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Question:
If memory serves me correctly, those terms (distance D-F, etc.) refer to the small plastic tool Clete designed for the measurements. The device looks kind of like a small protrator. – Hide quoted text — Show quoted text ->> STANFORD METHOD for predicting OSA >You’re right…it definitely is of interest! Thanks very much for >posting this. >By the way, would you happen to know and be able to describe what the >following mean? >Palatal Height (distance D – F) >Overjet (Angle AC is 20 degrees) >It would help me understand your article better. Thanks again for the >information! >Best Regards, >Tim >Sent via Deja.com http://www.deja.com/ >Share what you know. Learn what you don’t.
Response:
Hi Carolyn! In article <374DC239.10A17…@erols.com>, "Carolyn A. Slye" <cas…@erols.com> wrote: > I don’t remember where I picked up the following but thought it may be of > interest. > Carolyn > STANFORD METHOD for predicting OSA
You’re right…it definitely is of interest! Thanks very much for posting this. By the way, would you happen to know and be able to describe what the following mean? Palatal Height (distance D – F) Overjet (Angle AC is 20 degrees) It would help me understand your article better. Thanks again for the information! Best Regards, Tim Sent via Deja.com http://www.deja.com/ Share what you know. Learn what you don’t.
Response:
While I don’t intend to steal the thunder of your post, Tony, the research on craniofacial anomalies and their contributions to obstructive sleep apnea isn’t new material. About half of the literature you’ll find in the American Journal of Respiratory Critical Care related to OSA deals with some sort of bony or soft tissue structure like the pharynx, mandible, maxilla or nasal spine. (The other half is on the clinical presentation, effects, etc. or OSA.) Sadly, this information is SLOW to disseminate, so you will probably find physicians who still think snoring is a nasal problem, collapse is always behind the tongue and that only obese people get apnea (and that it’s caused by their weight). — ————————————————————– Kevin C Welch MCP-Hahnemann Medicine co/02 Theoretically there exists a perfect possibility of happiness: to believe in the indestructible element in oneself and not to strive after it. -Kafka, 66
Response:
On 28 May 1999 21:09:07 GMT, in alt.support.sleep-disorder kwe…@mail2.sas.upenn.edu (Kevin C Welch) wrote: >While I don’t intend to steal the thunder of your post, Tony, the >research on craniofacial anomalies and their contributions to obstructive >sleep apnea isn’t new material. >About half of the literature you’ll find in the American Journal of >Respiratory Critical Care related to OSA deals with some sort of bony or >soft tissue structure like the pharynx, mandible, maxilla or nasal spine. >(The other half is on the clinical presentation, effects, etc. or OSA.) >Sadly, this information is SLOW to disseminate, so you will probably find >physicians who still think snoring is a nasal problem, collapse is always >behind the tongue and that only obese people get apnea (and that it’s >caused by their weight).
Kevin, The previous research I have seen may only be a small sample, after all I am not medically qualified and have access only via Medline and N.A.P.S.. However what struck me about this Japanese research was not that it researched new parameters, but that it researched a highly comprehensive range of physiological parameters *at the same time*. The most innovative aspect of the research was actually the breadth of parameters studied together. If I may make a sweeping generalisation, it seems that previous (mainly Western) research has concentrated on finding simplistic indicators of what is an exceedingly complex problem. These indicators are sufficient to help a sleep doctor tell you why you have obstructive sleep apnea (and blame you, the patient, for your weight gain) but they are insufficient for any predictive technique that can contribute to preventative medicine. Imagine the day when physicians will be able accurately to predict who will, who may and who won’t suffer from obstructive sleep apnea, years before it would happen. Those who are certain to suffer from OSA in future years could have corrective surgery before apnea becomes a problem. Those who are at risk could enter a strict weight control program. These early interventions are what physicians must desire, rather than bolting a CPAP onto an already sick person or carrying out surgery whose crudeness is exceeded only by its low success rate. Trying to oversimplify a very complex morphological and structural problem into a simplistic scenario of "you’re fat and you have a receding jaw, so you’ve got OSA" is just an excuse to blame the patient for a problem that is (IMHO) extremely rarely of his/her making. The signal error that many physicians make is to conclude that a clear *statistical* link between obesity and OSA means that obesity *causes* OSA. This is a common error in drawing conclusions from research