Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Didgeridoo: Interesting but unconvincing
- hangwi tang (5 January 2006)
-
Low Energy Emission Therapy
- Edward J O'Hagan, N/A (5 February 2006)
-
Tubaplayer with Apnoea
- Patrick J. Votrian (5 March 2006)
-
The didgeridoo (and the clarinet ?) as neuropsychiatric treatment?
- Maurice Preter MD (12 March 2006)
-
Didgeridoo and vagal stimulation.
- Edward J. O'Hagan, n/a (16 March 2006)
|
|
|||
|
hangwi tang, sleep fellow Princess Alexandra Hosptial, Ipswich Rd, Woolloongabba, Q4102, Australia
Send response to journal:
|
I congratulate Puhan and colleagues for their interesting study on a novel treatment for obstructive sleep apnoea (OSA)1. At first glance, the study appears to have good internal validity and is persuasive. However, closer inspection reveals that the evidence is weak for the following reasons. Puhan selected non-obese participants (average BMI 25.8) with moderate OSA. The outcomes can be divided into subjective and objective measures. The Epworth sleepiness score is a subjective measure and showed the strongest positive effect in the trial. Those who use the Epworth regularly recognise that the score is dependent on many factors. Despite the title “randomised controlled trial”, this is not a “placebo controlled” trial. As acknowledged by the authors, the participants in the Didgeridoo arm were highly motivated and it would be surprising indeed if the Epworth did not show a strong placebo effect. The Apnoea Hypopnea Index (AHI) is an ‘objective’ outcome measure. However the AHI is an imperfect measure of OSA severity. The halving of AHI from 22.3 to 11.6 at 4 months may seem impressive. However Puhan’s paper doesn’t give enough details on whether this change is due to change in weight or night to night variability caused by differences in sleep stages, amount of supine versus non-supine sleep, prior sleep deprivation, degree of nasal congestion, prior alcohol use, biological variability and inter/ intra-scorer variability in marking apnoeas and hypopnoeas2. The study is very small size and some readers may misinterpret the p value of 0.05 for change in AHI as indicating that there is only 5% probability of the observed results being a chance finding. This is not so. The p value gives a falsely exaggerated impression that the ‘data speaks for itself’3. Using a Bayesian approach4: As there are no previous studies showing that upper airway muscle training would improve OSA, it is reasonable to assume a 90% pre-trial probability that the null hypothesis is correct (i.e. that Didgeridoo playing is no better than placebo). A p value of 0.05 approximates a Bayes Factor of 0.15. This gives a post-trial probability that the null hypothesis being correct as 57.4%. i.e. it is still more likely that the null hypothesis is correct. This highlights the importance of using the totality of evidence from other trials when interpreting p values in single trials5. The burden of OSA in the community is large and many patients tolerate continuous positive airway pressure poorly. New approaches to treatment are necessary. However, the data in this trial is unconvincing that the Didgeridoo will emerge as a useful therapy, especially in those with obesity and more severe disease. REF: 1. Puhan MA, Suarez A, Cascio CL, Zahn A, Heitz M, Braendli O. Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial. BMJ, doi:10.1136/bmj.38705.470590.55 (published 23 December 2005) 2. Le Bon O, Hoffmann G, Tecco J, Staner L, Noseda A, Pelc I, Linkowski P. Mild to moderate sleep respiratory events: one negative night may not be enough. CHEST 2000; 118: 353–359. 3. Goodman SN. Toward evidence-based medical statistics. 1: The p value fallacy. Ann Intern Med. 1999;130:995-1004. 4. Goodman SN. Toward evidence-based medical statistics. 2: The Bayes Factor. Ann Intern Med. 1999;130:1005-1013. 5. Lilford RJ, Braunholtz D. The statistical basis of public policy: a paradigm shift is overdue. BMJ 1996;313:603-607 Competing interests: None declared |
|||
|
|
|||
|
Edward J O'Hagan, Retired N/A, N/A
Send response to journal:
|
