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Biomedical subjects

E Seifritz

Publications and source records attributed to E Seifritz.

54 records · Page 3Linked to original sources
PubMed1996

Neuroendocrine effects of a 20-mg citalopram infusion in healthy males. A placebo-controlled evaluation of citalopram as 5-HT function probe.

Pharmacokinetic measurements, neuroendocrine responses, and side effects profiles of intravenous infusions of 20 mg citalopram over 30 minutes during the early afternoon have been studied. Eight healthy male volunteers were enrolled in a placebo- (saline) controlled, single-blind, cross-over protocol. Plasma concentrations of the parent compound showed a double exponential decay. Demethyl and didemethyl metabolites were not detectable, but low concentrations of the propionic acid derivative of citalopram were found. Determination of the citalopram enantiomers yielded a balanced S(+)/R(-) ratio of 0.9 to 1.2. The endocrine response to the drug was characterized by significant increases in plasma prolactin and cortisol. Except for one subject, who developed pronounced side effects, human growth hormone showed a surge following saline that was inhibited following citalopram. Rectal temperature and heart rate were not affected and tolerability was favorable. Because of citalopram's extremely high selectivity for the presynaptic 5-hydroxytryptamine nerve terminals, the present data suggest that it might be a promising tool for the investigation of serotonergic function in the human brain in vivo.

Citalopram↗
PubMed1995

[Sleep disorders in chronic pain and generalized tendomyopathy].

Patients with a chronic pain syndrome often suffer from sleep disturbance. As both symptoms are frequent in the fibromyalgia syndrome, these patients in particular have been examined in this regard. No clear polysomnographic evaluation of the subjectively experienced sleep disturbance in these patients has been done so far. Therefore, we recorded the sleep EEG of 13 patients with a fibromyalgia syndrome in order to objectively characterize their sleep. Furthermore, we were interested in the relationship between the sleep alterations and pain intensity. In a subsequent placebo-controlled study based on pathophysiological considerations, we attempted to beneficially influence the sleep disturbance and the pain syndrome with the 5-HT2-receptor antagonist ketanserine, as this system has been proved to play a major role in the regulation of both sleep and pain. The results of our studies in patients with fibromyalgia show that the alteration of sleep is mainly characterized by a disturbance of sleep continuity associated with the experience of pain intensity. The application of 5-HT-receptor-antagonists may be a new strategy for the common treatment of sleep disturbance and the pain syndrome which needs to be evaluated in further studies. Duration of the patients' illness seems to be a predictive value in relation to intensity of the symptoms and the therapeutic outcome.

Adult↗
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

Human plasma DSIP decreases at the initiation of sleep at different circadian times.

Nocturnal plasma delta sleep-inducing peptide-like immunoreactivity (DSIP-LI) was determined serially in seven healthy male subjects. Time courses during nocturnal sleep (2300-0800 h), nocturnal sleep deprivation (2300-0500 h), and morning recovery sleep (0500-0800 h) after sleep deprivation were compared. A significant decrease in plasma DSIP-LI was found at the transition from wakefulness to sleep in both evening sleep (2300 h) and morning recovery sleep (0500 h). Time courses were accompanied by physiological changes in sleep electroencephalographic slow-wave activity, and in plasma concentrations of cortisol and human growth hormone. No sleep stage specificity was found. It is concluded that DSIP is influenced by the initiation of sleep.

Adult↗
PubMed1995

Serial partial sleep deprivation as adjuvant treatment of depressive insomnia.

1. Sleep disturbance is a prominent symptom of major depression. Despite specific treatment with antidepressants, there is a substantial number of patients who improve in depressed mood but remain sleep disturbed. 2. Polysomnographic sleep (PSG) data and self reported sleep measures were assessed at baseline and after one week in 18 patients (35-65 years) randomly assigned to treatment with either trimipramine alone 200 mg/d (group 1) or trimipramine (200 mg/d) and additional serial partial sleep deprivation in the second half of the night (3x/week) (group 2). 3. In group 1 no marked changes between baseline and after treatment were found. 4. In group 2 the PSG data showed a significant increase of slow wave sleep and a compensatory decrease in stage 1. Sleep continuity improved in terms of numbers of awakenings, sleep onset latency and total sleep time. These changes were in parallel with the subjective estimation of sleep in group 2. 5. There was no significant difference in the Hamilton rating scale scores neither at baseline nor after treatment. 6. These observed effects on sleep following additional serial PSD therapy seem to occur independent from the antidepressive effect.

Adult↗
PubMed1995

Improving the diagnostic accuracy of the Mini-Mental State Examination.

INTRODUCTION: We determined the diagnostic accuracy of the Mini-Mental State Examination (MMSE) for dementia of the Alzheimer type (DAT) in an outpatient geriatric referral center in Switzerland. MATERIAL & METHODS: DAT patients and elderly controls were assigned to two groups: a validation sample (70 DAT patients; 50 controls) and a cross-validation sample (133 DAT patients; 43 controls). A Receiver Operating Characteristic curve was generated to derive the optimal MMSE cut-off score in the validation sample. RESULTS: The optimal MMSE cut-off was < 26/30 (sensitivity of 74%, specificity of 100%). Adjustments for age and education were necessary. The cross-validation confirmed these findings. CONCLUSION: iN A clinical setting the MMSE cut-off should be increased to < 26/30. A thorough neurobehavioral assessment is still necessary for a complete evaluation.

