What If Shigeru Miyamoto Had Become a Manga Artist?
Cover Story: A timeline from an alternative universe where gaming lacks input from one of its most prolific creators.
I
t's kind of a fascinating story really. Shigeru Miyamoto, maybe the most influential designer ever, had little interest in videogames until the late 1970s, when he played Space Invaders. Up until that point, he had wanted to be a manga artist. Well, what if he had followed his original dream and done just that? What would have happened to Nintendo? Or videogames in general? Here's one possible timeline.
1979 -- Miyamoto the Manga Artist: Shigeru Miyamoto graduates from the Kanazawa Munici College of Industrial Arts and Crafts. Because Miyamoto's father is a friend of Hiroshi Yamauchi, he soon receives an offer to work for Nintendo. But Miyamoto is something of a free spirit, and he has little interest in videogames. He decides instead to pursue a career as as manga artist.
Dead Island is set to be re-released in a Game of the Year Edition package next month, a fact that is the source of some complaints. It's not so much that the game is being bundled with its DLC that is the problem; it's the labeling of the game as Game of the Year, a title which many feel it is not deserving of.
It is completely understandable why a publisher would want a game re-release to be positioned as a "Game of the Year Edition." That title carries with it a certain connotation of quality, that it was among the very best, if not the best, games released during the year it originally came out. Game of the Year Editions are commonly associated with the likes of Morrowind, Oblivion, Fallout 3, Red Dead Redemption, and other critically acclaimed games. There is a certain expectation that a GotY Edition consists of a terrific game and bonus content (be it downloadable content or expansion packs) that early adopters had to pay extra for, with all of this often coming at a sub-$60 price.
What If the Cost of Games Continued to Rise Since the '80s?
Cover Story: A sad look at a hobby that became too damn expensive.
December 12, 1985
You'll never guess what I got for my birthday! I woke up this morning, walked into the living room, and saw Dad playing Nintendo in front of the TV! He was having trouble with the first level of Mario, so I sat down and helped him jump over the pits until we got to the flagpole at the end. After that, we brought out the Zapper and played Duck Hunt until dinner time. Mom got kinda mad at Dad for buying something so expensive, but he told her that my birthday only comes once a year.
What If the 1993 Video Game Violence Hearings Resulted in Government Censorship?
Cover Story: Peer into a dark and twisted present we'll (thankfully) never know.
I
n late 1993, state senators and certified oldsters Joseph Lieberman and Herb Khol got a whiff of this whole "video games" thing and decided to use their unholy powers to investigate the issue. While our friends in Germany and Australia often find amazing games banned outright or plagued with hilariously conspicuous censorship, we Americans escaped with a barely perceptible slap on the wrists thanks to the efforts of testifying industry vets who actually knew the subject at hand. But one can only wonder what the '90s gaming landscape (and beyond) would have looked like if the iron fist of government oppression punched the living daylights out of our beloved hobby...
Book Review: Exploring Video Gaming's Near-Death with "1983"
Cover Story: Thirty years ago, video games almost died. We examine the possibilities.
W
ith his latest book, 1983, game journalist and historian Chris Kohler has chosen to take a slightly different tack then he employed for his massive treatise Power Up: How America Gave Video Games an Extra Life a few years back. Rather than approaching the topic of video games from a wide-ranging, all-inclusive perspective, Kohler instead drills down here into a single crucial moment in time for the young medium: The near-crash of the industry in year 1983.
Despite the Orwellian overtones of the title Kohler has selected for his work, there's nothing ominous about the story contained herein -- perhaps, except, the idea that video gaming could have been snuffed out entirely a mere decade after Pong's debut. A combination of gold-rush greed, incompetence, and '80s corporate culture nearly suffocated the fledging entertainment medium just as it was hitting its stride. The Warner corporation's eagerness to cash in on their purchase of Atari, combined with the influx of low-quality, externally developed 2600 games after Activision broke away to become the first third-party developer, nearly buried the industry beneath a deluge of self-cannibalizing mediocrity.
I like to play games in what I imagine is an unusual manner, or at least I thought this to be the case until 1UP members revealed they share some of my habits. One of these things, my propensity for systematically exploring an area before moving on, has reared its head in particularly noticeable fashion as I make my way through Max Payne 3. Playing in this way was clearly something the game's designers accounted for, as evidenced by the collectables scattered throughout, and yet it feels almost as if I'm being punished for deciding to be a completionist.
My process for approaching each area in Max Payne 3 follows the same pattern, only being altered if I'm low on health and out of painkillers (health packs in Max Payne's world). I kill everyone and then proceed to sweep over the entire room, seeking out any hidden spots or areas which do not appear to lead to the next area. As I make my way from one combat area to the next, I'm mindful of my surroundings and am sure to double back to check behind staircases and to see which doors can be opened. I do this all while searching for golden gun components, painkillers, and clues which can be examined. The latter can fill in the backstory but is hardly needed to get the gist of the narrative. I'm able to comfortably do this because there is no ticking clock, even if what Max is doing at any given time suggests there should be, and because enemies come in limited numbers and only in certain areas.
What If?: Gaming's Alternate Realities
1UP explores what might have happened had video game history gone differently.
People love to look back at the past and ask, "What if things had gone differently?" Navel-gazing at history spans cultures and races. Whether it's author Harry Turtledove making a fortune by contemplating how differently the American Civil War would have gone if someone had time-traveled to give the Confederate Army machine guns, or the manga Konpeki No Kantai in which the Japanese navy beats up America in World War II before teaming up to kill Hitler, second-guessing ourselves seems to be human nature.
Maybe it's the competitive nature of the medium, but video gamers seem especially fond of revisiting the past and wondering about alternate outcomes. As the Three Fates in the image above suggest, games have woven a rich and complex tapestry in their mere half-century of existence -- a tapestry whose design and nature could have changed radically had things turned out differently.
