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Biomedical subjects

F Hohagen

Publications and source records attributed to F Hohagen.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Neurobiological aspects of the etiology and pathophysiology of obsessive-compulsive disorder].

Obsessive-compulsive disorder (OCD) is a common psychiatric illness characterized by intrusive, repetitive thoughts and behaviours which cause marked distress. During the last decade, different models were developed for the pathophysiology of the obsessive-compulsive-disorder. Three different neurobiological models are introduced in this article: 1. model of dysfunctional kortikostriatal circuitry, 2. amygdalocentric model, 3. neurochemical model. These models don't exclude themselves mutually but supplement themselves and should ideally be integrated into a biopsychosocial concept. Such increased understanding of the neurobiology can be translated into better diagnosis and treatment for those patients who suffer from obsessive-compulsive-disorder.

Humans↗
PubMed1999

The tryptophan depletion test. Impact on sleep in healthy subjects and patients with obsessive-compulsive disorder.

UNLABELLED: The tryptophan depletion test is a research tool to study the functional consequences of decreasing the brain serotonin metabolism. Since serotonin is involved in sleep regulation and assumed to be of high importance in the etiology of psychiatric disorders, the acute polysomnographic effects of tryptophan depletion were studied in healthy subjects and patients with obsessive compulsive disorder (OCD). According to the reciprocal interaction model of non-REM and REM-sleep regulation we expected that tryptophan depletion in healthy controls should provoke alterations of sleep similar to depression, whereas we assumed that these effects would be more pronounced in patients with OCD. METHODS: 12 healthy subjects with a mean age of 34 years and 12 patients suffering from OCD with a mean age of 30 years had 4 polysomnographic investigations. After 1 adaption and 1 baseline night subjects received a low protein diet on day 3 and 4 until midday. On day 4 at 18.00 h subjects ingested an aminoacid mixture devoid of tryptophan. This procedure resulted in a decrease of 85% in healthy subjects and 80% in OCD patients at 22.00 h. RESULTS: The tryptophan depletion led to more pronounced disturbances of sleep continuity in OCD patients than in healthy subjects in terms of an increase of wake time and a decrease of total sleep time. In both groups a decrease of sleep stage 2 could be observed. Healthy subjects showed significant alterations of phasic REM parameters as REM density and total number of rapid eye movements, what was not the case for OCD patients. CONCLUSIONS: Our results indicate the important role of the serotonergic system for sleep maintainance and the phasic aspects of REM sleep. Furthermore our data demonstrate that the tryptophan depletion test is a useful tool to evaluate the hypothesis of a serotonergic involvement in sleep regulation and the etiology of psychiatric disorders.

Adult↗
PubMed1999

[Management of mental health and primary care. Development and evaluation of a training program based on the PLISSIT approach].

Deficits in current approaches of psychosomatic and psychiatric education for general practitioners are reviewed. A skill-based training was developed in line with the four step counseling approach of the "PLISSIT" approach: The GP helps in first step ("permission") the patient to accept his problem and assesses informations about causing and maintaining factors of his symptomatology. In the second step he should provide information about the disorder and reverse misunderstanding and passivity (Limited Information). The GP's should develop preliminary strategies for change in the third step ("coping strategies", "symptom management", "special suggestions") and preparate the intensive phase of therapy as the last step. First results of the evaluation of the training program are presented demonstrate the effectiveness and acceptance of the education program.

Disease Management↗
PubMed1999

How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay.

Total sleep deprivation (TSD) leads to an immediate amelioration of depressed mood in approximately 70 % of patients with the melancholic subtype of depression. The clinical utility of this procedure is limited, as the improvement usually subsides after the next night of sleep. In the present study, 40 depressed inpatients, being free of psychoactive medication for at least 7 days and who had responded to a TSD were then distributed (according to a matched-pair design) to a sleep phase advance (SPA = time in bed scheduled from 1700-2400 hrs) or a sleep phase delay (SPD = time in bed from 0200-0700 hrs) with a succeeding shift back (for one hour in the SPA group per day) respectively shift forward (for 30 minutes in the SPD group per day), until the initial sleep phase (2300-0600 hrs) was reached after seven days again. Based on previous observations it was hypothesized that a phase advance of the sleep period should prevent responders to TSD from relapsing. Whereas 75% of the TSD responders were stabilized by the phase advanced condition and did not relapse over a period of seven days, only 40% of the patients in the phase delayed condition did not relapse. Polysomnography during the course of the study gave no evidence that the unusual sleep schedules caused prolonged sleep deprivation. Abnormalities of REM sleep persisted both in the clinical responders and non-responders after the sleep wake manipulation. It is concluded that the clinical effectiveness of TSD can be significantly improved by combining TSD with a following phase advance of the sleep period.

