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Biomedical subjects

D Riemann

Publications and source records attributed to D Riemann.

At least 145 records · Page 8Linked to original sources
PubMed1992

The effects of biperiden on nap sleep after sleep deprivation in depressed patients.

Sixteen patients with a major depressive disorder were allowed to take a nap at 5 A.M. after a period of total sleep deprivation. The patients were randomly assigned to biperiden or placebo treatment prior to the nap to test the hypothesis that anticholinergic medication is capable of preventing a nap-related worsening of mood. Total sleep deprivation positively influenced mood for the whole group. Contrary to expectations, the rate of nap-related relapses of mood did not differ between placebo- and biperiden-treated individuals, and biperiden did not significantly suppress rapid eye movement (REM) sleep. There was only a tendency for lower REM time after administration of biperiden compared to placebo. This unexpected result may be due to a high cholinergic tone in the patient group investigated and a high REM propensity in the early morning hours. Studies with more selective M1/M2 receptor antagonists are necessary to clarify whether nap-related changes of mood can be prevented by anticholinergic blockade.

Affect↗
PubMed1991

From early to late adulthood. Changes in EEG sleep of depressed patients and healthy volunteers.

In order to evaluate the impact of aging on EEG sleep patterns we investigated the polysomnograms of 74 patients with major depression and 51 healthy volunteers aged 18-65 years. In most of the EEG sleep parameters, age-related changes were obvious in both the depressives and the normals. In the patients, some of these alterations occurred earlier and were more pronounced. The amount of slow-wave sleep decreased with age, but no differences were found between the depressives and the healthy volunteers at any particular age. Rapid-eye-movement (REM) latency was clearly affected by age, but there were no significant differences between patients and controls until the middle of the fourth decade of life. On the other hand, REM density measures did not vary with age and were increased in the depressives. Therefore, REM density appears to be a more likely candidate for a biologic marker for major depression than is REM latency.

Adolescent↗
PubMed1991

The cholinergic REM induction test with RS 86 after scopolamine pretreatment in healthy subjects.

A shortened latency of rapid eye movement (REM) sleep is one of the most stable biological abnormalities described in depressive patients. According to the reciprocal interaction model of non-REM and REM sleep regulation, REM sleep disinhibition at the beginning of the night in depression is a consequence of heightened central nervous system cholinergic transmitter activity in relation to aminergic transmitter activity. A recent study has indicated that muscarinic supersensitivity, rather than quantitatively enhanced cholinergic activity, may be the primary cause of REM sleep abnormalities in depression. The present study tested this hypothesis by treating healthy volunteers for 3 days with a cholinergic antagonist (scopolamine) in the morning, in an effort to induce muscarinic receptor supersensitivity. On the last day of scopolamine administration, RS 86, an orally active cholinergic agonist, was administered before bedtime to test whether this procedure would induce sleep onset REM periods. Whereas scopolamine treatment tended to advance REM sleep and to heighten REM density in healthy controls in comparison to NaCl administration, the additional cholinergic stimulation did not provoke further REM sleep disinhibition. This result underlines the need to take a hypofunction of aminergic transmitter systems into account in attempts to explain the pronounced advance of REM sleep typically seen in depressives.

Adult↗
PubMed1991

Cholinergic drugs as diagnostic and therapeutic tools in affective disorders.

The hypothesis of a significant involvement of the cholinergic system in the pathogenesis of affective disorders still lacks strong experimental support. This is mainly because of missing specific peripheral markers of the central nervous activity of the cholinergic system and the lack of specific cholinergic agonists and antagonists without severe peripheral side effects. As the direct cholinergic agonist RS 86 seems to be more suitable because of its minor side effects, long half-life and oral applicability, it was tested for its antimanic property and its effect on the hypothalamo-pituitary adrenal system and the rapid eye movement (REM) sleep-generating system. RS 86 exhibited antimanic and REM sleep-inducing properties, but failed to stimulate the cortisol system.

Adult↗
PubMed1990

Neuroendocrinological investigations during sleep deprivation in depression. II. Longitudinal measurement of thyrotropin, TH, cortisol, prolactin, GH, and LH during sleep and sleep deprivation.

