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Biomedical subjects

J C Krieg

Publications and source records attributed to J C Krieg.

At least 109 records · Page 6Linked to original sources
PubMed1987

Enlargement of cerebrospinal fluid spaces in long-term benzodiazepine abusers.

In 17 benzodiazepine (BDZ) dependent in-patients a CT scan was performed before initiation of withdrawal therapy. The evaluation of the ventricular to brain ratio (VBR) by standardized and computerized measurements revealed significantly higher mean VBRs for both high- and low-dose BDZ-dependent patients compared to the mean VBR of an age- and sex-matched control group. In addition, the mean VBR of high-dose BDZ-dependent patients (N = 8) was significantly higher than the mean VBR of low-dose BDZ-dependent patients (N = 9). This difference could not be accounted for by the age of the patients or duration of BDZ-dependency and, therefore, suggests a dose-dependent effect of BDZs on the enlargement of internal CSF-spaces. On the other hand, higher values for the width of external CSF-spaces were found to be related to increasing age of the patients and duration of BDZ-dependency.

Adult↗
PubMed1987

Cranial computed tomography findings in bulimia.

In cranial computed tomography (CT), not only patients with anorexia nervosa but also patients suffering from bulimia, display enlarged external cerebrospinal fluid spaces. This was true for more than one third of the 28 bulimic patients studied, regardless of whether or not they had a past history of anorexia nervosa. As the bulimic patients had a near normal body weight, the observed structural changes cannot be attributed to underweight, as is commonly assumed to be the case in anorectic patients. These findings indicate that, in addition to underweight, other factors have to be considered as causing the morphological brain alterations present in patients with eating disorders.

Adolescent↗
PubMed1987

Anxiety disorders: a long-term prospective and retrospective follow-up study of former inpatients suffering from an anxiety neurosis or phobia.

Psychopathological status and psychosocial functioning of 40 former inpatients suffering from an anxiety neurosis (ICD 300.0) or phobia (ICD 300.2) were followed up over a period of 6-8 years using standardized instruments. In addition, the course of illness, the utilization of medical services and the periods of work disabilities were assessed. With regard to psychopathology, in more than half of the patients course and outcome could be regarded as chronic and severe; only one third of the patients were free of marked or severe psychopathological symptoms during the 12 months preceding the reexamination. Although on the psychosocial outcome level 67% of the 40 former inpatients showed marked or severe difficulties in most social role areas, especially in the field of personal interaction, the great majority of these patients seemed to have adapted somehow to their life situations. Only 13% could be regarded as severely impaired and in continuous need of supervision and guidance. Coping difficulties with everyday demands and dissatisfaction with their social functioning and their anxiety-related restrictions were most prominent in all anxious patients. In contrast to some other long-term follow-up studies, most of which were carried out on outpatients, the results suggest a rather unfavourable course and outcome of anxiety disorders.

Adolescent↗
PubMed1987

REM sleep and cortisol response to the cholinergic challenge with RS 86 in normals and depressives.

The influence of the muscarinic agonist RS 86 on rapid-eye-movement (REM) sleep and on hypothalamic-pituitary-adrenocortical (HPA) axis was studied in healthy subjects and in patients with a major depression. In both groups, RS 86 induced a shortening of REM latency and an increase in REM sleep; these effects were more pronounced in the depressives than in the controls. This finding supports the assumption that in depression the REM sleep regulating neurons are hypersensitive to cholinergic stimuli. However, neither in the healthy subjects nor in the depressed patients was an RS 86 induced increase in plasma cortisol seen. This observation does not agree with the assumption that, in humans, the HPA axis is stimulated by muscarinic neurons and that hypercortisolemia in depression is due to an overactivity of muscarinic neurons activating the HPA axis.

Adult↗
PubMed1987

Sleep and dreams in eating disorders.

The results of several studies on sleep EEG and dreams in patients with eating disorders are presented and compared with the data obtained in patients with a major depression. The sleep pattern, which is characteristic of depression, could not be found in the eating disorder group. Regarding the cholinergic REM induction test, the depressive displayed a pronounced shortening of REM sleep latency. However, this biological marker, indicating a cholinergic hyperactivity in depression, could not be observed in patients with eating disorders. The content analysis of laboratory-recorded dreams yielded several differences between depression and eating disorders and also, more subtle, between anorexia and bulimia.

