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Chapter 6: Adolescence Growth in Adolescence Puberty is a period of rapid growth and sexual maturation. These changes begin sometime l between eight and fourteen. Girls begin puberty at around ten years of age and boys begin approximately two years later. Pubertal changes take around three to four years to complete. Adolescents experience an overall physical growth spurt. The growth proceeds from the extremities toward the torso. This is referred to as distalproximal development. First the hands grow, then the arms, hand finally the torso. The overall physical growth spurt results in 10-11 inches of added height and 50 to 75 pounds of increased weight. The head begins to grow sometime after the feet have gone through their period of growth. Growth of the head is preceded by growth of the ears, nose, and lips. The difference in these patterns of growth result in adolescents appearing awkward and out-of-proportion. As the torso grows, so do the internal organs. The heart and lungs experience dramatic growth during this period. During childhood, boys and girls are quite similar in height and weight. However, gender differences become apparent during adolescence. From approximately age ten to fourteen, the average girl is taller, but not heavier, than the average boy. After that, the average boy becomes 223 both taller and heavier, although individual differences are certainly noted. As adolescents physically mature, weight differences are more noteworthy than height differences. At eighteen years of age, those that are heaviest weigh almost twice as much as the lightest, but the tallest teens are only about 10% taller than the shortest (Seifert, 2012). Both height and weight can certainly be sensitive issues for some teenagers. Most modern societies, and the teenagers in them, tend to favor relatively short women and tall men, as well as a somewhat thin body build, especially for girls and women. Yet, neither socially preferred height nor thinness is the destiny for many individuals. Being overweight, in particular, has become a common, serious problem in modern society due to the prevalence of diets high in fat and lifestyles low in activity (Tartamella et al., 2004). The educational system has, unfortunately, contributed to the problem as well by gradually restricting the number of physical education courses and classes in the past two decades. Average height and weight are also related somewhat to racial and ethnic background. In general, children of Asian background tend to be slightly shorter than children of European and North American background. The latter in turn tend to be shorter than children from African societies (Eveleth & Tanner, 1990). Body shape differs slightly as well, though the differences are not always visible until after puberty. Asian background youth tend to have arms and legs that are a bit short relative to their torsos, and African background youth tend to have relatively long arms and legs. The differences are only averages, as there are large individual differences as well. Sexual Development Typically, the growth spurt is followed by the development of sexual maturity. Sexual changes are divided into two categories: Primary sexual characteristics and secondary sexual characteristics. Primary sexual characteristics are changes in the reproductive organs. For males, this includes growth of the testes, penis, scrotum, and spermarche or first ejaculation of semen. This occurs between 11 and 15 years of age. For females, primary characteristics include growth of the uterus and menarche or the first menstrual period. The female gametes, which are stored in the ovaries, are present at birth, but are immature. Each ovary contains about 400,000 gametes, but only 500 will become mature eggs (Crooks & Baur, 2007). Beginning at puberty, one ovum ripens and is released about every 28 days during the menstrual cycle. Stress and higher percentage of body fat can bring menstruation at younger ages. Male Anatomy: Males have both internal and external genitalia that are responsible for procreation and sexual intercourse. Males produce their sperm on a cycle, and unlike the female's ovulation cycle, the male sperm production cycle is constantly producing millions of sperm daily. The main male sex organs are the penis and the testicles, the latter of which produce semen and sperm. The semen and sperm, as a result of sexual intercourse, can fertilize an ovum in the female's body; the fertilized ovum (zygote) develops into a fetus which is later born as a child. Female Anatomy: Female external genitalia is collectively known as the vulva, which includes the mons veneris, labia majora, labia minora, clitoris, vaginal opening, and urethral opening. Female internal reproductive organs consist of the vagina, uterus, fallopian tubes, and ovaries. The uterus hosts the developing fetus, produces vaginal and uterine secretions, and passes the male's sperm through to the fallopian tubes while the ovaries release the eggs. A female is born with all her eggs already produced. The vagina is attached to the uterus through the cervix, while the uterus is attached to the ovaries via the fallopian tubes. Females have a monthly reproductive cycle; at certain intervals the ovaries release an egg, which passes through the fallopian tube into the uterus. If, in this transit, it meets with sperm, the sperm might penetrate and merge with the egg, fertilizing it. If not fertilized, the egg is flushed out of the system through menstruation. Secondary sexual characteristics are visible physical changes not directly linked to reproduction but signal sexual maturity. For males this includes broader shoulders and a lower voice as the larynx grows. Hair becomes coarser and darker, and hair growth occurs in the pubic area, under the arms and on the face. For females, breast development occurs around age 10, although full development takes several years. Hips broaden, and pubic and underarm hair develops and also becomes darker and coarser. Acne: An unpleasant consequence of the hormonal changes in puberty is acne, defined as pimples on the skin due to overactive sebaceous (oil-producing) glands (Dolgin, 2011). These glands develop at a greater speed than the skin ducts that discharges the oil. Consequently, the ducts can become blocked with dead skin and acne will develop. According to the University of California at Los Angeles Medical Center (2000), approximately 85% of adolescents develop acne, and boys develop acne more than girls because of greater levels of testosterone in their systems (Dolgin, 2011). Experiencing acne can lead the adolescent to withdraw socially, especially if they are self-conscious about their skin or teased (Goodman, 2006). Effects of Pubertal Age: The age of puberty is getting younger for children throughout the world. According to Euling et al. (2008) data are sufficient to suggest a trend toward an earlier breast development onset and menarche in girls. A century ago the average age of a girl’s first period in the United States and Europe was 16, while today it is around 13. Because there is no clear marker of puberty for boys, it is harder to determine if boys are maturing earlier too. In addition to better nutrition, less positive reasons associated with early puberty for girls include increased stress, obesity, and endocrine disrupting chemicals. Cultural differences are noted with Asian-American girls, on average, developing last, while African American girls enter puberty the earliest. Hispanic girls start puberty the second earliest, while European-American girls rank third in their age of starting puberty. Although African American girls are typically the first to develop, they are less likely to experience negative consequences of early puberty when compared to European-American girls (Weir, 2016). Research has demonstrated mental health problems linked to children who begin puberty earlier than their peers. For girls, early puberty is associated with depression, substance use, eating disorders, disruptive behavior disorders, and early sexual behavior (Graber, 2013). Early maturing girls demonstrate more anxiety and less confidence in their relationships with family and friends, and they compare themselves more negatively to their peers (Weir, 2016). Problems with early puberty seem to be due to the mismatch between the child’s appearance and the way she acts and thinks. Adults especially may assume the child is more capable than she actually is, and parents might grant more freedom than the child’s age would indicate. For girls, the emphasis on physical attractiveness and sexuality is emphasized at puberty and they may lack effective coping strategies to deal with the attention they may receive. 