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PubMed2006

Periodic leg movements in sleep and periodic limb movement disorder: prevalence, clinical significance and treatment.

Periodic leg movements in sleep (PLMS) are a frequent finding in polysomnography. The prevalence of PLMS is estimated to be 4-11% in adults. In childhood, PLMS rarely occur although medical conditions like sleep apnea syndrome or neuropsychiatric disorders can lead to high rates of PLMS. In the elderly, PLMS are also common in subjects without sleep disturbances. In sleep studies, PLMS are found most frequently in restless legs syndrome (RLS) and often occur in narcolepsy, sleep apnea syndrome and REM sleep behavior disorder. Some patients with otherwise unexplained insomnia or hypersomnia reveal an elevated number of PLMS, a condition defined as periodic limb movement disorder (PLMD). PLMS were found also in various medical and neurological disorders that do not primarily affect sleep. A summary of these is presented. In sleep disorders related to dopaminergic dysfunction such as RLS, PLMS are considered to be a symptom of the disease. In other disorders like primary insomnia, the clinical relevance of PLMS is still being controversially discussed. Studies with findings both pro and contra are referred. To date, only a few studies have evaluated the efficacy of therapeutic substances in reducing PLMS in PLMD patients. Their results need to be confirmed in controlled randomized trials.

Aged↗
PubMed2006

Mood and sleep in Parkinson's disease.

OBJECTIVE: To determine whether severity of depression and severity of anxiety were associated with particular types of sleep disturbance in patients with Parkinson's disease. METHOD: 120 patients with a diagnosis of idiopathic Parkinson's disease were consecutively recruited from a movement disorders clinic from July 2004 to May 2005. Idiopathic Parkinson's disease was diagnosed by a board-certified neurologist (J.H.F) and defined by the presence of 3 of the 4 cardinal signs of Parkinson's disease: resting tremor, rigidity, bradykinesia, and postural instability. Patients were administered the Hamilton Rating Scale for Depression, Hamilton Rating Scale for Anxiety, Covi Anxiety Scale, Pittsburgh Sleep Quality Index (PSQI), and Epworth Sleepiness Scale (ESS). Patients were assessed for nightmares and rapid eye movement (REM) sleep behavior disorder (RBD) using a structured questionnaire and dream log. Multivariate analyses evaluated whether severity of depression and severity of anxiety correlated with the sleep outcome measures (PSQI, ESS, nightmares, and RBD). RESULTS: The mean +/- SD age of the patients was 71 +/- 10.8 years with a mean Parkinson's disease duration of 7.3 +/- 4.7 years. Thirty-eight percent were female, 41.7% had a psychiatric history, 53.3% had nightmares, and 30% had clinically defined RBD. Severity of depression and severity of anxiety significantly correlated with poor sleep quality, daytime somnolence, and nightmares. Severity of depression contributed significantly to the overall variance in poor sleep quality and nightmares. Severity of anxiety contributed significantly to the overall variance in daytime somnolence. CONCLUSIONS: Depressive and anxiety symptoms were associated with sleep disturbances in patients with Parkinson's disease. It is important to examine for the presence of depression and anxiety in patients presenting with sleep disorders, as depression and anxiety impair quality of life and are treatable conditions.

Aged↗
PubMed1992

Isolated sleep paralysis elicited by sleep interruption.

We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.

Adolescent↗
PubMed1992

Dissociated states of wakefulness and sleep.

Both sleep clinicians and basic science researchers have been witness to a wide variety of unusual clinical and experimental phenomena that represent admixtures, incomplete declaration, or rapid oscillations of the three states of being: wakefulness, rapid eye movement (REM) sleep, and nonrapid eye movement sleep. The concept of state dissociation provides an explanation for a wide variety of bizarre clinical phenomena, including the symptoms of narcolepsy, REM sleep behavior disorder, disorders of arousal (such as sleep terrors, sleepwalking, and sleep drunkenness), automatic behavior, and some "out-of-body" experiences. The purpose of this review is to provide an overview and perspective of such conditions, encourage systematic and detailed study of these "experiments in nature," and underscore the interdependence of clinicians and researchers.

Adolescent↗
PubMed2003

HLA and genetic susceptibility to sleepwalking.

