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By Jeffrey Burch, Certified Advanced Rolfer™
ABSTRACT The author provides a comprehensive view of sleep-disordered breathing (SDB), both sleep apnea and other syndromes, that may be factors behind our clients’ musculoskeletal issues. He gives specific attention to when a practitioner may suggest that a client should be assessed for SDB.
Introduction
This article will describe the several forms of sleep apnea and related conditions, how awareness of these conditions relates to structural integration (SI) practice, and how to recognize the sometimes-subtle signs that a client may have these conditions. In addition to how and why assessing for sleep-disordered breathing (SDB) is important in SI practice, I will detail:
Seven types of treatment for SDB
Here is why this understanding is important to SI practice. Clients come to us with a range of goals including athletic performance enhancement, recovery from injury or surgery, or personal growth. A very common presenting goal is reduction of chronic pain. When working with a client toward any goal, we like to see progress, and we usually do. We also like to see people continue to move forward toward their goals. If situations of reduced mobility, undesirable alignment, pain, or other problems repeatedly return, we investigate what is leading to the backsliding.
One line of questioning is, “What did I as a practitioner miss?” or, “What did I work on that was a compensation, leaving an underlying situation in place so that the body re-established the compensation?” Another line of questioning is, “What are the stressors in the client’s life that the body continues to respond to in this way?” There are many such possibilities having to do with many physical and emotional facets of life. To name a few:
One important factor is quality of sleep. Everything has a use and maintenance cycle. Printers need new toner cartridges, other parts, and cleaning on a regular basis. Automobiles have regularly scheduled maintenance. The maintenance schedule for humans is intensive. Each day we are on duty for about sixteen hours, followed by eight hours of sleep maintenance every night. One missed night of sleep leaves us feeling pretty bad. A week in a row of poor sleep leaves us physically, mentally, and emotionally ragged. Factors disturbing sleep can be large or small. I routinely work with people on what is called ‘sleep hygiene’ and its supporting factors:
An important factor of sleep is breath at night. There are distinct patterns of not breathing enough at night. The collective term for these conditions is sleep-disordered breathing. An estimated 20% of the general population does not breathe enough at night. The incidence of SDB among people with chronic pain is much higher. With all forms of SDB there are two physiologic problems: (1) not enough oxygen on an intermittent but frequent basis; and (2) frequent partial waking, so sleep is interrupted often, with a particular poverty of the deepest, most restorative sleep.
There are four forms of SDB, all of which I will lay out for you. If a person has SDB, his/her body is being beaten up every night. What should be the maintenance and restoration cycle of sleep literally becomes a damage cycle. This will affect some parts of the body more than others. Some features of this pattern of destruction are common, and some features can be very individual.
The internal organs in general and the brain in particular are quite vulnerable to low oxygen levels. Muscles and ligaments are less quickly damaged by low oxygen levels. When the brainstem registers low oxygen levels, an early response is to constrict arteries to the musculature to conserve the available oxygen for the brain and other organs. This arterial contracture usually starts at the periphery and, as the SDB event continues, progresses toward the core of the body.
The level of oxygen in the blood is measured as a percentage of maximum possible oxygen concentration where 100% is full oxygenation. The blood oxygen level is measurable by looking at the color of the blood: oxygenated blood is red, and as the oxygen level in the blood goes down, the color shifts toward blue. The oxygen concentration in blood is very well inferred by the color of the blood and this color measurement can be done with a simple device clipped on a finger called an oximeter.
Ideal blood oxygen levels are 96%-100%. Levels of 91%-95% are viewed with concern. A level of 90% is considered critically low. In a medical setting, if blood oxygen levels are persistently at 90% or lower, oxygen will be administered. During SDB episodes, levels will descend much lower than this, easily into the 80s in terms of blood oxygen percent, and may go as low as the 60s. The consequence of frequent low oxygen levels for body tissues is serious damage. Some tissues are more quickly damaged by low oxygen levels than others. Muscles and ligaments are more tolerant than some tissues, but prolonged
and/or repeated low oxygen levels still damage them. The nervous systems, both peripheral and central, is most easily damaged, and nervous system damage can be serious and permanent.