Anorexia Nervosa↗
PubMed1987

Hormonal and metabolic mechanisms in the development of cerebral pseudoatrophy in eating disorders.

Cranial computed tomography (CT) examinations performed on patients with schizophrenia, affective disorders or on patients with anorexia and bulimia nervosa revealed morphological brain alterations. In patients with eating disorders these structural changes were characterized by enlarged ventricles and sulci. Malnourishment-induced hormonal and metabolic disturbances may be responsible for this morphological brain alteration which, due to its reversibility after clinical remission, is frequently called 'pseudoatrophy'. As patients with alcohol dependency also display a cerebral pseudoatrophy, the search for similarities between alcoholics and patients with eating disorders may help to elucidate some of the pathogenetic factors which cause the CT findings in patients with different psychiatric or psychosomatic disorders.

Anorexia Nervosa↗
PubMed1985

The effect of weight loss and inappropriate plasma dexamethasone levels on the DST.

Recent studies from different research groups have raised fundamental questions about the postulated specificity of the dexamethasone suppression test (DST) for endogenous depression. Findings in 116 psychiatric inpatients and 24 semi-starved healthy volunteers underline the importance of weight loss as a factor affecting DST results. A study of 160 DSTs in 93 psychiatric inpatients further revealed a significant negative correlation of plasma cortisol and plasma dexamethasone levels 10 hours after oral administration of 1 mg of dexamethasone. These results suggest a decisive effect of the pharmacokinetics of dexamethasone, at least on the 1-mg DST.

Adolescent↗
PubMed1985

The influence of dieting on the menstrual cycle of healthy young women.

Nine normal young women of normal weight, aged 20-29 yr, who had regular menstrual cycles, dieted for 6 weeks (approximately 800-1000 kcal/day) and lost between 6 and 8 kg body wt. Half-hourly blood samples were taken from 1800-0530 h on two occasions before and after 1, 2, 3, 4, 5, and 6 weeks of dieting. In three women with anovulatory cycles the LH secretion pattern was not altered by dieting, but plasma estradiol levels decreased and reached menopausal concentrations during the final 2 weeks of dieting. In two of these three women the menstrual cycles were disrupted and regular cycles occurred only 3 and 6 months after dieting. Six women had regular ovulatory cycles. High progesterone values (greater than 3 ng/ml) were recorded in two cycles before the dieting period. While dieting, three women maintained ovulatory cycles and three women had no periovulatory hormone secretion pattern and/or a pattern characteristic of the luteal phase. No significant alterations of average LH concentrations and LH peak frequency developed. It is concluded that mild dieting does not suppress LH secretion in the manner found in anorexia nervosa or during total fasting. Dieting may interfere with gonadal steroid production, thus causing disturbances of the menstrual cycle. The effect described here may be responsible for the early onset of amenorrhea in patients with beginning anorexia nervosa.

Adult↗
PubMed1984

The limited utility of the dexamethasone suppression test for the diagnostic process in psychiatry.

In 231 psychiatric in-patients, the 1 mg or 1.5 mg DST with blood samples at 0900 h, 1600 h and 2300 h and a post-dexamethasone plasma cortisol threshold of greater than or equal to 5 micrograms/dl were tested for their differential diagnostic utility in clinical psychiatry. Neither test significantly separated endogenous depressed patients from patients with other depressive or non-depressive psychiatric disorders. Studies of the 1 mg or 1.5 mg DST in 75 healthy subjects revealed about 12% of cortisol non-suppressors, when a post-dexamethasone cortisol threshold of greater than or equal to 5 micrograms/dl was used. This seemed to be an unacceptably low specificity of the test in normal subjects. A threshold criterion of greater than or equal to 8 micrograms/dl, however, yielded only 2.7% of non-suppressed normal subjects. Analyses of the DST data of the psychiatric patients, using a cortisol threshold of greater than or equal to 8 micrograms/dl, also failed to reveal a significantly higher specificity of the DST for endogenous depression. However, it was demonstrated that intervening variables such as stress due to hospital admission, drug withdrawal, suicidal turmoil, weight loss, as well as a low dexamethasone plasma level, enhance the rate of abnormal DST results in psychiatric in-patients, regardless of their diagnostic classification.

Adult↗
PubMed1975

Particle-associated RNA dependent DNA polymerase and high-molecular-weight RNA in a human cell line derived from polycythemia vera bone marrow.

