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PubMed2001

Polysomnographic measures in Parkinson's disease: a comparison between patients with and without REM sleep disturbances.

STUDY OBJECTIVE: To assess the frequency of rapid eye movement (REM) sleep abnormalities in Parkinson's disease (PD) patients and compare polygraphic sleep measures in those with and without REM sleep disturbances. DESIGN: Polysomnographic recordings of 2 consecutive nights were performed in 45 patients with PD (mean age 65 years, mean Hoehn and Yahr stage 2.2). Twenty patients were treated with dopaminergic drugs, 10 were drug-free for two weeks and 15 had never been treated with L-dopa or dopamine agonists. According to the polysomnographic findings, the patients were divided into those with and without REM sleep abnormalities. Abnormal REM sleep features were defined as REM sleep without atonia (RWA) and REM sleep behavior disorder (RBD). RESULTS: Eighteen (40%) of the PD patients showed either RWA (24%; 6 men, 5 women) or RBD (16%; 6 men, 1 woman). Patients with REM sleep disturbances had a significantly longer duration of the disease (8.3 vs. 3.9 years), a more severe stage of the disease (2.6 vs. 2.0 Hoehn and Yahr stage) and were treated with a higher dosage of dopaminergic drugs (L-dopa, pergolide and bromocriptin). 67% of the patients with normal REM sleep were untreated at the time of the sleep study, but only 39% of those with REM sleep abnormalities. Sleep EEG measures (sleep efficiency, sleep onset latency, sleep period time, relative amounts of sleep stages) for the second night showed no significant differences between both groups apart from a significantly lower sleep period time in PD patients with RWA/RBD. CONCLUSIONS: Abnormal REM sleep features are a frequent finding in patients with PD. The prevalence seems to increase with a longer disease duration. Therefore, a careful follow-up is necessary. A sleep architecture not different from PD patients without RWA/RBD suggests that the underlying abnormality is confined to REM sleep.

Aged↗
PubMed2005

Relationship between hallucinations, delusions, and rapid eye movement sleep behavior disorder in Parkinson's disease.

Psychotic symptoms are the main and the most disabling "nonmotor" complications of Parkinson's disease (PD), the pathophysiology of which is poorly recognized. Polysomnographic studies have shown a relationship between visual hallucinations and rapid eye movement (REM) sleep. The objective of this study is to clarify the relationship between psychotic symptoms and REM sleep behavior disorder (RBD) in PD. In a Parkinson's disease outpatient unit, 289 consecutive subjects with idiopathic PD were administered (in the period from January to December 2002) a multiple-choice questionnaire and structured interview on sleep and mental disorders. RBD was diagnosed in accordance with the minimal diagnostic criteria of the International Classification of Sleep Disorders. Hallucinations and delusional disorders were diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders-IV criteria. The presence or absence of psychotic symptoms, of RBD, and of daytime sleepiness, as well as motor status, cognitive status, and mood were assessed. Approximately 32% (n = 92) of the subjects presented with psychotic disorders; 30% (n = 86) had experienced hallucinations; 2% (n = 6) had delusions without hallucinations. Sixty-two (72%) hallucinators reported nocturnal hallucinations. A total of 6.6% (n = 19) of the subjects complained of a delusional disorder. There were 26.6% (n = 77) of subjects who presented with RBD: 28 (36%) with onset before and 49 (63%) with onset after PD diagnosis. The presence of RBD was associated with an increased risk of manifesting hallucinations and delusions (odds ratio [OR], 2.73). Other independent clinical factors found to have an effect on psychotic disorders were cognitive impairment (OR, 3.92), disease duration (OR, 2.46), advanced age (OR, 2.34), and severity of motor symptoms (OR, 2.06). These results suggest that RBD is widely associated with psychosis in PD.

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PubMed2002

[Rapid-eye-movement sleep disorders in Parkinson's disease].

