Normal Sleep Spindles Research Articles

Extreme Sleep Spindles in Children with Autism Spectrum Disorder and Related Disorders—A Case Series

AbstractExtreme sleep spindles have fast activity and high amplitude, unlike normal sleep spindles. We report a case series of six children with autism and related disorders who had extreme spindles as noted on the sleep electroencephalogram recording at our center. We examine the types of extreme spindles, describe the clinical profiles of the 6 children, and discuss similar clinical and neurophysiological conditions.

Treatment Timing, EEG, Neuroimaging, and Outcomes After Acute Necrotizing Encephalopathy in Children.

Acute necrotizing encephalopathy (ANE) is a rare condition associated with rapid progression to coma and high incidence of morbidity and mortality. Clinical, electroencephalographic (EEG), and brain magnetic resonance imaging (MRI) characteristics and immunomodulatory therapy timing were retrospectively analyzed in children with ANE. ANE severity scores (ANE-SS) and MRI scores were also assessed. The associations of patient characteristics with 6-month modified Rankin scale (mRS) and length of hospitalization were determined using either univariate linear regression or one-way analysis of variance. 7 children were retrospectively evaluated. Normal EEG sleep spindles (P = .024) and early treatment (R2 = .57, P = .030) were associated with improved outcomes (ie, decreased mRS). Higher ANE-SS (R2 = .79, P = .011), higher age (R2 = .62, P = .038), and presence of brainstem lesions (P = .015) were associated with longer length of hospitalization. Other patient characteristics were not significantly associated with mRS or length of hospitalization. Early immunomodulatory therapy and normal sleep spindles are associated with better functional outcome in children with ANE.

Study of sleep spindle and K-complex characteristics on EEG during sleep in full-term infants from 2 weeks to 12 months of age

Background: Future neuronal development of the child is affected by the sleep characteristics during the infancy period. Proper development of sleep during early years of life is linked to mental and motor development. Hence, assessment of sleep during infancy is an opportunity to study the impact of sleep on the maturation of brain. Aim and Objective: The aim of the study is to estimate the development of sleep spindle characteristics and K-complex in sleep EEG in normal healthy infants, that is, from 2 weeks to 12 months of age. Materials and Methods: Our sample consisted of 50 healthy vaginally delivered full-term infants (27 boys and 23 girls) of both sexes with five repeated EEG assessments at 3-month intervals from 2 weeks to 12 months of age. Result: The K-complexes were absent up to 3 months started appearing after the age of 3 months. Sleep spindles were absent up to 2 weeks of age gradually established at 1 year of age in healthy full-term infants. Conclusion: The healthy full-term infants exhibited normal sleep spindles and K-complex development on EEG. Sleep EEG characteristics may be used as predictor for mental and motor development later in life.

Sleep spindles are resilient to extensive white matter deterioration.

Sleep spindles are an essential part of non-rapid eye movement sleep, notably involved in sleep consolidation, cognition, learning and memory. These oscillatory waves depend on an interaction loop between the thalamus and the cortex, which relies on a structural backbone of thalamo-cortical white matter tracts. It is still largely unknown if the brain can properly produce sleep spindles when it underwent extensive white matter deterioration in these tracts, and we hypothesized that it would affect sleep spindle generation and morphology. We tested this hypothesis with chronic moderate to severe traumatic brain injury (n = 23; 30.5 ± 11.1 years old; 17 m/6f), a unique human model of extensive white matter deterioration, and a healthy control group (n = 27; 30.3 ± 13.4 years old; 21m/6f). Sleep spindles were analysed on a full night of polysomnography over the frontal, central and parietal brain regions, and we measured their density, morphology and sigma-band power. White matter deterioration was quantified using diffusion-weighted MRI, with which we performed both whole-brain voxel-wise analysis (Tract-Based Spatial Statistics) and probabilistic tractography (with High Angular Resolution Diffusion Imaging) to target the thalamo-cortical tracts. Group differences were assessed for all variables and correlations were performed separately in each group, corrected for age and multiple comparisons. Surprisingly, although extensive white matter damage across the brain including all thalamo-cortical tracts was evident in the brain-injured group, sleep spindles remained completely undisrupted when compared to a healthy control group. In addition, almost all sleep spindle characteristics were not associated with the degree of white matter deterioration in the brain-injured group, except that more white matter deterioration correlated with lower spindle frequency over the frontal regions. This study highlights the resilience of sleep spindles to the deterioration of all white matter tracts critical to their existence, as they conserve normal density during non-rapid eye movement sleep with mostly unaltered morphology. We show that even with such a severe traumatic event, the brain has the ability to adapt or to withstand alterations in order to conserve normal sleep spindles.

