REM and NREM Sleep Parasomnia in Anti-NMDA Receptor Encephalitis.

OBJECTIVES: Encephalitis with anti-N-methyl-d-aspartate receptor antibodies (anti-NMDARe) is a rare disorder characterized by cognitive impairment, psychosis, seizures, and abnormal movements. Abnormal behaviors during REM sleep have not been described in anti-NMDARe. METHODS: Patients were monitored by video-polysomnography on a first night followed by multiple sleep latency tests and 18 hours of bed rest. RESULTS: Two patients with anti-NMDARe developed during the acute and postacute phase parasomnias including REM sleep behavior disorder and continuous finalistic quiet gesturing during a mixed N2/R sleep. The parasomnia disorder was improved by gabapentin and clonazepam. DISCUSSION: Video-polysomnography avoids misdiagnosing these parasomnia behaviors for seizure or movement disorders and allows adequate treatment.

"Catatrenia": un trastorno del sueño poco conocido: descripción de tres casos clínicos pediátricos / Catathrenia: unknown sleep disorder: report 3 cases in pediatric patients

Catatrenia (gemido nocturno) es una condición rara caracterizada por sonidos irregulares que ocurren durante el sueño. Los comportamientos ocurren intermitentemente durante cualquiera de las dos etapas de sueño, REM o NREM y se caracterizan por gemidos prolongados, a menudo muy fuertes, socialmente perturbadores, durante la expiración. Es poco conocido y espera más definición y estudios terapéuticos. Hay pocos reportes y en su mayoría de pacientes adultos. Se presentan 3 casos en pacientes pediátricos.

Catathrenia (nocturnal groaning) is a rare condition characterized by irregular sounds that occur during sleep. The behaviors occur intermittently during either REM or NREM sleep and are characterized by prolonged, often very loud, socially disruptive groaning sounds during expiration. It is poorly understood and awaits further definition and therapeutic studies. There are few reports mostly adult patients are presented below 3 cases in pediatric patients.

Perioperative Management of Insomnia, Restless Legs, Narcolepsy, and Parasomnias.

Obstructive sleep apnea (OSA) has been shown to increase risk of adverse perioperative events. More recently, investigators have begun to examine other common sleep disorders to assess how they may be impacted by the perioperative environment, as well as influence postoperative outcomes. There are a number of mechanisms by which such common sleep disorders (eg, insomnia, restless legs syndrome, narcolepsy, and parasomnias) may have consequences in the perioperative setting, both related to the underlying pathophysiology of the diseases as well as their treatments. This review will highlight the current state of the literature and offer recommendations for management of these conditions during the perioperative journey.

A 3-year observation of excessive daytime sleepiness after subthalamic deep brain stimulation in patients with Parkinson's disease.

OBJECTIVE: Subthalamic nucleus deep brain stimulation (STN DBS) has a positive effect on sleep quality, but its effect on wake functions is controversial. This study evaluated the longitudinal changes of the quality of sleep and excessive daytime sleepiness (EDS) in Parkinson's disease (PD) patients undergoing STN DBS and identify which factors are associated with the presence of EDS before and after STN DBS. PATIENT AND METHODS: A total of 33 PD patients who underwent bilateral STN DBS between July 2011 and October 2015 were recruited. We evaluated subjective sleep quality assessed by Parkinson's Disease Sleep Scale (PDSS) and EDS using Epworth Sleepiness Scale (ESS) preoperatively and 6 months, 1 year, and 3 years postoperatively. RESULTS: There is a significant improvement in PDSS, and a noticeable change occurs immediately after the surgery. After DBS, the number of patients with persistent EDS gradually decreased, but patients with newly developed EDS were added. Baseline ESS score was highly correlated with EDS at 6 months and 1 year postoperatively, and older age of PD onset was highly associated with EDS at 1 year after DBS. At 3 years after DBS, the total PDSS score is a main contributing factor for EDS. There was no significant difference in dopamine agonist dose (agonist LED) and levodopa equivalent daily dose (LEDD) between groups with and without EDS at any time points. CONCLUSION: Bilateral STN DBS improves the subjective sleep quality, but EDS may improve or worsen. The risk factors for EDS change over time after STN DBS. Interestingly, dopaminergic medication did not affect EDS in DBS-treated PD patients.

Adrenergic reactions during N3 sleep arousals in sleepwalking and sleep terrors: The chicken or the egg?

