Electrocortical Arousal Research Articles

Catathrenia in children: clinical presentation, polysomnographic features, natural history, and response to therapy.

To determine the clinical presentation, polysomnographic appearance, and the response to therapy of catathrenia in children. A retrospective analysis was performed in children referred or evaluated at the Boston Children's Hospital Sleep Center between 1998 and 2021 who were documented to have catathrenia either as a chief complaint or an incidental finding. Catathrenia was identified in 21 children. The age of onset by parent report was 6.4 ± 4.4 years (range: birth-14 years), but the diagnosis was at 8.3 ± 3.8 years (range: 1.5-14 years). Catathrenia was the chief complaint for 24% of patients and was incidentally identified in 76% referred for breathing concerns. Bruxism was observed in 62% of patients. Catathrenia events most often occur following an electrocortical arousal (79%) and are most common in the second half of the night (73%). Catathrenia was observed exclusively in rapid eye movement (REM) sleep (16%), exclusively in non-REM sleep (32%), and in both sleep states (52%). Treatment of obstructive sleep apnea resulted in resolution or improvement in the obstructive sleep apnea in all patients, but the catathrenia persisted at a reduced level. Most catathrenia in children is diagnosed incidentally during evaluation for sleep-disordered breathing, although the groaning often started many years earlier. Catathrenia events decreased considerably after treatment of obstructive sleep apnea, but persisted in all patients. Catathrenia was also observed in children without signs or symptoms of sleep-disordered breathing, indicating that these are distinct conditions. The majority of children with catathrenia had no sleepiness or behavioral concerns. Katz ES, D'Ambrosio C. Catathrenia in children: clinical presentation, polysomnographic features, natural history, and response to therapy. J Clin Sleep Med. 2023;19(8):1505-1511.

Arousal system stimulation and anesthetic state alter visuoparietal connectivity.

Cortical information processing is under the precise control of the ascending arousal system (AAS). Anesthesia suppresses cortical arousal that can be mitigated by exogenous stimulation of the AAS. The question remains to what extent cortical information processing is regained by AAS stimulation. We investigate the effect of electrical stimulation of the nucleus Pontis Oralis (PnO), a distinct source of ascending AAS projections, on cortical functional connectivity (FC) and information storage at mild, moderate, and deep anesthesia. Local field potentials (LFPs) recorded previously in the secondary visual cortex (V2) and the adjacent parietal association cortex (PtA) in chronically instrumented unrestrained rats. We hypothesized that PnO stimulation would induce electrocortical arousal accompanied by enhanced FC and active information storage (AIS) implying improved information processing. In fact, stimulation reduced FC in slow oscillations (0.3-2.5 Hz) at low anesthetic level and increased FC at high anesthetic level. These effects were augmented following stimulation suggesting stimulus-induced plasticity. The observed opposite stimulation-anesthetic impact was less clear in the γ-band activity (30-70 Hz). In addition, FC in slow oscillations was more sensitive to stimulation and anesthetic level than FC in γ-band activity which exhibited a rather constant spatial FC structure that was symmetric between specific, topographically related sites in V2 and PtA. Invariant networks were defined as a set of strongly connected electrode channels, which were invariant to experimental conditions. In invariant networks, stimulation decreased AIS and increasing anesthetic level increased AIS. Conversely, in non-invariant (complement) networks, stimulation did not affect AIS at low anesthetic level but increased it at high anesthetic level. The results suggest that arousal stimulation alters cortical FC and information storage as a function of anesthetic level with a prolonged effect beyond the duration of stimulation. The findings help better understand how the arousal system may influence information processing in cortical networks at different levels of anesthesia.

Trazodone Effects on Obstructive Sleep Apnea and Non-REM Arousal Threshold.

