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Biomedical subjects

F Hohagen

Publications and source records attributed to F Hohagen.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effect of tetrahydroaminoacridine on sleep in healthy subjects.

The present study investigated the impact of the cholinesterase inhibitor tetrahydroaminoacridine (THA; tacrine) on sleep in healthy subjects. According to the reciprocal interaction model of non-rapid eye movement (NREM) and REM sleep regulation, which postulates a primary role in cholinergic neurotransmission for the initiation and maintenance of REM sleep, it was expected that THA would lead to an earlier onset of REM sleep. In 12 healthy subjects aged from 21 to 50 years two different doses (20 mg, 40 mg) were administered 1 hour prior to bed time and compared to placebo. Only the higher dose of THA significantly shortened REM latency. No other significant effects on sleep architecture were observed, although administration of 40 mg tacrine was associated with a decrease in sleep efficiency and a prolongation of sleep latency. Blood plasma levels of tacrine and its metabolite 1-hydroxytacrine measured prior to sleep and during the first 90 min of sleep were significantly correlated with the onset of REM sleep in relation to the timing of drug administration (only for the 20 mg dose). The reversible cholinesterase inhibitor THA exerts effects on REM latency comparable to those observed with other cholinomimetic agents.

Adult↗
PubMed1996

Advanced vs. normal sleep timing: effects on depressed mood after response to sleep deprivation in patients with a major depressive disorder.

Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in patients with a major depressive disorder (MDD). Though approximately 50 to 70% of depressed patients improve after sleep deprivation, the majority relapse after recovery sleep, some even after a short nap. One theoretical model postulates a critical period in the early morning hours where sleep is likely to induce a relapse, and nap studies indicate that sleep may be particularly 'depressogenic' at this time of day. A second model attributes the relapse to the release of non-REM sleep. We therefore compared the impact of an advanced sleep period (17:00-24:00 h) to a normal sleep period (23:00-06:00 h) on mood in patients who had responded to sleep deprivation. Less relapses into depression occurred after advanced sleep. Polysomnographic data showed that, as expected, normal sleep was characterized by a more pronounced improvement of sleep continuity and increased slow-wave sleep. The normal sleep group showed a stronger decrease in REM sleep density than the advanced sleep group compared with baseline. These data add to a growing body of evidence that the timing of sleep following successful sleep deprivation may be crucial for a stabilization of its antidepressant effect. Thus, avoidance of sleep during a "critical period' for more than a single night is necessary to provide a longer-lasting treatment modality.

Adult↗
PubMed1996

[Organization of practice oriented knowledge structures by the "cognitive apprenticeship" method].

The introduction of the new German specialist for psychiatry and psychotherapy increased the requirement for more integrated and flexible clinical training programs for residents. The integration of this multitude of more sophisticated diagnostic and therapeutic strategies in an individualized treatment plan for each patient requires new teaching strategies. The instructional method "Cognitive Apprenticeship" in acquisition of treatment planning-competence is discussed within a curriculum framework.

Curriculum↗
PubMed1995

Induction of cytokine synthesis and fever suppresses REM sleep and improves mood in patients with major depression.

Beneficial effects of inflammatory events on certain psychiatric disorders, including depression, were reported sporadically by ancient Greek physicians, but have been described also in our times by a few psychiatrists during the past decades. During febrile inflammatory events, mediators of the immune system such as interleukin-1 can be detected in the brain and may act on their respective receptors which have also been demonstrated in the brain. Since cytokines such as interleukin-1 have been shown in animal studies to exert sedative behavioral effects, to be somnogenic, and to induce slow-wave sleep (SWS), we performed a pilot study to evaluate scientifically the anecdotically reported beneficial effects of inflammatory states on depressive disorders. Mood and sleep parameters were monitored in seven drug-free, severely depressed patients before, during, and after the administration of a single dose of endotoxin. All patients responded with a short pulse of increased synthesis of the cytokines tumor necrosis factor, interleukin-1, and interleukin-6 and elevated body temperature for several hours. During the night following endotoxin administration, rapid eye movement (REM) sleep was significantly suppressed, while changes in slow wave sleep were not significant. During the next day, all patients were in a significantly improved mood; however a rebound of REM sleep was observed in the second night after endotoxin administration and mood worsened again during the next days, indicating an only transient beneficial effect of the treatment.