At the end of each SDB event the person wakes up, either fully or partially. This is one of the ways that insomnia happens. Often this does not reach a level of memorable consciousness, but it takes people out of deeper sleep up into the lightest levels of sleep, or minimal wakefulness. This severely limits the amount of deep, restorative sleep a person can get. The combination of frequently repeated deoxygenation events and partial waking events is quite destructive.
Twin benefits of screening for SDB conditions and making a referral to sleep clinics for further evaluation are that: (1) we will see a lot less recurrence of the problems we strive to set right in our practices, and
Four Forms of SDB
Below I will discuss four forms of SDB. The first two are forms of sleep apnea. The two additional syndromes are not quite sleep apnea, but share the features of inadequate oxygenation during sleep and frequent waking. It is common for a person to have both types of sleep apnea, as will be discussed. In addition, a person can have any combination of any two, three, or all four of the SDB syndromes.
Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) is the most common kind of SDB. In OSA there is a mechanical closure of the airway in the throat that may last a variable amount of time. The medical criterion is that the throat closure must last at least ten seconds to qualify as an apneic event. This makes sense: holding one’s breath for ten seconds is not usually harmful. The longest recorded OSA event is almost four minutes long. Not breathing for thirty seconds to a few minutes is long enough to drive blood oxygen to
damagingly low levels. Obstructive apneic events may occur several times per hour. Medically, three or more events per hour is considered enough to warrant treatment. Insurance companies will often begin to pay for treatment if there are five or more events per hour. Five events per hour means the person is being de-oxygenated, and then partially woken up an average of once every twelve minutes. Consider how a night of that would feel, or how living with every night so disturbed would feel. Severe apnea is considered to be thirty or more events per hour, in other words every two minutes or less. Severe sleep apnea feels terrible and the damage from it soon leads to other serious health conditions.
There are several variations of how the mechanical closure of the throat can happen. The closure is always in the throat between the beginning of the oropharynx at the back of the mouth and the beginning of the trachea, where the cricoid cartilage marks the division between the trachea and the esophagus. The airway closure of OSA does not involve the nose. Nasal restrictions are important but are not in themselves part of OSA.
Closure can involve:
OSA is best described as a syndrome. Remember the distinction between a syndrome and a condition: in a medical condition there is a single situation with a particular cause (the disease malaria is an example); syndromes are presentations of symptoms that may have any of several different conditions creating the symptom picture (dementia is an example of a syndrome).
While OSA always involves closure of the airway in the throat, stopping breath intermittently during sleep, the exact mechanics of this stoppage are diverse. There is a characteristic breath pattern with OSA: breath stops; then after tens to hundreds of seconds breath restarts with a sharp inhale gasp; breath is then briefly faster than usual. While the sharp inhale gasp is the characteristic sign, sometimes it is subtle or even inaudible.
Central Sleep Apnea
Central sleep apnea (CSA) is the second most common type of sleep apnea. ‘Central’ here refers to the central nervous system. In CSA, the brainstem and pons do not send adequate signals to the person’s respiratory musculature to initiate breath. Central apneic events again can last from ten seconds to minutes and may be repeated several or many times per hour. While CSA does not usually involve closure of the throat, there are two things to know about this:
The breath pattern with CSA is simply stopping for ten or more seconds, then starting again. The sharp inhale on restart,
characteristic of OSA, is not heard. The restart will be softer and may be more gradual.
The brainstem problem can have any of several origins. The single most common source of CSA is central nervous system depressant medication or substances, such as opioids, benzodiazepines (Valium, Xanax, etc.), barbiturates (phenobarbital etc.), and alcohol. Other causes of CSA include stroke, traumatic brain injury, tumor, brain surgery, or history of other kinds of SDB which incrementally damage the brain.
Upper Airway Resistance Syndrome
Upper airway resistance Syndrome (UARS) is a partial closure of the airway similar to OSA, but not a complete closure. The airway in the throat may be closed 80%-90%, so that airflow is severely restricted. The breath sound is frequently raspy. The abrupt restarts of OSA are not heard, although a person may move in and out of having a raspy breath. Blood oxygen level with UARS may not go as low as with OSA or CSA but can remain low for longer periods of time. One minute of oxygen level at 80% is harmful. Ten minutes of 87% oxygenation may do as much damage.
