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Biomedical subjects

C J Lauer

Publications and source records attributed to C J Lauer.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effects of flumazenil on recovery sleep and hormonal secretion after sleep deprivation in male controls.

The effects of flumazenil, a benzodiazepine antagonist, on the sleep electroencephalogram (EEG) and neuroendocrine secretion in early morning recovery sleep (0500-0800 hours) following sleep deprivation (SD; 2300-0500 hours) were studied in seven healthy men. SD induced an increase in slow wave sleep (SWS), a decrease in sleep onset latency (SOL), an enhancement of EEG delta and theta power in non-rapid-eye-movement sleep, an increase in plasma human growth hormone (GH) concentration, and a decrease in plasma cortisol levels in recovery sleep (0500-0800 hours). Plasma GH, but neither plasma cortisol nor adrenocorticotrophic hormone (ACTH) concentration was attenuated during SD as compared to sleep (2300-0445 hours). The administration of flumazenil (3 x 1 mg intravenously) during recovery sleep resulted in an inhibition in SWS, an increase in stage 2 sleep, a selective reduction in delta and theta power, and a tendency to prolongation of SOL. Plasma GH concentration was decreased but plasma cortisol and ACTH remained unaffected. Since the SD-induced changes in sleep EEG and plasma GH secretion were antagonized by flumazenil, it is suggested that electrophysiological and hormonal effects of SD are mediated at least in part through GABAergic mechanisms.

Adrenocorticotropic Hormone↗
PubMed1995

gamma-Glutamylglutamine and taurine concentrations are decreased in the cerebrospinal fluid of drug-naive patients with schizophrenic disorders.

HPLC and gas chromatography-mass spectrometry analyses of 18 amino acids, N-acetylaspartate, N-acetylaspartylglutamate, and 5-hydroxyindoleacetic acid, derived from serotonin, and homovanillic acid, derived from dopamine, were performed in CSF collected from a group of patients with schizophrenia who either had been drug free for at least 1 year (n = 5) or were drug naive for psychotropic drugs (n = 21) and in 15 control subjects. Significant differences were found only for taurine (15% lower in the patients) and isoleucine (7% higher). A number of unidentified substances were detected, one of which proved to be markedly reduced (16%) among the schizophrenic patients. Liquid chromatography-mass spectrometry with continuous flow-fast atom bombardment interface allowed us to identify this substance as gamma-glutamylglutamine. The decreased level of gamma-glutamylglutamine may reflect a deficiency in the gamma-glutamyltransferase system, a system probably involved in glutamate uptake, or a deficiency in glutamine, an important precursor of releasable glutamate. Although glutamate was nonsignificantly reduced in the patients, it was one of the five substances (including gamma-glutamylglutamine) that were necessary for the best discrimination between the schizophrenic patients and the controls. These findings support the notion that the glutamatergic system is affected in schizophrenic disorders. In addition, they underscore the need to apply rigid bioanalytical techniques and use drug-naive patients to gain in-depth information on the pathophysiology of brain disorders such as schizophrenia.

Adult↗
PubMed1995

Cortisol, ACTH, and cardiovascular response to a cognitive challenge paradigm in aging and depression.

Aging and hypercortisolism may be associated with alterations of stress-induced hormone release. We therefore studied 20 normal controls of two different age groups (< 30 and > 60 yr of age) and 20 age-matched patients with major depression; baseline ACTH and cortisol secretion (between 1400 and 1700) as well as blood pressure and heart rate and their responses to a 45-min lasting signal detection task (1705-1750) were determined. No difference in basal hypothalamic-pituitary-adrenal (HPA) system activity between young and older healthy controls was noted. The cognitive challenge resulted in an increase in stress-induced hormonal secretion that was greater in the older controls than in their young counterparts. Basal hypercortisolemia and, at baseline, heart rates were higher in depressed patients, regardless of age. Blood pressure was elevated in older healthy controls as well as depressed patients. With the exception of the young depressed patients, all groups responded with an increase of the cardiovascular parameters during stress.

Adrenocorticotropic Hormone↗
PubMed1995

Altered hypothalamic-pituitary-adrenocortical regulation in healthy subjects at high familial risk for affective disorders.