During the past 10 years, there has been an increasing interest in the study of rapid-eye-movement (REM) sleep in neurodegenerative diseases and more particulary in Parkinson's disease (PD). This interest is justified by the strong association observed between these diseases and REM sleep behavior disorder (RBD). In the first section of this paper, a critical review of the literature on the presence of REM sleep disorders in PD is presented. Studies that show an association between PD and RBD are reviewed. Studies that report the presence of other REM sleep disorders in PD (short latency, abnormal length and/or proportion of REM sleep, increasing occurrence of hallucinations) are then discussed. Limitations of the criteria proposed by Rechtschaffen et Kales (1968) for the quantification of REM sleep are also presented. Some authors believe that dopaminergic (DA) agents used in the treatment of PD (levodopa, bromocriptine, pergolide, pramipexole and selegiline) could be a responsable factor for the occurence of REM sleep disorders observed in this disease. The literature concerning the impact of these DA agents on human REM sleep is therefore critically reviewed. It is concluded that DA agents cannot explain on their own the presence of REM sleep disorders in PD. Other causes, among which the disturbance of some neurochemical systems linked to the neuropathological process of the disease, must be considered in order to explain these REM sleep disorders. In the second section of this paper, we present the different pathophysiological hypotheses proposed to explain REM sleep disorders in PD, such as a dysfunction of the cholinergic, noradrenergic, serotonergic, dopaminergic or GABAergic neurons. Emphasis is placed on the role of cholinergic neurons of the pedunculopontine and laterodorsal tegmental nuclei, structures shown to be particularly impaired in PD. Neurophysiological, neuroanatomical and neuropharmacological studies demonstrate that these neurons are strongly implicated in the different REM sleep parameters (muscular atonia, electroencephalographic desynchronisation, ponto-geniculo-occipital spikes). Finally, future research directions are proposed.

Antiparkinson Agents↗
PubMed1998

[Screaming during sleep in patients with Parkinson disease].

We studied 12 patients with Parkinson disease who scream while sleeping. All 12 patients showed clinical manifestations and brain images of typical idiopathic Parkinson disease. On average, the screaming began 4.8 years after the onset signs and symptoms of Parkinson disease. In many cases, sleep talking started before the onset of Parkinson disease. All patients reported that the screaming disrupted the sleep of their families, and half of the patients reported that the screams disturbed their own sleep. The screams were incorporated into their dreams. Clonazepam was effective to alleviate this screaming in 8 out of 9 cases. We considered this screaming to be caused by similar mechanisms as rapid eye movement (REM) sleep behavior disorder in which muscle atonia characterizing normal REM sleep is absent. The screams were not accompanied by other abnormal behaviors. We postulate that the screaming is a symptom closely related to that of mid or lower brainstem lesion in Parkinson disease because the neural activity of the locus ceruleus or the pudunculopontine nucleus are responsible for muscle atonia in REM sleep.

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PubMed2001

Sleep disorders.

Many pharmacologic and nonpharmacologic strategies are available to treat sleep disorders successfully. Conventional stimulants and the new stimulant modafinil have roles to play in the management of narcolepsy and idiopathic hypersomnia. Knowledge of the properties and clinical effects of these drugs allows adequate doses of medications to be used with the goal of attaining as maximal alertness as possible. A range of dopaminergic agents is available to treat restless legs syndrome; other medications such as opiates, benzodiazepines, and anticonvulsants can also be used. Successful use of the dopaminergic agents depends on an understanding of the phenomena of augmentation, rebound, and tolerance. Arousal parasomnias can be treated with behavioral methods such as hypnosis and drug therapy. Clonazepam provides relief of the symptoms in most patients with REM sleep behavior disorder.

Disorders of Excessive Somnolence↗
PubMed2004

Serotonergic antidepressants are associated with REM sleep without atonia.

STUDY OBJECTIVES: Rapid eye movement (REM) sleep behavior disorder (RBD) is generally observed in older men and in individuals with specific neurologic diseases. There are case reports of RBD in individuals taking serotonergic antidepressants. Our objective was to assess electromyogram (EMG) activity during REM sleep in individuals taking serotonergic antidepressants and in a matched control group not on such medication. DESIGN: Chart review of clinical and polysomnographic data. SETTING: Sleep laboratory affiliated with a general hospital. PARTICIPANTS: 15 subjects taking a serotonergic antidepressant and 15 age-matched individuals not on such medication. MEASUREMENTS: Submental and anterior tibialis tonic and phasic EMG activity during REM sleep, REM latency, time in REM, apnea-hypopnea index, periodic leg movements of sleep index, and sleep-architecture measures. RESULTS: Tonic, but not phasic, submental EMG activity during REM sleep was significantly more common in the antidepressant-treated group than in the control group (P < .02). Tonic REM submental EMG activity correlated with REM latency (r = .42, P = .02) and inversely with REM time (r = -.36, P = .05). Subject age correlated with tonic REM submental EMG activity (r = .58, P = .02) in the antidepressant group There were also trends for more phasic activity in the anterior tibialis (P = .09) and submental (P = .07) EMG in REM sleep in the antidepressant group than in the control group. CONCLUSIONS: Subjects taking serotonergic antidepressants had more EMG activity in the submental lead during REM sleep than did controls. This correlated with measures of REM suppression and age. Individuals taking such medications may be at increased risk of developing REM sleep behavior disorder, particularly with increasing age.

