What can explain the lack of subjective sleep satisfaction among persons with mental illness on antipsychotics with objective evidence of actual sleep?
Maybe the sedative effect of antipsychotics can make them sleep better, but can still have an effect when they wake up, and influence their subjective state of not feeling refreshed
Pulsed magnetic fields in and around delta range will not only help guide (entrain) their brains to more sound sleep, but will improve neurochemical - neuroendocrine balance and neurotransmission. Fact. Not hearsay. If one is truly interested in solutions vs. Identification of issues and more drugging... I'd be glad to discuss.
That really depends on what type of mental disorders your patients suffer from and what type of antipsychotics they have taken. In general it is a well known phenomenon that for example many patients on a psychiatric ward do complain about poor sleep and non-refreshing sleep when questionned in the morning during a ward round. Interestingly, frequently, the night nurse, who has made her rounds through the patient rooms every 2 hours, will not confirm that, but may comment that she even heard patients snoring.
We also know that for insomnia in general there is frequently an even huge discrepancy between subjective self-reports of sleep quality and for example polysomnographic recordings, indication a strong amount of sleep state misperception or paradoxical insomnia in the sleep disordered patients. We have speculated that maybe the measurement of the macrostructureof sleep with polysomnography may not fully reflect sleep quality - maybe it is the microstructure, for example the spectral composition of frequency bands, which is important how sleep is perceived subjectively.
So summarizing: we still do not know exactly, how the subjective experience of sleep is generated or what it is really dependent on - especially in mental disorders a huge proportion of subjects complains about poor sleep and the complaints have to be taken seriously even if there are no objective signs of sleep loss. I have added some work from my group relating to this issue.
What do you consider 'actual sleep' - for example was this measured with polysomnography? And when you say 'actual sleep' are you also referring to good sleep quality on the PSG? As Nele said above the antipsychotic meds may provide 'actual sleep' but the poor sleep quality (as your post title mentions) could be contributing to the subjective complaints.Studies indicate that people with depression (and some other mental illnesses) have excessive REM sleep which can cause dissatisfaction and/or poor mood and motivation.
I agree with Dieter: it largely depends on the clinically predominant features ("diagnosis") of your patient(s). But yes, "sleep matters".
I could just give my personal, yet evidence-based, perspective for
BIPOLAR DISORDERS.
I'll attach you a passage from the introduction of one of my own papers (currently under-review: please let me know in the future if interested in the final PDF including a punctual referencing - if ever accepted...) which briefly considers some aspects I hope you could find of interest.
[..."The conceptualization of BD as a disorder of cycling, possibly based on disturbances in circadian rhythms has been suggested for centuries. Reports of impaired daily rhythms in “emotional disturbances” date back to Hippocrates, Galen, Aretaeus of Cappadocia: [“…vital tone was subject to typical circadian variations”], and later Kraepelin (10). However, it was not until after the discovery of melatonin in 1958 that the link between the pineal gland (and affective disorders) anticipated by 17thcentury Cartesian theories, found scientific biological support (11). More recently, these observations have been articulated into specific hypotheses of circadian rhythms as the bases for mood disorders (12, 13). Presently, changes in sleep are included in the DSM-IV criteria for major depressive episodes (MDEs), including those associated with BD, and sleep patterns have been proposed as predictors of manic relapses in BD (14). Melatonergic modulation has been shown to be relevant in regulating circadian rhythms and sleep patterns, both in MDD (15, 16) and BD (17), and ........................"]
AND (from the discussion...):
[.... "Sleep disturbances are a core aspect of BD and may often predict subsequent manic-switch (31). .................................................. While insomnia has been reported as a major predictor of depression (33), abnormalities in sleep architecture, including disturbances of sleep consolidation, slow-wave sleep and rapid eye movement (REM) sleep are common during antidepressant treatments, suggesting sleep quality and mood state are dissociable (34, 35). ............................"]