Sleep spindles are resilient to extensive white matter deterioration

Sleep spindles are an essential part of non-rapid eye movement sleep, notably involved in sleep consolidation, cognition, learning and memory. These oscillatory waves depend on an interaction loop between the thalamus and the cortex, which relies on a structural backbone of thalamo-cortical white matter tracts. It is still largely unknown if the brain can properly produce sleep spindles when it underwent extensive white matter deterioration in these tracts, and we hypothesized that it would affect sleep spindle generation and morphology. We tested this hypothesis with chronic moderate to severe traumatic brain injury (n = 23; 30.5 ± 11.1 years old; 17 m/6f), a unique human model of extensive white matter deterioration, and a healthy control group (n = 27; 30.3 ± 13.4 years old; 21m/6f). Sleep spindles were analysed on a full night of polysomnography over the frontal, central and parietal brain regions, and we measured their density, morphology and sigma-band power. White matter deterioration was quantified using diffusion-weighted MRI, with which we performed both whole-brain voxel-wise analysis (Tract-Based Spatial Statistics) and probabilistic tractography (with High Angular Resolution Diffusion Imaging) to target the thalamo-cortical tracts. Group differences were assessed for all variables and correlations were performed separately in each group, corrected for age and multiple comparisons. Surprisingly, although extensive white matter damage across the brain including all thalamo-cortical tracts was evident in the brain-injured group, sleep spindles remained completely undisrupted when compared to a healthy control group. In addition, almost all sleep spindle characteristics were not associated with the degree of white matter deterioration in the brain-injured group, except that more white matter deterioration correlated with lower spindle frequency over the frontal regions. This study highlights the resilience of sleep spindles to the deterioration of all white matter tracts critical to their existence, as they conserve normal density during non-rapid eye movement sleep with mostly unaltered morphology. We show that even with such a severe traumatic event, the brain has the ability to adapt or to withstand alterations in order to conserve normal sleep spindles.

Slow-wave activity preceding the onset of 10-15-Hz sleep spindles and 5-9-Hz oscillations in electroencephalograms in rats with and without absence seizures.

Cortico-thalamocortical networks generate sleep spindles and slow waves during non-rapid eye movement sleep, as well as paroxysmal spike-wave discharges (i.e. electroencephalogram manifestation of absence epilepsy) and 5-9-Hz oscillations in genetic rat models (i.e. pro-epileptic activity). Absence epilepsy is a disorder of the thalamocortical network. We tested a hypothesis that absence epilepsy associates with changes in the slow-wave activity before the onset of sleep spindles and pro-epileptic 5-9-Hz oscillations. The study was performed in the WAG/Rij genetic rat model of absence epilepsy and Wistar rats at the age of 9-12months. Electroencephalograms were recorded with epidural electrodes from the anterior cortex. Sleep spindles (10-15Hz), 5-9-Hz oscillations and their slow-wave (2-7Hz) precursors were automatically detected and analysed using continuous wavelet transform. Subjects with electroencephalogram seizures (the "epileptic" phenotype) and without seizure activity (the "non-epileptic" phenotype) were identified in both strains. It was found that time-amplitude features of sleep spindles and 5-9-Hz oscillations were similar in both rat strains and in both phenotypes. Sleep spindles in "epileptic" rats were more often preceded by the slow-wave (~4Hz) activity than in "non-epileptic" rats. The intrinsic frequency of slow-wave precursors of sleep spindles and 5-9-Hz oscillations in "epileptic" rats was 1-1.5Hz higher than in "non-epileptic" rats. In general, our results indicated that absence epilepsy associated with: (a) the reinforcement of slow waves immediately prior to normal sleep spindles; and (b) weakening of amplitude growth in transition "slow wave → spindle/5-9-Hz oscillation".

