evaluation is beneficial in answering questions. Parents should be tested to determine their chromosomal status. Genetic counseling could provide individuals and families with information on the nature, inheritance, and implications of DiGeorge syndrome to help them make informed medical and personal decisions. Current and future research using model organisms may help to explain the problems of phenotypic variability in DiGeorge syndrome.

Bibliography:

American Academy of Allergy Asthma & Immunology. "DiGeorge Syndrome (DGS)." AAAAI, 2013.

Emanuel, Beverly S., et al. “The 22q11.2 Deletion Syndrome.” Advances in Pediatrics 48 (2001): 33–73.

King, Richard A., Jerome I. Rotter, and Arno G. Motulsky, eds. The Genetic Basis of Common Diseases. 2d ed. New York: Oxford UP, 2002.

Maroni, Gustavo. Molecular and Genetic Analysis of Human Traits. Malden, Mass.: Blackwell, 2001.

McCoy, Krisha. "DiGeorge Syndrome." Health Library, Dec. 11, 2012.

Rimoin, David L., et al., eds. Emery and Rimoin’s Principles and Practice of Medical Genetics. 5th ed. Philadelphia: Churchill, 2007.

Stocker, J. Thomas, and Louis P. Dehner, eds. Pediatric Pathology. 2d ed. Philadelphia: Lippincott, 2001.

Turnpenny, Peter, and Sian Ellard. Emery’s Elements of Medical Genetics. 13th ed. New York: Churchill, 2007.

What are the ego, superego, and id?

Introduction

The ego, superego, and id are terms used by the father of psychoanalysis, Austrian Sigmund Freud, to describe the three components in the structural model of personality. He developed and wrote about this model in his classic work Das Ich und das Es (1923; The Ego and the Id, 1926).

Prior to the structural model, Freud’s focus was on understanding and differentiating conscious and unconscious processes. He came to realize that an additional model was needed to further elucidate the working of the mind and to describe the special functions that parts of the mind utilize. The structural model is not a replacement for his topographical model (unconscious and conscious), but rather it complements his previous work.

Freud’s structural model proposes that the personality has a definite structure, with three interacting components called the id, ego, and superego. The id is present from birth and is essentially a psychical representation of instincts or passions. The ego represents reason and thoughtful deliberation, while the superego represents the morals of society and ideal aspirations. These components are hypothetical and are not located in a specific region of the brain. Since Freud’s initial background and work were biologically based, this represented a major shift toward a more psychological understanding of human behavior.

Id

The id is present at birth, is totally unconscious, and contains everything inherited at birth, especially the innate instincts or impulses. The purpose of the id is to satisfy one’s innate urges. Freud theorized that the id operates according to the pleasure principle, seeking immediate gratification of wishes and a reduction of pain and tension. Since the id is infantile and primitive by nature, it attempts to satisfy its desires by what Freud termed primary process. This means that the id is illogical, asocial, impulsive, and demanding. Primary process means that there is action or discharge without thought or delay. There is no consideration of reality or the needs of others.

The id is instinctual and the source of all energy and passions. Freud proposed two classes of instincts: the sexual instincts, or eros, and the destructive instincts, or thanatos. Eros includes humans’ drives for self-preservation and the preservation of the species through sexuality. These instincts are life affirming, seeking development and renewal. In direct contrast, thanatos opposes life and seeks to bring about death and destruction. Freud viewed the death instinct (thanatos) as a desire to return to an earlier, inorganic state with an absence of undesired stimulation. Both classes of instincts can be directed inward toward the self or outward toward others. Eros and thanatos are typically fused (combined) together, thus modifying the potential destructiveness of thanatos.

Ego

The ego, according to Freud, is the component of the mind that is able to adapt to the demands of the external environment. The ego develops from the id and learns about the external world through the senses. As the child interacts with the world, the ego gains important perceptual and cognitive abilities.

Freud proposed that the ego operates according to the reality principle, replacing the id’s uninhibited search for gratification with thoughts and behaviors that take into account the conditions of real life and the needs of others. The ego uses a secondary process, a higher level of mental functioning, including intelligent reasoning and problem-solving skills, to mediate between the demands of the id, superego, and external reality. The ego therefore functions as the executive component of personality structure. The ego exercises delay and restraint in meeting the unrealistic demands of the id’s impulses. It considers how pleasure can be obtained without bringing harm to the self or others.

The metaphor of a horse and rider was used by Freud to describe the relationship between the ego and the id. The horse represents the power and strength of the id, while the rider (ego) attempts to guide the horse in an appropriate direction.

After Freud’s death, his daughter Anna and others focused their study on ego functioning in the personality. Ego psychology is a term used to describe the study of the ego and its role in adaptation and development.

Superego

Freud used the term superego, commonly referred to as conscience, to describe the third component of personality structure. The conscience is formed by the moral influences of parents and society, including rules and standards of conduct. It serves as the judge of what is right and wrong and can be quite harsh and perfectionistic.

The superego develops as children identify with parents and authority figures. Freud believed that the superego forms by an introjection (a process of taking inside or incorporating) of the values of the parents. It is interesting to note that this concept served as precursor to object relations theorists, who pay close attention to relationships between internal objects and external relationships. The superego, as an internal object, takes over the initial role of the parents by giving the ego orders, judging, and threatening it with punishments. Guilt feelings result when behavior does not live up to the expectations of the superego.

Integration of Id, Ego, and Superego

Freud theorized there would always be some conflict between the urges of the id, the morality of the superego, and the pressures of reality. The ego, as mediator, strives to fulfill the id impulses in a reasonable way while conforming to the superego’s moral standards. Impulsive, reckless behavior results when the id is too dominant, whereas a dominant superego leads to a loss of normal pleasure as impulses are too restricted.

Bibliography

Brenner, Charles. An Elementary Textbook of Psychoanalysis. Rev. ed. New York: Anchor, 1994. Print.

Diamond, Michael J., and Christopher Christian. The Second Century of Psychoanalysis: Evolving Perspectives on Therapeutic Action. London: Karnac, 2011. Print.

Elisha, Perrin. The Conscious Body: A Psychoanalytic Exploration of the Body in Therapy. Washington: American Psychological Association, 2011. Print.

Freud, Sigmund. The Ego and the Id. LaVergne: Pacific, 2011. Print.

Gay, Peter. Freud: A Life for Our Time. New York: Norton, 2006. Print.

Greenberg, Jay R., and Stephen A. Mitchell. Object Relations in Psychoanalytic Theory. Cambridge: Harvard UP, 2003. Print.

Webster, Jamieson. The Life and Death of Psychoanalysis: On Unconscious Desire and Its Sublimation. London: Karmac, 2011. Print.

What are tonsils? |

Structure and Functions

The palatine tonsils are the largest bodies of lymphoid tissue in Waldeyer’s ring. In contrast to the adenoid and lingual tonsil tissues, which are diffuse and adherent to the nasopharynx and the base of the tongue, the palatine tonsils are encapsulated by a specialized fascia and are easily dissected from their muscle beds. The tonsil tissues have ten to thirty deep crypts that extend into each tonsil and are lined by stratified squamous epithelium. Each tonsil sits in a tonsillar fossa in the lateral wall of the opening between the mouth and the pharynx. This tonsil bed is composed of three muscles that hold the tonsil in place. The anterior pillar of the tonsil is formed by the palatoglossus muscle, the posterior pillar is formed by the palatopharyngeal muscle, and the floor of the tonsil bed is formed by the superior constrictor muscle of the pharynx. The tonsils get their blood supply primarily at their lower pole from branches of the dorsal lingual and facial arteries. The tonsils’ main nerve supply is from the tonsillar branches of the glossopharyngeal
nerve.

