Affective Prosody and Depression After Stroke: A Pilot Study.

BACKGROUND AND PURPOSE: Poststroke depression (PSD) is a frequent complication of stroke with detrimental consequences in terms of quality of life and functional outcomes. In individuals with major depression, several studies have demonstrated an alteration of affective prosody. The aim of this study is to identify prosodic markers that may be predictive of PSD. METHODS: Patient voices were recorded at baseline and 3 months after stroke. We extracted prosodic parameters, including fundamental frequency, percentage of voice breaks, and shimmer. Depression and anxiety symptoms were assessed 3 months later. RESULTS: Among the 49 patients included in the study, 22.5% developed PSD 3 months after stroke. A significant decrease was observed concerning the fundamental frequency among patients who developed PSD. Discriminant analysis demonstrated that initial voice breaks coupled with shimmer are strongly predictive of subsequent PSD. CONCLUSIONS: Early alterations of affective prosody are associated with a higher risk of PSD 3 months after a stroke. This new physiological approach overcomes traditional barriers associated with clinical instruments and contributes to the prediction of this disorder.

Mood Influences the Concordance of Subjective and Objective Measures of Sleep Duration in Older Adults.

OBJECTIVE/BACKGROUND: Sleep plays a central role in maintaining health and cognition. In most epidemiologic studies, sleep is evaluated by self-report questionnaires but several reports suggest that these evaluations might be less accurate than objective measures such as polysomnography or actigraphy. Determinants of the discrepancy between objective and subjective measures remain to be investigated. The aim of this pilot-study was to examine the role of mood states in determining the discrepancy observed between objective and subjective measures of sleep duration in older adults. PATIENTS/METHODS: Objective sleep quantity and quality were recorded by actigraphy in a sample of 45 elderly subjects over at least three consecutive nights. Subjective sleep duration and supplementary data, such as mood status and memory, were evaluated using ecological momentary assessment (EMA). RESULTS: A significant discrepancy was observed between EMA and actigraphic measures of sleep duration (p < 0.001). The magnitude of this difference was explained by the patient's mood status (p = 0.020). No association was found between the magnitude of this discrepancy and age, sex, sleep quality or memory performance. CONCLUSION: The discrepancy classically observed between objective and subjective measures of sleep duration can be explained by mood status at the time of awakening. These results have potential implications for epidemiologic and clinical studies examining sleep as a risk factor for morbidity or mortality.

Circadian sleep/wake rhythm abnormalities as a risk factor of a poststroke apathy.

BACKGROUND: Poststroke apathy affects 19-55% of patients following stroke and has a negative impact on functional recovery, general health, and quality of life, as well as being a source of significant burden for caregivers. AIMS: A major clinical issue is the delayed diagnosis of poststroke apathy, and so the aim of our study is to evaluate the relationship between early poststroke alterations of circadian rhythms of sleep/wake cycles and the occurrence of poststroke apathy. METHODS: Forty-six patients with a recent magnetic resonance imaging confirmed stroke were included. Main exclusion criteria were a mild to severe disability impeding home discharge from the hospital and the presence of apathy or dementia before stroke. Cerebrovascular lesions were evaluated by magnetic resonance imaging. At hospital discharge, an actigraph was used to measure patient's global activity as well as parameters of circadian rhythmicity (relative amplitude, interdaily stability, intradaily variability) and sleep (sleep duration, sleep efficiency, fragmentation index) over seven-days. Apathy was assessed at hospital discharge as well as at three-months using the Apathy Inventory and the Lille Apathy Rating Scale. RESULTS: Of the 46 patients evaluated, 10 (22%) showed apathy three-months after stroke (median Apathy Inventory = 4·5). Before inclusion, these 10 subjects did not differ significantly from other patients concerning their sleep and, at inclusion, they did not differ concerning apathy, anxiety, depression, or cognitive and functional abilities. However, actigraphy measured at discharged identified significant alterations of sleep (P < 0·005). Future poststroke apathy patients exhibited a decrease in sleep efficiency (actual sleep time expressed as a percentage of time in bed) and an increase in the fragmentation index (degree of fragmentation during the sleep period) at three-months. No association was observed between poststroke apathy and the characteristics of cerebrovascular lesions (stroke location, extent of leucoencephalopathy, number of lacunes and microbleeds). CONCLUSION: These results indicate that early poststroke alterations of sleep/wake circadian rhythms--easily evaluated by actigraphy--are associated with a higher risk of poststroke apathy at three-months. In terms of clinical outcomes, our results provide targets for very early identification of patients at risk to develop apathy after stroke and for assessing when to start specific therapy to optimize rehabilitation efficiency.