First Hour Of Sleep Research Articles

EEG Characteristics Related to Educational Impairments in Children with Benign Childhood Epilepsy with Centrotemporal Spikes

Learning and behavioral difficulties often occur in benign childhood epilepsy with centrotemporal spikes (BCECTS). In recent years, several electroencephalogram (EEG) characteristics have been related to the occurrence of learning and behavioral problems. From 28 children medical, school and psychological reports were present and children were rated according to a 4-point scale for educational and behavioral impairment (Part 1). Thirty 24-h EEG recordings were reanalyzed for spike frequency, the presence of atypical EEG criteria, and the presence of a nondipole spike. EEGs were scored during wakefulness, first hour of sleep and whole night sleep (minus the first hour of sleep) separately (Part 2). The presence of I: an intermittent slow-wave focus during wakefulness, II: a high number of spikes in the first hour of sleep (and during whole night sleep), and III: multiple asynchronous bilateral spike-wave foci in the first hour of sleep correlates significantly with a sum score > or = 3 which indicates a complicated course with educational or behavioral impairment. It is sufficient to analyze an EEG during wakefulness and a sleep EEG for only the first hour of sleep instead of a whole night recording to demonstrate those EEG criteria. On basis of our reanalysis we can possibly conclude that the aforementioned EEG characteristics correlate with educational impairments, and that analysing an EEG recording during wake and the first hour of sleep is sufficient to look adequately for those EEG criteria in children with BCECTS.

Effects of Alcohol on Polysomnographically Recorded Sleep in Healthy Subjects

After studying the sleep of alcohol-dependent patients at the beginning and over the course of abstinence in earlier studies, our interest in the current study focused on the direct effect of 2 doses of alcohol [0.03 and 0.1% blood alcohol level (BAL)] on healthy sleep. This is the first polysomnographic study testing the impact of 2 doses of alcohol ingestion (thus reflecting "normal" social drinking and alcohol abuse) in a single-blind randomized design in healthy volunteers. The study evaluated a short-term acute drinking period for 3 and 2 days of withdrawal from alcohol not only for polysomnographic variables but also for subjective estimates of sleep quality. In a crossover design with a 1-week interval, healthy subjects received alcohol to raise their blood alcohol to either 0.03 or 0.1% BAL at bedtime for 3 consecutive nights after an alcohol-free baseline night. Objective (polysomnography) and subjective sleep (questionnaires) was recorded each night. During the following 2 days, alcohol was discontinued with simultaneous measurements of sleep to gauge withdrawal effects. At a dose of alcohol leading to BAL of 0.03%, no clear effects could be detected. Following an evening BAL of 0.1%, a hypnotic-like effect (shortened sleep latency, reduced number of wake periods, decreased stage 1 sleep) occurred primarily during the first half of the night with signs of rebound effects being already present during the second half of the night (increased stage 1 sleep). At this dose, alcohol significantly increased slow-wave sleep (SWS) in the first half of the night and reduced REM density in the beginning of the night. After discontinuation of the higher alcohol dose, REM sleep amount increased. No significant withdrawal or rebound effects could be observed for parameters of sleep continuity during the 2 nights after discontinuation from alcohol at a BAL of 0.1%. Owing to the small sample size, the results of this study need to be interpreted with caution. Short-term moderate alcohol consumption (BAL 0.03%) did not significantly alter objective or subjective parameters of sleep. Higher doses of alcohol resulting in a BAL level of 0.10% immediately before going to bed mainly influenced sleep in the first half of the night, resembling the effects of a short-acting hypnotic drug, including a suppression of phasic aspects of REM sleep (REM density). Interestingly, analysis of the latter part of these nights indicated the immediate presence of withdrawal effects (increased light sleep). No statistically significant effects on sleep parameters were observable during the 2 nights of withdrawal from alcohol at the higher BAL. Interpreted carefully, our data indicate that negative effects on sleep occur already with short-term use of alcohol at doses of BAL of 0.10%, despite hypnotic-like effects during the first hours of sleep, especially during the latter part of the night.

Sleep enhances nocturnal plasma ghrelin levels in healthy subjects.