The tonsils are immunologically active lymphatic organs. The lymphocytes of tonsil tissues are approximately composed of 60 percent B lymphocytes and 40 percent T lymphocytes. The location of the tonsils in the upper part of the aerodigestive tract exposes them to many airborne allergens. Tonsil crypts are able to trap foreign material and transport it to lymphoid follicles. When stimulated by antigens, B cells can proliferate in the germinal centers of the tonsils and produce all five major antibody classes. It has been shown that the immunologic activity of the tonsils and the adenoids in Waldeyer’s ring helps protect the entire upper aerodigestive tract. Tonsils are most immunologically active between the ages of four and ten. Although it has been a point of controversy over the years, there is no evidence that removing the tonsils results in any immunologic deficiency.

Disorders and Diseases

Acute tonsillitis is commonly caused by both virus and bacteria. Enlargement of the tonsils without exudates is common with the common cold virus. Epstein-Barr virus may cause mononucleosis with high fever, dysphagia, and tonsillitis characterized by thick gray exudates. The most common bacterial infection of the tonsils is group A streptococcus, which is most commonly seen in children at age five to six years. Before antibiotics, acute streptococcal tonsillitis was a frequent precursor of rheumatic fever.

Recurrent tonsillitis and chronic tonsil hypertrophy are the most common reason for performing tonsillectomy in children. Enlarged tonsils can contribute to airway obstruction and sleep apnea. A peritonsillar abscess is more likely to be seen in young adults. The abscess usually forms between the tonsil and the anterior pillar, causing pain, dysphagia, and drooling, and requires drainage. The combination of exudates and bacteria in the crypts of the tonsils can lead to the formation of plugs or stones called tonsilloliths that can cause pain and bad breath. In severe cases, this condition may also be an indication for tonsillectomy.

Cancer of the palatine tonsil accounts for less than 1 percent of all cancers. Men are affected four times more frequently than women, with an age range between fifty and seventy. More than 70 percent of malignancies are squamous cell carcinomas, with lymphoma accounting for most other tonsil malignancies. Risk factors for squamous cell carcinoma include smoking, drinking alcohol, and infection from HPV.

Perspective and Prospects

Tonsillectomy is one of the oldest recorded surgical procedures, with the first removal of tonsils being described by the Roman surgeon
Aulus Cornelius Celsus in 30 c.e. Between 1911 and 1917, Samuel J. Crowe, professor of otolaryngology at Johns Hopkins, reviewed one thousand tonsillectomies performed. His description of sharp dissection with low incidence of complications opened the way to common use of this procedure. By the middle part of the twentieth century, there were more than two million tonsillectomies being performed every year in the United States. Between 1915 and 1960, tonsillectomy and adenoidectomy was the most frequently performed surgery in the United States. Today that number has dropped to about 600,000 cases per year in the United States, according to the American Academy of Otolaryngology. The introduction of new techniques such as electrocautery, laser surgery, and high-frequency ablation have further contributed to lowering the complication rate associated with tonsillectomy to the point that about 80 percent of procedures are now done as outpatient surgery.

Recent research regarding cancers of the oral cavity including squamous cell tonsillar cancers has centered on the emerging role of HPV. HPV is one of the most common viruses in the world. In most cases, these viruses are relatively harmless. However, sexually transmitted types HPV 16 and 18 have been strongly linked to cervical cancer, and they are increasingly being recognized as a cause of oral cancer

as well. Smoking and drinking alcohol may promote the invasive ability of these viruses in the oral cavity. Recent studies suggest that as many as 25 percent of oral cancers may be positive for HPV. Some studies suggest that HPV-positive oral cancers have a better prognosis than HPV-negative cancers. Another recent study suggests that HPV-positive tumors are more likely to begin within the tonsillar crypts. Understanding the relationship and effect of HPV on tonsil cancer may lead to novel approaches for prevention, targeted therapy, and improved ability to predict the prognosis of these
tumors.

Bibliography

"Adenoid Removal." MedlinePlus. November 9, 2012.

Cummings, W. Charles, et al. Cummings Otolaryngology: Head and Neck Surgery. 4th ed. Philadelphia: Mosby/Elsevier, 2005.

Emery, Gene. "Surgery Offers Mixed Benefits For Kids' Sleep Apnea." MedlinePlus. May 21, 2013.

"Enlarged Adenoids." MedlinePlus. November 12, 2012.

Lalwani, K. Anil. Current Diagnosis and Treatment in Otolaryngology—Head and Neck Surgery. 2d ed. New York: McGraw-Hill, 2008.

Luginbuhl, A., et al. “Prevalence, Morphology, and Prognosis of Human Papilloma Virus in Tonsillar Cancer.” Annals of Otology, Rhinology, and Laryngology 118, no. 10 (October, 2009): 742-749.

Pasha, Raza. Otolaryngology: Head and Neck Surgery—A Clinical and Reference Guide. 2d ed. San Diego, Calif.: Plural, 2005.

"Tonsillectomy Facts In The U.S.: From ENT Doctors." American Academy of Otolaryngology–Head and Neck Surgery. July 22, 2013.

What are ergogenic aids? |

Introduction

In the history of sport, athletes have attempted to find a competitive advantage through advanced techniques in training, nutrition, and even in ergogenic aids, such as nutritional supplements and pharmacological aids. The use of these substances—such as anabolic-androgenic steroids (AAS), testosterone precursors (such as androstenedione), and nonsteroidal aids such as human growth hormone (GH) and creatine—have become increasingly popular in recent years, even without thorough scientific data supporting their efficacy and safety.

The population using such performance-enhancing drugs ranges from collegiate to professional athletes to adolescents and high school students. Recent meta-analyses estimate that 3 to 12 percent of adolescent boys have used an anabolic steroid
at least once, and 28 percent of collegiate athletes admit to taking creatine. Other studies have suggested that the number may be closer to 41 percent.

Though such ergogenic aids are thought to improve strength, endurance, agility, and overall performance, most athletic improvement is anecdotal at best. Scientific evidence supporting these ideas is scarce and incomplete. Even with aids that may improve strength and/or performance, the safety of these substances has been seriously questioned, such as with the use of AAS, GH, and ephedra.

Types of Ergogenic Aids

Anabolic-androgenic steroids (AAS) as ergogenic aids in sports are chemical compounds that resemble the structure of testosterone, the naturally occurring male sex hormone that affects muscle growth and strength. “Anabolic” refers to the growth of cells, and “androgenic” refers to the stimulation of the growth of male sex organs and masculine sex characteristics. AAS bind to cells that are used for muscle repair and that can transform into muscle fibers.

AAS has been one of the most studied ergogenic aids, yet many of its mechanisms and adverse effects are still not well understood. Studies have shown that increased doses of testosterone can decrease total body adipose tissue in the body and can increase strength and fat-free mass. Adverse effects of AAS use include hypothalamic-pituitary dysfunction, gynecomastia, severe acne, infection as a result of sharing needles, aggressive and depressive behavior, and a possible association with premature death.

Androstenedione (andro) is a testosterone precursor produced by the adrenal glands and gonads. Its ergogenic effect occurs after it is converted to testosterone in the testes as well as in other tissues. It can also be converted to estrone and estradiol, which are steroid compounds that are primary female sex hormones (found in both men and women). The creation of testosterone is regulated by the amount of testosterone precursors in the body. Theoretically, an increase in androstenedione would increase the production of testosterone and thus can increase protein synthesis, lean body mass, and strength.

Older studies showed that andro supplementation results in increased serum testosterone levels. However, more recent studies have shown that andro supplementation fails to directly improve lean body mass, muscular strength, or serum testosterone levels. Possible side effects to andro use are suppressed testosterone production, liver dysfunction, cardiovascular disease, testicular atrophy, baldness, acne, and aggressive behavior.

Similar to androstenedione, dihydroepiandrosterone (DHEA) is a precursor of testosterone and is also formed in the adrenal glands and gonads. DHEA is the most abundant steroid hormone in circulation and is a precursor to androstenedione and other testosterone precursors (such as androstenediol). Studies of DHEA supplementation have not been shown to increase lean body mass, strength, or testosterone levels. Possible side effects are similar to andro and AAS use.

