Search

Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues. The duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime and not with the length of prior wakefulness. Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm.

Ten male subjects were studied for a total of 306 days on self-selected schedules. Four of them developed bedrest-activity cycle period lengths very different from 24 hr (mean = 36.8 hr) despite the persistence of near-24-hr oscillations in other physiologic functions, including that of body temperature (mean = 24.6 hr). The percentage of sleep time spent in REM sleep varied significantly with the phase of that near-24-hr body temperature cycle. The peak in REM sleep propensity (RSP) occurred on the rising slope of the average body temperature curve, coincident with the phase of peak sleep tendency. This was associated with a significantly increased REM episode duration and shortened REM latency (including sleep-onset REM episodes), but without a significant change in the REM-NREM cycle length. We conclude that there is an endogenous circadian rhythm of REM sleep propensity which is closely coupled to the body temperature rhythm and is capable of free-running with a period different from both 24 hr and the average period of the sleep-wake cycle.

Plasma luteinizing hormone, follicle-stimulating hormone, and estradiol were measured at 20-minute intervals for 24-hours in seven pubertal premenarchal girls whose sleep was monitored polygraphically. A circadian variation in plasma estradiol was demonstrated with the highest values occurring during the day (1400-1600 hours) and lowest values during sleep, a time when gonadotropin secretion was augmented.

Plasma luteinizing hormone (LH) and testosterone (T) were measured by radioimmunoassay in nine pubertal boys and three sexually mature young men at 20-min intervals for 24 h. Plasma LH and T were also measured in one boy during a delayed sleep onset study. Polygraphic monitoring was carried out to identify precisely sleep onset. Wakefulness, and specific sleep stages. In all nine pubertal boys the plasma T concentration fluctuated and was significantly higher during normal nocturnal sleep as compared to daytime waking. This increased T secretion during sleep was temporally linked to the characteristic pubertal sleep augmentation of LH secretion. To define further the relationship of this increased T secretion to sleep, plasma LH and T were also measured in three of the pubertal boys after acute (1-day) reversal of the sleep-wake cycle. One of these boys was also studied after 3 days of sleep-wake cycle reversal. The results of these studies showed that plasma T was now augmented during the reversed daytime sleep period; the mean T concentrations during this period were significantly higher (P < 0.001) than during nocturnal waking in all four studies. Measurement of plasma LH and T in the three sexually mature young men showed episodic secretion of LH and T during both waking and sleep periods; there was no consistent significant augmentation of LH or T secretion during sleep. This study demonstrates that (a) in normal pubertal boys and sexually mature young men plasma T fluctuates episodically; (b) there is marked augmentation of T secretion during sleep in pubertal boys, which is dependent on increased LH secretion; (c) this pubertal LH-T secretory “program” is dependent on sleep, since it shifts with delayed sleep onset and reversal of the sleep-wake cycle; and (d) this demonstrable tropic effect of LH on T is evident only during puberty, since sexually mature young men fail to show any consistent relationship between LH and T secretion either awake or asleep.

A 6-year-old girl had subacute onset of hypoventilation and apnea during sleep. Diffuse dysautonomic changes were identified, including dilated, nonreactive pupils, decreased tearing and sweating, and abnormal temperature and cardiovascular control. All-night polysomnographic studies revealed frequent obstructive and central sleep apnea episodes. Her serum contained cytotoxic antineuroblastoma immunoglobulins. She died two years later during sleep. The general pathological examination revealed a ganglioneuroma originating in the sympathetic ganglia. Abnormalities in the brain were confined to the brainstem and consisted of complete loss of neurons with severe fibrillary gliosis in the region of the Edinger-Westphal nuclei as well as loss of neurons with gliosis in the locus ceruleus and in the reticular formation bilaterally.

On 4 separate occasions 17–20 mg of cortisol was given intravenously for 4.5 to 6.5 hr at different times of the day to an adult male. Endogenous cortisol secretion was suppressed for 4.5–5.5 hr following cessation of the infusion, and was reinitiated after this period of suppression of secretory activity in a pattern similar to that observed during the same portions of the control days. The study supports the concept that the episodic 24-hr ACTH-cortisol secretory pattern is not directly determined by a sequence of high or low plasma cortisol concentrations, but rather regulated or “programmed” for recurrent shorter time periods linked to the 24-hr sleep-wake cycle.

