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PubMed1993

A review of literature relating to sleep in hospital with emphasis on the sleep of the ICU patient.

The subject of this literature review is the sleep of hospitalised patients, with particular emphasis on the sleep of patients in intensive care units (ICUs). Initially there is an overview of the structure of sleep and the literature related to the main theories of sleep function in order to set the subject in context. A review of some of the work related to the sleep patterns of ICU patients outlines how severely sleep-deprived many patients are. Studies of sleep patterns implicate the environment of ICUs as an important factor in preventing sleep, but factors particular to patients which have an adverse effect on sleep are also reviewed, with particular reference to a study addressing the incidence of pain and discomfort of patients. Finally the sleep patterns of patients whose environment was carefully controlled to exclude factors known to disrupt sleep are reviewed. Thus the review moves from broad issues affecting sleep to the more focused issues personal to individual patients, with implications for nursing practice addressed as each point arises. In this way the complexity of the whole issue of sleep and the lack of sleep experienced by hospitalised patients is highlighted.

Health Facility Environment↗
PubMed1985

Obesity and hormonal factors in sleep and sleep apnea.

The presence of obesity, defined as weight 20 per cent or more above ideal body weight or increased body fat content, significantly increases risk of pulmonary, cardiovascular, metabolic, and gastrointestinal problems. Obesity is a major cause of shortened life expectancy. While obesity is not essential for the development of the obstructive sleep apnea syndrome, a significant percentage of patients with obstructive sleep apnea are obese. When evaluating these patients who have obstructive sleep apnea, it is important to search diligently for medical problems that are commonly found among the obese. While there is an increased incidence of obese patients among those who have obstructive sleep apnea, the exact reason for this is uncertain. The study of endorphins and enkephalins may expand our understanding of obesity, ventilatory regulation, and obstructive sleep apnea. This may, in fact, enable us to understand better the interrelationship between obesity and obstructive sleep apnea. The role that thyroid hormone, testosterone, and progesterone play in obstructive sleep apnea has also been reviewed. Patients who have obstructive sleep apnea should not be treated with testosterone. All patients given testosterone should be observed quite closely for the possible signs and symptoms of obstructive sleep apnea. Progesterone seems to be of some help in patients who have obesity hypoventilation syndrome. Its effectiveness in patients with obstructive sleep apnea is less clear. The obesity hypoventilation syndrome as described by Burwell is relatively uncommon. Many of the manifestations of the obesity hypoventilation syndrome, however, are found in patients with obstructive sleep apnea. The recognition that the symptoms stem from underlying obstructive sleep apnea offers great potential for therapy. Weight reduction is valuable therapy for patients with obesity and pulmonary dysfunction, obesity and obstructive sleep apnea, and obesity hypoventilation syndrome. Weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome. Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up.

Adult↗
PubMed2003

Differential increase in the expression of heat shock protein family members during sleep deprivation and during sleep.

Although sleep is thought to be restorative from prior wakeful activities, it is not clear what is being restored. To determine whether the synthesis of macromolecules is increased in the cerebral cortex during sleep, we subjected C57BL/6 mice to 6 hours of sleep deprivation and then screened the expression of 1176 genes of known function by using cDNA arrays. The expression of the heat shock proteins (HSP), endoplasmic reticulum protein (ERp72) and glucose-regulated protein (GRp78), was among the genes whose expression was significantly elevated in the cortex during sleep deprivation, whereas GRp78 and GRp94 mRNAs were elevated in the cortex during recovery sleep after sleep deprivation, as confirmed by conventional and quantitative real-time polymerase chain reaction and/or Northern analyses. A systematic evaluation of the expression of six heat shock protein family members (ERP72, GRp78, GRp94, HSP27, HSP70-1, and HSP84) in seven brain regions revealed increased mRNA levels in cortex, basal forebrain, hypothalamus, cerebellum and medulla during sleep deprivation, whereas increased mRNA levels during recovery sleep were limited to the cortex and medulla. Immunohistochemical studies identified increased numbers of GRp78-, GRp94-, and ERp72-immunoreactive cells in the dorsal and lateral cortex during sleep deprivation but, during recovery sleep, elevated numbers of these cells were found only in the lateral cortex. In the medulla, increased numbers of GRp94-immunoreactive cells were observed in nucleus tractus solitarius, dorsal motor nucleus of the vagus and the rostroventrolateral medulla during recovery sleep. The widespread increase of heat shock protein family mRNAs in brain during sleep deprivation may be a neuroprotective response to prolonged wakefulness. In contrast, the relatively limited heat shock protein family mRNA expression during recovery sleep may be related to the role of heat shock proteins in protein biogenesis and thus to the restorative function of sleep.