Human growth hormone (GH) is a metabolic hormone that is secreted into the blood by cells found in the anterior pituitary gland. After its secretion, GH stimulates the production of insulin-like growth factor (IGF)-1 in the liver. These hormones stimulate bone growth, protein synthesis, and the conversion of fat to energy. Athletes have been attracted to GH not only because of such theoretical benefits but also because of the limited techniques in detecting GH in the urine. GH levels vary in individuals of different, ages, sex, and activity and can vary throughout the day, so no reliable benchmark can be made to determine if illicit use has taken place.

Scientific studies have been unable to show that GH leads to increased muscle strength and exercise performance or changes in protein synthesis. Because of ethical limitations, it is difficult to study the effect of larger doses of GH on healthy individuals. Adverse effects of GH use include cosmetic damage, joint pain, muscle weakness, fluid retention, impaired glucose regulation (which may lead to diabetes mellitus), cardiomyopathy, hyperlipidemia, and possibly death.

Erythropoieten (EPO) is a hormone secreted by the kidneys that is a precursor to bone marrow. EPO increases the oxygen-carrying capacity of blood and, as a result, aids in endurance and aerobic respiration. The appeal of EPO among athletes is this endurance-enhancing effect. As a result, many users have been found to be skiers, cyclists, and other athletes who require high levels of endurance. Early use of EPO as an ergogenic aid, termed “blood doping,” came in the form of autologous blood transfusions, in which athletes would harvest their own red blood cells and reintroduce them into their systems before events. A synthetic form of EPO, recombinant human erythropoietin (r-HuEPO) became available in 1988.

Scientific studies have shown that EPO and r-HuEPO treatments do increase certain blood concentrations and can aid in endurance. EPO may also have serious and dangerous side effects, however, such as hypertension, seizures, thromboembolic events, and possibly death.

Creatine monohydrate is an amine synthesized in the kidneys, pancreas, and liver, and it can also be obtained through the diet from meat and fish. Approximately 90 to 95 percent of creatine in the body is found in skeletal muscle. Creatine, which is converted to creatine phosphate (PCr), is an important limiting factor in the resynthesis of adenosine triphosphate (ATP), which plays a significant role in energy reserves within the body. Theoretically, an increase of PCr in the body would increase the regeneration of ATP, resulting in an increase in sustained maximal energy production for short-term exercise. This could lead to increased intensity and repetition frequency, and thus possible increases in skeletal muscle mass.

In 2002, A. M. Bohn and colleagues argued in an article in Current Sports Medicine Reports that there are “no studies demonstrating benefit with the relatively indiscriminant use of variable amounts of creatine by large numbers of athletes on a specific team.” Nevertheless, creatine has been shown to enhance performance in small populations of athletes of various sports. Possible adverse effects of creatine include muscle cramping, dehydration, gastrointestinal distress, weight gain, increased risk of muscle tears, inhibited insulin and creatine production, renal damage, and possibly nephropathy.

Stimulants are drugs that increase nervous system activity. Examples of stimulants commonly used as ergogenic aids include the class of drugs called amphetamines, as well as specific chemical compounds such as caffeine and ephedrine. The use of caffeine has been shown to improve exercise time to exhaustion and may even significantly increase intestinal glucose absorption. It has been suggested that caffeine increases fat utilization for energy and delays the depletion of glycogen (the stored form of glucose). As a result, caffeine and other stimulants are popular ergogenic aids for extended aerobic activity.

Caffeine in small doses has been shown to increase performance. Possible adverse effects of caffeine may include anxiety, dependency, withdrawal, and possibly a diuretic effect (dehydration). Ephedrine may have similar adverse affects. Other stimulants, such as amphetamines or cocaine, have more serious and detrimental effects.

Perspective and Prospects

The use of ergogenic aids in the history of sport has progressively moved from primitive aids to more sophisticated performance enhancers. Crude natural concoctions and stimulants have paved the way for complex pharmacological agents (such as erythropoietin) and designer
anabolic steroids (such as tetrahydrogestrinone). Athletes and trainers have utilized any and all means to gain a competitive edge, even if that results in damage to health and even a risk of death.

The biggest problem stemming from the use of such aids is the difficulty in detecting them. This is evident in recent media attention given to ergogenic aids and their popularity, as seen through the 2007 Mitchell Report, an independent congressional investigation of the use of performance-enhancing drugs in Major League Baseball, as well as the 2012 discoveries of abuse by high-profile cyclists and athletes at the Summer Olympics held in London. This media attention has also shown the difficulties among investigators, such as the International Olympic Committee, the World Anti-Doping Agency, and the United States Anti-Doping Agency, in detecting the use of new designer steroids and new ergogenic aids among elite athletes.

Bibliography

Bhazin, S., et al. “The Effects of Supraphysiologic Doses of Testosterone on Muscle Size and Strength in Normal Men.” New England Journal of Medicine 335 (1996): 1–7.

Bohn, Amy Miller, Stephanie Betts, and Thomas L. Schwenk. “Creatine and Other Nonsteroidal Strength-Enhancing Aids.” Current Sports Medicine Reports 1, no. 4 (August, 2002): 239–245.

Foster, Zoë J., and Jeffrey A. Housner. “Anabolic-Andogenic Steroids and Testosterone Precursors: Ergogenic Aids and Sport.” Current Sports Medicine Reports 3, no. 4 (August, 2004): 234–241.

Graham, T. E. “Caffeine and Exercise: Metabolism, Endurance, and Performance.” Sports Medicine 31, no. 11 (November 1, 2001): 785–807.

Health Library. "Sports and Fitness Support: Enhancing Performance." Health Library, July 25, 2012.

Juhn, Mark S. “Ergogenic Aids in Aerobic Activity.” Current Sports Medicine Reports 1, no. 4 (August, 2002): 233–238.

Mayo Clinic. "Performance-Enhancing Drugs: Know the Risks." Mayo Clinic, December 12, 2012.

MedlinePlus. "Anabolic Steroids." MedlinePlus, June 17, 2013.

Powers, Michael E. “The Safety and Efficacy of Anabolic Steroid Precursors: What Is the Scientific Evidence?” Journal of Athletic Training 37, no. 3 (2002): 300–305.

Shekelle, Paul G., et al. “Efficacy and Safety of Ephedra and Ephedrine for Weight Loss and Athletic Performance: A Meta-analysis.” Journal of the American Medical Association 289, no. 12 (March 26, 2003): 1537–1545.

Singbart, G. “Adverse Events of Erythropoietin in Long-Term and in Acute/Short-Term Treatment.” Clinical Investigation 72 (1994): S36–S43.

Sotas, Pierre-Edouard, et al. "Prevlance of Blood Doping in Samples Collected from Elite Track and Field Athletes." Clinical Chemistry 57, no. 5 (May 2011): 762–769.

Stacy, Jason J., Thomas R. Terrell, and Thomas D. Armsey. “Ergogenic Aids: Human Growth Hormone.” Current Sports Medicine Reports 3, no. 4 (August, 2004): 229–233.

Yesalis, C. E., and M. S. Bahrke. “Doping Among Adolescent Athletes.” Baillieres Best Practice and Research in Clinical Endocrinology and Metabolism 14, no. 1 (March, 2000): 25–35.

What is neuroimaging? |

Indications and Procedures

Images of the living brain or other part of the central nervous system are indicated for any disorder anywhere in the body that may have neurological involvement or complications. Psychiatrists may also order neurological images for their patients whose mental disorders may have physical causes. Typical indications for neuroradiologic diagnosis include cancer, stroke, and head trauma, especially closed head injury.

Depending on what tissue is involved and what condition is suspected, the physician may order any of dozens of neuroimaging methods. The most common in the early twenty-first century are computed tomography (CT),
magnetic resonance imaging (MRI), positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetoencephalography (MEG). Additional methods include Electroencephalography (EEG), near infrared spectroscopy (NIRS), diffuse optical imaging (DOI), and other techniques.