In order to test the hypothesis that cortisol secretion is inhibited during sleep, six healthy young men (ages 18-24) were studied in a 4-day protocol. A baseline nocturnal sleep period was followed by one night's total sleep deprivation, then sleep at 180 degrees phase shift, and then return to a normal nocturnal sleep episode (SP-3). Plasma cortisol concentrations were measured every 20 min (obtained by an indwelling venous catheter), rectal temperature was measured every minute, and sleep was polygraphically defined. During the first 4 h of sustained sleep, cortisol secretion was decreased even when sleep occurred during a time when the subject was usually awake; conversely, it was elevated if awake at the usual daily time of sleeping. This was not the case for the last 4 h of sleep. Body temperature was also decreased but during each entire 7- to 8-h sleep period. Meals produced only a small brief rise of cortisol and produced no change in body temperature. Stage 4 sleep was increased during the 180 degrees inverted sleep episode and decreased during SP-3, REM sleep however was increased during SP-3. A reciprocal relationship was found between REM and stages 3 and 4 for the second, third, and fourth, and sixth h of sleep for SP-3. These results demonstrate the inhibitory effect of the behavioral complex of sleeping on cortisol secretion superimposed on its endogenous circadian and ultradian rhythm. These neurophysiological events may be used to entrain and time the period and phase of biological rhythms in relation to shift work, sleep deprivation, and transmeridian jet travel.

Investigations in recent years have shown that secretion of pituitary hormones is episodic rather than continuous, manifesting endogenous rhythms that are largely governed by the 24-hour sleep-wake cycle. Variance from normal secretory patterns has been observed in several clinical syndromes (among them acromegaly, Cushing's, and affective depressive illness) and already serves as a valuable diagnostic tool.

(1978). Polysomnographic Recording Techniques Used for the Diagnosis of Sleep Disorders in a Sleep Disorders Center. American Journal of EEG Technology: Vol. 18, No. 3, pp. 107-132.

During nonentrained sleep--wake conditions in man, healthy adult subjects spontaneously develop "long" biological days (greater than 35 hr) in addition to the normal, approximately 25 hr day. The ratio of sleep to total time remains constant (approximately 0.30), with long sleep episodes occurring approximately 180 degrees out of phase with the short sleep episodes. The timing and amount of REM sleep advance to an earlier time within the sleep episode during free-running, whereas stage 3 + 4 sleep is related to the initiation and course of the sleep process itself. The REM--NREM cycle length does not change, comparing entrained and nonentrained conditions. The study of the chronophysiology of humans under nonentrained conditions may serve as a model of the chronopathology of sleep--wake changes which occur in sleep disorders associated with depression, narcolepsy--cataplexy, sleep--wake dyssomnias, delayed sleep phase insomnia, and aging.

The relationship between plasma levels of the tricyclic antidepressant desmethylimipramine (DMI) and plasma levels of melatonin-like immunoreactivity was studied in 32 endogenously depressed patients. An inverse correlation between plasma levels of DMI and plasma levels of melatonin-like immunoreactivity was found in the group of clinical responders to the chronic administration of the drug. The nonresponders had higher levels of melatonin-like immunoreactivity at comparable levels of DMI. This findings is consistent with the hypothesis that chronic high plasma levels of DMI may down-regulate the β-adrenergic receptors in man. However, some other homeostatic mechanisms may be involved in the clinical response.

In a previous publication, prepubertal depressives were found not to exhibit a shortened REM period latency during active illness when compared with pathological and normal control groups. It was hypothesized that this might be due to a nonselective inhibition of REM sleep by slow-wave sleep (SWS), which is quite intense among prepubertal children, especially during the first 2 h of the sleep period. A number of polysomnographic signs normally associated with REM sleep were observed to occur periodically, prior to the beginning of the first REM period. It was thought that these signs might be indicative of "minor escapes" of REM sleep activity from the inhibitory influence of SWS. It was further hypothesized that differences among the experimental groups in the occurrence (timing and amount per minute) of these signs support the idea of an inhibitory effect of SWS on REM; and thus offer an explanation for the apparent dissociation between the depressive disorder among prepubertal children and a shortened REM period latency. The hypotheses were not supported by the results presented here indicating that the above dissociation is probably not due to inhibitory mechanisms of SWS on REM sleep.