of all kinds (*statistical* links are frequently – and incorrectly – interpreted as *causal* links through the whole spectrum of scientific research) and provides a neat get-out for the physician. In fact there is considerable evidence that OSA causes obesity, not the other way around. But this evidence is largely ignored because it points up the failure of preventative medicine to identify high risk groups and intervene well before the syndrome takes hold. Blaming patients for the very obesity that has likely been *caused* by underlying OSA is, in my opinion, one of the greatest lies ever perpetrated by the medical profession. It is also one of the greatest obstacles to prevention or early diagnosis of this devastating disorder. *************** A personal note *************** For what its worth, I will admit that my view of OSA prediction, diagnosis and treatment is heavily coloured by my own personal experience. However, as an experienced research professional (my job before I was retired by my employer on health grounds involved the creation and management of a $5 million per annum government research programme) I believe I am well qualified and able to identify the many fundamental and significant flaws in OSA research. When successive specialists (1 ENT and two pulmonary) were unable to understand why CPAP and, later, BiPAP treatment did not work for me, they merely *blamed* me for poor sleep hygiene and the consumption of caffeine. As it happened, my sleep hygiene was excellent and my caffeine consumption had dropped to zero to no avail. The pulmonary specialists also blamed an operation I had had at age 21 to correct an over-long lower jaw; this was a neat get-out as the reverse of this operation is sometimes used to treat OSA. When, following the end of my career, I moved to a different part of the UK, a new sleep specialist took a completely different approach. He instigated an investigation into the *root cause* of my sleep apnea, using detailed examination of my airway and its shape and form (morphology) and structure. This involved a maxillofacial specialist (using endoscopy and cephalometric X-ray) plus an ENT specialist. Jointly, working as a close knit team, these three specialists and their staff conducted a detailed survey and concluded that: My operation at age 21 was irrelevant as the airway behind the base of my tongue remained much larger than average; my site of obstruction was my soft palate, which on exhaling formed a seal which became ever firmer the more I tried to exhale; CPAP (at any pressure) was unable to maintain an airway under these conditions; Bi-level PAP was completely inappropriate as I needed my airway splinted on *exhalation* so the lower exhalation pressure of Bi-level PAP served only to make things worse. They also concluded (working together with absolutely no sign of wishing to compete for who got to treat the patient) that surgery was the only realistic option. As a result I had a tracheostomy three weeks ago. Here was an object lesson in how doctors could work together without a sign of professional jealousy to identify the problem. At no stage did anyone attempt to blame me for my weight or anything else. And the chosen treatment appears, at this very early stage, to have been the most appropriate so far. End of personal note *********************** Imagine how this sort of approach could be used to *screen* people (even at a relatively early age) for one of the many forms of predisposition to OSA. Whether through lack of airway structure or an ‘abnormal’ shape and form, early intervention in medium and high risk cases could decimate the number of people who suffer from this potentially devastating syndrome. I should include partners, offspring, friends, employers and work colleagues amongst those who suffer. I suppose progress towards this will be determined by who can make the most money out of a screening program, or whether it is more profitable to wait for the condition to develop to the point where it ruins people’s lives before intervening. — Tony Polson, North Yorkshire, UK
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Perhaps I’m biased, but not without merrit….I am being treated by Stanford, and they have been the breath of fresh air I’ve needed. They are also working with my 4 1/2 year old son, who unfortunatly also has OSA (small jaw alert). And check this out..my son had tagged along to my appt. to see Dr Guilleminault. I already knew my son had sleep apnea because I could hear it at night. I figured I’d have to go thru his pediatrician. Dr Guilleminault took one look at him, ONE and looked at me and said, "He has sleep apnea too…look at his chin…see it’s very small like yours…" Astounded I said, "As a matter of fact, he does…" The Dr. gave my son an examination right there, free of charge, and got his sleep study set up. Of course the study clearly showed apnea, and we go back in the end of June to discuss the results. Stanford also did all this without scarring the hell out of my child, which earns them