Homeopathy Papers

Causation in Sleep Apnea and its Significance in Homeopathic Case Analysis

sleep apnea awaerness kids

Homeopath Fatima Ho discusses sleep apnea, offers suggestions for repertorizing it and gives keynotes of some often indicated remedies.

 

2017 Independent Research Paper – Canadian College of Homeopathic Medicine

Table of Contents

  1. INTRODUCTION………………………………………………………………………………….2
  2. UNDERSTANDING SLEEP APNEA

CHAPTER 1: UNDERSTANDING SLEEP APNEA

  • Definition & Types……………………………………………………………………….3
  • Incidence & Prevalence…………………………………………………………………6
  • Predisposing Factors…………………..………………………………………………..7
  • Conventional Treatment of OSA and CSA in adults………………………………….9
  • Conventional Treatment of OSA in children…………………………………………….11

CHAPTER 2: CAUSATION or ETIOLOGY IN CSA

  • Freeze Response………………………………………………………………………13
  • Post-Traumatic Stress…………………………………………………………………14
  • The PTSD-Limbic System-Breathing Connection………………………………….15
  • Breathing-Related Trauma……………………………………………………………16
  • Head Trauma…………………………………………………………………………..19
  1. HOMEOPATHIC TREATMENT OF SLEEP APNEA

CHAPTER 3: SIGNS &SYMPTOMS & BEYOND

  • Symptoms of OSA and CSA…………………………………………………….……22
  • Symptoms specific tochildren………………………………………………………..23
  • Beyond signs & symptoms………………………………………..…………………..30
  • Flow-chart………………………………………………………………………………31

CHAPTER 4: RUBRICS & REPERTORIZATION

  • Rubrics for Symptoms…………………………………………………………………33
  • Rubrics and Remedies for Causation……………………………………………….36

CHAPTER 5: REMEDIES & DIFFERENTIAL DIAGNOSIS

  • Remedies……………………………………………………………….………………38
  • Differential diagnosis…………………………………………………………………..53
  1. SURVEY RESULTS……………………………………………………………………………54
  2. ..………………………………………………………………………………..56
  3. REFERENCES………………………………………………………………………………….58
  4. ONLINE RESOURCES………………………………………………………………………..66
  5. APPENDICES…………………………………………………………………………………..67

INTRODUCTION

Understanding the difference between obstructive sleep apnea (OSA) and central nervous system sleep apnea (CSA) can help homeopaths differentiate among the remedies that may be indicated. This is because the two types of sleep apnea are very different in origin. OSA occurs when the airway is narrowed or partially blocked e.g. when tissues at the back of the throat or the posterior soft palate over-relax or collapse during sleep or when enlarged tonsils or adenoids partially block the airway. CSA can occur for various reasons, one of which is related primarily to the breathing centre in the brainstem, and is not well understood by scientists despite considerable research.

Pioneering work by psychologist, Dr Damaris Drewry, has revealed that there is a type of CSA that is much more common than previously thought, and that it is often based on one or more traumatizing events. The effects of the trauma are imprinted in the autonomic nervous system as part of the fight/flight/freeze response and may lie dormant for varying periods of time until triggered by life stresses, resulting in the appearance of sleep apnea symptoms. By addressing these traumatizing events, Dr Drewry has been able to successfully resolve many cases of CSA.

While various techniques are used in homeopathic case analysis (e.g. totality of symptoms, keynotes, essence, organ specificity, or a combination of these), there are instances where causation is the only key that can unlock the puzzle of the case. Knowing the underlying cause of our patients’ symptoms can be invaluable in helping to guide us towards the correct group of remedies, especially when the seemingly well-indicated remedy (based solely on symptoms but not taking causation into consideration) fails to work.

While CPAP machines and intra-oral appliances may work for some patients, these are only symptomatic treatment options that do nothing to address the underlying root causes of the problem. In homeopathic terms, they are merely palliative as opposed to being curative. Knowing the cause of the problem may allow the homeopath to cure the patient who could otherwise be at increased risk of developing serious health complications such as hypertension and consequent cardiovascular morbidity.

As the diagnosis of sleep apnea has become more prevalent in recent years, research into this topic would be of increasing value as more people seek alternative or complementary help in the coming years, especially when Dr Drewry’s work* becomes more widely known and the general public comes to realize that there is the possibility of cure in many cases of trauma-basedCSA.

