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PubMed2004

Association between waking EEG slowing and REM sleep behavior disorder in PD without dementia.

OBJECTIVE: To compare nondemented patients with Parkinson's disease (PD) with and without REM sleep behavior disorder (RBD) to healthy controls on quantitative EEG characteristics for both wakefulness and REM sleep. METHODS: Fifteen patients with PD (7 patients with polysomnographic-confirmed RBD [PD-RBD] and 8 patients without RBD [PD-NRBD]) and 15 healthy control subjects were studied. Each subject underwent a quantitative EEG analysis of both wakefulness and REM sleep. RESULTS: During wakefulness, patients with PD-RBD showed a higher theta power in frontal, parietal, temporal, and occipital regions in comparison to patients with PD-NRBD and control subjects. Moreover, a slowing of the dominant occipital frequency was observed only in patients with PD-RBD (p < 0.02). Patients with PD-NRBD did not present any slowing of the EEG. No between-group difference in quantitative REM sleep EEG was observed. CONCLUSIONS: This study demonstrates that the EEG slowing reported during wakefulness in nondemented patients with PD is strongly related to the presence of RBD.

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PubMed2003

Melatonin for treatment of REM sleep behavior disorder in neurologic disorders: results in 14 patients.

OBJECTIVE: To describe the treatment response with melatonin for rapid eye movement (REM) sleep behavior disorder (RBD) associated with other neurologic disorders. BACKGROUND: Clonazepam has been considered the treatment of choice for RBD. However, an alternative treatment is desirable for those with RBD refractory to clonazepam, for those who experience intolerable side-effects with clonazepam, and for those in whom clonazepam precipitates or aggravates obstructive sleep apnea (OSA). To date, there is minimal published data and limited follow-up regarding the use of melatonin for patients with RBD associated with other neurologic syndromes and disorders. DESIGN/METHODS: The response to melatonin treatment for RBD was reviewed on consecutive patients the investigators treated with this agent at Mayo Clinic Rochester from January 2000 to June 2001. The coexisting neurologic disorders, reasons for using melatonin, effective doses, side-effects, and duration of follow-up were also reviewed on all patients. RESULTS: Fourteen patients were commenced on melatonin over the specified time period (13 male, median RBD onset age 56 years, range 20-77 years). The coexisting neurologic findings/disorders were dementia with Lewy bodies (n=7), mild cognitive impairment with mild parkinsonism (n=2), multiple system atrophy (n=2), narcolepsy (n=2), and Parkinson's disease (n=1). The reasons for using melatonin in these cases were incomplete response of RBD to clonazepam in six patients, existing cognitive impairment in five, intolerable side-effects with clonazepam in two, and presence of severe obstructive sleep apnea and narcolepsy in one. With seven patients continuing to use clonazepam at 0.5-1.0 mg/night, RBD was controlled in six patients, significantly improved in four, and initially improved but subsequently returned in two; no improvement occurred in one patient and increased RBD frequency/severity occurred in one patient. The effective melatonin doses were 3 mg in two cases, 6 mg in seven cases, 9 mg in one case, and 12 mg in two cases. Five patients reported side-effects, which included morning headaches (2), morning sleepiness (2), and delusions/hallucinations (1); these symptoms resolved with decreased dosage. The mean duration of follow-up was 14 months (range 9-25 months), with eight patients experiencing continued benefit with melatonin beyond 12 months of therapy. CONCLUSIONS: In this series, persistent benefit with melatonin beyond 1 year of therapy occurred in most but not all patients. Melatonin can be considered as a possible sole or add-on therapy in select patients with RBD. Prospective, long-term, controlled trials with melatonin are warranted in a larger number of patients with RBD associated with a variety of neurologic symptoms and disorders.

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PubMed2003

The effects of pramipexole in REM sleep behavior disorder.