226 Figure 6.4 Source Additionally, mental health problems are more likely to occur when the child is among the first in his or her peer group to develop. Because the preadolescent time is one of not wanting to appear different, early developing children stand out among their peer group and gravitate toward those who are older. For girls, this results in them interacting with older peers who engage in risky behaviors such as substance use and early sexual behavior (Weir, 2016). Boys also see changes in their emotional functioning at puberty. According to Mendle, Harden, Brooks-Gunn, and Graber (2010), while most boys experienced a decrease in depressive symptoms during puberty, boys who began puberty earlier and exhibited a rapid tempo, or a fast rate of change, actually increased in depressive symptoms. The effects of pubertal tempo were stronger than those of pubertal timing, suggesting that rapid pubertal change in boys may be a more important risk factor than the timing of development. In a further study to better analyze the reasons for this change, Mendle et al. (2012) found that both early maturing boys and rapidly maturing boys displayed decrements in the quality of their peer relationships as they moved into early adolescence, whereas boys with more typical timing and tempo development actually experienced improvements in peer relationships. The researchers concluded that the transition in peer relationships may be especially challenging for boys whose pubertal maturation differs significantly from those of others their age. Consequences for boys attaining early puberty were increased odds of cigarette, alcohol, or another drug use (Dudovitz, et al., 2015). Gender Role Intensification: At about the same time that puberty accentuates gender, role differences also accentuate for at least some teenagers. Some girls who excelled at math or science in elementary school, may curb their enthusiasm and displays of success at these subjects for fear of limiting their popularity or attractiveness as girls (Taylor et al/, 1995; Sadker, 2004). Some boys who were not especially interested in sports previously may begin dedicating themselves to athletics to affirm their masculinity in the eyes of others. Some boys and girls who once worked together successfully on class projects may no longer feel comfortable doing so, or alternatively may now seek to be working partners, but for social rather than academic reasons. Such changes do not affect all youngsters equally, nor affect any one youngster equally on all occasions. An individual may act like a young adult on one day, but more like a child the next. Adolescent Brain The brain undergoes dramatic changes during adolescence. Although it does not get larger, it matures by becoming more interconnected and specialized (Giedd, 2015). The myelination and 227 development of connections between neurons continues. This results in an increase in the white matter of the brain and allows the adolescent to make significant improvements in their thinking and processing skills. Different brain areas become myelinated at different times. For example, the brain’s language areas undergo myelination during the first 13 years. Completed insulation of the axons consolidates these language skills but makes it more difficult to learn a second language. With greater myelination, however, comes diminished plasticity as a myelin coating inhibits the growth of new connections (Dobbs, 2012). Even as the connections between neurons are strengthened, synaptic pruning occurs more than during childhood as the brain adapts to changes in the environment. This synaptic pruning causes the gray matter of the brain, or the cortex, to become thinner but more efficient (Dobbs, 2012). The corpus callosum, which connects the two hemispheres, continues to thicken allowing for stronger connections between brain areas. Additionally, the hippocampus becomes more strongly connected to the frontal lobes, allowing for greater integration of memory and experiences into our decision making. The limbic system, which regulates emotion and reward, is linked to the hormonal changes that occur at puberty. The limbic system is also related to novelty seeking and a shift toward interacting with peers. In contrast, the prefrontal cortex which is involved in the control of impulses, organization, planning, and making good decisions, does not fully develop until the mid-20s. According to Giedd (2015) the significant aspect of the later developing prefrontal cortex and early development of the limbic system is the “mismatch” in timing between the two. The approximately ten years that separates the development of these two brain areas can result in risky behavior, poor decision making, and weak emotional control for the adolescent. When puberty begins earlier, this mismatch extends even further. Teens often take more risks than adults and according to research it is because they weigh risks and rewards differently than adults do (Dobbs, 2012). For adolescents the brain’s sensitivity to the neurotransmitter dopamine peaks, and dopamine is involved in reward circuits, so the possible rewards outweighs the risks. Adolescents respond especially strongly to social rewards during activities, and they prefer the company of others their same age. Chein et al. (2011) found that peers sensitize brain regions associated with potential rewards. For example, adolescent drivers make risky driving decisions when with friends to impress them, and teens are much more likely to commit crimes together in comparison to adults (30 and older) who commit them alone (Steinberg et al., 2017). In addition to dopamine, the adolescent brain is affected by oxytocin which facilitates bonding and makes social connections more rewarding. With both dopamine and oxytocin engaged, it is no wonder that adolescents seek peers and excitement in their lives that could end up actually harming them. 228 Because of all the changes that occur in the adolescent brain, the chances for abnormal development can occur, including mental illness. In fact, 50% of the mental illness occurs by the age 14 and 75% occurs by age 24 (Giedd, 2015). Additionally, during this period of development the adolescent brain is especially vulnerable to damage from drug exposure. For example, repeated exposure to marijuana can affect cellular activity in the endocannabinoid system. Consequently, adolescents are more sensitive to the effects of repeated marijuana exposure (Weir, 2015). However, researchers have also focused on the highly adaptive qualities of the adolescent brain which allow the adolescent to move away from the family towards the outside world (Dobbs, 2012; Giedd, 2015). Novelty seeking and risk taking can generate positive outcomes including meeting new people and seeking out new situations. Separating from the family and moving into new relationships and different experiences are actually quite adaptive for society. Adolescent Sleep According to the National Sleep Foundation (NSF) (2016), adolescents need about 8 to 10 hours of sleep each night to function best. The most recent Sleep in America poll in 2006 indicated that adolescents between sixth and twelfth grade were not getting the recommended amount of sleep. On average adolescents only received 7 ½ hours of sleep per night on school nights with younger adolescents getting more than older ones (8.4 hours for sixth graders and only 6.9 hours for those in twelfth grade). For the older adolescents, only about one in ten (9%) get an optimal amount of sleep, and they are more likely to experience negative consequences the following day. These include feeling too tired or sleepy, being cranky or irritable, falling asleep in school, having a depressed mood, and drinking caffeinated beverages (NSF, 2016). Additionally, they are at risk for substance abuse, car crashes, poor academic performance, obesity, and a weakened immune system (Weintraub, 2016). Troxel et al. (2019) found that insufficient sleep in adolescents is a predictor of risky sexual behaviors. Reasons given for this include that those adolescents who stay out late, typically without parental supervision, are more likely to engage in a variety of risky behaviors, including risky sex, such as not using birth control or using substances before/during sex. An alternative explanation for risky sexual behavior is that the lack of sleep negatively affects impulsivity and decision-making processes. Figure 6.7 Source Why do adolescents not get adequate sleep? In addition to known environmental