*Information about Dr Drewry’s work can be found at BeyondTalkTherapy.com and SleepApneaSolution.org.

CHAPTER 1: UNDERSTANDING SLEEP APNEA

Definition of Sleep Apnea

The word “apnea” derives from Greek etymology and means “without breath“. Sleep apnea is the temporary cessation or suspension of breathing that occurs involuntarily and repeatedly during sleep.

Types of Sleep Apnea

There are 4 types of sleep apnea:

  1. obstructive sleep apnea (OSA),
  2. central sleep apnea (CSA),
  3. mixed sleep apnea (patient presenting with symptoms of both OSA and CSA), and
  4. complex sleep apnea (patient ending up with symptoms of both OSA and CSA following treatment)1,2.

Obstructive sleep apnea (OSA)

A disorder, first described in 1965, characterized by recurrent interruptions of breathing during sleep due to temporary obstruction of the airway by lax, excessively bulky, or malformed pharyngeal tissues (soft palate, uvula, and sometimes tonsils), with resultant hypoxemia and chronic lethargy. Sleep in the supine position predisposes apneic episodes.

Stedman’s Medical Dictionary © Wolters Kluwer Health.

OSA always involves blockage of the airway but there is continued respiratory effort3. The blockage is due to soft tissue sat the back of the throat collapsing and closing off the airway intermittently during sleep, or when enlarged tonsils and/or adenoids partially block the airway.The patient snores loudly or there are breathing pauses and, depending on the severity of the condition, either awakens partially or completely with a snort or gasping, smothering or choking.

Central sleep apnea (CSA)

Central sleep apnea (CSA) is characterized by a lack of drive to breathe during sleep, resulting in repetitive periods of insufficient ventilation and compromised gas exchange.4It comprises a heterogeneous group of conditions characterized by repeatedly suspended respiratory effort that is involuntary. In CSA, the problem arises primarily in the respiratory centre in the brainstem that is responsible for normal breathing or secondary to other conditions such as diseases, drugs (esp. chronic opioid use5,6), or high altitude.

The American Academy of Sleep Medicine’s International Classification of Sleep Disorders, 3rd edition (ICSD-3), distinguishes 5 subtypes of central sleep apnea (CSA) syndromes in adults:

  • primary CSA,
  • Cheyne-Stokes breathing-CSA pattern (e.g. patients with heart failure or stroke),
  • CSA due to medical conditions other than Cheyne-Stokes,
  • CSA due to drugs (narcotics/opioids), and
  • high altitude-induced periodic breathing.

Pathophysiology7,8.9

Normal ventilation is regulated to keep  arterial oxygen (PaO2) and carbon dioxide (PaCO2) levels within narrow ranges. This is achieved by feedback loops that involve chemoreceptors, intrapulmonary vagal receptors, respiratory control centers in the brain stem, and respiratory muscles. During wakeful periods, signals from the cerebral cortex influence respiration. This is known as behavioral control and involves nonchemical stimuli such as pulmonary mechanoreceptors. During sleep, behavioral control is lost and chemical control is the major mechanism regulating ventilation, with PaCO2 being the major stimulus. Reduction of PaCO2of just a few mmHg below the apneic threshold can result in apneas.

Two types of pathophysiological phenomena can cause central sleep apnea syndromes:

  1. ventilatory instability (either decreased or increased ventilator drive), or
  2. depression of the brainstem respiratory centers or chemoreceptors.

CSA patients fall into 2 groups based onPaCO2 level and ventilatory drive.

Group 1: presents with hypercapnia (abnormally elevated PaCO2 levels) with decreased ventilatory drive. Known causes include hypothyroidism and central lesions (e.g. brainstem infarctions, encephalitis).

Group 2: presents with eucapnia (a state in which the PaCO2 is optimal) or hypocapnia (less than the normal level of PaCO2) with increased ventilatory drive, but with episodes of apnea, periodic breathing, or both. This may be secondary to an existing medical condition such as stroke or heart failure, or due to the use of opioids, or resulting from a recent ascent to high altitudes.

While unstable ventilatory control during sleep is the hallmark of CSA, the pathophysiology and the prevalence of the various forms of CSA vary greatly.4Recent advances in scientific research have shown that the mechanisms responsible for CSA and OSA overlap, and patients with central apneas often have obstructive events, with the pharynx narrowing considerably during a central apneic event.10,11 The significance of this is that CSA can be mistaken for OSA and, in fact, is often treated as such.