What if Video Games Never Came Home?
Cover Story: A chilling glimpse into a world where the arcade still rules supreme.
1
UP's cover story this week revolves around the question, "What if?" In keeping with that theme, we'd like to offer this glimpse into one of many alternate realities of video gaming: A world where video games never came home. A world where the arcade still dominates gaming. How would a site like 1UP be different in such a place? We talk to our mirror universe counterparts about the state of gaming and their thoughts on the medium.
What If Third-Party Development Didn't Exist?
Cover Story: How Activision's 1982 win in court changed the industry.
L
et's be honest, when we think about Activision-Blizzard as a company, at least a few of us get a mental image of a dark overlord with hooked fingers looming over a burning landscape. This image is usually accompanied by a deep-voiced demand for sacrificial virgins. Given Activision-Blizzard's status as The Biggest Thing That Has Ever Existed in Gaming, it's easy to forget that prehistoric Activision fought for the right to develop third-party games on the Atari 2600 -- a battle that it eventually won in court.
Activision's victory essentially made it possible for third-party game designers to ply their trade on home game consoles.
Activision's drive for justice wasn't exclusively about being paid its deserved royalties, either. During the 2600 era, Atari had a nasty habit of not crediting its game developers (or even letting developers bring attention to themselves, which convinced Adventure developer Warren Robinett to bury his name in the game, possibly creating the first digital Easter Egg). When Activision won the right to make its own games for the 2600 in 1982, credit was no longer a problem.
What If Square Never Left Nintendo?
Cover Story: We look at how the RPG powerhouse would've fared without the PlayStation.
F
or RPG fans of the early 1990s, Square practically had their own branch on the Nintendo family tree. This held especially true on the Super NES, where Square came into its own with Final Fantasy IV and VI, Secret of Mana, Chrono Trigger, and wealth of Japan-only releases that loomed just out of reach for Americans. By the end of 1995, the union seemed solid. Nintendo's long-awaited Nintendo 64 system was on its way, and would be home to Square's next Final Fantasy.
There seemed no reason to worry until the spring of 1996, when those same RPG fans opened game magazines and learned that Final Fantasy VII wouldn't release in the form of a Nintendo 64 cartridge. It was now headed for the Sony PlayStation, as with every other game Square planned to make for the latest generation of consoles. By the end of the year, Square sewed up a publishing agreement with Sony, and their first PlayStation release, the fighter Tobal No. 1, sat on store shelves. It came as quite a surprise to players who'd effectively grown up with RPGs on Nintendo systems.
Final Fantasy VII didn't just amount to a critical PlayStation success; it was also instrumental in establishing the Japanese RPG in North America's mainstream game industry.
Knapsacks
Obstructive Sleep Apnea
The following is a discussion of obstructive sleep apnea (OSA); its content is not intended to be a medical primer nor meant to exhaustively cover all of the risks and complications possible with the disorder and its diagnosis, treatment, and non-treatment. The author stresses that this discussion does not substitute for the need to personally discuss all aspects of the health effects, diagnosis, and treatment of sleep apnea with a health care professional and, generally, with an expert in sleep disorders medicine. This review focuses on OSA in adults. Although some aspects of OSA in children are discussed here, the risks and benefits involved in the decision making process for testing for and treating OSA in children are substantially different than those for adults.
Introduction
Obstructive sleep apnea (OSA) is a condition of repetitive collapse of the soft air passage between the mouth and trachea (this passage is often termed the "upper airway") during sleep. "Apnea" means that there is a cessation of the flow of air from the environment to the lungs and from the lungs to the environment for at least 10 seconds. "Obstructive" means that the collapsed upper airway is responsible for the failure to move air in and out of the lungs. A person with OSA typically is seen to cycle between making reduced efforts to breathe as the upper airway begins to collapse, followed by increasingly strong breathing efforts, literally appearing to be choking as the chest and abdomen strain to pull air into the lungs while the soft upper airway airway remains blocked. The amount of oxygen entering the body is immediately diminished, while carbon dioxide is prevented from being exhaled. Finally, after as little as 10 seconds or as much as two consecutive minutes there is a sudden "arousal" of the brain and nervous system, often with an abrupt loud snoring, snorting, or choking sound as the airway reopens, and air again enters the body. Typically, another episode of upper airway blockage occurs immediately after. Sometimes these arousals from sleep are associated with confusion, anxiety or outright panic, and the person may describe awakening with feelings of suffocation or choking. Most of these obstructive episodes are not sensed by the sufferer, however. OSA is diagnosed when the frequency of air passage obstruction reaches five or more episodes per hour of sleep.
While the upper airway obstructions can occur in all "stages" of sleep, they tend to occur most frequently in light non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. REM sleep is also associated with a risk for longer apneas and more severe decreases in blood oxygen levels. Similarly, while OSA most frequently occurs in association with sleeping flat on the back (supine), it also commonly occurs in persons sleeping on their sides and face down (prone).
OSA a serious medical problem
The lack of oxygen and forceful efforts to breathe against the blocked air passage with each obstructive episode are, literally, periods of suffocation; each time this occurs there is slowing and speeding up of the heart rate, and a decrease in the amount of blood exiting from the heart to the body. When the brain abruptly arouses, there is a sudden increase in the blood pressure and heart rate as adrenaline surges, while the exit of blood from the heart continues to decrease. Many individuals have severe OSA, which is generally recognized as more than 30 of these obstructive episodes per hour of sleep, and/or frequent or prolonged blood oxygen saturation decreases to below 90% (normal for a healthy adult is well over 90%). See Figure 1 (right) for an example of repeated obstructive apneas recorded during a sleep study in a patient with severe OSA.