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been shown to promote slow-wave sleep (SWS, non-REM sleep stages 3 and 4). Plasma levels of ghrelin are dependent on food intake and increase in sleeping subjects during the early part of the night. It is unknown whether sleep itself affects ghrelin levels or whether circadian networks are involved. Therefore, we studied the effect of sleep deprivation on nocturnal ghrelin secretion. In healthy male volunteers, plasma levels of ghrelin, cortisol, and human growth hormone (hGH) were measured during two experimental sessions of 24 h each: once when the subjects were allowed to sleep between 2300 and 0700 and once when they were kept awake throughout the night. During sleep, ghrelin levels increased during the early part of the night and decreased in the morning. This nocturnal increase was blunted during sleep deprivation, and ghrelin levels increased only slightly until the early morning. Ghrelin secretion during the first hours of sleep correlated positively with peak hGH concentrations. We conclude that the nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences. During the first hours of sleep, ghrelin might promote sleep-associated hGH secretion and contribute to the promotion of SWS.

A sedentary day: effects on subsequent sleep and body temperatures in trained athletes

Exercise effects on sleep in fit healthy people have been difficult to determine because their sleep is close to optimal, leaving little room for improvement. Another method for assessing exercise effects on sleep is to significantly reduce the degree of activity in highly active people. Fifteen trained athletes who exercised daily at a moderate to high intensity were employed. By requesting that subjects remain sedentary in the laboratory for an entire day, the effect of reduced exercise on subsequent sleep parameters was assessed. Sleep and temperature were recorded after a sedentary day and after a normal day of moderate to high activity (control condition) in a counterbalanced design. In the sedentary condition, slow-wave sleep (SWS) decreased by a mean of 15.5±7.0 min and slow-wave activity (SWA) differed significantly ( P<.05) between conditions in the first hour of sleep only. Rapid eye movement (REM) sleep increased by a mean of 17.9±5.7 min in the sedentary condition, while sleep onset latency (SOL) to Stages 1 and 2 increased by 10.2 and 10.7 min, respectively, and REM sleep latency decreased by 24.0±6.8 min (all P<.05). Between conditions, there was no overall effect on total sleep time (TST), sleep efficiency, wake after sleep onset or core or foot temperatures ( P>.05). With reduced exercise load, SWS pressure may have been reduced, resulting in lower levels of SWS and increased REM sleep. Thus, the data indicate that reducing exercise has significant effects on sleep that may have implications for athletes tapering for competition.

Disturbances in hormonal profiles of night workers during their usual sleep and work times.

In a previous study, the authors reported that the 24-h rhythms of pituitary and adrenal hormones--that is, thyrotropin (TSH), prolactin (PRL), growth hormone, and cortisol--adapted only partially in a group of permanent night workers. However, the real impact of circadian rhythm alterations on the health and well-being of subjects is still unclear. In this study, the authors focus on an ergonomic field and address questions of adaptation of these hormones during the usual day sleep time (0700-1500 h) and during the usual night work time (2200-0600 h) in permanent night workers. Eleven night workers, working a night schedule for at least 2 years, submitted to a high-frequency blood sampling procedure (10 min) and to electroencephalographic recordings during sleep. The endocrine profiles of night workers were compared to those of day-active subjects studied during their usual sleep-wake schedule. During usual day sleep, despite an adapted sleep structure, cortisol levels among night workers were abnormally enhanced, whereas the TSH decreased in comparison to the plateau observed among day-active subjects. During usual work time, some hormonal disturbances persisted, in particular concerning cortisol and PRL (two hormones known to reflect the level of activation). Among night workers, the work time was associated with the quiescent period of cortisol secretion normally occurring during the first hours of sleep, and with a transient PRL increase. These results revealed altered hormonal profiles during the sleep time of night workers that do not result in an altered sleep pattern. The nocturnal work time, which requires a high level physical and mental performance, is associated with some endocrine alterations reflecting an eventual phase of hypovigilance.

Effects of overnight supplemental oxygen in obstructive sleep apnea in children.