Adult↗
PubMed1999

Independent sleep EEG slow-wave and spindle band dynamics associated with 4 weeks of continuous application of short-half-life hypnotics in healthy subjects.

OBJECTIVES: Habituation and adverse withdrawal reactions after prolonged medication with benzodiazepine (BZ) hypnotics are believed to play a role in dose escalation and the development of dependence. METHODS: In the current sleep EEG study in 43 healthy male subjects, the known property of BZ- and similar hypnotics to change the NREM sleep EEG spectrum is utilized for a detailed quantitative analysis across 4 weeks of continuous medication and a subsequent two-week withdrawal period. The BZ hypnotic triazolam and the non-BZ hypnotics zopiclone and zolpidem, differing in pharmacological properties and reported adverse effects, were examined in parallel to a placebo group. RESULTS: Reliably occurring spectral effects in the sleep stage 2 EEG were found in the 3 frequency bands 0.8-5 Hz, 5-10 Hz and 10-15 Hz. All 3 hypnotics showed the typical 'benzodiazepine signature', a 10-15 Hz increase and lower-frequency (<10 Hz) suppression relative to the preceding drug-free night. However, these effects developed differently across the first medication night, across the 4 medication weeks and after withdrawal: While the 5-10 Hz effect covaried with the blood presence of the drugs as estimated from the known plasma half-lifes, showed habituation and a rebound after withdrawal, the 10-15 Hz power increased across medication days and showed no rebound. Effects in the 0.8-5 Hz band in the first medication night correlated with the decrease of sleep efficiency at later withdrawal for triazolam and zolpidem.

Adult↗
PubMed1998

Magnesium therapy for periodic leg movements-related insomnia and restless legs syndrome: an open pilot study.

Periodic limb movements during sleep (PLMS), with or without symptoms of a restless legs syndrome (RLS), may cause sleep disturbances. The pharmacologic treatments of choice are dopaminergic drugs. Their use, however, may be limited due to tolerance development or rebound phenomena. Anecdotal observations have shown that oral magnesium therapy may ameliorate symptoms in patients with moderate RLS. We report on an open clinical and polysomnographic study in 10 patients (mean age 57 +/- 9 years; 6 men, 4 women) suffering from insomnia related to PLMS (n = 4) or mild-to-moderate RLS (n = 6). Magnesium was administered orally at a dose of 12.4 mmol in the evening over a period of 4-6 weeks. Following magnesium treatment, PLMS associated with arousals (PLMS-A) decreased significantly (17 +/- 7 vs 7 +/- 7 events per hour of total sleep time, p < 0.05). PLMS without arousal were also moderately reduced (PLMS per hour of total sleep time 33 +/- 16 vs 21 +/- 23, p = 0.07). Sleep efficiency improved from 75 +/- 12% to 85 +/- 8% (p < 0.01). In the group of patients estimating their sleep and/or symptoms of RLS as improved after therapy (n = 7), the effects of magnesium on PLMS and PLMS-A were even more pronounced. Our study indicates that magnesium treatment may be a useful alternative therapy in patients with mild or moderate RLS-or PLMS-related insomnia. Further investigations regarding the role of magnesium in the pathophysiology of RLS and placebo-controlled studies need to be performed.

Aged↗
PubMed1998

Cognitive frontal lobe dysfunction in obsessive-compulsive disorder.

BACKGROUND: There is evidence that dysfunction within associative frontostriatal circuits represents a feature of obsessive-compulsive disorder (OCD). Previous neuropsychologic studies have yielded diverging results, which may in part be explained by differences in the selection of subjects and methods. The present study focused on the question of cognitive frontal lobe performance in OCD. METHODS: Twenty-nine unmedicated OCD patients were compared to a double-size control group of normal subjects matched individually for age, sex, and intelligence. A series of 12 neuropsychologic tests was applied, most of which are thought to be sensitive to different aspects of cognitive frontal lobe function. RESULTS: OCD patients were unimpaired at tests of abstraction, problem solving, set-shifting, response inhibition, active memory search, and choice reaction speed. Deficits of approximately one standard deviation were observed at timed tests of verbal and nonverbal fluency, attentional processing, and weight sorting. CONCLUSIONS: OCD patients exhibited selective deficits in tasks involving controlled attentional processing and self-guided, spontaneous behavior. We discuss a link between this neuropsychologic profile and dysfunctioning within the anterior cingulate, but not the dorsolateral prefrontal circuit.

