Association of Central Hypersomnia and Fatigue in Patients With Multiple Sclerosis: A Polysomnographic Study.

OBJECTIVE: To evaluate sleepiness and central hypersomnia in multiple sclerosis (MS)-associated fatigue, we performed long-term polysomnography in patients with MS and healthy controls. METHODS: Patients with MS and healthy controls completed questionnaires on sleep, fatigue, sleepiness, and depression. They underwent nocturnal polysomnography, multiple sleep latency tests, and bed rest 24-hour polysomnography. Patients were divided into 3 groups (fatigue and sleepiness, fatigue and no sleepiness, neither fatigue nor sleepiness). RESULTS: Among 44 patients with MS, 19 (43.2%) had fatigue and sleepiness, 15 (34%) had only fatigue, and 10 (22.7%) had neither fatigue nor sleepiness. Compared to 24 controls, patients with fatigue and sleepiness had higher REM sleep percentages (median [interquartile range] 20.5% [19.6-24.7] vs 18.1% [12.6-20.6]), lower arousal indexes (12.7 [7.5-17.0] vs 22.4 [14.3-34.4]), and shorter daytime mean sleep latencies (8.6 [6.3-14.3] vs 16.6 [12.6-19.5] min). Restless leg syndrome, periodic leg movements, and sleep apnea had similar frequencies between groups. Central hypersomnia was found in 10 (53%) patients with fatigue and sleepiness (narcolepsy type 2, n = 2), in 2 (13%) patients with fatigue only, and in 3 (30%) patients with neither fatigue nor sleepiness. Patients with central hypersomnia were younger and sleepier than those without hypersomnia, but had similar levels of fatigue, disability, depression, cognitive performance, and frequencies of the human leukocyte antigen DQB1*0602 genotype. The severity of fatigue increased with higher depression scores, higher sleepiness severity, and lower sleep efficacy. CONCLUSION: Central hypersomnias are frequent in MS when fatigue and sleepiness are present. Screening them through polysomnography studies is recommended.

[Obstructive sleep apnea syndrome and cognition: A review]. / Syndrome d'apnées obstructives du sommeil et cognition : une revue.

Obstructive sleep apnea syndrome (OSAS) is a sleep-related breathing disorder characterized by repetitive episodes of airflow cessation, resulting in brief arousals and intermittent hypoxemia. OSAS is associated with a number of adverse health consequences, and cognitive difficulties. The overall pattern of cognitive impairment in OSAS is complex, and research in this field is mixed. On balance, OSAS have negative effects on cognition, most likely in the domain of attention/vigilance, verbal and visual delayed long-term memory, and executive functions. A still unanswered question is whether these deficits are primarily a consequence of sleep fragmentation and/or hypoxemia, or whether they coexist independently from OSAS. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment of OSAS. No consistent effect of CPAP use on cognitive performance was evident. This may be due, in part, to variability in study design and sampling methodology across studies. Structural changes have been reported in different brain regions, particularly in hippocampus and frontal cortex. Recent evidence suggests that the OSAS-related structural changes may improve with CPAP treatment. However, one of the challenges is to interpret the findings in light of comorbid conditions that also cause neural lesions. Animal models will be specifically useful to disentangle the different potential contributors to cognitive impairment in OSAS. The purpose of this article is to provide a review of the literature on cognition and neuroimaging in OSAS patients before and after CPAP treatment. We also discuss the mechanisms that have been proposed to explain cognitive deficits in OSAS patients.

Memory monitoring and memory control in patients suffering from obstructive sleep apnoea syndrome.

Patients with obstructive sleep apnoea syndrome exhibit memory deficit. The present study looked at whether this deficit is related to impaired memory monitoring and/or memory control. Here 25 patients and 26 healthy controls performed a paired-associate learning task. After participants had made a judgement of learning for each pair and performed an initial recall test they were free to restudy any items they wished, for as long or little as they wished, within a 5-minute period. They then performed a second recall test. Monitoring and control processes were assessed on the basis of judgements of learning, item selection, and study-time allocation. In spite of their memory impairment, patients accurately predicted their recall. For the restudy phase patients preferentially selected the judged-easy items, while controls selected the judged-difficult items. However, all the participants allocated more restudy time to the judged-difficult items than to the judged-easy ones. There were no significant correlations between memory performance, metamemory processes, and clinical measures (i.e., subjective sleepiness, subjective sleep quality, anxiety, and depression scores). Results suggested that both memory monitoring and memory control were preserved in our sample of patients with obstructive sleep apnoea.

Decision making is affected in obstructive sleep apnoea syndrome.

We assessed decision making in 20 patients newly diagnosed with obstructive sleep apnoea (OSA) and 20 healthy controls with the Iowa Gambling Task (IGT), which evaluates the ability to learn to sacrifice immediate rewards in favour of long-term gains. A standard neuropsychological battery was administered. Switching scores tended to be lower in patients. Patients persisted in selecting risky decks throughout the IGT, whereas controls behaved normally. Performance was correlated with hypoxaemia. Brain regions underlying decision making may be affected by OSA-related hypoxaemia.