If a person has more than one kind of SDB, these can interact synergistically to create more damage. For example, if a person has both UARS and CSA, many minutes of UARS-induced low oxygen levels may be followed by a CSA episode where the already low oxygen level falls to extremely low levels. Alternatively, a CSA episode with very low oxygen levels may be followed by a UARS episode giving the deoxygenation a long, if lesser, tail.
Obesity Hypoventilation Syndrome
Some, but not all, patterns of obesity can limit breathing at night. Obesity hypoventilation syndrome (OHS) is an insufficiency of breath not a stoppage of
breath. As it is a syndrome, there is more than one picture of this type of reduced breathing. One picture is enough fat inside the abdominal cavity to prevent the descent of the respiratory diaphragm or to at least seriously limit it. It is important to distinguish the anatomical picture of this. Fat on the outside of the abdominal wall does not do this. The picture is of a person with a bulging belly which, when palpated, has not so much fat outside the abdominal wall, but the muscular abdominal wall itself is bulged forward by the great amount of fat inside the abdomen in the greater omentum and in the mesenteries of the intestines. The other fat distribution possibility for OHS is a lot of fat on the chest wall so that the muscular effort required to elevate the ribs is greatly increased.
A person can have one, the other, or both of these obesity pictures. Either way, the person is not able to get a full enough breath. This may reduce oxygenation somewhat while awake, but usually while awake one is able to work through the resistance of the extra fat enough to stay adequately oxygenated. But, during sleep, without that conscious effort, oxygen falls to harmful levels. As with UARS, the blood-oxygen levels during an OHS event may not go as low as they do with OSA or CSA, but may stay low for a longer time, even for the whole night.
It is important to distinguish some things related to OSA. Obesity is correlated with OSA. Remember correlation is not causation. Here are two features of this complex correlation:
Speaking of epidemiologic relationships, it is well known that the incidence of all forms of SDB increases with age. Men are more likely to have SDB than women. However, it is important not to think that only fat old men have SDB. I have found SDB in slender little girls. Some babies are born with OSA, CSA, or UARS. Some babies grow out of these conditions. Others do not.
Potential SDB Signs and Symptoms
There are four kinds of SDB. There is testing, which I will describe, that can determine if a person has SDB or not, and if so which kind(s). Signs and symptoms that a client may report are useful, but very few of them are definitive for these conditions. Each person’s body has unique features. Each person’s awareness is unique. How SDB presents is highly variable. It is essential to look at many factors and to be alert to sometimes subtle signs a client may present. Since the presentation of these syndromes is highly variable, the description of signs and symptoms comes with ‘if’, ‘but’, and ‘maybe’.
Daytime sleepiness: People with all forms of SDB usually wake up slowly in
the morning, feeling groggy. They are likely to feel more focused and lively after being awake for about two hours, but usually feel somewhat sleepy all day. Falling asleep during the day while sitting, reading, watching TV, or even while driving is common. This daytime sleepiness is the single most common sign of SDB, but daytime sleepiness is neither a universal nor a definitive sign. People may be sleepy in the day for other reasons. Sleep may be disturbed by other things such as noise, a baby, or bodily pain. A person may have had the SDB condition for a long time, even his/her whole life, so s/he may not recognize the sleepiness. S/he won’t know what feeling really rested feels like; s/he has never experienced it.
Sudden falling asleep in the daytime can be mistaken for narcolepsy. Narcolepsy is a brain condition different from CSA. In apparent cases of narcolepsy, it is important to rule out SDB as there is some similarity in the presentation of the two conditions. It is also important to realize that a person can have both SDB and narcolepsy.
Three kinds of breath sounds: Next I’ll describe three kinds of breath sounds that may occur during sleep and may indicate SDB. Ask your clients about their awareness of their breath at night, and as they may not be aware, also ask them to ask their bed partners. Moreover, if your client falls asleep on your table, listen. Even falling asleep on your table is an indication of daytime sleepiness.
