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Sleep Medicine Reviews (2008) 12, 307 317

www.elsevier.com/locate/smrv

CLINICAL REVIEW

The relationship between insomnia and body temperatures

Leon C. Lacka,, Michael Gradisara, Eus J.W. Van Somerenb,c, Helen R. Wrighta, Kurt Lushingtond
School of Psychology, Flinders University, South Australia, Australia Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands c Departments of Clinical Neurophysiology, Neurology and Medical Psychology, VU University Medical Center, Amsterdam, The Netherlands d School of Psychology, University of South Australia, SA, Australia
b a

KEYWORDS
Sleep; Insomnia; Core body temperature; Circadian rhythms; Thermoregulation

Summary Sleepiness and sleep propensity are strongly inuenced by our circadian clock as indicated by many circadian rhythms, most commonly by that of core body temperature. Sleep is most conducive in the temperature minimum phase, but is inhibited in a wake maintenance zone before the minimum phase, and is disrupted in a zone following that phase. Different types of insomnia symptoms have been associated with abnormalities of the body temperature rhythm. Sleep onset insomnia is associated with a delayed temperature rhythm presumably, at least partly, because sleep is attempted during a delayed evening wake maintenance zone. Morning bright light has been used to phase advance circadian rhythms and successfully treat sleep onset insomnia. Conversely, early morning awakening insomnia has been associated with a phase advanced temperature rhythm and has been successfully treated with the phase delaying effects of evening bright light. Sleep maintenance insomnia has been associated not with a circadian rhythm timing abnormality, but with nocturnally elevated core body temperature. Combination of sleep onset and maintenance insomnia has been associated with a 24-h elevation of core body temperature supporting the chronic hyper-arousal model of insomnia. The possibility that these last two types of insomnia may be related to impaired thermoregulation, particularly a reduced ability to dissipate body heat from distal skin areas, has not been consistently supported in laboratory studies. Further studies of thermoregulation are needed in the typical home environment in which the insomnia is most evident. & 2008 Elsevier Ltd. All rights reserved.

Corresponding author. Tel.: +61 8 8201 2391;

fax: +61 8 8201 3877. E-mail address: leon.lack@inders.edu.au (L.C. Lack). 1087-0792/$ - see front matter & 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.smrv.2008.02.003

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308 L.C. Lack et al. Habitual wake up time usually occurs about 13 h after the CBTmin, when core body temperature begins to rise.7,8 These relationships can be seen in Figure 1. However, of particular relevance to insomnia are two zones of the CBT rhythm during which sleep is inhibited.9,10 One zone occurs in the early evening, about 69 h before the CBTmin and 14 h before habitual bedtime (18:0022:00). It has been termed a wake-maintenance zone,10 because sleep onsets are delayed during this period.8,11 Another zone occurs in the morning about 47 h after the CBTmin (typically between 08:00 and 11:00) and is associated with increasing wakefulness in sleep or with wake up.10,11 Therefore, if the timing of the individuals endogenous circadian temperature rhythm is timed relatively late or relatively early with respect to the attempted sleep period, difculty initiating or maintaining sleep can occur. The endogenous melatonin circadian rhythm is highly correlated with the CBT rhythm and is sometimes used to estimate the timing of the circadian system.12,13 Plasma melatonin level begins to increase in the evening typically about 23 h before habitual bedtime (about 21:00, see Figure 1). Levels peak between 02:00 and 04:00, the midpoint of the sleep period and about one to two hours before the CBTmin, decreasing to barely detectable levels before 09:00, about 1 h after habitual wake time.12,14

Insomnia
Insomnia is a very generic term with the criteria including difculty initiating sleep, maintaining sleep, and early morning awakening, accompanied by some form of daytime impairment (e.g., fatigue).1 This review will focus on these three areas of sleep difculties and the relationship with body temperatures. The International Classication of Sleep Disorders (ICSD-2)1 elaborates several categories of insomnia primarily on the basis of its etiology and contributing causes such as psychophysiological insomnia, inadequate sleep hygiene, etc. There are also insomnias arising from circadian rhythm sleep disorders described in a separate section of the ICSD. We will elaborate on the contribution of circadian rhythm timing disorders as indicated, in particular, by the timing of the core body temperature rhythm. These timing disorders will relate to both difculties initiating sleep (sleep onset insomnia) and early morning awakening insomnia. Difculty maintaining sleep and excessive nocturnal wakefulness will be related to nocturnal hyper-arousal as indicated primarily by elevated nocturnal core temperature. In addition, the review will look at the relationship of insomnia to the regulation of body temperature.

