The coeruleus/subcoeruleus complex in idiopathic rapid eye movement sleep behaviour disorder

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Abstract

Idiopathic rapid eye movement sleep behaviour disorder is characterized by nocturnal violence, increased muscle tone during rapid eye movement sleep and the lack of any other neurological disease. However, idiopathic rapid eye movement sleep behaviour disorder can precede parkinsonism and dementia by several years. Using 3 T magnetic resonance imaging and neuromelanin-sensitive sequences, we previously found that the signal intensity was reduced in the locus coeruleus/subcoeruleus area of patients with Parkinson's disease and rapid eye movement sleep behaviour disorder. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex with neuromelanin-sensitive imaging in 21 patients with idiopathic rapid eye movement sleep behaviour disorder and compared the results with those from 21 age- and gender-matched healthy volunteers. All subjects underwent a clinical examination, motor, cognitive, autonomous, psychological, olfactory and colour vision tests, and rapid eye movement sleep characterization using video-polysomnography and 3 T magnetic resonance imaging. The patients more frequently had preclinical markers of alpha-synucleinopathies, including constipation, olfactory deficits, orthostatic hypotension, and subtle motor impairment. Using neuromelanin-sensitive imaging, reduced signal intensity was identified in the locus coeruleus/subcoeruleus complex of the patients with idiopathic rapid eye movement sleep behaviour. The mean sensitivity of the visual analyses of the signal performed by neuroradiologists who were blind to the clinical diagnoses was 82.5%, and the specificity was 81% for the identification of idiopathic rapid eye movement sleep behaviour. The results confirm that this complex is affected in idiopathic rapid eye movement sleep behaviour (to the same degree as it is affected in Parkinson's disease). Neuromelanin-sensitive imaging provides an early marker of non-dopaminergic alpha-synucleinopathy that can be detected on an individual basis.

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A putative flip-flop switch for control of REM sleep.

Jun Lu, David Sherman, Marshall Devor … (2006)

Rapid eye movement (REM) sleep consists of a dreaming state in which there is activation of the cortical and hippocampal electroencephalogram (EEG), rapid eye movements, and loss of muscle tone. Although REM sleep was discovered more than 50 years ago, the neuronal circuits responsible for switching between REM and non-REM (NREM) sleep remain poorly understood. Here we propose a brainstem flip-flop switch, consisting of mutually inhibitory REM-off and REM-on areas in the mesopontine tegmentum. Each side contains GABA (gamma-aminobutyric acid)-ergic neurons that heavily innervate the other. The REM-on area also contains two populations of glutamatergic neurons. One set projects to the basal forebrain and regulates EEG components of REM sleep, whereas the other projects to the medulla and spinal cord and regulates atonia during REM sleep. The mutually inhibitory interactions of the REM-on and REM-off areas may form a flip-flop switch that sharpens state transitions and makes them vulnerable to sudden, unwanted transitions-for example, in narcolepsy.

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Rapid-eye-movement sleep behaviour disorder as an early marker for a neurodegenerative disorder: a descriptive study.

Mónica Serradell, Francesc Valldeoriola, Maria Martí … (2006)

Rapid-eye-movement (REM) sleep behaviour disorder (RBD) is a parasomnia characterised by dream-enacting behaviours related to unpleasant dreams and loss of muscle atonia during REM sleep. RBD may be idiopathic or associated with neurological disease. Available data suggest that in some cases RBD might be the initial manifestation of a neurodegenerative disease. We sought to determine the frequency and nature of neurological disorders developing in patients diagnosed with idiopathic RBD at our sleep centre. We retrospectively assessed 44 consecutive patients (39 men and five women with a mean age of 74 years), with at least 2 years of clinical follow-up after a diagnosis of idiopathic RBD, through a detailed clinical history, complete neurological examination, rating scales of parkinsonism, and neuropsychological tests. 20 (45%) patients developed a neurological disorder after a mean of 11.5 years from the reported onset of RBD and a mean follow-up of 5.1 years from the diagnosis of idiopathic RBD at our sleep centre. Emerging disorders were Parkinson's disease in nine patients, dementia with Lewy bodies in six, multiple system atrophy with predominant cerebellar syndrome in one, and mild cognitive impairment in four in whom visuospatial dysfunction was prominent. Patients with longer clinical follow-up developed a neurological disease (OR 1.512, 95% CI 1.105-2.069; p=0.010). Our study indicates that in people presenting to sleep centres, RBD often antedates the development of a neurodegenerative disorder. Close follow-up of patients with idiopathic RBD could enable early detection of neurodegenerative disease. This finding may be of great interest when early effective treatment strategies and neuroprotective drugs become available.

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Chronic behavioral disorders of human REM sleep: a new category of parasomnia.

Carlos H. Schenck, Scott R. Bundlie, Milton Ettinger … (1986)

Four men, aged 67-72 years, had 4-month to 6-year histories of injuring themselves or their spouses with aggressive behaviors during sleep, often during attempted dream enactment. A 60-year-old woman had disruptive though nonviolent sleep and dream behaviors. Polysomnography did not detect seizures but did document REM sleep pathology with variable loss of chin atonia, extraordinarily increased limb-twitch activity, and increased REM ocular activity and density. A broad range of REM sleep behaviors was recorded on videotape, including stereotypical hand motions, reaching and searching gestures, punches, kicks, and verified dream movements. Stage 3-4 slow wave sleep was elevated for age in all patients. NREM sleep was devoid of harmful behaviors, although three men had periodic myoclonus. There was no associated psychiatric disorder, whereas serious neurologic disorder was closely associated in four cases: olivo-ponto-cerebellar degeneration, Guillain-Barré syndrome, subarachnoid hemorrhage, and an atypical dementia. Two patients had immediate and lasting sleep behavioral suppression induced by clonazepam, and another patient had the same response with desipramine. All instances of drug discontinuation prompted immediate relapse. In four cases there was associated dream hyperactivity, which resolved with behavioral control. These REM sleep neurobehavioral disorders constitute another category of parasomnia, replicate findings from 21 years ago in cats receiving pontine tegmental lesions, and offer additional perspectives on human behavior, neurophysiology, pharmacology, and dream phenomenology.