and social factors, including work, homework, media, technology, and socializing, the adolescent brain is also a factor. As adolescent go through puberty, their circadian rhythms change and push back their sleep time until later in the evening (Weintraub, 2016). This biological change not only keeps adolescents awake at night, it makes it difficult for them to wake up. When they are awake too early, their brains do not function optimally. Impairments are noted in attention, academic achievement, and behavior while increases in tardiness and absenteeism are also seen. 229 To support adolescents’ later sleeping schedule, the Centers for Disease Control and Prevention recommended that school not begin any earlier than 8:30 a.m. Unfortunately, over 80% of American schools begin their day earlier than 8:30 a.m. with an average start time of 8:03 a.m. (Weintraub, 2016). Psychologists and other professionals have been advocating for later school times, and they have produced research demonstrating better student outcomes for later start times. More middle and high schools have changed their start times to better reflect the sleep research. However, the logistics of changing start times and bus schedules are proving too difficult for some schools leaving many adolescent vulnerable to the negative consequences of sleep deprivation. Troxel et al. (2019) cautions that adolescents should find a middle ground between sleeping too little during the school week and too much during the weekends. Keeping consistent sleep schedules of too little sleep will result in sleep deprivation but oversleeping on weekends can affect the natural biological sleep cycle making it harder to sleep on weekdays. Adolescent Sexual Activity By about age ten or eleven, most children experience increased sexual attraction to others that affects social life, both in school and out (McClintock & Herdt, 1996). By the end of high school, more than half of boys and girls report having experienced sexual intercourse at least once, though it is hard to be certain of the proportion because of the sensitivity and privacy of the information. (Center for Disease Control, 2004; Rosenbaum, 2006). Adolescent Pregnancy: As can be seen in Figure 6.8, in 2018 females aged 15–19 years experienced a birth rate (live births) of 17.4 per 1,000 women. The birth rate for teenagers has declined by 58% since 2007 and 72% since 1991, the most recent peak (Hamilton, Joyce, Martin, & Osterman, 2019). It appears that adolescents seem to be less sexually active than in previous years, and those who are sexually active seem to be using birth control (CDC, 2016). Figure 6.8 Source Risk Factors for Adolescent Pregnancy: Miller et al. (2001) found that parent/child closeness, parental supervision, and parents' values against teen intercourse (or unprotected intercourse) decreased the risk of adolescent pregnancy. In contrast, residing in disorganized/dangerous neighborhoods, living in a lower SES family, living with a single parent, having older sexually 230 active siblings or pregnant/parenting teenage sisters, early puberty, and being a victim of sexual abuse place adolescents at an increased risk of adolescent pregnancy. Consequences of Adolescent Pregnancy: After the child is born life can be difficult for a teenage mother. Only 40% of teenagers who have children before age 18 graduate from high school. Without a high school degree her job prospects are limited, and economic independence is difficult. Teen mothers are more likely to live in poverty, and more than 75% of all unmarried teen mother receive public assistance within 5 years of the birth of their first child. Approximately, 64% of children born to an unmarried teenage high-school dropout live in poverty. Further, a child born to a teenage mother is 50% more likely to repeat a grade in school and is more likely to perform poorly on standardized tests and drop out before finishing high school (March of Dimes, 2012). Research analyzing the age that men father their first child and how far they complete their education have been summarized by the Pew Research Center (2015) and reflect the research for females. Among dads ages 22 to 44, 70% of those with less than a high school diploma say they fathered their first child before the age of 25. In comparison, less than half (45%) of fathers with some college experience became dads by that age. Additionally, becoming a young father occurs much less for those with a bachelor’s degree or higher as just 14% had their first child prior to age 25. Like men, women with more education are likely to be older when they become mothers. Eating Disorders Figure 6.9 According to the DSM-5-TR (American Psychiatric Association, 2022), eating disorders are characterized by a persistent disturbance of eating or eating-related behavior that results in the altered consumption or absorption of food and that significantly impairs physical health or psychosocial functioning. Although eating disorders can occur in children and adults, they frequently appear during the teen years or young adulthood (National Institute of Mental Health (NIMH), 2016). Eating disorders affect both genders, although rates among women are 2½ times greater than among men. Similar to women who have eating disorders, men also have a distorted sense of body image, including muscle dysmorphia, which is an extreme desire to increase one’s muscularity (Bosson et al., 2019). The prevalence of eating disorders in the United States is similar among Non-Hispanic Whites, Hispanics, African-Americans, and Asians, with the exception that anorexia nervosa is more common among Non-Hispanic Whites (Hudson et al., 2007; Wade et al., 2011). Source Risk Factors for Eating Disorders: Because of the high mortality rate, researchers are looking into the etiology of the disorder and associated risk factors. Researchers are finding that eating disorders are caused by a complex interaction of genetic, biological, behavioral, psychological, and social factors (NIMH, 2016). Eating disorders appear to run in families, and researchers are working to identify DNA variations that are linked to the increased risk of developing eating 231 disorders. Researchers from King’s College London (2019) found that the genetic basis of anorexia overlaps with both metabolic and body measurement traits. The genetic factors also influence physical activity, which may explain the high activity level of those with anorexia. Further, the genetic basis of anorexia overlaps with other psychiatric disorders. Researchers have also found differences in patterns of brain activity in women with eating disorders in comparison with healthy women. The main criteria for the most common eating disorders: Anorexia nervosa, bulimia nervosa, and binge-eating disorder are described in the DSM-5-TR (American Psychiatric Association, 2022) and listed in Table 6.1. Table 6.1 DSM-5-TR Eating Disorders Anorexia Nervosa  Restriction of energy intake leading to a significantly low body weight  Intense fear of gaining weight  Disturbance in one’s self-evaluation regarding body weight Bulimia Nervosa Binge-Eating Disorder  Recurrent episodes of binge eating  Recurrent inappropriate compensatory behaviors to prevent weight gain, including purging, laxatives, fasting or excessive exercise  Self-evaluation is unduly affected by body shape and weight  Recurrent episodes of binge eating  Marked distress regarding binge eating  The binge eating is not associated with the recurrent use of inappropriate compensatory behavior Health Consequences of Eating Disorders: For those suffering from anorexia, health consequences include an abnormally slow heart rate and low blood pressure, which increases the risk for heart failure. Additionally, there is a reduction in bone density (osteoporosis), muscle loss and weakness, severe dehydration, fainting, fatigue, and overall weakness. Anorexia nervosa has the highest mortality rate of any psychiatric disorder (Arcelus et al., 2011). Individuals with this disorder may die from complications associated with starvation, while others die of suicide. In women, suicide is much more common in those with anorexia than with most other mental disorders. The binge and purging cycle of bulimia can affect the digestives system and lead to electrolyte and chemical imbalances that can affect the heart and other major organs. Frequent vomiting can cause inflammation and possible rupture of the esophagus, as well as tooth decay and staining from stomach acids. Lastly, binge eating disorder results in similar health risks to obesity, including high blood pressure, high cholesterol levels, heart disease, Type II diabetes, and gall bladder disease (National Eating Disorders Association, 2016). 232 Figure 6.10 Source Eating Disorders Treatment: To treat eating disorders, adequate nutrition and stopping inappropriate behaviors, such as purging, are the foundations of treatment. Treatment plans are tailored to individual needs and include medical care, nutritional counseling, medications (such as antidepressants), and individual, group, and/or family psychotherapy (NIMH, 2016). For example, the Maudsley Approach has parents of adolescents with anorexia nervosa be actively involved in their child’s treatment, such as assuming responsibility for feeding the child. To eliminate binge eating and purging behaviors, cognitive behavioral therapy (CBT) assists sufferers by identifying distorted thinking patterns and changing inaccurate beliefs

