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PubMed2007

[Sleep and movement disorders].

The three different states of being (wakefulness, NREM and REM sleep) are associated with profound neurophysiological and neurochemical changes in the brain. These changes explain the existence of movement disorders appearing only or preferentially during sleep, and the effects of sleep on movement disorders. Sleep-related movement disorders are of clinical relevance for multiple reasons: 1) high frequency (e.g. restless legs syndrome (RLS)); 2) diagnostic relevance (e.g. REM sleep behavior disorder (RBD) as first manifestation of Parkinson disorder); 3) diagnostic uncertainty (e.g. parasomnias vs nocturnal epilepsy); 4) association with injuries (e.g. RBD, sleepwalking), sleep disruption/daytime sleepiness (e.g. RLS), and psycho-social burden (e.g. enuresis); 5) requirement of specific treatments (e.g. nocturnal epilepsy, stridor, RBD). This article gives an overview on clinical manifestations, pathophysiology, work-up and treatment of sleep-related movement disorders (e.g. RLS, bruxism), parasomnias (e.g. sleepwalking, RBD), sleep-related epilepsies, and on sleep-associated manifestations of movement disorders (e.g. Parkinson disease, multiple system atrophy).

Adult↗
PubMed1994

Homicidal somnambulism: a case report.

A case of a homicide and an attempted homicide during presumed sleepwalking is reported in which somnambulism was the legal defense and led to an acquittal. Other possible explanations including complex partial seizures, dissociative state, rapid eye movement sleep behavior disorder and volitional waking behavior are discussed. The evidence supporting the probability that this act occurred during an episode of somnambulism and sleep-related confusional arousal is reviewed and weighed. This evidence includes personal and family history of somnambulism and related disorders; neurological, psychiatric and psychological assessments; presence of possible precipitating factors; and polysomnographic data.

Adult↗
PubMed2006

Sleep-wake habits and disorders in a series of 100 adult epilepsy patients--a prospective study.

The aim of the study was to assess sleep-wake habits and disorders and excessive daytime sleepiness (EDS) in an unselected outpatient epilepsy population. Sleep-wake habits and presence of sleep disorders were assessed by means of a clinical interview and a standard questionnaire in 100 consecutive patients with epilepsy and 90 controls. The questionnaire includes three validated instruments: the Epworth Sleepiness Scale (ESS) for EDS, SA-SDQ for sleep apnea (SA), and the Ullanlinna Narcolepsy Scale (UNS) for narcolepsy. Sleep complaints were reported by 30% of epilepsy patients compared to 10% of controls (p=0.001). The average total sleep time was similar in both groups. Insufficient sleep times were suspected in 24% of patients and 33% of controls. Sleep maintenance insomnia was more frequent in epilepsy patients (52% vs. 38%, p=0.06), whereas nightmares (6% vs. 16%, p=0.04) and bruxism (10% vs. 19%, p=0.07) were more frequent in controls. Sleep onset insomnia (34% vs. 28%), EDS (ESS >or=10, 19% vs. 14%), SA (9% vs. 3%), restless legs symptoms (RL-symptoms, 18% vs. 12%) and most parasomnias were similarly frequent in both groups. In a stepwise logistic regression model loud snoring and RL-symptoms were found to be the only independent predictors of EDS in epilepsy patients. In conclusion, sleep-wake habits and the frequency of most sleep disorders are similar in non-selected epilepsy patients as compared to controls. In epilepsy patients, EDS was predicted by a history of loud snoring and RL-symptoms but not by SA or epilepsy-related variables (including type of epilepsy, frequency of seizures, and number of antiepileptic drugs).

Adult↗
PubMed1983

Effect of methylmercury chloride on sleep-waking rhythms in rats.

Effects of methylmercury chloride (MMC) on circadian sleep-waking rhythms were examined in rats which had been chronically implanted with EEG and EMG electrodes. Bihourly distributions of wakefulness (W), slow wave sleep (SWS) and paradoxical sleep (PS) and 12-h amounts of W, SWS and PS during light and dark periods were measured before and after MMC administration for 2 successive days at 3 dose levels. A total dose of 10 mg MMC/kg body wt was found to be the threshold for inducing reversible changes in the sleep-waking patterns. A total dose of 30 mg MMC/kg produced an increase in both dark-phase SWS and PS as well as a decrease in light-phase PS at the expense of an increase in light-phase W and a delayed phase of the circadian PS rhythm. The delayed phase of the PS rhythm tended to persist after the increased SWS during the dark period returned to normal. Brain mercury concentrations were measured in order to find the dose-response relationship and the time dependence of the MMC-induced sleep disorder. The sleep-waking disorder was found to appear at lower levels of brain Hg and shorter latency than behavioral disorders of movement and postural maintenance previously reported [5-8].