HLA-DQB1 typing was performed in 60 Caucasian subjects with sleepwalking (SW) disorder and their families and 60 ethnically matched subjects without any diagnosed sleep disorder. A total of 21 sleepwalkers (35.0%) were DQB1*0501 positive vs eight (13.3%) controls (P = 0.0056; odds ratio = 3.5, 95% CI = 1.4-8.7). The family data for all HLA subtypes were further assessed for allelic association with SW using the transmission-disequilibrium test. A significant excess transmission was observed for DQB1*05 and *04 alleles in familial cases, strongly suggesting that a DQB1 polymorphic amino acid might be more tightly associated than any single allele. Sequence screening revealed that Ser74 in the second exon shared by all DQB1*05 and *04 was 20 times transmitted against 4 times non-transmitted (P = 0.001) in familial cases of SW. Thus, together with narcolepsy and REM sleep behavior disorder, these findings suggest that specific DQB1 genes are implicated in disorders of motor control during sleep.

Adolescent↗
PubMed2000

Rapid eye movement sleep behaviour disorder: demographic, clinical and laboratory findings in 93 cases.

We describe demographic, clinical, laboratory and aetiological findings in 93 consecutive patients with rapid eye movement (REM) sleep behaviour disorder (RBD), which consists of excessive motor activity during dreaming in association with loss of skeletal muscle atonia of REM sleep. The patients were seen at the Mayo Sleep Disorders Center between January 1, 1991 and July 31, 1995. Eighty-one patients (87%) were male. The mean age of RBD onset was 60.9 years (range 36-84 years) and the mean age at presentation was 64.4 years (37-85 years). Thirty-two per cent of patients had injured themselves and 64% had assaulted their spouses. Subdural haematomas occurred in two patients. Dream content was altered and involved defence of the sleeper against attack in 87%. The frequency of nocturnal events decreased with time in seven untreated patients with neurodegenerative disease. MRI or CT head scans were performed in 56% of patients. Although four scans showed brainstem pathology, all of these patients had apparently unrelated neurodegenerative diseases known to be associated with RBD. Neurological disorders were present in 57% of patients; Parkinson's disease, dementia without parkinsonism and multiple system atrophy accounted for all but 14% of these. RBD developed before parkinsonism in 52% of the patients with Parkinson's disease. Five of the 14 patients with multiple system atrophy were female, and thus the strong male predominance in RBD is less evident in this condition. Psychiatric disorders, drug use or drug withdrawal were rarely causally related to RBD. Clonazepam treatment of RBD was completely or partially successful in 87% of the patients who used the drug. We conclude that RBD is a well-defined condition and that descriptions from different centres are fairly consistent. It is commonest in elderly males and may result in serious morbidity to patients and bed partners. There is a strong relationship to neurodegenerative disease, especially Parkinson's disease, multiple system atrophy and dementia, and neurologists should explore the possibility of RBD in patients with these conditions. RBD symptoms may be the first manifestations of these disorders and careful follow-up is needed. Neuroimaging is unlikely to reveal underlying disorders not suspected clinically. We confirm the effectiveness of clonazepam, but note that attention to the safety of the bed environment may be sufficient for patients with contraindications to the drug.

Adult↗
PubMed1999

Narcolepsy.

Narcolepsy is a disabling, chronic sleep-wake disorder that typically starts in a patient's second or third decade of life. Its key features are hypersomnia and cataplexy. Sleep paralysis, hallucinations, and disrupted sleep are nonspecific symptoms and are not always present. Disability relates primarily to sleepiness- related cognitive impairment, accidents, and psychosocial problems. Treatment, which includes counseling, scheduled napping, and pharmacologic intervention, is effective for most patients. Hypersomnia is best treated with such indirect sympathomimetics as mazindol, pemoline, methylphenidate, and amphetamine. Modafinil may become the drug of choice because it has fewer side effects. Cataplexy, sleep paralysis, and hallucinations may be ameliorated by compounds, including clomipramine and imipramine, that suppress rapid eye movement (REM) sleep. Regular follow-up visits enable the clinician to recognize uncommon but serious side effects (tolerance, substance abuse, psychosis, and hypertension) and additional sleep disturbances (sleep apnea, periodic limb movements in sleep, REM sleep behavior disorder), which can be specifically treated.

Journal Article↗
PubMed2005

REM sleep behaviour disorder: clinical profiles and pathophysiology.

Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia characterized by the intermittent loss of electromyographic atonia normally present during REM sleep and the emergence of purposeful complex motor activity associated with vivid dreams. Rapid eye movement sleep behaviour disorder usually affects older males and can be either idiopathic or symptomatic of various underlying disorders, in particular neurodegenerative diseases; in the latter case, RBD may be a prodromal symptom of the neurological disease. Several brainstem regions have been implicated in RBD pathophysiology, although the exact mechanism of the disorder in humans remains to be clarified. On clinical grounds, differentiation of RBD should be made from several non-REM parasomnias and other aberrant behaviours occurring during sleep. Rapid eye movement sleep behaviour disorder can be diagnosed on the basis of a systematic medical, neurological and psychiatric evaluation of the patient, assisted by a standard polysomnographic recording that includes continuous overnight videotaping; a brain imaging study is mandatory when an underlying brain disease is being suspected. Clonazepam at bedtime is the treatment of choice for RBD; alternatively, melatonin or pramipexole can be administered when clonazepam is contraindicated.

Diagnosis, Differential↗
PubMed1997

Contributions of the pedunculopontine region to normal and altered REM sleep.

The pedunculopontine (PPN) region of the upper brainstem is recognized as a critical modulator of activated behavioral states such as wakefulness and rapid eye movement (REM) sleep. The expression of REM sleep-related physiology (e.g. thalamocortical arousal, ponto-geniculate-occipital (PGO) waves, and atonia) depends upon a subpopulation of PPN neurons that release acetylcholine (ACh) to act upon muscarinic receptors (mAChRs). Serotonin's potent hyperpolarization of cholinergic PPN neurons is central to present working models of REM sleep control. A growing body of experimental evidence and clinical experience suggests that the responsiveness of the PPN region, and thereby modulation of REM sleep, involves closely adjacent glutamatergic neurons and alternate afferent neurotransmitters. Although many of these afferents are yet to be defined, dopamine-sensitive GABAergic pathways exiting the main output nuclei of the basal ganglia and adjacent forebrain nuclei appear to be the most conspicuous and the most likely to be clinically relevant. These GABAergic pathways are ideally sited to modulate the physiologic hallmarks of REM sleep differentially (e.g. atonia versus cortical activation), because each originates from a functionally unique forebrain circuit and terminates in a unique pattern upon brain stem neurons with unique membrane characteristics. Evidence is reviewed that changes in the quality, timing, and quantity of REM sleep that characterize narcolepsy, REM sleep behavior disorder, and neurodegenerative and affective disorders (depression and schizophrenia) reflect 1) changes in responsiveness of cells in the PPN region governed by these afferents; 2) increase or decrease in PPN cell number; or 3) mAChRs mediating increased responsiveness to ACh derived from the PPN. Auditory evoked potentials and acoustic startle responses provide means independent from recording sleep to assess pathophysiologies affecting the PPN and its connections and thereby complement investigations of their role in affecting daytime functions (e.g. arousal and attention).

Acetylcholine↗
PubMed2001

Diffuse Lewy Body Disease.

Diffuse Lewy body disease (DLB) is a neurodegenerative disorder characterized by dementia, fluctuations in mental status, hallucinations, and parkinsonism. Diffuse Lewy body disease is the second most common cause of dementia, following Alzheimer's disease. The treatment of DLB includes cholinergic therapy for cognitive impairment, atypical neuroleptics to alleviate hallucinations, and levodopa/carbidopa to improve parkinsonism. The recognition and diagnosis of DLB has critical treatment implications. Centrally acting cholinesterase inhibitors, such as rivastigmine, donepezil, and galantamine partially reverse decreased cortical cholinergic activity and may improve cognition and neuropsychiatric symptoms in DLB. Rivastigmine has been demonstrated to improve cognition and neuropsychiatric symptoms in patients with DLB without worsening parkinsonian features. Due to the potential adverse events associated with neuroleptics in this population, treatment with cholinesterase inhibitors is currently considered first-line therapy in the treatment of hallucinations and mental status fluctuations in DLB. Exquisite sensitivity to neuroleptic medications is a hallmark of DLB and life-threatening complications have been reported. Caution should be exercised when implementing antipsychotic therapy for the treatment of behavioral disturbances of DLB. When required, atypical neuroleptics with the least extrapyramdial side effects, such as quetiapine, should be used. The parkinsonian features of DLB may respond to dopaminergic therapy with levodopa. If parkinsonian symptoms result in clinical disability, a trial of levodopa is warranted. Unfortunately, dopaminergic medications may worsen hallucinations. Because dopamine agonists have a greater tendency to induce hallucinations and somnolence, levodopa is the treatment of choice for parkinsonism in DLB. Rapid eye movement (REM) sleep behavior disorder (RBD) is now recognized as a feature of DLB. Awareness of the presence of this symptom in patients with DLB is important and treatment with low dose clonazepam may help. Cholinergic aumentation may also improve these symptoms in patients with DLB.