Adult↗
PubMed1995

A seizure, and electroencephalographic signs of a lowered seizure threshold, associated with fluvoxamine treatment of obsessive-compulsive disorder.

A 38-year-old patient with severe obsessive-compulsive disorder received fluvoxamine in a clinical study. Psychometric ratings showed marked clinical improvement in the third week of fluvoxamine administration, but after 8 weeks, at a dose of 300 mg per day, he suffered a grand mal seizure after drinking a glass of beer (0.2 liter). He had no history of previous epileptic seizures. Careful neurological evaluation including computer tomography and magnetic resonance imaging of the brain revealed no signs of acute disease. EEG before the fit did not show epileptiform activity; after the fit, spikes and spike-wave complexes appeared, which disappeared upon discontinuation of fluvoxamine. Since his obsessive-compulsive symptoms had responded well to fluvoxamine and worsened after its discontinuation, the drug was cautiously reintroduced. Improvement of the obsessive-compulsive symptoms was observed again, but spikes and spike-wave complexes reappeared at a dose of 50 mg per day. Under anticonvulsant treatment with carbamazepine, fluvoxamine was increased to 100 mg per day. No seizures occurred during a follow-up to two years.

Adult↗
PubMed1995

[Treatment of depression with sleep deprivation and sleep phase advancement].

Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in approximately 60% of the patients with a major depressive disorder (MDD). The positive effect of TSD is generally reversed after the next night of sleep. A pilot study of our group indicated that a consecutive one week phase advance of the sleep phase stabilized mood in more than half of the patients who responded to TSD. However, the majority of patients in our pilot study had been treated concomitantly with antidepressive medication. To exclude a possible synergistic effect of simultaneous antidepressive medication and the sleep-wake manipulation in the present study eleven medicated and sixteen drug-free depressed patients were investigated. In two thirds of the patients relapse into depression after successful TSD could be prevented. This effect seemed to be independent of adjunct antidepressant pharmacotherapy. Ten of these patients were studied polysomnographically prior to and during the treatment. Data analysis revealed that during the advance of the sleep phase no prolonged partial sleep deprivation took place. At the end of the study REM % had even increased and REM latency was still short in spite of clinical improvement, thus contradicting the assumption that REM sleep suppression is a necessary prerequisite for antidepressive therapy. The results support the hypothesis of a "critical phase" in the morning hours during which sleep can reinduce depressive mood and, vice versa, prevention of sleep during this time may act antidepressively.

Adult↗
PubMed1995

Mental comorbidity of chronic insomnia in general practice attenders using DSM-III-R.

The major aim of this study was to investigate links between chronic insomnia and mental and personality disorders using the DSM-III-R classification. Of a sample of 2512 general practice attenders, 105 with a chronic insomnia complaint over a 4-month period were evaluated for mental and personality disorders. In addition, the significance of other factors such as personality traits, social functioning and the patient's own estimation of sleep quality was studied. Sixty-six patients got a diagnosis of a current insomnia using a structured interview for DSM-III-R. Fifty percent of them had at least one additional current Axis I or II diagnosis. Affective disorders were most common as principal psychiatric diagnosis followed by substance use disorders. The general practitioners were poor in recognizing their patients' chronic insomnia complaints and the high percentage of substance abusers among them. The important role of psychopathology in chronic insomnia sufferers was indicated by the high number of patients who displayed prominent personality traits. The predominant personality pattern was characterized by a pattern of internalization of problems combined with an anxious-depressive reaction style. In summary, strong associations between chronic insomnia, mental disorders and psychopathology were confirmed by this investigation.