Mixed vs Complex Sleep Apnea     

Central and obstructive sleep apneas can occur together in one patient. When this happens spontaneously, prior to positive airway pressure therapy, it is termed mixed SA. When it happens subsequent to positive airway pressure therapy, it is termed complex SA. In the first instance, the patient presents with symptoms of both types of sleep apnea. In the second, the patient develops CSA or a Cheyne-Stokes breathing pattern while/after being treated for OSA using positive airway pressure therapy. In other words, a worse condition has been induced iatrogenically.

In 2006, Mayo Clinic researchers described a phenomenon12 in which a significant number of patients diagnosed with severe OSA(15 percent of 223 subjects) failed to breathe normally after undergoing positive airway pressure therapy. Instead, their sleep apnea assumed the characteristics of CSA. In other words, the therapy had induced CSA in OSA patients, culminating in iatrogenic complex SA. In homeopathic terms, the clinicians have suppressed their patients’ symptoms, resulting in a worsening of the patients’ condition.

As far back as 1991, researchers had published an article titled Occurrence of breathing disorders during CPAP administration in obstructive sleep apnoea syndrome13 in The European Respiratory Journal, in which they had noted an alarming trend:

We analysed the breathing pattern during sleep in forty patients while CPAP was administered. A regular breathing pattern throughout the sleep study was observed in 15 patients. In the remaining 25 subjects, one or more of the following events was observed: central apnoeas, hypopnoeas, periodic breathing, prolonged oxyhaemoglobin desaturations.

(Marrone et al., 1991)

Despite this and similar research, researchers keep coming up with ever more complicated methods to “treat” iatrogenic complex SA, often advocating the addition of drugs to CPAP use or alternative ventilatory assist modalities14,15. For instance, as recently as 2014, researchers Khan and Franco acknowledge the iatrogenic nature of complex sleep apnea in their article, Complex sleep apnea syndrome16, but then go on to advocate more complex “treatment” possibilities:

Complex sleep apnea syndrome is the diagnostic term for the form of central sleep apnea that persists or develops upon treatment of primarily obstructive sleep apnea with CPAP. The pathogenesis likely is related to a combination of the impact of CPAP therapy on ventilation, disturbed ventilatory control related to sleep and host response, and other medical comorbidities.

For those who are poor candidates for CPAP therapy and those who are CPAP therapy failures, more advanced respiratory assist devices including bilevel PAP-ST or adaptive servoventilation therapy can be effective. Other therapeutic medications such as acetazolamide or theophylline may offer an alternative when positive pressure devices of any type are ineffective or poorly tolerated.

(Khan and Franco, 2014)

In a similar vein, patients with upper airway resistance syndrome17(a condition in which patients snore, wake frequently during the night, and have excessive daytime sleepiness) have no breathing abnormalities that characterize sleep apnea and do not show a reduction in PaO2 levels. However, these patients are treated by conventional medicine as if they had sleep apnea, with CPAP devices. While this could result in “significant improvements in the excessive daytime sleepiness”, this is a typical short-sighted allopathic intervention that can have serious consequences on the patient’s overall health, conceivably giving rise to iatrogenic sleep apnea.

Incidence& Prevalence of OSA

  • OSA affectsabout 4% of menand 2% of women18, with the maximum prevalence in middle-aged men (45 to 64 years of age)19.
  • Sleep-disordered breathing is more severe in postmenopausal than in premenopausal women20.
  • OSA affects approximately 3% of children, with snoring being the most common presenting complaint, adenotonsillar hypertrophy being the most common cause, with obesity, hypotonic neuromuscular diseases, and craniofacial anomalies being other major risk factors21.
  • Obese children are 4-6 times more likely to have OSA, compared with lean subjects.22
  • The concurrent presence of adenotonsillar hypertrophy and obesity appears to facilitate the emergence of OSA in children.23
  • The prevalence of sleep apnea in non-obese and otherwise healthy children younger than 8 years old is estimated as 2-5%. OSA may develop in children of all ages, even in infants. Prematurely born infants are at a higher risk to develop sleep apnea.
  • SDB (sleep-disordered breathing) was 4 to 6 times more likely in black children compared with white children and almost 3 to 5 times more likely in former preterm compared with term children. The estimated population prevalence of SDB was 2.2%.24
  • SDB is a relatively common condition in 8- to 11-year-old children. Potentially vulnerable subgroups, black children, and former preterm infants, are at increased risk.24
  • Children with tonsillar hypertrophy had a 3.7 times higher risk of suffering SDB than those with normal size tonsils after adjustment for age, sex and body fat percentage.25
  • Abnormal craniofacial morphology (cross bite or convex facial profile), but not excess body fat, is associated with an increased risk of having SDB in 6-8-year-old Finnish children.25

