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New Treatments for Sleep Disorders

Functions of sleep? The easy answer is we donít know. We do know, like with most physiologic functions, how do we know what it does? We take it away and see what happens. When you take sleep away experimentally you do have impaired performance and you do have sleep cravings. If you stop sleep, you will crave it more and more, just like hunger. And eventually you will sleep. You are more likely to fall asleep in an inappropriate setting, as we will discuss. Selective REM deprivation, the classic question and the old teaching was if you deprive somebody of REM sleep selectively you cause psychosis.

Not true. The same thing you get with non-REM sleep you get REM fresher, you get REM rebound, you get more and more craving of REM sleep and eventually, whether you like it or not, you go in REM sleep. Thatís what people with narcolepsy do.

Sleep studies. Let me give you what you need to know about those. How do we sleep? How do we stage sleep? You need three things; EEG, EOG, EMG. The non-REM sleep stages is determined by EEG only. The reason we need those two is for REM sleep. Because REM sleep is defined by rapid eye movements and muscle atonia. So in order to make a comprehensive sleep staging you need all three. Technically you can do it with one EEG channel, in practice we like to have more. And especially central leads and occipital leads, which makes perfect sense. Central leads because the hallmark of non-REM sleep always.

Vertex, sharp waves, spindles, K-complexes and occipital leads because the hallmark of wakefulness is in the occipital region. Then EMG, technically one channel is enough. Iíll show you pictures of all that. You might be shown a few pictures. With a polysomnogram, which is a comprehensive recording of a whole night. What we do in addition to sleep staging, we measure what we are likely to find abnormal and since sleep apnea is so important, we measure respiration, airflow, respiratory effort, oxygen saturation, EKG, this is obviously to look for periodic leg movements of sleep or nocturnal myoclonus. And this is to look for penile tumescence or erection when we evaluate erectile function, which is a totally different study. This isnít done in a routine polysomnogram. Itís done when the indication is the assessment of impotence. They are usually referred by the urologist or the internist or the endocrinologist.

All they are asking me is, evaluate the erectile function at night. While we are on this topic, the only thing you need to know about this - which is common sense, I think - what we do is we do a polysomnogram and we look for penile tumescence, which is measured quantitatively, and if you have normal erection during REM sleep the erectile dysfunction or impotence is more likely to be psychogenic. If itís organic, you lose the REM-associated erection. You do a full polysomnogram because you want to make sure that there is REM sleep, because if somebody has severe sleep apnea and no REM sleep, then you cannot say the erectile dysfunction is psychogenic because they did not go into REM sleep and you are not expected to have erections.

Clinically, these are the three studies that we do. This is all you need to know about. The current thinking is that the majority of impotence is not psychogenic, so this is an important thing to do when people are making a diagnosis of psychogenic impotence. Now letís talk about the other two, which you are more likely to be asked about I think. Polysomnogram occurs all night, records sleep architecture and makes the diagnosis of the major sleep disorders, intrinsic sleep disorders, which are sleep apnea.

Narcolepsy is a major sleep disorder but the polysomnogram is usually normal during narcolepsy. First night effect: when we put somebody in the lab with leads all over the place and sometimes in unpleasant places, they donít sleep very well. So there is an artifact finding in every sleep study, which is: it is not a typical nightís sleep. We know that. How do we measure it? Itís called the first night effect. What happens if tomorrow you go to sleep in a lab with leads everywhere, it will take you longer to fall asleep. Youíll have an increased sleep latency. You will spend less time in REM sleep.

As a neurologist, you need to be familiar with the MSLT. This is the multiple sleep latency test. What it does is, we give the patients four or five opportunities to take a nap at 10, 12, 2, 4 and 6. And we measure how long it takes for them to fall asleep. By sleep staging criteria, how long it takes to go from awake to stage I sleep, to the beginning of sleep. And thatís called the sleep latency. The trial duration is 15 to 20 minutes. You have 15 to 20 minutes to fall asleep. If you donít fall asleep after that time, itís normal. We monitor sleep stages. In addition to how long it takes you to fall asleep, which stages do you go into? So the two things we measure are sleep latency - how long does it take you to go from awake to stage I - and do you go into REM sleep.

Thatís abnormal unless you are a newborn. Itís normal for a newborn - or actually almost the first year of life - to go into REM sleep very quickly. After that itís not normal. First leg of interpretation is mean sleep latency. You need to know these. These are numbers, these are agreed upon, these are guidelines. You will be asked. Normal mean sleep latency for a human is greater than 10 minutes. That means, the average of four or five naps where youíve tried to fall asleep should be greater than 10 minutes. Less than 10 is abnormal. Less than five is definitely abnormal and evidence of severe sleepiness. Between 5-10 is a gray zone, but nevertheless for purposes of the Boards, itís abnormal. Now that means that the person is sleepy. It doesnít tell you why, it could be any reason. The MSLT is not perfect but it is the only reliable measure we have to assess objectively sleepiness. But it has to be interpreted in the context of the previous nightís sleep, and for that reason, MSLTís should be done after a polysomnogram of the previous night. Because if the previous night shows terrible sleep architecture - for example, the person doesnít go into REM sleep, the person has severe sleep apnea, or the person was up most of the night - then in that context it means nothing. It has to be interpreted with caution. Your friends that you think fall asleep quickly will admit to you that if you do a MSLT they will have a sleep latency greater than 10 minutes.

Now the other leg of the interpretation is SOREMP, sleep onset REM period. Thatís abnormal. Unless you are in your first year of life. The reason we do this is because two SOREMPís - that means if it happens twice or more out of your four or five nights of MSLT - it is said to be highly specific and suggestive of narcolepsy. You as a neurologist, and a taker of neurology Boards, needs to know that. It is totally specific? Of course not. You know by now that you will never say something is 100% specific and 100% sensitive. They donít have to tell you that. But itís pretty good, 80%, 70%, whatever. The point is, if you get severely sleep deprived - you stay up all night because you are on call - you do a MSLT tomorrow, you may have sleep onset REM period. Again, it has to be interpreted in the context of the previous night, which is measured objectively by a polysomnogram. So severe obstructive sleep apnea.

Finally, Iím going to tell you this because it is important and weíll go back to it, drugs, very very important. Because drugs alter sleep. Whatís the strongest and most common REM-suppressing drug? You will be asked that question. Tricyclics. For that reason if you withdraw from tricyclics or another REM-suppression medication, you get a REM rebound. You will tend to get more REM.