To understand the mechanisms of N3 sleep interruptions in patients with sleepwalking episodes and/or sleep terrors (SW/ST), we evaluated whether autonomic reactions preceded or accompanied behavioural arousals from NREM sleep stage N3. In 20 adult patients with SW/ST and 20 matched controls without parasomnia, heart rate and pulse wave amplitude were measured beat-to-beat during the 10 beats preceding and during the 15 beats succeeding a motor arousal from N3 sleep. Respiratory rate and amplitude were measured during the same 25 successive beats. In patients with SW/ST, the N3 arousals were associated with a 33% increase in heart rate, a 57% decrease in pulse wave amplitude (indicating a major vasoconstriction), a 24% increase in respiratory rate and a doubling of respiratory amplitude. Notably, tachycardia and vasoconstriction started 4 s before motor arousals. A similar profile (tachycardia and vasoconstriction gradually increasing from the 4 s preceding arousal and post-arousal increase of respiratory amplitude, but no polypnea) was also observed, with a lower amplitude, during the less frequent 38 quiet N3 arousals in control subjects. Parasomniac arousals were associated with greater tachycardia, vasoconstriction and polypnea than quiet arousals, with the same pre-arousal gradual increases in heart rate and vasoconstriction. Autonomic arousal occurs 4 s before motor arousal from N3 sleep in patients with SW/ST (with a higher adrenergic reaction than in controls), suggesting that an alarming event during sleep (possibly a worrying sleep mentation or a local subcortical arousal) causes the motor arousal.

Sexsomnia in an Adolescent.

ABSTRACT: Sexsomnia has been reported and is well described in 115 prior cases in the literature. There have been associations with other sleep disorders serving as triggers for confusional arousals, thereby worsening sexsomnia episodes. We present a case of an adolescent boy with a history of resected and treated pineoblastoma who later developed sexsomnia marked by multiple episodes of masturbatory events per night. He had additional suspicions of obstructive sleep apnea. Polysomnography confirmed severe obstructive sleep apnea and captured multiple episodes of sexsomnia from both REM and NREM sleep. The patient also had daytime symptoms of severe anxiety and hypersomnia that required pharmacological intervention, cognitive behavioral techniques, and hypnosis. The patient showed improvement with hypnosis along with a multimodal approach to the treatment of sexsomnia.

A stereo EEG study in a patient with sleep-related hypermotor epilepsy due to DEPDC5 mutation.

PURPOSE: Dishevelled EGL-10 and pleckstrin domain-containing protein 5 (DEPDC5) mutations are found in a wide spectrum of focal epilepsies ranging from epilepsy caused by malformation of cortical development to non-lesional epilepsy, including sleep-related hypermotor epilepsy (SHE). A surgical approach has been anecdotally reported in patients with DEPDC5 mutations, but most of these cases had a lesional etiology. METHODS: We describe a stereo-EEG (SEEG) study in a patient with drug-resistant/non-lesional SHE. Patient was screened for known mutations associated with SHE. RESULTS: SEEG disclosed bilateral synchronous and independent activity prevailing on the right central-anterior cingulate cortex, without a clear spatially defined epileptogenic zone. Due to the lack of a clear epileptogenic zone, surgery was contraindicated. Years later a DEPDC5 mutation was identified. CONCLUSION: We suggest that genetic analysis should be considered before performing SEEG study in a patient with drug resistant non-lesional SHE, in the presence of seizures in wakefulness and unclear anatomo-electroclinical correlation. If DEPDC5 mutations are identified, the presurgical evaluation should be tailored to look for MRI-negative focal cortical dysplasia and a wide epileptogenic network. The appropriate management and potential benefit of surgery for genetic non-lesional epilepsy have yet to be clarified.

Sleep-related eating disorder and its associated conditions.

Sleep-related eating disorder (SRED) is a condition characterized by recurrent episodes of eating at the transition from night-time sleep to arousal. SRED patients describe eating in an out-of-control manner with preference for high-caloric foods and sometimes with inedible or toxic items. Level of consciousness during SRED episodes ranges from partial consciousness to dense unawareness typical of somnambulistic episodes. SRED is sometimes associated with psychotropic medication, in particular sedative hypnotics, and other sleep disorders, including parasomnias, narcolepsy, and restless legs syndrome. Night eating syndrome (NES) is another important condition in the disordered night-time eating spectrum showing hyperphagia episodes at full arousal from nocturnal sleep without accompanying amnesia. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset. The two conditions often overlap and possibly share a common pathophysiology. Studies have suggested that central nervous system serotonin modulation may lead to an effective treatment of NES, while the anti-seizure medication topiramate may be an effective SRED treatment.