Body temperature and circadian rhythm timing

Periodic circadian (24-h) variations or rhythms are ubiquitous in the human body and include physiological and behavioral rhythms of core body temperature, melatonin secretion, sleep propensity and subjective alertness. The sleepwake cycle and body temperature rhythms have a stable internal phase relationship in normally entrained conditions with the timing of sleep highly correlated with the timing or phase of the circadian body temperature rhythm.2 The temperature and melatonin circadian rhythms remain synchronized primarily by the entraining effects of the light/dark cycle. Endogenous core body temperature variations over time follow a near sinusoidal rhythm with the temperature minimum normally occurring between 04:00 and 06:00.3,4 Sleep propensity is closely linked to core body temperature. Sleep is typically initiated on the falling limb of the temperature rhythm, and about 56 h before the core body temperature minimum (CBTmin), with maximum circadian sleepiness occurring at the CBTmin.5,6 For an individual whose habitual sleep onset is 23:00, the CBTmin would occur between 04:00 and 05:00.

Sleep onset insomnia and delayed sleep phase disorder

Sleep onset difculties may occur when an individuals temperature rhythm is timed relatively late with respect to their attempted sleep period. In these cases the delayed temperature rhythm may result in a delay of the evening wake maintenance zone such that it coincides with the attempt to sleep. The evening wake maintenance zones of normal and sleep onset insomniacs are illustrated in Figure 2. Some studies have found that individuals experiencing sleep onset insomnia have a relatively delayed circadian rhythm. In one study,15 the sleep and temperature rhythm of 13 subjects (average age 33.7 years) who experienced sleep onset insomnia were compared to a similarly aged group of good sleepers. The polysomnographically measured (PSG) sleep onset latency of the insomnia group was 42 min compared to 11 min for the good sleepers. The insomniacs endogenous mean CBTmin, measured in a constant routine methodology, was at 07:18 and their typical

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The relationship between insomnia and body temperatures 309

Core Temperature

Sleep Propensity

Melatonin

SLEEP PERIOD

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21 22

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TIME (24 Hour Clock)

Figure 1 Diagrammatic representation of normally entrained endogenous rhythms of core body temperature (solid curve), plasma melatonin (dotted curve), and objective sleep propensity (dashed curve) placed in the context of the 24-h clock time and normal sleep period (shaded area).8,13

38 Wake Maintenance Zones

CORE BODY TEMP. C

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EMA Tmin

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SOI Tmin

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Figure 2 Diagrammatic representation of the circadian core body temperature rhythms of normally entrained good sleepers (solid line), sleep onset insomniacs (SOI, dotted line), and early morning awakening insomniacs (EMA, dashed line) showing their temperature minima, wake maintenance zones, and morning wake zones (thick dotted line).

bedtimes were at 24:00. Therefore, the insomnia group was attempting sleep within their wake maintenance zone estimated to occur between 22:18 and 01:18. On the other hand, the good

sleepers were attempting sleep at about 23:00, closer to their mean CBTmin of 03:15, and therefore, about 2 h after the evening wake maintenance zone.