A particle fraction with a density of 1.15-1.19 g/cm3 was isolated from the cytoplasm of a human cell line established in culture from the bone marrow of an untreated patient with polycythemia vera. Electron micrographs of cross sections of cells and cell homogenates revealed virus-like particles on which DNA could be synthesized. An RNA-dependent DNA polymerase, isolated from the particles, preferred poly(rA)-oligo(dT) over poly(dA)-oligo(dT) and was able to polymerize deoxyguanosine monophosphate in a reaction stimulated by poly(rC)-oligo(dG).

Bone Marrow↗
PubMedDate not supplied

Sleep electroencephalographic patterns and cranial computed tomography in anxiety disorders.

Sleep electroencephalogram (EEG) and cranial computed tomography (CT) were performed in 15 drug-free inpatients with an anxiety disorder. The sleep EEG of the patients was characterized by a decreased sleep efficiency and a shortened REM latency. Under visual inspection, four (27%) patients showed ventricular enlargement, while an increased ventricular brain ratio (VBR) was measured in five (33%). No clear associations between EEG sleep measures and ventricular size became obvious, although there is good evidence in the literature that sleep continuity, slow-wave sleep, or REM sleep are closely related to ventricular and/or sulcal widening in various neuropsychiatric disorders.

Adolescent↗
PubMedDate not supplied

Pain perception in psychiatric disorders: a review of the literature.

Aberrations of pain experience occur frequently in psychiatric disorders and hence pathological alterations in the basic mechanisms underlying pain experience can be expected. Nevertheless, pain perception, as one of the most important basic mechanisms of pain experience, has rarely been assessed experimentally in psychiatric disorders. The authors review the relevant experimental studies on pain perception in patients with anxiety disorders, schizophrenia, depression, eating disorders and personality disorders and suggest lines for future research. Finally, they point out that the experimental study of pain perception is useful not only in understanding aberrant pain experiences in psychiatric disorders but also in elucidating pathophysiological mechanisms because pain perception is controlled by neurochemical and neurohormonal functions known to be affected by psychiatric disease processes.

Arousal↗
PubMedDate not supplied

On the impact of episode sensitization on the course of recurrent affective disorders.

Sensitization of an organism by recurrent disease episodes is postulated as a key mechanism governing the progressive long-term course of affective disorders. The particular significance is that episode sensitization could underly the transition from externally triggered disease episodes to autonomous episode generation. Functionally, this transition might be explained by positive feedback between a disease episode and the activity state of an organism which includes the introduction of a memory trace for generated disease episodes. Here we consider the functional consequences of episode sensitization for the course of recurrent affective disorders. We use a computational approach and extend our previously introduced model for the course of affective disorders by a feedback mechanism for episode sensitization. Depending on sensitization timescale and amount, triggered episodes leave the model in a sustained sensitized state or induce autonomous disease progression. Runaway activation can end in saturation. Remarkably, however, over a broad parametric range the progression ends in intermediate states with fluctuating disease patterns. This behavior results from the model's nonlinear dynamics and represents a situation where the feedback intermittently changes between positive and negative directions. Our simulations strongly support episode sensitization as an important disease mechanism for affective disorders. From a nonlinear standpoint, this mechanism offers an explanation not only for autonomous disease progression but also for occurence and stability of irregular rapid-cycling disease states.

Feedback↗
PubMedDate not supplied

Alterations of blood platelet MAO-B activity and LSD-binding in humans after sleep deprivation and recovery sleep.

Sleep deprivation (SD) is an effective, however short-lived, method of treatment of depression. Preliminary findings suggest that the antidepressive effect of sleep deprivation is mediated by serotoninergic (5-HT) mechanisms. We therefore assessed serotoninergic activity before and after total SD (TSD) as well as after the following night sleep by investigating platelet LSD-binding, MAO B-activity, and 5-HT-content as well as plasma norepinephnne (NE) in 10 healthy men (age: 27.4 +/- 2.8 years). Blood samples were drawn on three consecutive days at 0700, 1300 and 1900 h, respectively. After TSD, a significant increase of LSD-binding KD and Bmax as well as of MAO-B KM and plasma NE could be observed, which, however, vanished after consecutive night sleep. Our findings favour an increased serotoninergic transmission after TSD and thus support the hypothesis, that sleep deprivation exerts its antidepressant effects by pro-serotoninergic mechanisms.

Adult↗