Incidence & Prevalence of CSA

CSA is generally considered to be less prevalent in the general population than OSA.26This is because researchers are mainly looking at one particular type of CSA—secondary CSA—found mostly in elderly males27who have certain co-morbid conditions, especially heart failure. In the next chapter, this idea—that CSA is rare and a disease of elderly men with failing hearts—will be refuted when the causation of a common type of CSAis revealed, showing that even young and otherwise healthy men and women can exhibit both signs and symptoms of CSA.

Predisposing/Risk factors

Predisposing factors for sleep apnea include those that contribute directly or indirectly to airway narrowing (e.g. obesity, craniofacial morphology, enlarged tonsils or adenoids), co-morbidities such as neuromuscular diseases, and habits such as smoking, alcohol and drug use.

The strongest risk factor is central obesity, reflected by BMI (body mass index), neck circumference (>17 inches for men, >15 inches for women), and waist-hip ratio. [Obesity contributes directly to upper airway narrowing by increased volume of pharyngeal fat deposits, under the mandible and within the tongue, soft palate, or uvula while excess fat-free muscular tissue increases the size of many upper airway structures, compressing lateral airway walls. Obesity contributes indirectly to upper airway narrowing, esp. during sleep, as lung volumes are markedly reduced by a combination of increased abdominal fat mass and recumbent posture.]

  • Obesity (more significant in adults than in children).
  • Aging (up to age 65).
  • Male gender.
  • Menopause20.
  • (Increased risk in African Americans appears to be independent of the effects of obesity or respiratory problems.28)
  • Abnormal craniofacial morphology (e.g. receding chin or mandible, or narrow or receding maxilla).
  • Large tonsils or adenoids (especially in children).
  • Upper and lower respiratory tract problems in children and adolescents.28
  • Allergies29 in children (Allergy is frequently present in pediatric patients with habitual snoring; presence of allergy is associated with an increased risk of OSA in this population.)
  • Neuromuscular disorders that affect the muscles in the airways.
  • Smoking30 (Cigarette smoking causes increased upper airway inflammation; even exposure to second-hand smoke is associated with habitual snoring).
  • Alcohol use30 (Ingestion of alcohol before sleep has been shown to increase upper airway collapsibility and to precipitate obstructive apneas and hypopneas during sleep.)
  • Drug use, esp. sedatives, sleeping pills, opioids, or heart medications.
  • Heart failure and stroke.
  • Family history of sleep apnea. (Genetic factors associated with craniofacial structure, body fat distribution and neural control of the upper airway muscles interact to produce the OSA phenotype.31)

Significance

People with untreated sleep apnea stop breathing repeatedly during sleep, sometimes hundreds of times during the night and often for a minute or longer each time. In most cases the sleeper is unaware of these breath stoppages because they don’t trigger a full awakening, but with each apnea event, the brain rouses the sleeper, albeit only partially, to signal breathing to resume. As a result, the patient’s sleep is extremely fragmented and of poor quality, never dropping into the deep stage of sleep (stage 4) that is required for detoxification of major organs and healing purposes. Patients with disrupted sleep stay within the shallower stages of sleep, with major repercussions on their physical, mental, and emotional well-being.

Complications

It is believed that many who have OSA do not seek treatment or even diagnostic confirmation of their symptoms. Reasons include lack of insurance, not wishing to increase insurance premiums, not wishing to use an oral appliance or CPAP machine or be told that they need surgery. Left untreated, OSA may predispose to serious health conditions, including hypertension and consequent cardiovascular morbidity32. It may also be associated with insulin resistance33, late-onset epilepsy34, cognitive impairment35 (e.g. difficulty in concentrating, increased forgetfulness, inability to make decisions), and peri-operative complications36. Sleep disorders in general have been associated with motor vehicle accidents36, workplace accidents, impaired cognition (reduced ability or inability to concentrate, think, or remember), mood changes, and decreased quality of life.