Theoretical and technical problems in using Nocturnal Penile Tumescence (NPT) measurements for the differential diagnosis of impotence are discussed and possible solutions are offered: 1) The basic assumption that NPT measurements can distinguish psychogenic from organic impotence has never been demonstrated in patients shown to be psychogenically and organically impotent independent of the NPT measurements themselves. Studies attempting to do this are necessary to determine definitively the limits of the clinical applicability of this important diagnostic tool. 2) Evidence is presented showing that though a direct observation of one of the patient's fullest erections is required for an adequate NPT evaluation, this is not always done. The danger of misdiagnosis if this step is omitted is illustrated with a case report. 3) Disagreements in the literature about NPT criteria for diagnosing psychogenic impotence are discussed and criteria are suggested that are based on demonstrating the intactness of the physiological mechanisms required for erection rather than on values recorded in normal subjects.

Plasma growth hormone measured at 20-min intervals across the night via indwelling venous cannula revealed a significant reduction in 16 healthy aged men as compared with 14 healthy young men. The decrease in growth hormone was entirely confined to the first 3 hours of the night (M +/- SEM for the integrated level was 5.0 +/- 1.2 and 21 +/- 4.2 ng . hr/ml). Growth hormone across the latter part of the night did not differ. Day and evening growth hormone levels measured hourly in five of the aged and nine of the young men failed to reveal an age effect. Growth hormone release is known to be associated with sleep onset, and particularly with slow wave sleep, stage 3 and 4, which was reduced in amount in these aged men (9.9 +/- 1.9 and 22.8 +/- 2.3% of time in bed for aged and young groups, respectively). Sleep stage 3 and 4 correlated significantly with growth hormone level (R = .463, p less than .01) for young and aged men combined, but not for either age group alone, indicating that growth hormone does not have a direct, simple relationship with slow wave sleep.

Prolactin secretion in normal adults is characterized by periods of episodic secretion which increase in magnitude during sleep. In this study, we report the 24-h mean prolactin concentrations, prolactin secretory patterns, and associated pituitary hormone function in nine patients (seven women and two men) with hyperprolactinemia of diverse etiologies. Four of the women and one of the men had clinically demonstrable pituitary tumors, one boy had a hypothalamic tumor, and the three other women had “functional” hyperprolactinemia. The 24-h mean prolactin concentrations derived from averaging the 20-min interval samples for 24 h ranged from 28.6 to 1,220 ng/ml. The plasma prolactin patterns in these patients showed persistence of episodic secretion in all and loss of the normal sleep-wake difference in plasma prolactin in seven of nine. Three of the patients with galactorrhea and comparable 24-h mean prolactin concentrations (58.3, 59.7, and 64.3 ng/ml) showed similar prolactin secretory patterns despite different etiologic mechanisms. Evaluation of the secretory patterns of luteinizing hormone (LH) in these patients showed loss of normal pulsatile LH release and a low 24-h mean LH concentration in the patient with the pituitary tumor, while the two patients without clinically demonstrable pituitary tumors (“post-pill” galactorrhea and “idiopathic” galactorrhea) showed normal LH secretory patterns and 24-h mean LH concentrations. The 24-h mean cortisol concentrations and secretory patterns were normal in five of the seven patients who had these parameters measured. The patient with the hypothalamic tumor had a low 24-h mean cortisol concentration and production rate and absent response to metyrapone. The patient with “idiopathic” galactorrhea had an elevated 24-h mean cortisol concentration but normal cortisol production rate and urinary 17-hydroxycorticoid excretion. Growth hormone secretion was abnormal in four of the patients (one with the hypothalamic tumor and three with pituitary tumors). Thyrotropin-releasing hormone (TRH) administration in four patients resulted in normal TSH release in two patients (one of whom developed galactorrhea after the test), an absent response in the patient with the hypothalamic tumor, and a blunted response in one of the women with a pituitary tumor. The two men had low 24-h mean plasma testosterone concentrations (69 and 30 ng/100 ml) and symptoms of impotence and loss of libido. Five of the women (four with pituitary tumors and one with Chiari-Frommel syndrome) had either low 24-h mean LH concentrations, abnormal LH secretory patterns, or both. These data indicate that patients with hyperprolactinemia encompassing a varied etiological range frequently show loss of the normal sleep-associated increase in prolactin secretion as well as abnormalities in the regulation of the other hypothalamic pituitary-regulated hormones. The finding that the abnormalities in LH, growth hormone, thyrotropin, and cortisol (adrenocorticotrophic) secretion were almost uniformly confined to the patients with the clinically demonstrable hypothalamic or pituitary tumors suggests that the size of the lesion is the critical factor.