Supplemental oxygen during sleep may be useful as a temporary palliative treatment in children with obstructive sleep apnea syndrome (OSAS) associated with significant hypoxemia. However, supplemental O2 may also blunt hypoxic ventilatory drive and worsen ventilation. To assess the safety of the use of supplemental O2 in children with OSAS, we studied 16 children ages 2-8 (mean: 4.28 +/- 2.88 yr) with OSAS secondary to adenotonsillar hypertrophy. Patients underwent two overnight polysomnograms within 1 mo, one on room air (RA) and one while receiving supplemental O2 via nasal cannula titrated by 1/4 lpm increments to achieve SpO2 > 95% during the first hour of sleep. Oxygenation measurements were significantly improved during supplemental O2 nights (average SpO2 increased from 89.5 +/- 4.8% on RA to 97.7 +/- 1.8% on supplemental O2 [p < 0.00001]) while alveolar ventilation remained unchanged (PETCO2 > 50 mm Hg: 3.6 +/- 8.9% total sleep time on RA and 3.3 +/- 6.3% total sleep time on supplemental O2 [p = NS]). Supplemental O2 significantly reduced hypopnea density, obstructive apnea index, and paradoxical breathing. The density and average duration of central apneas remained unchanged. In addition, supplemental O2 increased the percentage of REM sleep time and decreased the number of microarousals. We conclude that supplemental O2 might be a safe and beneficial temporary treatment in children with OSAS.

Caffeine reduces low-frequency delta activity in the human sleep EEG

In view of the hypothesis that adenosine is involved in sleep regulation, the effects of the adenosine antagonist caffeine on sleep and sleep EEG were investigated in eight young males. Compared to the placebo condition, caffeine (100 mg) administered at bedtime prolonged sleep latency and reduced sleep efficiency and stage 4 of non-rapid eye movement sleep (NREMS). Electroencephalographic slow-wave activity (SWA, spectral power density in the 1.75-4.5-Hz band) was reduced, whereas power density in the spindle frequency range was slightly enhanced. The suppression of SWA was limited to the first NREMS episode. Caffeine reduced the power density mainly in the lowest delta band, in contrast to the changes during physiological sleep that encompass both the delta and theta bands. Caffeine levels in saliva, assessed in a separate experiment, decreased from 7.5 mumol/l in the first hour of sleep to 3.5 mumol/l in the seventh hour. In the night following caffeine administration, stage 4 sleep had reverted to the baseline level, but sleep latency was still increased, and stage 2 sleep, as well as SWA in the first NREMS episode, were reduced. The data show that even a low dose of caffeine affects the sleep EEG. However, the effects of caffeine did not completely mimic the spectral changes observed during physiological sleep.

Effect of unilateral somatosensory stimulation prior to sleep on the sleep EEG in humans.

The hypothesis that local activation of brain regions during wakefulness affects the EEG recorded from these regions during sleep was tested by applying vibratory stimuli to one hand prior to sleep. Eight subjects slept in the laboratory for five consecutive nights. During a 6-h period prior to night 3, either the left or the right hand was vibrated intermittently (20 min on-8 min off), while prior to night 5 the same treatment was applied to the contralateral hand. The sleep EEG was recorded from frontal, central, parietal and occipital derivations and subjected to spectral analysis. The interhemispheric asymmetry index (IAI) was calculated for spectral power in nonREM sleep in the frequency range 0.25-25.0 Hz for 0.5-Hz or 1-Hz bins. In the first hour of sleep following right-hand stimulation, the IAI of the central derivation was increased relative to baseline, which corresponds to a shift of power towards the left hemisphere. This effect was most prominent in the delta range, was limited to the first hour of sleep and was restricted to the central derivation situated over the somatosensory cortex. No significant changes were observed following left-hand stimulation. Although the effect was small, it is consistent with the hypothesis that the activation of specific neuronal populations during wakefulness may have repercussions on their electrical activity pattern during subsequent sleep.

Effects of pulsatile cortisol infusion on sleep-EEG and nocturnal growth hormone release in healthy men.

This study investigates the short-term effects of pulsatile cortisol administrations upon sleep electroencephalogram (EEG) and spontaneous release of growth hormone (GH) in humans. Ten young healthy male volunteers received intravenous injections of either placebo or cortisol every 60 min between 17.00 hours and 06.00 hours (1 mg kg-1 BW with a loading dose of 20% starting at 17.00 hours, followed by a dose of 6% every hour until 06.00 hours). The amount of rapid eye-movement (REM) sleep was significantly reduced (placebo: 19.9 +/- 1.8; cortisol: 12.2 +/- 1.5%; P < 0.05), whereas the time spent in slow-wave sleep (SWS) was significantly increased (placebo: 9.4 +/- 1.6; cortisol: 13.9 +/- 1.9%; P < 0.05). The SWS-promoting effect was most prominent during the first hours of sleep, but tended to persist also during the second half of the night. The pulsatile cortisol administration augmented the total amount of plasma GH concentrations (mean area under the time course curve, AUC, placebo: 3.2 +/- 0.5; cortisol: 4.4 +/- 0.6 [ng x 1000 x ml min-1]; P < 0.05) due to an increase of GH release before sleep onset, and during the second half of the night, while the GH surge at sleep onset remained unchanged. Our data are in accordance with the hypotheses that cortisol-induced changes of both sleep-EEG and GH secretion involve a common mechanism that includes activation of the hypothalamic-somatotrophic (growth hormone releasing hormone-growth hormone) system.