the number one spot in my book right there. I only have medicare and state medicaid (from disability from osa)…they aren’t making diddley off me, and they are changing the lives of this family by treating my children and myself. Hopefully the baby won’t have it too, but he’s got a good chance. And of course I didn’t know I would pass it on. But I suppose there are worse things to pass on genetically, so *shrugs*. I trust Stanford. -sheila Carolyn A. Slye <cas…@erols.com> wrote in message news:374DC239.10A17C7D@erols.com… – Hide quoted text — Show quoted text -> Tony, > I don’t remember where I picked up the following but thought it may be of > interest. > Carolyn > STANFORD METHOD for predicting OSA > The Stanford Method predicts which patients will have Obstructive Sleep > Apnea. > BMI = Body Mass Index = (Weight in Kilograms) / (Height in meters)2 > NC = Neck circumference measured at a point 2 cm below the Adam’s apple > Craniofacial > Measurements > Palatal Height (distance D – F): > mm = P > Maxillary Intermolar Distance: > mm = Mx > Mandibular Intermolar Distance: > mm = Mn > Overjet: mm = OJ > (Angle AC is 20 degrees) > 1.Kushida CA, Efron B, Guilleminault C. A Predictive Morphometric Model > for the Obstructive Sleep Apnea Syndrome Ann Intern Med 1997; 127:581 – > 587. > The Stanford Score = {P + (Mx – Mn) + 3 x OJ} + {[Max(BMI - 25, 0)] x > (NC/BMI)} > = {Craniofacial Score} + {Obesity Score} > If > 70 patient has OSA; and if < 70, there is a 10% > chance of OSA > What this equation says is the following: > 1.If the jaw is too small, there will not be enough room for the tongue. > This is reflected in the Craniofacial Score. > 2.If the person is obese and/or has a very thick neck (such as a > weightlifter or bodybuilder), thickening of the muscles around the spine and > the weight of the jaw on the throat can lead to collapse of the throat > during sleep. This is reflected in the Obesity Score. > This equation does not fully account for individuals who have a large and > heavy lower jaw who are also at increased risk for breathing problems during > asleep. This may explain the 10 % chance of having OSA when the score is > less than 70. > These measurements are very simple to make using calipers and a tape > measure. This can be done by a family doctor or by a dentist. In a full – > grown individual, the mouth measurements only need to be made every 5 – 10 > years. When the score is less than 70, tracking the BMI and NC on an annual > basis will allow for the early detection and treatment of OSA before it can > lead to serious health problems. > Tony Polson wrote: > > A group of researchers in Japan have investigated the relationship > > between (A) the shape and structure of the face and skull and > > (B) the presence (and severity) of obstructive sleep apnea syndrome > > (OSAS).
Response:
Tony, I don’t remember where I picked up the following but thought it may be of interest. Carolyn STANFORD METHOD for predicting OSA The Stanford Method predicts which patients will have Obstructive Sleep Apnea. BMI = Body Mass Index = (Weight in Kilograms) / (Height in meters)2 NC = Neck circumference measured at a point 2 cm below the Adam’s apple Craniofacial Measurements Palatal Height (distance D – F): mm = P Maxillary Intermolar Distance: mm = Mx Mandibular Intermolar Distance: mm = Mn Overjet: mm = OJ (Angle AC is 20 degrees) 1.Kushida CA, Efron B, Guilleminault C. A Predictive Morphometric Model for the Obstructive Sleep Apnea Syndrome Ann Intern Med 1997; 127:581 – 587. The Stanford Score = {P + (Mx – Mn) + 3 x OJ} + {[Max(BMI - 25, 0)] x (NC/BMI)} = {Craniofacial Score} + {Obesity Score} If > 70 patient has OSA; and if < 70, there is a 10% chance of OSA What this equation says is the following: 1.If the jaw is too small, there will not be enough room for the tongue. This is reflected in the Craniofacial Score. 2.If the person is obese and/or has a very thick neck (such as a weightlifter or bodybuilder), thickening of the muscles around the spine and the weight of the jaw on the throat can lead to collapse of the throat during sleep. This is reflected in the Obesity Score. This equation does not fully account for individuals who have a large and heavy lower jaw who are also at increased risk for breathing problems during asleep. This may explain the 10 % chance of having OSA when the score is less than 70. These measurements are very simple to make using calipers and a tape measure. This can be done by a family doctor or by a dentist. In a full – grown individual, the mouth measurements only need to be made every 5 – 10 years. When the score is less than 70, tracking the BMI and NC on an annual basis will allow for the early detection and treatment of OSA before it can lead to serious health problems. – Hide quoted text — Show quoted text -Tony Polson wrote: > A group of researchers in Japan have investigated the relationship > between (A) the shape and structure of the face and skull and > (B) the presence (and severity) of obstructive sleep apnea syndrome > (OSAS).