A low respiratory arousal threshold is a physiological trait involved in obstructive sleep apnea (OSA) pathogenesis. Trazodone may increase arousal threshold without compromising upper airway muscles, which should improve OSA. We aimed to examine how trazodone alters OSA severity and arousal threshold. We hypothesized that trazodone would increase the arousal threshold and improve the apnea/hypopnea index (AHI) in selected patients with OSA. Subjects were studied on two separate nights in a randomized crossover design. Fifteen unselected subjects with OSA (AHI ≥ 10/h) underwent a standard polysomnogram plus an epiglottic catheter to measure the arousal threshold. Subjects were studied after receiving trazodone (100 mg) and placebo, with 1 week between conditions. The arousal threshold was calculated as the nadir pressure before electrocortical arousal from approximately 20 spontaneous respiratory events selected randomly. Compared with placebo, trazodone resulted in a significant reduction in AHI (38.7 vs. 28.5 events/h, P = 0.041), without worsening oxygen saturation or respiratory event duration. Trazodone was not associated with a significant change in the non-REM arousal threshold (-20.3 vs. -19.3 cm H2O, P = 0.51) compared with placebo. In subgroup analysis, responders to trazodone spent less time in N1 sleep (20.1% placebo vs. 9.0% trazodone, P = 0.052) and had an accompanying reduction in arousal index, whereas nonresponders were not observed to have a change in sleep parameters. These findings suggest that trazodone could be effective therapy for patients with OSA without worsening hypoxemia. Future studies should focus on underlying mechanisms and combination therapies to eliminate OSA. Clinical trial registered with www.clinicaltrials.gov (NCT 01817907).

An examination of the association between chronic sleep restriction and electrocortical arousal in college students

ObjectiveThe deleterious neurocognitive effects of laboratory-controlled short-term sleep deprivation are well-known. The present study investigated neurocognitive changes arising from chronic sleep restriction outside the laboratory. MethodsSleep patterns of 24 undergraduates were tracked via actigraphy across a 15-week semester. At the semester beginning, at a midpoint, and a week before finals, students performed the Psychomotor Vigilance Test (PVT) and cortical arousal was measured via event-related potentials (ERP) and resting state electroencephalography (EEG). ResultsAverage daily sleep decreased between Session 1 and Sessions 2 and 3. Calculated circadian rhythm measures indicated nighttime movement increased and sleep quality decreased from Sessions 1 and 2 to Session 3. Parallel to the sleep/activity measures, PVT reaction time increased between Session 1 and Sessions 2 and 3 and resting state alpha EEG reactivity magnitude and PVT-evoked P3 ERP amplitude decreased between Session 1 and Sessions 2 and 3. Cross-sectional regressions showed PVT reaction time was negatively associated with average daily sleep, alpha reactivity, and P3 changes; sleep/circadian measures were associated with alpha reactivity and/or P3 changes. ConclusionsSmall, but persistent sleep deficits reduced cortical arousal and impaired vigilant attention. SignificanceChronic sleep restriction impacts neurocognition in a manner similar to laboratory controlled sleep deprivation.

Esophageal sensation in premature human neonates: temporal relationships and implications of aerodigestive reflexes and electrocortical arousals

Electrocortical arousal (ECA) as an effect of visceral provocation or of its temporal relationships with aerodigestive reflexes in premature neonates is not known. We tested the hypothesis that esophageal provocation results in both esophageal reflex responses and ECAs during sleep and that ECAs are dependent on the frequency characteristics of esophageal neuromotor responses. We defined the spatiotemporal relationship of ECAs in relation to 1) spontaneous pharyngoesophageal swallow sequences and gastroesophageal reflux (GER) events and 2) sensory-motor characteristics of esophageal reflexes. Sixteen healthy premature neonates born at 27.9 ± 3.4 wk were tested at 36.8 ± 1.9 wk postmenstrual age. Ninety-five midesophageal and 31 sham stimuli were given in sleep during concurrent manometry and videopolysomnography. With stimulus onset as reference point, we scored the response latency, frequency occurrence and duration of arousals, peristaltic reflex, and upper esophageal sphincter contractile reflex (UESCR). Changes in polysomnography-respiratory patterns and esophageal sensory-motor parameters were scored by blinded observers. Significantly (for each characteristic listed, P < 0.05), swallow sequences were associated with arousals and sleep state changes, and arousals were associated with incomplete peristalsis, response delays to lower esophageal sphincter relaxation, and prolonged esophageal clearance. GER events (73.5%) provoked arousals, and arousals were associated with response delays to peristaltic reflexes or clearance, sleep state modification, and prolonged respiratory arousal. Midesophageal stimuli (54%) provoked arousals and were associated with increased frequency, prolonged latency, prolonged response duration of peristaltic reflexes and UESCR, and increased frequency of sleep state changes and respiratory arousals. In human neonates, ECAs are provoked upon esophageal stimulation; the sensory-motor characteristics of esophageal reflexes are distinct when accompanied by arousals. Aerodigestive homeostasis is defended by multiple tiers of aerodigestive safety mechanisms, and when esophageal reflexes are delayed, cortical hypervigilance (ECAs) occurs.

