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Biomedical subjects

D Riemann

Publications and source records attributed to D Riemann.

At least 127 records · Page 7Linked to original sources
PubMed1994

Sleep onset insomnia, sleep maintaining insomnia and insomnia with early morning awakening--temporal stability of subtypes in a longitudinal study on general practice attenders.

The present study investigated the temporal stability of insomnia patterns during a 4-month study period, classifying insomnia as sleep-onset insomnia, sleep-maintaining insomnia or insomnia with early morning awakening. In a longitudinal study design, 2,512 general practice attenders were investigated at the time of the first inquiry (T1) with a questionnaire. Four months later (T2), all patients complaining of difficulties in initiating and/or maintaining sleep and/or early morning awakening (n = 328) were again contacted by mail and received the same questionnaire as at T1. According to the reported symptoms, patients were assigned to the different subtypes of insomnia. The diagnosis at T1 was then compared with the diagnosis at T2 4 months later. Only about half of all patients who complained of difficulties in initiating sleep at T1 still exclusively reported sleep-onset insomnia 4 months later, whereas the remaining patients were distributed to different subtypes. The stability of sleep-maintaining insomnia and insomnia with early morning awakening was even lower. Comorbidity with a somatic or psychiatric disorder at T1 and change in hypnotic treatment did not account for the instability of the respective subgroup of insomnia. These findings illustrate that cross-sectional studies focusing on subtypes of insomnia, e.g. sleep-onset insomnia, may lead to erroneous results.

Adolescent↗
PubMed1994

[REM sleep parasomnia].

The parasomnias consist of a heterogenous group of sleep behaviour disorders with different etiologies and various symptomatologies. By employing polysomnography and the simultaneous video recording of behaviour during sleep, it is possible to associate behavioral disturbances during sleep with specific sleep stages. In the present case study, a patient with a REM (rapid eye movement) sleep behaviour disorder is discussed. This rare form of parasomnia is characterized by motor enactment of vivid and striking dreams. Underlying disease in the present case involved bilateral lacunar ischemic infarcts in the brain stem. Under the combined psychotropic medication of carbamazepine and amitriptyline, the behaviour disorder during REM sleep remitted markedly.

Amitriptyline↗
PubMed1993

REM sleep parameters in the discrimination of probable Alzheimer's disease from old-age depression.

Thirteen dementia of the Alzheimer type (DAT) patients and fifteen old-age major depressive disorder (OAD) patients were investigated by polysomnography. The sleep was recorded during two nights after a 1 week wash-out period of psychotropic drugs. No statistically significant differences between the two groups were found concerning sleep continuity or architecture. The amount of REM sleep was significantly lower in DAT in comparison with OAD patients (11.7% verses 18.5%). Also, total REM density as well as the density of the first REM period were significantly lower in the DAT compared with the OAD patient group (15.8% verses 32.5%, 14.9% verses 38.1%, respectively). REM latency did not differ between both groups. Because REM latency is known from other studies to be shortened in depressed patients due to a cholinergic hyperactivity, the opposite finding, i.e., prolongation of REM latency, was expected for DAT patients. This assumption, however, could not be confirmed in the present study. It is concluded that REM density may better differentiate between DAT and OAD.

Aged↗
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

Prevalence and treatment of insomnia in general practice. A longitudinal study.

The aim of the study was to assess prevalence and treatment modalities of insomnia in general practice. To investigate the course of insomnia, a longitudinal study design was adopted. Two thousand five hundred and twelve patients (age 18-65 years) were investigated with a questionnaire in general practice (T1). Four months later (T2) and again 2 years later (T3) a questionnaire was sent to all patients who had complained about severe insomnia at the time of the first inquiry. To assess insomnia, operationalized diagnostic criteria were applied (DSM-III-R). Eighteen point seven percent suffered from severe, 12.2% suffered from moderate and 15% suffered from mild insomnia. In the course of 2 years insomnia appeared as a chronic health problem. A high comorbidity of severe insomnia was found with chronic somatic and psychiatric disorders, especially with depression. Of the severely insomniac patients, 23.9% used prescribed hypnotics habitually, mainly benzodiazepines. The use of prescribed hypnotics remained rather stable during the whole study period. More than half of the patients reported a daily use of the hypnotics for 1-5 years or longer, but only 22% of the severely insomniac patients reported at the time of the third inquiry a significant improvement of insomnia due to the administration of sleeping pills. Thus, the long-term administration of benzodiazepine hypnotics seems to be an inadequate treatment strategy in chronic insomnia. Whether the occurrence of rebound insomnia after benzodiazepine withdrawal may be one of the main factors for chronic hypnotic use requires discussion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

