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Biomedical subjects

E D Weitzman

Publications and source records attributed to E D Weitzman.

At least 37 records · Page 2Linked to original sources
PubMed1982

Effects of flurazepam on sleep and growth hormone release during sleep in healthy subjects.

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.

Adult↗
PubMed1982

Mathematical model of the human circadian system with two interacting oscillators.

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.

Body Temperature↗
PubMed1982

Respiratory and cardiac events observed and recorded during and following a "near miss" for Sudden Infant Death Syndrome episode.

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.

Bradycardia↗
PubMed1981

Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia.

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.

Adolescent↗
PubMed1981

Sleep apnea and hypoventilation syndrome associated with acquired nonprogressive dysautonomia: clinical and pathological studies in a child.

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.

Antibodies, Neoplasm↗
PubMed1981

Lack of an effect of melatonin on the basal and L-dopa stimulated growth hormone secretion in men.

The oral administration of melatonin to men has been reported to cause a rapid and significant elevation of serum GH, and to inhibit GH release after stimulation by L-Dopa. We studied the effect of melatonin i.v. on the basal and L-Dopa stimulated GH secretion in four young men. Each subject's control response to L-Dopa was first studied by an oral administration to 500 mg of L-Dopa under a placebo infusion and was followed 2 weeks later by a similar study under melatonin infusion, 2.1 mg/min (total dose of 500 mg). The infusion of melatonin was given for a 4-hour period, 2 hours before and 2 hours after the L-Dopa stimulation. Blood samples for GH were obtained at 30-min intervals. Basal values of serum GH did not rise under the melatonin infusion and peak GH values following L-Dopa stimulation during the control infusion and the melatonin infusion also did not differ (2 +/- 0.5 to 22 +/- 6 and 2 +/- 0.8 to 25 +/- 4 ng/ml respectively). Our data suggest that under an acute constant infusion melatonin does not stimulate GH secretion, nor does it interfere with the L-Dopa stimulated GH response in men.

Adult↗
PubMed1981

An inverse correlation between serum levels of desmethylimipramine and melatonin-like immunoreactivity in DMI-responsive depressives.

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 finding is consistent with the hypothesis that chronic high plasma levels of DMI may down-regulate the beta-adrenergic receptors in man. However, some other homeostatic mechanisms may be involved in the clinical response.

Adolescent↗
PubMed1981

Chronotherapy: resetting the circadian clocks of patients with delayed sleep phase insomnia.

We report here the development of a brief drug-free rescheduling treatment ("chronotherapy") for Delayed Sleep Phase (DSP) insomnia, a syndrome characterized by sleep-onset insomnia with difficulty in morning awakening. We postulated that patients with DSP insomnia had an inadequate capacity to achieve phase advance shifts of the circadian pacemaker which times the sleep-wake cycle. Chronotherapy was therefore designed to reset these patients' biological clocks by the phase delay route. This single 5-6 day treatment was tested in 5 patients with a 4-15 year history of DSP insomnia. All 5 patients reported a lasting resolution of their symptoms substantiated by systematic long-term self-reports and objective polygraphic recording before and after treatment (average follow-up of 260 days; range, 42-910 days). The average sleep onset advanced from 4:50 a.m. before treatment to 12:20 a.m. afterwards, and wake times advanced from 1:00 p.m. to 755 a.m. (for both, p less than 0.001), with no reduction in sleep efficiency. As a result, all 5 patients were able to end their chronic dependence on hypnotic medications.

Adult↗
PubMed1981

Effect of phenobarbital on sleep and nighttime plasma growth hormone and cortisol levels.

The acute and chronic effects of phenobarbital and phenobarbital withdrawal on sleep patterns and on plasma growth hormone (GH) and cortisol fluctuations occurring during sleep were studied. Before bed, five healthy men, aged 21 to 25, were given a placebo on three baseline nights, phenobarbital (100 mg p.o.) for nine nights, and a placebo on a final withdrawal night. Beginning on the third of three consecutive nights in the laboratory, all-night polygraphic sleep recordings and blood samples (obtained every 20 min through indwelling venous cannulae) were collected for the placebo, acute phenobarbital, chronic phenobarbital, and phenobarbital withdrawal conditions. Blood phenobarbital levels ranged between 5 to 9 micrograms/100 mL across all hours of the chronic drug night. At this low sedative dose, latency to sleep onset and stage 4 sleep were significantly reduced in the chronic drug condition, but REM sleep was not significantly reduced. No significant sleep change was observed on the withdrawal night. Both peak GH level and total integrated GH across the night were unaffected by the acute, chronic, and withdrawal conditions. The pattern of GH release appeared to be altered on the phenobarbital and phenobarbital withdrawal nights as compared with placebo. Nighttime plasma cortisol levels were not significantly altered by any experimental condition.

Adult↗
PubMed1981

Sleep and its disorders.

The advances in research on sleep an biological rhythms have recently been applied to the diagnosis and treatment of sleep disorders. A new clinical specialty has developed with the establishment of sleep disorder centers and a diagnostic classification of sleep and arousal disorders. This new nosological approach has evolved from an extensive base of new scientific information concerning descriptive polygraphic and analysis of clinical case series. Four major categories have been defined: (a) disorders of initiating and maintaining sleep (insomnias), (b) disorders of excessive somnolence, (c) disorders of the sleep-wake schedule, and (d) dysfunctions associated with sleep. Within this comprehensive classification certain major pathophysiological advances are described for the "insomnias." These include polysomnographic identification of altered sleep stage patterns in the major effective illnesses, insomnias related to hypnotic drugs and alcohol, sleep disturbances associated with sleep-induced respiratory impairment, and sleep-related periodic movements during sleep (nocturnal myoclonus). Excessive daytime somnolence is primarily associated with the hypersomnia sleep-apnea syndrome and with narcolepsy. The relationship between biological rhythms (chronobiology) and disorders of the human sleep-wake schedules is very actively investigated. The recognition that sleep length, internal organization, and timing within neurophysiological circadian time-keeping systems has lead to better diagnosis of these sleep-wake disorders and new chronotherapeutic regimens. Finally, increasing identification and description of "parasomnias," i.e. dysfunctions associated with sleep, has led sleep research into important new areas that are of general physiological interest. It is now clear that sleep disorders medicine has become a new scientific and clinical discipline in its own right.

Arousal↗
PubMed1981

The developmental pattern of in vitro rat liver melatonin degrading activity.

The developmental pattern of the in vitro rat liver melatonin degrading activity was studied. Livers from rats 3, 12, 16, 21, 30 and 90 days old were incubated with [3H] melatonin. A high pressure liquid chromatography (HPLC) technique was used to determine the appearance of melatonin metabolic product--6-hydroxymelatonin--in the liver extract. Catabolic activity belong very low at age 3 days, increased rapidly with age and reached maximum activity between the ages 21 to 30 days.

Aging↗
PubMed1981

Sleep apnea studies in an infant with congenital primary hypoventilation ("Ondine's curse").

Recurrent apneic episodes were typically associated with sleep, not wakefulness, in an infant with congenital primary hypoventilation ("Ondine's Curse"). Quiet sleep (SLQ) was shown to constitute a higher risk condition than active sleep (SLA) at the ages she was recorded polygraphically (2-4 months old). This infant's respiratory disorder was complicated by recurrent pneumonia, seizures and deficient growth which resulted in death at the age of eight months. Necropsy revealed bronchopulmonary dysplastic fibrosis and cor pulmonale. Neuropathologic examination failed to reveal pathologic changes in the brainstem.

Autonomic Nervous System Diseases↗