PBT4 - Anticancer and Cancer Etiology

LESSON 11: Speech and Language Disorders and Etiology of Speech and Language Disorders

EPIDEMIOLOGY & ETIOLOGY OF MALOCCLUSION

Etiology, Medications

Epidemiology and Etiology of Schizophrenia

The American Sleep Disorders Association, in 1990, initiated a 5 year process to develop the widely used International Classification of Sleep Disorders (ICSD). The original ICSD listed 84 sleep disorders, each with descriptive details and specific diagnostic, severity, and duration criteria. The ICSD had 4 major categories: (1) dyssomnias, (2) parasomnias, (3) disorders associated with medical or psychiatric disorders, (4) "proposed" sleep disorders. The ICSD has since been revised twice. The second edition, ICSD-2 was released in 2005 which contains a list of 77 sleep disorders. That new list was broken down into 8 sub-categories: (1) Insomnia; (2) Sleep-related breathing disorder; (3) Hypersomnia not due to a sleep related breathing disorder; (4) Circadian rhythm sleep disorder; (5) Parasomnia; (6) Sleep-related movement disorder; (7) Isolated Symptoms, apparently normal variants, and unresolved issues; and (8) Other sleep disorders. A third edition of the ICSD was released in 2014. The major clinical divisions were unchanged in the third edition from the 2nd version, but there was an addition of variations in the diagnostic criteria for pediatric patients with obstructive sleep apnea, and there was a heading of Developmental Issues added to each section of disorders that have developmentally-specific clinical features in order to aid physicians in diagnosing those patients (specifically 9-CM and 10 CM). Sleep Disorders Categories The ICSD-3 lists about 77 sleep disorders which are divided into the following categories: Insomnia Sleep-related breathing disorder Central Disorders of Hypersomnolence Circadian rhythm sleep disorder Parasomnias Sleep-related movement disorder Some of the above categories have a section for isolated Symptoms, apparently normal variants, and unresolved issues Other sleep disorders There are some other sleep disorders that are divided into two appendices of the ICSD-2 manual. They are as follows: Sleep Related Medical and Neurological Disorders; and ICD-10-CM Coding for Substance-induced Sleep Disorders Study the disorders listed under each of the above categories until you have a good idea of what is included in each. There is a complete list of all the current classified sleep disorders in chapter 27, beginning on page 476 of your Sleep Disorders Medicine, 4th edition textbook. Insomnias Insomnias are disorders that usually produce complaints of not enough sleep, poor quality of sleep. Patient perception can play a role in the complaints. Occasionally, a patient may perceive that they are getting poor quality or not enough sleep even though they may be getting what we think is a normal night’s rest. Insomnias are defined by a repeated difficulty initiating sleep, not sleeping long enough, or poor quality sleep regardless of the amount of sleep time. Primary insomnia would not be due to another sleep disorder. If another sleep disorder such as OSA is causing the insomnia, then we call that secondary insomnia. These disorders may require medical treatment if they are long-lasting. Temporary insomnia due to a stressful situation or life event may correct itself with time. The types of insomnia are covered on pages 476 and 480 of your textbook. Sleep-Related Breathing Disorders These are disorders that involve disordered respiration, or breathing during sleep. These may be obstructive or not. There can be various causes of both. Central apnea syndromes include Cheyenne-Stokes breathing pattern and high-altitude periodic breathing. Cheyenne-Stokes is usually associated with either congestive heart failure or a traumatic brain injury which would actually be called secondary Central Sleep Apnea because it is secondary to another problem. It can also occur due to extreme old age, or a “worn-out” heart (a pacemaker may be needed for this type of patient). You will see patients like this occasionally. Primary Central Sleep Apnea has no apparent cause but still results in an irregular breathing pattern. These patients are not necessarily good candidates for CPAP because their breathing problem may not involve an obstruction. If not, you will likely see an increase in the number or length of central apneas after placing them on CPAP. There are newer PAP technologies that have been developed in recent years that do have some effect on the regulation of these types of patients’ breathing pattern but may show limited success in extending life expectancy. The obstructive type of breathing disorders, on the other hand, do respond well to treatment. These will likely make up the vast majority of patients that you will encounter in the sleep laboratory. Refer to pages 476 and 481 for more detailed examples of these disorders. Central Disorders of Hypersomnolence If you break down the word “hypersomnia” into its root terms as you did in medical terminology, it should be apparent that these disorders involve excessive sleepiness. However, the excessive sleepiness cannot be the result of another class of disorder. If a patient has another such disorder, that disorder must be effectively treated before a diagnosis of hypersomnia not due to a sleep-related breathing disorder can be made. These patients may have nights of uninterrupted sleep, but they still have unintended or unwanted lapses into sleep during the day. There can be many different causes of this; some of which are very interesting. Narcolepsy and Kleine-Levin Syndrome fall into this category along with some neurologic or psychiatric disorders. Circadian Rhythm Sleep Disorder Circadian rhythm sleep disorders are sleep disorders related to the internal clock of the human body resulting in an irregular sleep-wake cycle. Patients with these sleep disorders have circadian rhythms that make it difficult for them to function in society. The three extrinsic circadian rhythm sleep disorders are the time zone change syndrome, shift work sleep disorder, and irregular sleep-wake pattern (secondary circadian rhythm disorders). Three intrinsic circadian rhythm sleep disorders are delayed sleep phase syndrome, advanced sleep phase syndrome, and non-24-hour sleep-wake disorder (primary circadian rhythm disorders). For Circadian Rhythm disorders, refer to page 482 of your textbook. Time Zone Change Syndrome (Jet Lag Syndrome): Jet lag is experienced as a result of eastward or westward jet travel, after crossing several time zones, disrupting synchronization between the body's inner clock and its external cues. Symptoms do not occur after north-south travel. jet lag symptoms consist of difficulty in maintaining sleep, frequent arousals, and excessive daytime somnolence. Delayed Sleep Phase Syndrome: The ICSD-2 defines delayed sleep phase syndrome (DSPS) as a condition in which a patient's major sleep episode is delayed in relation to a desired clock time. This delay causes symptoms of sleep-onset insomnia or difficulty awakening at the desired time. Typically, patients go to sleep late (between 2:00 am and 6:00 am) and awaken during late morning or afternoon hours (between 10:00 am and 2:00 pm). Patients cannot function normally in society due to disturbed sleep schedules. Patients may try hypnotic medications or alcohol in attempts to initiate sleep sooner. DSPS patients may be treated by the use of chronotherapy (intentionally delays sleep onset by 2-3 hours on successive days until the desired bedtime has been achieved) or phototherapy (exposure to bright light on awakening). Advanced Sleep Phase Syndrome: Advanced sleep phase syndrome is characterized by patients going to sleep in the early evening and wake up earlier than desired in