Effects in Infants and Children

Consequences of OSA in children include failure to thrive (young children failing to gain weight or grow at a normal rate; parents of infants with significant OSA may report difficulty with feeding37), enuresis, behavioural issues such as attention-deficit disorder and hyperactivity, poor academic performance, and cardiopulmonary disease.38 In fact, children with undiagnosed sleep apnea may be misdiagnosed with attention-deficit and hyperactivity39 disorder (ADHD).

Confounding Factors

While some articles have linked OSA with increased risk of cardiovascular events and of stroke, some researchers, e.g. Hermann and Bassetti40, urge caution and further research due to confounding factors such as hypertension, hyperlipidemia, diabetes mellitus, and smoking:

Despite considerable progress regarding our understanding about the role of SDB in vascular disease, further studies are needed to determine whether cerebrovascular morbidity is related to SDB independent of associated vascular risk factors, whether SDB has indeed a negative impact on stroke progression and whether CPAP treatment ameliorates stroke outcome.

(Hermann and Bassetti, 2003)

Ethical Considerations

While many researchers recommend weight loss as first line treatment of OSA in the obese patient, researchers sponsored by manufacturers of  CPAP machines(e.g. Respironics and Resmed) and those who hold patents for similar equipment are the ones who, perhaps unsurprisingly, come up with rather dire conclusions41 and highly recommend CPAP usage:

Sleep-disordered breathing is associated with all-cause mortality and specifically that due to coronary artery disease, particularly in men aged 40–70 with severe sleep-disordered breathing.

(Punjabi et al., 2003)

Conventional Diagnosis

Diagnosis rests on the basis of history and clinical findings, confirmed by polysomnography, which is completed via overnight observation in a sleep laboratory. Testing may not be done if CSA causes no symptoms or is clearly related to an identifiable disorder (e.g. heart failure, chronic opioid use). To diagnose causes of CSA, brain or brain stem imaging may be indicated.

Conventional Understanding

Conventional medicine considers all types of sleep apnea to be incurable, so treatment is “supportive”.  In homeopathic terms, it is palliative as opposed to being curative. Patients with moderate to severe sleep apnea are often traumatized by the dire prognosis given to them by sleep doctors—that they will “get a stroke in 5 years without a CPAP machine”, and that it is their only option for the rest of their lives.

Conventional Treatment for OSA& CSA in Adults

Conventional treatment in OSA includes non-invasive therapies as well as surgery. Where obesity is an issue, it should be, but often is not, addressed. Cases of mild to moderate OSA are sometimes treated using oral appliances. These arecustom-made by dentists who are trained, often in one short course, in “dental sleep medicine”, and are intended to improve breathing by holding the tongue in place or by forward positioning of the lower jaw using a mandibular advancement device to, theoretically, improve the patency of the upper airway during sleep.

Recent research by Park and colleagues42 (2016) has shown that the mandibular advancement device (MAD) has been successful in the treatment of OSA, but only in a subset of patients:

The OSA patients who had lower body mass index and upper airway narrowing at the level of palate and tongue base showed relatively higher rates of a satisfactory outcome even in cases of moderate or severe OSA. These results suggest that the use of a MAD may be an alternative treatment option in OSA patients with retropalatal and retroglossal area narrowing regardless of disease severity. Additionally, MADs can be recommended as an initial treatment modality, and the effectiveness of MADs in achieving success may not be inferior to CPAP.

(Park et al., 2016)

Patient compliance with oral appliances is not high, as might be expected, and tooth movement such as changes in overbite and overjet, as well as TMJ pain and dysfunction, can result.

Almost all cases of moderate to severe OSA are told that a CPAP (Continuous Positive Air Pressure) machine is their only option for life, despite the fact that both CPAP and BiPAP devices have been shown to cause CSA in OSA patients.43

In secondary CSA, first line of treatment is management of underlying conditions and avoidance of opioids and other sedatives if relevant. Second line of treatment is CPAP or ASV and oxygen or, if none of these work, BiPAP in cases if CHF, or drugs if PAP therapy is not tolerated. Most concerning is the treatment outlined for idiopathic primary CSA: not just PAP therapy but dangerous drugs that have “limited supportive evidence44.

Surgery for adultsshould be considered only as a last resort for patients who cannot tolerate CPAP use, as it is fraught with complications, especially in the case of soft tissue surgery such as uvulopalatopharyngoplasty (UPPP), the most widely performed surgery in adultswith OSA, despite research by Boyd and colleagues who concluded in their article, Comparative Effectiveness of Maxillomandibular Advancement and Uvulopalatopharyngoplasty for the Treatment of Moderate to Severe Obstructive Sleep Apnea45, that:

MMA (maxillomandibular advancement) should be the surgical treatment option of choice for most patients with moderate to severe OSA who are unable to adequately adhere to CPAP.