Adult↗
PubMed1999

Therapy of behavioral disorders in Parkinson's disease.

Behavioral disturbances in Parkinson's disease (PD) are a common source of disability to both patients and their families, but there is a considerable controversy regarding their frequency and their neuropathological and neurochemical bases. Since they are so common, the disorders associated with PD should be well recognized, and proper management by neurologists is required. The most frequent behavioral disturbances encountered in patients with PD are depression, anxiety, cognitive impairment and dementia. Also frequent are sleep disorders such as sleep fragmentation, REM sleep behavior disorder, insomnia and altered dreaming. The most troublesome situations come from drug-induced psychiatric states, such as delusional states, hallucinations, paranoid ideation, delirium, and confusion. The treatment of these behaviors is reviewed here.

Behavioral Symptoms↗
PubMed2001

[Sleep talking].

Sleep talking is very common in the general population. Its prevalence remains stable from childhood through adulthood. Sleep talking is often associated with other parasomnias: sleep walking, sleep terrors or REM sleep behavior disorders. It may arise from either REM or non REM sleep, when associated with REM sleep it is more comprehensible and often associated with clear sentences and recall of sleep mentation. Sleep talking is a benign entity and does not require any treatment; however an exceptional organic cause or psychopathology should be suspected if the onset is late (after 25 years); if the mental content is too violent or too emotional.

Adult↗
PubMed1998

Nocturnal wandering and violence: review of a sleep clinic population.

Sleep consists of two complex states--NREM and REM sleep--and disturbances of the boundaries between the states of sleep and wakefulness may result in violence. We investigated our population for reports of violence associated with sleep. REM behavior disorder is rarely associated with injury to the sufferer or others. NREM sleep related nocturnal wandering associated with self-inflicted injuries has variable etiologies. In the elderly, it is associated with dementia. In young individuals, it may be associated with mesio-temporal or mesio-frontal foci and an indication of a complex partial seizure. It also may be related to abnormal alertness and is associated with excessive daytime sleepiness, micro-sleeps, and hypnagogic hallucinations in sleep disorders such as narcolepsy or sleep disordered breathing.

Adult↗
PubMed2007

Dementia with Lewy bodies.

Synucleinopathies, with and without dementia, encompass a wide range of diseases including Parkinson's disease, multiple system atrophy, rapid eye movement (REM) sleep behavior disorder, and dementia with Lewy bodies (DLB). DLB is a neurodegenerative disorder resulting in slowly progressive and unrelenting dementia until death. Prevalence studies suggest that it is the second most common dementing illness in the elderly. The neuropathologic findings of DLB show a wide anatomic range. Lewy bodies and Lewy-related pathology are found from the brain stem to the cortex and, in many cases, associated with concurrent Alzheimer's disease pathology. A recent international consortium on DLB has resulted in revised criteria for the clinical and pathological diagnosis of DLB incorporating new information about the core clinical features and improved methods for their assessment. The presentation of DLB is typically one of cortical and subcortical cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer's disease. There may be relative sparing of memory especially in the early stages. Core clinical features of DLB include fluctuating attention, recurrent visual hallucinations, and parkinsonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuroimaging. Additional supportive features that commonly occur in DLB, but with lower specificity, include repeated falls and syncope, transient, unexplained loss of consciousness, severe autonomic dysfunction, hallucinations in other modalities, systematized delusions, depression, relative preservation of medial temporal lobe structures on structural neuroimaging, reduced occipital activity on functional neuroimaging, prominent slow wave activity on electroencephalogram, and low uptake myocardial scintigraphy. Management of DLB includes pharmacological and nonpharmacological interventions for its cognitive, neuropsychiatric, motor, and sleep disturbances.

Brain↗
PubMed2002

Study of image findings in rapid eye movement sleep behavioural disorder.

