xxx. Light Therapy, Practice Parameters, 1999

23 February 2007 at 11:37 | Posted in Circadian rhythm | Leave a comment
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Practice Parameters for the Use of Light Therapy in the Treatment of Sleep Disorders appeared in SLEEP, Vol. 22, No. 5, 1999. The authors, Chesson et al, were all connected to universities and medical institutions in the USA. 

The clinical guidelines developed by the Standards of Practice Committee were reviewed and approved by the Board of Directors of the American Academy of Sleep Medicine. The guidelines provide recommendations for the practice of sleep medicine in North America regarding the use of light therapy for treatment of various sleep disorders.  

 “These practice parameters define principles of practice that should meet the needs of most patients in most situations.” 

As the PDF apparently no longer is available on the Internet and the document is found only in Google’s html version, I’m offering some excerpts here. I’m leaving out altogether the sections on shift work and other voluntary shifts of sleep-wake schedules, sleep disturbances in the elderly, jet lag and Seasonal Affective Disorder (SAD).  Update, December 2010:  the PDF is now here, hat tip to ttt.

Almost 10 years old, the guidelines can hardly be said to be up-to-date. Much of the information is, however, correct, and it is interesting to see what doctors “should have known” at the turn of the century, at least in the USA. [Emphasis, bold, is mine.] 

From the INTRODUCTION: Endogenous circadian rhythms are in large part regulated by the hypothalamic suprachiasmatic nuclei (SCN). The SCN are key regulators of sleep, as they regulate rhythms that promote sleep and wakening. It is now recognized that a number of sleep disorders are linked to abnormal circadian rhythms or to a lack of coordination of the sleep-wake cycle with the individual’s circadian rhythms. One of the most potent external factors that can alter the period of the SCN is light exposure. 

From BACKGROUND: Over the past two decades, laboratory studies have demonstrated that scheduled light exposure can produce a dose-dependent phase shift in the endogenous circadian rhythms of a variety of variables. These variables include plasma or saliva melatonin, core body temperature, cortisol and a propensity to sleep. 

The rationale for the use of light therapy evolves from the observation that circadian rhythms in humans can be phase-shifted by scheduled exposure to light. Because of an endogenous pattern of light sensitivity, the direction of the phase shift varies with the timing of the light exposure. The responses of circadian rhythms to light exposure have been summarized in Phase Response Curves (PRC).  The PRC appears phase-locked to the core body temperature and plasma melatonin concentration rhythm. In healthy young subjects, with a normal sleep pattern and temperature curve, the core body temperature minimum typically occurs about two hours before habitual wake time (around 4 to 5 a.m.).

  • Light exposure prior to the endogenous minimum of the core body temperature will shift rhythms to a later clock time (i.e., will delay rhythms).
  • Light exposure just after the endogenous circadian body temperature minimum will shift rhythms to an earlier clock time (i.e., will advance rhythms).

From SAFETY and SIDE EFFECTS:

Light therapy appears to be a generally safe treatment option for some circadian rhythm disorders…  

Rarely, light therapy may provoke a hypomanic state in patients with bipolar affective disorders.

TREATMENT OBJECTIVES, INDICATIONS and FOLLOW-UP: Treatment is indicated only if there is a desire on the patient’s part to resolve symptoms. The objective is to achieve a sleep onset at either a more socially acceptable time or at a time that provides sufficient sleep in keeping with the work schedule or lifestyle. 

Objective documentation is generally limited to a shift in the core body temperature minimum, a shift in the onset of dim light melatonin secretion or in the peak of the melatonin rhythm, information the patient has recorded in diaries, or actigraphic measurement of rest/activity patterns.

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Next page:

RECOMMENDATIONS FOR SPECIFIC DISORDERS:

1. Delayed Sleep-Phase Syndrome (DSPS)

2. Advanced Sleep-Phase Syndrome (ASPS)

3. Non-24-Hour Sleep-Wake Syndrome (NON-24)

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Next:  xxxi. Light Therapy Recommendations, 1999

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xix. Phase Response Curve (2)

12 December 2005 at 15:46 | Posted in Circadian rhythm | 2 Comments
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 PRCmelaMIDT-rev
 
 
I can’t yet leave the subject of the PRC, even if it is a bit technical.  Not all researchers say that we have a long “dead zone” mid-day in regard to our response to bright light.  The figure above shows the phase response of melatonin in the blood to light administered at various times.  From a study at Harvard published in 2003, it is somewhat simplified here.
 
