Posted by Craig on April 01, 2002 at 17:19:45:
In Reply to: Re: SL in narcolepsy on MSLT posted by jkhan621 on March 30, 2002 at 16:49:10:
Unfortunately, evaluating for REM suppressing medications is difficult. A large amount of the medications that we use for medical and psychiatric disorders (not only sleep) will suppress REM.
If we are worried about a man with the diagnosis of hypersomnia or narcolepsy, we should think of the most common medications for this:
1. Amphetamines (Only somewhat REM suppressing, and withdrawal should also be characterized by EDS-which this patient's sleep latency did not show.)
2. TCA (unfortunately no real test for these medications. Widening of an EKG is consistant with "toxicity," but does not necessarily tell us usage.)
3. SSRI (Most readily identified by the "Prozac eyes" in EOG of PSG/MSLT. This actually may be a factor. Would cause REM withdrawal....and actually the ocular findings can be mistaken for rapid eye movements at time.)
Remember though, I was focusing on etiologies that are associated with medications that PHYSICIANS may have given him for his current complaints of EDS. Other things:
1. Alcohol (People's favorite sleeping drug, and the most common drug of abuse. Best diagnosed with a blood test and looking at sleep stages.)
2. Illicit stimulants and hypnotics. (Who knows what else he uses to maintain vigilence...or even to sleep. Most are tested by the urine toxicology. Look at his spindles...remember benzodiazepines are REM suppressive.)
I hate to admit this, but I am a pessimist both about my patient's telling me the truth and my interpretative abilities.
When I get something which I cannot explain such as this, I will commonly do a urine toxicology both at an office visit (random) and at the polysomnography appointment. Occationally I will also do a blood test for alcohol, and when I am concerned enough for this I will check APAP and ASA levels. (The only effect of ASA that I know on sleep is a question of effecting SWS, but APAP and ASA are commonly mixed and used with other medications.) An EKG would only be helpful if he was taking excessive amounts of TCA.
Now my pessimism about my diagnostic abilities with this case gets manifested two fold:
1. Repeating the NPSG and MSLT to repeat my findings. I would also favor using videotaping if not standard in you lab to ensure not eyes open awake rapid eye movements. Since we also have such a high suspicion of SOREM, I might think of inferior ROC and superior LOC in addition to my standard leads EOGs. (Since if I did not see the SOREM on the repeat, I would want to be sure I did not miss them [pessimist remember].)
2. Start thinking about things that may provide some signs that look like "wake" into his early sleep (ie did I miss read his sleep onset?) For example , did we misinterpret "Prozac eyes" for slow rolling eye movements of drowsiness? Is there a reason for alpha intrusion?
The secondary gain issue may be able to get you some compliance with follow-up (which is good). I guess by your concerns about secondary gains that there are no other evidence of REM sleep intrusion? Was there any further evidence of narcolepsy on your PSG? (ex: Non-ICSD criteria like decreased sleep efficiency, increased arousals...etc)? Was there evidence of other disorders that can cause SOREM without EDS (ex: early morning awakings such as depression)?
Last piece of personal pessimism: I also pay special attention to the SWS percentage of the NPSG the night before an MSLT. If I see an inappropriately large amount of slow wave sleep for a patient's age, I start considering "Slow wave rebound" and "REM sleep rebound" from simply sleep deprivation/insufficient sleep sydrome previous to the night of the study. (Remember, classically after sleep deprivation, first night SWS rebound, second night REM rebound...but since the patient is napping the next day...maybe next day REM rebound.)
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