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Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 235 records · Page 13Linked to original sources
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

Childhood obsessive-compulsive disorder.

The authors collected clinical diagnostic, neurophysiological, electrophysiological, and biochemical data on 9 adolescents who had primary obsessive-compulsive disorder. The results indicate considerable descriptive validity of the syndrome in childhood and its independence from obsessional traits; however, all of the children had a history of major depressive disorder, and their sleep EEG measures resembled those of young adults with primary depressive disorder. The patients' families did not have a more consistent pattern of anxiety disorder or any other psychiatric disorder than do families of adult obsessive patients. Psycholinguistic test results showed a lack of normal laterality, which has been reported for other psychiatric illness.

Adolescent↗
PubMed1981

Wheat gluten challenge in schizophrenic patients.

Eight chronic schizophrenic patients were maintained on a diet free of gluten, cereal grains, and milk (CM-F diet) and challenged in a double-blind manner with dietary wheat gluten and placebo. While on the CM-F diet, each patient received a daily challenge of 30 g of gluten for 5 weeks and a placebo challenge for 8 weeks. No deterioration in clinical status as measured by the BPRS was noted on gluten challenge. Serum alpha 1 acid glycoprotein measurement demonstrated no evidence of inflammatory response to gluten challenge. The data suggest that sensitivity to dietary gluten is not characteristic of young chronic schizophrenic patients.

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

Changes of hippocampal Met-enkephalin content after recurrent motor seizures.

Kainic acid (KA), a powerful neurotoxic analogue of glutamate, has been extensively used as a tool for selectively lesioning neuronal cell bodies; however, axons or nerve terminals are spared from damage in the area injected with kainic acid. Injections of this neurotoxin in various brain regions were successfully used to locate cell bodies of neurones containing substance P, enkephalin and other putative neurotransmitters. While attempting to locate the cell bodies of the enkephalin containing neurones present in hippocampus using KA injections, we found that a few days after intracerebral injections of KA a drastic increase in the Met-enkephalin (ME) content of hippocampus occurs. We now describe the delayed increase in hippocampal ME content elicited by intracerebral KA injections and examine the possible mechanism that is operative in causing this increase. Moreover, we provide some evidence suggesting that the increase in ME content elicited by intracerebral injections of KA may be related to the recurrent motor seizures elicited by intracerebral injections of KA.

Animals↗
PubMed1980

Faster cholinergic REM sleep induction in euthymic patients with primary affective illness.

Arecoline, a cholinergic muscarinic receptor agonist, induced rapid eye movement sleep significantly more rapidly in patients with primary affective illness in remission than in normal control subjects matched for age and sex. These results, and others, suggest that patients with primary affective illness may have a supersensitive cholinergic system both when they are ill and when their symptoms are in clinical remission.

Adult↗
PubMed1980

Childhood enuresis. I. Sleep patterns and psychopathology.

Forty severely enuretic boys (mean age, 10.8 years) were selected; 20 had associated psychiatric disturbance and 20 had enuresis as an isolated symptom. Psychiatrically disturbed enuretics had both slightly higher scores on a neurological examination for "soft signs" and more "stressful" background events. Enuretic events were not associated with a particular sleep stage; disturbed and nondisturbed enuretics did not differ from each other with respect to the distribution of enuretic events by sleep stage. The results do not support the concepts of enuresis as an arousal disorder or of there being different sleep profiles of enuresis in relation to behavioral pathology.

Adolescent↗
PubMed1980

Childhood enuresis. II. Psychopathology, tricyclic concentration in plasma, and antienuretic effect.

The efficacy of treatment with imipramine hydrochloride, desipramine hydrochloride, methscopolamine bromide, and placebo was compared in a study with 40 severely enuretic boys. Both tricyclic antidepressants were superior to placebo and methscopolamine, but they did not differ from each other. Psychiatric disturbance, sleep measures, and other clinical parameters did not predict antienuretic response to tricyclics nor was there a psychotropic response. Plasma concentrations of imipramine and desipramine showed a significant correlation with clinical effect. However, true nonresponders were found, and tolerance to the antienuretic drugs developed in some boys.

Child↗
PubMed1980

Production of convulsions in mice by the combination of methionine and homocysteine.

Behavioral effects of methionine have been attributed to either increased availability of methyl groups for the production of methylated amines or accumulation of convulsive metabolites. If the second hypothesis is correct, methionine would be expected to have convulsive properties either by itself or in combination with subconvulsive dosages of other known convulsants. Methionine alone did not induce convulsions when administered by various routes in dosages of 250--13,000 mg/kg, although larger doses of methionine (500--4,000 mg/kg) decreased behavioral activity. However, methionine pretreatment (125--1,000 mg/kg) markedly enhanced convulsions in animals challenaed with subconvulsine dosages of homocysteine. Pentylenetetrazol was less effective than homocysteine in promoting convulsions in methionine-pretreated animals. Although the convulsive effects of methionine were not shared by other natural amino acids (glutamate, asparate, cysteine, tryptophan, and others), ethionine enhanced homocysteine-induced convulsions almost as effectively as did methionine. Methionine thus promotes convulsions under certain conditions, plerhaps due to an accumulation of homocysteine or of other metabolites with convulsive properties.U

Animals↗
PubMed1980

Anomalous behavioral response to imidazoleacetic acid, a GABA agonist, in animals treated chronically with haloperidol.

Short-term haloperidol treatment decreases the stimulant effects of drugs with dopaminelike actions, while withdrawal from long-term haloperidol treatment enhances the effects of such drugs. In the present study, we have shown that withdrawal from long-term haloperidol treatment decreases or eliminates the tendency for imidazole-4-acetic acid, a GABA agonist, to decrease the locomotor activity of mice. Acute haloperidol treatment did not duplicate these effects. It is suggested that chronic administration of haloperidol causes changes in a variety of systems in the brain, and that the GABA system in particular is profoundly altered by such treatment.

Animals↗