Reassessment of the structural basis of the ascending arousal system

The "ascending reticular activating system" theory proposed that neurons in the upper brainstem reticular formation projected to forebrain targets that promoted wakefulness. More recent formulations have emphasized that most neurons at the pontomesencephalic junction that participate in these pathways are actually in monoaminergic and cholinergic cell groups. However, cell-specific lesions of these cell groups have never been able to reproduce the deep coma seen after acute paramedian midbrain lesions that transect ascending axons at the caudal midbrain level. To determine whether the cortical afferents from the thalamus or the basal forebrain were more important in maintaining arousal, we first placed large cell-body-specific lesions in these targets. Surprisingly, extensive thalamic lesions had little effect on electroencephalographic (EEG) or behavioral measures of wakefulness or on c-Fos expression by cortical neurons during wakefulness. In contrast, animals with large basal forebrain lesions were behaviorally unresponsive and had a monotonous sub-1-Hz EEG, and little cortical c-Fos expression during continuous gentle handling. We then retrogradely labeled inputs to the basal forebrain from the upper brainstem, and found a substantial input from glutamatergic neurons in the parabrachial nucleus and adjacent precoeruleus area. Cell-specific lesions of the parabrachial-precoeruleus complex produced behavioral unresponsiveness, a monotonous sub-1-Hz cortical EEG, and loss of cortical c-Fos expression during gentle handling. These experiments indicate that in rats the reticulo-thalamo-cortical pathway may play a very limited role in behavioral or electrocortical arousal, whereas the projection from the parabrachial nucleus and precoeruleus region, relayed by the basal forebrain to the cerebral cortex, may be critical for this process.

The effects of acute nicotine administration on electrocortical arousal in patients with schizophrenia

The effects of acute nicotine administration on electrocortical arousal in patients with schizophrenia

Adenosinergic modulation of rat basal forebrain neurons during sleep and waking: neuronal recording with microdialysis.

1. The cholinergic system of the basal forebrain (BF) is hypothesized to play an important role in behavioural and electrocortical arousal. Adenosine has been proposed as a sleep-promoting substance that induces sleep by inhibiting cholinergic neurons of the BF and brainstem. However, adenosinergic influences on the activity of BF neurons in naturally awake and sleeping animals have not been demonstrated. 2. We recorded the sleep-wake discharge profile of BF neurons and simultaneously assessed adenosinergic influences on wake- and sleep-related activity of these neurons by delivering adenosinergic agents adjacent to the recorded neurons with a microdialysis probe. Discharge rates of BF neurons were recorded through two to three sleep-wake episodes during baseline (artificial cerebrospinal fluid perfusion), and after delivering an adenosine transport inhibitor (s-(p-nitrobenzyl)-6-thioinosine; NBTI), or exogenous adenosine, or a selective adenosine A1 receptor antagonist (8-cyclopentyl-1, 3-dimethylxanthine; CPDX). 3. NBTI and adenosine decreased the discharge rate of BF neurons during both waking and non-rapid eye movement (NREM) sleep. In contrast, CPDX increased the discharge rate of BF neurons during both waking and NREM sleep. These results suggest that in naturally awake and sleeping animals, adenosine exerts tonic inhibitory influences on BF neurons, supporting the hypothesized role of adenosine in sleep regulation. 4. However, in the presence of exogenous adenosine, NBTI or CPDX, BF neurons retained their wake- and sleep-related discharge patterns, i.e. still exhibited changes in discharge rate during transitions between waking and NREM sleep. This suggests that other neurotransmitters/neuromodulators also contribute to the sleep-wake discharge modulation of BF neurons.

A psychophysiological investigation of fluctuating consciousness in neurodegenerative dementias

Fluctuating levels of consciousness (FC) are a key feature in neurodegenerative dementias, yet clinical identification is poor, hindering accurate diagnosis. One hundred and nineteen patients (32 Dementia with Lewy Bodies (DLB), 57 Alzheimer's disease (AD) and 30 controls) with clinical scores of FC were assessed using an attentional task. Cortical arousal was assessed in 25 of these patients using electroencephalography. Over 90 s both variability in attention (p<0·0001) and fluctuations in electrocortical activity (p<0·0001) correlated with clinical FC scores, and with each other (p<0·0001). Variability in attention and electrocortical arousal are accurate FC markers and can assist differential diagnosis of AD and DLB. Previous work has underestimated the intensity and hence impact of FC in dementia. Copyright © 1999 John Wiley & Sons, Ltd.