48-hour rapid cycling: results of psychopathometric, polysomnographic, PET imaging and neuro-endocrine longitudinal investigations in a single case.

We report a 64-year-old patient suffering from rapid cycling bipolar disorder who was studied by means of polysomnography, neuroendocrine tests and PET (positron emission tomography) imaging. In a manner only partly compatible with the cholinergic-aminergic imbalance model of mania and depression, a linkage of REM sleep disinhibition and depressive mood was observed, but no decisive REM sleep delay was seen on manic days. Growth hormone secretion after clonidine stimulation was blunted on depressive and hypomanic days. A series of total sleep deprivations led to a positive effect on psychopathology for about two weeks. Carbamazepine treatment normalized REM sleep variables, damped the amplitude of mood cycling of the patient, increased TSH and decreased FT4.

Bipolar Disorder↗
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↗
PubMed1993

Demonstration of CD13/aminopeptidase N on synovial fluid T cells from patients with different forms of joint effusions.

Cytofluorometric analysis was performed to characterize the immunophenotype of lymphocytes of the synovial fluid (SF) and the peripheral blood (PB) from patients suffering from juvenile chronic arthritis (JCA) or rheumatoid arthritis (RA). The most obvious difference could be found in expression of the surface protease aminopeptidase N (AP N/CD13). Whereas monoclonal antibodies specific to CD13 failed to reveal surface expression on lymphocytes of the PB; 63 +/- 15% of SF T cells gave positive staining for CD13 using Leu-M7. No correlation between CD13 expression and joint disease could be found in patients who had different types of inflammatory joint effusions. CD13 expression of T cells was also found in synovial tissue and inflammatory serous cavity effusions. Fixation of T cells revealed the presence of intracellular CD13 antigen already located in the PB T cells of healthy individuals. Induction of CD13 expression on PB T cells could be demonstrated after incubation with Con A/IL-2 or SF from patients with RA. Our findings suggest a role for AP N as a new activation-associated molecule of T lymphocytes.

Aminopeptidases↗
PubMed1993

Influence of the cholinergic agonist SDZ 210-086 on sleep in healthy subjects.

The administration of 1.0 mg SDZ 210-086, an orally acting muscarinic agonist, shortened rapid-eye movement (REM) latency, increased REM percent of sleep period time and the total duration of REM sleep, and decreased slow-wave sleep in 12 healthy male subjects. The administration of 0.5 mg SDZ 210-086 had no statistically significant effect on sleep variables. Although the tonic components of REM sleep (REM duration, the REM percent of sleep period time) were increased, REM density percent (total) was significantly decreased due to the prolongation of total REM duration (in minutes) and a parallel reduction of the total number of eye movements. This finding is in contrast to studies using other cholinomimetics (i.e., physostigmine, arecoline, and RS 86) and may implicate different generating systems of phasic and tonic REM sleep components.

Adult↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: REM sleep in depression-an overview.

Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a major depressive disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state- or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well-known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.

Journal Article↗
PubMed1993

Treatment of narcolepsy-cataplexy syndrome with the new selective and reversible MAO-A inhibitor brofaromine-a pilot study.