Untreated OSA has been shown to be associated with an increased risk of each of the following:
High blood pressure (hypertension)
Damage to the arteries which carry blood and oxygen to the tissues of the body
Progressive heart enlargement and eventual heart failure
Stroke
Coronary artery disease and heart attack
Heart rhythm disturbances including atrial fibrillation
Pulmonary hypertension
Problems with blood sugar control (including diabetes mellitus)
Problems with appetite control
Untreated OSA has been estimated to cost the United States an excess of several billions of dollars per year to treat the medical complications of the disorder. Persons with OSA are considered to have an increased mortality risk associated with compromise of the cardiovascular (heart and major arteries) and cerebrovascular (major vessels of the brain) systems (9). The risk for suddenly dying of heart problems has been shown to be increased in OSA patients when they sleep (2). Further, the brain arousal which is typical of each obstructive episode causes brief sleep fragmentation which is usually unrecognized by the person suffering, but in fact can lead to a loss of restorative sleep, even though the person is in bed and "sleeping" for many hours. The combination of repeated sleep disruption and decreased oxygen to the brain during sleep likely contributes to the characteristic and sometimes severe daytime sleepiness of OSA. Associated mood changes including feeling depressed, as well as lack of energy, and failure of memory and concentration, all may occur. The poorly controllable sleepiness of untreated OSA is considered to cause the United States thousands of lives annually in motor vehicle accidents (14, 17).
While all of these medical problems are most likely to be found in association with severe OSA, even mild OSA (for example, less than 10 obstructive episodes per hour of sleep) has been associated with an increased risk of having or developing some form of heart disease compared with the risk of persons without OSA (12, 15).
OSA is a common disorder
OSA is one of the most common of chronic medical conditions to affect humans. It has been found in at least 9-26% of middle aged persons unselected for symptoms (18). Persons who are 65 years or older are even more likely to have OSA. OSA is much more common in adult men than women, but post-menopausal women have a high frequency of OSA as well. Persons with a blood relative with diagnosed OSA are almost twice as likely to have OSA compared with persons without relatives with the disorder. OSA appears to be common in children as well. In adults, overweight status (not necessarily obesity), particularly with excess weight and soft tissue around the mid section and neck, is probably the most common condition associated with OSA; in children, enlarged tonsils and/or adenoids is the most frequently associated condition.
Common symptoms and signs of OSA
The most common symptoms (what the patient feels) and signs (what is seen and heard) of OSA are understandable from the discussion above, and are as follows:
Snoring, particularly occurring as interrupted, abrupt snoring, snorting, or choking sounds. The patient with OSA may occasionally be aware of the snoring, although it is more typically the bed partner, housemate, or even neighbor who is most aware of it
Witnessed struggling to breathe alternating with shallow breathing during sleep
Awakening with a choking sensation or feeling that the breathing was blocked
Excessive daytime sleepiness: that is, dozing off, even for a microsecond, unexpectedly and uncontrollably during usual awake time behavior. This typically occurs when the person is sedentary, such as at a meeting, movie, watching TV, or driving. With severe OSA, naps tend not to be refreshing any more than nighttime sleep is.
Restless sleep, often with frequent kicking or jerking of the arms or legs, and/or night sweats
Impaired ability to maintain attention, concentration, and memory
Mood changes including depression
Increased frequency of nighttime need for urination
Insomnia: that is, difficulty falling asleep or staying asleep due to the airway closing when the person tries to sleep. The patient with OSA may be particularly aware of difficulty falling or staying asleep when flat on his/her back (supine)
Sleep walking and sleep talking (each with the OSA sufferer having "aroused" from an obstructive event during sleep in a confused state)
Gastroesophageal refux (GERD)
Awakening with headaches at night or in the morning
Occasional episodes of breathing pauses, snoring, irregular breathing, and awakenings with a snort or choking sensation occur in almost all individuals in sleep; these may even be associated with anxiety or panic as noted above, and are not necessarily dangerous or associated with OSA. Persons with upper respiratory infections or suffering from allergic nasal congestion may have an increased frequency of such events, which may resolve when the congestion clears. Further, not all snoring means that OSA is present; it is abrupt and interrupted loud sounds that are more characteristic of OSA, rather than continuous snoring.
In adults, severe OSA is not difficult to spot: a very common example is an overweight middle aged man with a thick neck and high blood pressure, who bothers anyone near him at night with his repetitive explosive airway sounds and restless sleep, and who is noted to become drowsy or even nod off when the lights go down in a meeting, or behind the wheel of a car. Conversely, the absence of snoring, obvious breathing problems in sleep, and daytime sleepiness makes the presence of OSA unlikely, even in an overweight person. Children with OSA commonly display hyperactivity rather than unexpected sleep episodes.
Other Major Risk Factors for OSA
Adults are also more likely to have OSA if they have one or more of the following medical or anatomic conditions:
High blood pressure, particularly if it has been difficult to control with medications
Heart failure
A history of stroke or "transient ischemic attack" (TIA)
A seizure disorder which has been difficult to control with medication
Chronic headache, particularly awakening at night or in the A.M. with headache
Endocrine disorders such as acromegaly and hypothyroidism, and "metabolic syndrome", the combination of high blood pressure, obesity, and poorly controlled blood sugar
There are numerous anatomic factors which predispose to OSA, and the presence of any of the following in addition to any of the symptoms or signs of OSA noted earlier makes the presence of OSA likely:
Obesity
Thick neck
Chronic nasal congestion (including due to allergies), nasal septal deviation, past nasal fracture
Small and/or backward jaw
Large tongue and/or large soft palate and uvula
In children with OSA, the following are commonly found:
Large tonsils and adenoids
Deformities of the facial bones, jaw, or skull
Past cleft palate surgery
Down syndrome is associated with a high incidence of OSA in children and adults in part due to the characteristic palate and facial structure.