There are many aspects of BD and sleep quality (and quantity) mutually connected. I would suggest you an excellent review by Murray et.:"Murray G, Harvey A. Circadian rhythms and sleep in bipolar disorder. Bipolar disorders. 2010; 12:459-72."
Hope this was helpful, regards, Michele Fornaro, MD.
Having that premised, considering a hypothetical BD patient experiencing your symptoms, just consider the following:
1) Not all the antipychotics are the same: the anti-Ach, anti-H1, anti-alpha1 or specific binding of D1/D2-like receptors could produce different effects in terms of sedation or sleep impairment.
2) In case of first generation antipsychotic administered without an anti-Ach drug, it may happen "akathisia" including the very disturbing, self-reported, inner tension and agitation of the patient ("psychic experience of pseudo-akathisia") which may contribute to explain why a patient with a "normal" sleep may self-report "rest-less" or poor life (including sleep) quality.
3) Quantity does not necessarily mean "quality". The patient could have a "normal" total number of hours of sleep, but a disrupted sleep architecture (e.g. REM period).
4) Most bipolar patients receiving an acute administration of antipsychotics are currently manic: they feel a reduced need for sleep but also they consider their "manic states" as 'normal" or as the optimal mood state to achieve, so that this could contribute to understand why they subjectively rate their sleep as poor: "simply because they are forced to sleep with antipsychotics!".
Yes it is well known in mental disorders (depression, bipolar disorder and schizophrenia) that subjective sleep might be worse than "objective" sleep. An hypothesis might be that our "objective" assessments (polysomno, actigraphy, ...) might be not enough accurate in this population but also in others sleep disorders without psychiatric comorbidity.
I don't know if it is replicated yet, but an actigraphic study in Bipolar disorder found that actigraphic measures in bipolar patients were independent of the type and dose of concurrent psychotropic medication.
Bipolar Disord. 2008 Mar;10(2):256-65.
Circadian activity rhythm abnormalities in ill and recovered bipolar I disorder patients.
Had you not added "...with objective evidence of actual sleep" I would have proposed a hypothesis of mine concerning people with ASD. Their sleeplessness seems to be pretty well documented but not explained. I read an article about sleep problems of the elderly which are attributed to changes in the retina which block relevant parts of the light specter. Subsequently, in the daytime, the pineapple gland is under-stimulated and the production of melatonin is insufficiently suppressed, thereby hampering the sleep-cycle. Combine this mechanism with the equally well documented fact that many people with ASD avoid sunlight: eureka!
Who knows which other psychiatric syndromes (or indeed psychotropic drugs) tend to stimulate sufferers from avoiding sunlight?
Perhaps continued daytime sedation holds a key explanation for the lack of subjective sleep satisfaction. Interesting answers overall, but what is the way out in managing these group of patients (schizophrenia, bipolar disorders and depression). Do we make them wake up earlier? reduce their dosage? switch over to atypicals?
Indeed it wouldn't surprise me at all if exposure to sunlight was diminished among the patient groups you mention, as is my hypothesis for Asd-patients. So step one: let's test this hypothesis by simply counting the number of minutes patients are in sunlit rooms (if possible taking account of time spent in sunlit parts of rooms) and see if there is a correlation with (subjective) sleeping problems. One should take care to correct for intervening variables, indicative of a disturbed sleep-cycle in order to rule out spurious correlations of this kind. (People sleeping in the daytime behind closed curtains probably don’t sleep as well during the night, but attributing this to lack of sunlight would be stretching it, to say the least.) In case there is indeed evidence for this idea (probably in some measure specific to various patient groups) one can consider measures. It’s my understanding glass is available which filters out the ‘unpleasant’ aspects of daylight but not the part of the specter which influences melatonin production/release. Daylight lamps seem to have have similar qualities. Again research is necessary to get beyond speculation (which sometimes seems the main pastime here on ResearchGate).