A field study of sleep disturbance: effects of aircraft noise and other factors on 5,742 nights of actimetrically monitored sleep in a large subject sample.

This field study assessed the effects of nighttime aircraft noise on actimetrically measured sleep in 400 people (211 women and 189 men; 20-70 years of age; one per household) habitually living at eight sites adjacent to four U.K. airports, with different levels of night flying. Subjects wore wrist-actimeters for 15 nights and completed morning sleep logs. A sample of 178 nights of sleep electroencephalograms (EEGs) were recorded synchronously with actigrams. The EEG was used to develop filters for the raw actigrams, in order to: (1) estimate sleep onset and (2) compare actigrams with aircraft noise events (ANEs). Actigrams, filtered to detect the onset of discrete movements, were able to detect 88% of all EEG-determined periods of interim wakefulness of > 15 seconds and periods of movement time of > 10 seconds. The main findings were: (1) actimetry and self-reports showed that only a minority of ANEs affected sleep, and, for most of our subjects, that domestic and idiosyncratic factors had much greater effects; (2) despite large between-site variations in ANEs, the difference between sites in overall sleep disturbance was not significant; (3) there was a diminished actimetric response to ANEs in the first hour of sleep and, apparently, also in the last hour of sleep; and (4) men had significantly more discrete movements than women and were more likely to respond to ANEs.

Sleep and wakefulness affect the responsiveness of the pituitary-adrenocortical axis to arginine vasopressin in humans.

The secretory activity of the pituitary-adrenocortical axis at night is characterized by a quiescent period during the first hours of sleep, preceding a period of enhanced activity in the early morning hours. It is still controversial whether the typical nocturnal secretory pattern of adrenocorticotropic hormone (ACTH) and cortisol is a mere reflection of a circadian rhythm or whether mechanisms associated with the state of sleep influence the nocturnal secretion of these hormones. Here, we administered arginine vasopressin (AVP) to normal men during the first part of nocturnal sleep and compared the release of ACTH and cortisol with the release after a second administration during the second part of the same night and also with the release after administration of AVP at identical points of nighttime while subjects were kept awake in another night. Compared with wakefulness, the cortisol release in response to AVP was significantly lower during sleep, with this effect restricted to the early part of sleep. The ACTH release was lower after the first AVP administration during the early part of sleep as compared with the AVP injection during the second part of the same night. Our data demonstrate a sleep-associated inhibition of stimulated ACTH and cortisol release, suggesting a period of decreased responsiveness of the pituitary-adrenocortical axis during early sleep.

Nasal capnography in children: automated analysis provides a measure of obstruction during sleep

A detailed analysis was made of nasal capnograms obtained from sleeping children with differing degrees of sleep-induced respiratory obstruction, the severe form being known as obstructive sleep apnoea. Clinical observations of these children were compared with analyses of nasal capnography data. During periods when the degree of obstruction was consistent throughout the first hour of sleep, the means and coefficients of variation of several parameters, derived from the capnograms were calculated. The coefficients of variation showed a close relationship to the degree of obstruction. In comparison, measures of end-tidal carbon dioxide concentration proved to be a very insensitive index of the degree of obstruction. The conclusion is that the usefulness of nasal capnography in predicting and grading obstruction can easily be extended by the use of statistical measures of dispersion and that this concept warrants further work.

Cytokine production during sleep and wakefulness and its relationship to cortisol in healthy humans.