Snoring: A majority of people with OSA or UARS also snore. On the other hand, a large minority of people who snore also have OSA or UARS. Snoring is a yellow flag for OSA. The correlation between these forms of SDB and snoring is large enough that people who snore should be screened for SDB.
Snort-restart of breath: People with OSA will usually have the characteristic sharp restart of breath. Most of the time this does not wake them up enough for them to remember it. But if the person has heard it in themselves even once . . . as it’s said, where there’s smoke there’s fire. A bed partner is usually more informative than the client. Like other signs, the sharp breath restart may not be present. I know a couple where the woman had insomnia for many years, a pattern where she would sleep about two hours, followed by two hours of wakefulness, repeating this pattern twenty-four hours a day. Many
things were tried to resolve her insomnia with little success. Her husband is a health-care provider very well attuned to SDB. The woman did not snore, and was not obese. One night the husband heard his wife give a very subtle snort-restart of breath. He recommended she be tested for SDB, and the results showed she averaged thirty-five OSA events per hour (severe OSA). What had apparently been happening was she would get two hours of low-quality sleep followed by two hours of adequate oxygen, on a repeated cycle. Anyone who has displayed even one apneic snort restart of breath should be screened for SDB. People will often say, ‘Oh, it just happens once in a while’, but a person with OSA will usually not wake fully enough to hear the snort-restart. If the person hears it occasionally, it is happening frequently and should be evaluated.
Raspy breath: As described above, people with UARS will have intermittently raspy breath during sleep. Usually this will be frequent. The person may or may not be aware of it but their bed partners will. Raspy breath while sleeping is a red flag for UARS. Anyone exhibiting this sign should be screened for SDB.
Undershot jaw: Among the many features of facial structure, there is the prominence of the jaw. There is a big range from protruding ‘lantern’ jaws to receding jaws. Jaws that protrude more forward tend to hold the throat more open; receding jaws tend to let the throat close more, predisposing to OSA and UARS and adding to the possibility of OHS. Lengthening undershot jaws is one of the more successful surgeries for OSA and UARS. Having an undershot jaw adds some weight to the scale toward screening for OHS.
Dental development: There is an interesting economic and cultural correlate. The incidence of OSA and UARS is much lower in developing countries than in the industrial world. If a child frequently eats food that requires more chewing, teeth will end up more splayed out with more space between them. This positioning holds the upper part of the throat more open. Children who grow up eating soft food, requiring little chewing, develop dental occlusal patterns where the teeth are relatively angled in and crowded. This positioning does not hold the throat as open. Another dental issue is that some orthodontic procedures have involved pulling some teeth and then drawing the others in. There is an aesthetic
preference among orthodontists to have little space between teeth. Thus, a history of receiving orthodontia may predispose to OSA or UARS, or both, and even make OHS a little more likely. How crowded versus open the dental line is, or a history of orthodontia, or both, tips the scales towards screening for SDB.
Gastroesophageal reflux disease (GERD) and heartburn: Dysfunction of the gastroesophageal (GE) sphincter is well correlated with OSA and UARS. The interactions between GE sphincter dysfunction and SDB are complex and not fully understood. One feature is that when the GE sphincter spends too much of the time open, hydrochloric acid fumes flow up the esophagus to the throat, pharynx, and mouth. This is known to cause tooth decay and chronic sinus inflammation. The chronic presence of hydrochloric acid fumes will etch the inside of the throat and pharynx, often contributing heavily to OSA and UARS. Both heartburn and GERD are yellow flags for SDB. It is my considered opinion that people with chronic heartburn or GERD should be evaluated for SDB.
Musculoskeletal pain:
Back pain: I mentioned that with all SDB conditions the brainstem will direct arterial contracture to reduce blood flow to the musculoskeletal system, sending the blood instead to the brain and other internal organs. Usually this blood flow reduction starts with the hands and feet and progresses toward the trunk. However, different people’s systems are tuned differently, and there may be other underlying vascular damage or occlusion so that trunk muscles may be affected earlier. This is one cause of back pain.