Animals↗
PubMed2004

Caffeine attenuates waking and sleep electroencephalographic markers of sleep homeostasis in humans.

Prolonged wakefulness increases electroencephalogram (EEG) low-frequency activity (< 10 Hz) in waking and sleep, and reduces spindle frequency activity (approximately 12-16 Hz) in non-rapid-eye-movement (nonREM) sleep. These physiologic markers of enhanced sleep propensity reflect a sleep-wake-dependent process referred to as sleep homeostasis. We hypothesized that caffeine, an adenosine receptor antagonist, reduces the increase of sleep propensity during waking. To test this hypothesis, we compared the effects of caffeine and placebo on EEG power spectra during and after 40 h of wakefulness. A total of 12 young men underwent two periods of sleep deprivation. According to a randomized, double-blind, crossover design, they received two doses of caffeine (200 mg) or placebo after 11 and 23 h of wakefulness. Sleep propensity was estimated at 3-h intervals by measuring subjective sleepiness and EEG theta (5-8 Hz) activity, and polysomnographic recordings of baseline and recovery nights. Saliva caffeine concentration decreased from 15.7 micromol/l 16 h before the recovery night, to 1.8 micromol/l 1 h before the recovery night. Compared with placebo, caffeine reduced sleepiness and theta activity during wakefulness. Compared with sleep under baseline conditions, sleep deprivation increased 0.75-8.0 Hz activity and reduced spindle frequency activity in nonREM sleep of the recovery nights. Although caffeine approached undetectable saliva concentrations before recovery sleep, it significantly reduced EEG power in the 0.75-2.0 Hz band and enhanced power in the 11.25-20.0 Hz range relative to placebo. These findings suggest that caffeine attenuated the build-up of sleep propensity associated with wakefulness, and support an important role of adenosine and adenosine receptors in the homeostatic regulation of sleep.

Adult↗
PubMed2002

Evolution of sleep and sleep EEG after hemispheric stroke.

The evolution of subjective sleep and sleep electroencephalogram (EEG) after hemispheric stroke have been rarely studied and the relationship of sleep variables to stroke outcome is essentially unknown. We studied 27 patients with first hemispheric ischaemic stroke and no sleep apnoea in the acute (1-8 days), subacute (9-35 days), and chronic phase (5-24 months) after stroke. Clinical assessment included estimated sleep time per 24 h (EST) and Epworth sleepiness score (ESS) before stroke, as well as EST, ESS and clinical outcome after stroke. Sleep EEG data from stroke patients were compared with data from 11 hospitalized controls and published norms. Changes in EST (>2 h, 38% of patients) and ESS (>3 points, 26%) were frequent but correlated poorly with sleep EEG changes. In the chronic phase no significant differences in sleep EEG between controls and patients were found. High sleep efficiency and low wakefulness after sleep onset in the acute phase were associated with a good long-term outcome. These two sleep EEG variables improved significantly from the acute to the subacute and chronic phase. In conclusion, hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities. High sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.

Adolescent↗
PubMed1992

T-sleep: an improved method for scoring breathing-disordered sleep.

We developed a new method to score sleep fragmented by respiratory events that we call the T-sleep (transitional sleep scoring) method. Five control polysomnograms from subjects without sleep-related breathing abnormalities were scored by the Rechtschaffen and Kales (R&K) method, and 10 polysomnograms from patients with severe obstructive sleep apnea were scored by both the R&K and the T-sleep method. Comparative analyses were performed on sleep variables of the control and apnea polysomnograms, and interscorer correlations were assessed for sleep and apnea variables. The interscorer correlations were high for both R&K control scoring and for apnea recordings scored by the T-sleep method. The number of sleep stage events documented for the 10 apnea recordings was significantly less for the T-sleep method than the R&K method (36, SD 17.0 vs. 332, SD 144.0; p = 0.0002). The T-sleep method was shown to be an effective, accurate and quick method for scoring sleep in patients with sleep-related breathing disorders.

Adult↗
PubMed1999

Validation of the sleep-EVAL system against clinical assessments of sleep disorders and polysomnographic data.

