Considering the association of sleep disturbance and fatigue in multiple sclerosis (MS), we investigated the presence of sleep disturbances that may be related to fatigue by using objective and subjective measures. We included 27 MS patients with fatigue, 10 MS patients without fatigue and 13 controls. The Pittsburgh sleep quality index score showed significant differences between patient groups and controls. Beck depression inventory scores were significantly higher in fatigued than non-fatigued patients. Comparison of patient groups and controls revealed significant differences for time in bed, sleep efficiency index, sleep continuity index, wake time after sleep onset, total arousal index and periodic limb movement arousal index. Our study confirms that MS causes sleep fragmentation in terms of both macro and microstructure. Fatigue in MS could be partially explained by disruption of sleep microstructure, poor subjective sleep quality and depression.
Sleep disturbances and daytime sleepiness are well-known phenomena in Parkinson's disease (PD). Fifteen previously untreated PD patients underwent clinical evaluation, subjective sleep evaluation and polysomnographic evaluation (PSG) before and after a treatment period of mean 8+/-3.1 months with dopaminergic drugs. Both mean Unified Parkinson's Disease Rating Scale (UPDRS) total score and mean subset III of the UPDRS were significantly improved with dopaminergic treatment. PSG revealed that administration of dopaminergic drugs resulted in significant increase in mean percentage of stages 1 and 2. The mean Epworth Sleepiness Scale (ESS) score was significantly increased and mean Multiple Sleep Latency Test (MSLT) score was significantly decreased after dopaminergic treatment indicating subjective and objective daytime sleepiness. The differences in MSLT scores were best explained by a higher dose of L-dopa, whereas other variables such as disease duration, treatment duration, Hoehn and Yahr stage, sleep efficiency index or dopamine agonists did not increase the significance. In contrast, any of the variables appeared to explain ESS score variability. This study demonstrates that daytime sleepiness is not present in untreated patients but emerges later during dopaminergic treatment. Total daily L-dopa dose is predictive of objective daytime sleepiness. Furthermore, subjective assessment of sleepiness may cause underestimation of the severity of daytime sleepiness.
Morning headache is accepted as part of clinical findings of obstructive sleep apnoea syndrome (OSAS). The prevalence of morning headache is at variable levels from 18% to 74% in patients with OSAS. However, there is controversy over the association of morning headache and OSAS. We studied morning headache prevalence and characteristics in 101 controls with apnoea-hypnoea index (AHI) < 5 and 462 OSAS patients with AHI > or = 5. Morning headache was reported by only nine (8.9%) subjects in a control group compared with 156 (33.6%) of OSAS patients (P < 0.01). Morning headache prevalence was significantly higher in severe and moderate OSAS groups. AHI was significantly higher in OSAS patients with morning headache compared with patients without morning headaches. Oxygen saturation nadir during rapid eye movement and non-rapid eye movement sleep as well as mean oxygen saturation value during total sleep time were also found to be significantly lower in morning headache group. However, none of the sleep parameters was found to be determinants of morning headache. Morning headache was more frequently reported by patients of female gender and with primary headache history. Morning headache was totally resolved in 90% of patients treated with nasal continuous positive airway pressure. The history of OSAS should be considered in the differential diagnosis of morning headache.
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