The authors evaluated the effects of pramipexole, a dopaminergic D2-D3 receptor agonist, on eight patients with idiopathic REM sleep behavior disorder. Five patients reported a sustained reduction in the frequency or intensity of sleep motor behaviors, which was confirmed by video recording, although no change was observed for the percentage of phasic EMG activity during REM sleep. Surprisingly, a decrease in the percentage of time spent with REM sleep muscle atonia was observed with treatment. The treatment did not modify the indexes of periodic leg movements.

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PubMed2003

Mirtazapine induces REM sleep behavior disorder (RBD) in parkinsonism.

Shortly after initiation of mirtazapine (a noradrenergic and serotonergic antidepressant) treatment in four patients with parkinsonism, the authors observed the appearance of REM sleep behavior disorder (RBD). In the two patients with severe motor symptoms, RBD was accompanied by hallucinations and confusion. These disturbances resolved with drug discontinuation, and remained resolved by 12- to 24-month follow-up, suggesting that RBD can be triggered by a drug lacking anticholinergic activity.

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PubMed2002

Periodic leg movements in REM sleep behavior disorder and related autonomic and EEG activation.

OBJECTIVE: To assess the frequency of periodic leg movements (PLM) in idiopathic REM sleep behavior disorder (RBD) and to analyze their polysomnographic characteristics and associated autonomic and cortical activation. BACKGROUND: PLM during sleep (PLMS) and wakefulness (PLMW) are typical features of restless legs syndrome (RLS), but are also frequently observed in patients with RBD. METHODS: Forty patients with idiopathic RBD underwent one night of polysomnographic recording to assess PLMS frequency. PLM features, PLMS-related cardiac activation during stage 2 sleep, and EEG changes were analyzed in 15 of these patients with RBD. Results were compared with similar data obtained in 15 sex- and age-matched patients with primary RLS. RESULTS: Twenty-eight (70%) of 40 patients with RBD showed a PLMS index greater than 10. No between-group differences were found in sleep architecture or indexes of PLMW and PLMS during non-REM sleep, but a trend for a higher PLMS index during REM sleep was found in patients with RBD. PLM mean duration and interval in the two conditions were similar. A transient tachycardia followed by a bradycardia was observed in close association with every PLMS in both groups, but the amplitude of the cardiac activation was significantly reduced in patients with RBD. In addition, significantly fewer PLMS were associated with microarousal in this condition. CONCLUSIONS: Periodic leg movements are very common in idiopathic RBD, occurring in all stages of sleep, especially during REM sleep. In idiopathic RBD, the reduction of cardiac and EEG activation associated with PLMS suggests the presence of an impaired autonomic and cortical reactivity to internal stimuli.

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PubMed2006

Insights into REM sleep behavior disorder pathophysiology in brainstem-predominant Lewy body disease.

BACKGROUND AND PURPOSE: Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia reflecting changes in the brain, but which specific neuronal networks are involved in human RBD pathogenesis has not yet been determined. To date, only one case of idiopathic RBD has undergone autopsy, in which "incidental Lewy body disease" was found. Due to the severe neuronal loss and gliosis in the substantia nigra (SN) and locus ceruleus (LC) in this case, degeneration of brainstem monoaminergic neurons was postulated as the underlying substrate for RBD. Additional cases of idiopathic RBD with neuropathologic examination may help clarify which key brainstem structures are involved. PATIENT AND METHODS: Case report with neuropathologic analysis. RESULTS: A man with polysomnographically proven RBD (onset age 57 years), but no other neurologic signs or symptoms, underwent neuropathologic examination upon his death at age 72. Histopathologic analysis showed Lewy body disease, but no significant neuronal loss or gliosis was present in the SN or LC. CONCLUSIONS: This case represents another example of Lewy body disease associated with RBD. The minimal degenerative changes in the SN and LC call into question the role of these nuclei in RBD, at least in our case. We suggest additional cases of idiopathic RBD undergo neuropathologic analyses to better delineate the neurologic substrate of this intriguing parasomnia.