21 carefully chosen persons were kept in dim light, then just once exposed to nearly 7 hours of bright light at different points in their personal cycles on the 6th day of a 10-day study.  The timing of each individual’s melatonin secretion was determined at the beginning and again at the end of the experiment.  All results are combined in the curve shown.
 
An interesting point: the midpoints of the individual melatonin profiles were found to be within a range of 2½ to 6 hours prior to these persons’ habitual awakening times. 
 
The horizontal line, about a half an hour below zero, shows how great the delay would have been anyway during the course of the experiment, due to the built-in pacemaker’s longer-than-24-hour period, had there been no light exposure at all. 
   
Phase shifts, from the beginning to the end of the study, are shown in clock time (vertical axis; phase delays are the negative values).  Here, the falling slope in the daytime is only slightly slacker than the rising slope in the night, and the true “dead zone” is only momentary, twelve hours before (or after) the core body temperature minimum. 
 
It is not difficult to explain the long mid-day “dead zone” found by earlier research.  Since bright light has only slight effect in the middle of the day, the effects of light before and after that magic moment will cancel each other out.  Unless, one could imagine, someone consistently is exposed to darkness for an appreciable period just before or just after.  How about someone working in darkness in the projection room of a cinema for the afternoon show, for example — might a phase advance be the result? 
 
The authors state: “These data provide a comprehensive characterization of the human PRC under highly controlled laboratory conditions.”  So this is perhaps the last word on that matter. 
 
Honors for inventing the Phase Response Curve in 1960 go to Patricia DeCoursey.  The “daily” activity rhythms of her flying squirrels, kept in constant darkness, responded to pulses of light exposure.  The response varied according to the time of day — that is, the animals’ subjective “day” — when light was administered.  When DeCoursey plotted all her data relating the quantity and direction (advance or delay) of phase-shift on a single curve, she created the PRC.  It has since been a standard tool in the study of biological rhythms.

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Next post:  xx. Entrainment

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xvi. Treatment

28 November 2005 at 23:35 | Posted in Circadian rhythm | 13 Comments
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  My light box 
 
It sounds so simple.  Take no naps.  Take melatonin at about 9 p.m.  To bed after 10.  Sleep soundly until about 7.  Turn on the light box, which stands on a shelf above the monitor, and do e-mail and stuff for almost an hour with 10000 lux entering the eyes at the slight angle from above. 
 
Keep a sleep diary showing exact sleep times (including the occasional nap).  Analyze it together with the sleep specialist every 5th week.  Hear him say “You’re doing well,” even when that seems to be more than slightly exaggerated.  
 
Never mind the occasional 36-hour trick.  Many patients never do stop staying up all night and all the next day now and then.  Seems to be a necessary adjustment, not just an old habit. 
 
Melatonin does make one sleepy.  Morning bright light does, apparently, shift the body temperature minimum earlier, so that it is not difficult to awaken at about 7. 
 
So it is that simple, when it works. 
 
The doctor does admit (reluctantly, I think) that some patients never do adjust to this regimen.  I understand that.  My body knows that it is being fooled.  Appetite (and who knows what else) has not shifted.  I’ve lost the creative, productive hours of 1-4 a.m., and they haven’t popped up anywhere else. 
 
Conclusion after a year:  it is possible, but no more.  Might it have been satisfactory, if tried at a much younger age?  I do suspect that it might have been…
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Next post:  xvii. Coffee break
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xii. Circadian rhythm disorders

27 November 2005 at 11:14 | Posted in Circadian rhythm | 6 Comments
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There are a great many sleep disorders. I read recently that an official list of them had been pared down to about 70. Many have to do with not getting enough sleep, or getting sleep of poor quality by several criteria. Some have obvious causes, such as chronic pain, frequent stops in breathing etc.

My interest is in the timing of sleep as my sleep seems otherwise normal. As the experts put it, I have normal “sleep architecture”. (For a good, short explanation of sleep architecture — stages and brain waves — see this page from Feinberg School of Medicine at Northwestern University in the USA.)

Nearly all of us can reset our clocks daily, adjusting the various rhythms to 24 hours. As much as I’ve read about it, I’ve not found a good enough explanation for being able to adjust to 24 hours while not being able to adjust to sleeping midnight to eight or so.

I’m not immune to the light/dark cycle. I need to get up at noon. I fly 8 hours east or west, go through jet lag like anyone else and within days I need to get up at noon in the new location. This is built in. I’m not the only one. I’d just like to understand it better.

A Japanese paper (2004) suggests these possible mechanisms:

  • reduced sensitivity of the oscillator to photic entrainment,
  • an intrinsic period beyond the range of entrainment to the 24 hour day, and
  • abnormal coupling of the sleep/wake cycle to the circadian rhythm.

