SUMMARY

The syndrome of Periodic Leg Movements of Sleep (see Glossary), occurring often in the elderly and in association with sleep apnea syndrome, is thought to be one major cause of daytime sleepiness. When coexisting with sleep apnea, the movements may occur at the same time as the respiratory events, or indepently of them, or both. CPAP can increase PLMS. Some patients with apnea and PLMS whose sleepiness persists with CPAP respond quickly to L-dopa (Sinemet), used to treat the PLMS. The authors decided to study nocturnal leg movements in apnea patients before and during CPAP. Instead of limiting their observations to periodic leg movements, which they consider poorly defied, they included non-periodic movements as well. They would label muscle activity in the legs as “periodic” only when there was a rhythmic pattern lasting at least five movements. They further classified movements as to whether they occurred at the same time as a respiratory event or separately from any respiratory event. A consecutive series of 19 male patients referred because of excessive daytime sleepiness and found on polysomnography to have AHIs (see Article #13), especially if the inter-movement interval is long (50-60 secs). This would indicate a need for readjustment of pressure. Shorter (30-40 sec) intervals seem more typical of true PLMS, which is an indication to start drug treatment such as L-dopa, bromocriptine, or clonazepam. Non-periodic movenets, strongly associated with apneas, are reduced by CPAP, while periodic movements remained the same or even increased.

COMMENTS

This study goes into more detail, in its hypothetical subclasses of movements, than the average apnea patient needs to know. What the patient needs to know is (1) with CPAP, leg movements may persist or increase, fragmenting sleep and causing daytime sleepiness much as respiratory events do; (2) when the pattern of leg movements is clearly periodic, the treatment of choice is one of a variety of medications; (3) if there is a less typical pattern of movements, they may be arising in relation to episodes of upper airway resistance, which can be checked for by intraesophageal pressure monitors or other approaches that are being devised. In this case, the first approach should be one of readjusting, presumably increasing, CPAP pressure until not only apneas and hypopneas, but upper airway resistance episodes are suppressed. These points, while plausible and supported by a variety of studies, are not all demonstrated in this one study. Two aspects of this study which gave me reservations were the use of oximetry only to diagnose the sleep apneics and the absence of rating of arousals, which seem to me the key mechanism by which either respiratory events or leg movements exert much of their harmful effects. Leg movements of sleep are not necessarily something either the patient or the bed partner would notice. Neither can the patient assume that the doctor will be alert to this as a matter of course. Doctors enter sleep medicine through various routes, and a pulmonologist might have considerably more interest in respiratory events than in other factors disrupting sleep. I have elsewhere remarked on my own experience receiving a hard copy of my own sleep study with CPAP as an example of “normal sleep” and then reviewing it with a technician at a course, only to discover that PLMS were causing frequent arousals, a fact that the original doctor later freely admitted when reexamining the record later. Lab errors occur everywhere, but especially when dealing with such complex data as the sleep polysomnogram.





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