the morning (2:00 am-4:00 am). Because the patients have early morning awakenings, they experience sleep disruption and daytime sleepiness if they don't go to sleep at early hours. ASPS is most commonly seen in elderly individuals. Diagnosis is based upon sleep logs and characteristic actigraphic recordings made over several days. Chronotherapy may be used to treat ASPS; however, this therapy is not as successful in ASPS as in DSPS. Bright light exposure in the evening has been successful in delaying sleep onset. Non-24-Hour Sleep-Wake Disorder: Also known as Non-entrained, free running, or hypernychthemeral syndrome, is a disorder characterized by a patient's inability to maintain a regular bedtime and a sleep onset that occurs at irregular hours. Patients display increases in the delay of sleep onset by approximately one hour per sleep-wake cycle, causing an eventual progression of sleep onset through the daytime hours and into the evening. These individuals fail to be entrained or synchronized by usual time cues such as sunlight or social activities. This disorder is extremely rare and is most often associated with blindness. Parasomnia The parasomnias are a class of sleep disorders associated with arousals, partial arousals, and sleep stage transitions. They are dysfunctions (including movements and behaviors) that are associated with sleep, or that occur during sleep. Most parasomnias occur during delta sleep or slow wave sleep, although some can occur during any stage. REM Behavior Disorder, Nightmare Disorder, and Recurrent Isolated Sleep Paralysis are also included in this group although they are all associated with REM sleep. Rem Behavior Disorder (RBD) may involve a very drastic or sometimes violent dream enactment. Approximately 88% of known cases are in males. Elderly patients (over the age of 60) make up a high percentage of known cases (60%). RBD is now considered to be a possible indication of a future neurodegenerative disease such as Parkinson’s. Around 50% of patients with REM parasomnias also have some type of central nervous system disorder, and almost 10% have a psychiatric disorder. The treatment for these disorders is usually limited to securing the environment, but can also include the prescription of clonazepam. Think of parasomnias as things that patients may also do while sleeping, excluding movement disorders (other than RBD) which used to be included in this category as well. Examples would be Night Terrors, Nightmares, Hallucinations, Sleepwalking, or Enuresis (bed-wetting), etc. Parasomnias are covered in your text book on pages 482 - 484. Sleep-Related Movement Disorders Bruxism: Bruxism (teeth grinding) occurs most commonly in individuals between ages 10 and 20 years and is commonly noted in children with mental retardation or cerebral palsy. Bruxism is noted most prominently during NREM stages I and II and REM sleep. Episodes are characterized by stereotypical tooth grinding and are often precipitated by anxiety, stress, and dental disease. Occasionally, familial cases have been described. Usually, no treatment is required, but in extreme cases, dental reconstruction and appliances such as mouth guards may be needed. Periodic Limb Movement Disorder: Periodic limb movement disorder (PLMD, or PLMS for Periodic Limb Movements in Sleep) is a common sleep disorder affecting approximately 34% of people over the age of 60 years. PLMD can be defined as repetitive, involuntary limb movements during sleep. These movements are seen mostly in stage II sleep, and not in REM sleep due to muscle atonia in REM. The criteria for the leg movements to qualify as PLMS, the leg movements must last from 0.5 seconds to 5 seconds in duration each, there must be a gap of 5 to 90 seconds between each one, and there must be a cluster of at least 4 of these movements. Symptoms of PLMS often include frequent EEG arousals, fragmented sleep architecture, daytime sleepiness, and a disturbed bed partner. Treatment of PLMS usually includes medications. However, if the leg movements are related to respiratory events, they usually disappear when the respiratory events are corrected via CPAP, BiPAP, dental appliances, etc. The most common medications used to treat PLMS include Clonazepam, Dopamine Agonists, Anticonvulsants, and Opiates. Restless Legs Syndrome: Restless Legs Syndrome (RLS) is a disorder that causes discomfort in the legs and an irresistible urge to move them. This scenario can occur while the patient is asleep or awake. Patients often describe this discomfort as an itching, crawling, or creeping sensation in their legs. RLS is a common disorder, and affects more than 5% of the total population. Most RLS patients begin having symptoms before the age of 20, and continue to have these symptoms throughout their lives. Most patients with RLS also have PLMS. The most common treatments for these disorders are medications, including benzodiazepines, dopamine, opiates, and alpha-adrenergic blockers. Nocturnal Leg Cramps: Nocturnal leg cramps are intensely painful sensations that are accompanied by muscle tightness occurring during sleep. These spasms usually last for a few seconds but sometimes persist for several minutes. Cramps during sleep are generally associated with awakening. Many normal individuals experience nocturnal leg cramps. Causes remain unknown. Local massage or movement of the limbs usually relieves the cramps. Rhythmic Movement Disorder: Rhythmic movement disorder occurs mostly in infants younger than 18 months of age, is occasionally associated with retardation, and is rarely familial. It is comprised of three characteristic movements: head rolling, headbanging, and body rocking. These episodes are usually not remembered once the person awakens. It affects approximately three times as many males as females. Treatment for rhythmic movement disorder usually includes behavior modification, benzodiazepines, and antidepressants. Rhythmic movement disorder is a benign condition, and usually, the patient outgrows the episodes. Other rhythmic movement disorders can be related to the use of a drug or substance, or to another medical condition. Isolated Symptoms, Apparently Normal Variants, and Unresolved Issues This category includes disorders that are borderline normal or are normal variants. These include such examples as long sleeper, short sleeper, hypnic jerks, and other types of twitching or jerking movements that may only occur at sleep onset or in newborns. You have probably seen someone display a hypnic jerk as they fell asleep, or you may have woken yourself jerking because you felt like you were falling. Things like snoring or sleep-talking could be included in this case if they are not causing symptoms of insomnia or excessive daytime sleepiness but are disturbing to the patient or other people. Other Sleep Disorders A diagnosis in this category gives the physician an option for when the diagnosis may not be clear or too unusual to clearly fit into one of the other categories. This diagnosis may often be used as a temporary diagnosis until the actual cause of the disorder is determined. Environmental Sleep Disorder could be something in the surrounding environment, such as a barking dog, that is disturbing the patient's sleep enough to cause symptoms. Appendix A: Sleep-Related Medical and Neurological Disorders This category includes disorders that sometimes occur unrelated to sleep, but are related to sleep in these cases. Examples are sleep-related epilepsy, headaches, Sleep-related Myocardial Ischemia, or gastroesophageal reflux. Fibromyalgia used to be included in this section. While fibromyalgia is not necessarily a disorder that is only related to sleep, it can cause arousals, or disruptions of the patient's sleep and is a common diagnosis of patients that you will see. Appendix B: Other Psychiatric/Behavioral Disorders Frequently Encountered in the Differential Diagnosis of Sleep Disorders This section includes mood disorders, anxiety disorders, schizophrenia, or any other psychiatric diagnosis that may affect the patient's quality of sleep. Therefore, you will also likely see patients who have been referred by a psychiatrist on occasions. Intrinsic and Extrinsic Sleep Disorders These are terms that were previously used to differentiate between disorders that originated from within the body and those that were caused by something in the outside environment. However, I think that you could still see these terms again, so I think it is a good idea for you to be familiar with this terminology. INTRINSIC DISORDERS Intrinsic disorders include various types of insomnia and restless legs syndrome. Narcolepsy and recurrent