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PubMed2004

Neuropsychological assessment in idiopathic REM sleep behavior disorder (RBD): does the idiopathic form of RBD really exist?

OBJECTIVE: To evaluate the cognitive performance of patients with idiopathic REM sleep behavior disorder (RBD). METHODS: The authors studied 17 consecutive patients with idiopathic RBD vs 17 age- and education-matched control subjects. Tests given to each patient and control included Mini-Mental State Examination, verbal and spatial short-term memory, visual selective attention, verbal fluency, prose memory, visuoconstructional abilities, spatial learning, and executive function tests. A self-administered depression rating scale was also used. RESULTS: RBD patients had significantly lower scores than control subjects in two tests: copy of Rey-Osterrieth Figure and Corsi Supraspan Learning. No correlation was found between the results of neuropsychological tests and RBD duration or with polysomnographic findings. CONCLUSIONS: Visuospatial constructional dysfunction and altered visuospatial learning may be present in idiopathic RBD. A neuropsychological assessment may be indicated in RBD patients.

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PubMed2006

REM sleep behavior disorder, hallucinations, and cognitive impairment in Parkinson's disease.

The objective of this study was to evaluate the relationship between REM sleep behavior disorder (RBD), hallucinations, and cognitive impairment in Parkinson's disease (PD). One hundred and ten PD patients, divided into three groups (without RBD or hallucinations; with RBD but no hallucinations; with RBD and hallucinations), were submitted to neuropsychological evaluation. The group without RBD and hallucinations showed normal neuropsychological tests when compared to normal controls. The group with hallucinations was characterized by a more severe cognitive impairment affecting both short- and long-term memory, logical abilities, and frontal functions, while the RBD-only group presented frontal impairment. The hypothesis that RBD in PD can be considered a risk factor not only of the hallucinations but also of more severe and diffuse cognitive abnormalities needs to be strengthened through a longitudinal evaluation.

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PubMed1992

[REM-sleep behavior disorder and olivo-ponto-cerebellar atrophy: a case report].

The authors report the observation of REM-sleep behavior disorder in a patient also suffering from an olivo-ponto-cerebellar atrophy. They discuss the place of this sleep disorder among the parasomnias, its pathophysiological basis and its features similar to those of the somnambulism. Only a polysomnography study can help to make the diagnosis.

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PubMed1999

REM sleep behavior disorder and dementia: cognitive differences when compared with AD.

OBJECTIVE: To determine whether the dementia associated with REM sleep behavior disorder (RBD) differs from Alzheimer's disease (AD) and, if so, whether differences in cognitive performance between RBD/dementia and AD resemble reported differences between dementia with Lewy bodies (DLB) and AD. METHODS: This retrospective study compares neurocognitive performance between 31 patients with degenerative dementia and polysomnography-confirmed RBD and 31 patients without brainstem Lewy body pathology who met Consortium to Establish a Registry for Alzheimer's Disease (CERAD) clinical and neuropathologic criteria for AD. The patient groups did not differ in dementia severity (based on Global Deterioration Scale score) or duration. RESULTS: RBD preceded or coincided with the onset of cognitive decline in 94% of the patients. All but one patient with RBD/dementia had one or more of the following clinical features of DLB: visual hallucinations, extrapyramidal signs, or fluctuating cognition/alertness. The data revealed significantly worse performance on attention, perceptual organization, visual memory, and letter fluency for the RBD/dementia group, whereas the AD group showed significantly worse performance on confrontation naming and verbal memory. CONCLUSIONS: Patients with RBD and degenerative dementia demonstrate a significantly different pattern of cognitive performance from patients with AD. Most of the patients in the RBD/dementia sample also meet criteria for possible or probable DLB, and the pattern of cognitive differences from AD is similar to reported comparisons between DLB and AD. The cognitive and clinical data provide evidence to suggest that the dementia associated with RBD may represent DLB.

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PubMed1997

Subclinical REM sleep behavior disorder in a patient with corticobasal degeneration.