We have observed three children who developed obstructive sleep apnea immediately following construction of pharyngeal flaps designed to improve the speech of these patients with velopharyngeal incompetence. Postoperatively the patients were noted to have repeated episodes during sleep of strong respiratory efforts without airflow. Sleep apnea can be debilitating and lethal, and should be looked for following surgery of the upper airway. Respiratory depressants should be avoided. Airway intubation, revision of the surgery, or tracheostomy may be necessary.

Obstructive sleep apnea syndrome was studied in 32 children, aged 2 to 14 years, in the sleep-wake disorders center at Montefiore Hospital and Medical Center during the years 1977 to 1980. All children under-went all-night polysomnograms; 17 of these children had surgery to relieve airway obstruction and seven had a repeat polysomnographic study 4 to 6 weeks following the surgery. There was a significant improvement in the number of obstructive apneas and in other apnea indices following surgery. There was no significant effect on the durations and the proportions of the various sleep stages, on sleep efficiency, or on the number of awakenings.

The temporal pattern of growth hormone release at sleep onset was studied in six adult human subjects by frequent blood sampling combined with polygraphic sleep recording. HGH release was associated with sleep onset but not with the transition from waking to sleep. Delta activity consistently preceded the first elevation of plasma HGH.

To evaluate the secretory patterns of luteinizing and follicle-stimulating hormones in various forms of sexual precocity, plasma levels of these hormones were measured every 20 minutes for 24 hours in six patients and nine normal pubertal children. Three patients with "idiopathic" precocious puberty and one boy with a hypothalamic tumo rand precocious puberty exhibited fluctuating plasma concentrations that resembled findings in normal pubertal children in that they had significantly increased luteinizing hormone concentrations during sleep. Two boys with congenital adrenal hyperplasia and advanced bone age also showed episodic fluctuation of both hormones and augmented luteinizing hormone concentrations during sleep. These findings show that patients with precocious puberty related either to Central-nervous-system stimulation or to a primary adrenal disorder can exhibit the normal pubertal luteinizing hormone pattern of augmented secretory activity synchronous with sleep. (N Engl J Med 289:282–2...

Polygraphic recording is presented of the sleep pattern in a young male who developed nystagmus and oscillopsia associated with a remittent CNS demyelinating disease. The vestibular nystagmus observed during wakefulness disappeared during all stages of sleep, including rapid eye movement sleep (REM). Since vestibular nystagmus experimentally induced in wakefulness is also absent during all phases of sleep, these findings suggest that during sleep similar suppressive mechanisms are operative.

It has recently been demonstrated that the total daily production of cortisol by normal man is accomplished in a series of discontinuous secretory episodes (Fig 1) separated by periods of quiescence of the adrenal cortex (1). In the normal it was shown that the adrenals did not secrete cortisol for about 18 hours of each day. The proof was based upon measurement of the specific activity of plasma cortisol in association with rises and falls in the plasma cortisol concentration measured at brief intervals. Rises in plasma level were accompanied by drops in cortisol specific activities while falls were associated with unchanged specific activity. It was also demonstrated that this episodic secretory activity persisted throughout the 24 hour sleep-awake cycle. It was of considerable importance to establish whether a similar pattern of secretion existed in Cushing's syndrome due to bilateral adrenal hyperplasia. It has been possible to study a carefully selected patient and to resolve the problem with the fin...