hypersomnia are disorders of excessive sleepiness. Hypersomnolence can also be caused by narcolepsy, apnea, sleep disordered breathing, or periodic limb movements in sleep. EXTRINSIC DISORDERS Extrinsic sleep disorders include those that originate or develop from causes outside the body. Some of these dyssomnias found within this category include: conditions of inadequate sleep hygiene, altitude insomnia, food allergy insomnia, nocturnal eating, limit-setting sleep disorder, and sleep-onset association disorder. Sleep apnea is a disorder that commonly afflicts more than 12 million people in the United States. The word apnea is of Greek origin and means "without breath." Patients diagnosed with sleep apnea will literally stop breathing numerous times while they are asleep. The apneas on average can last from ten seconds to longer than a minute. These events can occur hundreds of times during a single night of sleep. Obstructive sleep apnea (OSA) is the most common type of apnea found within the category of sleep disordered breathing. OSA is caused by a complete obstruction of the airway, while partial closure is referred to as a hypopnea. The hypopnea is characterized by slow, shallow breathing. There are three types of apneas: obstructive, central, and mixed. So, sleep disordered breathing may be due to an airway obstruction (OSA), an abnormality in the part of the brain that controls respiration (central sleep apnea), or a combination of both ( mixed sleep apnea). This lesson will concentrate on obstructive sleep apnea. OSA occurs in approximately two percent of women and four percent of men over the age of 35. Check out this video for a good example of an OSA patient: Sleep Apnea - Hard to Watch... (Links open in a new window. Right click on link and choose "open in a new window") Obstructive Sleep Apnea sufferers are not always the ones that you would expect. Check out this video of an Asian woman, especially near the end: Sleep Apnea Causes of Obstructive Sleep Apnea The exact cause of OSA is difficult to pinpoint. The site of obstruction in most patients is the soft palate, extending to the region at the base of the tongue. There are no rigid structures, such as cartilage or bone, in this area to hold the airway open. When a patient is awake, muscles in the region keep the passage open. However, a patient who tests positive for OSA will experience a collapsing of the airway when they are asleep. Thus, the obstruction occurs, and the patient awakens to open the airway. The arousal from sleep lasts only a few seconds, but brief arousals disrupt continuous sleep. When the sleep architecture is fragmented, the patient will be prevented from obtaining SWS and REM sleep ( these stages of sleep are needed by the body to replenish its strength ). Once normal breathing is restored, the person falls asleep only to repeat the cycle throughout the night. Typically, the frequency of waking episodes is somewhere between 10 and 60. A patient with severe OSA may have more than 100 waking episodes in a night of sleep. Often, the OSA patient will complain of nonrestorative sleep and excessive daytime sleepiness. Risk Factors The primary risk factor for OSA is excessive weight gain. The accumulation of fat on the sides of the upper airway causes it to become narrow and predisposed to closure when the muscles relax. Age is another prominent risk factor. Loss of muscle mass is a common occurrence associated with the aging process. If muscle mass decreases in the airway, it may be replaced with fat, leaving the airway narrow and soft. Men have a greater risk for OSA. Male hormones can cause structural changes in the upper airway. Below are other common predisposing factors associated with OSA: Anatomic abnormalities, such as a receding chin Enlarged tonsils and adenoids ( the main causes of OSA in children) Family history of OSA ( However, there has been no medically documented facts stating a generic inheritance pattern ) Use of alcohol and sedative drugs, which relax the musculature in the surrounding upper airway Smoking, which can cause inflammation, swelling, and narrowing of the upper airway Hypothyroidism, acromegaly, amyloidosis, vocal cord paralysis, post-polio syndrome, neuromuscular disorders, Marfan's syndrome, and Down syndrome Nasal and sinus congestion or problems Symptoms of OSA The nightly disruption and fragmentation of normal sleep architecture will cause the patient to experience the feeling of nonrestorative sleep. The most common complaint from someone who suffers from OSA is excessive daytime sleepiness (EDS) . The numerous disruptions and arousals will prevent the patient from obtaining a continuous deep sleep. Thus, the individual could also be prone to automobile accidents, personality changes, decreased memory, impotence, and depression. Patients are rarely aware or recall the frequent awakenings that occur following the obstructive episodes. EDS may be mild, moderate, or severe. Some patients will complain of falling asleep in a non stimulating environment, such as reading a book or a newspaper in a quiet room. Severe OSA patients may complain of falling asleep in a stimulating environment, such as during business meetings, eating, or casual conversation. One of the most dangerous scenarios is patients who suffer from OSA can fall asleep behind the wheel. Patients will often complain of feeling like they have not slept at all no matter of the length of time in bed. The same holds true for napping. Other indicators or symptoms of possible OSA include morning headaches and frequent urination during the night. Physical signs that coincides with characteristics of OSA patients include snoring, witnessed apneic episodes, and obesity. Not every individual who snores will test positive for OSA, but most patients who have OSA will snore with moderate to loud levels. Hypertension is prevalent in patients with OSA, although the exact relationship is unclear. It has been medically proven that treating OSA can significantly lower blood pressure. Complications The most prevalent complication for patients who suffer from OSA is a diminished quality of life due to chronic sleep deprivation and previous described symptoms. Coronary artery disease, cerebral vascular accidents (strokes), and congestive heart failure are being evaluated to define the exact nature of their connection to OSA. Still, it has documented that there is a relation between these complications and OSA. Obstructive sleep apnea aggravates congestive heart failure (CHF) by placing stress on the heart during sleep. Statistics show there is a high prevalence of OSA in patients with CHF. Central sleep apnea may be prominent in patients with CHF. Diagnosis The most universal method for diagnosing OSA is to have the patient undergo a sleep study. The technical name for the procedure is nocturnal polysomnograph. The first priority with any procedure is patient safety. A thorough analysis of the information gathered prior to beginning the test will give the technician an opportunity to determine the reason for testing, to verify all necessary monitoring parameters, and to determine the possible need for ancillary equipment. The technician must be aware of any precautions or special patient needs during testing. An understanding and knowledge of the signs, symptoms, and findings of a variety of sleep disorders and sleep related breathing disorders is necessary to ensure patient safety and recording requirements during polysomnography testing. Various medical problems will be encountered with the patients undergoing a sleep study. Examples of these complications include: asthma, COPD, cardiac arrhythmias, carbon dioxide narcosis, and abnormal breathing. Numerous cardiac arrhythmias may occur and they include: asystole, ventricular tachycardia or fibrillation, bigeminy, trigeminy, multi-focal PVC's, heart blocks, atrial fibrillation, bradycardia, or tachycardia associated with sleep apnea. Some of these cardiac arrhythmias are life threatening and require technician intervention. Others are relatively benign and require only that the technician watch the patient closely. Thus, all polysomnography technicians will be required to be certified in Basic Life Support. The polysomnography testing will include recording of multiple physiological parameters in sleep. These parameters usually include EEG, EKG, eye movements, respiration, muscle tone, body position, body movements, and oxygen saturation. The electroencephalogram (EEG) measures brain electrical activity. The brain activity during different stages of sleep as compared to wake is distinctly different. The electrooculogram (EOG) monitors eye