 

The least common and most debilitating circadian disorder is the one where body temperature, melatonin secretion, sleep and other rhythms vary several times a day, in and out of phase with one another, so called Irregular Sleep/Wake Disorder. This has been reported in humans who’ve been in accidents and had physical injuries to the hypothalamus. It’s also been provoked by surgery in lab animals.

One of the most rare disorders which occurs naturally is called Non-24. Sufferers simply(?) live on a 23, 25 or 26 hour cycle, getting up one hour later each day for example, thus coming in sync with the earth’s rotation every few weeks. Their rhythms are in sync internally, just not with the light/dark cycle outside. Most, but not all, of these people are blind. 

ASPS, Advanced Sleep-Phase Syndrome, is also rare. These people fall asleep and awaken much earlier than normal. The disorder runs in families, and an American family has been studied intensively the last few years. Research on their genetic mutation was published in 2001. “Detailed sequence studies of the candidate human gene, hPer2, in the affected family members, revealed a key change in a single amino acid — from serine to glycine — at position 662 in the hPer2 protein.” The alteration “occurred in the portion of the hPer2 protein that governed binding to an enzyme called casein kinase one-epsilon (CK1e ).” In animal models, this enzyme regulates “proteins involved in controlling the length of circadian rhythms.”

Now this is beyond me, but it would appear that these disorders may be genetically programmed. Though ASPS is rare, it seems reasonable that researchers start there, since one can compare the DNA of people who are related to one other.

DSPS, Delayed Sleep-Phase Syndrome, is a bit more common. Studies indicate that somewhat more than one in a thousand adults have DSPS (Japan 0.13%, Norway 0.17%). It runs less commonly in families, but it doesn’t seem unreasonable to guess that its cause may be similar to that of ASPS.
 
Clearly, anyone whose health cannot tolerate frequent forced awakening earlier than 10 a.m., will have few real choices in our society. Thus, hardcore (inflexible) DSPS must be considered a disability.

Another disorder which may be related to the others is Seasonal Affective Disorder, SAD. Sufferers are normal in summer, have problems of mood, weight gain etc. when days get shorter and can often be treated successfully by bright light therapy. It seems likely that they may have a mild form of ASPS or DSPS which is “treated” by morning/evening daylight when days are long.

Diurnal preference, spoken of as “morningness”, larks, and “eveningness”, owls, is also a subject of study, the field of chronobiology. This is, reasonably enough, connected to one’s circadian rhythms. However, it does not appear that ASPS is an extreme morningness chronotype nor DSPS an extreme eveningness chronotype. The internal relationships among the various rhythms do not place these conditions on a simple continuum.

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Next post:  xiii. DSPS-sleep

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xi. My diagnosis!

27 November 2005 at 04:22 | Posted in Circadian rhythm | 7 Comments
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 (No, this isn’t my sleep specialist, but he does look like him :-))

Through a 15 year period, my present doctor had tested me for thyroid etc., sent me to a neurologist for overnight sleep analysis with all the attached equipment, sent me to a series of time-consuming and useless psychologists, had my throat operated (probably unnecessarily) for apnea and put me on a pill for depression.
 
Finally, he said he wanted to send me to a specialist to see if the depression diagnosis was correct.  The specialist he chose is a professor of psychiatry and the co-founder of a sleep clinic where he works one afternoon and evening a week.  I feared, and fully expected, a new and expensive round of psychologist-type time-wasting.
 
Dr. Holsten asked the many questions you’d expect to get from any new doctor:  health, job, living arrangements.  A great many questions, very quickly.  I should have taped the interview so I could analyze at what point it dawned on me that these aren’t questions to just any and every patient — this guy is circling me in!  He asked unexpectedly about several things which applied to me, but which I’d never connected to sleep problems.  It was rather exhilarating, like the experience some people rave about after having their fortunes told.
 
Unlike most doctors today he wasn’t staring at a computer screen, but he wasn’t looking at me either.  He was placing dots on a tiny grid about 8×10 cm.  Suddenly he looked up and said “You have DSPS!”  Of which I’d never heard.  He drew curves showing the timing of normal sleep related to body temperature, said he’d have my regular doctor put me on 100% sick leave for two months, gave me a sleep diary form to fill out every day, wrote the application and prescription for melatonin, arranged for me to borrow a light box, gave instructions (NO naps!), said it wouldn’t hurt to keep taking the depression medication and made an appointment for the first follow-up three weeks later.  I was out of there within 30 minutes with my head swimming.
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Next post:  xii. Circadian rhythm disorders
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