Response:
A group of researchers in Japan have investigated the relationship between (A) the shape and structure of the face and skull and (B) the presence (and severity) of obstructive sleep apnea syndrome (OSAS). This is important research because, generally speaking, sleep apnea is treated only after it occurs. Little or no effort appears to have been made towards the development of predictive methods and preventative techniques. This is particularly strange, given the high incidence of OSAS and its well documented effects on highway accident rates, poor performance at work and thus significantly lowered GDP. Physicians make gross assumptions about the reasons for OSAS being present in individual patients. Personally I have been variously accused by two sleep specialists of *causing* my own OSAS through weight gain, poor sleep hygiene, and/or caffeine consumption. I have asked both specialists how they expected me to cope with severe and increasing daytime sleepiness as caffeine and raised levels of blood sugar both enabled me to continue my work in the absence of any significant help from my CPAP machine. Sleep specialists, as well as doctors in General Practice, need to be educated not only in the outward signs of OSAS but also in the underlying causes. One reason they are not better informed about the underlying causes is the paucity of research in this field. Yet many sleep specialists are prepared to categorise us by appearance; excess body weight and receding lower jaw being the usual simplistic data on which major decisions are made about treatment. The Japanese research should contribute to the fundamental knowledge needed to help medics identify those with a physical predisposition toward OSAS long before OSAS actually occurs. Knowledge of a higher than normal risk of developing OSAS and the consequences of taking no action will help those who can prevent OSAS merely by avoiding weight gain. Future severe cases may be able to contemplate interventions that will prevent, or at least ameliorate the consequences of, the onset of this potentially devastating syndrome. Note that the research is reported to show agreement with similar measurements taken of Caucasians. As usual, the medical abstract below comes from the excellent N.A.P.S. service which I strongly recommend to all who subscribe to this newsgroup. **************************** Eur Respir J 1999;13(2):403-10. Cephalometric abnormalities in non-obese and obese patients with obstructive sleep apnoea. SAKAKIBARA H, TONG M, MATSUSHITA K, HIRATA M, KONISHI Y, SUETSUGU S. Dept of Internal Medicine, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan The aim of this work was to comprehensively evaluate the cephalometric features in Japanese patients with obstructive sleep apnoea (OSA) and to elucidate the relationship between cephalometric variables and severity of apnoea. Forty-eight cephalometric variables were measured in 37 healthy males and 114 male OSA patients, who were classed into 54 non-obese (body mass index (BMI) <27 kg x m(-2), apnoea-hypopnoea index (AHI)=25.3+/-16.1 events x h(-1)) and 60 obese (BMI > or = 27 kg x m(- 2), AHI=45.6+/-28.0 events h(-1)) groups. Diagnostic polysomnography was carried out in all of the OSA patients and in 19 of the normal controls. The non-obese OSA patients showed several cephalometric defects compared with their BMI-matched normal controls: 1) decreased facial A-P distance at cranial base, maxilla and mandible levels and decreased bony pharynx width; 2) enlarged tongue and inferior shift of the tongue volume; 3) enlarged soft palate; 4) inferiorly positioned hyoid bone; and 5) decreased upper airway width at four different levels. More extensive and severe soft tissue abnormalities with a few defects in craniofacial bony structures were found in the obese OSA group. For the non-obese OSA group, the stepwise regression model on AHI was significant with two bony structure variables as determinants: anterior cranial base length (S-N) and mandibular length (Me-Go). Although the regression model retained only linear distance between anterior vertebra and hyoid bone (H-VL) as an explainable determinant for AHI in the obese OSA group, H-VL was significantly correlated with soft tissue measurements such as overall tongue area (Ton), inferior tongue area (Ton2) and pharyngeal airway length (PNS-V). In conclusion, Japanese obstructive sleep apnoea patients have a series of cephalometric abnormalities similar to those described in Caucasian patients, and that the aetiology of obstructive sleep apnoea in obese patients may be different from that in non-obese patients. In obese patients, upper airway soft tissue enlargement may play a more important role in the development of obstructive sleep apnoea, whereas in non-obese patients, bony structure discrepancies may be the dominant contributing factors for obstructive sleep apnoea. ******************** — Tony Polson, North Yorkshire, UK