movements and allows the examiner to determine REM sleep and wake. The electromyogram (EMG) monitors muscle tone, and the EMG helps to differentiate REM sleep from wake because the muscles relax to a state of paralysis in REM sleep. The electrocardiogram (EKG or ECG) monitors heart rate and graphs the electrical signal as it is conducted through the heart. Respiratory effort belts are placed around the patient's chest and abdomen to detect and record the rising and falling movements associated with respiration. A pulse oximeter is attached to the finger to record oxygen saturation levels in the blood. Leg leads or electrodes are attached to record leg movements which may determine the patient has periodic limb movement disorder. A thermistor is used to monitor breathing. Obstructive sleep apnea is diagnosed if the patient has an apnea/hypopnea index (AHI) of 5 or greater an hour. The respiratory disturbance index (RDI) is sometimes used in place of the AHI and essentially refers to the same data. However, in the recent past, RDI was an index that also included the number of respiratory effort related arousals(RERAS) per hour in addition to the hypopneas and apneas. Some sleep centers may still do this, but most are currently not scoring the RERAS due to non-coverage of insurance. An RDI from five to ten per hour would be a positive finding for OSA as well. Clinically speaking, an obstructive apnea is defined as a complete cessation of airflow for 10 seconds or more with persistent respiratory effort. An obstructive hypopnea is defined as a partial reduction in airflow of at least 30 percent followed by a drop in SaO2 of at least 3% or an arousal from sleep, or an alternate definition of 50 percent reduction in nasal pressure airflow signal followed by at least a 4% drop in SaO2(desaturation). Medicare still requires the 4% drop in SaO2 for their patients, but the first definition is recommended by the American Academy of Sleep currently. SaO2 refers to the amount of Oxygen in the blood being carried by the red blood cells. This will always drop when a patient stops breathing. The many physiological measurements taken usually enable the physician to diagnose or reasonably exclude OSA. Certain scenarios may prove a more difficult diagnosis. Such as, a patient who may have mild OSA at home, or only after using certain medications or alcohol but does not experience any episodes during the sleep study. Thus, the sleep study results must be interpreted with the entire clinical picture in mind. Another condition, called upper airway resistance syndrome, cannot be seen on polysomnography. This syndrome is characterized by repetitive arousals from sleep that probably result from increasing respiratory effort during narrowing of the upper airway. These patients suffer the same sleep disruption and deprivation as other sleep apnea patients. In such cases, the only alarming indicator that is recorded is the recurrent arousals. Ultimately, patients suffering from upper airway resistance syndrome may not test positive for OSA with standard polysomnography testing. Treatment A patient suffering from OSA has several treatment options that include: weight reduction, positional therapy, positive pressure therapy, surgical options, and oral appliances. Significant weight loss has shown tremendous improvement and possible elimination of OSA. The amount of weight a patient needs to lose to achieve noticeable benefits varies. However, one will not need to achieve "ideal body weight" to see improvement. Positional therapy is a method of treatment used to treat patients whose OSA is related to body positioning during sleep. A OSA patient who sleeps flat on their back, or in supine position, will experience worse symptoms in general. This type of therapy has its limits, but some patients have experienced benefits. Some of the strategic methods include: a sock filled with tennis balls is sewn into their shirt to make it uncomfortable for the sleeper to lie on their back, and positional pillows to assist in sleeping on their side. Positive pressure therapy is one of the most if not the best methods of treatment for obstructive sleep apnea. There are three different types of devices: continuous positive airway pressure (CPAP), autotitration, and bi-level positive airway pressure. CPAP, the more common of the three therapy modes, is the most prescribed method of treatment for OSA. A facial or nasal mask is worn by the patient while they sleep. The mask is connected to the CPAP machine with tubing. Positive air pressure is delivered from the machine to the mask and continues to the upper airways establishing a "pneumatic splint" that prevents collapsing of the airways. Autotitration devices are designed to provide the minimum necessary pressure at any given time and change that pressure as the needs of the patient change. Bi-level positive airway pressure differs from the CPAP by reducing the level of positive pressure upon exhalation. Oral appliances are another avenue a patient can try as a therapeutic device. Generally, there are two categories, mandibular advance devices and tongue-retaining devices. Mandibular advance devices are similar to athletic mouth guards. They differ in the mold for the lower teeth is advanced further forward than the mold for the upper teeth. This will cause the jawbone to remain forward and prevent the collapse of the airway. It is effective in mild cases of OSA, particularly if the patient's OSA is positional. Tongue-retaining devices also resemble an athletic mouth guard. It acts as a suction cup and is placed between the upper and lower teeth. The tongue is positioned forward and obstructions caused by the tongue should be minimized. First described in 1981, CPAP therapy has become the most preferred treatment for patients with OSA. CPAP flow generators or machines maintain a constant, controllable pressure to prevent blockage of the upper airway. The positive air pressure travels through the nostrils by a nasal or facial mask. This airflow holds the soft tissue of the uvula, palate, and pharyngeal tissue in the upper airway in position so the airway remains open while the patient progresses into deeper stages of sleep and REM sleep. The CPAP device can be described as a "pneumatic splint." Variations to the CPAP machine are available to help with compliance. BPAP, Bi-PAP or bi-level positive airway pressure is another option for treatment. Those three are one and the same. They are just different ways that you might see this term. The AASM guidelines uses "BPAP" in their protocol publications. BiPAP is a trademarked term by a company named Respironics. Anyway, most of the problems patients experience with CPAP are caused by having to exhale against a high airway pressure. Because the air pressure required to prevent respiratory obstruction is typically less on expiration than on inspiration, Bi-PAP machines are designed to detect when the patient is inhaling and exhaling and to reduce the pressure to a preset level on exhalation. Patients with severe OSA may require maximum levels of pressure to eliminate the obstructive apnea. Bi-PAP may be the chosen method of treatment with this scenario, and Bi-PAP may be used when the patient has more than one respiratory disorder. Regardless of the mechanism used, the goal of the technician should always be to titrate the machine to the lowest possible pressure to eradicate the sleep apnea. Each individual patient with OSA will present a different scenario for the attending polysomnography technician. The sleep study with positive airway pressure titration will need to achieve the optimal pressure for the specific patient. The sleep study with CPAP/Bi-PAP will show not only when the respiratory events have ceased, but also when the arousals from the respiratory events occur. The ultimate goal for the technician during a titration process is to achieve the minimal optimum pressure to eliminate all obstructive events and snoring during all stages of sleep and all body positions while sleeping. Compliance Mask fitting is an essential element of a patient's success with positive airway pressure therapy since it affects compliance and effectiveness of treatment. The higher pressures used during CPAP/Bi-PAP therapy can cause a significant air leak with the mask. The leak can also emerge from the patient's mouth if they are using a mask that doesn't cover the mouth. This can startle a new CPAP user. The leak can wake the patient from sleep. Thus, the mask stability is tested with higher pressures. Higher pressures may also require tighter head gear to maintain an adequate seal. Adversely, this will contribute