Individual spindle detection and analysis in high-density recordings across the night and in thalamic stroke.

Sleep spindles are thalamocortical oscillations associated with several behavioural and clinical phenomena. In clinical populations, spindle activity has been shown to be reduced in schizophrenia, as well as after thalamic stroke. Automatic spindle detection algorithms present the only feasible way to systematically examine individual spindle characteristics. We took an established algorithm for spindle detection, and adapted it to high-density EEG sleep recordings. To illustrate the detection and analysis procedure, we examined how spindle characteristics changed across the night and introduced a linear mixed model approach applied to individual spindles in adults (n = 9). Next we examined spindle characteristics between a group of paramedian thalamic stroke patients (n = 9) and matched controls. We found a high spindle incidence rate and that, from early to late in the night, individual spindle power increased with the duration and globality of spindles; despite decreases in spindle incidence and peak-to-peak amplitude. In stroke patients, we found that only left-sided damage reduced individual spindle power. Furthermore, reduction was specific to posterior/fast spindles. Altogether, we demonstrate how state-of-the-art spindle detection techniques, applied to high-density recordings, and analysed using advanced statistical approaches can yield novel insights into how both normal and pathological circumstances affect sleep.

Sodium oxybate in narcolepsy with cataplexy: Zurich sleep center experience.

Sodium oxybate (SO; Xyrem®) has been approved in most countries for treatment of narcolepsy and cataplexy. In this study, we present a single-center experience of a series of 18 patients with narcolepsy with cataplexy (18/18 DQB1*0602 positive, 17/17 with low/absent cerebrospinal fluid hypocretin) in whom SO was prescribed. After 26 ± 13 months, 13/18 patients were still on SO at a mean dosage of 6.1 ± 1.2 g (in 8 of them in combination with stimulants). The following significant effects were observed: improved subjective sleepiness (12/13), cataplexy (13/13; median number of attacks from 20 to 1/month), hallucinations (8/10) and sleep paralysis (8/8); increase in mean sleep latency on the Maintenance of Wakefulness Test (from 5.5 to 17.4 min) and sleep/rest efficiency on actigraphy (from 61 to 76%); decrease in Epworth Sleepiness Scale score (from 18 to 14), sleep onset REM periods on the Multiple Sleep Latency Test (from 3.6 to 2.4) and errors in the Steer-Clear Test (from 11 to 2%). Five patients discontinued SO because of insufficient compliance (n = 2), lack of efficiency (n = 1) and side effects (n = 1). These data confirm and expand previous reports on the good effects and tolerability of SO as a treatment for narcolepsy with cataplexy.

Laughing as a manifestation of rapid eye movement sleep behavior disorder.

BACKGROUND: Among the range of sleep-related behavior displayed by patients with rapid eye movement (REM) sleep behavior disorder (RBD), aggressive acts are particularly common, while pleasant behaviors have rarely been reported. We aimed at identifying the frequency and characteristics of patients who displayed laughing as a pleasant, nonviolent manifestation of RBD. METHODS: We reviewed 67 consecutive polysomnographic recordings of patients with RBD, obtained in our sleep laboratory between July 2004 and July 2009. RESULTS: We identified 14 patients (21% of our RBD patients with degenerative parkinsonism: 10 males, mean age 63 ± 11 years) who repeatedly laughed during REM sleep. Ten patients had idiopathic Parkinson's disease, 3 suffered from multisystem atrophy and 1 patient was diagnosed with dementia with Lewy bodies. Other RBD-associated behaviors included smiling, crying, aggressive behavior, screaming, and somniloquia. Nine of the 14 patients were depressed during daytime. CONCLUSION: Laughing belongs to the spectrum of behavioral manifestations of RBD. Many of our patients with RBD-associated laughter were depressed, suggesting a dissociation between emotional expression during daytime and REM sleep.

Non-fluent aphasia and neural reorganization after speech therapy: insights from human sleep electrophysiology and functional magnetic resonance imaging.

Stroke is associated with long-term functional deficits. Behavioral interventions are often effective in promoting functional recovery and plastic changes. Recent studies in normal subjects have shown that sleep, and particularly slow wave activity (SWA), is tied to local brain plasticity and may be used as a sensitive marker of local cortical reorganization after stroke. In a pilot study, we assessed the local changes induced by a single exposure to a therapeutic session of IMITATE (Intensive Mouth Imitation and Talking for Aphasia Therapeutic Effects), a behavioral therapy used for recovery in patients with post-stroke aphasia. In addition, we measured brain activity changes with functional magnetic resonance imaging (fMRI) in a language observation task before, during and after the full IMITATE rehabilitative program. Speech production improved both after a single exposure and the full therapy program as measured by the Western Aphasia Battery (WAB) Repetition subscale. We found that IMITATE induced reorganization in functionally-connected, speech-relevant areas in the left hemisphere. These preliminary results suggest that sleep hd-EEGs, and the topographical analysis of SWA parameters, are well suited to investigate brain plastic changes underpinning functional recovery in neurological disorders.

Excessive daytime sleepiness in Parkinson's disease: characteristics and determinants.

BACKGROUND/AIMS: Excessive daytime sleepiness (EDS) is frequent in patients with Parkinson's disease (PD). Occasionally, EDS in PD exhibits narcolepsy-like features. We aimed to assess characteristics and determinants of EDS in consecutive patients with PD. METHODS: Thirty consecutive patients with PD underwent a detailed clinical examination. EDS was assessed using the Epworth Sleepiness Scale (ESS) and Multiple Sleep Latency Test (MSLT). Sleep was assessed using video-polysomnography. Cerebrospinal fluid (CSF) hypocretin-1 levels were obtained in 3 patients. RESULTS: ESS was >10 in 17 patients (57%). Mean sleep latency (MSL) on MSLT was <5 min in 11 patients (37%). There was a significant negative correlation between ESS and MSL. None of the 11 patients with MSL <5 min showed a sleep onset REM (SOREM) episode. Patients with EDS had higher dopamine agonists/levodopa equivalent doses, higher apnea/hypopnea index and exhibited wearing-off symptoms more often. Hypocretin-1 was normal in 3 patients tested. CONCLUSION: EDS, which can sometimes be severe, is common in PD patients even in the absence of SOREM and detectable CSF-hypocretin deficiency. In PD, EDS is a multifaceted phenomenon, the determinants of which include severity of PD, wearing-off symptoms, dosage of antiparkinsonian drugs and sleep-disordered breathing.

[Sleep and movement disorders]. / Schlaf und Bewegungsstörungen.

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).