OBJECTIVES: To validate the Sleep-EVAL expert system, a computerized tool designed for the assessment of sleep disorders, against polysomnographic data and clinical assessments by sleep specialists. DESIGN: Patients were interviewed twice, once by a physician using Sleep-EVAL and again by a sleep specialist. Polysomnographic data were also recorded to ascertain diagnoses. Agreement between diagnoses generated by Sleep-EVAL and those formulated by sleep specialists was determined via the kappa statistic. SETTINGS: Sleep disorder centers at Stanford University (USA) and Regensburg University (Germany). PATIENTS: 105 patients aged 18 years or over. INTERVENTIONS: NA. RESULTS: Sleep-EVAL made an average of 1.32 diagnoses per patient, compared with 0.93 for the sleep specialists. Overall agreement on any sleep-breathing disorder was 96.9% (Kappa .94). More than half of the patients were diagnosed with obstructive sleep apnea syndrome (OSAS); the agreement rate for this specific diagnosis was 96.7% (Kappa .93). CONCLUSIONS: The findings indicate that the Sleep-EVAL system is a valid instrument for the recognition of major sleep disorders, particularly insomnia and OSAS.

Adult↗
PubMed2004

Twenty-four-hour disruption of the sleep-wake cycle and sleep-onset REM-like episodes in a rat model of African trypanosomiasis.

STUDY OBJECTIVES: Patients with human African trypanosomiasis (sleeping sickness) due to the inoculation of Trypanosoma brucei gambiense or rhodesiense show a major disruption of the 24-hour sleep-wake distribution, accompanied by the occurrence of sleep-onset rapid-eye-movement (REM) sleep episodes, proportional to the severity of the illness. Although animal models of human African trypanosomiasis have been developed to understand the pathogenic mechanisms leading to immune alterations, the development of an animal model featuring the alterations of endogenous biologic rhythms remains a necessity. ANIMALS: Sprague-Dawley rats (N = 10) entrained to a 12:12-hour dark-light regimen. INTERVENTIONS: Rats were infected with Trypanosoma brucei brucei AnTat 1.1E and instrumented with electrocorticographic and electromyographic electrodes. Polysomnography was recorded continuously from 2 days before infection until the animal's death. MEASUREMENTS AND RESULTS: The analysis of the spontaneous sleep-wake architecture revealed an increased proportion of slow-wave sleep (SWS) and a decreased amount of wakefulness 2 days before death. Considerable sleep fragmentation was observed in the infected rats, with numerous changes in sleep-wake stages and an increased number of episodes of wakefulness and SWS. Infected rats presented a fragmented pattern of SWS and a marked reduction in the mean paradoxical-sleep (PS) latency, resulting in a considerable disruption of the PS-SWS sequences. Abnormal transitions, particularly the appearance of sleep-onset REM episodes, marked the disruption of the internal sleep structure. The electrocorticogram traces were modified during SWS, with the occurrence of abnormal hypersynchronic slow waves and a disappearance of spindles. CONCLUSION: The Trypanosoma brucei brucei-infected rat is a good model of the syndrome seen in human African trypanosomiasis, ie, the 24-hour disruption of the sleep-wake cycle and the occurrence of sleep-onset REM-like sleep episodes.

Animals↗
PubMed1999

Effect of wake-sleep transitions and rapid eye movement sleep on pharyngeal muscle response to negative pressure in humans.

1. Genioglossus (GG) activation in response to upper airway negative pressure may be an important mechanism in the maintenance of airway patency. This reflex occurs during wakefulness but is diminished during stable non-rapid eye movement (NREM) sleep. Since obstructive events occur more commonly at wake-sleep transitions and during rapid eye movement (REM) sleep than during stable NREM sleep, we assessed the GG reflex during these two vulnerable states. 2. Seventeen healthy adults were studied throughout one evening and overnight. Electroencephalograms (EEGs), electro-oculograms (EOGs), submental electromyogram (EMG), GG EMG (intramuscular electrodes), and choanal plus epiglottic pressures were recorded. The GG reflex response to pulses of -8 cmH2O choanal pressure applied via nose mask during early inspiration was quantified repeatedly during relaxed wakefulness, within five breaths of wake-sleep transition (EEG alpha-theta transition) and during REM sleep. Only trials without EEG arousal were analysed, resulting in data from 14 subjects during sleep onset and 10 subjects during REM sleep (overall, 174-491 trials per state). 3. During wakefulness there was brisk GG reflex activation in response to negative pressure (amplitude: +78.5 +/- 28.3 % baseline (mean +/- s.e.m.); latency to maximal response: 177 +/- 16 ms). 4. At sleep onset, although there was marked variability among individuals, there was no significant reduction in the magnitude of the GG reflex for the group as a whole (amplitude: +33.2 +/- 8.2 % baseline; latency: 159 +/- 15 ms). 5. In contrast, during REM sleep there was a reduction of GG reflex (amplitude: -12.6 +/- 8.3 % baseline (P = 0.017 vs. awake); latency: 160 +/- 10 ms (n.s. vs. awake)) and greater airway collapsibility during the applied pressures (P = 0.043 vs. awake). 6. We conclude that there was no systematic reduction in the GG reflex to negative pressure at sleep onset. Nonetheless, it remains possible that sleep-deprived normal subjects and patients with sleep apnoea could react differently. 7. The apparent inhibition of the GG reflex during REM sleep may help explain why the upper airway is vulnerable to collapse during this state.