Plasma LH and FSH concentrations were measured every 20 min for 24 hr in 3 patients with gonadal dysgenesis (12, 18, and 26 yr old). A 12-yr-old girl with Turner's syndrome showed augmented LH and FSH secretory activity synchronous with sleep similar to normal pubertal girls, but with gonadotropin levels in the castrate range. An 18-yr-old girl with pure gonadal dysgenesis had a statistically significant higher mean LH concentration during sleep compared with waking; however, the difference was less striking compared with the 12-yr-old. This diminution in the sleep-wake LH difference is also characteristic of normal late adolescents. A 26-yrold woman with Turner's syndrome did not show increased LH or FSH secretory activity during sleep which is similar to what has been reported in normal women. These findings suggest that patients with gonadal dysgenesis follow a qualitative pattern of gonadotropin secretion during sexual maturation which is similar to normal, but the concentrations of gonadotro...

The recent development of precise and sensitive radioimmunoassay methods for the measurement of human prolactin has resulted in a large body of data concerning the regulation of this hormone in phy...

The amount of time that monkeys (Macaca mulatta) slept was reduced after they were given p-chlorophenylalanine, a selective depletor of serotonin in animal tissues. The time spent in the rapid eye movement stage of sleep was unchanged, but the time in other sleep stages decreased. Seven regions of the brain had a 31 to 46 percent decrease in serotonin content; the concentration of cerebellar serotonin increased by 44 percent.

A case of impotence with significantly impaired nocturnal penile tumescence (NPT) following transurethral resection of the prostate (TURP) is described. The patient was studied with polysomnographic recording including measurements of NPT for three consecutive nights at nine months after surgery and showed a total absence of full erections. Possible causes of his impotence are discussed. It is concluded that the total clinical picture strongly suggests that the erectile dysfunction was a result of physiologic complications of the surgery. Methodologic problems in past work are discussed, and the need for detailed diagnostic studies is stressed. The sleep studies that should be a part of this comprehensive evaluation are described.

We studied the effect of flurazepam, a known suppressor of stages 3 and 4 of sleep, on nocturnal sleep patterns and on growth hormone release immediately following sleep onset in normal young adults. Polysomnography and sampling of growth hormone (every 20 min for 26 h) were performed before and after 2 weeks of nightly flurazepam (30 mg, 8 subjects) or placebo (8 subjects) administration. There were no significant changes in growth hormone release in spite of a significant decrease in stage 4 sleep (69%) and total waking time (46%) and an increase in total sleep time (23%) in the drug group. REM sleep was not changed. These results indicate that the normal GH release following sleep onset continues to occur despite stage 4 suppression by pharmacological means.

The acute and chronic effects of alcohol and alcohol withdrawal on sleep patterns and plasma GH and cortisol fluctuations occurring during sleep were studied. Five healthy men, aged 21-26 yr, consumed a placebo drink for 3 baseline nights, alcohol (0.8 g/kg) for 9 nights, and a placebo drink on final withdrawal night. All-night polygraphic sleep recordings and blood samples (every 20 min with a venous catheter) were collected for 1 placebo, 1 acute alcohol, 1 chronic alcohol (night 9), and 1 alcohol withdrawal night. Acute and chronic alcohol consumption reduced rapid eye movement sleep nonsignificantly during the first half of the night, whereas slow wave sleep (stages 3 and 4) was increased significantly after acute alcohol, returning to baseline values on the chronic alcohol night. On the withdrawal night, rapid eye movement sleep and slow wave sleep were not significantly different from placebo sleep. Alcohol significantly suppressed plasma GH values (70-75%) on acute and chronic nights. All measures of GH, including total integral for bedtime hours, mean hourly rate, and peak level, were similarly affected by alcohol. GH returned to placebo values on the withdrawal night. Measures of nighttime plasma cortisol were not significantly altered by alcohol or alcohol withdrawal at this dose level.

An electromyographic study of nonmimetic skeletal muscles was carried out in 8 normal adults and 4 patients with spastic hemiparesis during all stages of sleep for a total of 21 nights. All normal subjects showed absence of tonic electromyographic activity in all nonmimetic skeletal muscles in all stages of sleep. Also, during quiet, relaxed wakefulness, tonic muscle discharges disappeared in the normal subjects. Three patients with upper motor neuron spasticity demonstrated results during sleep similar to those obtained in the normal subjects. In the fourth patient, tonic muscle discharges persisted into stage 2 non-REM sleep, disappeared within 30 to 240 seconds following the onset of stage 2 sleep, and were absent during stages 3 and 4 sleep and REM sleep.