Age Factors↗
PubMed1994

Increased trimipramine plasma levels during fluvoxamine comedication.

A depressive patient, a non-responder to trimipramine (TRI), was comedicated first with citalopram (CIT) and then with fluvoxamine (FLUV). Both the TRI-CIT and TRI-FLUV combination treatments led to a worsening of the depressive state and to the appearance of panic attacks. The addition of FLUV to TRI resulted in a twofold increase of the plasma levels of TRI and to a slight increase of its N-demethylated and 2-hydroxylated metabolites. These results suggest that the interaction between FLUV and TRI occurred at the level of cytochrome P-450IID6 and cytochrome P-450meph in this patient, phenotyped as an extensive metabolizer of both dextromethorphan and mephenytoin. The adverse effects were possibly due to (a) a pharmacokinetic interaction between CIT and FLUV with TRI and/or (b) alterations in serotonergic and/or dopaminergic neurotransmission.

Aged↗
PubMed1994

[Cortisone-induced delusional depression in systemic lupus erythematosus].

A case of systemic lupus erythematodes (SLE) with development of a delusional depression is presented. Psychiatric symptoms in patients with SLE and in patients treated with glucocorticoids are discussed. The main psychiatric side effects of a therapy with steroids are a dose-dependent, reversible dementia like syndrome and a probably not dose-dependent provocation of psychosis. Furthermore the role of the dysregulation of the limbic-hypothalamic-pituitary-adrenocortical axis in major depression is stressed and consequences for psychopharmacological treatment are emphasized.

Adult↗
PubMedDate not supplied

Detection of BOLD changes by means of a frequency-sensitive trueFISP technique: preliminary results.

A new method is introduced to detect magnetic field modulation arising from brain activation-induced BOLD effects. This approach uses a two-dimensional high-bandwidth, high-resolution conventional gradient-echo steady-state imaging sequence known as TrueFISP. The ability to visualize changes in oxygen saturation comes from the fact that the method is sensitive to the local field. As is well known, as the oxygen saturation changes so does the local field associated with the venous blood. We demonstrate that it is possible to visualize not only venous blood with this approach on a macroscopic level for major veins, but also to measure conventional oscillatory like signal changes during activated and resting states. Unfortunately, the method has two major drawbacks. First, a long TR is needed to maximize signal changes and, second, the field must be very well shimmed or numerous experiments need to be run to find the activation, as the signal response is sensitive to the starting frequency in the resting state. Nevertheless, these images can be compared directly with anatomical images collected with the same method without the need for distortion correction.

Brain↗
PubMedDate not supplied

Hydro-MRI for the visualization of gastric wall motility using RARE magnetic resonance imaging sequences.

BACKGROUND: Although different imaging techniques such as conventional X-ray, ultrasonography, and hydro-computed tomography are available for the imaging of the stomach, none can depict this organ in full size without radiation. Therefore, the study of the entire gastric wall motility of the stomach is difficult and in principle only performable with rapid magnetic resonance imaging (MRI) techniques. T1-weighted imaging sequences have been used for the dynamic study of gastric wall motility. This technique was combined with the oral intake of para- or superparamagnetic contrast agents to achieve sufficient intraluminal contrast. The technique described in the present study is based on a different contrast mechanism. METHODS: The stomach was filled with 500 mL of 10% of aqueous dextrose solution, and a strongly T2-weighted fast rapid acquisition with relaxation enhancement (RARE) type imaging sequence was used for data acquisition. No other contrast agents were applied. An ultrafast RARE imaging sequence with an asymmetric phase-encoding scheme was developed to achieve a high temporal and spatial resolution. The scanning time per image was approximately 1 s. RESULTS: The stomach was imaged in full size. The concentric constrictor rings moved from the proximal part of the body toward the antrum. The mean duration for one contraction cycle was approximately 17.9 +/- 2.5 s, the mean contractile frequency was 3.4 +/- 0.5 s, and the mean spreading velocity was 65.5 +/- 3.6 cm/min. CONCLUSIONS: The purpose of this study was to demonstrate a new technical approach for a noninvasive dynamic study of gastric motor function with hydro-MRI. This robust method may have clinical application, e.g., in the diagnosis of gastroparesis, and may be extended to the rest of the gastrointestinal tract.

Administration, Oral↗
PubMedDate not supplied

Sleep deprivation and bright light as potential augmenters of antidepressant drug treatment--neurobiological and psychometric assessment of course.