Adult↗
PubMed1997

Effects of sleep and sleep stage on epileptic and nonepileptic seizures.

PURPOSE: Previous studies of patients with epilepsy and animal models of epilepsy suggest that sleep increases the frequency, duration, and secondary generalization of seizures. This information is, however, incomplete. METHODS: We retrospectively examined video-EEG monitoring reports from our comprehensive epilepsy center. We recorded seizure type, site of onset (for partial seizures), sleep state at onset, and whether partial seizures secondarily generalized. Seizures arising from sleep were then reviewed to determine sleep state. RESULTS: We analyzed 1,116 seizures in 188 patients. Thirty-five percent of complex partial seizures (CPSs) starting during sleep underwent secondary generalization compared with 18% in wakefulness (p < 0.0001). Frontal lobe CPSs secondarily generalized at equal rates during sleep (22%) and wakefulness (20%), but temporal lobe CPSs generalized much more frequently during sleep (45%) than in wakefulness (19%; p < 0.0001). Frontal lobe seizures were more likely to occur during sleep (37%) than were temporal lobe seizures (26%; p = 0.0068). CPSs were more frequent in stages 1 and 2 and occurred rarely during REM. Seizures starting during slow-wave sleep were significantly longer than seizures starting during wakefulness or stage 2 sleep. Psychogenic nonepileptic seizures (PNESs) were rare between midnight and 6 a m. and never occurred during sleep. CONCLUSIONS: Sleep has a pronounced effect on secondary generalization of partial seizures, especially those of temporal lobe origin. Frontal lobe seizures occur more often during sleep than do temporal lobe seizures, and occurrence during sleep helps to distinguish PNESs from CPSs.

Brain↗
PubMed1994

Non-invasive beat to beat arterial blood pressure during non-REM sleep in obstructive sleep apnoea and snoring.

BACKGROUND: Obstructive sleep apnoea, and possibly snoring, are associated with a poorly understood increase in cardiovascular mortality which may be explained by their effects on systemic blood pressure during sleep. This study compares changes in mean blood pressure during obstructive sleep apnoea and snoring without apnoeas with those in matched control subjects during non-REM sleep. METHODS: Eighteen men with obstructive sleep apnoea, 16 men who snored without apnoeas, and 34 control subjects matched for age, sex, obesity, smoking, and alcohol intake were studied. During polysomnography non-invasive mean blood pressure (Finapres) was recorded from each cardiac cycle during non-REM sleep and averaged over a 10 minute period. This was compared with the blood pressure during 10 minutes before sleep onset. The changes in the patients' sleeping blood pressure were compared with those in their individually matched control subjects. RESULTS: Compared with the control subjects the change in mean (SD) arterial blood pressure between being awake and asleep was higher during obstructive sleep apnoea (+6.5 (9) mm Hg v-2 (6.5), difference 8.5 (11)), and the rise from wakefulness to sleep in the obstructive sleep apnoea group was itself significant. The average mean arterial pressure was not raised in those who snored without apnoeas compared with either the control subjects or during wakefulness. CONCLUSIONS: Average mean arterial pressure is higher during obstructive sleep apnoea than it is during wakefulness, while normal subjects show a fall in blood pressure at sleep onset. This sleep related rise in blood pressure may contribute to the excess cardiovascular morbidity and mortality experienced by patients with this condition.

Blood Pressure↗
PubMed2002

Selective REM sleep deprivation during daytime. II. Muscle atonia in non-REM sleep.