Adolescent↗
PubMed1995

[Chronotherapeutic approaches in depressive disorders].

Sleep deprivation has been regarded as a beneficial treatment modality for about 60% of patients with Major Depressive Disorder. Unfortunately, however, more than 80% of the improved patients relapse into depression after the next night of sleep. In the present study we tried to prevent relapses into depression after successful total sleep deprivation (TSD) by treating 27 patients suffering from a Major Depressive Disorder according to DSM-III-R with a combination of sleep deprivation with consecutive sleep phase advance for 1 week. Advancing the sleep period to 5.00 p.m. until 12.00 p.m. following TSD and then gradually shifting back by 1 h daily the sleep period to the normal phase position (11.00 p.m. until 6.00 a.m.) prevented 61% of these patients from relapsing into depression. Thus, the combination of sleep deprivation with consecutive sleep phase advance has been proven to be an effective antidepressant treatment besides other well established antidepressive treatment modalities.

Adult↗
PubMed1995

[Approximation of sleep duration and sleep efficiency using actography].

The actography is a cost-effective semiobjective method to measure sleep/wake-cycles. This is the reason why the actography should be used first. The actography is after the cost-intensive polysomnography the best method in diagnosis of sleep disorders and monitoring of sleep disorder therapy. Actography over several days allows a precise estimation of total sleep time and sleep efficiency and makes possible an analysis of sleep/wake in natural conditions. The estimation is better if the patient is in high wake body activity and the recording time is longer. The mean values of total sleep time and sleep efficiency from polysomnography and actography are congruent.

Adult↗
PubMed1994

Sleep EEG of patients with obsessive-compulsive disorder.

Twenty-two patients suffering from an obsessive and compulsive disorder (OCD) according to DSM-III-R were investigated by polysomnographic sleep EEG recordings under drug-free conditions and compared to age- and sex-matched healthy controls. Sleep efficiency was significantly lower and wake % SPT was significantly increased in the patient group compared to healthy subjects. Sleep architecture did not differ among the two samples. Especially REM sleep measures, in particular, REM latency did not differ among the groups. No positive correlation was found between sleep variables and rating inventories for obsession and compulsions (Y-BOCS), depression (Hamilton) and anxiety (CAS). A secondary depression did not influence sleep EEG variables. The results of this study contradict the assumption that OCD patients show REM sleep and slow wave sleep abnormalities similar to those shown by patients with primary depression.

Adult↗
PubMed1994

Sleep in depression: the influence of age, gender and diagnostic subtype on baseline sleep and the cholinergic REM induction test with RS 86.

One hundred and eight healthy controls and 178 patients with a major depressive disorder according to DSM-III were investigated in the sleep laboratory after a 7-day drug wash-out period. Subsamples of 36 healthy controls and 56 patients additionally took part in the cholinergic rapid eye movement (REM) sleep induction test with RS 86. Data analysis revealed that age exerted powerful influences on sleep in control subjects and depressed patients. Sleep efficiency and amount of slow wave sleep (SWS) decreased with age, whereas the number of awakenings, early morning awakening, and amounts of wake time and stage 1 increased with age. REM latency was negatively correlated with age only in the group of patients with a major depression. Statistical analysis revealed group differences for almost all parameters of sleep continuity with disturbed indices in the depressed group. Differences in SWS were not detected. REM latency and REM density were altered in depression compared to healthy subjects. Sex differences existed for the amounts of stage 1 and SWS. The cholinergic REM induction test resulted in a significantly more pronounced induction of REM sleep in depressed patients compared with healthy controls, provoking sleep onset REM periods as well in those depressed patients showing baseline REM latencies in the normal range. Depressed patients with or without melancholia (according to DSM-III) did not differ from each other, either concerning baseline sleep or with respect to the results of the cholinergic REM induction test. The results stress the importance of age when comparing sleep patterns of healthy controls with those of depressed patients. Furthermore they underline the usefulness of the cholinergic REM induction test for differentiating depressed patients from healthy controls and support the reciprocal interaction model of nonREM-REM regulation and the cholinergic-aminergic imbalance hypothesis of affective disorders.