(Boyd et al., 2013)

The extremely poor prognosis of UPPP is often attributed to the patient gaining weight and “the natural aging of the body and increase in tissue collapsibility46.

Compliance with CPAP devices is poor and other conventional treatment options often ineffective, as pointed out by Dempsey and colleagues in the article Physiology in Medicine: Obstructive sleep apnea pathogenesis and treatment—considerations beyond airway anatomy.47

Given that several non-anatomical determinants of cyclical airway obstruction are prevalent in many patients with OSA, that appropriate CPAP therapy is not acceptable to about one-half of patients diagnosed with OSA, and that oral appliances and surgical therapies are not always effective, alternative therapies or combination of therapies are needed, preferably tailored to specific risk factors of a patient.

(Dempsey et al., 2014)

The American Academy of Sleep Medicine updated their clinical guidelines48 in 2015 with statements that appear excessive, e.g.: “We recommend sleep physicians prescribe oral appliances, rather than no therapy, for adult patients who request treatment of primary snoring (without obstructive sleep apnea)”, especially when we consider that a recent (2015) well-designed Swedish study49 by Marklund and colleagues has concluded that while a custom-made, adjustable oral appliance may reduce OSA and snoring, it does so without any positive effect on daytime sleepiness, headaches, insomnia, or quality of life.

However, while less effective than CPAP, oral appliances are more effective than surgery such as UPPP, as noted by Hoffstein in his 2007 meta-analysis, Review of oral appliances for treatment of sleep-disordered breathing.50

ConventionalTreatment for OSA in Children

In a recent (2016) article, Non-surgical management of obstructive sleep apnoea: a review51, published in the journal Pediatrics and International Child Health, researchers examined recent literature on non-surgical management of paediatric obstructive sleep apnoea (OSA) and concluded that interventions all have their limitations.

In mild cases of OSA, intra-nasal steroids and other anti-inflammatory medications may give relief, but the long-term safety of these treatments has not been established. Weight loss in obese children has been shown to be effective in selected patients but is limited in practice. Non-invasive ventilation may be effective but compliance can be a major obstacle. Oral appliances are effective by stenting the pharyngeal airway, but research in this area is limited.

CONCLUSION:There are number of potential, if not proven, alternative management strategies for children with OSA, which could be considered in the absence of early surgical intervention.

(Whitla and Lennon, 2016)

Children with swollen tonsils and/or adenoids often have these surgically removed as a first line of treatment52 even though this does not work for every child .In their well-researched article, Pediatric Obstructive Sleep Apnea. Complications, Management, and Long-term Outcomes39, Capdevila and fellow researchers note that surgery do not always improve outcome in certain groups of children:

The recommended initial treatment, even in obese children, consists of surgical removal of the adenoids and tonsils. However, not all children who undergo adenotonsillectomy (T&A) for OSA are cured. In a meta-analysis of the published literature, the success rate for T&A in the context of OSA was approximately 85%. This figure may actually be lower, particularly among obese children with OSA, or among children with severe OSA

(Capdevila et al., 2008)

In the article, Risk factors and treatment for obstructive sleep apnea amongst obese children and adults53, researcher Kohler points out that obesity as a predisposing factor of OSA is less significant in children than in adults, and that conventional treatment (including surgical removal of tonsils and adenoids) may not give rise to optimal outcome unless the obesity is addressed.

In view of recent findings, a direct association between body mass and upper airway obstruction should be viewed with caution. Obesity may play a more significant role in the predisposition to OSA amongst particular subgroups of the population, such as adults, and those with particular craniofacial and upper airway morphology…Further, commonly used treatment methods for OSA (such as adenotonsillectomy for children and continuous positive airway pressure for adults) may be less effective for obese individuals. Weight-reduction strategies appear important for an optimal outcome…

(Kohler, 2009)

SUMMARY of Conventional Treatment

NON-INVASIVEINVASIVE/SURGERY
§  Obesity management

§  Oral appliances:

o   in adults, e.g. MAD

o   in children, rapid maxillary expansion (orthodontic procedure to widen palate); functional appliances

