Lifespan and the Circadian Insomnias

One obvious feature of the circadian insomnias apparently not commented on previously is their relationship to age. In Figure 2 the insomnias are arranged not in the order presented in the diagnostics manual (63) but according to time of life. It becomes clear that there is a progressive change with age that parallels changes tothe circadian pacemaker evident from animal studies though not necessarily yet demonstrated in humans. A review of sleep disturbances, changes to circadian rhythmicity and the chronobiotic potential of MLT in retarding aging has been given elsewhere (12,42). Briefly, a large body of evidence, mainly animal but some human, indicates that with age: circadian period is altered, amplitude is reduced, alpha-rho loses its definition, stability to environmental challenge is reduced (e.g. phase shifts of the zeitgeber), internal desynchrony (humans) and splitting (rodents) increases. In addition, a number of changes to the circadian organization of the sleep-wake cycle (as distinct from sleep mechanisms per se) occur. Taken together, the single underlying variable tying all these appears to be amplitude of the circadian clock. It is also interesting to note the interrelationship between the occurrence of circadian insomnias, changes with age of circadian variables (Figure 2) and the occurrence of depressive illness (Figure 3).

The classic cases of DSPS occur in adolescence and teenage years but could occur earlier (the possible confounding of childhood DSPS as Idiopathic Insomnia has been raised above). In contrast, ASPS is found commonly in seniors. Clinical observations suggest exaggerated evening tiredness and dozing (particularly in front of TV) starts in the mid-forties and fifties, and by the sixties early morning awakening is apparent. ASPS is rare in younger individuals (unless they are suffering from diagnosed/undiag-nosed major depression where terminal insomnia is common). Thus, there is a trend from a delayed clock in youth to an advanced clock in old age; a phase-lag of "normal" bedtime becomes a phase-lead.

Whereas ASPS occurs in seniors, ISWP is more likely found in the nursing home and geriatric population. The fragmented sleep of the demented, nocturnal wanderings and Sundowner's syndrome are all suggestive of a fragmented sleep-wake cycle due to a low amplitude clock. However, non-demented nursing home residents are also obvious targets for ISWP. Indeed, in the nursing home, lack of bright light input to the circadian clock could exacerbate reduced clock amplitude as would lack of strong secondary zeitgebers. In addition to lack of light, an important health parameter would be change in visual sensitivity to light with age.

In assessing clock amplitude in the elderly, it is advantageous to measure more than one variable, e.g. core temperature nadir and circulating MLT levels. Impaired thermoregulation on the one hand, and potential pathology to the pineal gland and the circuitous pathway from the suprachiasmatic nuclei (SCN) (including autonomic innervation) on the other, makes hazardous single variable amplitude estimation in the aged.

It is well established that after puberty MLT levels reduce with age and therefore the changes summarized in Figure 2 covary with a reduction in circulating MLT levels.1 The pertinent question is: What do reduced MLT levels do, if anything, to the integrity of the SCN pacemaker? One can speculate on possible changes by observing the effects of Px on rest-activity rhythms. This is best done, not by looking primarily at mammals but by reverting to our knowledge of birds and lizards.

1 If the approach outlined here is substantially correct, it only accounts for sleep phase changes post-puberty: it implies that the relationship between the SCN and circulating MLT feedback changes dramatically after puberty. The highest levels of melatonin are found pre-puberty, yet, as far as is known, these high levels have no major influence on sleep. Perhaps the dynamics of Process S and C (19) are different in pre-puberty with the homeostatic aspect dominating.

Figure 2. Relationship between the circadian insomnias and changes to the circadian pacemaker with age in the normal population.

Figure 2. Relationship between the circadian insomnias and changes to the circadian pacemaker with age in the normal population.

Figure 3. Circadian Sleep Disorders Occurrence in Psychiatric Populations.
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