Sleep spindles and spike–wave discharges in EEG: Their generic features, similarities and distinctions disclosed with Fourier transform and continuous wavelet analysis

Epileptic activity in the form of spike–wave discharges (SWD) appears in the electroencephalogram (EEG) during absence seizures. A relationship between SWD and normal sleep spindles is often assumed. This study compares time–frequency parameters of SWD and sleep spindles as recorded in the EEG in the WAG/Rij rat model of absence epilepsy. Fast Fourier transformation and continuous wavelet transformation were used for EEG analysis. Wavelet analysis was performed in non-segmented full-length EEG. A specific wavelet-based algorithm was developed for the automatic identification of sleep spindles and SWD. None of standard wavelet templates provided precise identification of all sleep spindles and SWD in the EEG and different wavelet templates were imperative in order to accomplish this task. SWD were identified with high probability using standard Morlet wavelet, but sleep spindles were identified using two types of customized adoptive ‘spindle wavelets’. It was found that (1) almost 100% of SWD (but only 50–60% of spindles) were identified using the Morlet-based wavelet transform. (2) 82–91% of sleep spindles were selected using adoptive ‘spindle wavelet 1’ (template's peak frequency ∼12.2 Hz), the remaining sleep spindles with ‘spindle wavelet 2’ (peak frequency ∼20–25 Hz). (3) Sleep spindles and SWD were detected by the elevation of wavelet energy in different frequencies: SWD, in 30–50 Hz band, sleep spindles, in 7–14 Hz. It is concluded that the EEG patterns of sleep spindles and SWD belong to different families of phasic EEG events with different time frequency characteristics.

Extreme spindles: A distinctive EEG pattern in Mycoplasma pneumoniae encephalitis

Extreme spindles are diffuse, continuous, high voltage, frontocentral, 8- to 15-Hz spindles thought to be an unusual exaggeration of normal sleep spindles.1 Historically, this EEG pattern was described and termed extreme spindles by Gibbs and Gibbs in 1962.1 Extreme spindles typically occur in children aged 1 to 12 years. They have been associated with such conditions as cerebral palsy, residual brain damage, undefined infections, infantile neuroaxonal dystrophy, Menkes’ kinky-hair syndrome, and congenital muscular dystrophy.2–4 There is one case report of extreme spindles in a 4-year-old Japanese boy during a subacute phase of mycoplasma encephalitis.5 We report a previously healthy child with an acute Mycoplasma pneumoniae encephalitis whose early EEG demonstrated extreme spindles before the pneumonia diagnosis was confirmed by mycoplasma antibodies. An 11-year-old boy presented with a new onset seizure. He was in good health when he …

Sleep architecture and its clinical correlates in first episode and neuroleptic-naive patients with schizophrenia

The goal of the present study was to characterize sleep organization in first episode and neuroleptic-naive patients with schizophrenia and to evaluate relationships between those sleep parameters and clinical symptoms. Eleven patients with acute schizophrenia never treated with neuroleptics were compared to 11 healthy controls. Sleep stages and phasic events (sleep spindles and rapid-eye-movements during REM sleep (REMs) were visually identified. Clinical symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS). Compared to controls, patients with schizophrenia had difficulty initiating sleep, decreased stage 4 duration, reduced rapid eye movement (REM) sleep latency, and normal sleep spindles and REMs densities. Positive symptoms correlated negatively with REM sleep latency. The BPRS total score correlated negatively with REM sleep duration and REMs density. The present results indicate that first episode and neuroleptic-naive patients with schizophrenia have difficulties initiating, but not maintaining, sleep. These results also confirm that the duration of stage 4 and REM sleep latency are reduced in first episode and neuroleptic-naive patients with schizophrenia. The fact that measures of REM sleep correlate with clinical scales of schizophrenia suggests that REM sleep physiology shares common substrates with symptoms of this disease.