Respiratory and Arousal Responses to Acoustic Stimulation

Although sleep-related obstructive apnea is most often associated with transient arousal, the impact of this arousal on respiratory control remains unclear. We tested the hypotheses that acoustic arousing stimulation can generate a significant respiratory response during sleep in healthy subjects and that the magnitude or timing of this response is affected by the presence of electrocortical arousal or inhaled carbon dioxide. We employed binaural tone bursts (0.5-s duration, 4-KHz center frequency, 99-s interstimulus interval) to elicit repetitive transient arousals from sleep during nocturnal polysomnographic recordings beginning at 10 PM and ending at 6 AM. Recordings were conducted in five healthy adult volunteers aged 24 to 37 years. Inspired gas was alternated between room air and 3% to 7% CO2 (titrated to yield an approximate 50% increase in minute ventilation) at 1-h intervals. Each 30-s epoch was scored for sleep/wake stage according to standard criteria. Only results obtained during nonrapid eye movement sleep are presented herein. Tone-evoked arousals were detected by computer analysis as increased EEG frequency occurring within 3 s of acoustic stimulation. For each tone, respiratory parameters for each of three prestimulus and four poststimulus breaths were normalized to the overall mean of prestimulus breaths measured during room air breathing for each subject. Tone bursts elicited repetitive transient arousals with a mean duration of approximately 10 s from all stages of sleep. With respect to the three prestimulus breaths, acoustic stimulation was associated with increased tidal volume and decreased inspiratory duration for at least four breaths. These respiratory responses to acoustic stimulation were not significantly influenced by either presence of transient arousal from sleep or inspired gas. We conclude that transient EEG arousal may be repeatedly evoked from nonrapid eye movement sleep by transient acoustic stimulation in normal sleepers. This sensory stimulation is associated with augmented ventilation, a response that is not significantly affected by inspired hypercapnia or the presence of generalized EEG arousal.

Ventilatory dynamics during transient arousal from NREM sleep: implications for respiratory control stability.

The polysomnographic and ventilatory patterns of nine normal adults were measured during non-rapid-eye-movement (NREM) stage 2 sleep before and after repeated administrations of a tone (40-72 dB) lasting 5 s. The ventilatory response to arousal (VRA) was determined in data sections showing electrocortical arousal following the start of the tone. Mean inspiratory flow and tidal volume increased significantly above control levels in the first seven breaths after the start of arousal, with peak increases (64.2% > control) occurring on the second breath. Breath-to-breath occlusion pressure 100 ms after the start of inspiration showed significant increases only on the second and third postarousal breaths, whereas upper airway resistance declined immediately and remained below control for > or = 7 consecutive breaths. These results suggest that the first breath and latter portion of the VRA are determined more by upper airway dynamics than by changes in the neural drive to breathe. Computer model simulations comparing different VRA time courses show that sustained periodic apnea is more likely to occur when the fall in the postarousal increase in ventilation is more abrupt.

POSTNATAL DEVELOPMENT OF RESPONSES TO AIRFLOW OBSTRUCTION

1. Obstruction of the upper airway could be an initiating factor in the Sudden Infant Death Syndrome (SIDS). Responses to upper airway obstruction include augmentation of respiratory efforts, active dilation of the upper airway and electrocortical arousal. Vulnerable individuals may fail to mount these responses effectively. 2. Respiratory and arousal responses to obstruction of the upper airway have been investigated in newborn lambs. In conscious lambs, nasal obstruction causes a profound augmentation of inspiratory efforts, mild asphyxiation and eventual formation of an oral airway. The ability to establish an oral airway involves both chemoreception and mechanoreception and improves with age. 3. In sleeping lambs, obstruction of tidal airflow leads to progressive hypoxaemia, augmentation of inspiratory efforts, bradycardia and arousal. Arousal occurs earlier and with less hypoxaemia and bradycardia in non-REM sleep than in REM sleep. Arousal occurs after inspiratory efforts have increased to the same extent during both sleep states, suggesting that mechanoreception, or a sense of inspiratory effort, is important in initiating arousal. 4. Obstruction of nasal tubes tends to cause arousal from sleep earlier, and with less hypoxaemia and less augmentation of inspiratory effort, than when a more compliant face mask is obstructed. This supports the suggestion that mechanoreception, which may be involved in the perception of inspiratory effort, is a determinant of arousal. 5. With increasing postnatal age, lambs become less arousable in response to airflow obstruction when in REM sleep. This suggests that lambs may become progressively more vulnerable to the effects of airway obstruction during the immediate newborn period.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence that nitric oxide is involved in the control of electrocortical arousal.