OSA is not simply an "anatomic" problem of airway closure in adults
While one or more of the anatomic factors listed above inevitably play a role in the final result of the airway closing, OSA is actually a very complicated process in which the breathing control mechanisms of the central nervous system themselves are prone to cyclic breathing and obstruction of the upper airway once the brain transitions from being alert and awake to becoming drowsy and then lapsing into sleep. Thus, while nasal decongestants, sleeping out of the supine position, and surgeries to widen the airspace often help, they are not necessarily curative in adults, particularly those who are very overweight or who have severe OSA. In contrast, tonsillectomy and adenoidectomy are very often curative in children with enlarged tonsils and adenoids.
How is OSA diagnosed?
The diagnosis of OSA ideally begins in the home, with the identification of any of the signs and symptoms described above, particularly in association with any of the risk factors as outlined above. Such identification should bring the possibility of OSA to medical attention often through initial consultation with a primary care provider or sleep specialist. It has been shown that for most health care visits health care providers don't ask about OSA and most patients don't tell (13). The next step should be to attempt to make a diagnosis by polysomnography ("PSG") which is, literally, a test of multiple parameters during sleep. This test is usually involves all night monitoring (ideally obtaining 6 to 7 hours of sleep) in a sleep center as an outpatient procedure. If OSA is clearly present during the first few hours of the test, treatment may be tried during the remainder of the test with positive airway pressure (this is referred to as a "split night" study). The test is not dangerous and usually does not involve any "invasive" monitoring such as intravenous lines or blood testing. A typical PSG includes the following:
Electrodes on the scalp and forehead with a special paste, to determine brain wave activity and the stages of sleep
Electrodes with paste on the skin at the side of the eyes to determine eye movements of REM sleep
Electrodes with paste on the skin under the chin to determine muscle activity of breathing and sleep
Soft sensors in front of the nose and mouth to measure the degree of airflow into the body, and carbon dioxide levels in the airway
Soft belts around the rib cage and abdomen to measure breathing efforts
Electrodes with paste on the chest (electrocardiogram) to measure heart rhythm
A soft probe on the finger to monitor continuous oxygen saturation levels
A soft probe on the throat to measure snoring activity
Audiovisual recording with a camera and sound system
Many patients are initially put off by the thought of such testing and probes, and are skeptical that they can sleep in such a setting, or that such sleep would be representative of their sleep at home such that the findings would be legitimate. A sleep expert will in fact be able to accurately determine whether and to what extent OSA is present with such a test in the vast majority of cases, as well as in many cases what treatment is necessary or best. In particular, the amount of positive airway pressure which optimally improves the breathing can be determined on such a test (see below, Treatment of OSA). Through this sophisticated testing set up the sleep expert will in particular determine the following:
The frequency of total obstructions (apnea) and partial obstructions (hypopnea) of the airway per hour of sleep (apnea+hypoppnea index, or "AHI")
The length of these obstructive events
The degree to which the oxygen saturation levels of the blood decrease, including the lowest level and the time the oxygen saturation is below 90%, a usual cut-off for physiologically significant decrease in blood oxygen levels
The degree to which carbon dioxide levels in the body increase
The stages of sleep in which the OSA was improved or worsened
The positions of sleep (supine, prone, side) in which the OSA was improved and worsened
The degree to which sleep, particularly deep sleep, is disrupted by the breathing disorder
OSA is generally considered "mild" when the AHI is less than 15 events per hour and the oxygen saturation does not fall below 89-90%. OSA is considered "severe" when the AHI is at least 30 events per hour and/or oxygen saturation falls to below 89% frequently. Even mild OSA should be treated if the patient is symptomatic.
Testing may be performed at home rather than in a sleep center under certain circumstances, and if advised and planned by an expert in sleep disorders medicine. For example, for those with suspected OSA who have symptoms of falling asleep in dangerous situations such as driving, or those having chest pain, or symptoms of impending stroke, treatment must be obtained urgently, and this may mean bypassing the usual wait for a sleep test in a sleep center. Tests at home which generally do not involve all the electrodes to record sleep as noted above may be used, but such testing has a greater risk than in-laboratory PSG to give inaccurate findings, and generally cannot provide a treatment regimen which the in-laboratory PSG with positive airway pressure "titration" can. In some circumstances the sleep expert can devise a reasonable positive airway pressure level prescription without testing of breathing parameters; this may involve positive pressure machines which can diagnose the amount of pressure needed automatically while the patient sleeps at home, or be devised solely based on the patient's signs and symptoms (10).
Other Sleep Disorders To Be Aware Of
There are many serious disorders of breathing which occur during sleep other than OSA, to which a person may be particularly predisposed due to certain medical conditions, which may mimic the signs and symptoms of OSA, and which may only be correctly diagnosed and treated after proper sleep testing is designed and performed. Such conditions and breathing disorders include the following:
"Central" rather than "obstructive" sleep apnea, in which the breathing decreases, stops, and increases again periodically in sleep without the upper air passage being blocked. This is seen commonly in persons with heart failure and stroke, but is also possible in infants, children, and adults with brainstem disorders.
Oxygen level decreases and carbon dioxide level increases due to:
Chronic obstructive lung disease (COPD)
Restrictive lung disease (such as with patients with pulmonary fibrosis, or sarcoidosis)
Nocturnal asthma
Cystic fibrosis
Neuromuscular disorders such as muscular dystrophy and amyotrophic lateral sclerosis,
Spine and chest wall deformities (for example, kyphoscolioisis)
Obesity without OSA
Often these types and patterns of breathing abnormality overlap with OSA or with each other. Further, OSA is not the only disorder which can cause poor or unrefreshing sleep or daytime sleepiness : for example, insufficient sleep time, narcolepsy (this is an uncommon, specific condition of the central nervous system in which severe sleepiness occurs unrelated to having a breathing disorder), chronic insomnia, shift work, and other "circadian rhythm" disorders. The possible presence of all of these breathing and sleep disorders should be considered when considering the diagnosis of OSA. Therefore, OSA is not necessarily straight-forward to diagnose or treat in many persons, and the testing for OSA is best designed in most cases by a sleep medicine expert who has planned for using the information to prescribe or suggest a treatment fashioned for the particular patient. This is the reason why a consultation with the sleep expert prior to undergoing such testing is recommended.