The improvement of movement and speech during rapid eye movement sleep behaviour disorder in multiple system atrophy.

Multiple system atrophy is an atypical parkinsonism characterized by severe motor disabilities that are poorly levodopa responsive. Most patients develop rapid eye movement sleep behaviour disorder. Because parkinsonism is absent during rapid eye movement sleep behaviour disorder in patients with Parkinson's disease, we studied the movements of patients with multiple system atrophy during rapid eye movement sleep. Forty-nine non-demented patients with multiple system atrophy and 49 patients with idiopathic Parkinson's disease were interviewed along with their 98 bed partners using a structured questionnaire. They rated the quality of movements, vocal and facial expressions during rapid eye movement sleep behaviour disorder as better than, equal to or worse than the same activities in an awake state. Sleep and movements were monitored using video-polysomnography in 22/49 patients with multiple system atrophy and in 19/49 patients with Parkinson's disease. These recordings were analysed for the presence of parkinsonism and cerebellar syndrome during rapid eye movement sleep movements. Clinical rapid eye movement sleep behaviour disorder was observed in 43/49 (88%) patients with multiple system atrophy. Reports from the 31/43 bed partners who were able to evaluate movements during sleep indicate that 81% of the patients showed some form of improvement during rapid eye movement sleep behaviour disorder. These included improved movement (73% of patients: faster, 67%; stronger, 52%; and smoother, 26%), improved speech (59% of patients: louder, 55%; more intelligible, 17%; and better articulated, 36%) and normalized facial expression (50% of patients). The rate of improvement was higher in Parkinson's disease than in multiple system atrophy, but no further difference was observed between the two forms of multiple system atrophy (predominant parkinsonism versus cerebellar syndrome). Video-monitored movements during rapid eye movement sleep in patients with multiple system atrophy revealed more expressive faces, and movements that were faster and more ample in comparison with facial expression and movements during wakefulness. These movements were still somewhat jerky but lacked any visible parkinsonism. Cerebellar signs were not assessable. We conclude that parkinsonism also disappears during rapid eye movement sleep behaviour disorder in patients with multiple system atrophy, but this improvement is not due to enhanced dopamine transmission because these patients are not levodopa-sensitive. These data suggest that these movements are not influenced by extrapyramidal regions; however, the influence of abnormal cerebellar control remains unclear. The transient disappearance of parkinsonism here is all the more surprising since no treatment (even dopaminergic) provides a real benefit in this disabling disease.

Metamemory beliefs and episodic memory in obstructive sleep apnea syndrome.

This study assessed metamemory and its role in actual episodic memory performance in 26 patients with obstructive sleep apnea syndrome and 27 healthy controls. Metamemory knowledge and memory beliefs were assessed using the Metamemory Inventory in Adulthood. Episodic memory performance was investigated with the Remember/Know paradigm. Subjective sleepiness was evaluated. Patients underwent a polysomnographic assessment. In contrast to the control group's more stable memory beliefs, patients self-assessed their memory as declining across time, and felt more anxious about their memory. There was only a modest difference between patients' self-perceptions of their memory capacities and those of the control group, but patients' actual memory performance was strongly disturbed. While the latter was significantly correlated with severity of obstructive sleep apnea, scores on the Metamemory Inventory in Adulthood scales were not correlated with physiological measures, subjective sleepiness, or episodic memory performance. Obstructive sleep apnea may affect prefrontal cortex functioning and hence the ability to assess one's own memory impairment.

Spatial and temporal memories are affected by sleep fragmentation in obstructive sleep apnea syndrome.

This study evaluated episodic memory, with an emphasis on the recollection of spatial and temporal contexts, in 28 patients suffering from obstructive sleep apnea syndrome and 29 healthy controls. Recollection was assessed by means of the R/K paradigm and the process-dissociation procedure. Attentional abilities were also evaluated. A polysomnographic assessment, including nocturnal oxygen saturation and daytime sleepiness, was conducted. Recollection was strongly disturbed in patients, the number of microarousals being the best predictor of the memory deficit. Attention was only slightly disturbed. Results suggest a link between episodic memory deficit and those areas of the brain that are particularly sensitive to sleep fragmentation, in particular the hippocampus.

Slow wave sleep and recollection in recognition memory.

Recognition memory performance reflects two distinct memory processes: a conscious process of recollection, which allows remembering specific details of a previous event, and familiarity, which emerges in the absence of any conscious information about the context in which the event occurred. Slow wave sleep (SWS) and rapid eye movement (REM) sleep are differentially involved in the consolidation of different types of memory. The study assessed the effects of SWS and REM sleep on recollection, by means of the "remember"/"know" paradigm. Subjects studied three blocks of 12 words before a 3-h retention interval filled with SWS, REM sleep or wakefulness, placed between 3 a.m. and 6 a.m. Afterwards, recognition and recollection were tested. Recollection was higher after a retention interval rich in SWS than after a retention interval rich in REM sleep or filled with wakefulness. The results suggest that SWS facilitates the process of recollection in recognition memory.