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310 In another pilot study we assessed the circadian timing of the melatonin rhythm and sleep of 16 participants (average age 29 years) with sleep onset insomnia.16 The timing of salivary dim light melatonin onset (DLMO)17 which is estimated to occur about 7 h before the CBTmin18,19 was used as an indicator of the timing of their circadian rhythm.17,20 The time of DLMO for this group was later than 24:00, indicating a delayed circadian rhythm. Their average bedtime was 00:30 and average sleep onset time was 01:45. As in the previous study these subjects were also attempting to fall asleep during their predicted wake maintenance zone. Cases with more severely delayed circadian rhythms can result in delayed sleep phase disorder (DSPD), previously known as delayed sleep phase syndrome.1 Weitzman and colleagues21 rst described the syndrome of delayed sleep phase insomnia in patients who were unable to fall asleep until about 02:00 or even as late as 06:00, and therefore had chronic difculty falling asleep at the desired time necessary to meet their daily commitments. When ambulatory core body temperature was monitored in individuals with DSPD, their CBTmin was approximately 2 h later when compared to a control group of good sleepers.22 Watanabe and colleagues23 assessed the sleep and circadian rhythm of individuals with DSPD. Their ambulatory core body temperature minimum occurred at 07:43, over 2.5 h later than the control group. On the two nights of PSG, their sleep onset latency was over 100 min and they were not able to fall asleep until 02:15. In contrast, the control group had a latency of only 5 min and a sleep onset time at 23:30. Those individuals with DSPD were attempting sleep in their wake maintenance zone that would have extended from about 23:0002:00, and hence had difculty falling asleep at their chosen bedtime. Therefore, considerable evidence relates sleep onset insomnia and a delayed sleep onset time with a delayed core body temperature rhythm and late timed circadian clock in general. L.C. Lack et al. and wake times at 03:00. If the person tries to obtain more sleep in the morning by staying in bed, frequent unsuccessful attempts to reinitiate sleep may lead to conditioned insomnia.1,24 An advanced sleep phase is associated with an advanced circadian core body temperature rhythm25,26 and melatonin rhythm.27 In individuals with ASPD, Jones and colleagues25 found their mean temperature and melatonin rhythms were timed about 4 h earlier than normal. This would place their typical wake up time of 04:18 at about the start of their morning wake zone. Those who present symptoms of early morning awakening insomnia (i.e., chronic difculty waking before intended, getting inadequate sleep, and reporting daytime tiredness) may also show an advanced temperature rhythm. Using a laboratory controlled constant routine procedure to eliminate external masking effects28 we evaluated the endogenous core body temperature timing of individuals who experienced early morning awakening insomnia.29 Individuals with early morning awakening insomnia were compared with an agematched group of good sleepers. The mean CBTmin of the insomnia group occurred at 00:20, almost 4 h earlier than the control group. The wake up time of the insomnia group at 04:49 occurred in their estimated morning wake zone preventing them from falling back to sleep and limiting their total sleep amount to less than 6 h. In a further constant routine study evaluating the effectiveness of light therapy for early morning awakening insomnia,24 participants average baseline CBTmin occurred at 01:40 with the wake zone estimated to start before 06:00. This coincided closely with their subjective (sleep diary) wake up time at about 05:45 and an objective wake up time (actigraphy) at 06:15. Again, participants were unable to sleep-in later and could obtain no more than 6 h total sleep. Therefore, ASPD and early morning awakening insomnia are associated with an early timed temperature rhythm that would predictably limit the ability to extend sleep in the morning. The relatively early timed temperature rhythm and associated morning wake zone of early morning awakening insomniacs is illustrated in Figure 2 as the dashed curve advanced about 3 h earlier than normal.

Early morning awakening insomnia and advanced sleep phase disorder

The ICSD-2 nosology describes advanced sleep phase disorder (ASPD), or earlier terminology syndrome, as a disorder in which the major sleep period is early (advanced) with respect to the desired sleep/wake period.1 Individuals with ASPD have overwhelming early evening sleepiness, an early sleep onset and early morning awakenings. For example, bedtimes could be as early as 19:00

The treatment of insomnia by phase shifting (re-timing) circadian rhythms

If treatments that appropriately shift the rhythms of sleep onset and early morning awakening insomnia are efcacious, it would support the