Evidence that nitric oxide is involved in the control of electrocortical arousal.

Acoustically induced cortical arousal increases phasic pharyngeal muscle and diaphragmatic EMG in NREM sleep.

Six healthy subjects (3 males, 3 females) were studied to assess phasic inspiratory responses of upper airway (UA) and diaphragm muscles to electrocortical arousal independent of other potential respiratory stimulation. Transient electroencephalographic (EEG) arousal (abrupt EEG frequency shift > or = 3 s without awakening) was induced during supine stage 2 non-rapid-eye-movement (NREM) sleep with binaural tone bursts (0.5 s, 4 kHz, 25-95 dB). Electromyograms (EMG) of levator veli palatini (EMGlvp) and genioglossus (EMGgg) were obtained with intramuscular electrodes, and EMG of diaphragm (EMGdi) was obtained with esophageal electrodes. EMG signals were processed as moving time-averaged inspiratory activity over 100-ms windows. For each arousal, each of five consecutive postarousal breaths (R1-R5) was scored for peak inspiratory phasic EMG and normalized as percent averaged EMG of the three prearousal breaths for all muscles. After arousal, EMGlvp was increased for R1-R5 and EMGgg and EMGdi were increased for R1-R4. The increase in EMGlvp was greater than those of EMGgg and EMGdi for all response breaths. There was a significant increase in EMGlvp in all subjects, and EMGgg and EMGdi were significantly increased in three and two subjects, respectively. These data indicate that isolated transient electrocortical arousal is generally associated with phasic inspiratory recruitment of UA and diaphragm muscles in normal humans during NREM sleep; velopharyngeal muscle recruitment appears to be more consistent and of greater magnitude and duration than that of oropharyngeal muscle or diaphragm. We speculate that transient arousal from sleep may contribute to UA patency independent of chemical and mechanical respiratory stimuli.

Inhibition by Nω‐nitro‐L‐arginine methyl ester of the electrocortical arousal response in rats

In rats chronically implanted with cannulae into one lateral cerebral ventricle and recording electrodes onto the fronto-parietal cortex, the effects of systemic or intraventricular administration of the nitric oxide (NO) synthesis inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), on electrocortical (ECoG) arousal response evoked by sound stimulation were studied. In control animals, a single acoustic stimulation (80 dB for 15 s) produced a significant decrease in ECoG total voltage power lasting approximately 25 s. No tolerance developed after repeating the same sound stimulation at 15, 30, 60 min and 24 h intervals. Under these experimental conditions, pretreatment with L-NAME, given systemically (10 mg kg-1, i.p.) or intracerebroventricularly (300 micrograms), significantly reduced the sound-evoked arousal response 1 h and 15 min later, respectively. In conclusion, the present data are in favour of a physiological role of NO in the control of arousal mechanisms.

The neurological development of grasping

1.1. The primary responses evoked in the sensori-motor cortex by single shock stimulation of n. ventralis posterolateralis, n. ventralis posteromedialis and n. ventralis lateralis of thalamus are not affected by electrocortical arousal, induced either by sensory or reticular stimulation.2.2. The augmenting responses, induced by low frequency repetitive stimulation of the same thalamic nuclei, are strongly reduced during cortical arousal. The late components of the augmenting potential show a greater susceptibility.3.3. Unlike the primary responses evoked by thalamic stimulation, similar potentials elicited by peripheral excitation are definitely decreased during cortical arousal.

Postlunch smoking for pleasure seeking or arousal maintenance?