A growing body of evidence indicates that cytokines, especially interleukin-1 beta, are involved in the regulation of sleep and wakefulness. The aim of the present pilot study was to investigate the relationship between interleukin-1 beta (IL-1 beta) and gamma-interferon (gamma-IFN) production and the regulation of sleep and wakefulness. Four healthy male volunteers were investigated. After one adaptation night, beginning at 8 a.m. in the morning, the EEG was recorded by means of a mobile long-term EEG and blood samples were drawn every 45 min for the analysis of IL-1 beta, gamma-IFN and cortisol for 24 h. For the analysis of cytokines whole blood cultures were established. After 48 h of incubation in the presence of endotoxin Salmonella typhimurium, IL-1 beta and gamma-IFN levels were measured in the culture supernatants using specific immunodetection assays. Methods of stochastic time series analysis were adopted to evaluate the biochemical data. Our results show the capability of cultured blood cells to produce cytokines upon endotoxin challenge to be at a maximum around the time of sleep onset and during the first hours of sleep, declining during the night to a minimum level in the morning hours. The opposite was observed for cortisol. The analysis of autocorrelation functions gives evidence of a 24-hour rhythm of cortisol and cytokines. The results indicate that the cytokines IL-1 beta and gamma-IFN may play a role in sleep regulation.

Effect of awakening on aldosterone.

Overnight studies conducted in 10 male volunteers showed that the effect of awakening on aldosterone and its main regulatory hormonal systems depends on the time of its occurrence. Waking periods in the latter half of the night induced concomitant increases in plasma levels of aldosterone and ACTH, whereas plasma renin activity tended to decrease. No effect was apparent, when subjects were awoken during the first hours of sleep, which is known to be a quiescent period of adrenocorticotropic activity. These results provide evidence of the dominant influence of ACTH during the second half of the night insuring the regulation of aldosterone during waking periods.

Effects of evening bright light exposure on melatonin, body temperature and sleep.

Five male subjects were exposed to a single 2-h period of bright (2500 lux) or dim (<100 lux) light prior to sleep on two consecutive nights. The two conditions were repeated the following week in opposite order. Bright light significantly suppressed salivary melatonin and raised rectal temperature 0.3 degrees C (which remained elevated during the first 1.5 h of sleep), without affecting tympanic temperature. Bright light also increased REM latency, NREM period length, EEG spectral power in low frequency, 0.75-8 Hz and sigma, 12-14 Hz (sleep spindle) bandwidths during the first hour of sleep, and power of all frequency bands (0.5-32 Hz) within the first NREMP. Potentiation of EEG slow wave activity (0.5-4.0 Hz) by bright light persisted through the end of the second NREMP. The enhanced low-frequency power and delayed REM sleep after bright light exposure could represent a circadian phase-shift and/or the effect of an elevated rectal temperature, possibly mediated by the suppression of melatonin.

Diurnal variation of plasma atrial natriuretic peptide in normals and patients with enuresis nocturna

The circadian variation of plasma atrial natriuretic peptide (ANP) in relation to urinary excretion of sodium (UNa) and potassium (UK) as well as clearance of creatinine (Ccrea) was assessed in 15 juvenile patients with enuresis nocturna and compared with 11 age-, sex-, and weight-matched normal subjects. Normal juveniles showed a highly significant diurnal variation (p less than 0.001) of plasma ANP with diurnal peak levels at midnight (0000 hours) and minimum levels at 0400 hours. Enuretic patients showed a similar diurnal rhythmicity with normal levels during day and night. In normals both UNa and UK showed significant diurnal rhythmicity with a marked reduction from daytime to night-time. Although the total diurnal excretions of UNa and UK were similar to normals, patients with enuresis showed abnormal diurnal variation in both UNa (p less than 0.05) and UK (p less than 0.01). The abnormal circadian rhythm of UNa and UK in enuretics seemed to be caused by abnormal tubular handling as similar abnormalities were found in the fractional excretions and as the circadian variation of Ccrea was normal. Especially during the first hours of sleep (2200 hours to 0000 hours), the patients showed polyuria (230 +/- 138 ml vs 116 +/- 58 ml, p less than 0.01), natriuresis (20.9 +/- 16.3 mmol l-1 vs 10.7 +/- 6.8 mmol l-1, p less than 0.01), and kaliuresis (7.3 +/- 6.3 mmol l-1 vs 3.7 +/- 2.3 mmol l-1, p less than 0.05), despite normal levels of plasma ANP. In conclusion, the study describes the diurnal variation of plasma ANP in relation to urinary excretion of sodium and potassium in a juvenile normal population. Patients with nocturnal enuresis show abnormal diurnal rhythmicity in the urinary excretion of sodium and potassium that is not correlated to the plasma levels of ANP.