Various neurodegenerative diseases have been reported to be associated with rapid eye movement (REM) sleep behavior disorder (RBD). This is the first report of a patient with corticobasal degeneration (CBD) associated with subclinical RBD. A 72-year-old woman was admitted complaining of fine tremor of the right hand and weakness of the right lower extremity. She was diagnosed as having CBD on the basis of clinical features and neuroimaging studies. Her family noticed snoring and increase in sleep talk, but they did not regard them as pathological. All-night polysomnography (PSG) revealed REM sleep without atonia (RWA) during which 14 episodes of talking and singing were observed. They ranged from the utterance of one word to that of comprehensible words of a song for about 3 minutes accompanied by various nonpurposeful movements of the mouth, hands, and limbs. These episodes were not associated with any sleep-disturbed breathing. Future PSG studies on CBD patients together with postmortem analysis of brain stem structures that are crucial for generating REM sleep-related atonia are warranted for further understanding of the pathophysiological mechanism of RBD.

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PubMed1995

Incidental Lewy body disease in a patient with REM sleep behavior disorder.

We studied an 84-year-old man with a 20-year history of nocturnal violent behavior during sleep, but no other clinically evident neuropsychiatric disorders. Polysomnographic investigations confirmed that he suffered from REM sleep behavior disorder (RBD). Histopathologic examination revealed he had Lewy body disease with a marked decrease of pigmented neurons in the locus ceruleus and substantia nigra. These histologic findings represent the first documented evidence of a loss of brainstem monoaminergic neurons in clinically idiopathic RBD and suggest that Lewy body disease might provide an explanation for idiopathic RBD in the aged.

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PubMed2002

Remitting REM sleep behavior disorder as the initial sign of multiple sclerosis.

We report a case of a 25-year-old woman presenting with a 6 month history of REM sleep behavior disorder (RBD), confirmed by video-polysomnography. A brain MRI disclosed multiple cerebral periventricular and pontine non-gadolinium-enhancing hyperintensities and CSF isoelectric focusing showed oligoclonal bands, consistent with a diagnosis of probable multiple sclerosis (MS). RBD episodes disappeared after ACTH treatment, but clinical relapses and MRI follow-up confirmed the diagnosis of MS. Although RBD has been described in association with MS, it has not been reported as a heralding sign, nor related to MS brainstem lesion. Our case emphasizes the value of RBD as a clinical tell-tale sign: when isolated RBD appears in a young subject, brain-imaging studies and long-term follow-up are warranted.

Journal Article↗
PubMed2005

Severe obstructive sleep apnea/hypopnea mimicking REM sleep behavior disorder.

OBJECTIVE: To describe the clinical and video-polysomnographic (VPSG) features of a group of subjects with severe obstructive sleep apnea/hypopnea (OSAH) mimicking the symptoms of REM sleep behavior disorder (RBD). DESIGN: Evaluation of clinical and VPSG data. SETTING: University hospital sleep laboratory unit. PARTICIPANTS: Sixteen patients that were identified during routine first evaluation visits. Patients' PSG measures were compared with those of 20 healthy controls and 16 subjects with idiopathic RBD of similar age and sex distribution and apnea/hypopnea index lower than 10. INTERVENTIONS: NA. RESULTS: Sixteen subjects were identified presenting with dream-enacting behaviors and unpleasant dreams suggesting the diagnosis of RBD, in addition to snoring and excessive daytime sleepiness. VPSG excluded RBD showing REM sleep with atonia and without increased phasic EMG activity, and was diagnostic of severe OSAH with a mean apnea-hypopnea index of 67.5 +/- 18.7 (range, 41-105) demonstrating that the reported abnormal sleep behaviors occurred only during apnea-induced arousals. Continuous positive airway pressure therapy eliminated the abnormal behaviors, unpleasant dreams, snoring and daytime hypersomnolence. CONCLUSIONS: Our study shows that severe OSAH may mimick the symptoms of RBD and that VPSG is mandatory to establish the diagnosis of RBD, and identify or exclude other causes of dream-enacting behaviors.