Interactions between smoking and eating might be expected, since the craving to smoke increases after a meal, since smokers tend to have a lower body weight and since they have also been suggested to differ from nonsmokers with respect to metabolism. Further, both eating and smoking have been reported to affect mental performance. In the first experiment the influences of a heavy meal, a light meal and no meal on smoking behavior and subjective ratings were compared in 15 subjects. Whereas puffing behavior was not affected by the meal conditions, craving and smoking enjoyment increased after the meals. In the second experiment the effects of smoking on postlunch performance and concomitant central and peripheral physiology were investigated. Postlunch smoking (compared to postlunch no smoking) distinctly showed the usual increases in heart rate, peripheral vasoconstriction and electrocortical arousal, but it failed to affect rapid information processing performance and its concomitant event-related EEG potentials as well as several indices of metabolic activity. It appears, thus, that under the conditions of the present experiments, pleasure seeking may be a more important factor in postmeal smoking than the effects on performance, EEG or metabolism.

The effects of smoking on electrocortical arousal in coronary prone (type A) and non-coronary prone (type B) subjects.

Twenty-nine Type A subjects, (greater than 75 percentile on the Jenkins Activity Survey) and 28 Type Bs (less than 25 percentile of the survey) were asked to smoke one cigarette (1.0 mg nicotine, 16 mg tar, 14 mg CO) using a standardized smoking procedure. Significant differences between baseline and smoking conditions were noted in the distribution of electrocortical activity for both groups. In addition, a shift from EEG low frequency high amplitude (alpha) events to high frequency low amplitude activity (beta) was noted for the As, while the Bs showed enhanced very low frequency high amplitude (theta) activity. A striking parallel was observed between the behavioral predisposition of the subject (A/B) and the possible function of the underlying neurological structure mediating the observed EEG changes. It is suggested that the electrocortical changes observed for the As during smoking are mediated by reticular (ARS I) arousal. Enhanced reticular activity may coincide with an increased rate of information processing, attention and vigilance. On the other hand, the electrocortical changes observed for the Type Bs may represent enhanced activity of the limbic system (ARS II) with could coincide with stimulation of the reward/pleasure centers. Smoking may produce a pattern of neurophysiological arousal which parallels the behavioral tempo of the individual. Possible differences in in vivo regulation of nicotine cholinergic binding sites are also discussed.

Cognitive Processes During Self-Paced Motor Performance: An Electroencephalographic Profile of Skilled Marksmen

In the initial phase of the study (Study 1) electrocortical arousal (EEG alpha activity) was assessed at four standardized sites (T3, T4, 01, and 02) from male and female (N = 17) international-caliber marksmen during rifle shooting performance. The task consisted of the execution of 40 shots at a conventional indoor target from the standing position. During each shot preparation, a significant increase in left temporal and occipital alpha activity was demonstrated, while the right hemispheric activity remained constant. Hemispheric laterality ratios (T4:T3) evidenced a significant shift toward right-brain dominance as the time to trigger pull approached. In the second phase of the study (Study 2) male and female (N = 15) marksmen performed the same shooting task and, additionally, the resultant EEG performance patterns were contrasted to those observed during the mental processing of sterotyped left-brain and right-brain mental tasks. Observed EEG patterns, that is, temporal ratios, during shooting replicated the results of Study 1, and furthermore, indicated that the laterality indices derived during shooting exhibited a more pronounced shift to right-brain processing than did those derived during right-brain mental task performance. The EEG data obtained during the comparative mental task states were used to interpret the shooting performance EEG findings in terms of the implications from bilateral or split-brain cognitive process theory.

Electrocortical activity and related phenomena associated with meditation practice: a literature review.

The state effects of meditation appear to include decreased electrocortical arousal. There is also evidence that meditators more readily demonstrate alpha and theta activity than nonmeditators, even when not meditating. It is not clear whether prospective meditators as a group already possessed this characteristic, or whether the state effects of meditation practice eventually generalize to become traits. However, certain individuals, namely the psychologically "healthy" and those with a capacity for relaxed absorbed attention, appear to be more favourably disposed to meditation. Meditators appear to show both stronger orienting and recovery responses to stressors while meditating than controls. Meditation practice may begin with left hemisphere type activity, which gives way to functioning more characteristic of the right hemisphere. However, it appears that during advanced meditation ("no thought") both left and right hemisphere activity are largely inhibited or suspended. Depending on the individual, inexperienced meditators may report sleep, hypnogogic reverie, trance or abreaction during practice. The evidence to date does not support the notion of unique state effects associated with the practice of meditation.