Animals↗
PubMed2006

Paroxysmal motor disorders of sleep: the clinical spectrum and differentiation from epilepsy.

The diagnosis of paroxysmal events in sleep represents a significant challenge for the clinician, with the distinction of nocturnal epilepsy from nonepileptic sleep disorders often the primary concern. Diagnostic error or uncertainty is not uncommon in this situation, particularly with respect to nocturnal frontal lobe epilepsy (NFLE), which has a variable and often unusual presentation. Such errors can be minimized if the range of nonepileptic disorders with motor activity in sleep is fully appreciated. Here we review these disorders, before discussing the important clinical and electrographic features that allow their accurate differentiation from seizures. Particular emphasis is placed on the differentiation of nocturnal frontal lobe epilepsy from non-rapid eye movement (NREM) arousal disorders and other parasomnias. The value of recording episodes with video EEG polysomnography is discussed.

Adolescent↗
PubMed2006

Promoting adjustment of the sleep-wake cycle by chronobiotics.

Chronobiotics are substances that adjust the timing of internal biological rhythms. Many classes of drugs have been claimed to possess such properties and arouse growing interest as the circumstances for their use in sleep disturbances caused by circadian rhythms alterations (delayed or advanced sleep-phase syndromes, non-24-h sleep-wake disorders, jet lag, shift work sleep disorders and so on) have become progressively more frequent. Amongst the substances potentially presenting chronobiotic properties, a consensus seems to be reached on the possible use of melatonin or its agonists to shift the phase of the human circadian clock, but optimizing the dose, formulation and especially the time of administration require further studies.

Chronobiology Phenomena↗
PubMed2001

[Photoperiod phototherapy and wakefulness-sleep rhythm disorders].

Bright light therapy is a recent physical treatment in chronodisabled situations. The most recognized indication is the seasonal affective disorder. However, any disease or dysfunction where a misalignment of sleep-wake and circadian rhythms may be suspected is a potential tool for this treatment. Analyses of the literature throughout the interpretation methods of the evidence based medicine indicate that bright light therapy, if not a standard, could be recommended in a number of circadian rhythm sleep disorders, mainly the delayed and advanced sleep phase syndromes. Time aspects are essential for the success of phototherapy. From this point of view, easy and practical technological means or methods, allowing to shape a Phase Response Curve in each individual to be treated, should be clear progress. A future extension of indications will also depend on the checking of essential hypotheses linking circadian and sleep-wake rhythms in diseases such as psychophysiological insomnia, multiple sclerosis, brain dysgeneses or dementias. At last, a non negligible advantage of bright light therapy appears to be its relative safety.

Humans↗
PubMed2000

Neuroanatomical and neurophysiological aspects of sleep: basic science and clinical relevance.

This is an exciting period for basic sleep research, because we are now beginning to understand some of the mechanisms controlling the changes in consciousness associated with sleep and wakefulness. Witness the recent discoveries of a probable genetic involvement in narcolepsy, the identification of hypothalamic structures promoting sleep, and the mounting evidence that adenosine is an endogenous sleep factor. We review these and other recent developments that help us understand the neuroanatomical and neurophysiological basis of some sleep disorders. For a detailed discussion of specific sleep disorders and clinical issues, the reader is referred to other sources. Overviews are also available covering rapid eye movement (REM) and non-REM sleep physiology, the role of humoral factors in sleep, and the relationship between the immune system and sleep. In fact, where appropriate, here we draw directly on material from our earlier summaries of work in the field. We begin with a brief review of the organization of sleep and wakefulness to provide the background for the subsequent discussions of the anatomy and neurophysiology of the neural control of different vigilance states and associated sleep disorders. For example, a brief description of the neural mechanisms of REM sleep will be followed by an outline of selected sleep disorders related to REM sleep. In summary, we make no attempt here to include all sleep disorders and only review a few selected examples, those in which there is an understanding based on knowledge of central nervous system physiology. Unfortunately we are not now able to include sleep apnea, because the discovery of sleep apnea not only was a defining moment for clinical sleep research, but to this day remains the principal presenting complaint at some sleep disorder clinics.

Brain↗
PubMed2004

Systemic growth hormone corrects sleep disturbance in Smith-Magenis syndrome.