Treatment of OSA
OSA can be treated safely and effectively in the vast majority of cases, and is done ideally with the direct input of a sleep expert familiar with the particular factors associated with an individual's OSA. OSA is not "cured" in the usual sense of the term in medicine, and once developed in the adult form, it is usually present for life unless major anatomic changes occur such as tonsillectomy/adenoidectomy in children or weight loss in adults. The overweight adult diagnosed with OSA, and in particular the obese patient, should feel empowered that weight loss can significantly decrease the frequency of upper airway obstructions during sleep, as well as decrease the severity of oxygen level decreases associated with the OSA, and may in some cases eliminate the disorder (19). Weight loss has been shown to be effective as a treatment in OSA whether achieved through diet and exercise or weight-reduction ("bariatric") surgery; however, the safety and long term effectiveness of bariatric surgery in OSA has not been established, and such surgery is not recommended as first line therapy for OSA at this time.
All overweight persons diagnosed with OSA should be considered for a weight loss program. Further, sleep positioning out of the flat on the back (supine) position, by elevating the head of the bed, and using body pillows propped behind the patient to prevent rolling over to his/her back, or using a tennis ball sewed into the back of the nightshirt, or an inflated beach ball held in a knapsack around the back, may also greatly decrease the severity of OSA in certain cases, and such positioning should be considered for adult patients diagnosed with OSA.
Positive airway pressure, usually delivered as a continuous pressure at the nose or mouth (thus, Continuous Positive Airway Pressure, or "CPAP") is the recommended treatment for most patients with OSA, particularly patients with severe OSA or who have underlying heart or blood pressure problems (6, 8). CPAP is a safe, direct, and immediately applicable method of allowing the OSA sufferer to resume being able to move air in and out of his/her body during sleep. There are a great deal of convincing data which document the efficacy of this treatment in ameliorating the severe consequences of OSA including the heart and blood vessel problems and the excessive sleepiness, if the patient is willing and able to use it diligently (1, 11, 14 ).
To use CPAP, the person wears a soft headstrap which holds a gel foam or air cushioned soft plastic mask snugly in place around the nose, or in some cases the nose and mouth, while he/she sleeps. There are also "nasal pillows" which are soft tubes which fit into the nostrils and thus avoid pressing onto the skin of the face and bridge of the nose. The mask, or nasal pillows, is attached via plastic tubing to a small machine which is, basically, an airflow generator, and which delivers a level of air pressure to the nose or nose and mouth. Figure 2(ab0ve) is an illustration of a patient wearing such a nasal mask which is attached to a CPAP machine. The sleep expert prescribes the best pressure level usually based on a adjusting, or "titrating" the minimal amount of airway pressure necessary to allow for a consistently unblocked upper air passage and thereby no snoring, no decreases in oxygen levels, no great fluctuations in heart rate and blood pressure, and no episodes of sleep disruption associated with the closure of the airway during a night of sleep. The titration initially occurs either in the sleep center during the same night as the diagnostic study (a "split night" study as noted above) or during a second night in the center; CPAP titration may also be performed with an "autotitrating" machine at home as noted earlier. Most CPAP prescriptions fall in the 6 to 12 cmH20 range, but this varies widely among different patients. The person using the CPAP and the prescribing clinician can then keep track of the amount of time the CPAP is used each night, and how effectively the pressure was delivered during that time, with most CPAP machines. CPAP allows the patient with OSA to breathe more normally and inspire air such that oxygenation of the blood is normal, and therefore no additional source of oxygen is necessary in the majority of cases. Oxygen may be added directly to the CPAP circuit in the infrequent cases when necessary. Oxygen alone is usually not prescribed as treatment for OSA, as it is not usually effective, and can in some cases cause longer apneas.
Most patients note immediate and lasting improvement in their daytime sleepiness and alertness using CPAP; the disappearance of the snoring and struggling to breathe sometimes prompts the bed partner to believe the patient is no longer breathing at all. The CPAP should not make much noise; the noise is a soft sound of air intake with inspiration, and a soft flow of air out of the exhalation opening in the tubing just beneath the mask. Any louder sounds suggest an air leak from the mask or the patient's mouth, each of which should be adjusted through the night. The treatment can be immediately and lastingly effective. The mask and headgear, hoses, and filters need to be changed every 6 months; water in the humidifer needs to be changed daily, and all tubing rinsed out and dried after each use. The machine itself varies in size and weight, but all are now small, lightweight, and suitable for being placed on a nightstand by the bed. There are small and very lightweight machines which can be held easily in the palm of the hand, ideal for traveling. The prescribed pressure settings are generally made by a respiratory technologist who delivers the machine to the home of the patient, and the patient does not need to make adjustments to the machine itself.
While CPAP, with which the patient feels a constant pressure at the airway during inhaling (inspiration) and exhaling (expiration) is the therapy of choice for most patients with OSA using positive pressure, "bilevel pressure" delivers two levels of pressure, whereby the pressure inspired is higher than the pressure when the patient expires.
