Perpetual, Shifting Jet Lag: Non-24-Hour Sleep-Wake Syndrome and Corollary Discharge

The United States (and much of the rest of the world) times work and school days in relation to the 24 hour solar day. In order to be awake at socially acceptable times for work and school, then, a person's internal clock, or circadian rhythm, must also conform to the 24-hour day. Common thinking holds that cycles may vary considerably within that 24 hour framework- hence "night owls" and "morning people"- but no one can completely diverge from the 24 hour pattern.

Or can they? Today, psychiatrists and sleep specialists have identified many types of circadian rhythm disturbances and disorders. Some are relatively mild- jet lag following travel across time zones, for instance- and generally remedy themselves within a few days <a href="/exchange/#4">(4)</a> Others, however, are more debilitating. Possibly the most debilitating of all is non-24-hour sleep-wake syndrome. People with this disorder, instead of having a 24-hour circadian rhythm, have an internal clock that runs in cycles of 25 hours or more, which may or may not begin in alignment with the 24-hour day. The result (if the condition is left untreated) is a pattern known as free-running, where a person's sleep cycle shifts a few hours later each day, never settling consistently; this pattern makes school, regularly scheduled work, and other daily routines generally taken for granted very difficult <a href="/exchange/#4">(4)</a>. One source describes the pattern as "a state of perpetual, shifting jet lag" <a href="/exchange/#3">(3)</a>

People could easily question why this disorder is often so devastating. Maybe the concepts of 24 hour days and sleep disorders are purely socially constructed, they might say; why not simply allow for more flexible work and school schedules to reflect a diversity of circadian rhythm patterns? But while such changes could certainly be useful to non-24-hour sleep-wake syndrome patients, long-established social patterns are incredibly hard to deconstruct. So long as most of the world adheres to the 24-hour clock, and so long as the non-24-hour sleep-wake syndrome patient needs to interact with others not on their sleep cycle, all the flexible scheduling in the world cannot solve the problem. I became especially interested in non-24-hour sleep-wake syndrome after letting a friend of mine, who has the syndrome, stay with me on a night when he felt he was too impaired from sleeplessness to navigate public transit home. At roughly 8 PM, a time that should be early for most twenty-somethings, he could not walk twenty feet to my doorway without staggering. "I fail the sobriety test," he joked as he settled in for the night, but I thought his offhand remark was a striking analogy; he had consumed no alcohol that night, but an outside observer noting his age, his gait, and the time of night might automatically assume drunkenness rather than sleep deprivation.

It's also tempting to label non-24-hour sleep wake syndrome as an entirely biological disorder. Indeed, neurologists can now name many of the areas of the brain responsible for regulating circadian rhythms, and provide some explanations as to how those areas might be disrupted in those with non-24-hour sleep-wake syndrome. The most important area in these explanations is a pair of small cell clusters in the hypothalamus known as the superchiasmatic nucleus, or SCN. Photoreceptors in the retina receive sensory input of light and transmit this input through the optic nerve to the SCN, which uses the light cues to entrain, or "set," the person's biological clock <a href="/exchange/#2">(2)</a>. Since light comes and goes in 24 hour cycles as per the rotation of the Earth, it follows that human sleep-wake cycles, which depend on light cues, should also be roughly 24 hours long. The SCN also uses these light cues to regulate cycles of melatonin, a hormone produced in the pineal gland. In a person with normal sleep cycles, melatonin levels peak in the middle of the night, lowering throughout the day and rising as darkness begins again; shifting levels of melatonin are associated with overall shifts in sleep patterns <a href="/exchange/#2">(2)</a>. Using this model, one could interpret non-24-hour sleep-wake syndrome as an inability to process these light cues "normally," or as a reduced sensitivity to light cues. This inability or reduced sensitivit, then, encourages underproduction of melatonin at night and over-production during the day, resulting in unusually timed sleep cycles. However, there are undoubtedly institutions in society that encourage abnormal sleep patterns on some level, in addition to physical factors like melatonin problems. Consider American high schools which start at 7 or 7:30 in the morning, forcing students to wake up at 5 or 6. For much of the academic year, there is little natural light at 5 or 6 in the morning. This discrepancy between sensory input and alertness is hard enough on teenagers with normal circadian rhythms<a href="/exchange/#1">(1)</a>; for those with non-24-hour sleep-wake syndrome, it must be especially difficult to adjust to.

The best model for explaining non-24-hour sleep-wake syndrome then, I believe, is one based on the principle of corollary discharge. Corollary discharge, as we discussed in class, is a mechanism that allows humans to distinguish between internal and external sensorimotor input; discrepancies between sensory and motor inputs lead to various forms of discomfort. Explaining non-24-hour sleep wake syndrome in terms of corollary discharge problems emphasizes the complex relationships between biological and societal factors in the disorder. On one level, the discrepancy between non-24-hour sleep-wake syndrome sufferers' internal melatonin levels and outside light cues surely plays a role in creating their irregular sleep patterns. This biological explanation also explains why blind people tend to have non-24-hour sleep-wake syndrome at far higher rates than sighted people; since they take in no light through the retina, the SCN cannot register light cues, which in turn inhibits its ability to regulate the pineal gland's melatonin release cycles <a href="/exchange/#3">(3)</a>. But institutions with rigid, early start times, like some jobs or schools, also create corollary discharge problems, since they force people to be awake at times when light cues and melatonin cycles would otherwise indicate the need for sleep <a href="/exchange/#1">(1)</a>. This discharge explains why shift workers, who may alternate between very early and very late work hours, often have disrupted sleep patterns (although they will rarely have true non-24-hour sleep-wake syndrome, which is a very rare condition.)

Non-24-hour sleep wake syndrome cannot be cured, only controlled. It's interesting to note, though, that common methods of controlling the condition attack both the biological and the social underpinnings. To regulate internal circadian rhythms, non-24-hour sleep-wake syndrome patients can take melatonin supplements before bed, bringing their nighttime melatonin levels up to "normal" and, hopefully, encouraging sleep at socially acceptable hours. In addition, sighted patients may use light therapy: exposure to a bright, full-spectrum light early in the day, in an attempt to mimic the bright light of the afternoon hours when the person might naturally wake up <a href="/exchange/#4">(4)</a>. But social factors, like career choice, can also help in the management of the disorder; having a job where one can work from home and choose one's own hours makes the erratic sleep schedule a bit less problematic.

This disorder is a perfect illustration of why it is problematic to claim that disabilities are entirely biologically based or entirely socially constructed. Claiming biological basis alone completely ignores the fact that institutions like high school may aggravate existing disorders. But claiming only social construction leaves little room for interventions based in biology, such as attempts to alter melatonin cycles in non-24-hour sleep-wake patients; while fighting to change the social bases of the disorder is certainly admirable, there's no denying that it cannot produce the immediate effects of melatonin or light therapy. Balance between these two aspects of the disorder seems to be the key; hopefully, medical professionals and social scientists working together can help to shed more light on this condition, as it were.

Web Sources

2. "Information About Sleep."
http://science.education.nih.gov/supplements/nih3/sleep/guide/info-sleep.htm

3. "Pathophysiology and Treatment of Circadian Rhythm Sleep Disorders"
http://www.medscape.com/viewarticle/465494_30

4. Sleep Disorder Primer
http://health.discovery.com/centers/sleepdreams/sleepdisorders/sleepdisorders.html#3