Adolescent↗
PubMed1994

Treatment of primary insomnia with trimipramine: an alternative to benzodiazepine hypnotics?

A group of 19 middle aged patients suffering from primary insomnia according to the DSM-III-R were treated in a single-blind study with trimipramine, a sedating antidepressant. A total of 15 patients completed the study protocol and were evaluated. The present pilot study aimed at investigating the sleep-inducing properties of trimipramine, and at clarifying the question of whether short- or long-term rebound insomnia occurs after discontinuation of this drug. At four measurement points, i.e. under baseline conditions, under treatment and 4 and 14 days after drug discontinuation, sleep was recorded with an ambulatory-electroencephalogram (EEG) monitoring device in the patient's home environment. Simultaneously, psychometric tests were applied to measure withdrawal symptoms, subjective sleep quality and well-being during daytime. Trimipramine at a mean dose of 166 +/- 48 mg led to a significant increase in sleep efficiency, total sleep time, and stage 2% sleep-period time (SPT), whereas a significant decrease in wake time and stage 1% SPT was noted. Insomniac patients reported an improvement in subjectively perceived sleep quality following trimipramine. Additionally, an improvement in well-being during the daytime occurred. Negative side effects were limited to dry mouth due to the anticholinergic properties of the drug. Discontinuation of trimipramine did not provoke either short- or long-term rebound insomnia in objective and subjective sleep measurements considering mean values of the whole sample, although a subgroup of patients did display total sleep times below baseline values during short- and long-term withdrawal, but generally without a concomitant worsening of sleep quality according to the sleep questionnaire.

Adult↗
PubMed1994

Cholinergic neurotransmission, REM sleep and depression.

It is known from animal experiments that the regulation of REM and Non-REM sleep is governed by cholinergic and serotonergic/adrenergic neurons in the brain stem. Cholinergic neurons in the gigantocellular field of the tegmentum seem to be responsible for the triggering and maintenance of REM sleep. These findings are of special interest for interpreting abnormalities of REM sleep in depression. Psychiatric sleep research in the last two decades has demonstrated that an early onset of REM sleep and heightened REM density frequently occurs in patients suffering from depression. Extrapolating from animal data on REM sleep regulation, the premature onset of REM sleep in depression may be interpreted as the consequence of a central nervous cholinergic overactivity or muscarinic supersensitivity. In our experimental work we have tested assumptions of the so-called reciprocal interaction model of NonREM and REM sleep by cholinergic/anticholinergic stimulation strategies of sleep in healthy subjects. Furthermore, the impact of cholinergic stimulation on sleep in depression, healthy control subjects and other psychopathological conditions was investigated. These studies demonstrated that the most pronounced REM sleep response to cholinergic stimulation occurred in depression.

Adolescent↗
PubMed1994

Influence of biperiden and bornaprine on sleep in healthy subjects.

Biperiden, 4 mg, an anticholinergic drug that is relatively selective for the M1 receptor subtype, and bornaprine, 4 mg, a nonselective M1 and M2 antagonist, were administered orally in a randomized, double-blind design to twelve healthy volunteers to investigate the effect on polysomnographically recorded sleep. Both drugs suppressed rapid eye movement (REM) sleep as reflected by an increase of REM latency and a decrease in the percentage of REM sleep period time with the effects of biperiden being more pronounced. No significant effect on slow wave sleep was observed. The results of this study support the hypothesis that both the M1 and the M2 receptor subtype are involved in the regulation of REM sleep in humans.

Adult↗