Q: Just wondered what you know about sleep studies for kids. One of the children in my practice sounds like he has some nasal obstruction, but no snoring that the parents have detected, and he is not heavy. So I have my doubts about tonsils, but I have not examined him. Wonder if he is more like UARS? Do you know anything about CPAP for kids? Oh, and he also sleepwalks.

Dr. Smith: No experience at all with childhood epilepsy and OSA. However, yes, I treat children with OSA…had one in today with great parents who both come with him at appointments. Mom was going in to hold his jaw forward for at least an hour every night to get him at least SOME restful sleep. Sleep centers are very comfortable with studies on children. Sleep walking shows no neurological effects or predispositions, so no worries there.

Children do not have to snore at all to have OSA, and when they do, the palatine tonsils are rarely (about 2% of the time) the cause. MUCH more common to have adenoidal obstruction (about 38% of the time, if memory serves), so his nasal obstruction is likely the source. I would get him in to see about the adenoids, then get a sleep study if this does not appear to be the problem. They put CPAPs on small children, but I doubt he will need that.

Q: I was told that a mandibular advancement device will not help central sleep apnea. Is this true?

Dr. Dmith:
1. From Sleep and Breathing (When we remove obstructions and anatomically reorient the mandible, we can be surprised at the benefits)

The aim of the present study was to investigate the effect of a mandibular advancement device (MAD) for the treatment of sleep apnea (SA) on plasma brain natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), and health-related qualify of life (HRQL) in patients with mild to moderate stable congestive heart failure (CHF). Seventeen male patients aged 68.4±5.5 with an apnea–hypopnea index (AHI) 10 were equipped with an individually fitted MAD. SA was evaluated using a portable respiratory multirecording system before and after the initiation of treatment. Eleven patients completed follow-up and were evaluated after 6 months of treatment. The AHI reduced from 25.4±10.3 to 16.5±10.0 (p=0.033) compared to baseline and mean plasma BNP levels decreased from 195.8±180.5 pg/ml to 148.1±139.9pg/ml (p=0.035). SA-related symptoms, e.g., excessive daytime sleepiness, were also reduced (p=0.003). LVEF and HRQL were unchanged. We conclude that SA treatment with a MAD on patients with mild to moderate stable CHF appears to result in the reduction of plasma BNP levels. Further studies to investigate if the observed reduction in BNP concentrations also result in improved prognosis are warranted.

2. From articles like this one, it becomes clear that a) Obstructions that create a decrease in respiratory motor output will b) decrease respiratory drive, leading to c) CSA. Therefore, anything that removes obstructions, such as a MAD, can improve CSA.

3. Additionally, OSA leads to arousals, which leads to hyperventilation, which leads to hypocapnia, which leads to a decreased respiratory drive, which leads to CSA. So, control OSA with a MAD, and you can lessen the likelihood of CSA manifestation.

Q: Can a MAD improve CSA as opposed to OSA?

Dr. Smith: Yes, there is more and more literature coming out showing that not only can mandibular advancement devices improve obstructive sleep apnea, but they can have a positive effect on central sleep apnea as well.

From articles like this one, it becomes clear that a) Obstructions that create a decrease in respiratory motor output will b) decrease respiratory drive, leading to c) CSA. Therefore, anything that removes obstructions, such as a MAD, can improve CSA.

Additionally, OSA leads to arousals, which leads to hyperventilation, which leads to hypocapnia, which leads to a decreased respiratory drive, which leads to CSA. So, control OSA with a MAD, and you can lessen the likelihood of CSA manifestation.