Bilevel pressure may be prescribed to treat additional breathing disorders seen in the patient during the sleep test, but is generally neither necessary nor effective in the majority of patients with OSA. Patients often initially feel that the expiratory pressure they are breathing against is troublesome, and that they are at risk of suffocating; the patient should understand that this pressure in fact is preventing the airway from collapsing and thus actually preventing sleep-related suffocation; the pressure should be set at the minimum pressure to keep the airway unblocked during the expiration phase of breathing, and therefore in most cases cannot and should not be decreased at that point. However, if the patient feels that it is a problem, the prescribing clinician may want to reassess the prescription with another sleep test in the laboratory, or possibly at home using an auto-adjusting machine. CPAP which allows breath by breath auto-adjustment in the level of pressure based on changes in the patient's tendency to collapse the airway is also available (4); while this may have a great deal of utility in both diagnosing and treating patients out of the sleep center, such a machine has not been shown to have more efficacy than CPAP itself for treating OSA, and is more expensive. Timing of the expiratory pressure such that it decreases earlier than typical is also available in some models of CPAP.
CPAP is usually most effective when delivered via a nasal interface, even when there is considerable nasal congestion. Heated humidification, which comes as an option with most current CPAP machines, which is easily attached in line with the breathing circuit is often very helpful in patients who experience coldness or dryness of the air being delivered to the nose and throat, and also may improve nasal and sinus congestion.
The patient using nasal CPAP must become used to breathing in and out against the pressure at the nose and airway while keeping the mouth as closed as possible; opening the mouth will allow air leak and decrease the effectiveness of the pressure to keep the airway unblocked. A soft chin strap, which reaches across the head and under the jaw, can help to keep the mouth closed if necessary. The patient must try to keep the interface on properly throughout sleep, particularly after changes in position the bed partner can be very helpful in this regard, and in fact may well notice increased sounds suggesting air leak from the mask or mouth, or outright return of snoring.
When nasal positive airway pressure is ineffective due to nasal or sinus congestion, nasal deformities, or inability to keep the mouth effectively closed, a larger mask which surrounds the nose and mouth, thus allowing breathing both through the nose and mouth, can be used. Such a "full face mask" is generally more bulky and uncomfortable, and carries with it the increased tendency to swallow air and thus have gastric bloating.
Problems reported by patients using positive airway pressure include the following, listed in approximate order of how commonly they tend to be reported:
Inability to keep the mask on all night due to air leak, discomfort from the pressure or mask, or removing the mask during the night without being aware of doing so
Too much pressure at the nose or mouth to breathe against (as noted above)
Pain, pressure, and irritation from the mask, including a rash, or sore, which can leave permanent marks, generally on the skin around the nose and at the bridge of the nose
Dry mouth, nose, and throat
Claustrophobia with the mask
Nasal congestion and discharge
Stomach and bowel distention, bloating, and gas
Pain and pressure behind the head or at the side of the head where the headgear rests
Irritation or sores within the nostrils particularly with the nasal pillows form of interface
Headache
Eye irritation from air leak
Ear and sinus infections
Lung infection, thought to be due primarily from not changing the water in the humidifier daily or otherwise poor hygiene with the equipment is occasionally seen with CPAP. Patients occasionally note that they have increased upper respiratory infections with CPAP. Vomiting and aspirating this into the lungs is considered a potential and life threatening adverse effect, particularly when using a tight fitting full face mask.
Most if not all of these problems can be avoided or at least lessened with careful attention to proper selection and fitting of the mask and headgear, use of humidification, education including an acclimatization session to the equipment in the sleep laboratory or at home with the respiratory technologist, and of course careful and expert titration and adjustment of the pressure levels themselves are necessary to allow continued use of the CPAP. If the patient has difficulty adjusting to the level of pressure when trying to fall asleep, a "ramp" function is available which allows the pressure to increase gradually over 10 to 20 minutes until the set pressure is reached. This has the possible adverse effect of leaving the patient with too little pressure for too long, and thus the use of this function should be discussed with the prescribing clinician. Initial follow up within 30 days is important. CPAP prevents the airway from being blocked but does not otherwise greatly change the patient's tendency to have such obstruction when he/she is not wearing the device during sleep; therefore, it must be worn during all sleep episodes, not just for several nights a week, and should not be discontinued without the informed advice of the prescribing clinician (5).
Other treatments for OSA
A mandibular advancement device, which ideally is individually fashioned by a dental expert to be worn in the mouth and push the jaw forward to widen the upper air passage, can be considered for patients who do not have severe OSA, or whose OSA is primarily related to supine sleep (7), or who cannot tolerate CPAP. CPAP is generally more effective than a mandibular advancement device for treatment of OSA (3). Adverse effects include temperomandibular joint pain, gum pain, and malocclusion of the jaw. Patients who receive this treatment should be tested in the sleep center with polysomnography with the device in place to determine its efficacy; this can only occur after the patient has gone to the trouble and expense of getting fitted for the device; some insurers have not agreed to reimburse for this treatment.
Tracheostomy is not performed in most patients with OSA, although this is sometimes considered in patients with very severe OSA who do not have a favorable response to CPAP, or who have another major heart or respiratory disorder. Surgical procedures including surgical removal of the soft tissue at the back of the throat, ("uvulopalatopharyngoplasty") radiofrequency or laser assisted reduction of palate and/or tongue tissue, and tongue advancement have not been shown to have sufficient benefit in patients with OSA to recommend their use as first line treatment for OSA (16), particularly for severe OSA or OSA associated with heart, blood vessel, or cerebrovascular disorders. Further, there are potential serious side effects of surgical procedures for OSA including pain and hemorrhage as well as the risks of anesthesia. Palatal stiffening procedures have not been studied sufficiently to warrant consideration as first line treatment at this time. Simple "snoring" treatments are unlikely to be sufficient to treat underlying OSA unless it is very mild.
While using a heart pacemaker to treat OSA has received considerable attention over the last several years, such therapy has not been shown to be an effective strategy for OSA treatment.