Thyrotropin (TSH), thyroxin (T4), triiodothyronine (T3), free T3 (fT3), cortisol, prolactin, and human growth hormone (HGH) were measured every 2 hr during a night of sleep, the following day, and a night of sleep deprivation (SD) in 14 patients with major depressive disorder. In subgroups fT4 (n = 5), reverse T3 (rT3), and luteinizing hormone (LH) (n = 6) were also investigated. Significant increases in TSH, T4, fT4, T3, fT3, rT3, and cortisol and decreases in prolactin levels occurred during the night of SD, compared to the pattern during the night of sleep. The pre-SD T4 and T3 levels of the responders to SD were already higher than in the nonresponders, and increased less during SD. The cortisol and HGH concentrations of the responders rose higher during SD than those of the nonresponders. Changes in TSH and prolactin were not correlated to clinical response. Analysis of possible neurochemical mechanisms underlying this "pattern" of changes in different endocrine profiles suggests that enhanced noradrenergic activity might play a role in the changes in TSH, cortisol, thyroid hormones, and possibly HGH secretion during SD, and increased dopaminergic tone probably induced the decline in prolactin levels. Additional effects of the serotonergic system cannot be excluded at present. In conclusion, the data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD. This mechanism could well be involved in the antidepressant effect of this therapy.

Adult↗
PubMed1990

A polysomnographic study in young psychiatric inpatients: major depression, anorexia nervosa, bulimia nervosa.

The baseline EEG sleep patterns of 10 young depressed patients, 20 patients with anorexia nervosa, 10 patients with bulimia nervosa, and 10 healthy subjects were found to be indistinguishable, except for an increased REM density in the depressed patients. In eating disorder patients, a concomitant major depressive episode had no influence on EEG sleep. The results of the cholinergic REM sleep induction test revealed a significantly faster induction of REM sleep in the depressed patients when compared with the eating disorder patients and the control subjects. This indicates a subthreshold hypersensitivity of the REM sleep triggering cholinergic transmitter system in depressives, but not in eating disorder patients.

Adolescent↗
PubMed1990

REM-suppressing effects of amitriptyline and amitriptyline-N-oxide after acute medication in healthy volunteers: results of two uncontrolled pilot trials.

Almost all tricyclic and tetracyclic antidepressants as well as the MAO (monoamineoxidase) inhibitors suppress REM sleep significantly and sustainedly. This does not seem to be an epiphenomenon of antidepressant pharmacotherapy, since initial REM sleep suppression during pharmacological treatment correlated positively with antidepressant effect after three weeks. Furthermore, selective REM-sleep deprivation (by waking patients) had a marked antidepressive effect in depressed patients. The present study used rapid eye movement (REM) sleep suppression in healthy volunteers as a marker to compare the central nervous effects of 150 mg amitriptylineoxide (AMINO) with those of 75 mg amitriptyline (AMI). Both compounds exerted comparable sleep-inducing effects; suppression of REM sleep tended to be more pronounced after application of AMI, despite the higher dose of AMINO used. While this result is evidence of the immediate central nervous effects of a single dose of AMINO, they seem less marked than those of AMI.

Adult↗
PubMed1990

The effects of total sleep deprivation and subsequent treatment with clomipramine on depressive symptoms and sleep electroencephalography in patients with a major depressive disorder.

In the present study patients with a major depressive disorder were first subjected to total sleep deprivation (TSD) and then treated with clomipramine. Sleep electroencephalography (EEG) was registered prior to and after TSD, during the 2 initial nights of antidepressive treatment and after 19 days. A negative correlation between response to TSD and clomipramine was found. TSD did not differentially influence the sleep EEG (responders vs nonresponders): responders tended, however, to show a more classical depressive sleep pattern prior to TSD. Clomipramine profoundly suppressed rapid eye movement (REM) sleep; the amount of initial REM sleep reduction, however, did not correlate significantly with therapy response after 3 weeks of treatment.

Adolescent↗
PubMed1990

Ion channels in human endothelial cells.

Ion channels were studied in human endothelial cells from umbilical cord by the patch clamp technique in the cell attached mode. Four different types of ion channels were recorded: i) potassium channel current that rectifies at positive potentials in symmetrical potassium solutions (inward rectifier); ii) low-conductance non-selective cation channel with a permeability ratio K:Na:Ca = 1:0.9:0.2; iii) high-conductance cation-selective channel that is about 100 times more permeable for calcium than for sodium or potassium; iv) high-conductance potassium channel with a permeability ratio K:Na = 1:0.05. The extrapolated reversal potential of the inwardly rectifying current was near to the potassium equilibrium potential. The slope conductance decreased from 27 pS in isotonic KCl solution to 7 pS with 5.4 mmol/l KCl and 140 mmol/l NaCl in the pipette but 140 mmol/l KCl in the bath. The low-conductance non-selective cation channel showed a single-channel conductance of 26 pS with 140 mmol/l Na outside, 28 pS with 140 mmol/l K outside, and rectified in inward direction in the presence of Ca (60 mmol/l Ca, 70 mmol/l Na, 2.7 mmol/l K in the pipette) at negative potentials. The current could be observed with either chloride or aspartate as anion. The high-conductance non-selective channel did not discriminate between Na and K. The single-channel conductance was about 50 pS. The extrapolated reversal potential was more positive than +40 mV (140 K or 140 Na with 5 Ca outside). Both the 26 and 50 pS channel showed a run-down, and they rapidly disappeared in excised patches. The high-conductance potassium channel with a single-channel conductance of 170 pS was observed only rarely. It reversed near the expected potassium equilibrium potential. The 26 pS channel could be stimulated with histamine and thrombin from outside in the cell-attached mode. Both the 26 pS as well as the 50 pS channel can mediate calcium flux into the endothelial cell.