Eighteen narcoleptic patients were treated in a single-blind study with brofaromine, a new selective and reversible MAO-A-inhibitor. After a drug-free period of seven days, brofaromine was administered for two weeks. Patients were treated with 75 mg brofaromine for the first week and with 150 mg brofaromine for the second week of the study. After an adaptation night nocturnal sleep EEGs were recorded under placebo before brofaromine was given, one week later under 75 mg, and another week later under 150 mg brofaromine. Excessive daytime sleepiness (EDS) was evaluated under placebo at the beginning of the study, under 75 mg at the end of the first week, and under 150 mg brofaromine at the end of the second week by means of the Multiple Sleep Latency Test (MSLT) and the Maintenance of Wakefulness Test (MWT). The number of cataplexies was protocolled by the patients. Compared to placebo the administration of 150 mg brofaromine led to a significant increase of sleep latency in the MLST as well as in the MWT. REM sleep was significantly suppressed in the nocturnal sleep EEG, in the MSLT and in the MWT. The number of cataplexies protocolled by the patient was significantly decreased under 150 mg of brofaromine compared to placebo. Improvement of vigilance and cataplexy occurred in dose-dependent manner. No serious side effects were observed. The results of the present single-blind study indicate that brofaromine seems to be a well-tolerated and effective drug for the treatment of excessive daytime sleepiness and cataplexy in narcoleptic patients.

Journal Article↗
PubMed1993

The influence of total sleep deprivation on urinary excretion of catecholamine metabolites in major depression.

To elucidate the influence of total sleep deprivation (TSD) on catecholaminergic neurotransmission, which is assumed to be disturbed in depression, 9 depressive patients collected consecutive 24-h urine samples prior to (baseline), during (TSD) and following total sleep deprivation (post-TSD). Urine samples were analysed for total MHPG (3-methoxy-4-hydroxyphenylglycol), conjugates of MHPG (glucuronide and sulfate), excretion of HVA (homovanillic acid) and VMA (3-methoxy-4-hydroxymandelic acid). TSD increased the urinary excretion of MHPG-sulfate as a marker of the central norepinephrine metabolism and the excretion rates of VMA and HVA as indices of the peripheral catecholamine metabolism. Patients with higher VMA values prior to TSD reacted worse, and the VMA increase due to TSD was positively correlated with the response. The results demonstrate that TSD, besides acting as a stimulus on the peripheral sympathetic nervous system, influences central nervous noradrenergic neurotransmission, as reflected by the increase of MHPG-sulfate.

Adult↗
PubMed1993

The effect of carbamazepine on endocrine and sleep EEG variables in a patient with 48-hour rapid cycling, and healthy controls.

Carbamazepine treatment of a patient with 48-hour rapid cycling led to a dampening of mood cycling, and prolonged rapid eye movement (REM) sleep latency. No effect on central alpha-receptors as measured by growth hormone (GH) secretion after clonidine stimulation or on spontaneous 48-hour GH secretion was observed. In 12 healthy subjects given 400 mg carbamazepine daily for a period of 5 days, improved sleep continuity and increased slow-wave sleep occurred with treatment. REM sleep percentage and REM latency remained uninfluenced, whereas REM density decreased. GH secretion after clonidine stimulation was not altered. Data from the single-case longitudinal study emphasize that carbamazepine is effective in treating rapid-cycling affective psychosis. Furthermore, neuroendocrine and sleep EEG data from the study in healthy subjects indicate a different profile of action for carbamazepine compared to most other antidepressants or antimanic drugs.

Adult↗
PubMed1993

Effects of single and repeated clonidine administration on the properties of central and peripheral alpha 2-adrenoceptors in man.

