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The Relationship Between Cognitive Impairments and Sleep Quality Measures in Persistent Insomnia Disorder
STUDY OBJECTIVES: Persistent insomnia disorder (pID) is linked to neurocognitive decline and increased risk of Alzheimer’s Disease (AD) in later life. However, research in this field often utilizes self-reported sleep quality data - which may be biased by sleep misperception - or uses extensive neur...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10319274/ https://www.ncbi.nlm.nih.gov/pubmed/37408565 http://dx.doi.org/10.2147/NSS.S399644 |
Sumario: | STUDY OBJECTIVES: Persistent insomnia disorder (pID) is linked to neurocognitive decline and increased risk of Alzheimer’s Disease (AD) in later life. However, research in this field often utilizes self-reported sleep quality data - which may be biased by sleep misperception - or uses extensive neurocognitive test batteries - which are often not feasible in clinical settings. This study therefore aims to assess whether a simple screening tool could uncover a specific pattern of cognitive changes in pID patients, and whether these relate to objective aspect(s) of sleep quality. METHODS: Neurocognitive performance (Montreal Cognitive Assessment; MoCA), anxiety/depression severity, and subjective sleep quality (Pittsburgh Sleep Quality Index: PSQI; Insomnia Severity Index: ISI) data were collected from 22 middle-aged pID patients and 22 good-sleepers. Patients underwent overnight polysomnography. RESULTS: Compared to good-sleepers, patients had lower overall cognitive performance (average: 24.6 versus 26.3 points, Mann–Whitney U = 136.5, p = <0.006), with deficits in clock drawing and verbal abstraction. In patients, poorer overall cognitive performance correlated with reduced subjective sleep quality (PSQI: r(42) = −0.47, p = 0.001; and ISI: r(42) = −0.43, p = 0.004), reduced objective sleep quality (lower sleep efficiency: r(20) = 0.59, p = 0.004 and less REM-sleep: r(20) = 0.52, p = 0.013; and increased sleep latency: r(20) = −0.57, p = 0.005 and time awake: r(20) = −0.59, p = 0.004). Cognitive performance was not related to anxiety/depression scores. CONCLUSION: Using a simple neurocognitive screening tool, we found that pID patients showed cognitive deficiencies that related to both subjective/self-reported and objective/polysomnographic measures of sleep quality. Furthermore, these cognitive changes resembled those seen in preclinical non-amnestic AD, and thus could indicate incumbent neurodegenerative processes in pID. Interestingly, increased REM-sleep was correlated with better cognitive performance. However, whether REM-sleep is protective against neurodegeneration requires further investigation. |
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