Uses and Complications

Besides clinical uses in diagnosing disease in individual patients, neuroimaging is also valuable as a research tool for studying Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, epilepsy, and other degenerative and acute conditions that affect the central nervous system. It can also increase the understanding of drug effects on the brain, natural aging processes, brain function localization, autism, psychiatric disorders, and many other kinds of physiological events. Well-funded initiatives exist for “brain mapping” to create precise, molecular-level, function-specific atlases of the human brain, as well as the brains of mice, rats, and many other animals. The Laboratory of Neuro Imaging (LONI) at the University of California, Los Angeles (UCLA) is the world leader in this kind of research.

Risks are minimal for patients undergoing brain scans. Usually the worst that can happen is that the scan may provide inadequate diagnosis. The physical dangers are generally the same as for CT or MRI scans on other parts of the body. Occasionally, CT brain scans trigger seizures, especially in children. The chance of these inadvertent seizures is much less with MRI. Another safety advantage of MRI over CT is that MRI does not use radioactive materials. On the other hand, MRIs can be harmful if there is metal inside the body, such as from bone or joint repair, or a pacemaker; doctors must be notified of this ahead of time.

Perspective and Prospects

Neuroimaging began almost immediately after German physicist Wilhelm Conrad Röntgen discovered x-rays in 1895. The limits of using plain film x-rays to diagnose nervous system diseases and other soft tissue disorders soon became apparent. Nevertheless, because of its simplicity and thanks to the pioneering work of Austrian neurologist Artur Schüller and Swedish radiologist Erik Lysholm, physicians until the early 1970s generally preferred plain film to the three other methods available for intracranial and spinal diagnosis: pneumography, radiopaque myelography, and cerebral angiography. These other three all involved using contrast media to improve the detail in the x-ray.

American physician Walter Dandy invented pneumography at Johns Hopkins University in 1918. After observing that x-rays show air as black, soft tissue as gray, and bone as white, Dandy developed techniques to inject air into the central nervous system to serve as a contrast medium. The resulting x-rays clearly highlighted abnormalities such as tumors, but the technique was very dangerous. French scientists Jean Athanase Sicard and Jacques Forestier developed radiopaque myelography, the use of contrast media in spinal x-rays, in the early 1920s.

In the 1920s, Portuguese physician António Egas Moniz developed cerebral angiography, a technique in which a rapid series of skull x-rays were taken immediately after injecting a radioactive contrast medium into both carotid arteries. This proved to be an excellent method of showing abnormalities and displacements caused by tumors, but was disfavored because of its significant danger to the patient and the ugly surgical scars left on the patient’s neck.

British physicist Godfrey Newbold Hounsfield and his team of radiologists built the first practical clinical CT scanning machine in 1971. Between 1971 and 1977, several scientists developed practical MRI from facts about the magnetic properties of atomic nuclei that had been known since the 1950s. These two methods soon superseded both plain film and cerebral angiography as the preferred methods of neuroimaging. Today, there are a great variety of specialized MRI techniques geared toward different kinds of body imaging and diagnosis; an especially important one for brain imaging is functional MRI (fMRI), which can measure neural activity.

Bibliography

Cabeza, Roberto, and Alan Kingstone, eds. Handbook of Functional Neuroimaging of Cognition. 2d ed. Cambridge, Mass.: MIT Press, 2006.

Carter, Rita, and Christopher D. Frith. Mapping the Mind. Rev. ed. Berkeley: University of California Press, 2010.

Clarke, Edwin, and Kenneth Dewhurst. An Illustrated History of Brain Function: Imaging the Brain from Antiquity to the Present. 2d rev. ed. San Francisco: Norman, 1996.

Damasio, Hanna. Human Brain Anatomy in Computerized Images. 2d ed. New York: Oxford University Press, 2005.

D’Esposito, Mark. Functional MRI: Applications in Clinical Neurology and Psychiatry. Boca Raton, Fla.: Taylor & Francis, 2006.

Dumit, Joseph. Picturing Personhood: Brain Scans and Biomedical Identity. Princeton, N.J.: Princeton University Press, 2004.

Mori, Susumu, et al. MRI Atlas of Human White Matter. Boston: Elsevier, 2005.

"Neuroimaging and Mental Illness: A Window into the Brain." National Institutes of Mental Health, 2013.

"Neurological Imaging." National Institutes of Health, March 29, 2013.

Taveras, Juan M. “Diamond Jubilee Lecture: Neuroradiology—Past, Present, and Future.” Radiology 175 (1990): 593–602.

Toga, Arthur W., and John C. Mazziotta, eds. Brain Mapping: The Methods. 2d ed. Boston: Academic Press, 2002.

Toga, Arthur W., and John C. Mazziotta, eds. Brain Mapping: The Systems. San Diego, Calif.: Academic Press, 2000.

Toga, Arthur W., John C. Mazziotta, and Richard S. J. Frackowiak, eds. Brain Mapping: The Disorders. San Diego, Calif.: Academic Press, 2000.

Van Bruggen, Nick, and Timothy P. L. Roberts, eds. Biomedical Imaging in Experimental Neuroscience. Boca Raton, Fla.: CRC Press, 2003.

What is generalized anxiety disorder (GAD)?

Introduction

Generalized anxiety disorder (GAD) is characterized by excessive worry about a variety of topics. This anxiety occurs every day, over a period of at least six months. The worries tend to be difficult to control and to diminish the person’s quality of life. Signs and symptoms of GAD include restlessness, difficulty concentrating, fatigue, irritability, impatience, being easily distracted, muscle tension, trouble falling asleep or staying asleep, excessive sweating or hot flashes, shortness of breath, diarrhea, headache, stomachache, having trouble swallowing, feeling light-headed, and having to go to the bathroom frequently.

Possible Causes

The cause of generalized anxiety disorder is not known, although there are a number of theories as to its cause. There may be a hereditary tendency to develop GAD. Some of the causative theories are based on experiences in the person’s life, such as traumatic events occurring in childhood, serious illness, and stressful life experiences. Anxiety may be an inherent part of the person’s personality. Some medications and medical conditions can cause GAD. It is also theorized that persons with GAD may produce low levels of brain chemicals such as serotonin, gamma-aminobutyric acid (GABA), norepinephrine, and dopamine, which are thought to improve mood. It is thought that the amygdala, a small structure within the brain, is a depository for memories of frightening and other highly emotional events. Persons with GAD may have an overly sensitive amygdala that tends to react to situations that are not actually threatening. Questions remain as to whether physical changes in the brain lead to anxiety or whether stressful situations and the resulting anxiety lead to changes in the brain.

Diagnosis

In 2013, the American Psychiatric Association published its most recent edition of the DSM (Diagnostic and Statistical Manual of Mental Disorders). The DSM-5 describes all currently identified mental health problems that may receive a formal medical diagnosis in the United States. In this edition, the section on anxiety disorders is split into twelve individual sub-disorders: separation anxiety disorder, selective mutism, specific phobia, social anxiety disorder, panic disorder, panic attack, agoraphobia, generalized anxiety disorder, substance/medication-induced anxiety disorder, anxiety disorder due to another medical condition, other specified anxiety disorder, and unspecified anxiety disorder.

The diagnosis of GAD is a subjective one and is based on the patient’s reporting of excessive worrying about a variety of topics that has lasted at least six continuous months. GAD can develop in people of all ages, including children. However, all anxiety disorders, including GAD, are more common in women and in older persons.

Treatment Options

The treatment for GAD is antianxiety medications, cognitive behavior therapy(CBT), or both. Antianxiety medications used to treat GAD include benzodiazepines, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, and an azpirone derivative.

Benzodiazepines are the first medications prescribed for GAD. They cause mental and physical relaxation by increasing levels of GABA in the brain. They include alprazolam (Xanax), lorazepam (Ativan), clonazepam (Klonopin), and diazepam (Valium). Benzodiazepines are highly addictive and their use should be monitored.