The present study was designed to investigate the clinical efficacy of trimipramine with adjunct sleep deprivation (SD) or bright light (BL) and to evaluate psychometric and neurobiological variables that might be of predictive value for treatment response. We used (1) the combined dexamethasone-corticotropin releasing hormone test (DEX-CRH test) to characterize alterations of the hypothalamic-pituitary-adrenal (HPA) system; (2) polysomnography to evaluate sleep disturbances; and (3) a standardized test battery to assess cognitive psychomotor functions after study initiation and after 5 weeks of treatment. The overall response rate (> or = 50% decrease in score on Hamilton Rating Scale for Depression [HRS]) was 55% (N = 42). The response rate in the group with trimipramine monotherapy (N = 14) was 79%, whereas in the groups with adjunct SD (N = 14) and BL (N = 14), respectively, it was only 43%. All three groups showed significant improvement at the end of the third week of treatment. Neither of the adjunct treatments hastened the onset of antidepressant action as measured by HRS. A significantly higher proportion of nonresponders than responders (p < .05) had HPA dysregulation, disturbed rapid eye movement (REM) sleep (REM latency, REM% first third of night) and decreased non-REM sleep (% stage 2). The non-responders showed significantly more corticotropin (ACTH) secretion after CRH stimulation in the DEX-CRH test than the responders and a less rapid normalization of the neuroendocrine dysregulation (cortisol secretion) (p < .01). In addition, REM latency was significantly shorter in the BL group than in the monotherapy group and estimated duration of illness significantly longer in the SD group than in the monotherapy group. REM latency, percentage of REM sleep during the first third of the total sleep period, percentage of non-REM sleep stage 2 and ACTH release after a DEX-CRH challenge predicted response across all three treatment groups. The neurobiological symptoms were unevenly distributed, among the three groups, thus creating heterogeneity in these measures. This heterogeneity may have contributed to the different treatment response rates as defined by psychopathology (HRS). In contrast, the neuropsychological tests and some of the sleep-EEG investigations revealed different response patterns for different groups: The onset of improvement in simple cognitive functions and in sleep continuity was earlier in the adjunct treatment groups. This study underlines the need for a multidimensional approach including use of neurobiological and neuropsychological measures to identify the therapeutic profiles of different treatment strategies and predictors of outcome.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Differential mood response to natural and synthetic corticosteroids after bilateral adrenalectomy: a case report.

A 48-year-old woman who had had a bilateral adrenalectomy for Cushing's syndrome developed severe psychotic symptoms that were unresponsive to psychotropic drugs as long as she was taking prednisone (PRED) as replacement therapy. However, after she was switched to a regimen of cortisol (CORT) and fludrocortone (FLUD) the psychopathology disappeared. Mechanisms related to the differences in the interaction of natural (e.g. CORT) and synthetic (e.g. PRED) corticosteroids with the central glucocorticoid and mineralocorticoid receptors may explain the different effects upon psychopathology.

Adrenalectomy↗
PubMedDate not supplied

Hypothalamic-pituitary-adrenal system function in patients with Alzheimer's disease.

The neuropathologic hallmarks of Alzheimer's disease (AD) are very prominent in the hippocampus, a brain site which is pivotal for the regulation of the hypothalamic-pituitary-adrenal (HPA) system. Thus, the combined dexamethasone-suppression/CRH-stimulation-test outcome in patients with AD was compared to that of healthy elderly controls to assess--with a more refined neuroendocrine challenge procedure--HPA function in AD. Cortisol secretion after dexamethasone (DEX) pretreatment and before CRH was increased in Alzheimer's patients and 21% of this group were DST-nonsuppressors. None of the healthy control subjects escaped DEX-induced suppression of cortisol. However, after additional CRH administration, AD patients released significantly less cortisol and ACTH than the control subjects. No correlations were found between any of the endocrine parameters and degree of severity of dementia. It is concluded that the DST part of the DEX/CRH test better reflects glucocorticoid feedback disturbances, probably at a suprapituitary level. The CRH part of the DEX/CRH-test outcome might indicate the loss of endogenous CRH-Arginine-Vasopressin (AVP) synergism of the HPA system of these patients.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Effect of sleep deprivation on neuroendocrine response to a serotonergic probe in healthy male subjects.

Neuroendocrine responses to stimulation with a selective serotonin reuptake inhibitor (citalopram) were measured to investigate the effects of all-night sleep deprivation on serotonergic function in healthy male subjects (n = 7). We studied citalopram-stimulated prolactin and cortisol plasma concentrations in a placebo-controlled cross-over protocol following sleep and sleep deprivation. Citalopram infusion (20 mg i.v. at 14:20-14:50 h) after a night of undisturbed sleep prompted robust increases in both plasma prolactin and cortisol concentrations. Following a night of sleep deprivation, by contrast, the citalopram-induced prolactin response was blunted, but the cortisol response was not significantly altered. This differential response pattern relates to the distinct pathways through which serotonin may activate the corticotrophic and the lactotrophic systems. While an unchanged cortisol response does not indicate (but also does not refute the possibility of) an altered serotonergic responsivity following sleep deprivation, the suppressed prolactin response could reflect a downregulation of 5-HT1A or 2 receptors. An alternative, not mutually exclusive, explanation points to the possibility that sleep deprivation activates the tubuloinfundibular dopaminergic system, the final inhibitory pathway of prolactin regulation.

Adult↗