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The real Professor(s) Higgins: Section 1–a professor of Phonetics: Henry Sweet, phonetician: The whole point of his “Current shorthand” is that it can express every sound in the language perfectly, vowels as consonants, and that your hand has to make no stroke except for the easy and current ones with which you write m, n, l, p and q, scribbling them at whatever angle comes easiest to you, his unfortunate determination to make this remarkable and quite legible script serve also as a Shorthand reduced it in his own practice to the most inscrutable of cryptograms. HIS TRUE OBJECTIVE WAS the provision of a full, accurate. Legible script for ur noble but ill-dressed language; but he was led past by his contempt for the popular Pitman system of Shorthand, which he called the Pytfall system. —> the triumph of Pitman was because of business organisation: cheap textbooks and exercise books were available in this and school where experienced teachers coached you up to the necessary sufficient. Sweet couldn’t organise his market in that fashion—> he was angry at Oxford for the failure of it to do justice to his eminence. Such people as phoneticians are among the most important people in England right now. Pygmalion (1938-12) shows the figure of a Phoenician, a linguist who studies languages scientifically and whose existence is usually confined to the knowledge of very few people belonging to the field, emerged publicly for the first time. Section 2.2– The Philological Society Established in 1830 it is the oldest learned society in Great Britain devoted to the scholarly study of language and languages. It had a particular interest in historical comparative linguistics and maintains its traditional interest in the structure, development and varieties of Modern English. The society experiences a period of heightened success in the 1860’s-70s with phoneticians suc as Alexander John Ellis and Henry Sweet — through the years it continued to attract known scholars like Bopp and Grimm. The greatest achievement to date is what has since remained the foremost authoritative dictionary of the English language: Oxford English Dictionary, whose first official dictionary was Augustus Henry Murray. Daniel Jones: played a key role in the development and Institutionalisation of the study of phonetic in England. In 1907 he secured a part-time lectureship in phonetics at University College in London —> his reputation soon expanded and in 1911 he was named Britain’s first Professor of Phonetics. He produced an extremely large number of publications and transcripts which offered meticulous descriptions of English phonetics ì, especially directed at second language learners, and explanations of other languages such as Cornish, Sindhi and Ga. Besides, he published analyses of French, Spanish, Italian, Russian and Cantonese. He identified and systemised the eight Cardinal vowels. He was also interested in the improvement of orthography. He was more concerned about practical matters, he developed a new concept of phoneme, considering phonemes as families of sounds, each appropriate to a specific phonetic context. He also distinguished prosodic features from phonemes and coined the terms chroneme and toneme to denote differences in length and pitch. he invested time in scientific descriptions of his analyses by means of photos of his own lip movements, X-rays of his tongue positions, oscillograms. He recorded his voice, and in 1956 he recorded his pronunciation of the Cardinal Vowels on gramophone records (Thomas 2011). The next paragraphs will illustrate some of these descriptions concerning Cardinal Vowels in detail, and one of Daniel Jones's major works, the English Pronouncing Dictionary (1917), which both students and teachers, native and non-native speakers of English, still use nowadays (almost 100 years later!) as a major reference for the pronunciation of the English language. One of the main aims characterizing his works was to provide the learner with a scientific study of the English speech sounds and their distribution in connected speech. It is, indeed, with this idea in mind that he identified and systematized the eight Cardinal Vowels as a technique for characterizing the vowel inventories of language (i.e. of all languages), and illustrated the speech sounds of English to give foreigners the scientific information needed in order to learn educated Southern English, in an appreciably lighter fashion ones 1922: Il. The general idea behind the concept of Cardinal Vowels is that they demarcate the articulatory vowel space that speakers have at their disposal; consequently, such vowels can be regarded as reference points for the phonetic description and transcription of any language. For this purpose, and with the firm conviction that these vowel sounds can only be learnt from a teacher who knows how to make them or from a gramophone record or tape record, Daniel Jones recorded his pronunciation of the Cardinal Vowels on gramophone records'". The following extract describes their use as presented by Daniels Jones himself in the booklet which accompanied his two-record set in 1956: + ++ Section 4–playing Mr. Higgins: Praat (Dutch for talk) is a freeware program for the analysis and reconstruction of acoustic speech signals. Student could use it for: Recording themselves in order to compare their English to other’s Explore varieties of English Become more familiar with the language features studied theoretically during linguistic courses. 4.1.1–The Praat windows: A variety of windows will open, it is better to explore the main windows before starting to use the actual Spectrogram. Praat objects windows: is used to open, create and save files, as well as, to open the various editors and queries which will be needed to work with sound files. Praat picture windows: used to create and display publication-quality images. Praat editor windows: mostly used when examining a sound file, the spectrogram on the bottom, and selections and measurements can be taken by using the cursor. Praat info windows: will pop up with the specific result when a query is made either in the editor window or the objects window. TO KNOW: Pitch: quality of a sound governed by the rate of vibrations producing it; the degree or highness or lowness of a tone. The intensity of a sound wave: is measured in decibels and represents the power and loudness of the wave. A dormant (called f1, f2, f3, f4 —> voice) is a concentration of acoustic energy around a particular frequency in the speech wave, it emphasises the harmonic, with higher amplitudes of a speech sound. —> f0 is the lowest frequency of a complex sound and is equal to the Pitch of one’s voice. F1 and F2 are important for vowels, while using dormant patterns, acoustic phonetics makes it possible to define specific vowels and differentiate them from one another. F1 describes the height of the tongue when the vowel is being produced, whereas f2 reflects the place of the tongue and the rounding of the lips —> will be further apart for front vowels and closer together for back vowels. Pulses: are single vibrations or short bursts of sound which produce variations in air pressure —> occur in pulse-like manner, pushing the air out of the mouth or nose and displacing air with pulse. —> can be represented as a waveform. 