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The relationship between insomnia and body temperatures prediction that temperature rhythm de-synchrony contributes to the etiology of these two insomnias. Initial studies have demonstrated that bright light can phase shift circadian rhythms,3032 with bright light presented before the CBTmin delaying the circadian rhythm and bright light administered after the CBTmin advancing the rhythm.3337 Morning bright light has advanced the sleep and temperature rhythm of individuals with DSPD3840 and DSPD with associated sleep onset insomnia.4143 Conversely, evening bright light has been shown to be effective in phase delaying the sleep and body temperature rhythms of insomniacs with an early CBTmin (before 02:30) and lengthening the sleep of early morning awakening insomnia.24,44 A nal example is an experimental study in hemodialysis patients demonstrating that early morning awakening is associated with an early morning advanced drop in skin temperature.45 If the early morning drop in skin temperature is prevented by conditioning of the dialysate temperature, the patients sleep better in the early morning. 311

Practice points
1. Sleep onset insomnia can be caused by a delayed circadian rhythm and can be treated with morning bright light therapy. 2. Early morning awakening insomnia can be caused by an early timed circadian rhythm that can be treated with evening bright light therapy.

Insomnia from hyper-arousal

Independent of circadian factors, it is clear that insomnia can arise from a wide range of stimuli that promote arousal. These include environmental (e.g., noise, elevated ambient temperature), social (e.g., poor sleep habits, shiftwork), psychological (e.g., conditioned responses, anxiety) and physiological (respiratory impairment, restless legs, pain) stimuli. At a broad conceptual level it is generally held that such stimuli lead to a hyper-aroused state that is the immediate cause of poor sleep and secondary daytime symptoms of insomnia (e.g., fatigue, impaired mood).4650 However, whether the secondary daytime symptoms associated with poor sleep arise from the poor sleep or chronic hyper-arousal separately or in combination remains contentious.

From a series of studies, Bonnet and Arand47,51,52 suggested that the secondary symptoms of insomnia (e.g., fatigue, cognitive impairment, and general dysphoria) are not due to loss of sleep per se, but may be better explained instead by persistent hyper-arousal. For example, disrupting the sleep of normal sleepers to simulate that of a typical insomniac resulted in increased sleepiness that is not usually associated with chronic insomnia despite their reduced total sleep.47 In another study where sleep maintenance insomniacs had their poor sleep further disrupted by articially increasing their wakeful periods they showed increased sleepiness rather than the more typical secondary symptoms of insomnia.51 By contrast, when hyper-arousal was induced in a group of 12 good sleepers over a week by administering a total of 1200 mg of caffeine across each day, they found the changes in physiological, sleep, and daytime functioning measures were comparable to those seen in chronic primary insomnia.52 Further support for the hyper-arousal model of insomnia has come from evidence showing that physiological arousal (e.g., adrenocortical activity, catecholamine levels, electrodermal conductance, frontalis muscle tension, heart rate, metabolic rate, and peripheral vasoconstriction) is raised in insomniacs compared to controls.46,49,5364 A particular focus in the arousal and sleep literature has been an exploration of the relationship between nocturnal core body temperature and sleep onset. Compared to controls, insomniacs are reported to have higher oral pre-sleep onset temperatures58 and, under ad lib sleep conditions, both higher rectal61 and oral49 temperatures over the sleep period. Finally, consistent with the inverse relationship reported between core body temperature and distal peripheral temperature,4 insomniacs are also reported to have lower nger temperatures in the minutes prior to sleep onset.56 By contrast, two studies reported no difference between insomniacs and controls in core body temperature and other correlates of arousal. Adam et al.58 observed no signicant difference under ad lib sleep conditions in either post-sleep onset oral temperature or daytime adrenocortical activity in middle-aged to elderly insomniacs compared to controls. Similarly, Freedman and Sattler56 observed no difference in a variety of autonomic activity measures (e.g., EMG, heart rate, nger temperature) between young sleep onset insomniacs and controls during ad lib sleep. However, it is to be noted in both cases that the trends were in the expected direction. Despite evidence of an association between physiological arousal and insomnia it is noteworthy