Progesterone for hot flush and night sweat treatment--effectiveness for severe vasomotor symptoms and lack of withdrawal rebound.

A controlled trial recently showed that oral micronized progesterone (Progesterone, 300 mg at h.s. daily) was effective for vasomotor symptoms (VMS) in 133 healthy early postmenopausal women. Here, we present subgroup data in women with severe VMS (50 VMS of moderate-severe intensity/wk) and also 1-mo withdrawal study outcomes. Women with severe VMS (n = 46) resembled the full cohort but experienced 10 VMS/d of 3 of 4 intensity. On therapy, the progesterone VMS number (#) decreased significantly more than placebo # to 5.5/day (d) versus 8/d (ANCOVA -2.0 95% CI: -3.5 to -0.4). Just after trial mid-point, a withdrawal substudy (D/C) was added--56 women were invited and 34 (61%) took part (progesterone 17; placebo 17). Those in the D/C cohort resembled the whole cohort. On stopping, VMS gradually increased--at D/C week 4, on progesterone, VMS daily # reached 78% and significantly less than baseline (-3.0 to -0.8) but placebo VMS # did not differ from run-in. In summary, progesterone is effective for severe VMS and does not cause a rebound increase in VMS when stopped. That progesterone may be used alone for severe VMS and unlike estrogen does not appear to cause a withdrawal rebound increases VMS treatment options.

The two main theories on dental bruxism.

Bruxism is characterized by non-functional contact of mandibular and maxillary teeth resulting in clenching or grating of teeth. Theories on factors causing bruxism are a matter of controversy in current literature. The dental profession has predominantly viewed peripheral local morphological disorders, such as malocclusion, as the cause of clenching and gnashing. This etiological model is based on the theory that occlusal maladjustment results in reduced masticatory muscle tone. In the absence of occlusal equilibration, motor neuron activity of masticatory muscles is triggered by periodontal receptors. The second theory assumes that central disturbances in the area of the basal ganglia are the main cause of bruxism. An imbalance in the circuit processing of the basal ganglia is supposed to be responsible for muscle hyperactivity during nocturnal dyskinesia such as bruxism. Some authors assume that bruxism constitutes sleep-related parafunctional activity (parasomnia). A recent model, which may explain the potential imbalance of the basal ganglia, is neuroplasticity. Neural plasticity is based on the ability of synapses to change the way they work. Activation of neural plasticity can change the relationship between inhibitory and excitatory neurons. It seems obvious that bruxism is not a symptom specific to just one disease. Many forms (and causes) of bruxism may exist simultaneously, as, for example, peripheral or central forms.

Lifetime prevalence and incidence of parasomnias in a population of young adult Nigerians.

Lifetime prevalence, incidence, and risk factors for parasomnias were determined. Past experiences of non-REM, REM, and sleep-transition parasomnias were recorded. Diaries of night sleep duration, parasomnias, perception of aliens, levels of physical activity, headaches and intake of all substances, drugs, and tobacco were kept for 14 consecutive days. A total of 276 subjects were studied. Lifetime prevalences (95% CI) were 725 (668-776) for occurrence of any parasomnia, 43 (25-74) for sleepwalking, 112 (80-155) for sleep terror, 475 (416-533) for nightmares, 225 (179-277) for sleep paralysis, 43 (25-74) for sleep starts, 322 (270-380) for sleep talking, and 344 (291-402) for enuresis. Incidences (95% CI) were 210 (166-262) for occurrence of any parasomnia, 14 (6-37) for sleepwalking, 11 (4-31) for sleep terror, 170 (131-219) for confusional arousal, 18 (8-42) for nightmares, 14 (6-37) for sleep paralysis, 33 (17-61) for sleep starts, and 4 (1-20) for sleep enuresis. Multivariate analysis showed associations of increase occurrence of parasomnias and duration of sleep >7 h (p < 0.05) and intake of alcohol (p < 0.001), but heavy workload before sleep was associated with decreased occurrence of parasomnias (p < 0.01). Gender, smoking, caffeinated drinks, hypnotics, and headaches were not associated with parasomnias. Incidence of presence of aliens (95% CI) in the room was 25(0/infinity) (12-51). This study shows that more than 70% of the population have experienced parasomnias at any time in the past. Nightmares, enuresis, sleep paralysis and night terrors are the commonest parasomnias experienced in the past, while confusional arousal, sleep starts, and nightmares are the commonest parasomnias currently experienced. Incidence estimates show that all parasomnias persist into adulthood at reduced rates, but reduction of occurrence was greatest for enuresis. Long duration of night sleep and intake of alcohol predisposed subjects to higher occurrence of parasomnias.