To elucidate the cause of idiopathic rapid eye movement (REM) sleep behavior disorder (RBD), magnetic resonance imaging and single-photon emission computed tomography of the brain were conducted on 20 patients with RBD. Blood flow in the upper portion of both sides of the frontal lobe and pons was significantly lower in patients with RBD than in the normal elderly group. Among the patients with RBD, decreased blood flow in the frontal lobe showed no correlation with the extent of frontal lobe atrophy. Decreased blood flow in the upper portion of the frontal lobe and pons might be associated with the pathogenesis of idiopathic RBD.

Aged↗
PubMed2005

Parkinsonism with excessive daytime sleepiness--a narcolepsy-like disorder?

BACKGROUND: Parkinsonian patients with excessive daytime sleepiness (EDS), hallucinations, REM sleep behavior disorder (RBD), short mean sleep latencies, and sleep-onset REM periods (SOREMP) on multiple sleep latency tests (MSLT) have been reported. In these patients a narcolepsy-like pathophysiology of sleep-wake disturbances has been suggested. PATIENTS AND METHODS: We studied 14 consecutive patients with Parkinsonism and EDS. Standard studies included assessment of duration and severity of Parkinsonism (Hoehn & Yahr score), Epworth sleepiness score (ESS), history of "REM-symptoms" (RBD/hallucinations/sleep paralysis/cataplexy-like episodes), polysomnography (PSG), MSLT, and measurement of cerebrospinal fluid (CSF) levels of hypocretin-1 (orexin A). RESULTS: There were 12 men and 2 women (mean age 69 years; range 54-82). The mean duration and the Hoehn&Yahr score were 6.3 years and 2.2, respectively. Diagnoses included idiopathic Parkinson's disease (IPD, n = 10), dementia with diffuse Lewy bodies (n = 3), and multisystem atrophy (n = 1). The ESS was > or = 10 in all patients (mean 12; range 10-18). "REM-symptoms" were reported by all but two patients (hallucinations: n = 9; RBD: n = 9). None of the patients reported cataplexy-like symptoms or sleep paralysis. On PSG sleep apnea (apnea hypopnea index > 10/h, n = 7), periodic limb movements during sleep (PLMS-index > 10/h, n = 6), and features of RBD (n = 5) were found. On MSLT mean sleep latency was < 5 minutes in 10 patients, and SOREMP were found in two patients. When compared with controls (n = 20, mean 497 pg/ml; range 350-603), CSF hypocretin-1 levels were normal in 8 patients and low in 2 patients (221 and 307 pg/ml, respectively). CONCLUSION: These findings do not support the hypothesis of a "final common pathway" in the pathophysiology of narcolepsy and Parkinsonism with EDS. Sleep apnea and PLMS may play a so-far underestimated role in the pathogenesis of EDS in Parkinsonian patients.

Aged↗
PubMed2005

Abnormal sleep architecture is an early feature in the E46K familial synucleinopathy.

We examined 7 patients from a family harboring a novel mutation in the alpha-synuclein gene (E46K) that segregated with a phenotype of parkinsonism and dementia with Lewy bodies. An abnormal restless sleep was the presenting symptom in 2 of them. Polysomnographic (PSG) studies were performed in 4 of the 7 patients and in 2 asymptomatic carriers of the mutation. A severe loss of both rapid eye movement (REM) and non-REM sleep was observed in 2 patients complaining of insomnia and in a third parkinsonian member of the family who did not complain of trouble with sleeping. Another parkinsonian family member had a mild disorganization of the sleep architecture. The 2 asymptomatic carriers also had minor changes in the PSG findings. Episodes of bizarre behavior at night were reported historically in the 2 symptomatic patients, but we did not observed the behaviors during the PSG studies. REM sleep behavior disorder could not be recorded in any case. Our findings expand the spectrum of sleep disorders reported in synucleinopathies whether sporadic or familial.

Adult↗
PubMed1991

Injurious sleep behavior disorders (parasomnias) affecting patients on intensive care units.