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312 that the majority of studies have measured arousal under ad lib sleep conditions. This methodological limitation may account for some of the group differences reported between insomniacs and controls. For example, group differences in physical activity and posture rather than sleep quality may account for temperature differences.6568 Similarly, core temperature may be elevated in insomniacs compared to controls during ad lib sleep conditions simply because temperature is elevated during wakefulness and by denition insomniacs spend a greater period of the night awake.69 In brief, it could be argued that elevated core body temperature is simply a result of sleepwake state rather than an endogenous contributor to insomnia as the hyper-arousal model would suggest. More direct evidence that core body temperature is elevated in insomniacs has come from work by our group70 where we examined temperature under wakeful constant routine conditions. In our study we found that aged insomniacs (primarily sleep maintenance insomniacs) compared to controls had higher core body temperatures prior to their habitual sleep onset time at home and that this persisted across the wakeful constant routine night until early morning when both groups converged and showed similar core temperature values across the remainder of the day. These ndings suggest that aged sleep maintenance insomniacs are not chronically hyper-aroused across the 24-h period but are endogenously hyper-aroused at night. It should be noted that one other study of core temperature evaluated in a constant routine protocol failed to nd differences between good sleepers and insomniacs during the day or at night.71 Whether this lack of difference arose from the use of a younger age group or smaller differences in objective sleep parameters between groups needs further investigation. Our data support Sewitchs50 proposition that insomnia is characterized by a failure to down regulate temperature at night. It is also consistent with a large body of evidence that a rise in distal peripheral temperature and a concomitant fall in core body temperature presages successful sleep onset.7276 This last nding anticipates the next section that reviews the possible relationship of insomnia to abnormal thermoregulation. In conclusion, there is some evidence to suggest that hyper-arousal can account for the sleep loss and perhaps the daytime symptoms of insomnia. What remains to be more fully determined is whether hyper-arousal is simply restricted to the L.C. Lack et al. night time period or whether it persists over the day in insomnia.

Practice points
1. Considerable evidence supports the chronic hyper-arousal model of insomnia. 2. The evidence from constant routine studies of core body temperature only supports nocturnal elevated CBT in aged sleep maintenance insomniacs.

Thermoregulation and Insomnia

Skin temperatures role in thermoregulation
We have already described the relationships between core body temperature and poor sleep. However, a review of insomnia and temperature would be incomplete without reference to the role of skin temperature in thermoregulation. The regulation of core body temperature occurs as a combination of heat production and heat loss.3 When heat production is greater than heat loss, core body temperature increases and, conversely, when heat loss exceeds heat production, as in the late evening, it decreases. As the circadian rhythm of heat loss is phase advanced with respect to heat production, this has led many researchers to conclude that the process of heat loss rather than changes in heat production primarily drives the circadian rhythm of core body temperature.3,4 With regards to insomnia and in particular, sleep onset insomnia, the mid to late evening could be considered the critical part of the circadian body temperature rhythm. Prior to retiring to bed, the core temperature rhythm should be on the decline. However, this requires heat loss from the core through the transference of heated blood to various blood vessels located in the skin. The vessels most effective at rapidly losing heat are known as arterio-venous anastomoses (AVAs), and are concentrated in more distal regions of the skin (i.e., hands, feet, nose, lips, and ears).75,77 Increased transference of blood to distal skin regions can be indirectly measured via increases of distal skin temperatures. Since the proximal skin region (i.e., forehead, abdomen, thigh, and infraclavicular) blood vessels are less involved with thermoregulation,78,79 this section will focus on distal skin temperature in relation to insomnia.

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The relationship between insomnia and body temperatures 313