SSRIs (selective serotonin reuptake inhibitors) are drugs, developed in the 1990s, that interfere with the reabsorption (reuptake) of serotonin in the brain, leading to higher levels of serotonin in the body. These medications are less habit-forming than the benzodiazepines and have fewer side effects than older antidepressant medications. SSRIs include fluoxetine (Prozac), paroxetine(Paxil), citalopram (Celexa), sertraline (Zoloft), and escitalopram (Lexapro).

Serotonin-norepinephrine reuptake inhibitors (SNRIs) interfere with the reabsorption of both serotonin and norepinephrine in the brain. There are two drugs in this group: venlafaxine (Effexor) and duloxetine (Cymbalta).

Tricyclic antidepressants (TCAs), which were developed in the 1970s, interfere with the reabsorption of serotonin and norepinephrine in the brain, and they increase the sensitivity of the serotonin and norepinephrine receptors. TCAs have more side effects and more serious side effects than SSRIs, including altering the rhythm of the heart. TCAs include amitriptyline (Elavil), clomipramine (Anafranil), and imipramine (Tofranil).

There is only one azapirone derivative, buspirone (BuSpar). Buspirone increases the activity of serotonin and decreases the activity of dopamine. It accomplishes this by binding to the serotonin and dopamine receptors in the brain. Buspirone has few side effects compared with other drugs used to treat GAD.

Cognitive behavior therapy increases the levels of serotonin and norepinephrine in the body by changing the negative thought patterns of the patient. Persons with anxiety disorders, including GAD, tend to get caught up in their excessive reactions to stressful situations. Cognitive behavior therapy teaches them to stop these negative thoughts and to evaluate the validity of their fears.

Bibliography

Baldwin, David S., and B. E. Leonard. Anxiety Disorders. New York: Karger, 2013. Print.

Bourne, Edmund J., and Lorna Garano. Coping with Anxiety: Ten Simple Ways to Relieve Anxiety, Fear, and Worry. Oakland, Calif.: New Harbinger, 2003. Print.

Dugas, Michel J., and Melisa Robichaud. Cognitive-Behavioral Treatment for Generalized Anxiety Disorder: From Science to Practice. New York: Routledge, 2007. Print.

Gliatto, Michael F. “Generalized Anxiety Disorder.” American Family Physician 62 (2000): 1509–600, 1602. Print.

Graham, P. J., and Shirley Reynolds. Cognitive Behavioral Therapy for Children and Families. Cambridge: Cambridge UP, 2013. Print.

McKay, Dean, and Eric A. Storch. Handbook of Assessing Variants and Complications in Anxiety Disorders. New York: Springer, 2013. Print.

Mufson, Michael, et al., eds. Coping with Anxiety and Phobias. Boston: Harvard Medical School, 2002. Print.

Rugh, Jayne L., and William C. Sanderson. Treating Generalized Anxiety Disorder: Evidence-Based Strategies, Tools, and Techniques. New York: Guilford Press, 2004. Print.

What are genital herpes? |

Definition

Genital herpes is a highly contagious infection
that is caused by a virus. Genital herpes causes fluid-filled blisters or sores on
the skin of the genitals (areas on or around the vagina or penis). The infection
can also cause blisters at the anal opening, on the buttocks or thighs, inside the
vagina on the cervix, or in the urinary tract of women and men.

Causes

The infection is caused by the herpes simplex virus (HSV), of which
there are two kinds: herpes simplex type 1 (HSV-1) and herpes simplex type 2
(HSV-2). HSV-2 is usually the cause of genital herpes, but the disease can also be
caused by HSV-1, the virus that is associated with oral herpes (cold sores on
the mouth).

Genital herpes is a common virus. In the United States, forty-five million people, or one of every five adolescents and adults, ages twelve years and older, are infected with HSV-2.

HSV is transmitted from skin-to-skin contact, especially in places that are warm and moist. The virus enters the body through a cut or opening in the skin or through mucous membranes, the moist inner lining of the urinary tract (in the vaginal area), or the digestive system that includes the mouth, esophagus, stomach, intestines, and anus. The virus stays in the nerve cells of the body, even if a person does not have symptoms or signs of genital herpes. Genital herpes is a chronic, life-long infection with symptoms that will come and go (be active and inactive) throughout a person’s life.

Risk Factors

Genital herpes is considered a sexually transmitted disease. One can
spread the virus by touching, kissing, or having sexual contact, including
vaginal, anal, and oral sex. Several factors lead to the spread of HSV, including
having sexual contact with someone who does not have any obvious sores and with
someone who has a clear outbreak of the virus. An outbreak means that the sexual
partner has visible sores or blisters in the genital area. These sores give off
(or shed) some of the virus that can infect the other partner. The virus is most
contagious when the sores are visible and open and are producing a discharge.

Symptoms

Once someone is infected, symptoms begin to appear within two to twenty days. The first outbreak is usually the most severe and lasts the longest. Early symptoms can last two to three weeks and can include discomfort (itching, burning, or pain) in the genital or anal area, discharge from the vagina, and a feeling of pressure in the abdomen.

Risk Factors

It is possible to develop genital herpes with or without the risk factors discussed here; however, the more risk factors one has, the greater the likelihood of becoming infected with genital herpes. Studies have found that cases of genital herpes have continued to increase. From the 1970’s to the 1990’s, the incidence of HSV-2, the virus that causes genital herpes, has increased by 30 percent.

Anyone who is sexually active (has vaginal, oral, or anal contact with others) can get genital herpes. If a person has oral herpes and performs oral sex, it is possible for that person’s partner to develop genital herpes from that contact.

The following factors can increase the risk of becoming infected with genital herpes:

Behaviors. Having unprotected sex, becoming sexually active at a young age, having been sexually active for many years, having had several sexual partners, having a partner who is infected with genital herpes, and anal sex.

Gender. Women (one of every four women) are more likely than men (one of every five) to become infected with genital herpes.

Socioeconomics. The majority of new infections occur in adolescents and young adults (ages twenty to forty years). In young adults, HSV-1 infection is becoming a more common cause of genital herpes.

Health. Persons with a higher risk of genital herpes are those
with human
immunodeficiency virus infection, a history of other sexually
transmitted infections, and a weak immune system.

Outside factors. Studies suggest there are several things that can trigger the virus and make it active, including stress, excessive sunlight, menstruation, and vigorous sexual activity.

Symptoms

Not all persons are aware they have genital herpes, mostly because they may not have symptoms. They may also not recognize the symptoms if they have them. When first infected, a person has the following symptoms, which appear within two to ten days:

Early symptoms that can last two to three weeks include itching, burning, and pain in the genital or anal area; discharge from the vagina; flulike symptoms, such as fever and swollen glands; and pressure in the abdomen (the area below the stomach).

As the infection progresses, symptoms of an outbreak include sores that start to form on the part of the body where the virus was contracted; sores that begin as small red bumps, develop into blisters, and then become painful open sores; sores or blisters that appear and occur in clusters or small groupings; vaginal discharge; pain when urinating; and flulike symptoms, including fever, muscle aches, swollen glands, and headache.

The outbreak is coming to an end when, after a few days, the sores form a scablike outer layer and then fall off. The virus will recur and become active and inactive over time. The frequency of these recurrences varies from person to person. One may experience symptoms a number of times throughout a given year or may experience an outbreak only once or twice in a lifetime. Doctors and researchers do not yet know why these recurrences happen.

Every case of genital herpes is unique. The average number of outbreaks that a person experiences each year is about four or five. The first year of the virus is usually the worst. The first outbreak is usually the most severe and painful, with the second occurrence often happening only a few weeks later. As time goes on, the frequency of outbreaks lessens and the outbreaks become much less severe. Recurrences tend to become milder and last usually only a week.

Genital herpes also can result in no symptoms. One can still spread genital herpes even if he or she does not experience symptoms or if the symptoms are inactive.

Many people fail to recognize the symptoms of genital herpes. Women often
confuse the discomfort with their menstrual period or with an itchy yeast
infection. Men often confuse the symptoms with jock itch or
friction burn. Symptoms of genital herpes have also been mistaken for insect bites
or hemorrhoids.