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PubMed2005

Brainstem 1H-MR spectroscopy in patients with Parkinson's disease with REM sleep behavior disorder and IPD patients without dream enactment behavior.

OBJECTIVES: The objective of our study was to evaluate brainstem involvement by 1H-MR spectroscopy (1H-MRS) method in patients with idiopathic Parkinson's disease (IPD) with REM sleep behavior disorder (RBD) and IPD without dream enactment behavior. PATIENTS AND METHODS: We prospectively studied 12 IPD (3 females, 9 males) with a clinically and electrophysiologically confirmed RBD and 12 IPD (3 females, 9 males) patients without dream enactment behavior followed in Outpatient Clinics for Movement Disorders of Department of Neurology, Haseki Hospital. Using long and short TE single voxel 1H-MRS directed at ventral and dorsal pons, long TE NAA/Cr, Ch/Cr and short TE NAA/Cr, Ch/Cr, MI/Cr values of both groups were compared. RESULTS: Although no difference was found between groups with RBD and IPD without dream enactment behavior in demographic characteristics, duration of disease, mean levodopa dosage and duration of levodopa use, all UPDRS scores (total, motor and cognitive) were worse in RBD group (p<0.05). There was no statistically significant difference in long TE NAA/Cr, Ch/Cr and short TE NAA/Cr, Ch/Cr, MI/Cr values obtained in both groups (p>0.05). CONCLUSION: 1H-MRS does not detect marked metabolic differences in the pons in subjects with IPD with RBD and IPD without dream enactment behavior. This finding suggests either that present methodologies are not sensitive to detect subtle metabolic changes in the pons of subjects with RBD or that the primary lesion of RBD exists in other REM sleep-related brain regions beyond the pons such as the substantia nigra, the basal ganglia or the limbic system.

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PubMed1992

Prominent eye movements during NREM sleep and REM sleep behavior disorder associated with fluoxetine treatment of depression and obsessive-compulsive disorder.

The clinical polysomnographic (PSG) reports of 2,650 consecutive adults studied during 41 months were reviewed retrospectively to identify all patients treated with fluoxetine or tricyclic antidepressants. The PSG reports of four other adult groups were also reviewed: periodic limb movement (PLM) disorder (n = 28); sleep terror/sleepwalking (ST/SW) (n = 54); rapid eye movement (REM) sleep behavior disorder (RBD) (n = 70); patients with clinically unremarkable sleep during two consecutive PSG studies (n = 30). Standard PSG recording and scoring methods were employed. A total of 1.5% (n = 41) and 2.0% (n = 52) of patients were receiving fluoxetine or tricyclics (amitriptyline or nortriptyline, n = 31; imipramine or desipramine, n = 16; protriptyline or trimipramine, n = 5). A selective association between fluoxetine and extensive, prominent eye movements in nonrapid eye movement (NREM) sleep was detected, utilizing Fisher's exact one-tailed statistic (p less than 0.00001 for each comparison). The detection rates were fluoxetine, 48.8% (20/41); tricyclics, 5.8% (3/52); RBD, 4.3% (3/70); objectively normal sleepers, 3.3% (1/30); PLM, ST/SW, 0% (0/82). These groups had similar mean ages (31.5-45.4 years) and gender distributions (50.0-60.7% male), apart from RBD. The effect of fluoxetine, a potent and specific serotonin reuptake inhibitor, on NREM eye movements is postulated to derive from potentiation of serotonergic neurons that inhibit brainstem "omnipause neurons", which, in turn, inhibit saccadic eye movements, thus resulting in disinhibited release of saccades. In addition, a 31-year-old man with obsessive-compulsive disorder developed RBD soon after starting fluoxetine therapy, which persisted at PSG study 19 months after fluoxetine discontinuation.

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