Skin temperature and the sympathetic nervous system

Heat loss from distal skin areas occurs most rapidly when AVAs are maximally dilated.4,77 Conversely, when vasoconstriction occurs, the amount of blood ow is restricted causing distal skin temperature values to decrease towards ambient air temperature (e.g., 2022 1C in a laboratory). Vasomotor activity of AVAs is directed primarily from sympathetic nervous system constrictor neurons. When these neurons are activated, smooth muscles around AVAs constrict causing vasoconstriction, sometimes to the point of ceasing blood ow.77 Alternatively, when there is reduced activation of these sympathetic constrictor neurons, the smooth muscles relax, vasodilation takes place, and blood ow increases.77 As a result, skin temperature rises towards values close to core body temperature and heat loss occurs through convection to cooler ambient air. Many studies of good sleepers have found a close association between distal skin temperature increases and the onset of sleep.76,8085 Some pathological conditions also support this relationship. Pache et al.86 found that those with vasospastic syndrome from chronic peripheral vasoconstriction causing cold hands and feet also suffer from difculty initiating sleep. At the other extreme narcoleptics who have abnormally short sleep onset latencies also have chronically elevated distal/proximal skin temperature gradients (DPG) and showed increases of DPG during sleep arising mainly from robust increases in distal skin temperature.87 A suggested causal mechanism involves warm sensitive neurons in the pre-optic area/anterior hypothalamus that receive input from skin and that are also involved in sleep initiation.79,8890 This suggestion is consistent with recent evidence that inducing an elevation in skin temperature promotes sleep onset,90,91 and enhances sleep depth both in normal sleepers and elderly insomniacs.92 However, these processes have received little attention in insomniacs. It has been postulated that distal skin temperatures around sleep onset for insomniacs may undergo a different process.76,93

within a reasonable amount of time (e.g., within 1015 min). In contrast, insomniacs take longer to fall asleep initially and following awakenings from sleep.15,50,56,58 Unlike good sleepers, insomniacs are not relaxed, even to the point of being anxious when attempting sleep.58,94 This view has been supported very recently with the nding that the normal reduction of cognitive arousal and alertness at bedtime is attenuated in those with sleep onset insomnia.95 Their anxiety and alertness may be associated with an activation of their sympathetic nervous system, resulting in vasoconstriction of AVAs, and indicated by decreased distal skin temperatures. Some studies have found relationships between anxiety-provoking stimuli and lower nger skin temperatures in good sleepers.96 Hence, if insomniacs nd that the attempt to sleep produces even mild anxiety, it would be expected to increase sympathetic nervous system activation and lower skin temperatures (at least compared to good sleepers).

Supporting research
The rst study to investigate the skin temperatures of insomniacs attempting sleep was conducted in 1979 by Brown97 who found that insomniacs did show increases in toe skin temperature when attempting sleep, but that sometimes there was no observable change. Yet, when toe temperature increases were observed, they were more variable, and took twice as long to reach the same amount of temperature change compared to good sleepers. Freedman and Sattler56 found that compared to good sleepers insomniacs have signicantly lower nger skin temperatures from lights out through to Stage 2 sleep onset. However, it appears that once sleep is achieved, differences in distal skin temperatures between insomniacs and good sleepers disappear, suggesting a critical period between lights out and sleep onset. It is worth noting that Freedman and Sattler56 found their insomniacs scored signicantly higher on measures of general anxiety and worry compared to good sleepers, providing support for a link between anxiety, insomnia and lower distal skin temperature. More recent attempts to investigate the notion that insomniacs have attenuated distal skin temperature increases when attempting sleep have found conicting results. Research by our group conrmed that middle-aged insomniacs with sleep onset and maintenance difculties reported both higher levels of general anxiety and sleep anticipatory anxiety in their home environments compared to good sleepers.98 Surprisingly though, we

Does insomnia limit the down regulation of core temperature as a result of impaired distal skin vasodilation?
Good sleepers are typically known to be relaxed when attempting sleep, and manage to fall asleep