Cells, Cultured↗
PubMed1990

Prospective study of concurrent ploidy analysis and routine cytopathology in body cavity fluids.

A total of 390 body cavity fluids were analyzed by both cytopathologic examination and flow cytometric DNA analysis. The two methods gave compatible results in analyses of 304 fluids (78%). In 24 patients, cytopathologic studies found the specimens to contain malignant cells, but the DNA content was diploid. This illustrates an area where flow cytometric studies do not extend tumor detection. In 56 fluids from 48 patients, cytologic methods revealed no malignant cells but flow cytometry distinguished aneuploid cell populations; additional clinical information allowed the identification of malignant tumors in 24 (50%) of these patients. Because flow cytometry was able to detect aneuploidy in cases where conventional cytologic examination could not detect malignant cells, the number of patients with tumors detected was increased by 39% beyond those detected by cytologic methods alone in this series.

Aneuploidy↗
PubMed1990

[Restless legs and sleep apnea syndrome--random coincidence or causal relation?].

We report three cases of restless-legs syndrome in which by polygraphic sleep recordings an accompanying sleep-apnea syndrome was detected. Etiopathological factors, in particular a dysfunction of the sleep regulating centers in the brain stem as a cause of both diseases are discussed. Our observations suggest that a polysomnographic recording including respiration parameters should be carried out in every patient suffering from restless-legs syndrome.

Arousal↗
PubMed1990

Investigations of morning and laboratory dream recall and content in depressive patients during baseline conditions and under antidepressive treatment with trimipramine.

REM sleep abnormalities like shortened REM (rapid eye movement) latency, prolongation of the first REM period and heightening of REM density often found in patients with a major depression have prompted an increasing number of studies investigating the neurobiology and neurophysiology of REM sleep in depressive patients, as well as in healthy humans and animals. On the other hand, since the early 1970s investigation of the psychological concomitant of REM sleep, i.e., dreaming, in depressive patients has been extremely sparse. The present study aimed at investigating morning and laboratory dream recall and content in patients with a major depressive disorder to shed more light on this neglected area. In short, morning as well as laboratory dream recall in depressive inpatients was drastically reduced. The low number of scorable dream reports collected did not reveal a heightened incidence of "masochistic" or "negative" content, indeed were rather mundane. In contrast, depressive outpatients (probably less depressed) had a higher rate of morning dream recall. Interestingly, antidepressive treatment with trimipramine (an antidepressant which does not suppress REM sleep) led to a positive influence on patients' mood that was paralleled by a change of dream mood in a positive direction.

Adult↗
PubMed1990

[Dream interpretation and experimental dream research: a comparison].

Since the discovery of REM sleep, many experimental studies have focused on dream recall, dream function and dream analysis in the sleep laboratory. The present article gives an overview of the results of experimental dream research and tries to evaluate the relevance of these results for psychoanalytical dream theory. Two theories originating from psychophysiological dream research are discussed in detail and compared with formulations stemming from psychoanalytical oriented dream theory.

Cerebral Cortex↗
PubMed1989

The cholinergic rapid eye movement sleep induction test with RS-86. State or trait marker of depression?

Rapid eye movement (REM) sleep disinhibition at the beginning of the night is one of the most frequently described biologic abnormalities in depression. As REM sleep in animals and humans seems to be facilitated by cholinergic neuronal activity, it has been postulated that REM sleep disinhibition in depression is a consequence of cholinergic neuronal overactivity. The current study with the newly available cholinergic agonist RS-86, which is orally active, has a half-life of six to eight hours, and exhibits only minor peripheral side effects, supports this assumption. The application of this compound before sleep led to a significantly faster induction of REM sleep at the beginning of the night in patients with major depressive disorders compared with healthy subjects and patients with other nondepressive psychiatric diseases, such as eating disorders. Whereas 14 of 16 depressed patients displayed sleep-onset REM periods after the administration of RS-86, this happened only in three of the 16 healthy controls and in one of the 20 patients with other diagnoses. The increased susceptibility of REM sleep to cholinergic stimulation was limited to the state of depression and was not observed in a group of remitted depressed patients.

Adolescent↗