The centrally acting alpha 2-adrenoceptor agonist clonidine was used to assess the sensitivity of alpha 2-adrenergic neurotransmission in man, using receptor-binding studies and clonidine-induced growth hormone response. Neither acute (2 micrograms/kg body weight) nor subchronic (3 days, 2 x 150 micrograms/kg body weight) administration of clonidine affected platelet alpha 2-adrenoceptor number in humans as judged by 3H-yohimbine and 3H-UK-14,304 binding. The same treatment also did not modify central postsynaptic alpha 2-adrenoceptor function in the same individuals as assessed by clonidine-induced growth hormone responses. Similarly, subchronic (3 days, 500 micrograms/kg body weight, i.p.) or chronic (14 days, 500 micrograms/kg, i.p.) administration of clonidine to mice failed to change 3H-yohimbine or 3H-UK-14,304 binding sites in membranes prepared from frontal cortex. On the other hand, in vitro experiments using mouse frontal cortex or human platelet membranes showed pronounced reduction of 3H-UK-14,304 but not of 3H-yohimbine binding sites after incubation with several adrenoceptor agonists. The data indicate that acute and subchronic clonidine treatment may not change alpha 2-adrenoceptor sensitivity in humans or mice as assessed both at the functional and receptor level.

Adaptation, Physiological↗
PubMed1993

Test-retest reliability and validity of the Structured Interview for Sleep Disorders According to DSM-III-R.

OBJECTIVE: The purpose of this study was to evaluate the reliability of sleep disorder diagnoses in DSM-III-R by using a newly developed interview, the Structured Interview for Sleep Disorders According to DSM-III-R (SIS-D) and to evaluate the concordance between these diagnoses and sleep laboratory data. In addition, the sources of disagreements between two interviewers in the diagnoses given to the same patient were determined. METHOD: Two different interviewers used the SIS-D to diagnose 68 patients with complaints of sleep disorders. The concordance between these interviewers' diagnoses and polysomnographic findings was investigated by using kappa statistics. RESULTS: There were excellent reliabilities for almost all current main diagnostic categories and good concordance between diagnoses made on the basis of the structured interview and polysomnographic data. The main source of disagreement between interviewers was found in the symptom information given by the patient. CONCLUSIONS: These findings provide support for the utility of DSM-III-R sleep disorder diagnoses and for their retention in DSM-IV. These findings also accord well with a recent literature review of the DSM-III-R diagnosis of primary insomnia by the DSM-IV Work Group on Sleep Disorders. The good concordance between interview diagnoses and polysomnographic data suggests that a structured interview such as the SIS-D may be a useful screening instrument. The authors discuss the implications of these findings for the polysomnographic evaluation of chronic insomnia.

Adult↗
PubMed1992

The sleep structure of patients with anxiety disorders in comparison to that of healthy controls and depressive patients under baseline conditions and after cholinergic stimulation.

This study investigated sleep EEG during placebo and after cholinergic stimulation with RS 86 in 36 healthy subjects, 34 patients with major depression and 20 patients with anxiety disorders. Cholinergic stimulation with RS 86 led to a decrease of slow wave sleep and REM latency. RS 86 had a more profound impact on REM latency in patients with major depression than in healthy controls and patients with anxiety disorders. Six out of 36 healthy controls, three out of 20 patients with anxiety disorders and 24 of 34 patients with depression displayed sleep onset REM periods after cholinergic stimulation. Also effects on REM density and duration of the first REM period were more pronounced in major depression. Even in those patients with anxiety disorders and a secondary major depression no depression-like sleep abnormalities could be provoked. The results underline the usefulness of the cholinergic REM induction test to differentiate patients with major depression from those with other psychiatric disorders. The results can be interpreted as further evidence for the cholinergic-aminergic imbalance model of depression and for the reciprocal interaction model of nonREM-REM regulation.

Adult↗
PubMed1992

Sleep, age, depression and the cholinergic REM induction test with RS 86.

1. Healthy volunteers and patients with a major depressive disorders were administered 1.5 mg RS 86 (a cholinergic agonist) and placebo in a randomized double-blind cross-over design at 10 p.m. prior to bedtime. 2. Polysomnographic recordings demonstrated a significantly more pronounced shortening of REM latency after cholinergic stimulation in depressed patients compared to healthy subjects. 3. Even those depressed patients displaying placebo REM latencies in the normal range showed sleep onset REM periods after cholinergic stimulation. 4. The results support the reciprocal interaction model of NonREM-REM sleep regulation and the cholinergic-aminergic imbalance model of depression.

Adult↗