4.1.2—Recording, opening, and saving sounds: To record sounds using Praat, a microphone, sound card, or external ADC (Analog-Digital Conversion) box will have to be plugged in to a computer before starting Praat, and then: Objects → New → Record Mono (at this stage the Sound recorder window will pop up, see Figure 32). The Sound recorder window Through the Sound recorder window it will be possible to choose the sampling frequency (the default, 44100 Hz, is fine for most purposes), the microphone or other sound source, and whether to record a mono or stereo sound. In order to record and then to stop the recording, Record and Stop will have to be pressed respectively, being careful that the sound level ar stays within the green range to avoid clipping"?. Once a recordinglas been made, it will have to be named and saved, It will then show up in the Praat objects window where it's ready for editing. Praat can only record one minute long chunks, to record longer sounds, the buffer size in Praat → Preferences → Sound Recording Preferences will have to be changed, otherwise another software program to record the session can be used and then the sounds can be imported into Praat for analysis and manipulation. If there is no need to record a sound because one has already been recorded lin aif, wav or flac format®, there are two ways to open it in Praat: on Mac OS X, the supported files can be dragged onto the Praat icon in the dock, otherwise: Objects → Open → Read trom File... as it works for other operating systems. Once the files have been uploaded, they will appear in the Objects window for further use. To save a file, given that files are never saved by default by Praat, the file in the Objects window will have to be selected, then: Objects → Save → Save as file. 4.1.3–Measuring waveforms and spectrograms: Once a sound has been recorded and/or opened in Editor window via Objects → View & Edit, the Waveform of the sound will be represented as in Figure 25 above and, if the sound is sufficiently short, a broadband Spectrogram showing the spectral energy of the sound over time, will be displayed. In addition, a series of red dots (representing the Formants), blue lines (representing the speaker's Pitch), and a yellow line (representing the Intensity) might also be present. These can be enabled and disabled in the Editor → View → Show Analyses menu. The cursor will spawn two dotted lines by clicking within the Editor window. A vertical bar will show the time within the sound where it has been clicked (labeled at the top in seconds) and, by clicking within the Spectrogram, a horizontal bar will show the frequency at the cursor (labeled on the left in red). If the Pitch or Intensity tracks are displayed where the cursor is placed, values at the time the cursor represent will be given on the left side of the editor window. In addition, portions of the sound can be selected by clicking and dragging them (or by using the Select menu). The time of the start and finish of the selection will be displayed in red, and the duration of the selection (in seconds) will be displayed in the top of the bar. The three gray bars at the bottom of the editor window can be used to play a sound in the editor window. The bottom-most bai (Total Duration) will play the entire sound. The middle bar (Visible Part) will play only the visible portion of the sound. The different sections of the top bar (split by the cursor or selection), when clicked, will play the corresponding pieces of the visible portions of the sound file. Hitting < tab> also plays the visible portion of the file. To view some analyses and to get a closer look at the data, the five buttons in the bottom left corner of the window will have to be selected: all shows the entire file, in and out zoom in and out, sel zooms to make the current selection fill the window, and bak zooms back to the previous zoom level. When dealing with long sound files, in order to view analyses like the spectrogram and formants, zooming in will have to be selected to show only a pre-defined amount of time. The Group setting in the bottom right corner of the window will ensure that if two sounds are open in Editor windows at once, they will share the same zoom characteristics. This is best used to compare two versions of the same file, say, an original versus one with an acoustic modification made. 4.1.4– Viewing Pitch via a Narrowband Spectrogram: The most reliable way of getting a sense of the Pitch through the course of the word in Praat is by examining a narrowband Spectrogram 2 with a reduced visible range 0 - 400 Hz for speech). This can be done by editing the Spectrogram settings as described here: To make changes to the spectrogram settings, Editor → Spectrum → Spectrogram Settings will have to be selected. This will pull up the Spectrogram settings window where there are two very important settings: the window length and view range. Window length (given in seconds) controls how large of a chunk of the sound Praat will examine when trying to find the frequencies present at a given moment in the signal. Looking at a larger window of the sound will give more accurate information about the frequencies present, but will also reduce the accuracy of the temporal information given. Varying the window length enables one to choose between Broadband and Narrowband spectrograms. View range controls how much of the spectrum is visible. For speech, one is likely be interested in the range from 0 to 5000 or 6000 Hz, but if examining fricatives, it might be interesting to look as high as 15,000 Hz. For music, instead, one may focus on the area from 100 to 2000 Hz. If the sound files have a relatively small or large dynamic range (the difference in volume between the loudest and quietest parts), or if the spectrograms seems too light or too dark, the dynamic range setting can be adjusted here, but 50 dB is usually safe. The contours of the harmonics will accurately represent the Pitch contours of the voice during the word, and doing this will offer a sense of the contour before using the Pich tracker for more precise measurement. Praat also has the ability to provide a Pitch track in the Editor window: Editor → Pich → Show Pitch will select it in the Editor window. At this point, a blue line will be placed on top of the Spectrogram representing the Pitch (see Figure 33). Once the Pitch track is placed, the cursor can be used to check the Pitch at any given point in the word by placing it and checking the middle blue number on the right side of the window. The cursor can also be placed at a given point in the file and Editor → Pitch → Get Pitch. Running Editor → Pitch → Get Pitch when a chunk of the sound is collected will return the average pitch during that selection
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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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