LH (luteinizing hormone) secretion in pubertal individuals has been previously reported to be augmented during nocturnal sleep. The present paper attempts to clarify the relationship of this phenomenon to sleep. Two 24-hr periods of blood sampling every 20 min were carried out in each of 4 boys who were 14–15 yr old. The first study was during a normal sleep-wake cycle while the second study was during an acute sleep-wake reversal (or, in one subject, sleep delay). Each blood sample was assayed for LH and sleep was recorded polygraphically. The control study confirmed the association of LH secretory enhancement with nocturnal sleep at puberty while the reversal proved that a rise in LH secretion is also associated with daytime sleep. LH plasma concentrations remained elevated during nocturnal waking, as opposed to daytime waking, showing that acute sleep-wake reversal does not eliminate increased LH secretion at night in pubertal subjects.

Six young men with idiopathic hypogonadotropic hypogonadism had 24-h frequent blood sampling studies for measurement of LH, FSH and testosterone. Five of the patients had LH and FSH measured after administration of 100 mug LH-RH during waking and then during sleep. Four of the patients had testicular biopsies performed. The results of the present studies showed that 4 of the patients had no evidence of episodic LH, FSH, or testosterone secretion. The two patients who showed significant sleep related pulses of LH had the highest 24 h mean testosterone concentrations, the best responses to exogenous LH-RH and the most differentiated testicular biopsies. Sleep had no effect on the release of LH or FSH in response to LH-RH. These sutdies suggest that the clinical and laboratory heterogeneity of idiopathic hypogonadotropic hypogonadism may be the result of differences in the degree of endogenous LH-RH deficiency.

We describe a new syndrome called "delayed sleep phase insomnia." Thirty of 450 patients seen for a primary insomniac complaint had the following characteristics: (1) chronic inability to fall asleep at a desired clock time; (2) when not on a strict schedule, the patients have a normal sleep pattern and after a sleep of normal length awaken spontaneously and feel refreshed; and (3) a long history of unsuccessful attempts to treat the problem. These patients were younger than the general insomniac population and as a group did not have a specific psychiatric disorder. Six patients' histories are described in detail, including the successful nonpharmacological chronotherapy regimen (resetting the patients' biological clock by progressive phase delay). Delayed sleep phase insomnia is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.

Human subjects during extended isolation from environmental time cues show complex variations in timing and duration of sleep with a progressive pattern, which eventually results in rest-activity and body temperature rhythms having different average periods. We present a model where temperature and rest-activity are each governed by an oscillator of the van der Pol type, denoted x and y, respectively. The oscillators affect one another through “velocity” type coupling, the effect of x on y being about four times greater than y on x. Periodic zeitgeber, z, is modeled as forcing only on y. We find that the entire pattern sequence can be realistically reproduced by causing only the intrinsic period of the y oscillator to increase while that of x remains stable. Desynchronization between x and y is the result of the intrinsic periods of the two oscillators becoming so disparate that the coupling is no longer able to enforce synchrony. Prior to desynchronization both human subjects and our model exhibit “phase trapping” wherein the relative phase of x and y is slowly modulated although the average x and y periods match. The model phase relations between temperature and both the timing and duration of sleep are, throughout, in good agreement with entrained and free-running human data. Most importantly, the model shows that the dramatic change in the length of the rest-activity cycle when desynchronization occurs is actually due to a relatively small variation in the governing variable, y.

To the Editor. —We read with interest the two recent articles by Kales et al on narcolepsy (Archives1982;39:164-168, 169-171). The authors stated that the presence of cataplexy allows the physician to proceed with treatment "solely on the basis of the clinical picture, without sleep laboratory evaluation." We agree that a skilled clinician can easily and accurately diagnose narcolepsy when the symptoms are classic. However, it has been our experience that recording sleep patterns in the clinical sleep laboratory is important for several reasons other than just diagnosis. First, the clinical diagnosis of narcolepsy is based on the patient's subjective symptoms and is a subjective conclusion by the clinician, as there are no objective clinical signs. Although the clinician may be confident in making the assessment, the patient recognizes that the clinician is not infallible and frequently desires objective documentation of the disorder. We have studied many patients with narcolepsy

The concentration of PRL was measured every 20 min for 24 h in six prepubertal and three adolescent boys. In both groups, PRL secretory episodes occurred throughout the 24-h period. In all subjects, the mean concentration of PRL was significantly higher during sleep than during wakefulness; the mean concentration during the entire 24-h period, during sleep or during wakefulness, was not different between the prepubertal subjects and the adolescents. These data suggest the absence of an ontogenetic change for PRL secretion in boys. During acute sleep-wake reversal, two of three pubertal boys showed significantly higher PRL during daytime sleep than during nocturnal wakefulness. This suggests that PRL release in adolescent boys is linked with sleep, rather than with clock time.