Low Energy Emission Therapy (LEET) was a term employed by Dr. Boris Pasche in describing his invention of a spoon-like radio-wave transmitter, which he designed to treat insomnia.(Interested readers should visit http://www.personalmd.com/news/a1997043004.shtml for further information.) In anticipation of sleep, the spoon is hooked up to a small bedside transmitter, and is understood to be emitting low -level radio frequencies into the brain via the roof of the mouth . Tests conducted at both the Scripps Institute in California, and at Denver's University of Colorado Health Sciences Center, concluded that troubled sleepers who were using the LEET device, fell asleep 18 minutes earlier than those using a 'sham' device. While the device was deemed effective in treating insomnia in some circumstances, the big mystery remained as to how low-leve(Hz) frequencies could possibly help in inducing sleep. Based on a theoretical model of sleep and arousal which I have constructed I would propose that the assumption that LEET activity is signalled DIRECTLY into the brain, is incorrect. Instead, application of the model would imply that the LEET stimulates the downward efferent pathway of the pharyngeal vagus; and in a manner comparable to the low Hz. intonations of Bhuddist monks when they employ their deep sounding OMMMMM utterances during mediation... and beyond that to even lower Hz. vibratory accomplishments via attaining the ability to perform what is described as 'Tibetan stomach-singing'. Likewise, I submit,the low Hz. vibrations of the diggeridoo are conducted downward along the efferent vagal pathway, and in common with the Pasche spoon, the OMMMM utterances and the 'Tibetan stomach singing', they result in reduction of abdominal afferential vagal signalling back to the nucleus tractus solitarius (NTS) in the brainstem.The overall result is that SNS input is decreased, and in the case of insomnia this facilitates sleep onset. The model supports the conclusions of the authors, but inasmuch as the foregoing may be relevant, it is suggested that it may merit consideration. Edward J.O'Hagan, Niagara Falls, Canada Competing interests: None declared |
|||
|
|
|||
|
Patrick J. Votrian, tubaplayer The Netherlands
Send response to journal:
|
and now for a word from the battle front... I am a professional tuba player of 43yrs and have played the tuba since the age of 12 (also known as bass tuba or contrabass tuba). I have a light form of Apnoea and have been under observation/treatment since 2002 via the Sloterdijk Hospital (Ziekenhuis) in Amsterdam, the Netherlands. My response is more of 2 questions. 1.If the pure low vibrations of didgeridoo playing are assisting in the reduction of Apnoea symptoms, than why isn't the same affect achieved by playing the tuba? 2.If the pure physical playing of a didgeridoo reduces Apnoea symptoms, than how does it differ from that of playing the tuba? The usage of the circular breathing technique on the didgeridoo is the only difference between the two playing techniques that I am aware of. (circular breathing involves filling the cheeks with air from the lungs, then expelling this air by contracting the cheeks. At the precise moment of check contraction a second action is performed of filling the lungs with air through the nose. In this way, a continuous stream of air is pressed through the lips, allowing them to continually vibrate thus producing a continuous sound. Generally speaking, a tuba is mostly played by simply filling the lungs with air, expelling that air directly, and stopping the sound production to fill the lungs once again with air.) Competing interests: None declared |
|||
|
|
|||
|
Maurice Preter MD, Neurologist and psychiatrist; Assistant Professor of Clinical Psychiatry, Columbia University New York, NY 10028
Send response to journal:
|
This study is of great interest, especially given the lack of alternatives to CPAP. As correctly pointed out by the authors, given CPAP's lack of appeal, "[o]ne of the challenges in the treatment of sleep disorders is poor compliance". In neuropsychiatry, the human cost of disrupted sleep in terms of potentially reversible cognitive deficits and disordered mood (primarily depression, but also elevation) is staggering. Epileptic patients with OSA may become intractable just because of disrupted sleep.
All caveats to this innovative approach mentioned in prior comments certainly apply: Need for replication, sample bias etc. Also, waitlisting is problematic as a control [corrected from "not a bad control" on 14 March] in a syndrome that fluctuates over time, such as mild-moderate sleep apnea. Given the realities of medicine at least in the U.S., well-designed large scale studies are unlikely to surface as there is no monetary incentive. The last comment from Patrick J. Votrian, the Dutch tuba player is interesting in that it seems to stress the central role of circular breathing in upper airway retraining. This should not be too difficult to test in an experimental model. Also, unlike tuba players, clarinetists use circular breathing (a technique that takes many months to master). What is the prevalence of UERS/OSA in clarinet players? Maurice Preter, M.D.