Screening and Diagnosis

Sometimes genital herpes is easy to diagnose because the blisters or open sores around the genital area are easily visible, but oftentimes, for an adequate diagnosis, one will need more than an examination. Also, one can have genital herpes yet display no visible sores.

During an examination, laboratory tests will be done to determine if HSV is in the body. These tests will also determine whether the infection is caused by HSV-1 or by HSV-2.

The following tests are used to check for genital herpes:

Viral culture. If the infection is visible, the doctor will rub a
swab over an open sore or blister to collect some cells. The cells are then tested
to see if the virus is present in those cells. It is recommended that this culture
test be taken within the first forty-eight hours after symptoms appear. The
problem with this test is that if the body’s immune system
already killed the herpesvirus from that sore, the test
may come back negative for genital herpes, leading to a false-negative
diagnosis.

Blood tests. These blood tests are also called antibody tests
because they measure HSV antibodies, the disease-fighting
substances in the blood. If the blood tests show HSV antibodies, the affected
person is most likely infected with HSV. Newer tests can even distinguish between
HSV-1 and HSV-2. It is recommended that one wait a minimum of twelve to sixteen
weeks from possible exposure to herpes so that the body has enough time to develop
antibodies. This will ensure a more accurate blood test.

Specific blood tests include a point of care test, in which the physician gets a small blood sample from the patient (by pricking the skin). Results are available in less than ten minutes. This blood test checks for the presence of HSV-2 antibodies. The HerpeSelect ELISA (enzyme-linked immunoabsorbent assay), the HerpeSelect Immunoblot, and Captiva HSV IgG Type Specific ELISA all involve the patient going to a lab, where blood will be drawn from a vein for testing for HSV-1 or HSV-2 antibodies. Results are available in approximately one to two weeks. None of these tests, however, can pinpoint the site of the infection.

Treatment and Therapy

There is no cure for genital herpes and no surgical option for treatment. There are, however, medications that treat the symptoms and help prevent future outbreaks.

Prevention and Outcomes

Because there is no cure, behavioral change is the best way to lower the risk of contracting the virus and spreading it to others. Abstaining or refraining from sex is the most certain way to avoid contracting genital herpes. Another preventive measure is to have a long-term mutually monogamous (only one exclusive sexual partner) with someone who does not have genital herpes. Persons should avoid sexual contact with others during a genital herpes outbreak, and one should always use a condom during sex. Persons with cold sores (a blister caused by HSV-1 infection) should avoid kissing other people and should avoid oral sex.

One should recognize when the disease is most contagious and know that the virus can be spread even if the person does not have visible sores or is not experiencing an outbreak. One should not touch any visible sores or blisters and should wash hands thoroughly with soap and warm water if a sore or blister is touched. One can ensure against spreading the virus to other parts of the body, such as the mouth or eyes, by not touching sores and then touching these uninfected areas.

One can also take medications, such as valacyclovir, that are approved by the
U.S. Food and
Drug Administration for use in preventing the spread of
genital herpes. Taking valacyclovir only reduces the risk of transmission by 50
percent. A better way to protect oneself and one’s partner is to take valacyclovir
and use a condom.

Bibliography

American Academy of Dermatology. “Herpes Simplex.” Available at http://www.aad.org. A brief but comprehensive discussion of the herpes simplex virus and its dermatological manifestations.

Drake, S., et al. “Improving the Care of Patients with Genital Herpes.” British Medical Journal 321 (2000): 619-623. A clinician’s guide to caring for persons with HSV genital infection.

Groves, M. J. “Transmission of Herpes Simplex Virus via Oral Sex.” American Family Physician 73 (2006): 1153. Discusses how HSV infection, including cold sores, is transmissible through oral sex.

“Herpes Simplex.” In Ferri’s Clinical Advisor 2011: Instant Diagnosis and Treatment, edited by Fred F. Ferri. Philadelphia: Mosby/Elsevier, 2011. Provides recommendations on clinical treatments for HSV infections.

Langlais, Robert P., and Craig S. Miller. Color Atlas of Common Oral Diseases. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2009. Provides six hundred color photographs of the most commonly seen oral conditions, including HSV infections, and descriptive text for each condition.

What is phenytoin? How does it interact with other drugs?

Ginkgo

Effect: Possible Harmful Interaction

The herb ginkgo (Ginkgo biloba) has been used to
treat Alzheimer’s disease and ordinary age-related memory loss, among many other
conditions. Seizures have been reported with the use of ginkgo leaf extract in
people with previously well-controlled epilepsy; in one case, the seizures were
fatal. One possible explanation is contamination of ginkgo leaf products with
ginkgo seeds. It has also been suggested that ginkgo might interfere with the
effectiveness of some antiseizure medications, including phenytoin.
Finally, it has been noted that the drug tacrine (also used to improve memory) has
been associated with seizures, and ginkgo may affect the brain in ways similar to
tacrine.

Glutamine

Effect: Possible Harmful Interaction

The amino acid glutamine is converted to glutamate in the body. Glutamate
is thought to act as a neurotransmitter (a chemical that enables nerve
transmission). Because anticonvulsants work (at least in part) by blocking
glutamate pathways in the brain, high dosages of the amino acid glutamine might
theoretically diminish an anticonvulsant’s effect and increase the risk of
seizures.

Ipriflavone

Effect: Possible Harmful Interaction

Ipriflavone, a synthetic isoflavone
that slows bone breakdown, is used to treat osteoporosis. Test-tube studies
indicate that ipriflavone might increase blood levels of the anticonvulsants
phenytoin and carbamazepine when they are taken therapeutically.
Ipriflavone was found to inhibit a liver enzyme involved in the body’s normal
breakdown of these drugs, thus allowing them to build up in the blood. Higher drug
levels increase the risk of adverse effects.

Because anticonvulsants are known to contribute to the development of osteoporosis, a concern is that the use of ipriflavone for this drug-induced osteoporosis could result in higher blood levels of the drugs, with potentially serious consequences. People taking either of these drugs should use ipriflavone only under medical supervision.

Hops, Kava, Passionflower, Valerian

Effect: Possible Harmful Interaction

The herb kava (Piper methysticum) has a sedative
effect and is used for anxiety and insomnia. Combining kava with anticonvulsants,
which possess similar depressant effects, could result in add-on or excessive
physical depression, sedation, and impairment. In one case report, a
fifty-four-year-old man was hospitalized for lethargy and disorientation, side
effects attributed to his having taken the combination of kava and the antianxiety
agent alprazolam (Xanax) for three days.

Other herbs having a sedative effect that might cause problems when combined with anticonvulsants include ashwagandha, calendula, catnip, hops, lady’s slipper, lemon balm, passionflower, sassafras, skullcap, valerian, and yerba mansa.

Because of the potentially serious consequences, one should avoid combining these herbs with anticonvulsants or other drugs that also have sedative or depressant effects, unless advised by a physician.

White Willow

Effect: Possible Harmful Interaction

The herb white
willow (Salix alba), also known as willow
bark, is used to treat pain and fever. White willow contains a substance that is
converted by the body into a salicylate similar to aspirin. Higher doses of
aspirin may increase phenytoin levels and toxicity during long-term use of both
drugs. This raises the concern that white willow might have similar effects on
phenytoin, though this has not been proven.

Biotin

Effect: Supplementation Possibly Helpful, but Take at a Different Time of Day

Anticonvulsants may deplete biotin, an essential water-soluble B
vitamin, possibly by competing with it for absorption in the intestine. It is not
clear, however, whether this effect is great enough to be harmful. Blood levels of
biotin were found to be substantially lower in 404 people with epilepsy on
long-term treatment with anticonvulsants, compared with 112 untreated people with
epilepsy. The effect occurred with phenytoin, carbamazepine, phenobarbital, and
primidone. Valproic acid appears to affect biotin to a lesser extent than other
anticonvulsants.

A test-tube study suggested that anticonvulsants might lower biotin levels by interfering with the way biotin is transported in the intestine.