§  Drugs/Medications

§  Ventilators (e.g. CPAP, BiPAP, APAP, ASV)

 

§  Adenotonsillectomy in children

§  Orthognathic/craniofacial surgery, e.g. MMA

§  Nasal surgery (e.g. deviated septum, turbinates, sinus disease)

§  Surgery of nasopharynx, e.g. UPPP

§  Tongue surgery

§  Bariatric surgery (weight loss)

§  Tracheostomy (in COPD, CHF)

 

  • APAP: adjustable positive airway pressure
  • ASV: adaptive servo-ventilation
  • BiPAP: bi-level positive airway pressure
  • CHF: congestive heart failure
  • COPD: chronic obstructive pulmonary disease
  • CPAP: continuous positive airway pressure
  • MAD: mandibular advancement device
  • MMA: maxillomandibular advancement
  • UPPP: uvulopalatopharyngoplast

Alternative/Complementary/Preventative Treatment of OSA in Children

While obesity as a risk factor for sleep apnea is one issue that must be addressed, abnormal cranial morphology is an even more significant risk factor that needs to be understood. Narrow maxillae and receding mandibles are not inevitable genetic expressions but are amenable to epigenetic influences. Dr. Weston Price’s pioneering work in the 1930s shows how a poor diet can affect the size and shape of the oral cavity, which not only results in crowded teeth but affects tongue placement that can lead to poor breathing habits such as mouth-breathing as well as dysfunctional swallowing patterns. Poor nutrition and lack of breastfeeding over several generations can lead to sub-optimal orofacial growth, as breastfeeding guides and promotes the development of an infant’s palate, helping create adequate width and patency of the upper airway. Children with a diet high in processed foods simply do not chew enough, and masticatory muscles that pull on muscle attachments become under-utilized, resulting in sub-optimal jaw development.

Also, “tongue-tie” or a short lingual frenulum54 can predispose to abnormal tongue function which in turn can impact orofacial growth that can lead to disordered breathing during sleep. Dentists, pediatricians and otolaryngologists should assess the lingual frenulum in a child with difficulties such as mouth-breathing, snoring, tooth grinding and clenching, speech impediments, and feeding problems. While frenulum removal can help, it may not resolve all abnormal breathing patterns, in which case orofacial myofunctional therapy, both pre- and post-surgery, is recommended to restore normal breathing through the nose. Alternatively, the Buteyko Methodcan help both children and adults learn how to breathe properly through the nose. This method has helped both asthma and sleep apnea patients of all ages.

CHAPTER 2: CAUSATION IN CSA

Freeze Response

Coined by Cannon in the ’20s, the phrase “fight or flight” in the context of human response to perceived threat has been influential in subsequent work on anxiety and anxiety disorders. In their article Exploring Human Freeze Responses to a Threat Stressor55, Schmidt and fellow researchers refer to Barlow’s treatise, Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic,and elaborate on the “freeze response”.

Part of Barlow’s (2002) description of an adaptive alarm model suggests that a freeze response may occur in some threatening situations. Specifically, freezing — or tonic immobility — may overwhelm other competing action tendencies. For example, when fleeing or aggressive responses are likely to be ineffective, a freeze response may take place. Similar to the flight/fight response, a freeze response is believed to have adaptive value. In the context of predatory attack, some animals will freeze or “play dead.” This response, often referred to as tonic immobility (Gallup, 1977), includes motor and vocal inhibition with an abrupt initiation and cessation.

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About the author

Fatima Ho

Fatima Ho

Fatima Ho has a background in dentistry and homeopathy, formal training in hypnosis and emotional health, as well as research into sleep disorders. This has given her a special interest in dental-related issues such as tooth grinding, TMJ dysfunction, and sleep apnea. She also teaches dental health professionals how to integrate homeopathy within their dental practice. Her work with parents and children addresses the underpinnings of emotional health. By learning Emotional Intelligence and stress management techniques, both children and adults acquire life-skills such as resilience, self-mastery and self-confidence that are so crucial to our ability to cope with the stresses of everyday life. By getting to the root causes of health problems, she is able to help her patients improve not just their health but also their relationships and quality of life.

2 Comments

  • I am so glad that I was alerted to this valuable overview of sleep apnea, different types and causations, and differential description of remedies. I was not at all aware of the connection between sleep apnea and trauma, nor did I know how the condition commonly manifests in children. I will refer back to this paper many times in the future when treating children with sleeping and breathing difficulties.

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