Sleep Mechanisms and Pathophysiology: Some Clinical Implications of the Reciprocal Interaction Hypothesis of Sleep Cycle Control

Ja, Hobson

doi:10.1097/00006842-198305000-00005

Cited by 48 publications

(5 citation statements)

References 22 publications

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“…Reynolds and Kupfer [1987] posited that redistribution of REM time to later portions of the sleep period, combined with relatively higher phasic REM activity, may explain patient reports of increased dreaming or nightmares while receiving antidepressants. Finally, basic investigations of the neurobiological mechanisms regulating sleep implicate several neurotransmitter systems in the control of REM onset and offset [Hobson, 1983] (Fig. 1).…”

Section: Tricyclic Antidepressant Compounds (Tcas)mentioning

confidence: 99%

Depression, sleep physiology, and antidepressant drugs

et al. 2001

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This review summarizes current findings regarding effects of antidepressant compounds on sleep architecture and interprets their clinical relevance. Effects of the major classes of antidepressant drugs on sleep properties are presented, with the antidepressant compounds organized into categories based primarily on their putative mechanism of action. The majority of antidepressant compounds, across several different categories, exhibit robust suppression of REM sleep. Others, such as bupropion and nefazodone, lack REM suppressant effects. Such findings support the idea that critical neurochemical mechanisms involved in the regulation of discrete sleep stages can be elucidated by means of polysomnographic investigations utilizing pharmacologically targeted agents. Clinicians have appreciated the importance of antidepressant drug effects on sleep when considering therapeutic options for patients. While such decisions in the past were based on empirical observations, an increasing amount of information regarding specific effects of different antidepressant drugs on sleep continuity and sleep architecture is available. Thus, clinicians may choose to consider profiles of sleep effects for different antidepressant drugs in the initial selection of an antidepressant compound.

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Section: Tricyclic Antidepressant Compounds (Tcas)mentioning

confidence: 99%

Depression, sleep physiology, and antidepressant drugs

et al. 2001

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“…There is some evidence for the reciprocal interaction hypothesis published by Hobson [23], postulating a subtle aminergic and cholinergic interaction during REM sleep. If these cholinergic mechanisms might influence sleep and dreaming of MG patients is still not known.…”

Section: Introductionmentioning

confidence: 96%

“…The main symptom is an abnormal and fluctuating weakness of certain voluntary muscles requiring therapy with anticholinesterase inhibi- [21][22][23][24][25][26][27] Happe/Klösch/Zeitlhofer tors [1]. Acetylcholine is also an important neurotransmitter in the central nervous system: cholinergic neurons are located in the brainstem, as a main part of the ascending reticular activating system and in the cerebrum (e.g.…”

Section: Introductionmentioning

confidence: 99%

Perception of Dreams and Subjective Sleep Quality in Patients with Myasthenia gravis

2004

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Objectives: Recent reports have led to the hypothesis of a central nervous system involvement in myasthenia gravis (MG). As the central cholinergic system also plays an important role in sleep/wake rhythms and in the regulation of REM sleep, sleep perception and dreaming may be altered in MG patients. Patients and Methods: Seventeen consecutive patients with MG (mean age 49.5 ± 13.6 years) and 14 healthy controls (mean age 50.5 ± 16.0 years) were investigated by means of the Self-Rating Depression Scale, Self-Rating Anxiety Scale, Quality of Life Index, Pittsburgh Sleep Quality Index, and Epworth Sleepiness Scale as well as a self-rating questionnaire for sleep and awakening quality and dreaming for 2 weeks. Results: Subjective sleep and awakening quality and sleep efficiency were reduced (p < 0.05), and the number of nocturnal awakenings (p = 0.02) as well as dream recall frequency (p = 0.02) were increased in patients with MG. Patients reported more often body-related and tactile sensations during dreaming (p = 0.001) and dreamed less often visually (p = 0.04). Dream content, emotions, and dream sources did not differ between both groups. Whereas the number of awakenings was related to dream recall frequency in healthy controls, no such a relationship was found in the patient group. Conclusion: There is no clear evidence for the arousal-retrieval model of dream recall in patients with MG, but more for the continuity hypothesis of dreaming. Other factors such as the functional state of the brain, possibly related to a central cholinergic involvement in MG or its anticholinesterase treatment, may be important in explaining dream recall in this patient group.

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“…Furthermore, when aggravated by age or obesity, the obstructive sleep apnea may become gravely disabling and even fatal ( 194 ). The understanding of sleep disorders may be informed by a pathophysiological approach that integrates clinical and basic biological science ( 195 ). For the mind–brain integrationist this—and other sleep disorders—provide an interdisciplinary bridge for neurologists, psychiatrists and internists.…”

Section: Discussionmentioning

confidence: 99%

Minds and Brains, Sleep and Psychiatry

Hobson

Gott

Friston

2020

Psychiatr. res. clin. pract.

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Objective This article offers a philosophical thesis for psychiatric disorders that rests upon some simple truths about the mind and brain. Specifically, it asks whether the dual aspect monism—that emerges from sleep research and theoretical neurobiology—can be applied to pathophysiology and psychopathology in psychiatry. Methods Our starting point is that the mind and brain are emergent aspects of the same (neuronal) dynamics; namely, the brain–mind. Our endpoint is that synaptic dysconnection syndromes inherit the same dual aspect; namely, aberrant inference or belief updating on the one hand, and a failure of neuromodulatory synaptic gain control on the other. We start with some basic considerations from sleep research that integrate the phenomenology of dreaming with the neurophysiology of sleep. Results We then leverage this treatment by treating the brain as an organ of inference. Our particular focus is on the role of precision (i.e., the representation of uncertainty) in belief updating and the accompanying synaptic mechanisms. Conclusions Finally, we suggest a dual aspect approach—based upon belief updating (i.e., mind processes) and its neurophysiological implementation (i.e., brain processes)—has a wide explanatory compass for psychiatry and various movement disorders. This approach identifies the kind of pathophysiology that underwrites psychopathology—and points to certain psychotherapeutic and psychopharmacological targets, which may stand in mechanistic relation to each other.

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Sleep Mechanisms and Pathophysiology: Some Clinical Implications of the Reciprocal Interaction Hypothesis of Sleep Cycle Control

Cited by 48 publications

References 22 publications

Depression, sleep physiology, and antidepressant drugs

Depression, sleep physiology, and antidepressant drugs

Perception of Dreams and Subjective Sleep Quality in Patients with Myasthenia gravis

Minds and Brains, Sleep and Psychiatry

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