Sleep abnormalities in individuals at clinical high risk for psychosis

Mayeli, Ahmad; LaGoy, Alice D.; Donati, Francesco; Kaskie, Rachel; Najibi, Seyed Morteza; Ferrarelli, Fabio

doi:10.1016/j.jpsychires.2021.03.006

Cited by 13 publications

(10 citation statements)

References 55 publications

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“…An increase in fast frequency activity may also reflect a more disrupted, fragmented sleep. Consistent with this assumption, in a recent sleep study, we found that higher gamma activity was associated with WASO in both healthy and clinical groups [26]. While in this study, we found a higher average sigma power spectra as well as higher sigma power in right frontal/prefrontal areas, a previous sleep study conducted on eight healthy individuals found a lower sigma power in two specific channels [12].…”

Section: Discussionsupporting

confidence: 90%

“…Further, the percentages of good NREM epochs for each night were as follows: Night 1: 79% ± 2% and Night 2: 79% ± 3%. NREM absolute EEG power from good channels and good epochs was then averaged across six frequency bands of interest, delta (1-4.5 Hz), theta (4.5-8 Hz), alpha (8-12 Hz), sigma (12-15 Hz), beta (15-25 Hz), and gamma (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40), and compared between nights in study participants to assess for FNE.…”

Section: Sleep Hd-eeg Data Processingmentioning

confidence: 99%

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Examining First Night Effect on Sleep Parameters with hd-EEG in Healthy Individuals

et al. 2022

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Difficulty sleeping in a novel environment is a common phenomenon that is often described as the first night effect (FNE). Previous works have found FNE on sleep architecture and sleep power spectra parameters, especially during non-rapid eye movement (NREM) sleep. However, the impact of FNE on sleep parameters, including local differences in electroencephalographic (EEG) activity across nights, has not been systematically assessed. Here, we performed high-density EEG sleep recordings on 27 healthy individuals on two nights and examined differences in sleep architecture, NREM (stages 2 and 3) EEG power spectra, and NREM power topography across nights. We found higher wakefulness after sleep onset (WASO), reduced sleep efficiency, and less deep NREM sleep (stage 3), along with increased high-frequency NREM EEG power during the first night of sleep, corresponding to small to medium effect sizes (Cohen’s d ≤ 0.5). Furthermore, study individuals showed significantly lower slow-wave activity in right frontal/prefrontal regions as well as higher sigma and beta activities in medial and left frontal/prefrontal areas, yielding medium to large effect sizes (Cohen’s d ≥ 0.5). Altogether, these findings suggest the FNE is characterized by less efficient, more fragmented, shallower sleep that tends to affect especially certain brain regions. The magnitude and specificity of these effects should be considered when designing sleep studies aiming to compare across night effects.

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Section: Discussionsupporting

confidence: 90%

Section: Sleep Hd-eeg Data Processingmentioning

confidence: 99%

Examining First Night Effect on Sleep Parameters with hd-EEG in Healthy Individuals

et al. 2022

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“…We could find only two polysomnography studies, which revealed that the UHR group presented significantly more Wake After Sleep Onset (WASO) ( 21 ) and increased sleep latency (i.e., more difficulty falling asleep) than HC ( 32 ). Zanini et al ( 32 ) did not find significant differences in the polysomnographic sleep efficiency percentages, WASO scores, and total sleep time and of UHR participants relative to controls.…”

Section: The Nature Of Sleep Disturbances In Uhr Individualsmentioning

confidence: 95%

“…We could find only one previous review that included data prior to February 2020 to examine sleep disturbances in the UHR state, with the specific goal of exploring the relationships between sleep and psychotic symptoms, functioning and quality of life (18). Some interesting new studies have emerged since then [e.g., (19)(20)(21)(22)]. This, along with the identified knowledge gaps, have motivated the present review aiming at synthetizing the existing literature to update and extend our understanding of: (1) the nature of sleep disturbances, (2) their underlying mechanisms, (3) their clinical and functional consequences, as well as (4) the prevention and intervention strategies in the at-risk for psychosis population.…”

