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PubMed2006

Rapid eye movement sleep behavior disorder and potassium channel antibody-associated limbic encephalitis.

Of six patients registered in our center with nonparaneoplastic limbic encephalitis associated with antibodies to voltage-gated potassium channels, the five men had rapid eye movement sleep behavior disorder (RBD) coincident with voltage-gated potassium channel antibody-associated limbic encephalitis onset. In three patients, immunosuppression resulted in resolution of RBD in parallel with remission of the limbic syndrome. RBD persisted in two patients with partial resolution of the limbic syndrome. Our findings suggest that RBD is frequent in the setting of voltage-gated potassium channel antibody-associated limbic encephalitis and can be related to autoimmune-mediated mechanisms. In addition, these observations suggest that impairment of the limbic system may play a role in the pathogenesis of RBD.

Aged↗
PubMed2004

Review of rapid eye movement behavior sleep disorders.

The spectrum of rapid eye movement behavior disorders (RBD) spans various age groups, with the greatest prevalence in elderly men. Major diagnostic features include harmful or potentially harmful sleep behaviors that disrupt sleep continuity and dream enactment during rapid eye movement sleep. In RBD patients, the polysomnogram during rapid eye movement sleep demonstrates excessive augmentation of chin electromyogram or excessive chin or limb phasic electromyogram twitching. RBD may be associated with various neurodegenerative disorders, such as multiple system atrophy, Parkinson's disease, and dementia with Lewy bodies. Other co-morbid conditions may include narcolepsy, agrypnia excitata, sleepwalking, and sleep terrors. RBD is hypothesized to be caused by primary dysfunction of the pedunculo-pontine nucleus or other key brainstem structures associated with basal ganglia pathology or, alternatively, from abnormal afferent signals in the basal ganglia leading to dysfunction in the midbrain extrapyramidal area/ pedunculo-pontine nucleus regions.

Adolescent↗
PubMed2002

Presumed rapid eye movement behavior disorder in Machado-Joseph disease (spinocerebellar ataxia type 3).

Rapid eye movement behavior disorder (RBD) is a recently recognized sleep disorder in which patients are occasionally not paralyzed during the dream portions of sleep. When not idiopathic, this state has been associated primarily with parkinsonian conditions but also with a small number of medications and other neurodegenerative disorders. Dopamine deficiency may play a role in some patients. This report describes the occurrence of a syndrome that appears to be RBD in 6 of 7 patients followed with Spinocerebellar ataxia type 3 (Machado-Joseph disease). Polysomnography was normal in 1 patient. Two of these patients had had single photon emission computed tomographic imaging of the dopamine transporter 1 year previously.

Adult↗
PubMed2005

Rapid eye movement-related disordered breathing: clinical and polysomnographic features.

OBJECTIVE: The existence of a rapid eye movement (REM)-specific sleep-disordered breathing (SDB) has been suggested based on the finding of an association between sleepiness and respiratory disturbances confined primarily to REM sleep. The aim of the study was to define the frequency and the clinical and polysomnographic features of REM SDB in a large clinical population. METHODS: Anthropometric, clinical, and polysomnographic characteristics of 415 patients undergoing polysomnography for SDB were examined. For all patients the apnea-hypopnea index (AHI) during total sleep time, the AHI during REM (AHI-REM), and the AHI during non-REM sleep (AHI-NREM) were calculated. REM SDB was defined as an AHI-REM/AHI-NREM ratio >2. Patients were stratified according to the severity of disease in mild, moderate, and severe cases. Daytime sleepiness was assessed subjectively by the Epworth sleepiness scale (ESS), and objectively, in a subgroup of 228 patients, by the maintenance wakefulness test (MWT). RESULTS: Of the initial sample, 36.4% of cases (n = 151) fulfilled the REM SDB criteria. No significant differences in subjective complaints, medical history, and drug intake were present between REM and non-REM SDB patients, and no significant differences were found in ESS scores and mean sleep latency of the MWT between groups. A high occurrence of REM SDB was found in mild (73.1%) and moderate cases (47.2%). While in the entire group and in non-REM SDB patients a strong male prevalence was found, the incidence of REM SDB was similar in men and women. CONCLUSION: Our results show that neither clinical history nor daytime sleepiness differentiate patients with REM SDB from non-REM SDB patients. The disorder is more common in mild and moderate cases; there is an equal incidence in women and men. These findings may suggest that REM-related SDB is a part of the spectrum of SDB.

Adult↗
PubMed2006

Visual hallucinations in Parkinson's disease: clues to separate origins.

Our paper discusses two experimental studies suggesting that Visual Hallucinations (VH) in Parkinson's Disease (PD) may have separate origins. The first is a prospective 8years study evaluating the appearance of VH, visual abnormalities assessed by Visual Evoked Potentials (VEPs) and REM sleep Behaviour Disorder (RBD), in 80 PD patients treated with l-Dopa and Dopaminoagonists (DA). In chronically treated, cognitively unimpaired, PD patients VH were statistically related (p=0.001) to RBD occurrence and high DA doses. Visual abnormalities were significantly reduced by l-Dopa or DA intake, and were statistically unrelated to VH. The second study involved PD patients placed in a Virtual Reality Environment, to decontextualize visual input. When motor symptoms worsened and VEP abnormalities developed patients consistently described hallucinatory dysperceptions of the virtual environment. The two studies therefore show that VH can occur in two seemingly distinct conditions, one is related to chronic treatment and to a sleep disorder frequently observed in PD, the other is probably related to a hypodopaminergic state. Our studies support a recently proposed integrative model of VH, and show that the neural circuits purported to explain VH must include the retinal dopaminergic system and the REM sleep regulatory system.

