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Biomedical subjects

N Sitaram

Publications and source records attributed to N Sitaram.

79 records · Page 5Linked to original sources
PubMed1978

The switch process in manic-depressive illness. Circadian variation in time of switch and sleep and manic ratings before and after switch.

Research data collected on 75 Bipolar I patients, hospitalized at the NIMH between 1963 and 1975, were reviewed to identify "switches" into and out of mania. There were 27 "slow" switches (i.e. occurring over a period of 2--6 days) in 14 patients and 89 "rapid" switches (i.e. occurring in 24 hours or less) in 35 patients. No patient showed both "rapid" and "slow" switches during his hospitalization. Among the 89 rapid switches, 52 switches were into mania and 37 were out of mania. Rapid switches into and out of mania occurred significantly more often in the morning (7 a.m. to 3 p.m.) than at night (11 p.m. to 7 a.m.) or in the evening (3 p.m. to 11 p.m.). Estimated average sleep time on the night prior to switch into mania showed a significant drop as compared to sleep time on the second, third and fourth nights prior to switch. Patients who switched into mania at night were rated as significantly more manic during the 4 days following the switch than patients who switched in the morning or evening. Patients who switched into mania at night and evening were rated as sleeping significantly less during the 4 days following the switch than patients who switched in the morning.

Bipolar Disorder↗
PubMed1978

Methoscopolamine inhibition of sleep-related growth hormone secretion. Evidence for a cholinergic secretory mechanism.

We have examined the effects of cholinergic blockade with 0.5 mg methscopolamine bromide, intramuscularly, on sleep-related and insulin-induced growth hormone (GH) secretion. 17 normal young men were studied; 8 had sleep studies, and 12 (including 3 who also had sleep studies) had insulin tolerance tests (ITT) with 0.1 U/kg of regular insulin. After an adjustment night in the sleep laboratory, saline control night and methscopolamine night studies were done in random sequence; study procedures included electroencephalographic, electromyographic, and electrooculographic recordings, and blood sampling every 20 min for hormone radioimmunoassays. Prolactin levels were also measured during sleep. For methscopolamine night studies, the mean overall control GH level of 2.89+/-0.44 ng/ml and the mean peak control GH level of 11.09+/-3.11 ng/ml were dramatically reduced to 0.75+/-0.01 and 1.04+/-0.25 ng/ml, respectively (P<0.0001 and <0.001). Despite virtual absence of GH secretion during the night in every study subject, no measured sleep characteristic was affected by methscopolamine, including total slow-wave sleep (12.1+/-2.6% control vs. 10.3+/-2.5% drug, P>0.2). Sleep prolactin levels were not changed by methscopolamine. In contrast to the abolition of sleep-related GH secretion, administration of methscopolamine had only a marginal effect on the GH response to insulin hypoglycemia. None of nine time points differed significantly, as was also the case with peak levels, mean increments, and areas under the curves (P>0.2). Analysis of variance did, however, indicate that the lower GH concentrations achieved during ITT after methscopolamine (average 31.7% below control) were significantly different than control concentrations. We conclude that the burst of GH secretion which normally occurs after sleep onset is primed by a cholinergic mechanism which does not influence slow-wave sleep. Cholinergic mechanisms do not appear to play an important role in sleep-related prolactin secretion. The contrast between the complete suppression of sleep-related GH release and the relatively small inhibitory effect on ITT-induced GH secretion suggests that the neurotransmitter mechanisms, and presumably the pathways, which subserve sleep-related GH secretion in man may be different from those which mediate the GH response to pharmacologic stimuli such as insulin.

Adult↗
PubMed1978

Circadian variation in the time of "switch" of a patient with 48-hour manic-depressive cycles.

A 43-year-old patient with regularly occurring 48-hr manic depressive cycles was studied intensively for about 2 years. While she was hospitalized, she was rated for manic behavior on a 15-point scale every 2 hr. Using predefined criteria, we have systematically analyzed 173 switches into mania and 171 switches out of mania with respect to their time of occurrence during the 24-hr day and the influence of time of switch on the intensity and duration of mania. A significantly higher number of switches into mania occurred at night (12 midnight to 8 AM) with peak incidence between 4 AM and 6 AM. Switches out of mania peaked between 10 PM and 12 midnight and also between 6 AM and 8 AM. Night switches into mania were also associated with a significantly higher peak mania rating than morning (8 AM to 4 PM) switches and higher rate of mania increment than morning and evening (4 PM to 12 midnight) switches. This indicates that time of day or circadian factors may determine the frequency and intensity of the manic process in this patient.

Adult↗
PubMed1977

Physostigmine analgesia and somatosensory evoked responses in man.

14 normal volunteers were given 0.5 mg physostigmine or saline placebo i.v. in a randomized double blind trial. Subjects were pretreated with 0.5 mg methscopolamine i.m. on both days. Pain ratings and average evoked responses were obtained to brief electrical stimuli administered to the forearm. Pain response criterion was significantly higher on physostigmine than on placebo. Average evoked response component P100 was significantly smaller on physostigmine than placebo, especially for higher intensity stimuli. These results are consistent with central cholinergic modulation of pain and arousal systems in man.

Adult↗
PubMed1976

REM sleep induction by physostigmine infusion during sleep.

Physostigmine (an anticholinesterase agent that increases acetylcholine at the synapse), in a dose of 0.5 milligram, was given intravenously to seven normal human volunteers. When injected during rapid eye movement (REM) sleep, physostigmine woke the subjects, and when injected during non-REM sleep, it induced REM sleep. This result suggests that cholinergic mechanisms play a role in the induction of REM sleep and in modulating cortical arousal mechanisms.

Acetylcholine↗