Section: Introductionmentioning

confidence: 99%

The nature, consequences, mechanisms, and management of sleep disturbances in individuals at-risk for psychosis

et al. 2022

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There is strong evidence that sleep disturbances are commonly experienced by people with psychosis. Evidence has also shown that sleep disturbances are present since the very early stages of the disease, even during the pre-diagnostic phase. More recently, research involving young individuals at ultra-high risk (UHR) for psychosis documented frequent occurrence of sleep disturbances in this group. The very early onset of sleep disturbances in the course of psychosis has drawn attention to the possible links between sleep parameters and the risk of psychosis. To date, the nature of sleep disturbances characterizing the UHR stage remains unclear, with available studies having yielded mixed findings. In this regard, we performed this review to update the body of literature on the nature of sleep disturbances, their underlying mechanisms, their clinical and functional consequences, the prevention and intervention strategies in the at-risk for psychosis population. Our findings provided further support to the presence of disturbed sleep in UHR individuals as evidenced by subjective and objective sleep measures such as polysomnography, sleep electroencephalograms, and actigraphy. Reviewing the possible mechanisms underlying the relationship between sleep and psychosis emphasized its complex and multifactorial nature which is yet to be determined and understood. Further research is warranted to determine which facets of sleep disturbances are most detrimental to this specific population, and to what extent they can be causal factors or markers of psychosis.

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“…In many neuropsychiatric illnesses, including schizophrenia, sleep disorders and deficits in attention-related sensorimotor and cognitive integration processes are common. These disorders insidiously start to occur during the prodromal phase (McGhie & Chapman, 1961; Lunsford-Avery et al ., 2013; Manoach et al ., 2014; Zanini et al ., 2015; Mayeli et al ., 2021). Administration of the non-competitive NMDA receptor antagonist ketamine at a subanesthetic dose can, after the administration of a subanesthetic dose, induce a psychosis-relevant mental state in healthy humans (Krystal et al ., 1994; Hetem et al ., 2000; Anticevic et al ., 2015; Hoflich et al ., 2015; Rivolta et al ., 2015; Grent-’t-Jong et al ., 2018) and other species, including rodents (Chrobak et al ., 2008; Pinault, 2008; Pitsikas et al ., 2008; Ehrlichman et al ., 2009; Hakami et al ., 2009; Kocsis, 2012).…”

Section: Introductionmentioning

confidence: 99%

The psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network

Qin

Mahdavi

Bertschy

et al. 2022

Preprint

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In prodromal and early schizophrenia, disorders of attention and perception are associated with structural and chemical brain abnormalities, and with dysfunctional, highly distributed corticothalamic networks exhibiting disturbed brain rhythms. The underlying mechanisms are elusive. The non-competitive NMDA receptor antagonist ketamine simulates the symptoms of prodromal and early schizophrenia, including the disturbances in ongoing and task/sensory-related broadband gamma frequency (30-80 Hz) oscillations in corticothalamic networks. In normal healthy subjects and rodents, complex integration processes, like sensory perception, induce transient, large-scale synchronized gamma oscillations in a time window of a few hundreds of ms (200-700 ms) after the presentation of the object of attention (e.g., sensory stimulation). Our goal was to use an electrophysiological multisite network approach to investigate, in lightly anesthetized rats, the effects of a single psychotomimetic low-dose (2.5 mg/kg, subcutaneous) of ketamine on sensory stimulus-induced gamma oscillations. Ketamine transiently increased the power of baseline gamma oscillations and decreased sensory-induced gamma oscillations. In addition, it disrupted information transferability in both the somatosensory thalamus and the related cortex and decreased the stimulus-induced gamma-frequency band thalamocortical connectivity. In conclusion, the present findings support the hypothesis that NMDA receptor antagonism disrupts the transfer of perceptual information in the somatosensory cortico-thalamo-cortical system.

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Sleep abnormalities in individuals at clinical high risk for psychosis

Cited by 13 publications

References 55 publications

Examining First Night Effect on Sleep Parameters with hd-EEG in Healthy Individuals

Examining First Night Effect on Sleep Parameters with hd-EEG in Healthy Individuals

The nature, consequences, mechanisms, and management of sleep disturbances in individuals at-risk for psychosis

The psychotomimetic ketamine disrupts the transfer of late sensory information in the corticothalamic network

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