Antiparkinson Agents↗
PubMed2006

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

BACKGROUND: 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. METHODS: 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. FINDINGS: 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). INTERPRETATION: 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.

Aged↗
PubMed2003

HLA typing does not predict REM sleep behaviour disorder and hallucinations in Parkinson's disease.

HLA-DR2 haplotype and DQ1 DNA alleles, characterizing 90 to 100% of all narcoleptic patients, were found to be equally distributed in 20 Parkinson's disease (PD) patients with early hallucinations, rapid eye movement (REM) sleep-related behaviour disturbances (RBD), and sleep onset in REM (SOREM), and in 20 PD patients without hallucinations, despite 10 to 15 years of treatment, and no RBD or SOREM.

Aged↗
PubMed2005

Parkinson's disease and sleep.

Sleep disorders are common in PD and many factors can contribute to disturbed nocturnal sleep and daytime sleepiness. Factors contributing to sleep disturbance include the presence of insomnia, mood or anxiety disorders, dementia, specific sleep disorders, PD motor disorders, and the effects of PD or medications. Patients who have PD should be interrogated about sleep disturbance and daytime sleepiness and preferably, because of underestimation of the severity of sleepiness or lack of awareness, patients should be interviewed in the presence of a close friend or relative. The ability to drive, if sleepiness is present, should be assessed and appropriate recommendations made. Treatment of sleepiness involves treating any underlying sleep disturbance and may involve the use of stimulant or alerting medications in the daytime.

Aged↗
PubMed2003

Interobserver reliability of ICSD-R criteria for REM sleep behaviour disorder.

We estimated the interobserver reliability (IR) of the diagnosis of rapid eye movement (REM) Sleep Behaviour Disorder (RBD) among trained neurologists, with the application of International Classification of Sleep Disorders Revised (ICSD-R), by means of videotaped interviews of people with motor sleep behaviour disorders of different nature. IR of clinical judgement for the diagnosis of RBD was "substantial" (Kappa 0.65); nevertheless, some criteria ('limb or body movement associated with dream mentation', criterion B, and 'sleep behaviours (that) disrupt sleep continuity', criterion C3) showed a 'moderate' IR, resulting from the intrinsic limitations of the patient report and terminological ambiguity. Further clarification of terminology of the ICSD-R criteria would be useful to improve the reliability.

Female↗
PubMed2004

Abnormal motor behavior during sleep.

Abnormal motor behaviors during sleep can be classified into four categories, ranging from myoclonic jerks to complex and integrated motor behaviors There have been recent developments in several of these conditions, in particular restless legs syndrome (RLS) and rapid-eye-movement sleep behavior disorder (RBD). RLS is one of the major causes of insomnia. Familial aggregation of RLS has been demonstrated by several groups, and molecular genetics studies have suggested the presence of susceptibility genes on chromosomes 12q and 14q. Pharmacologic and brain imaging studies suggest the involvement of dopaminergic mechanisms in RLS, but recent work has focused on brain iron metabolism. Studies indicate that RBD patients may eventually develop Parkinson's disease (PD). Conversely, RBD has been found in patients already diagnosed with PD. Single-photon emission computed tomography and positron emission tomography studies have shown a decrease in binding to presynaptic dopamine transporter in both idiopathic RBD and PD. Patients with RBD (associated or unassociated with PD) also have neuropsychological deficits. RBD may therefore represent the prodrome of a neurodegenerative disease leading to multiple system atrophy and Lewy body dementia. Understanding the underlying pathophysiology of abnormal sleep motor behaviors may prove useful in the management of insomnia.

Brain↗
PubMed2006

Absence of rapid eye movement sleep behavior disorder in 11 members of the pallidopontonigral degeneration kindred.