Altered negative feedback control of the hypothalamic-pituitary-adrenocortical (HPA) system is a frequent laboratory sign of major depression. It coincides with depressive episodes and partially reverses after recovery from psychopathology. Such an HPA disturbance in feedback control can be acquired as a result of stressful life experiences and be compounded by age or it can be genetically predetermined at all levels involved in fine-tuned neuroendocrine regulation. Major psychiatric disorders run in families and a high familial load for an affective illness therefore increases an individual's risk of becoming affected. We investigated whether the HPA feedback disturbance observed among patients with depression is present in otherwise healthy individuals who are at high risk for psychiatric disorders because they have a first-degree relative with an affective illness. Using rigid psychodiagnostic techniques, we screened 431 consecutively admitted patients with depression and identified 35 families with one or more high-risk probands (HRPs). The results of a combined dexamethasone/human corticotropin-releasing hormone (DEX-CRH) test showed that the group of dexamethasone-pretreated (1.5 mg; 23.00 h) HRPs released more cortisol after stimulation with human CRH (100 micrograms; 15.00 h the next day) than a control group (CPs), but less than a group of patients with an acute major depressive episode (DPs). The peak cortisol values were 146.1 +/- 147.7 nmol/l (mean +/- SD) (HRPs), 75.3 +/- 47.9 nmol/l (CPs) and 278.2 +/- 199.2 nmol/l (DPs), yielding significant (F = 9.66, p < 0.001) group differences, with values for HRPs vs. CPs and HRPs vs. DPs being significant at the 1% level (t test).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Flumazenil exerts intrinsic activity on sleep EEG and nocturnal hormone secretion in normal controls.

The physiological function of benzodiazepine (BDZ) receptors includes regulation of sleep and neuroendocrine activity. Most of the pharmacological effects of BDZ are blocked by flumazenil. However, recent neurological and behavioral studies suggest that flumazenil has its own central intrinsic activity. This issue was addressed in a study of the sleep EEG and the nocturnal secretion of growth hormone and cortisol in ten normal male controls, who were given flumazenil either alone or in combination with the BDZ agonist midazolam, placebo and midazolam alone. Flumazenil prompted an increase in sleep onset latency, a decrease in slow wave sleep and an increase in wakefulness. Plasma cortisol concentrations after flumazenil administration were lower than after midazolam. Both flumazenil and midazolam decreased nocturnal growth hormone secretion. After simultaneous application of both BDZ receptor ligands the growth hormone blunting was amplified. Our study demonstrates that at the level of the sleep EEG and neuroendocrine activity flumazenil is capable of exerting both agonistic and inverse agonistic or antagonistic effects.

Adult↗
PubMed1994

Effects of 5HT3 receptor antagonism by tropisetron on the sleep EEG and on nocturnal hormone secretion.

Two dosages (5 mg and 25 mg) of the selective 5HT3 receptor antagonist tropisetron (ICS 205-930) were administered to healthy male controls, and the effects on the sleep EEG and nocturnal secretory activity of growth hormone (GH) and cortisol were evaluated. The lower dosage was administered to four subjects and the higher dosage to eight on 5 consecutive days, preceded and followed by 2 days of placebo treatment. After 25 mg of tropisetron, there was a slight increase in REM sleep in the first part of the sleep period, and stage 2 was decreased during the total night. In addition, plasma cortisol levels increased earlier than under placebo, and plasma GH levels were reduced in the second part of the night. Thus, only discrete effects of tropisetron upon sleep-endocrine activity were noted, making it unlikely that serotoninergic neurotransmission exerts its well-documented effects upon sleep through 5HT3 receptors.

Adult↗
PubMed1993

Effect of morning and afternoon naps on mood after total sleep deprivation in patients with major depression.

In 30 depressed patients who had responded to total sleep deprivation therapy, morning naps led more frequently to relapses into depression than did afternoon naps. Longer naps were less detrimental than shorter ones, and there was no significant relationship between the effect of a nap on mood and its content of slow-wave-sleep. The amount of the rapid eye-movement sleep, too, was unrelated to clinical nap effects. Thus, some of the current theories on the relationship between sleep and depressive symptomatology are not supported by the data. Our results demonstrate the importance of nap timing, suggesting a circadian variation of propensity to relapse into depression.

Adult↗
PubMed1993

Naps after total sleep deprivation in depressed patients: are they depressiogenic?

Total sleep deprivation (TSD) exerts beneficial but transient effects on mood in approximately 60% of patients with a major depressive disorder. The positive effects of a night of total sleep deprivation are generally reversed after the next night of sleep. Several anecdotal reports and a pilot study by our group indicated that even short naps during the period of sleep deprivation are capable of re-inducing depressive mood in responders to TSD. The present study explored whether the structure of naps at 9 a.m. was crucial for the "depressiogenic" impact of naps on mood. A negative effect on mood was replicated, but this effect was not related to any of the nap sleep variables. The effect of naps on mood was attenuated in the early afternoon. The results support the assumption of a "depressiogenic" effect of naps in patients with major depression after successful TSD.