Biotin supplementation may be beneficial for persons on long-term anticonvulsant therapy. To avoid a potential interaction, one should take the supplement two to three hours apart from the drug. It has been suggested that the action of anticonvulsant drugs may be at least partly related to their effect of reducing biotin levels. For this reason, it may be desirable to take enough biotin to prevent a deficiency but not an excessive amount.

Folate

Effect: Possible Benefits and Risks

Folate (also known as folic acid) is a B vitamin that plays
an important role in many vital aspects of health, including preventing neural
tube birth defects and possibly reducing the risk of heart disease. Because
inadequate intake of folate is widespread, if one is taking any medication that
depletes or impairs folate even slightly, one may need supplementation.

Most drugs used for preventing seizures can reduce levels of folate in the body. Phenytoin in particular appears to decrease folate levels by interfering with its absorption in the small intestine, as well as by accelerating its normal breakdown by the body. The low blood levels of folate caused by anticonvulsants can raise homocysteine levels, a condition believed to increase the risk of heart disease.

Adequate folate intake is also necessary to prevent neural tube birth
defects, such as spina bifida and anencephaly (absence of a
brain). Because anticonvulsant drugs deplete folate, babies born to women taking
anticonvulsants are at increased risk for such birth defects. Anticonvulsants may
also play a more direct role in the development of birth defects.

However, there can be problems with using folate supplements. High folate levels may speed up the normal breakdown of phenytoin. This can lead to breakthrough seizures. For this reason, folate supplementation during phenytoin therapy should be supervised by a physician.

Calcium

Effect: Supplementation Probably Helpful, but Take at a Different Time of Day

Anticonvulsant drugs may impair calcium absorption and, in this way, increase the risk of osteoporosis and other bone disorders. Calcium absorption was compared in twelve people on anticonvulsant therapy (all taking phenytoin and some also taking phenobarbital, primidone, and/or carbamazepine) and twelve people receiving no treatment. Calcium absorption was found to be 27 percent lower in the treated participants.

An observational study found low blood calcium levels in 48 percent of 109 people taking anticonvulsants. Other findings in this study suggested that anticonvulsants might also reduce calcium levels by directly interfering with parathyroid hormone, a substance that helps keep calcium levels in proper balance.

A low level of blood calcium can itself trigger seizures, and this might reduce
the effectiveness of anticonvulsants. Calcium supplementation may be beneficial
for people taking anticonvulsant drugs. However, some studies indicate that
antacids containing calcium carbonate may interfere with the absorption of
phenytoin and perhaps other anticonvulsants. For this reason, one should take
calcium supplements and anticonvulsant drugs several hours
apart if possible.

Carnitine

Effect: Supplementation Possibly Helpful

Carnitine is an amino acid that has been used for heart
conditions, Alzheimer’s disease, and intermittent claudication. Long-term therapy
with anticonvulsant agents, particularly valproic acid, is associated with low
levels of carnitine. However, it is not clear whether the anticonvulsants cause
the carnitine deficiency or whether it occurs for other reasons. It has been
hypothesized that low carnitine levels may contribute to valproic acid’s damaging
effects on the liver. The risk of this liver damage increases in children younger
than twenty-four months, and carnitine supplementation does seem to be protective.
However, in one double-blind crossover study, carnitine supplementation produced
no real improvement in “well-being” as assessed by parents of children receiving
either valproic acid or carbamazepine.

L-carnitine supplementation may be advisable in certain cases, such as in infants and young children (especially those younger than two years) who have neurologic disorders and are receiving valproic acid and multiple anticonvulsants.

Vitamin D

Effect: Supplementation Possibly Helpful

Anticonvulsant drugs may interfere with the activity of vitamin D. As
proper handling of calcium by the body depends on vitamin D, this may be another
way that these drugs increase the risk of osteoporosis and related bone disorders.
Anticonvulsants appear to speed up the body’s normal breakdown of vitamin D,
decreasing the amount of the vitamin in the blood. A survey of forty-eight people
taking both phenytoin and phenobarbital found significantly lower levels of
calcium and vitamin D in many of them, compared with thirty-eight untreated
people. Similar but lesser changes were seen in thirteen people taking phenytoin
or phenobarbital alone. This effect may be apparent only after several weeks of
treatment.

Another study found decreased blood levels of one form of vitamin D but normal levels of another. Because there are two primary forms of vitamin D circulating in the blood, the body might be able to adjust in some cases to keep vitamin D in balance, at least for a time, despite the influence of anticonvulsants. Adequate sunlight exposure may help overcome the effects of anticonvulsants on vitamin D by stimulating the skin to manufacture the vitamin. Of 450 people on anticonvulsants residing in a Florida facility, none was found to have low blood levels of vitamin D or evidence of bone disease. This suggests that environments providing regular sun exposure may be protective. People regularly taking anticonvulsants, especially those taking combination therapy and those with limited exposure to sunlight, may benefit from vitamin D supplementation.

Vitamin K

Effect: Supplementation Possibly Helpful for Pregnant Women

Phenytoin, carbamazepine, phenobarbital, and primidone speed up the normal
breakdown of vitamin K into inactive byproducts, thus depriving the body
of active vitamin K. This can lead to bone problems, such as osteoporosis. In
addition, use of these anticonvulsants can lead to a vitamin K deficiency in
babies born to pregnant women taking the drugs, resulting in bleeding disorders or
facial bone abnormalities in the newborns. Women who take these anticonvulsants
may need vitamin K supplementation during pregnancy to prevent these conditions in
their newborns.

Bibliography

De Vivo, D. C., et al. “L-carnitine Supplementation in Childhood Epilepsy: Current Perspectives.” Epilepsia 30 (1998): 1216-1225.

Granger, A. S. “Ginkgo biloba Precipitating Epileptic Seizures.” Age and Ageing 30 (2001): 523-525.

Gregory, P. J. “Seizure Associated with Ginkgo biloba?” Annals of Internal Medicine 134 (2001): 344.

Kupiec, T., and V. Raj. “Fatal Seizures Due to Potential Herb-Drug Interactions with Ginkgo biloba.” Journal of Analytical Toxicology 29 (2006): 755-758.

How did "bunburying" end up playing a major role in The Importance of Being Earnest by Oscar Wilde?

Bunburying is a word Algernon coins to represent the act of using a fictitious person as an excuse to avoid unpleasant interactions with others or to gain a sense of freedom for a short time.

Algernon invented his dear friend "Bunbury," a man prone to sudden, unexplained illnesses, as a means of avoiding social engagements with his Aunt Augusta and her family. He soon discovers his friend Jack has likewise used a nonexistent brother named...

Bunburying is a word Algernon coins to represent the act of using a fictitious person as an excuse to avoid unpleasant interactions with others or to gain a sense of freedom for a short time.

Algernon invented his dear friend "Bunbury," a man prone to sudden, unexplained illnesses, as a means of avoiding social engagements with his Aunt Augusta and her family. He soon discovers his friend Jack has likewise used a nonexistent brother named Ernest to gain freedom from his duties in the country. As Jack is spending an evening under the alias of Ernest in the city, Algernon stumbles upon his real identity and proclaims, "I have always suspected you of being a confirmed and secret Bunburyist; and I am quite sure of it now." He uses this information to bunbury in the country to meet Cecily.

The problem arises because both women the men desire to marry believe they are engaged to Ernest. Gwendolyn believes Jack's name is actually Ernest. Cecily, Jack's ward, is made to believe Algernon's name is Ernest when he makes his bunburying trip to the country to meet her. Both men have to come clean about their deceit.

Without the concept of bunburying, Cecily would have never met Algernon. While Jack and Gwendolyn would have met, Jack likely would have never learned his true identity as Algernon's brother. Most importantly, he would have never learned "the vital Importance of Being Earnest." 

What does the term "coming out" mean?

"Coming out" is a figure of speech that refers to the process of openly identifying as a lesbian, gay, bisexual, or transgender (LGBT) person. Coming out is not a single event. Rather, it is a lifelong process of learning to understand and acknowledge one’s sexuality and feeling comfortable expressing it in private and public.

