A Preliminary Fluorodeoxyglucose Positron Emission Tomography Study in Healthy Adults Reporting Dream-Enactment Behavior

Caselli, Richard J.; Chen, Kewei; Bandy, Dan; Smilovici, Oded; Boeve, Bradley F.; Osborne, David; Alexander, Gene E.; Parish, James M.; Krahn, Lois E.; Reiman, Eric M.

doi:10.1093/sleep/29.7.927

Cited by 48 publications

(27 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As summarized in the Table, cross-sectional studies in patients with iRBD have shown that a significant proportion of them have detectable abnormalities on measures of smell testing, 64–69 color vision and discrimination, 17, 69 cardiac autonomic activity, 17, 70, 71 cardiac (123)I-metaiodobenzylguanidine (MIBG) imaging, 72–74 motor and gait functioning, 17 neuropsychological testing, 75–78 electroencephalography (EEG), 79–81 transcranial sonography (TCS), 15, 22, 66, 68, 82 magnetic resonance imaging (MRI)/magnetic resonance spectroscopy (MRS), 83–86 single photon emission computed tomography (SPECT), 87, 88 dopamine transporter imaging using SPECT, 15, 16, 22, 64, 66, 89–91 fluoro-deoxyglucose positron emission tomography (FDG-PET), 92, 93 and dihydrotetrabenazine (DTBZ) PET. 94 .…”

Section: Longitudinal Assessment Of Irbd Subjects – Testing the Braakmentioning

confidence: 99%

Idiopathic REM sleep behaviour disorder in the development of Parkinson's disease

Boeve

2013

The Lancet Neurology

168

View full text Add to dashboard Cite

Summary Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with Lewy body disease (LBD) pathology in central and peripheral nervous system structures. While the etiology of PD is not fully understood, recent clinicopathologic analyses by Braak and colleagues have led to the development of a staging system of LBD pathology in the evolution of prototypical PD. This system posits a relatively predictable topography of progression of LBD pathology in the central nervous system, from olfactory structures and the medulla, which then progresses rostrally from the medulla to the pons, then midbrain/substantia nigra, then limbic, and then neocortical structures. If this topography and temporal evolution of LBD pathology indeed occur, one could hypothesize that other manifestations of LBD which reflect degeneration of olfactory and pontomedullary structures may begin many years prior to the development of prominent nigral degeneration and the associated parkinsonian features of classic PD. One such manifestation of prodromal PD is rapid eye movement (REM) sleep behavior disorder (RBD), which is a parasomnia manifested by vivid dreams associated with dream enactment behavior during REM sleep. Animal and human studies have implicated lesions or dysfunction in REM sleep and motor control circuitry in the pontomedullary structures cause RBD phenomenology, and degeneration of these structures could explain the presence of RBD years or decades prior to the onset of parkinsonism in those who develop PD. This review incorporates the rapidly growing literature on RBD and other prodromal features of PD as it pertains to the Braak staging system, and presents a framework from which many hypotheses can be (and already are being) tested. An important outcome of this framework will be to determine the natural history of RBD and associated features in the evolution to PD in the current era of no disease-modifying therapies – these natural history data will permit the development of clinical trail methodology with key measures and adequate power to detect if such therapies delay the onset or prevent the development of PD and associated morbidity.

show abstract

Section: Longitudinal Assessment Of Irbd Subjects – Testing the Braakmentioning

confidence: 99%

Idiopathic REM sleep behaviour disorder in the development of Parkinson's disease

Boeve

2013

The Lancet Neurology

168

View full text Add to dashboard Cite

show abstract

“…These findings may help further explain the clinical differences between RBD and TSD. Cerebral hypometabolism in occipitoparietal, paralimbic, and anterior temporal cortices has been reported on PET scans of patients with RBD 29,30 In a study of combat-related PTSD with patients who reported DNB, cerebral hypermetabolism was detected in brainstem regions, such as the midbrain reticular formation, locus ceruleus, and the pedunculopontine tegmentum, as well as regions involved in the threat response (e.g., amygdala, dorsal cingulate, and hippocampus) during wakefulness and REM sleep. 31 Hyperactivity in these neuroanatomical regions during REM may result in RWA and DNB, including dream enactment behaviors.…”