Competing interests: None declared |
|||
|
|
|||
|
Edward J. O'Hagan, Retired elementary school principal n/a, n/a
Send response to journal:
|
http://aboriginalart.com.au/didgeridoo/dig_background.html The above website provides both listening and learning instructions on didgeridoo playing. Other related websites refer to the abilty of the instrument to influence vagal involvement. An online search for 'digeridoo vagus' will provide a wide range of associated information in that regard. In my first response, I stated that a theoretical model of sleep and arousal which I have constructed, suggests that the low Hz. vibrations of the didgeridoo are conducted downward along the efferent vagal pathway, and in common with the Pasche spoon, the OMMMM utterances and the 'Tibetan stomach singing', they result in reduction of abdominal afferential vagal signalling back to the nucleus tractus solitarius (NTS) in the brainstem.The overall result is that SNS input is decreased, and in the case of insomnia this facilitates sleep onset. Now may be the appropriate time to provide additional and more detailed information in that regard. The following has been copied directly from the relevant section of the model's text: Research conducted by Hawthorn et al (1988) on the ferret showed that electrical stimulation of the abdominal afferent vagus nerve caused the release of increased levels of vasopressin (AVP) but not oxytocin (OT) in the NTS. Independent of their individual roles peripherally, central involvement of both AVP and OT as regulatory neurotransmitters of the autonomic system was clearly demonstrated by Landgraf et al.(1990) using anaesthetized rats. Electrical stimulation of the ipsilateral paraventricular nucleus (PVN) of the hypothalamus, resulted in a 5-fold increased level of OT and AVP, recovered and measured in a push-pull perfusate of the NTS and dorsal motor vagus (DMV) area. After stimulation, the peptides were found to return to the level of controls. An osmotic stimulus failed to increase AVP and OT levels in the NTS/DMV perfusate. The authors concluded that their results were consistent with the view that both peptides are centrally involved as neurotransmitters in autonomic regulation. Central oxytocinergic neurons had also been hypothesized to influence gastric motility and secretion by increasing the excitability of central vagal neurons in the NTS and the nucleus of the DMV. Support for this hypothesis was evidenced in a study using the rat by McCann and Rogers (1990). In the following year Nordmann and Steunkel (1991) demonstrated that Na+ acts directly in releasing AVP from rat isolated neurohypophysial nerve endings. The secretory elevation was dose dependently related to Na+ and could occur in the absence of Ca++. The authors concluded that Na+ per se may be an intrinsic regulator of basal neurosecretion. A study by Raggenbass et al. (1992) carried the work forward by elucidating the roles played by both Na+ and Ca++ in the regulation of vagal neurotransmission in the brainstem. These investigators studied the effect of OT on brainstem slices of vagal neurons of the rat. OT induced current was concluded to be inward and voltage dependent since its magnitude moved from the resting potential toward less negative potentials. Regulation of the OT induced current in response to membrane potential suggested that OT acts by effecting opening of voltage dependent channels, which can exist in either of two states ...open or closed. Extracelluar calcium (Ca++) in lowered concentration enhanced the OT response, while raising the Ca++ concentration reduced it. Partial replacement of ECF Na+ was shown to reversibly attenuate or suppress the OT current. The authors concluded that OT increases the excitability of vagal neurons by generating a voltage-gated current, which is modulated by divalent cations and carried by Na+. More recently, a paper dealing with peptides as neurotransmitters in vascular autonomic neurons (Morris,1995) stated that neuropeptides are present in the majority of autonomic neurons projecting to blood vessels, where they work in conjunction with non- peptide transmitters and sometimes with other peptides in regularly producing potent effects on vascular tone, which often are restricted to selected regions in the vasculature. Neuropeptides can thus be regarded also as being important contributors to the regional regulation of the vasculature in selectively responding to various physiological stimuli. From the foregoing it is hypothesized that an increasing concentration of Na+ perfusing the abdominal afferent collaterals of the vagus nerve in humans would likewise produce current and stimulate the release of AVP but not OT in the NTS, in a manner analogous to that demonstrated by Hawthorn et al.(1988) in the ferret. This in turn should lead to a corresponding lowering of OT voltage-gating current, a reduction in membrane permeability and lessening of the excitability of efferent vagal neurons, as was described by Raggenbass et al.(1992) in the rat- tissue demonstration in vitro, thus leading to a reduction in parasympathetic activity. Hence , by combining the outcomes of these two studies, it becomes possible to suggest how the regulation of parasympathetic outflow from the brainstem along the efferent vagal pathway can be directly influenced by the effects of a concentration dependent sodium carried current acting along the abdominal afferent vagus nerve. References Hawthorn J, Andrews PL, Ang VT, Jenkins JS. (1988) Differential release of vasopressin and oxytocin in response to abdominal vagal afferent stimulation or apomorphine in the ferret. Brain Research (Netherlands) 1988 (Jan 12); 438(1-2):193-8 Nordmann JJ, Steunkel EL. (1991) Ca++ independent regulation of neurosecretion by intracelluar Na+. FEBS Letters; 292: 1,2: 37-41 Raggenbasss M, Dreifuss J J. (1992) Mechanism of action of oxytocin in ratvagal neurons: induction of a sustained sodium-dependent current. J.Physiology (London, England), 457: Nov. 1992, 131-42 Morris JL. (1995) Peptides as neurotransmitters in vascular autonomic neurons. Clinical Experimental Pharmacology and Physiology 1995 (Nov);22:.792-802 Competing interests: None declared |
|||