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Biomedical subjects

W B Mendelson

Publications and source records attributed to W B Mendelson.

At least 127 records · Page 7Linked to original sources
PubMed1982

Disturbances of sleep and cognitive functioning in patients with dementia.

The relationship of sleep, circadian rhythms, and cognitive impairment in dementia patients is briefly reviewed. All-night sleep EEG data were collected in relatively young and relatively unimpaired patients with presumptive Alzheimer's disease and eight age-matched controls. Delta sleep time and Delta sleep % (Stages 3 and 4)--but not REM sleep measures--were significantly reduced in the patients. Implications of these findings are discussed.

Aged↗
PubMed1982

A clinical study of flurazepam.

Eleven patients suffering from chronic insomnia were given 30 mg flurazepam for 28 nights. While EEG measures of total sleep time and sleep efficiency were improved, changes in sleep latency and intermittent waking time were small and nonsignificant. Subjective benefits in sleep were confined to the first 2 nights. There was neither increased nor decreased daytime sleepiness. Cognitive functioning was significantly decreased during the first 2 days, and patients were unaware of these changes. Simple motor tasks were relatively unaffected. Desalkylflurazepam concentrations showed significant accumulation over time, but were not predictive of sleep measures or daytime performance in individual subjects. The withdrawal period was characterized by subjectively disturbed sleep and daytime dysphoria.

Clinical Trials as Topic↗
PubMed1982

Topographic cortical mapping of EEG sleep stages during daytime naps in normal subjects.

Computer-generated cortical maps of power spectral estimates derived from 16 leads were drawn based on daytime sleep recordings in four normal volunteers. These data were compiled from nine 10-s artifact-free, EEG epochs from awake, stages 1-4 and REM sleep in each volunteer. EEG leads were placed on the left hemisphere and midline according to the 10-20 system with four additional interpolated posterior locations. Magnitude spectral estimates with 1 Hz resolution and adjacent frequencies (delta 2-4, alpha 8-12, beta 13-18) were analyzed with two-way ANOVA (lead by sleep stage). Delta activity was relatively uniform and of low amplitude in awake, eyes-closed subjects, and REM. Delta power increased at the vertex in stage 1. With progressing, non-REM sleep stages, it increased in power and enlarged radially to the intraparietal sulcus posteriorly, and the superior frontal gyrus anteriorly. Comparison of maps with ear and a computed average reference yielded similar topographic patterns. Alpha activity was expectedly maximal occipitally in awake subjects, but surprisingly a frontal area appeared in slow wave sleep. Beta activity in awake subjects was low and maximal parietally; stages 1 and REM showed even lower and more uniform distribution. Stage 2 showed the greatest power, concentrated at the vertex, with stages 3 and 4 diminishing. These data suggest that sleep stages are not completely uniform electrophysiologically across the cortex. This opens the possibility for a new method for the diagnosis of sleep disorders and alternatives in sleep staging.

Adult↗
PubMed1981

Speaking, thinking, and blinking.

The effect of several mental tasks on the spontaneous eye blink rate in 36 normals was examined. The blink rate during silence was 19.0 blinks/minute. This was significantly lower than the mean blink rate during speech (24.7 blinks/minute) and while listening to a paragraph to be memorized (27.6 blinks/minute). Reading reduced the blink rate to 12.3 blinks/minute. Men were more able to suppress and speed up blinking than women.

Adult↗
PubMed1981

Flurazepam-induced sleep apnea syndrome in a patient with insomnia and mild sleep-related respiratory changes.

Sleep EEG and respiratory measures were examined in a 38-year-old man with a long-standing history of insomnia and daytime sleepiness. He was found to have seven to 18 primarily obstructive apneas per night on four baseline recordings, a finding not generally considered to be indicative of pathology. On the first two nights on which he received 30 mg of the benzodiazepine hypnotic flurazepam, there were 22 and 100 apneas, and during the daytime he became extremely sleepy. Upon cessation of medication, his clinical condition improved, and the number of apneas decreased to 11 and 6 on withdrawal nights 4 and 6. Although respiratory depression is neither invariable nor unique to flurazepam, this case suggests that it may be a clinically significant problem with recommended oral doses in some individuals.

Adult↗
PubMed1981

Piperidine enhances sleep-related and insulin-induced growth hormone secretion: further evidence for a cholinergic secretory mechanism.

Piperidine, a nicotinic cholinergic receptor stimulator, was used in paired design studies of sleep-related and insulin-induced GH and PRL secretion. For the sleep studies, 100 mg piperidine or an equal volume of saline were infused for 30 min starting at sleep onset in eight normal volunteers. The same dose of piperidine was infused for 30 min (beginning 15 min before insulin injection) in an additional eight volunteers undergoing insulin tolerance tests. After piperidine administration, there was a significant (P less than 0.01) enhancement of sleep-related GH secretion, abut no change in PRL. GH concentrations during the first 2 h of sleep were 7.2 +/- 1.2 ng/ml after saline and 15.2 +/-2.9 ng/ml after piperidine (P less than 0.01). No alteration in any measured sleep parameter was noted with the drug. Piperidine did not affect the daytime insulin-induced secretion of either GH or PRL, as assessed by an analysis of variance. However, paired analysis of increments and areas under the response curves indicated a statistically significant effect for GH but not PRL. The maximum GH increment with piperidine was 48.0 +/- 4.3 ng/ml, compared to 36.8 +/- 3.6 ng/ml with saline (P less than 0.01). Piperidine given alone did not influence daytime concentrations of GH. These data are consistent with the view proposed by us, on the bass of methoscopolamine inhibition of nocturnal GH secretion, that cholinergic pathways play a facilitatory role in sleep-related and insulin-induced GH secretion. Thus, cholinergic mechanisms stimulate GH secretion. Nicotinic as well as muscarinic pathways appear to be involved, although the quantitative nicotinic contribution seems to be smaller than the associated with muscarinic sites.

Adolescent↗
PubMed1980

Effects of melatonin and propranolol on sleep of the rat.

Melatonin and L-propranolol, which inhibits melatonin synthesis, were administered to rats at 07.45 h and 19.45 h. Melatonin given in the morning decreased non-REM sleep, but when given at night had no effect on sleep stages. L-propranolol given in the morning had no effect on non-REM sleep, but increased it at night. L-propranolol produced decreased in percentage REM sleep at both times.

Animals↗
PubMed1980

Sleep in Gilles de la Tourette syndrome.

The sleep of six Tourette patients (drug-free and while taking haloperidol was compared with that of nine normal volunteers. The untreated patients had 30% less delta sleep, which returned to values indistinguishable from those of volunteers when they received haloperidol.

Adolescent↗
PubMed1980

The effect of growth hormone administration on human sleep: a dose-response study.

Human growth hormone and saline were administered for one night each to normal volunteers in a cross-over study. A dose of 2 units im given 15 min before bedtime had no effect on sleep EEG parameters. In contrast, 5 units resulted in a 19% decrease in slow-wave sleep (p < 0.01) and a 13% increase in REM sleep (p < 0.05). Neither doe, when given during daytime, affected tests of affect or serial learning.

Adolescent↗
PubMed1979

Sleeping pills.

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Anti-Anxiety Agents↗