RESUMEN
STUDY OBJECTIVES: Sleep issues are common for people with neurodegenerative conditions, yet research has focused on specific aspects of sleep. While important, a more holistic approach to investigating sleep, termed "sleep health," considers sleep's positive and negative aspects. Current studies exploring sleep health have lacked a control group for reference. For the first time, this study investigated the sleep health of people living with multiple sclerosis and Huntington's disease (HD) and compared it with a community sample. METHODS: 111 people, including 43 with multiple sclerosis, 19 with HD, and 49 from a community sample, participated in this study. The data, including actigraphy, Pittsburgh Sleep Quality Index, and Epworth Sleepiness Scale, were collected as part of ongoing research studies. Seven sleep health domains were determined from the collected data, and a composite sleep health score was developed. Analysis of variance and independent t tests were performed to identify population and sex differences. RESULTS: The HD group had higher sleep regularity and lower sleep rhythmicity than the multiple sclerosis and community sample groups. The HD group had significantly less sleep duration than the multiple sclerosis group. No significant differences between the groups were observed in the sleep health composite score. Males had significantly higher sleep regularity within the HD group but significantly lower sleepiness scores in the community sample. CONCLUSIONS: These findings indicate that people with HD may experience greater variance in their wake times, therefore decreasing the consistency of being awake or asleep 24 hours apart. Understanding the mechanisms for this should be explored in people with HD. CITATION: Turner M, Griffiths M, Laws M, Vial S, Bartlett D, Cruickshank T. The multidimensional sleep health of individuals with multiple sclerosis and Huntington's disease and healthy controls. J Clin Sleep Med. 2024;20(6):967-972.
Asunto(s)
Actigrafía , Enfermedad de Huntington , Esclerosis Múltiple , Trastornos del Sueño-Vigilia , Humanos , Enfermedad de Huntington/complicaciones , Enfermedad de Huntington/fisiopatología , Masculino , Femenino , Esclerosis Múltiple/complicaciones , Esclerosis Múltiple/fisiopatología , Persona de Mediana Edad , Actigrafía/estadística & datos numéricos , Trastornos del Sueño-Vigilia/fisiopatología , Trastornos del Sueño-Vigilia/complicaciones , Adulto , Calidad del Sueño , Sueño/fisiologíaRESUMEN
Numerous studies have reported the negative impacts of poor sleep on work productivity in the general population. However, despite the known sleep issues that individuals living with neurological conditions experience, no study has explored its impact on their work productivity. Sleep health is a concept that includes multiple domains of sleep, measured with a combination of objective and subjective measures. Therefore, this study aimed to ascertain the associations between sleep health and its domains and work productivity in individuals with neurological conditions. Sleep health domains were determined through actigraphy data collected over 1 week and sleep questionnaires. Work productivity was assessed via the Work Productivity and Activity Impairment Questionnaire. A comparison of sleep health scores between demographic variables was performed using Mann-Whitney U and Kruskal-Wallis tests. Associations between the sleep health domains and work productivity were performed using linear regression models. There were no significant differences in sleep health scores between sex, smoking status, education level, employment status or any work productivity domain. Individuals with non-optimal sleep timing had greater absenteeism (22.99%) than the optimal group. Individuals with non-optimal sleep quality had an increase in presenteeism (30.85%), work productivity loss (26.44%) and activity impairment (25.81%) compared to those in the optimal group. The findings from this study highlight that self-reported sleep quality has the largest impact on work productivity. Improving individuals' sleep quality through triage for potential sleep disorders or improving their sleep hygiene (sleep behaviour and environment) may positively impact work productivity.
RESUMEN
Both motor and non-motor symptoms of Parkinson's disease (PD), a progressive neurological condition, have broad-ranging impacts on nutritional intake and dietary behaviour. Historically studies focused on individual dietary components, but evidence demonstrating ameliorative outcomes with whole-of-diet patterns such as Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) is emerging. These diets provide plenty of antioxidant rich fruits, vegetables, nuts, wholegrains and healthy fats. Paradoxically, the ketogenic diet, high fat and very low carbohydrate, is also proving to be beneficial. Within the PD community, it is well advertised that nutritional intake is associated with disease progression and symptom severity but understandably, the messaging is inconsistent. With projected prevalence estimated to rise to 1.6 million by 2037, more data regarding the impact of whole-of-diet patterns is needed to develop diet-behaviour change programmes and provide clear advice for PD management. Objectives and Methods: Objectives of this scoping review of both peer-reviewed academic and grey literatures are to determine the current evidence-based consensus for best dietary practice in PD and to ascertain whether the grey literature aligns. Results and Discussion: The consensus from the academic literature was that a MeDi/MIND whole of diet pattern (fresh fruit, vegetables, wholegrains, omega-3 fish and olive oil) is the best practice for improving PD outcomes. Support for the KD is emerging, but further research is needed to determine long-term effects. Encouragingly, the grey literature mostly aligned but nutrition advice was rarely forefront. The importance of nutrition needs greater emphasis in the grey literature, with positive messaging on dietary approaches for management of day-to-day symptoms.
RESUMEN
Personality factors have been associated with Alzheimer's disease (AD) and dementia, but they have not been examined against markers of regional brain glucose metabolism (a primary measure of brain functioning) in older adults without clinically diagnosed cognitive impairment. The relationship between personality factors derived from the five-factor model and cerebral glucose metabolism determined using positron emission tomography (PET) with [18F]-2-fluoro-2-deoxy-D-glucose (18F-FDG-PET) was examined in a cohort of 237 non-demented, community-dwelling older adults aged 60-89 years (M ± SD = 73.76 ± 6.73). Higher neuroticism and lower scores on extraversion and conscientiousness were significantly associated with decreased glucose metabolism in brain regions typically affected by AD neuropathological processes, including the hippocampus and entorhinal cortex. Furthermore, while there were significant differences between apolipoprotein E (APOE) ε4 allele carriers and non-carriers on 18F-FDG-PET results in the neocortex and other brain regions (p < 0.05), there was no significant difference between carriers and non-carriers on personality factors and no significant interactions were found between APOE ε4 carriage and personality factors on brain glucose metabolism. In conclusion, we found significant relationships between personality factors and glucose metabolism in neural regions more susceptible to AD neuropathology in older adults without clinically significant cognitive impairment. These findings support the need for longitudinal research into the potential mechanisms underlying the relationship between personality and dementia risk, including measurement of change in other AD biomarkers (amyloid and tau imaging) and how they correspond to change in personality factors. Future research is also warranted to determine whether timely psychological interventions aimed at personality facets (specific aspects or characteristics of personality factors) can affect imaging or other biomarkers of AD resulting in delay or ideally preventing the onset of the cognitive impairment.