One of the hallmarks of rapid eye movement (REM) sleep is muscle atonia. Here we report extended epochs of muscle atonia in non-REM sleep (MAN). Their extent and time course was studied in a protocol that included a baseline night, a daytime sleep episode with or without selective REM sleep deprivation, and a recovery night. The distribution of the latency to the first occurrence of MAN was bimodal with a first mode shortly after sleep onset and a second mode 40 min later. Within a non-REM sleep episode, MAN showed a U-shaped distribution with the highest values before and after REM sleep. Whereas MAN was at a constant level over consecutive 2-h intervals of nighttime sleep, MAN showed high initial values when sleep began in the morning. Selective daytime REM sleep deprivation caused an initial enhancement of MAN during recovery sleep. It is concluded that episodes of MAN may represent an REM sleep equivalent and that it may be a marker of homeostatic and circadian REM sleep regulating processes. MAN episodes may contribute to the compensation of an REM sleep deficit.

Adult↗
PubMed1996

The effect of sleep deprivation on sleep states, breathing events, peripheral chemoresponsiveness and arousal propensity in healthy 3 month old infants.

We wished to investigate the effects of sleep deprivation on sleep, arousal propensity, respiratory events and peripheral chemoresponses in healthy infants, since these effects might be relevant to mechanisms concerned with some cases of sudden infant death syndrome. Paired observations were made overnight during natural sleep and following sleep deprivation, in a randomized fashion, in 15 healthy infants aged 78 (7) days (mean (SD)). Polysomnograms were recorded and sleep was scored using Anders' criteria. Respiratory events were categorized into central, mixed and obstructive apnoeas. Peripheral chemoresponses were measured during quiet sleep from the respiratory response to two-breath alternations in fractional inspiratory oxygen (F1, O2) (0.42 and 0.00). Arousal propensity was determined from awakening and arousal thresholds to graded photic and auditory stimuli during quiet sleep, and from spontaneous awakenings and limb movements. Compared with natural sleep, following sleep deprivation infants maintained a greater proportion of quiet sleep (39 vs 44%). There was no measurable change in arousal propensity. During quiet sleep, obstructed breathing events tended to be more common after sleep deprivation (0.1 vs 0 events.h-1) and the expiratory time during baseline breathing increased significantly (1.27 vs 1.58 s) although the decrease in respiratory rate was not significant (32 vs 30 breaths.min-1). Peripheral chemoresponses altered significantly, alternations in tidal volume/inspiratory time (VT/tI) as a measure of inspiratory drive increased after sleep deprivation (9 vs 21%). In conclusion, following short-term sleep deprivation in infancy, respiratory control alters, peripheral chemoresponsiveness increases in magnitude and the timing of baseline breathing alters, without any detectable alteration in arousal propensity. This state may be associated with an increased vulnerability to obstructive respiratory events.

Arousal↗
PubMed2004

Sleep hygiene and sleep quality in Italian and American adolescents.

This study investigated cross-cultural differences in adolescent sleep hygiene and sleep quality. Participants were 1348 students (655 males; 693 females) aged 12-17 years from public school systems in Rome, Italy (n = 776) and Southern Mississippi (n = 572). Participants completed the Adolescent Sleep-Wake Scale and the Adolescent Sleep Hygiene Scale. Reported sleep hygiene and sleep quality were significantly better for Italian than American adolescents. A moderate linear relationship was observed between sleep hygiene and sleep quality in both samples (Italians: R =.40; Americans: R =.46). Separate hierarchical multiple regression analyses showed that sleep hygiene accounted for significant variance in sleep quality, even after controlling for demographic and health variables (Italians: R(2) =.38; Americans: R(2) =.44). The results of this study suggest that there are cultural differences in sleep quality and sleep hygiene practices, and that sleep hygiene practices are importantly related to adolescent sleep quality.

Activities of Daily Living↗
PubMed1977

Effects of thyrotropin-releasing hormone on sleep and sleep-related growth hormone release in normal subjects.