There are no previous reports on parasomnias (sleep behavior disorders) affecting patients on intensive care units (ICUs). During 8 years of clinical practice, we evaluated over 200 adults with complaints of injurious, sleep-related behaviors, 20 of whom had ICU admissions while their parasomnias had been active and generally undiagnosed/untreated. Mean age during ICU confinement was 62.8 (+/- SD 13.1) years; 85.0% (17/20) were males. Patients underwent comprehensive clinical examinations along with extensive polysomnographic and audiovisual monitoring (electrooculogram, 9 channel EEG with paper speeds of 15 and 30 mm/sec, electromyogram [submental and 4 limbs], EKG, airflow). The polysomnographic studies were diagnostic for the REM sleep behavior disorder (vigorous dream-enactment during rapid eye movement [REM] sleep) in 85.0% (17/20) of patients, and for night terrors/sleepwalking in 15.0% (3/20). Three groups of parasomnia-ICU relationships were identified: i) Parasomnias originating in ICUs, stroke-induced (n = 3); ii) Admission to ICUs resulting from parasomnia-induced injuries: C2 odontoid process fracture and C3 spinous process fracture with severe concussion (n = 2); iii) Parasomnias in patients admitted to ICUs for various other medical problems (n = 15). Physicians should be thus alerted about the possibility of injurious, but usually treatable, parasomnias in ICU patients.

Adult↗
PubMed2006

Sleep disturbances and excessive daytime sleepiness in Parkinson disease: an overview.

Sleep disturbances are frequent in Parkinson disease. These disorders can be broadly categorized into those that involve nocturnal sleep and excessive daytime sleepiness. The disorders that are often observed during the night in PD include sleep fragmentation that may be due to recurrent PD symptoms, sleep apnea, Restless Leg Syndrome/ periodic limb movements and REM sleep behavior disorder. Excessive daytime sleepiness is also a common occurrence in PD. EDS can arise from several etiologies, and patients may have more than one etiology responsible. The causes of EDS include nocturnal sleep disorder with sleep deprivation and resulting daytime somnolence, the effect of drugs used to treat PD, and possibly neurodegeneration of central sleep/wake areas. Appropriate diagnosis of the sleep disturbance affecting a PD patient can lead to specific treatments that can consolidate nocturnal sleep and enhance daytime alertness.

Animals↗
PubMed2006

Parasomnias.

Parasomnias are undesirable behaviors that arise from sleep but are not fully under voluntary control. Parasomnias are grouped broadly according to whether they arise from non-rapid eye movement (NREM) or rapid eye movement (REM) sleep. NREM parasomnias are disorders of arousal that occur along a continuum of behavioral, affective, and autonomic activation. REM-related parasomnias include REM sleep behavior disorder, sleep paralysis, and nightmare disorder. Parasomnias can often be managed successfully using behavioral and pharmacologic therapies.

Arousal↗
PubMed2000

[Consideration on neuroimaging and functional diagnosis in cerebrovascular disorder].

The electroencephalogram(EEG) has been one of the important clinical examination in cerebrovascular disorder(CVD). Since X-ray computed tomography(CT) was introduced in the 1970's, the numbers of EEG examination decreased in Japan. In the present, the diagnosis of acute CVD is done by neuroimaging examinations which generally are CT, magnetic resonance imaging(MRI) and at times, single photon emission computed tomography(SPECT). But EEG examination is necessary for estimate of brain function in acute and/or chronic CVD. Only EEG examination is able to confirm epileptic seizure, sleep-wake disorder and disturbance of consciousness. alpha-coma and spindle coma are peculiar disturbance of consciousness and appear in acute CVD. REM sleep behavior disorder(RBD) sometimes appear in chronic CVD. The characteristic of RBD is violent or injurious behavior during REM sleep. Polysomnography demonstrates abnormal REM sleep without loss of atonia. Both neuroimaging and functional diagnosis have been to perform to estimate in CVD same as in the other central nervous disorders.

Cerebrovascular Disorders↗
PubMed2001

Parasomnia as an occasion for the diagnosis of Parkinson's disease.

We report a case of Parkinson's disease (PD) diagnosed by REM sleep behavior disorder (RBD). The patient was a 68-year-old man. On admission, rigidity in the left upper and lower extremities, bradykinesia, and gait disturbance were noted. In addition, polysomnography revealed REM sleep without atonia (RWA), and a diagnosis of untreated PD associated with RBD was made. Polysomnographic data showed that REM density decreased and RWA tended to increase after administration of a combination of L-DOPA and DCI (L-DOPA/DCI). Thus, we considered that the pathophysiological mechanism of RBD in this case was based not only on the dysfunction of the brainstem mechanism of RWA, but also on the impairment of dopaminergic neuron.

Aged↗