Compensatory rebound of body movements during sleep, after asphyxia in neonatal rats / Resposta compensatória dos movimentos corporais do sono após a asfixia em ratos recém-nascidos

PURPOSE: The usefulness of body movements that occur during sleep when assessing perinatal asphyxia and predicting its long-term consequences is contradictory. This study investigated whether neonatal rats manifest these movements in compensatory rebound after asphyxia, and if these alterations play an important role in its pathogenesis. METHODS: Eight neonatal rats (aged 6-48h) were implanted with small EMG and EKG electrodes and sleep movements were recorded over a 30-minute control period. Recordings were continued during asphyxia caused by the enclosure of the animal in a polyvinyl sheet for 60 minutes, followed by a 30-minute recovery period. RESULTS: Heart rate was lowered to bradycardic level during asphyxia causing behavioral agitation and increased waking time during the initial phase (30 minutes). Sleep-related movements were also significantly reduced from 12.5 ± 0.5 (median ± SE/2min) to 9.0 ± 0.44 in the final half of the period (Anova, p<0.05). Movement frequency increased in the recovery period to 15.0 ± 0.49 (Anova, p<0.05). CONCLUSION: These data show that newborn rats present compensatory rebound of body movements during sleep which may help in the diagnosis of asphyxia and other problems related to sleep parameters.

OBJETIVO: A utilidade dos movimentos corporais (MC) que ocorrem durante o sono para diagnosticar e predizer as conseqüências, em longo prazo, da asfixia perinatal é contraditório. Este estudo investigou se ratos recém-nascidos (RN) manifestam MC em resposta compensatória à asfixia, e se estas alterações podem ter alguma importância na sua patogênese. MÉTODOS: Oito ratos RN (6-48h de vida) foram submetidos à implantação de pequenos eletrodos para registros da eletromiografia e eletrocardiografia. Os MC e a freqüência cardíaca (FC) foram registrados durante períodos de 30 min: fase controle (F1), fases de asfixia (F2; F3) e fase de recuperação pós-asfixia (F4). A asfixia foi promovida pelo envolvimento completo do animal com uma lâmina de polivinil. RESULTADOS: A FC diminuiu progressivamente durante F2 e F3 até a bradicardia. Em F2 houve grande agitação dos animais e aumento dos períodos de vigília. Em F3 houve redução significante dos MC de 12,5 ± 0,5 (Md ± SE/2min) para 9,0 ± 0,44 (P<0,05). A freqüência dos MC aumentou em F4 para 15,0 ± 0,49. CONCLUSÃO: Estes dados mostram que ratos RN com asfixia apresentam MC compensatórios durante o sono que podem ajudar no diagnóstico desta afecção e de outros problemas relacionados aos parâmetros do sono.

Parasomnias. Things that go thump in the night.

BACKGROUND: General practitioners are well versed with patients presenting to the surgery with sleep symptoms, however, the approach to evaluating these symptoms is often haphazard. Insomnia is the commonest presenting complaint. Sleep apnoea, although readily treatable, carries with it significant morbidity and mortality. OBJECTIVE: This article aims to highlight those disorders that occur infrequently during the night but which interrupt sleep--the parasomnias. DISCUSSION: Knowledge of the spectrum of parasomnias and their symptoms usually allows a reasonably accurate clinical diagnosis and the assistance of a sleep physician or sleep laboratory is not often required. Parasomnias may be classified by the sleep phase during which they occur. Nonrapid eye movement (NREM) parasomnias are most likely to occur during the first episode of stages 3 and 4 of NREM sleep (slow wave sleep) which is approximately one hour after sleep onset. Rapid eye movement (REM) sleep density is usually greatest in the last few hours of sleep, therefore REM sleep parasomnias are most likely to occur during this time.