Effects of TRH on sleep and sleep-related growth hormone (GH) release were examined in four normal volunteers. A bolus of 500 microgram of synthetic TRH was injected iv at the onset of sleep, followed by continuous iv infusion of 1000 microgram of TRH dissolved in saline for 3 h on two nights. Saline alone was infused on two control nights in each of these subjects. Polygraphic sleep records showed that TRH transiently interrupted sleep on both nights in all of the four subjects. The arousal phenomenon was observed from 80 to 151 min after the start of TRH administration until 20 to 212 min after the end of TRH infusion. The mean (+/-SE) percentage of awakening on the nights of TRH administration was significantly larger than on the control nights (36.4 +/- 1.9% vs. 1.3 +/- 0.8%, P less than 0.001). Plasma GH increased in close relationship to the initial appearance of slow wave sleep (SWS) within 40 min after sleep onset on both control nights in all four subjects. On nights of TRH administration, however, plasma GH levels during the initial 80 min of sleep were significantly lower (P less than 0.005) than on control nights, whereas SWS was demonstrated before the interruption of sleep. On nights when sleep was interrupted by forced wakefulness 1 h after sleep onset, plasma GH rose to levels comparable to those on control nights during early sleep periods in all subjects examined. These results suggest that TRH inhibits sleep and sleep-related GH release in normal subjects.

Adult↗
PubMed2005

Cystic fibrosis patients have poor sleep quality despite normal sleep latency and efficiency.

STUDY OBJECTIVES: Cystic fibrosis (CF) patients may be predisposed to poor sleep quality due to upper and lower airway abnormalities and impaired gas exchange. Previous sleep investigations of CF patients using single-night polysomnography have reported conflicting results. We hypothesized that sampling sleep for a prolonged period in a patient's normal environment may give a more representative assessment of sleep quality than a single-night polysomnogram, and that impaired sleep quality would correlate with pulmonary disease severity and self-assessed sleep quality. DESIGN: Using wrist actigraphy, we measured sleep quality in clinically stable CF patients and age-matched control subjects. In addition, each CF patient and control subject completed the following three questionnaires: the Epworth sleepiness scale; the Pittsburgh sleep quality index (PSQI); and the Medical Outcomes Study 36-item short form. RESULTS: Twenty CF patients and control subjects were enrolled in the study, and were well-matched for age, sex, and body mass index. The mean (+/- SD) FEV(1) for CF patients was 61.0 +/- 20.1% predicted. CF patients and control subjects had similar sleep duration, sleep latency, and sleep efficiency. However, CF patients had higher PSQI scores (6.45 vs 4.55, respectively; p = .04), a higher fragmentation index (FI) [31.72 vs 18.02, respectively; p < 0.001], and less immobile time (88.87 vs 91.89, respectively; p = 0.02). There was a significant correlation of FI with FEV(1) and PSQI scores. CONCLUSIONS: Stable CF patients have disrupted sleep, and sleep disruption may in part be related to the severity of pulmonary disease. In addition, the PSQI may be useful in detecting CF patients with poor sleep quality.

Adult↗
PubMed1987

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea.

Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (greater than 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

Achondroplasia↗
PubMed2004

Does sleep or sleep deprivation increase epileptiform discharges in pediatric electroencephalograms?

OBJECTIVE: Sleep deprivation before obtaining an electroencephalogram (EEG) is believed both to increase the likelihood of sleep during an EEG and to increase the detection of interictal epileptiform discharges. However, depriving a child of sleep poses a burden on both the parent and the child. The objective of this study was to compare the effects of sleep, standard sleep deprivation, partial sleep deprivation, and no sleep deprivation on the odds of an epileptiform abnormality in outpatient pediatric EEGs. METHODS: Data were collected from all pediatric EEGs performed at a busy, university-based neurologic practice during two 2-month periods. During the first period, all EEGs were performed as ordered, either standard sleep-deprived (SSD) or non-sleep-deprived (NSD). During the second 2 months, SSD EEGs were performed per routine. However, non-SSD families were instructed to keep their children awake 2 hours later the night before the EEG. Those who complied were classified as partially sleep-deprived (PSD). Patient characteristics across protocols were compared with chi(2) and analysis of variance tests as appropriate. The odds of epileptiform and abnormal findings associated with sleep, NSD, PSD, and SSD EEGs were calculated using logistic regression. RESULTS: Of 820 eligible EEGs, sleep occurred in 22% of NSD, 44% of PSD, and 57% of SSD EEGs. The sample size of this study allowed for an 85% power, with alpha of.05, to detect an absolute increased EEG yield of 10%. Neither the presence of sleep (odds ratio [OR]: 0.99; 95% confidence interval [CI]: 0.69-1.42) nor the use of PSD (OR: 0.90; 95% CI: 0.50-1.62) or SSD (OR: 0.96; 95% CI: 0.63-1.47) protocols increased the odds of epileptiform EEGs. CONCLUSIONS: Sleep deprivation should not be used routinely to increase the yield of pediatric EEGs.

Adolescent↗