Journal Article↗
PubMed2005

Non-movement disorder heralds symptoms of Machado-Joseph disease years before ataxia.

We describe three patients with the Machado-Joseph disease (MJD) genetic abnormality who had non-movement disorder neurological symptoms or signs that preceded the gait ataxia by several years. This implies that some clinical manifestations other than ataxia may be considered part of the herald symptoms of MJD, especially in the setting of a positive family history.

Adult↗
PubMed2000

[Dementia with Lewy bodies].

Dementia with Lewy bodies (DLB) is the second most frequent neuropathologically diagnosed degenerative dementing illness. The clinical characteristics are progressive dementia, parkinsonian syndrome, fluctuations of cognitive functions, alertness, and attention, visual hallucinations (usually detailed and well described), depression, REM sleep behavior disorder, adverse responses to standard neuroleptics doses, falls, syncopes, systematized delusions, and other modalities of hallucinations. Specificity of the clinical diagnostic criteria is high (95%), and sensitivity is considerably lower. Mean age at disease onset ranges between 60 and 68 years. The male gender prevails. Disease duration is 6 to 8 years. The differential diagnoses of DLB are dementia of the Alzheimer type, Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy, multiple system atrophy, and rarely Creutzfeldt-Jakob disease. The genetic background of the disease is unclear. Magnetic resonance imaging and single photon emission tomography can contribute to the diagnosis. Controlled pharmacological studies have so far not been published. The disease is treated with L-dopa, atypical neuroleptics, acetylcholine esterase inhibitors, antihypotensive agents, and peripheral anticholinergic and alpha receptor-blocking medications to improve neurogenic bladder dysfunction.

Aged↗
PubMed2002

Sleep and periodic limb movements in corticobasal degeneration.

Corticobasal degeneration (CBD) exhibits distinct features of akinesia, the 'alien limb' sign and cortical myoclonus. We report a 63-year old woman with a history of CBD for 18 months who was studied twice using all-night polysomnography with an interval of 13 months. Both recordings revealed frequent periodic arm and leg movements predominantly during non-REM sleep. To our knowledge this has not been described in a patient with CBD so far. Similar to a previous report we found REM sleep without atonia (RWA) in all REM episodes. However, the patient showed RWA and some non violent movements that fulfilled the diagnosis of subclinical REM sleep behavior disorder only in the second investigation. These observations may be due to the underlying degenerative process that involves not only cortical but also thalamic and brainstem structures.

Journal Article↗
PubMed2002

[Dementia with Lewy bodies].

Dementia with Lewy bodies (DLB) is the second most frequent neuropathologically diagnosed degenerative dementing illness. The clinical characteristics are progressive dementia, Parkinson syndrome, fluctuations of cognitive functions, vigilance and attention, visual hallucinations (usually detailed and well described), depression, REM-sleep behavior disorder, adverse responses to standard doses of neuroleptics, falls, syncopes, systematized delusions, and non-visual hallucinations. Mean age at disease onset ranges between 60 and 68 years. Male persons are more frequently affected than female. Disease duration is six to seven years. The differential diagnoses of DLB are dementia of the Alzheimer-type, Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy, multiple system atrophy, and, in rare cases, Creutzfeldt-Jakob disease. The genetic background of the disease is unclear. Magnetic resonance imaging and single photon emission tomography can contribute to the diagnosis. The disease is treated with L-dopa, atypical neuroleptics, acetylcholine esterase inhibitors, antihypotensive agents, and peripheral anticholinergic and alpha-receptor-blocking medicaments to improve neurogenic bladder dysfunction.

Aged↗
PubMed1996

Fear of suicide during sleepwalking.