to the discomfort from wearing the mask. When selecting a CPAP mask the following factors should be considered: comfort quality of air seal convenience quietness air venting CPAP/Bi-PAP machines are also available with humidity. Nasal congestion and dryness are very common complaints with positive airway pressure therapy. Humidification can also be heated. These features have proven to help with patient compliance. Ultimately, the biggest obstacle with compliance is getting patients to comply with their own treatment. Without the patient's willingness to use it, CPAP will not provide effective therapy. Studies have shown that CPAP compliance varies from approximately 65% to 85%. The bottom line for the patient to experience the benefits and relief of complaints is they must use the machine on a nightly basis. Information regarding the degree to which a patient is compliant with CPAP is essential for assessment of therapeutic impact. If problems persist after implementation of CPAP, the causes could include: delivery of insufficient pressure to maintain upper airway patency during sleep misdiagnosis of the etiology of the individual's symptoms failure to use the device for a sufficient duration on a regular basis Possible Side Effects The principal side effects with CPAP/Bi-PAP use include: contact dermatitis nasal congestion rhinorrhea dry eyes mouth leaks nose bleeds (rare) tympanic membrane rupture (very rare) chest pain aerophagia (the excessive swallowing of air, often resulting in belching) pneumoencephalitis (air in the brain, which is extremely rare, reported in a patient with a chronic cerebral spinal fluid leak) claustrophobia smothering sensation Actions can be taken to counteract some of the side effects. Nasal congestion or dryness often can be reduced or eliminated with nasal sprays or humidification. Rhinorrhea can be eliminated with nasal steroid sprays or ipratropium bromide nasal sprays. Epistaxis (nose bleeds) is usually due to dry mucosa and can be treated with humidification. Skin irritation can be combated with different mask materials. Dry eyes are usually caused by mask leaks and can be eliminated by changing to a better fitting mask. Attempts to reduce claustrophobic complaints have resulted in the patient using nasal pillows or prongs as opposed to the nasal or facial mask. Mouth leaks can be reduced or eliminated by using a chin strap. A small number of patients complain of chest pain or discomfort with CPAP use. This can probably be attributed to increased end-expiratory pressure and the consequent elevation of resting lung volume, which stretches wall muscles and cartilaginous structures. The resulting sensation that is created is due to chest wall pressure that persists through the hours of wakefulness. Any complaints of chest pain should always be taken seriously. However, if the complaint by the patient on CPAP proves to be nondiagnostic, Bi-PAP therapy may prove to be an option since expiratory pressure can be reduced. Sometimes it pays for the technologist to develop some psychological skills in order to convince the patient to use the device. I have found that a patient who doesn't seem to believe they need CPAP tends to change her/his mind when they see the data that shows him not breathing. Keep in mind that your patients can't see themselves sleep. They may also not be aware of all the possible complications of OSA down the road. Another area of concern for OSA patients using CPAP/BPAP devices is the negative effects on arterial blood gases and oxyhemoglobin saturation. Studies have reported severe oxyhemoglobin desaturation during nasal CPAP therapy in a hypercapnic (elevated levels of carbon dioxide in the blood) sleep apnea patients. Studies have also shown significant oxygen desaturations with CPAP administration with supplemental oxygen. The exact cause has yet to be determined. This occurrence may be due to the following factors: worsening hypoventilation related to the added mechanical impedance to ventilation associated with exhalation against increased pressure increased dead-space ventilation a decrease in venous return and cardiac output due to increased intrathoracic pressure during CPAP administration in patients with impaired right or left ventricular function and inadequate filling pressure One more possibility is when the optimal pressure setting has not been reached yet. Therefore, a ten second apnea may have turned into a 90 second hypopnea. The patient may not arouse from sleep as quickly to get a breath since the airway is not completely closing off as it was without therapy. This should improve once enough pressure is added, however. Despite the above scenarios and problematic experiences, CPAP/Bi-PAP administration has been reported to improve awake arterial blood gases in OSA patients with hypercapnia and cor pulmonale. Traditional and Evolving Methods of Initiating CPAP/BPAP Different methods have been established for implementation of positive airway pressure therapy. Traditionally, patients have undergone a technician attended PSG-monitored trial of CPAP. Split-night studies are now conducted more frequently. Home CPAP trials is another avenue that is being investigated. Use of predictive formulas to estimate or establish optimal level for CPAP therapy has been investigated. Each scenario has advantages and disadvantages. CPAP Therapy of Nonapneic SDB There are numerous documentations of patients with congestive heart failure (CHF) suffering from sleep-disordered breathing (SDB). Most often the respiratory events will be central in nature (no effort, brain not sending signal to breathe) resembling Cheyne-Stokes respiration (CSR). CSR is defined as a breathing pattern characterized by regular "crescendo-decrescendo" fluctuations in respiratory rate and tidal volume. The presence of SDB was associated with sleep-fragmentation and increased nocturnal hypoxemia. The conclusions from the findings are stated below: There is a high prevalence of daytime sleepiness in patients with CSR in conjunction with CHF. Patients with CHF who also have CSR have a higher mortality than patients who have CHF without CSR. CSR, AHI (apnea/hypopnea index), and the frequency of arousals were correlated with mortality. Furthermore, research has found CPAP has been noteworthy and effective on breathing in patients with CHF and CSR. The results of several studies showed an increase in cardiac output and stroke volume and a reduction in left ventricular wall tension during application of CPAP. The improvements seen in CHF patients with CSR regarding cardiac function during sleep is believed to carry over to wakefulness. Possible factors contributing to the improvements seen include: sleep-related reduction of left ventricular transmural pressure improved oxygenation during sleep reduced sympathetic nervous system activation during sleep CPAP machines have become a lot more sophisticated during the past decade. One of these updates is the ability of some machines to generate an algorithm that can predict the next breath of these central sleep apnea patients. These machines will adjust how much air is delivered during each breath based on this prediction. This has the effect of making the breathing pattern more consistent. You may see this denoted as Auto-SV, or servo-ventilation. We will talk about this more later, but I just wanted you to be aware that there are more sophisticated machines for patients with CHF and irregular breathing patterns that are not due to obstructions. Effects of Altitude Changes and Alcohol Consumption Older CPAP machines will not adjust to changes in altitude. As altitude increases, the older CPAP devices will deliver progressively lower than prescribed pressure. The more modern devices will detect altitude changes and make the appropriate adjustments. The polysomnography technician would benefit from information regarding a patient relocating from a high altitude location to lower altitude or vice versa if there are complaints of the CPAP therapy being nontherapeutic. Alcohol consumption can present further complications for a patient suffering from OSA. Alcohol suppresses the arousal response. The patient may experience a greater frequency and duration of apneas and hypopneas and increased snoring. Excessive alcohol use also increases sleep fragmentation. Taking a sedative can cause these effects to be imitated or exacerbated. Still, there are reports stating moderate alcohol consumption did not significantly alter the level of pressure required to eliminate the obstructive events. Nonetheless, OSA patients should avoid alcohol

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