Depressive Disorder↗
PubMed1992

Cholinergic REM sleep induction test in subjects at high risk for psychiatric disorders.

The influence of the cholinergic agonist RS 86 on electroencephalographic (EEG) sleep was investigated in 21 healthy members of families identified as being at high risk for psychiatric disorders and in 17 healthy control subjects without any personal or family history of a psychiatric illness. In comparison to the placebo night, the administration of RS 86 led to a shortening of rapid eye movement (REM) latency in both groups. This effect, however, was much more pronounced in the high-risk group, whereas in the control subjects the arousal system and the slow-wave sleep during the first nonREM period were more affected. These observations suggest that the cholinergic action on sleep regulating mechanisms has differing preferential targets in high-risk probands and in control subjects.

Adult↗
PubMed1992

All-night electroencephalographic sleep and cranial computed tomography in depression. A study of unipolar and bipolar patients.

All-night electroencephalographic (EEG) sleep recording and cranial computed tomography were performed in 24 inpatients with major depression (14 unipolar, 10 bipolar). The patients showed the characteristic "depression-like" EEG sleep alterations and their ventricular brain ratio (VBR) was increased compared with the control subjects. No major differences were found between the unipolar and the bipolar groups. There was a close and positive association between the VBR values and several measures of slow wave sleep. It is hypothesized that this relationship is due to an altered function of the limbic-hypothalamic-pituitary-adrenocortical axis in depression that affects both EEG sleep and brain morphology.

Adult↗
PubMed1992

Panic disorder and major depression: a comparative electroencephalographic sleep study.

Family studies suggest some common etiological factors in panic disorder and depression. The observation of characteristic depression-like polysomnographic alterations in panic disorder patients would further underline the assumed biological interface between the two psychiatric disorders. In a polysomnographic study of 22 inpatients with panic disorder, 12 inpatients with major depression, and 12 control subjects, we found that both groups of patients had one major feature of depression-like sleep: a shortened rapid eye movement (REM) latency. However, the patterns of the first hours of polysomnography showed more differences than similarities between these psychiatric disorders, indicating that the shortened REM latency apparently is merely a common final pathway of different alterations in sleep regulation. Our findings, therefore, provide more evidence against than for a significant biological interface between panic disorder and depression.

Adolescent↗
PubMed1992

Brofaromine in panic disorder: a pilot study with a new reversible inhibitor of monoamine oxidase-A.

The therapeutic efficacy of brofaromine--a new reversible and short acting MAO-A inhibitor--was evaluated in 14 inpatients with a panic disorder. In an open trial, the patients were treated with placebo during the first week and with 150 mg brofaromine per day during the following four weeks. In all patients a distinct improvement in both anxiety and depressive symptoms was observed under the active drug. Treatment outcome was the same in patients with and without a concomitant major depressive episode. No side-effects of any note were reported. Our findings suggest that the MAO-A inhibitor brofaromine is an effective drug in the treatment of anxiety disorders.

Adult↗
PubMed1992

On the issue of drug washout prior to polysomnographic studies in depressed patients.

In psychoneurobiological studies it is a point of controversy how long psychoactive medication has to be withdrawn to exclude drug effects on the variables to be investigated. In order to answer the question of whether the generally assumed two-week washout of psychoactive medication is sufficient for polysomnographic studies, we computed a post hoc analysis of EEG sleep recordings in 61 newly admitted depressed patients. The results indicate that after a 2-week withdrawal of tricyclic antidepressants and/or benzodiazepines there are no major drug effects on visually scored polysomnograms. In addition, the observations raise the question of whether even a 1-week drug washout may be sufficient to exclude confounding effects of prior psychoactive medication on EEG sleep.

Adolescent↗
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

Nocturnal sleep in Huntington's disease.

Nocturnal sleep was studied in 16 inpatients with Huntington's disease. In comparison with healthy controls, patients exhibited a disturbed sleep pattern with increased sleep onset latency, reduced sleep efficiency, frequent nocturnal awakenings, more time spent awake and less slow wave sleep. These abnormalities correlated in part with duration of illness, severity of clinical symptoms, and degree of atrophy of the caudate nucleus. Patients showed an increased density of sleep spindles.

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↗