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314 found the rapid increases in nger temperature of the insomniacs to be greater than those of good sleepers when they were falling asleep. However, it should be noted that in the laboratory the insomniacs fell asleep as quickly as the good sleepers and, in that sense, were not displaying their characteristic insomnia. The insomniacs did have signicantly higher core body temperatures (by approximately 0.2 1C) throughout the circadian rhythm thus supporting the chronic hyper-arousal theory for those suffering combined sleep onset and sleep maintenance insomnia. It would have been of interest for this study98 to have measured proximal skin temperature, as, along with core temperature, it would be likely to be higher in the insomniacs prior to the sleep attempt. If so, this would produce a lower distal/ proximal skin temperature gradient associated with longer sleep latencies in normal sleepers.82 However, such a result would not negate the nding of a robust increase of distal skin temperature when insomniacs fell asleep. The chronically higher core temperature also suggests that there was a greater need for the insomniacs to lose core heat via the ngers and they appeared able to do so in the laboratory free of their previous insomnia symptoms. On the other hand, a recent study by van den Heuvel et al.99 suggested that insomniacs have less ability to vasodilate in distal skin. They found that younger sleep onset insomniacs had no greater nger temperature increase when challenged by a warm (45 1C) contralateral hand bath than a neutral bath (3035 1C), whereas good sleepers showed a greater increase to the warm bath. However, because the baseline nger temperatures were not reported, it is not possible to rule out the possibility that the attenuated response in the insomnia group was due to a ceiling effect in their nger temperature. Regardless of whether insomniacs show attenuated vasodilation responses, it is still relevant, at least from a clinical perspective, to investigate whether skin warming would facilitate sleep onset. Raymann et al.100 have recently found that foot (distal) skin warming signicantly facilitated shorter sleep onsets in young and elderly healthy sleepers, but not signicantly in sleep disturbed elderly. Interestingly though, this elderly insomnia group showed the greatest slowing of reaction speed during proximal skin warming.100 Reaction speed and the ability to maintain wakefulness have also been shown to be sensitive to mild skin warming in narcolepsy.101 Therefore, in good sleepers, narcoleptics and possibly in insomniacs skin warming seems conducive to sleepiness which L.C. Lack et al. is consistent with the earlier suggested link between warm sensitive and sleep inducing neurons in the hypothalamus. However, as in the two previous studies this one was also conducted in the laboratory during the day without insomnia evident according to their relatively short sleep latencies. Further research is needed to determine whether vasodilation attenuation or non-reactivity to skin warming can be demonstrated in the bedroom environment where, presumably, their sleep onset is typically impaired and delayed. There are now wireless skin temperature sensors that would facilitate such home based studies.102

Practice points
1. While there is considerable understanding of the normal role of distal skin vasodilation in body heat loss and down regulation of core body temperature prior to bedtime and with the attempt to sleep, the few relevant studies have not consistently shown this process to be abnormal with insomnia. 2. One of these studies, however, has supported the chronic hyper-arousal model of combined sleep onset and maintenance insomnia.

Conclusion
Insomnia subtypes may be differentiated in terms of the aspect of sleep that is the predominant chronic difculty (difculty falling asleep, waking frequently for long periods during the night, early nal awakening before sufcient sleep is obtained). There appear to be specic abnormalities of body temperature associated with some of these subtypes. Difculty initiating sleep at a normal time (sleep onset insomnia) is associated with a circadian core body temperature rhythm that is delayed from normal timing indicating a delayed circadian clock likely to be a contributor to the insomnia. Morning bright light therapy has been used to phase advance the circadian rhythm and treat this type of insomnia. Early awakening insomnia has been associated with a circadian temperature rhythm timed much earlier than normal. Evening bright light therapy has been used to delay the circadian rhythms and treat this type of insomnia. Difculty with excessive nocturnal wakefulness has been

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The relationship between insomnia and body temperatures associated with elevated nocturnal core temperature, even in controlled laboratory constant routines, suggesting an endogenous nocturnal hyperarousal state at least in sleep maintenance insomnia. There is some evidence that the combination of sleep onset and maintenance insomnia is associated with elevated core temperature throughout the 24-h period and supports the chronic hyper-arousal model of insomnia. The possibility that elevated core temperature reects an impairment of the distal skin regions to vasodilate and dissipate body heat has received inconsistent support. Further research is needed to explore the etiological role of body temperature and thermoregulation under the conditions in which chronic insomnia is manifest in the home setting. 315

Research agenda
Future research should: 1. Examine further the 24-h core, proximal, and distal skin temperature rhythms and other correlates of arousal under controlled conditions for the differing insomnia subtypes compared to controls. 2. Extend the chronobiologic treatment research of those insomnia types showing an apparent mis-timing etiology (sleep onset, early morning awakening) in order to optimize treatment methods (e.g., timing and type of light therapy and other chronobiotic effectors). 3. Measure subjective arousal/anxiety in conjunction with sleep latency and distal skin temperature for sleep attempts of insomniacs in the typical home environment in which the insomnia is evident.

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