Waking with stiff, achy hands is a sign of SDB. Again, the sign is common but neither universal nor definitive. The damage to the hands and wrists, including the nerves to them, often leads to carpal tunnel syndrome, de Quervain’s tenosynovitis, or ulnar neuropathy. Of course, repetitive strain is a player in these conditions also. Either repetitive strain or SDB can cause carpal tunnel syndrome. Often there is a synergistic combination of both. It is my considered opinion that all cases of hand neuropathies and tendinopathies should be evaluated for SDB.
Waking with stiff, achy feet is similarly common with SDB, but again neither definitive nor universal. There is a strong correlation between plantar fasciitis and
SDB. If the feet are oxygen deprived every night, the foot tissue is damaged. SDB by itself can cause plantar fasciitis. Foot overuse or misuse patterns or poor shoes can by themselves cause plantar fasciitis. SDB and dysfunctional use patterns are synergistic to cause plantar fasciitis. It is my considered opinion that all cases of plantar fasciitis should be evaluated for SDB.
Chronic pain returning after SI: While musculoskeletal pain is more common in the periphery with SDB, due to the quirks of individual nervous systems and circulatory systems the musculoskeletal pain may be anywhere in the body. Chronic musculoskeletal pain is one of the most common reasons for people to present for SI. Often, we are successful at resolving these complaints. If we see musculoskeletal pain returning after our work, and movement habit sources of this pain are ruled out, then SDB is a likely culprit and should be investigated. Recall that 20% of the population has some form of SDB. The incidence of SDB among people with chronic pain is much higher. Since chronic pain is the most common reason for people to seek SI, it follows that a substantial percentage of our clients have one or more forms of SDB. In my practice it is a rare week in which I don’t ferret out SDB in at least one client.
Chronic fatigue syndrome (CFS): CFS is a syndrome, which is to say it is not a single condition; rather, it is a symptom picture that can be the presenting feature of any of several different conditions. As its name indicates, people with CFS are tired all the time. The single most common disorder presenting as CFS is SDB. Chronic fatigue syndrome is a red flag for SDB. All persons with CFS should be screened for SDB.
Fibromyalgia is a common comorbidity of CFS. Again, this is a syndrome, not a specific condition. The symptom picture is a set of tender points on the body. A lot of different things can create tender points on the body. The single most common disorder presenting as fibromyalgia is SDB. Fibromyalgia is a red flag for SDB. All persons with fibromyalgia should be screened for SDB.
Myofascial pain syndrome (MPS): The presentation of MPS is similar to fibromyalgia, but is more specifically muscularly located. As with fibromyalgia, the correlation of MPS with SDB is substantial. MPS is a red flag for SDB. It is my considered opinion that all persons
with myofascial pain syndrome should be screened for SDB.
Heart rate response to SDB events: If heart rate and breathing are recorded together, the usual pattern in an SDB event is that the breathing stops or is diminished, soon followed by an increase in heart rate up to twice normal. During each SDB event the brainstem measures less oxygen in each unit of blood. An early solution the brainstem tries is to direct the heart to pump more units of blood, and heart rate will commonly double. If the SDB event continues, eventually there is not enough oxygen in the blood to support heart muscle activity and the heart rate may fall to half of normal. Somewhere along this course the person’s system will be alarmed enough that the person will at least partially wake up. If the person wakes earlier in this cycle, they will wake with their heart pounding. They will usually wake with some sense of struggling for breath.
Attention deficit disorder syndrome (ADD): There are many causes of ADD. The single most common driver of ADD is SDB. It is easy to see how, if a person has not had a good night’s sleep in years, or ever, they will have difficulty staying focused. ADD is a red flag for SDB. All persons with ADD should be screened for sleep apnea.