It is generally accepted that sleepwalking (SW) is a state of automatism in which an individual is unaware of, and has no control of, his or her behavior. Recently, Broughton et al. (1994) reported a case of a homicide and an attempted homicide during SW in which somnambulism was a legal defense and led to an acquittal. The wide variety in the clinical manifestations of SW and sleep terrors (ST) may sometimes lead to difficulties in diagnosing these treatable entities. The present case illustrates a diagnostic and clinical problem, deciding between histrionic behavior, suicidal acting out, REM-sleep behavioral disorder, and SW; and assessing the risk of suicide during SW.

Adult↗
PubMed2004

Definition and diagnosis of dementia with Lewy bodies.

Significant advances have been made in neuropathologic identification procedures for dementia with Lewy bodies (DLB), but difficulties remain in clinical diagnosis. Consensus criteria state that the core features of DLB are fluctuating cognition with pronounced variation in attention and alertness, recurrent visual hallucinations and spontaneous motor features of parkinsonism. At least two of these features must be present for the diagnosis of probable DLB. Assessments of the validity of the consensus criteria against autopsy generally indicate high specificity but varying sensitivity. More detailed assessments of core diagnostic features or better operationalization, particularly of fluctuating cognition, may help improve the diagnostic guidelines. Greater utilization of some features described as supporting the diagnosis (such as auditory hallucinations) and the potential inclusion of additional symptoms (such as REM sleep behavioral disorder) also may be useful. In addition, the potential role of more detailed neuropsychology and neuroimaging in the diagnostic process needs to be evaluated, although it is important that changes to the diagnostic criteria are based on empirical evidence. Other key issues pertain to the classification of DLB patients with concurrent Alzheimer's disease and the differentiation of DLB and Parkinson's disease dementia based on less than a 1-year history of parkinsonism preceding the dementia.

Aged↗
PubMed1999

Report of the second dementia with Lewy body international workshop: diagnosis and treatment. Consortium on Dementia with Lewy Bodies.

BACKGROUND/OBJECTIVE: The second International Workshop of the Consortium on Dementia with Lewy Bodies (DLB) met to review developments since publication of consensus guidelines for the clinical and pathologic diagnosis of DLB in 1996. The specificity of a clinical diagnosis of probable DLB, made using consensus criteria, is generally high (>85%), but sensitivity of case detection is lower and more variable. Inter-rater reliability for the core clinical features-recurrent visual hallucinations and spontaneous motor features of parkinsonism-is acceptable, but reliable identification of fluctuating cognition remains problematic. Depression and REM sleep behavior disorder may be additional features supportive of a diagnosis of DLB that were not included in the original guideline. RESULTS: It is recommended that the clinical consensus criteria continue to be used in their current format with research efforts focused on increasing sensitivity of case detection. Antiubiquitin immunocytochemistry is the method of choice for routine detection of Lewy bodies for diagnostic purposes in research and clinical practice. The use of alpha-synuclein antibodies to label Lewy bodies and Lewy neurites represents a major methodologic advance since the first DLB workshop. alpha-Synuclein-based methods are likely to be most useful in research laboratories, particularly for clinicopathologic correlative studies. CONCLUSION: Clinical management of DLB patients usually centers on the treatment of noncognitive features. There is now a pressing need to establish appropriately designed randomized controlled trials in DLB. Collaboration between dementia and movement disorder specialists is essential for rapid progress in research and clinical management protocols.

Dementia↗
PubMed2004

The two faces of Eve: dopamine's modulation of wakefulness and sleep.

In Parkinson's disease (PD), waking is frequently punctuated by sleep episodes, including rapid eye movement (REM) (i.e., dream) sleep, and sleep is interrupted by motor activities such as periodic limb movements and REM sleep behavior disorder. Because these pathologic behaviors are unaccounted for by contemporary models, this review summarizes the complex effects of dopamine (DA) on normal and pathological waking-sleeping. Maintenance of wakefulness is probably promoted by mesocorticolimbic DA circuits, and suppression of nocturnal movement appears to be influenced by indirect pathways linking midbrain DA neurons with pre-motor structures in the mesopontine tegmentum and ventromedial medulla. A diencephalospinal DA system may have an additional important role in mediating state-specific sensorimotor activity that is relevant to periodic limb movements and restless legs syndrome.

Arousal↗