Smith-Magenis syndrome (SMS) is a multiple congenital anomaly syndrome characterized by an interstitial deletion of chromosome 17p11.2. Sleep problems such as nocturnal awakening and abnormality in the percentage of rapid eye movement (REM) sleep are frequently observed in patients with SMS, and several medications have been administered to improve the sleep disorders. Here we present a female case of SMS showing early waking and reduction of REM sleep, which were corrected by human growth hormone (GH) replacement for her dwarfism. Also, we report changes in the sleep-wakefulness circadian rhythm and polysomnographical data before and after the start of human GH replacement. It is speculated that GH deficiency could be involved in sleep disturbance in SMS.

Abnormalities, Multiple↗
PubMed2003

[Sleep rhythm disturbances in Alzheimer's disease].

PURPOSE: Sleep-wake rhythm disturbances observed in Alzheimer's disease are correlated with the severity of cognitive impairment and often result in institutionalization. These disturbances are also a major cause of psychotropic medication misuse. We report age-related physiologic and disease related pathologic changes in sleep-wake rhythms and propose chronobiological treatment approaches in patients with Alzheimer's disease. CURRENT KNOWLEDGE AND KEY POINT: Alzheimer patients show a greater breakdown of the circadian sleep-wake cycle compared to similarly aged non demented controls. Demented patients spend their nights in a state of frequent restlessness and their days in a state of frequent sleepiness. These sleep-wake disturbances became increasingly more marked with progression of the disease. The architecture of sleep in Alzheimer's disease is marked by further decreases of slow wave sleep (SWS) and rapid eye movement (REM) sleep, and increases of time and frequency of awakening compared to age-matched control subjects. The sleep-wake disturbances in elderly people and particularly Alzheimer patients may result from changes at different levels: a reduction of environmental synchronizers or their perception, a lack of mental and physical activity, an age or disease related anatomical changes with loss of functionality of the biological clock(s). FUTURE PROSPECTS AND PROJECTS: In Alzheimer patients, controlling sleep-wake disturbances with sedative drugs often increases both sleep disturbance and cognitive dysfunction. A chronobiological approach with bright-light therapy, melatonin administration, restricted time in bed, and diurnal activity may be an interesting therapeutic alternative in the management of sleep-wake disorders in Alzheimer patients. The aim of these therapeutics is to improve sleep and diurnal activity and consequently to increase the quality of life in Alzheimer patients.

Aged↗
PubMed1987

Sleep disorders in kindled cats differ according to the timing of polygraphic recordings and of seizures in the sleep-wake cycle.

Sleep disorders in amygdala-kindled cats differ according to the sleep or waking state in which seizures occur and the time lapse between seizures and polygraphic recordings. Twelve-hour polygraphic recordings were initiated at the following times: (i) before kindling (N = 8 cats); (ii) just after kindled convulsions during waking, slow-wave sleep (SWS), rapid-eye-movement sleep (REMS), or in transition from SWS to REMS (N = 8 cats per state), and (iii) 24 h after state-specific seizures (N = 8 cats per state). Rapid onset SWS and delayed REMS occurred in records started immediately after seizures in waking, SWS, or REMS; in contrast, seizures during transitions from SWS to REMS produced early onset REMS and SWS. Finally, records begun 24 h after seizures always revealed prolonged sleep onset and generalized sleep suppression regardless of the state in which seizures occurred. The timing of seizures and of polygraphic recordings may explain discrepancies in the literature on the type of sleep disorders seen in secondary generalized temporal lobe epilepsy.

Animals↗
PubMed1979

Hypersomnia with simultaneous waking and sleep patterns in the electroencephalogram. A case report with neurotransmitter studies.

A mildly dyslexic boy of 11 years, with no neurological deficit or history of epileptic seizures, had marked hypersomnia for 2 years, which was most pronounced in the morning hours. Repeated EEG studies and power spectral analysis revealed simultaneous posterior alpha rhythm and sleep patterns (spindles, vertex waves, K complexes) over vertex and frontocentral regions, while the patient was behaviorally awake. Bilateral synchronous anterior spikes were frequently noted in association with sleep patterns. A polysomnogram over 24 h confirmed excessive sleep, night and day (especially morning hours) and there was evidence of a large REM sleep percentage (on EMG and EOG basis) while the EEG had predominantly non-REM sleep patterns. Special neurotransmitter studies were performed in view of a presumed disturbance affecting the neurobiochemical sleep regulation. These studies were based on CSF metabolite levels and provided evidence for a high serotonin metabolite (5HIAA) level. It is tempting to hypothesize that the biochemical disturbance has led to encroachment of non-REM sleep patterns on both wakefulness and REM sleep. Further discussion deals with the bilateral-synchronous spike activity and its relationship to arousal patterns in sleep.

Child↗