The time course of ‘process S’: comparison of visually scored slow wave sleep and power spectral analysis

The sleep of 4 groups (N = 8) of young healthy subjects was recorded during naps at either 09.00, 14.00, 19.00 or 24.00 h. For the first hour of sleep, conventionally scored slow wave sleep SWS) and computed EEG power density (0–25 Hz) were found to increase exponentially as a function of prior wakefulness (range 3–18 h). The equations based on SWS and spectral analysis of the sleep EEG gave values for r′ (the growth rate of the function) that were similar to each other (0.038 and 0.039, respectively) and to that reported by Daan et al. (1984; 0.055). These data are consistent with the proposal that process S, 1 of 2 processes believed to regulate sleep and wakefulness, increases exponentially during the waking day (Daan et al. 1984). In addition, they indicate that in this context SWS and spectral analysis provide measures of slow wave activity that are equally sensitive to changes in prior wakefulness.

Supervision of ambulatory cassette EEG screening: a strategy based on the temporal distribution of epileptiform abnormalities

The interposition of screening personnel in the analysis of extended cassette EEG recordings requires a method for supervision by the responsible electroencephalographer. To this end, analysis was undertaken of the temporal distribution of epileptiform abnormalities and seizures on cassette EEG in 40 epilepsy unit inpatients for whom these abnormalities were confirmed by simultaneous cable telemetry. Epileptiform abnormalities were noted in the hour following sleep onset in 38 patients (92%). Seizures occurred primarily in wakefulness. One hundred cassette EEG tapes obtained for clinical purposes and previously found to contain evidence of epilepsy were then subjected to an abbreviated review. Eighty-seven contained epileptiform abnormalities in the first hour of sleep, and 7 additional tapes contained only EEG seizure activity coincident with reported clinical events. Considering that fewer than 20% of cassette recordings obtained in unrestricted clinical use are likely to harbor epileptiform abnormalities or seizures, correct identification of about 99% of tapes as normal or abnormal can be anticipated with an abbreviated review consisting of (1) analysis of the first hour of sleep; and (2) analysis of reported clinical events if no abnormalities are noted in the first hour of sleep. Such a review is sufficiently accurate to serve as a supervisory analysis of cassette EEG tapes that have been previously screened and reported to lack evidence of epilepsy.

Alcohol, snoring and sleep apnea.

We studied the effect of alcohol ingestion on sleep-induced breathing abnormalities and arterial oxyhaemoglobin saturation in seven patients with a range of sleep-induced upper airway occlusion. The characteristics of each patient's sleep-induced breathing abnormality was established on one or more control all-night studies, and then a further all-night study was done immediately following alcohol ingestion. Alcohol increased the duration and frequency of the occlusive episodes in five patients with obstructive sleep apnoea, and resulted in a marked increase in the degree of hypoxaemia in the first hour of sleep. In two patients with benign chronic snoring, alcohol induced frank obstructive sleep apnoea during the first hour of sleep. We suggest that the increased tendency to develop obstructive apnoea after alcohol is the result of alcohol-induced oropharyngeal muscle hypotonia, while the increased duration of obstructive apnea is the result of alcohol-induced depression of arousal mechanisms.

ARMAND TROUSSEAU ON THE TREATMENT OF ENURESIS (c1850)

Armand Trousseau (1801-1867), in his time considered the foremost clinician of the Hôtel-Dieu (the oldest hospital in Paris), made many significant advances in the treatment of diphtheria, scarlet fever, typhoid fever, and rickets. In one of his clinical lectures at the Hôpital des Enfants-Malades, Trousseau gave the following suggestions for the treatment of enuresis. This infirmity [enuresis] I consider a neuralgia or névrose, and it is much more common than is generally believed. It has been thought nearly incurable, but with belladonna, is one of the most easily cured of all diseases. Those children who are troubled in the daytime are not cured by belladonna. A child going to bed with an empty bladder will pass his water during the first two hours, sometimes during the first hour; placed in bed at 9 o'clock, the bladder will throw off its contents at 10 o'clock, and then retain them until 8 o'clock the following morning, being full at that time. The accident generally happens once only during the night, but sometimes twice. During the first hours of sleep, you generally find in young men and children an erection. The question may be asked, whether something of the same kind may not take place in the bladder. This complaint is most common among young girls, and is generally cured spontaneously at the age of puberty; but when this is not the case, do what chance has shown to be efficacious. Treatment—The first precaution is to break up the bad habit of the organs. Wake the child at the end of an hour, and make him pass his water; after several days, make him at the end of an hour and a half. This is only accessory.