Section: Discussionmentioning

confidence: 99%

Trauma Associated Sleep Disorder: A Proposed Parasomnia Encompassing Disruptive Nocturnal Behaviors, Nightmares, and REM without Atonia in Trauma Survivors

Mysliwiec¹,

O’Reilly

Polchinski

et al. 2014

Journal of Clinical Sleep Medicine

101

View full text Add to dashboard Cite

S C I E N T I F I C I N V E S T I G A T I O N SD isruptive nocturnal behaviors (DNB) consisting of excessive movements, autonomic hyperarousal, abnormal vocalizations and complex motor behaviors, and nightmares which are replays of traumatic experiences are frequently reported sleep disturbances in combat veterans and trauma survivors with and without posttraumatic stress disorder (PTSD).1-6 Despite their frequent occurrence, there is no established diagnosis that accurately encompasses these sleep disturbances. Lack of diagnostic criteria is likely secondary to the discrepancy between frequent self-reported DNB and the rare occurrence of DNB in laboratory settings. 1,7,8 Thus, the exact nature of DNB in terms of their sleep stage, electromyographic (EMG) characteristics, and physiologic parameters are relatively unknown.Nightmare disorder is reported in up to 80% of patients with PTSD.9 This diagnosis does not acknowledge the presence of the DNB that trauma survivors frequently report.2,4,9 Secondary REM behavior disorder is reported to occur in patients with PTSD when REM without atonia (RWA) is present on a polysomnogram (PSG) and dream enactment behaviors are reported or are present on PSG 4,10 ; however, the onset of DNB and nightmares after an inciting traumatic event and the autonomic hyperactivity reported with trauma associated sleep disturbances are clinical and physiologic abnormalities that are not associated with REM behavior disorder (RBD).

show abstract

“…However, imaging studies show reduced blood flow and glucose metabolism in frontal, parietal, and temporal regions in RBD (Shirakawa et al, 2002;Caselli et al, 2006;Mazza et al, 2006). These areas also have reduced EEG activity during waking and NREM in RBD patients.…”

Section: Inhibition and Eeg Slowing In Rbdmentioning

confidence: 99%

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Brooks¹,

Peever²

2011

J. Neurosci.

116

View full text Add to dashboard Cite

Rapid eye movement (REM) sleep behavior disorder (RBD) is a neurological disease characterized by loss of normal REM motor inhibition and subsequent dream enactment. RBD is clinically relevant because it predicts neurodegenerative disease onset (e.g., Parkinson's disease) and is clinically problematic because it disrupts sleep and results in patient injuries and hospitalization. Even though the cause of RBD is unknown, multiple lines of evidence indicate that abnormal inhibitory transmission underlies the disorder. Here, we show that transgenic mice with deficient glycine and GABA transmission have a behavioral, motor, and sleep phenotype that recapitulates the cardinal features of RBD. Specifically, we show that mice with impaired glycine and GABA A receptor function exhibit REM motor behaviors, non-REM muscle twitches, sleep disruption, and EEG slowing-the defining disease features. Importantly, the RBD phenotype is rescued by drugs (e.g., clonazepam and melatonin) that are routinely used to treat human disease symptoms. Our findings are the first to identify a potential mechanism for RBD-we show that deficits in glycine-and GABA A -mediated inhibition trigger the full spectrum of RBD symptoms. We propose that these mice are a useful resource for investigating in vivo disease mechanisms and developing potential therapeutics for RBD.

show abstract

A Preliminary Fluorodeoxyglucose Positron Emission Tomography Study in Healthy Adults Reporting Dream-Enactment Behavior

Abstract: These preliminary findings suggest that cognitively normal persons with DEB have reduced CMRgl in brain regions known to be metabolically affected by DLB, supporting further study of DEB as a possible risk factor for the development of DLB.

Cited by 48 publications

References 48 publications

Idiopathic REM sleep behaviour disorder in the development of Parkinson's disease

Idiopathic REM sleep behaviour disorder in the development of Parkinson's disease

Trauma Associated Sleep Disorder: A Proposed Parasomnia Encompassing Disruptive Nocturnal Behaviors, Nightmares, and REM without Atonia in Trauma Survivors

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Contact Info

Product

Resources

About