The role of thalamic IGABAb in generating spike-wave discharges during petit mal seizures

Recent studies have suggested that 7-14 Hz spindle rhythms which appear during slow wave sleep and the 3 Hz spike-wave discharge accompanying petit mal seizures share common thalamocortical circuitry. A computational model was used to investigate the manner in which differential changes in the synaptic currents, IGABAA and IGABAB, observed in these cells can transform normal sleep spindles into the pathological oscillations recorded in primate exhibiting generalized petit mal epilepsy. The model suggests that inhibition by GABAergic interneurons and possibly nucleus reticularis thalami cells which reduce IGABA, increases the amplitude of the slower IGABAB. These events produce an extended inhibitory period in relay cells and also lead to the exaggerated post-inhibitory rebound Ca(2+)-dependent burst observed during seizures.

Aberrant transients in the EEG of epileptic rats: A spectral analytical approach

Aberrant transients in the cortical electroencephalogram of rats of the epileptic WAG/Rij strain were studied by means of spectial analysis. The EEG of rats of this strain contains, besides normal sleep spindles, high-voltage spiky phenomena, epileptic spike-wave discharges, and deviant intermediate stage. Spectral analysis of these transient phenomena shows that some features, like their peak frequency, are alike, but that they differ in other spectral characteristics, as in the first harmonic of the peak frequency and in the domain of the high frequencies. The results provide arguments for the view that spike-wave discharges might be considered as unique aberrant phenomena, presumably related but dissimilar to the high-voltage spiky phenomena and intermediate stage. Next to this, spectral analysis was used to study the intraphenomenal dynamics of spike-wave discharges. The peak frequency was found to decrease monotonously from about 10 Hz at the beginning of the spike-wave discharge to about 8 Hz at the end. Other spike-wave discharge frequency bands showed an intraphenomenal increase followed by a decrease. These time-variant EEG dynamics in spike-wave discharges might correlate with the cognitive disturbances during absence seizures in man.

Cortical activity and sleep in the rat lateral hypothalamic syndrome

Continuous EEG recordings were performed in lateral hypothalamic (LH) damaged rats from day 1 post-lesion when totally aphagic and adipsic until complete recovery of their feeding and drinking. During the early post-operative stage (days 1–3 post-lesion), LH rats showed a complete disorganization of their basal EEG which was characterized by two superimposed activities, a constant rapid low voltage activity modulated by high voltage low frequency waves. Except in the case of intense illumination, several arousing stimuli did not affect this activity. By day 4 post-lesion, the two overlapping activities were replaced by less abnormal waves on top of which the first normal sleep spindles appeared. Sleep increased gradually and normal amounts of both slow-wave and paradoxical sleep were observed during ‘stage 4’ of recovery when rats again ate food and drank water. During this stage, and contrary to normal rats, meal size was correlated only with sleep events occurring within the intermeal interval following the next meal, when most of the ingested nutrients reached the systematic compartment. The effect on sleep of intragastric or intravenous caloric repletion was, at least in part, in agreement with the view of indirect effect of LH lesions on sleep through metabolic impairment. Whatever the mechanism underlying sleep deficits, these are one of the major symptoms of the lateral hypothalamic syndrome.

Neuroanatomical and Electroencephalographic Correlations in Sanfilippo Syndrome, Type A

Waking and all-night-sleeping electroencephalographic recordings were obtained on a boy with Sanfilippo disease, type A. The most striking abnormalities were noted during sleep and included (1) lack of progression through normal sleep stages, (2) absence of vertex waves and normal sleep spindles, (3) inability to stage sleep by the usual criteria, and (4) an unusual alteration of low-amplitude (12 to 15 Hz) activity with generalized delta frequencies. Subsequently, neuropathological examination was performed. The electrophysiological phenomena may be correlated with severe cortical involvement.

A fast and spikey spindle variant in children with organic brain disease

A fast spikey variant of sleep spindles was observed in four patients (age 3–13 years) with clinical evidence of residual or progressive brain disease. This pattern can be separated from normal sleep spindles, sharp and asynchronous spindles of infancy and from the 14 and 6/sec positive spike discharge. The spikey component is predominantly negative and its distribution shows most common involvement of the central areas; there is no vertex maximum.