Expert guidance should be the key to choosing treatment which is optimal for a given patient, and in all cases expert follow up consultation is recommended; for example, follow up should begin generally within 30 days of prescribing CPAP and then at 3 to 6 month intervals for the first year of treatment. Ongoing adjustments in any treatment should be made based on response, and particularly in light of weight change. Repeat sleep studies to objectively document efficacy of the treatment chosen should be considered, as deemed necessary, in consultation with the sleep expert. Prior to any testing and treatment procedures, one should check with his/her insurer to see to what extent these costs will be covered. For the signs and symptoms of OSA described above, most insurers reimburse for diagnostic testing, and once the testing establishes the diagnosis of OSA, most insurers reimburse for CPAP.
Medications which may improve OSA
There are no medicines which are curative or exert proven sufficient benefit in treating the breathing disorder of OSA such that they are first line treatment in most cases. However, antidepressant medications are generally regarded safe in patients with OSA, and some of these antidepressant medications, including selective serotonin reuptake inhibitors ("SSRIs") and tricyclic antidepressants, have been shown to be of at least limited benefit in decreasing the severity of OSA in small studies. Women who are post-menopausal may achieve amelioration of their OSA if undergoing hormone replacement therapy. Stimulants may be prescribed if necessary for the OSA patient who has been successfully treated for the breathing disorder of OSA but remains too drowsy to function safely. All such medications should be considered as having potential serious side effects in the populations noted.
Medications which may worsen OSA
Alcohol and benzodiazepines may worsen OSA and should be avoided in the hours prior to sleep in patients not using CPAP or other treatment for the OSA. Although some sleeping aids appear to have little direct effect on breathing and OSA, all sedatives and anti-anxiety agents should be considered as having the potential of worsening the OSA, and their use should be checked with an expert health care provider in this setting.
Other considerations
Persons with OSA or with risk factors for OSA should be considered at increased risk for airway collapse and inability to breathe if undergoing in-patient or out-patient procedures which involve any type of sedation or anesthesia, and should consult with a sleep expert or their primary care physician, as well as the anesthesiologist, and clinician performing the procedure, prior to undergoing such procedure.
It must be emphasized that persons with OSA, particularly severe OSA, should be aware that they are at risk of suffering a sudden episode of "microsleep" when driving, even when they take precautions, which may result in death or injury to themselves or someone else. Legal experts suggest that such an occurrence involves significant risk of legal liability for the person with OSA.
To learn more about OSA
Recommended readings and sources:
A detailed overview of OSA and its treatment with CPAP for clinicians by the current author can be found in: Basner, R.C. Continuous Positive Airway Pressure for Obstructive Sleep Apnea. Clinical Therapeutics. N. Engl. J. Med. 2007;356:1751-1758 (www.nejm.org). This article includes a computer animation of a patient during upper airway obstruction in sleep, and subsequent reopening of his airway with CPAP, as well as a photo of a patient wearing a nasal CPAP mask.
An excellent and comprehensive review of OSA is:
Caples SM, Gami AS, Somers VK. Obstructive sleep apnea. Ann Intern Med 2005;142:187-197.
Other extensive and specific discussions of all aspects of OSA, other sleep-related breathing disorders, other disorders of sleepiness, and a patient information summary of sleep apnea, may be found in the online version of the medical journal UpToDate (www.uptodate.com). Note that access to some of this information requires a subscription to the journal.
The web sites of the following major organizations involved with obstructive sleep apnea are highly recommended:
Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N et al. Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure. Chest 2005;128:624-633.
Gami AS, Howard DE, Olson EJ, Somers VK. Day-night pattern of sudden death in obstructive sleep apnea. N Eng J Med 2005; 352:1206-1214.
Giles TL, Lasserson TJ, Smith BJ, et al. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database of Systematic Reviews 2006; :CD001106.
Hailey D, Jacobs P, Mayers I, et al. The current status of autotitrating continuous positive airway pressure systems in the management of obstructive sleep apnea. Can Respir J 2005;12:271-276.
Kribbs, NB, Pack, AI, Kline, LR, et al. Effects of one night without nasal CPAP treatment on sleep and sleepiness in patients with obstructive sleep apnea. Am Rev Respir Dis 1993; 147: 1162-1168.
Kushida CA, Littner MR, Hirshkowitz M et al. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. Sleep 2006; 29:375-380.
Kushida CA, Morgenthaler TI, Littner MR et al. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances: an update for 2005. Sleep 2006; 29: 240-243.
Loube DI, Gay PC, Strohl KP, Pack AI, White DP, Collop NA. Consensus statement Indications for positive airway pressure treatment of adult obstructive sleep apnea patients. Chest 1999; 115: 863-866,
Marin JM, Carrizo SJ, Vicente E, Agusti AGN. Long-term cardiovascular outcomes in men with obstructive sleep-apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046-1053.
Masa JF, Jimenez A, Duran J et al. Alternative methods of titrating continuous positive airway pressure. A large multicenter study. Am J Respir Crit Care Med 2004;170:1218-1224.
Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med 2003;163:565-571.
Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Eng J Med 2000;342:1378-1384.
Rahaghi, F., and R.C. Basner. Delayed diagnosis of obstructive sleep apnea: Don't ask, don't tell. Sleep and Breathing 3:119-124, 1999.
Sassani A, Findley LJ, Kryger M, Goldlust E, George C, Davidson TM. Reducing motor-vehicle collisions, costs, and fatalities by treating obstructive sleep apnea syndrome. Sleep 2004;27:453-458.
Shahar E, Whitney CW, Redline S et al. Sleep-disordered breathing and cardiovascular disease: cross sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163:19-25.
Sundaram S, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database of Sytematic Reviews 2005, Issue 4. Art No: CD001004.DOI: 10.1002/14651858.CD001004.pub2.
Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. N Engl J Med 1999;340:847-851.
Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-1235.