BACKGROUND: Rapid eye movement sleep behavior disorder (RBD) is a parasomnia that is manifested by dream enactment behavior. The electrophysiologic substrate for RBD on polysomnography is rapid eye movement sleep without atonia. Rapid eye movement sleep behavior disorder likely stems from neuronal network dysfunction in the brainstem, although it is not yet clear which specific networks are involved. Rapid eye movement sleep behavior disorder is often associated with the sporadic synucleinopathies but rarely associated with the sporadic tauopathies. There are no reports on the possible association of rapid eye movement sleep without atonia and RBD with any familial tauopathy. OBJECTIVE: To characterize the clinical sleep and polysomnography features in a kindred with a familial tauopathy. METHODS: We performed standard polysomnography in 11 members of the pallidopontonigral degeneration kindred irrespective of any sleep-related complaints. Neuropathologic findings were analyzed in those who subsequently underwent autopsy. RESULTS: Six affected and 5 genealogically at-risk family members were studied. None of the 11 had a history of dream enactment behavior. Nine of the 11 members attained sufficient rapid eye movement sleep on polysomnography, and the electrophysiologic features of rapid eye movement sleep without atonia and behavioral manifestations of RBD were absent in all subjects. Neuropathologic examination of 4 affected individuals revealed marked nigral degeneration in 3 along with mild degenerative changes in the locus coeruleus, pontine nuclei and tegmentum, and medullary tegmentum. CONCLUSIONS: These findings argue against nigral degeneration being the primary cause of RBD. The absence of the historical, electrophysiologic, and behavioral manifestations of RBD in this kindred provides further evidence that RBD is rare in the sporadic and familial tauopathies. The difference in frequencies of RBD associated with the synucleinopathies compared with the tauopathies suggests differences in the selective vulnerability of brainstem circuits between the synucleinopathies and tauopathies.

Adult↗
PubMed2005

Rapid eye movement sleep deprivation induces changes in the high-affinity binding of [3H]-ouabain to the rat cortical membranes.

Rapid eye movement sleep (REMS) suppresses seizures. On the other hand, REMS deprivation (REMSD) increases brain susceptibility to seizures. Sodium-potassium/ATPase is involved in the control of brain excitability. Ouabain, a cardiotonic glycoside, binds to a regulatory extracellular allosteric site in the sodium-potassium/ATPase inhibiting/stimulating its activity depending on its concentration. Endogenous ouabain-like substances exist in the brain; therefore, changes in the ouabain binding site may be involved in the increased brain excitability induced by REMSD. Adult, Wistar male rats were deprived of REMS for 96 hours by the flower-pot method (REMSD). A stress control group was kept in the same environment on a larger platform (LP). A third group of rats was kept in the same room in their home-cages (CONTROL). After REMSD all rats were sacrificed by decapitation and their cerebral cortex dissected. High-affinity [3H]-ouabain binding was carried out in cortical crude membrane preparation using 8 concentrations of [3H]-ouabain (1-24 nM). The results show a statistically significant increase of KD in the REMSD rats compared to both CONTROL and LP groups. There were no statistically significant differences in the Bmax among the experimental groups. There was also no change either in cortical activity of K+ stimulated p-nitrophenylphosphatase, the dephosphorylation reaction of phosphorylated sodium-potassium/ATPase or in Mg2+-stimulated p-nitrophenylphosphatase. An increase in the KD of [3H]-ouabain binding to the sodium-potassium/ATPase in REMSD rats indicates a lower affinity to the endogenous inhibitors/stimulators of the enzyme. Therefore, this decreased affinity of the endogenous ouabain-like substances may be involved in the increased excitability induced by REMSD.

Animals↗
PubMed1992

Narcolepsy.

The symptom of excessive sleepiness in children and adolescents does not necessarily cause great concern to families and professionals involved in their care. Children may deny the symptom and minimise the adverse effects. These factors contribute to an underdiagnosis of narcolepsy in this age group when clinical diagnosis is difficult as associated symptoms may not have appeared or are hard to elicit. In this paper three children whose difficult behaviour contributed to the presentation of their sleep disorder are described.

Child↗
PubMed2005

Altered sleep regulation in leptin-deficient mice.

Recent epidemiological, clinical, and experimental studies have demonstrated important links between sleep duration and architecture, circadian rhythms, and metabolism, although the genetic pathways that interconnect these processes are not well understood. Leptin is a circulating hormone and major adiposity signal involved in long-term energy homeostasis. In this study, we tested the hypothesis that leptin deficiency leads to impairments in sleep-wake regulation. Male ob/ob mice, a genetic model of leptin deficiency, had significantly disrupted sleep architecture with an elevated number of arousals from sleep [wild-type (WT) mice, 108.2 +/- 7.2 vs. ob/ob mice, 148.4 +/- 4.5, P < 0.001] and increased stage shifts (WT, 519.1 +/- 25.2 vs. ob/ob, 748.0 +/- 38.8, P < 0.001) compared with WT mice. Ob/ob mice also had more frequent, but shorter-lasting sleep bouts compared with WT mice, indicating impaired sleep consolidation. Interestingly, ob/ob mice showed changes in sleep time, with increased amounts of 24-h non-rapid eye movement (NREM) sleep (WT, 601.5 +/- 10.8 vs. ob/ob, 669.2 +/- 13.4 min, P < 0.001). Ob/ob mice had overall lower body temperature (WT, 35.1 +/- 0.2 vs. ob/ob, 33.4 +/- 0.2 degrees C, P < 0.001) and locomotor activity counts (WT, 25125 +/- 2137 vs. ob/ob, 5219 +/- 1759, P < 0.001). Ob/ob mice displayed an attenuated diurnal rhythm of sleep-wake stages, NREM delta power, and locomotor activity. Following sleep deprivation, ob/ob mice had smaller amounts of NREM and REM recovery sleep, both in terms of the magnitude and the duration of the recovery response. In combination, these results indicate that leptin deficiency disrupts the regulation of sleep architecture and diurnal rhythmicity.

Animals↗