In the past, coming out was prohibited due to social prejudices and laws against homosexuality. Due to the efforts of gay activists, many Americans have become accepting of LGBT people and homosexuality. The experience of coming out is very personal and can be difficult.

Overview

Historically, society has discouraged LGBT people from coming out. In twentieth-century America, every state with the exception of Illinois had laws that expressly prohibited homosexual behavior. Homosexual activity was punishable by fines and prison sentences, even if such acts occurred in private homes. Additionally, the American Psychiatric Association classified homosexuality as a mental disorder, cementing the idea that LGBT behavior was inherently wrong. Mainstream religion almost universally condemned homosexuality. As a result, LGBT people were often harassed, tormented, or imprisoned. Coming out safely was not an option during this time.

Gay Rights Activism

The Stonewall riots are widely regarded as the spark for the LGBT civil rights movement and gay acceptance in the United States. The riots began on June 28, 1969, when police raided a popular gay bar in New York City called the Stonewall Inn. Although police actions against gay bars were common at the time, the bar’s patrons were infuriated by the invasion. They resisted arrest and fought with the police. The fighting spilled into the streets of Greenwich Village and became violent. Protests and demonstrations lasted for the next six days.

The riots inspired LGBT people in America to organize to support the rights of gay people, sparking the gay rights movement. The first gay pride march was held in New York City in 1970 to commemorate the riots. This became an annual event that eventually spread to other major cities. Within two years, gay rights groups had organized in nearly every large city in the United States. From the 1970s onward, these organizations helped to keep gay rights issues at the forefront of the media and government. Eventually, these groups paved the way for acceptance of civil protections, same-sex marriage, and a widespread—but not universal—acceptance of LGBT people in America.

A Deeply Personal Process

Although much of American society has become tolerant and accepting of LGBT people, coming out is still a deeply personal process and carries a risk of rejection. All LGBT people must decide if and how they will come out. It is important for an individual to feel that he or she is in control of the process. Additionally, LGBT people can choose to come out only to certain people or in certain groups. It is not necessary to be "out" in all places at all times. For example, one person might choose to come out to his or her family but not to coworkers. Another might feel comfortable living openly in all areas of his or her life.

For some people, coming out is a positive experience. These individuals feel confident in their sexual identity and have the support of their loved ones. They have no problem opening a conversation with family and friends and find comfort and understanding with them.

Not everyone finds the process easy, however. Some LGBT people may be confused about their sexual identity and unsure where they fit in society. They may feel undermined or dismissed by parents or teachers who try to convince them they are in a "phase." They may worry about being bullied by their peers or be concerned about risking their professional careers. All of these factors can impact the experience of coming out.

Why Come Out?

Most people who come out do so because they are tired of hiding their true selves. They want to express their real identities openly and honestly. They want the opportunity to explore and develop meaningful relationships with others, both platonically and romantically. They feel it is important for other people to know who they really are. This is a very natural feeling.

Coming out can have many benefits, such as feeling like part of a larger community. Additionally, coming out often reduces the stress that LGBT people feel about hiding the truth about themselves, stress that shows LGBT individuals are at a higher risk for mental health issues.

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Dealing with the Risks

Coming out has risks, too. Although many Americans say they are tolerant of LGBT people, that tolerance is not universal. Not everyone will be accepting or supportive. Some people may be hostile. Physical safety may even be a concern in certain environments. Sometimes close friends or family members may react negatively. They may be shocked or confused. They may refuse to acknowledge or accept the truth. Some families may withdraw financial support or even ask their LGBT children to move out of their homes. This situation can be painful and dangerous for the LGBT individual.

Some LGBT people experience bullying, harassment, or discrimination when they come out. These incidents can occur anywhere and can be problematic at school or in the workplace.

Resources

Many resources are available, both online and offline, to help LGBT people, especially young people, learn about coming out safely. National movements, such as the Human Rights Campaign and the It Gets Better Project, provide information about the process and can help LGBT people decide if coming out is right for them. Professional counseling can also be helpful, especially when family members or friends are not be supportive or in cases of bullying or discrimination.

Bibliography

"Coming Out." Gender Equity Resource Center. UC Berkeley Gender Equity Resource Center. Web. 6 Nov. 2014. http://geneq.berkeley.edu/lgbt_resources_coming_out#1

"Resource Guide to Coming Out." Human Rights Campaign. Human Rights Campaign. Apr. 2013. Web. 6 Nov. 2014. http://www.hrc.org/resources/entry/resource-guide-to-coming-out

"Introduction: Stonewall Uprising." PBS. WGBH Educational Foundation. Web. 7 Nov. 2014. http://www.pbs.org/wgbh/americanexperience/features/introduction/stonewall-intro/

What is Hirschsprung's disease? |

Causes and Symptoms

Hirschsprung’s disease is caused when the lower part of the large intestine (colon), including the rectum, does not have the ganglion nerve cells to control the muscles that produce the contractions necessary for a bowel movement. Occasionally, the whole large intestine and even portions of the small intestine may be missing these nerve cells. The disease develops prior to birth. In the normal development of a fetus, the ganglion nerve cells grow from the top of the intestine down to the anus. For some unknown reason, the nerve cells stop growing at some distance down the intestine in children who are born with Hirschsprung’s disease.

The disease manifests itself most often in young children, although it can appear when an individual is a teenager or an adult. In an individual with Hirschsprung’s disease, the healthy upper portion of the colon pushes stool down until it reaches the affected part. The stool then stops. New stool backs up behind it. Severe constipation results. In some cases, the victim may not be able to have any bowel movements at all. Babies with Hirschsprung’s disease often vomit up bile and experience swollen abdomens after eating. Infections, particularly enterocolitis, may develop in the intestines, which has the potential of bursting the colon.

Treatment and Therapy

Diagnosis of the disorder is confirmed by a barium enema x-ray and a biopsy of the rectum. Barium makes the intestine show up better on an x-ray. Manometry is also often used by the doctor to diagnose the disease. In this procedure, a small balloon is inflated inside the rectum. If the anal muscle does not relax, the patient may have Hirschsprung’s disease.

A pull-through operation removes the affected area of the intestine. The remaining ends are joined together. After this surgery, 85 to 90 percent of the patients pass feces normally, although some may experience diarrhea or constipation for a period of time. Eating high-fiber foods can help reduce diarrhea and constipation. Since the intestine is shortened by the surgery, not as much fluid is absorbed by the body. Consequently, the patient will need to drink plenty of fluids.

Perspective and Prospects

Hirschsprung’s disease occurs in approximately 1 out of every 5,000 births. About 80 percent of patients are boys. Children with Down syndrome are at a high risk for developing the disorder.

Hirschsprung’s disease has been found to be hereditary, with the risk greater if the mother has the condition. Even if the parents have not had the disorder develop in their own lives, they may pass it on to their children. If one child in a family has the disease, other children are at greater risk to be born with it.

Bibliography

Eichenwald, Heinz F., Josef Ströder, and Charles M. Ginsburg, eds. Pediatric Therapy. 3d ed. St. Louis, Mo.: Mosby Year Book, 1993.

Holschneider, Alexander M., and Prem Puri, eds. Hirschsprung’s Disease and Allied Disorders. 3d ed. New York: Springer, 2008.

Kaneshiro, Neil K. "Hirschsprung Disease." MedlinePlus, November 13, 2011.

Icon Health. Hirschsprung’s Disease: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, Calif.: Author, 2004.

Núñez Núñez, Ramón. Hirschsprung's Disease: Diagnosis and Treatment. New York: Nova Biomedical Books, 2006.

Parisi, MA. "Hirschsprung's Disease Overview." NCBI, November 10, 2011.

Wallace, A. S., and R. B. Anderson. "Genetic Interactions and Modifier Genes in Hirschsprung's Disease." World Journal of Gastroenterology 17, 45. (December 7, 2011): 4937–4944.