Young T, Peppard PE, Taheri WS. Excess weight and sleep disordered breathing. J Appl Physiol 2005;99:1592-1599.
Figure Legends:
Figure 1: Displayed is a continuous 2.5 minute segment of non-rapid eye movement (NREM) sleep during a polysomnogram in which the patient suffers repetitive obstructive apneas of greater than 30 seconds each, with severe oxygen desaturation with each event, along with slowing down and speeding up of the heart rate. Each apnea is characteristic obstructive apnea as seen in the flat airflow signal ("nasal press") which signifies absent air flow through the upper air passage, with progressively rapid attempts to move the chest ("Thorax") and abdominal ("Abdomen") muscles against the blocked airway. There is speeding up of the heart rate ("EKG") at "arousal" as airflow resumes for 4 breaths; then another apnea begins. There is a severe decrease in the oxygen saturation in the blood ("SpO2") which decreases to as low as 72%, which means that the ability to deliver oxygenated blood to the major organs of the body, including the heart and brain, is severely compromised at that time.The chin muscles ("chin") abruptly increase their activity at the end of each apnea, signifying an arousal and sleep disruption, although the electroencephalogram is not displayed here.
Figure 2: This is a drawing of a patient wearing a nasal mask and headgear attached to a CPAP machine.
B&A: what kind of reader/writer are you?
I thought, for kicks and because I've got the Wednesday blues, I'd write a little questionnaire for your entertainment. It's a bit lengthy, so answer as many or as few of the questions as you'd like. My own answers are in parentheses.
PART 1: READER
A) What genres are you drawn to? What do you usually read?
("Lit fic"/quasi-pretentious MFA stuff or "classic" literature (particularly drawn to magical realism and modernist novels), some poetry, and occasional fantasy-- but only if it's really exceptional; poorly-done stuff gives me the angry reds.)
B) Your plane crashes in Siberia (because desert islands are so last year). What are the three books in your knapsack?
(The complete works of Shakespeare, Northanger Abbey, and Grimm's Fairy Tales; two for pleasure, one for inspiration.)
C) Are you a "visual" reader? Do you get strong 'pictures' in your head of characters and settings, or is it more nebulous?
(Not visual at ALL, actually. The words in my head represent only the words themselves, as pure concepts, if that makes sense. Probably to do with having a photographic memory.)
D) Favourite author?
(Changes daily; today it's George Saunders.)
5) Favourite poet?
(Either Roethke or Rita Dove)
E) Most-loathed genre? (I loooaaathe most Westerns. Urgh. No THANK you.)
F) Literary pet peeve?
(Uninspired, cryptic waffling that's only PRETENDING to be deep/ obvious award-bait. If you have nothing to say, don't say anything.)
PART TWO: WRITER
A) When did you begin writing?
(I was about three. :S I loved books and stories even then. Apparently I taught myself to read, and then write, out of frustration that my parents wouldn't sit down and read to me whenever I liked. But I didn't start SERIOUSLY thinking about being a 'writer', per se, until I was around nine or ten.)
B) What genre(s) do you write?
(All sorts, although I wouldn't say any of it could be strictly considered 'genre' fiction, anymore. That said, I definitely don't tend to be a realist.)
C) What medium do you write? (Novels, short stories, poetry, etc.)
(Mostly short stories, which I am best at, with aspirations to one day finish a novel, and occasional side excursions into poetry as my college courseload demands.)
D) Describe your style in seven words or less.
(Clawed-apart, f**ked-up fairy tales)
E) Describe your eventual, highest goals as a writer
(I want to be masterful at what I do, not merely competent. My stories are developing in complexity but I still feel that the layering is clumsy, and the characterization is sometimes not to my standards. I think a beautiful short story should be like looking through very thin, black ice into a pond, as the sun is shining down directly overhead-- there is a kind of clarity, but distorted by the layer of ice. You make out shapes and forms which are significant, but unclear. It's an aesthetic that doesn't poke you so hard in the eyes, is what I think I'm trying to say.)
Why loving Christians would create sick torture instruments?
In a recess in the subterranean vault, next to the private hall where the interrogations were conducted, stood a wooden figure, carved by the monks, and representing the Virgin Mary. A gilded halo encompassed her head, and in her right hand she held a banner extolling the glory of her Faith.
It appeared to us at first sight that, despite the silken robe adorning her, she wore some kind of breastplate which, on closer examination, was seen to be stuck full of extremely sharp, narrow knife-blades, the points being directed towards the spectator. The arms and hands were jointed, controlled by machinery concealed behind a curtain.
One of the Inquisition staff was commanded to set it in motion, and when the figure extended its arms, as though to press someone most lovingly to its heart. For the victim the effigy hugged it closer and closer, and when finally it was made to unclasp its arms, the knapsack had been perforated to a depth of two or three inches, and remained hanging on the points of the projecting daggers.
Persons accused of heresy, or of blaspheming God or the Saints, and obstinately refusing to confess their guilt, were conducted into this cellar, at the furthest end of which, numerous lamps placed around a recess, threw a variegated illumination of the gilded halo, and on the figure with a banner in her right hand. At a little altar standing opposite to her, and hung with black, the prisoner received the sacrament, and two ecclesiastics earnestly besought him, in the presence of the Mother of God, to make a confession. "See," they said, "how lovingly the blessed Virgin opens her arms to thee! On her bosom thy hardened heart will be melted; there thou wilt confess."
All at once the figure began to extend its arms; the prisoner was led to her embrace; she drew him nearer and nearer, pressed him almost imperceptibly closer and closer, until the spikes and knives just pierced his chest.
Do Libertarians fantasize about getting Alexander Hamilton off our currency and replacing him with Ron Paul?
Or would they rather abolish the US Dollar currency altogether, and have us carry gold bullion around in knapsacks, because the colonial-era Founding Fathers presumably did so?