After 1 week of a normal control (baseline) period, 7 healthy young adult subjects were subjected to a 3-hr sleep-wake schedule, (ultradian) which was adhered to for 10 days. They were allowed eight 1 hr sleep times, equally spaced throughout each 24 hr period. They were then allowed a normal nocturnal 8-hr sleep time for 7 days. During all lights-out sleep periods, poly-graphic definition of sleep stages and waking time was made. On the sixth 24-hr period of the first week (baseline) and on the eighth 24-hr period of the ultradian period, sequential 20-min plasma samples were obtained by means of an indwelling intravenous catheter. Rectal temperature was obtained at regularly spaced frequent intervals. Despite significant sleep deprivation, a circadian pattern of total sleep time persisted throughout the 10-day ultradian condition. The distribution and amount of REM sleep time was most affected with stages 3–4 sleep least affected. The time of maximum sleep was delayed by approximately 6 hr. The...

Documented observations of a 5-week-old infant during a "near miss" for a Sudden Infant Death Syndrome (SIDS) episode by a physician were carried out during an in-hospital physiological recording of respiratory and cardiac activity. This "near miss" event occurred during quiet sleep and was characterized by a prolonged apneic attack with marked bradycardia, cyanosis and limpness which required immediate vigorous resuscitative efforts by a physician and trained nurse. Parental descriptions of similar events parallel these documented sudden unexpected changes in cardiorespiratory parameters. Objective polygraphic data were obtained immediately following the episode and at later ages during 24 and 48 hour continuous recordings of respiration, heart rate, sleep/wake and behavioral activity. The data show that numerous apneic episodes occurred following the "near miss" event, many accompanied by marked bradycardia. The moderately severe hypoxemia noted during these sleep-related apneas indicate that immediate intervention is required to prevent significant hypoxia and central depression in such infants.

Periodic movements in sleep (PMS) are stereotyped, repetitive, nonepileptiform movements of the lower extremities. A total of 409 sleep disorder patients were studied with all-night polysomnogram recording, and 53 (13%) had PMS. Such movements occurred in a wide variety of sleep-wake disorders in addition to insomnia. The prevalence and magnitude of PMS were not statistically greater in patients with insomniac disorders than in those with syndromes of excessive daytime sleepiness or other sleep-wake disorders. The results suggest that although PMS is responsible for disturbed sleep in relatively few patients, chronic sleep-wake disturbance is associated with PMS and may lead to the development of these movements.

It has been postulated that the sudden infant death syndrome (s.i.d.s.) may sometimes be due to abnormal maturation or injury to the brain stem centres that regulate respiration. This functional abnormality of the brain stem respiratory centres may result in the interruption of the automatic inspiratory/expiratory cycle by recurrent periods of apnoea. There is a subgroup of infants known as ‘near-miss’ for s.i.d.s., who survived a prolonged apnoeic episode during sleep which may have resulted in death. In a number of recent studies, the near-miss infant has been clearly identified as an infant at high risk for s.i.d.s. Clinical studies conducted by using polygraphic and behavioural monitoring of near-miss infants have revealed numerous apnoeic episodes during sleep. Consequently, the clinical necessity of monitoring these babies in a paediatric care unit has become well established both for diagnostic purposes and for subsequent outpatient care. In view of these findings, it has become increasingly more important to develop advanced sophisticated computer methods for the on-line detection and processing of apnoeas during in-hospital monitoring of infants. This paper describes a digital computer method of on-line apnoea processing for application during the in-hospital monitoring of infants. The method is based on the application of Walsh transformations to the expired CO2 signal measured in infants using a Beckman CO2 analyser.