Cognitive impairment is a frequent feature of rapid eye movement sleep behavior disorder (RBD). The cognitive profile of RBD patients is heterogeneous, with impairments in attention, executive functions, episodic memory, and visuospatial abilities. Moreover, over 50% of RBD patients meet the diagnostic criteria for mild cognitive impairment (MCI). Although a comprehensive neuropsychological assessment remains the most sensitive way to detect MCI, three cognitive screening tests have been validated in RBD. The Montreal Cognitive Assessment was found to be the most appropriate screening test for detecting MCI in RBD. In addition RBD in Parkinson’s disease may be a risk factor for MCI and dementia.
相似文献Parasomnia Overlap Disorder (POD) was described and named in 1997 with a series of 33 cases of rapid eye movement (REM) sleep behavior disorder (RBD) combined with a disorder of arousal from non-rapid eye movement (NREM) sleep (sleepwalking, sleep terrors) that emerged idiopathically or symptomatically with neurological and other disorders. POD is a subtype of RBD in the International Classification of Sleep Disorders Diagnostic and Coding Manual, second edition (ICSD-2). An updated classification of POD also includes subclinical RBD-NREM parasomnia, RBD-sleep-related eating disorder, RBD-sexsomnia, RBD-rhythmic movement disorder, and status dissociatus (SD), which is another subtype of RBD in the ICSD-2. Similar to POD, a core feature of SD is sleep motor-behavioral dyscontrol, with release of dream-related behaviors suggestive of RBD, but with nearly continuous ambiguous polygraphic sleep precluding the identification of NREM/REM sleep states. SD exemplifies extreme state dissociation. SD is always a symptomatic disorder, and is causally associated with a broad range of neurologic disorders, often with thalamic, limbic, striatal, and pontine involvement. The parasomnia behaviors associated with POD and SD — typical RBD behaviors — can often be controlled with bedtime clonazepam therapy, including the abnormal dreaming.
相似文献Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). The neuronal dysfunctions responsible for RBD are not known. In the present review, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD. We propose that RBD appears based on a specific degeneration of PS-on glutamatergic neurons localized in the caudal pontine sublaterodorsal tegmental nucleus or the glycinergic/GABAergic premotoneurons localized in the medullary ventral gigantocellular reticular nucleus.
相似文献The basal forebrain (BF) plays an important role in regulating cortical activity and sleep/wake states. Both cholinergic and non-cholinergic neurons of the BF project to the cerebral cortex and hippocampus, whereas the hypothalamus and brainstem nuclei are mostly innervated by non-cholinergic BF neurons. Neurons in the BF show various discharge profiles in relation to cortical activity and behavioral states and are differentially modulated by neurotransmitters of other sleep/wake regulatory neurons. Recent technical advances have made it possible to correlate discharge profiles of single BF neurons during sleep/wake states with their neurochemical phenotypes, and to make selective lesions of certain cell types. The goal of this review is to summarize the current knowledge of the anatomy and sleep/wake regulatory functions of cholinergic and non-cholinergic BF neurons. We will first review the anatomical heterogeneity of BF neurons, and then discuss recent evidence for the firing patterns of BF cholinergic and non-cholinergic neurons during natural sleep–wake patterns, and finally, discuss their roles in sleep homeostasis. It is proposed that through different neurotransmitters, projections, and state-regulated activity, the cholinergic and non-cholinergic BF neurons collectively and differently regulate cortical activity and sleep-wake states.
相似文献Rapid eye movement (REM) sleep behavior disorder (RBD) and hypnagogic hallucinations are salient symptoms of abnormal and dissociated REM sleep that are frequently associated in serious neurological diseases. RBD is a strong, independent risk factor for hallucinations in narcolepsy (odds ratio: 4.3) and in Parkinson’s disease (odds ratio: 2.7). In Parkinson’s disease, RBD also predicts incident hallucinations and psychosis in prospective cohorts. Status dissociatus (a mixture of hallucinations, RBD, and dissociated sleep-wake states) is observed in patients with Guillain-Barré when hallucinating, but also in Lewy bodies dementia, delirium tremens, fatal familial insomnia, and Morvan’s chorea. This co-occurrence of RBD and visual hallucinations suggests a common, extensive lesion within REM sleep executive systems.
相似文献Rapid eye movement sleep behavior disorder (RBD) frequently occurs in synucleinopathies including multiple system atrophy, Parkinson’s disease, and dementia with Lewy bodies despite the clinical course of RBD being different between these disorders. Comparatively, the existence of RBD symptoms is relatively rare in patients with progressive supranuclear palsy, a tauopathy showing atypical parkinsonism compared with Parkinson’s disease. Moreover, in patients with Alzheimer’s disease, which is another tauopathy, RBD symptoms are less frequent than dementia with Lewy bodies, although both disorders share commonalities in terms of the existence of cortical dementia. Thus, RBD is thought to be relatively specific to synucleinopathies.
相似文献Economo observed in 1930 that many cases of lethargy begin with a severe insomnia and fever followed by a long-lasting hypersomnia. We confirmed this evidence in animal cases where chemical lesions of the preoptic region resulted in severe insomnia accompanied with fever. Moreover, a subsequent pharmacological inhibition of neuronal activity of the posterior ventrolateral hypothalamus caused transient hypersomnia in these insomniac animals. However, vigilance states of the experimental animals returned to normal after several weeks, suggesting that the irreversible Economo’s lethargy may be due to the damage of passing fibers in the ventral hypothalamus. Similarly, chemical lesions of neurons of the midbrain reticular formation did not induce coma nor hypersomnia, which is inconsistent with lesion studies reported by Lindsley et al. using electrolytic coagulation. This fact further supports the importance of passing fibers in the midbrain. In addition, Mauthner in 1890 observed hypersomnia and abnormal eye movements in lethargic patients infected by “nona”, suggesting the implication of the periaqueductal gray in the vicinity of the 3rd nerve. We confirmed this hypothesis: hypersomnia was accompanied by a significant increase in REM sleep after chemical inactivation of a small part of the ventrolateral periaqueductal gray and dorsal portion of the subjacent reticular formation. On the other hand, removal of the tele- and di-encephalon caused an irreversible coma and abolished the daily rhythm of REM. This state of sleep is also regulated by forebrain structures and internal clocks in the suprachiasmatic nucleus.
相似文献Rapid eye movement sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment behavior during rapid eye movement sleep, which is generally related to damage of pontomedullary structures. Idiopathic RBD is a well-established risk factor for neurodegenerative disease; at least 40-65% of patients with idiopathic RBD will develop a defined neurodegenerative phenotype over 10 years. This is almost always a “synucleinopathy” (Parkinson’s disease, dementia with Lewy bodies, or multiple system atrophy). Often, patients develop a syndrome with overlapping parkinsonism and cognitive impairment. The ability of RBD to predict disease has major implications for development of neuroprotective therapy, by providing a high-risk prodromal group for neuro-protective trials. In addition, it allows testing of other predictive markers of neurodegeneration. Recent prospective studies found that idiopathic RBD patients with abnormal olfaction at baseline had a 65% 5-year risk of developing neurodegenerative disease, compared with a 14% risk in those with normal olfaction. Those with abnormal color vision had a 74% risk of neurodegenerative disease compared with 26% in those with normal vision. Additionally, neuroimaging markers of the sub-stantia nigra including dopaminergic functional imaging and transcranial ultrasound have been able to predict imminent development of defined neurodegenerative disease in RBD, although sensitivity and lead time have not been established. Future studies will continue to expand the list of predictive markers of neurodegeneration and will better define specificity, sensitivity, and lead time of prodromal markers.
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