Atrial fibrillation: Atrial fibrillation is strongly correlated with SDB. As mentioned earlier, as the blood oxygen level falls at the beginning of an SDB event, the heart accelerates to about twice its normal rate. Then, as the blood oxygen level falls farther, the heart rate falls to half of normal as the heart muscle is not adequately supported with oxygen. Repeated over time, this deoxygenation can damage heart muscle. As mentioned earlier, the nervous system is particularly vulnerable to low oxygen levels. This includes the sinoatrial node, which is the metronome for the heart. Medically, it is recognized that even if SDB is not the original cause of atrial fibrillation, use of a CPAP machine as supportive therapy is usually beneficial. Atrial fibrillation is a red
flag for SDB. It is my considered opinion that all persons with atrial fibrillation should be screened for sleep apnea.
Heart failure is a description of weakened heart muscle, so that the heart cannot pump out as much blood as arrives at the heart. This condition can range from very mild to fatally severe. Many different things can weaken heart muscle. As mentioned in the discussion of atrial fibrillation, SDB is one of these things. If a person has heart failure, then the weakly- pumped blood arrives late at the blood oxygen sensors in the brainstem. Seeing older blood, the brainstem lacks current information about the blood and will not recognize that the blood oxygen level is a little low; thus, it does not direct the body to breathe. This is a common way for OSA to occur. There is a nasty feedback loop where the low blood volume pumped by the heart misleads the brainstem, so the brainstem fails to request breathing; the resultant low blood oxygen level can further damage heart muscle. Any degree of heart failure is a red flag for SDB. It is my considered opinion that all persons with heart failure should be screened for sleep apnea.
Type II diabetes: There is a strong correlation between SDB and Type II diabetes. It appears that the low blood oxygen levels and sleep deprivation of SDB often trigger Type II diabetes. The mechanism is not well understood, yet the causation is clear. This includes but is not limited to the interaction of obesity, which is known to trigger Type II diabetes. SDB-induced obesity may further cascade into Type II diabetes. There are certainly other causes of Type II diabetes, including genetic propensities and persistent dietary indiscretions. Type II diabetes is a yellow flag for SDB. The correlation is strong enough that people with Type II diabetes should be screened for SDB.
Type I diabetes: While Type II diabetes has long been recognized as having a strong correlation with SDB, more recently Type I diabetes has been found
to have a 30% correlation with SDB. While the mechanisms of this are even less clear than with Type II diabetes, the correlation is strong enough to wave a red flag. Anyone with Type I diabetes should be screened for SDB.
Insomnia is another syndrome and has many causes. With insomnia it may be difficult to fall asleep; or initially falling asleep may be easy, but it is hard to stay asleep. A person can experience both. With SDB a person is partially woken often during the night; this can look like the kind of insomnia where it is difficult to stay asleep. Since sleep is literally dangerous to a person with SDB, a kind of sleep-phobia can set in making it hard to fall asleep. Insomnia is a yellow flag for SDB. Testing for SDB may not be the first line of investigation for a sleep doctor looking at a patient with insomnia, but as other lines of investigation prove fruitless, SDB rises as a possibility. Or, if a person has insomnia and one or more other signs of SDB, then SDB becomes an earlier candidate to investigate.
Adrenal exhaustion syndrome: There are many ways to arrive at adrenal exhaustion. If a person has not had a good nights’ sleep in years, this can easily present as adrenal exhaustion. Adrenal exhaustion is a yellow flag for SDB. The correlation is strong enough that people with adrenal exhaustion should be screened for SDB.
Kidney Disease: We are born with much more kidney function capacity than we need. A measure of kidney function capacity is glomerular filtration rate (GFR), which is measured with a blood test. As we age, our kidney function capacity decreases. At age twenty, we have a GFR of about 140. We only need 70 to function well. On average, our GFR decreases one point per year (10 points per decade). No problem is noted with kidney function until the GFR falls below
GFR is falling early in life, this is a yellow flag for SDB. It is my considered opinion that people with kidney disease should be screened for SDB.
Depression and anxiety are two of the most common psychological syndromes. They are both syndromes, as these psychological pictures can represent many different underlying situations. Not sleeping well for years leaves one depleted. This can fit the diagnostic criteria for depression. If the person still has some fight left in them, SDB may leave the person anxious. Consider how irritable you can feel after missing a night’s sleep. The correlation between both depression and anxiety and SDB is strong enough that it is my considered opinion that people with either of these conditions should be screened for SDB. Many conditions are multi-causal. A person may have emotional history that makes good sense for developing depression or anxiety. That does not rule out the possibility that s/he could also have SDB.
