Friday, August 31, 2007

 

apneu

EDS = excessive daytime sleepiness

OSA= obstructive sleep apneu

The Causes of EDS

Once EDS has been identified through clinical assessment and the use of specific tools, if needed, the clinician can proceed to the next step, determining whether the EDS is related to insufficient sleep time, disrupted sleep, or a shift in circadian timing, or whether the EDS is a reflection of true hypersomnia and an increased need for sleep during a 24-hour period. In most cases, further probing will direct the need for additional testing.

Failure to allow sufficient time for sleep is a fairly common cause of EDS. In general, this can be attributed to a variety of behavioral and lifestyle issues. Each individual carries a certain sleep need as defined above (usually 7-9 hours for adults, longer for adolescents and children, and slightly shorter for older adults). A failure to meet this "quota" will lead to an increase in daytime sleepiness. This may be most noticeable during "down" times when external stimulation diminishes. A particularly vulnerable period will also occur in the middle of the afternoon, a time that is related to circadian factors. The resolution to this problem is to adjust schedules to meet this sleep need. Unfortunately, lifestyle patterns are often difficult to change and may require the persistence of the clinician.

Disrupted or inefficient sleep, even in the context of a full night of sleep, may also lead to EDS. As noted, the patient may not always be aware of the extent of the disruption. At times, other medical conditions may contribute. Chronic pain, frequent urination, and muscle cramps are a few examples. In dealing with EDS, the clinician should always look for those factors that may suggest the possibility of OSA. EDS, obesity, systemic hypertension, heavy snoring, and male gender all fit into the typical profile for OSA. On the other hand, these are relative risk factors and young, thin, normotensive women may also present with OSA. The critical diagnostic study for OSA is the overnight polysomnogram. Various treatment options are available, but continuous positive airway pressure is often the treatment of choice. Interestingly, an occasional patient may have persistent EDS even after relatively adequate treatment of OSA.

Disturbances in the circadian timing system may also play a role in EDS. At times, a shift in the timing system relative to the daily lifestyle schedule occurs, involving either a delay or advancement. This results in a situation where the individual is attempting to sleep when the circadian system is prepared for wakefulness or the individual is planning for wakefulness when the circadian system is prepared for sleep. A special case can be seen in shift workers who may suffer from a shift work sleep disorder. In some respects, these patients actually suffer from a combination of insufficient sleep and fragmented sleep, as well as the difficulties of functioning in opposition to the circadian rhythm. In some sense, they experience ongoing "jet lag." Scheduling issues frequently lead to a shortened time in bed, and sleep during the day is often fragmented. Work time function is often suboptimal because of the effects of sleep deprivation, sleepiness, and the limitations of trying to function "out of rhythm."

Finally, some patients seem to get an adequate amount of efficient sleep without a circadian disturbance, but still exhibit evidence of EDS. Obviously, the clinician should always be wary of toxic-metabolic disorders and the effects of medications and drugs. Several neurologic conditions, including certain neurodegenerative disorders and disorders with lesions of the hypothalamus, have been associated with EDS. On occasion, EDS may be a feature of a depressive syndrome. Narcolepsy, with or without cataplexy, refers to a disorder of EDS that is independent of all of the above. In addition to EDS, these patients may also complain of sleep paralysis or sleep-onset hallucinations. Cataplexy refers to a transient, emotion-induced atonia. The diagnosis is made on the basis of a clinical evaluation coupled with a polysomniogram and MSLT.

Conclusion

This walk through the identification and assessment of EDS should be viewed as something more than an academic exercise. These are disorders that may often remain undiagnosed and may lead to obvious morbidity. Although the causes may be diverse, most can be managed and treated -- but the first step requires a clinician who is alert to the possibilities and who knows the right questions to ask.

Supported by an independent educational grant from Cephalon


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