How the Various Forms of SDB Are Diagnosed
In the presentation so far, I have made it clear that while there are many correlates of the four SDB syndromes there are few definitive signs. The snort-restart of breath is definitive for OSA; raspy breathing is strongly suggestive of UARS; and that is about it. Many health and behavioral situations can point to SDB. The demographic correlates of greater age, male gender, and obesity are useful for describing populations, but are not definitive for any individual. As I mentioned earlier, there are skinny young children with raging SDB. There are also fat old men who do not have any form of SDB.
Diagnosis requires testing. There are three levels of testing: (1) The simplest test is two nights of wearing a recording pulse oximeter. This test provides enough information to recognize that a person has some form of SDB and a general idea of how severe it is, but this test alone cannot distinguish between the four forms a person might have. Overnight
oximetry is useful as a screening test. It is easy and cheap. If a person has one or two yellow flags, this simple test may be a good starting place. (2) A home test is often used, in which the person wears a recording pulse oximeter and a band around the chest which monitors breath movement, plus a nasal canula similar to those used to give a person oxygen, but which instead measures the oxygen concentration in the exhaled air. This kind of test usually gives enough information to make a diagnosis of whether or not a person has any form of SDB, if so which kind(s) of SDB the person has, and how severe the condition is. (3) Overnight in a hospital wearing all the gear from #2, an electroencephalogram net on the head, and a night vision camera with technicians monitoring live. Results from this type of testing are highly definitive.
Treatment of SDB
Several approaches to treating the various forms of SDB have been tried with varying success. These are discussed below.
Muscular retraining: Some versions of OSA and UARS have a muscular tone component. Retraining these muscles can reduce the severity of the disorder. Speech therapists are skilled at assessing facial structure and use of muscles associated with speech to design and implement muscle retraining programs. Many studies have been published in the speech therapy literature on corrective exercises for SDB. A meta-analysis of this literature suggests that speech therapy can reduce the number of incidents per hour in OSA by about 30%, and reduce the level of de-oxygenation in events by 2-3 percentage points.
Manual therapy: SI and other forms of manual therapy have been tried for OSA and UARS with little success. There are occasional case reports of success. Since use of manual therapy methods is likely to improve other things including neck range of motion and comfort, it is worth trying. Since the success rate of manual therapy is low, the client should not wait to pursue other methods of treatment. Our principal task is to look for signs and
symptoms from which to make referrals to sleep doctors.
Central nervous system (CNS) medication abatement: Recall that taking CNS depressant medication is the single greatest cause of CSA. It follows that if a person is diagnosed with CSA and is currently taking CNS depressant medication, it is valuable to take a look at the medical condition(s) for which this medication is prescribed and to refer them to a physician to seek other ways of managing those situations without CNS depressant medication.
Weight loss: If a person has one of the patterns of obesity known to create an SDB syndrome, i.e., deep belly fat, chest- wall fat, double chin, or a fat tongue, then weight loss may be useful. Since SDBs also commonly cause weight gain there may be staged treatment where other methods are used for a period of time to mitigate the effects of the SDB so that weight loss becomes possible. Trying to lose weight while suffering from an untreated SDB is like trying to walk up a down escalator.
Positive air pressure devices: These are portable, nightstand supported electromechanical devices that supply air under carefully regulated, modest pressure to the patient’s nose or mouth or both. The air pressure flowing through the throat with each breath reduces the likelihood of the throat closing and can gently blow the throat open if it does close. The original devices blew air at a constant pressure and were known as continuous positive airway pressure (CPAP) devices. Over time, continuous pressure devices evolved into bi-level positive airway pressure (BiPAP) devices, which offered two pressure levels: a higher level of pressure as the person inhaled and a lower level of pressure as they exhaled. The next generation of devices has sensors that can vary the pressure level depending on how a person is breathing. Variable positive airway pressure (VPAP) devices, in addition to lowering pressure on exhale, also notice if a person stops breathing and respond by gradually increasing pressure until the airway is blown open.
Although most PAP devices today are VPAP, they are still commonly referred to as CPAP as this is the commonly known name. VPAP machines are adjustable for the needs of each person. Some now have smart computer chips that adjust the pressure as the person’s condition evolves over the years. In addition to the variable pressure, modern devices also warm and humidify the air. Masks, nose pillows, and headgear have evolved to be lighter weight and more comfortable, considerably improving patient compliance. Many different versions of headgear are available to meet the needs of each person. Sometimes it takes trying several types to find the best individual solution. PAP machines are the most common and highly successful treatment for all forms of SDB.
Oral appliances: Dentists with specialized training will craft carefully constructed bite guards that bring the mandible forward enough to hold the throat open wider, without being so forward as to harm the temporomandibular joints. In milder cases of OSA and UARS, these mandibular repositioning devices provide effective treatment. In more severe cases, these devices alone are not effective. In the worst cases, a patient may both wear an oral appliance and use a VPAP machine. Patient compliance tends to be better with oral appliances than with VPAP machines. In situations where a patient can’t or won’t tolerate a VPAP machine, an appliance may provide at least partial correction, reducing the number and length of apneic events.
Surgery: For OSA and UARS, various surgeries have been tried. The type of surgery used varies with both the particular biomechanics of the condition and the understanding of each surgeon. Success rates with such surgeries are low. One sleep doctor whose presentation I attended described success rates for surgeries for SDB as around 10%.
Relationships of SDB and COVID-19
Clinical monitoring has shown an elevated incidence of OSA among patients with COVID-19. It appears that having OSA is a risk factor for COVID-19. (I am not aware of studies correlating other forms of SDB and COVID-19.) In addition to OSA being a risk factor for getting COVID-19, having any form of SDB would complicate treatment of COVID-19 and could easily
lead to a poorer outcome. The symptoms of COVID-19 vary from person to person but more often than not include difficulty breathing. If the person already has a condition that makes breathing more difficult, such as SDB, emphysema, or obstructive pulmonary disorder, the combined reduction in oxygenation from two or more conditions would easily lead to a poorer outcome.
Some COVID-19 patients need assistance breathing. This may include being put on a respirator. Some hospitals have been overwhelmed with COVID-19 patients, with not enough ventilators available. One solution is to use CPAP machines. CPAP machines provide less robust breathing assistance than a ventilator, but are valuable for some patients, certainly more valuable than no breathing assistance. A problem with use of CPAP machines for COVID-19 patients is air filtration. CPAP machines filter the incoming air so the patient has cleaner air to breath, but do not filter exhaled air. Thus a CPAP machine used by a COVID-19 patient will actively blow virus-laden exhaled air into the room, increasing the risk of infection among attending health-care workers. If a CPAP machine is used for a COVID-19 patient either as a substitute for an unavailable ventilator, or due to the patient having an SDB comorbidity, the CPAP machine must be adapted with additional air filtration for the exhaled air.
Jeffrey Burch received a BA in biology from the University of Oregon in 1975, after which he trained at The Dr. Ida Rolf Institute® in Boulder, Colorado, receiving his Certification as a Rolfer in 1977. He has been in continuous practice since then. Jeffrey received his Rolfing Advanced Certification in 1990, after which he again began studying at the University of Oregon where he received a second BA in psychology in 1993 and a Master of Science in Counseling in 1995. His master’s thesis “Alexithymia and Dissociation” explores topics related to psychosomatic conditions. In 1998, Jeffrey began intensively studying craniosacral therapy through the Upledger Institute, cranial manipulation with French osteopath Alain Gehin, and visceral manipulation with Jean- Pierre Barral and his associates. Jeffrey completed the apprenticeship to teach visceral manipulation. He independently offers specialized courses in visceral manipulation with the permission of Jean- Pierre Barral. He also offers foundational courses in assessment methods and treatment methods. Starting in 2010 he began to develop groundbreaking new methods to assess and release adhesions and contractures in joint capsules, bursas, and tendon sheaths. In 2015 he began to teach these methods to other therapists.
Assessing for Sleep- Disordered Breathing[:]
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