Adolescent↗
PubMed1998

Impact of experimentally induced serotonin deficiency by tryptophan depletion on sleep EEG in healthy subjects.

The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism. Because serotonin is involved in sleep regulation and the regulation of affective states, we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients. A total of 12 healthy subjects (mean age 34 +/- 3 years) had eight polysomnograms, divided in two blocks of 4 consecutive nights. After one adaptation and 1 baseline night, subjects received a low-protein diet on day 3 and 4 until midday. On day 4 at 18.00 h, they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan (placebo control) in randomized and double-blind order, resulting in an 85% decrease (tryptophan depletion) and a 144% increase (placebo control) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo, significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement (REM) density compared with baseline. REM latency was not altered, however the first and second REM period interval were significantly shorter after tryptophan depletion. This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep.

Adult↗
PubMed1998

A 19-h spontaneous sleep period in idiopathic central nervous system hypersomnia.

Reports of prolonged sleep periods in idiopathic central nervous system hypersomnia, as shown by ad libitum sleep recordings, are rare. A patient with idiopathic hypersomnia with extremely long sleep periods and sleep drunkenness after awakening is described. Polysomnographic recordings showed a spontaneous sleep period of 19.4 h and a normal Multiple Sleep Latency Test. These polysomnographic findings are clearly abnormal but essentially different form those of narcolepsy. Unlike narcolepsy, 'idiopathic hypersomnia' does not seem to be a distinct clinical entity but a category for different heterogenous subtypes.

Adolescent↗
PubMed1998

Sleep and the cholinergic rem sleep induction test in patients with primary alcoholism.

Sleep disturbances of alcoholics while actively drinking and at the beginning of, and during, abstinence were frequently reported. Recently, Gillin et al. (1994) showed that a high "REM sleep pressure" at the time of admission to a 1-month inpatient alcohol treatment program predicted the relapse in nondepressed patients with primary alcoholism at 3 months following hospital discharge. We investigated 24 patients with primary alcoholism after 2-3 weeks abstinence in the sleep laboratory; in 15 of these patients the cholinergic REM sleep induction test (CRIT) with 10 mg galanthamine was performed additionally. In comparison with an age- and sex-matched healthy control group, patients had a heightened "REM sleep pressure" including shortened REM latency and increased REM density. A decrease of serotonergic neurotransmission is proposed as being the neurochemical mechanism to explain the results in alcoholic subjects. Follow-up investigations will clarify whether the sleep abnormalities in alcoholism are state- or trait-markers and whether they are suitable to predict the relapse risk.

Adult↗
PubMed1998

Combination of behaviour therapy with fluvoxamine in comparison with behaviour therapy and placebo. Results of a multicentre study.

BACKGROUND: We investigated whether the combination of multi-modal behaviour therapy (BT) with fluvoxamine is superior to BT and placebo in the acute treatment of severely ill in-patients with obsessive-compulsive disorder (OCD). METHOD: In a randomised, double-blind design, 30 patients were treated for nine weeks with BT plus placebo and 30 patients with BT plus fluvoxamine (maximum dosage 300 mg, mean dose 288.1 mg). BT included exposure with response prevention, cognitive restructuring and development of alternative behaviours. RESULTS: Both groups showed a highly significant symptom reduction after treatment. There were no significant differences between the groups concerning compulsions. Obsessions were significantly more reduced in the fluvoxamine and BT group than in the placebo and BT group. Furthermore, the group BT plus fluvoxamine showed a significantly higher response rate (87.5 v. 60%) according to a previously defined response criterion. Severely depressed patients with OCD receiving BT plus placebo presented a significantly worse treatment outcome (Y-BOCS scores) than all other groups. CONCLUSIONS: The results suggest that BT should be combined with fluvoxamine when obsessions dominate the clinical picture and when a secondary depression is present.

Adult↗
PubMed1997

1H-magnetic resonance spectroscopy in obsessive-compulsive disorder: evidence for neuronal loss in the cingulate gyrus and the right striatum.

We compared 12 patients with obsessive-compulsive disorder (OCD) and six control subjects by 1H-magnetic resonance spectroscopy. Significantly lower relative N-acetyl-aspartate (NAA) levels were found in the right striatum of OCD patients, as well as a decrease of anterior cingulate NAA that correlated with severity of illness. Age and sex were correlated to striatal NAA levels.

Adult↗
PubMed1997

Sleep deprivation combined with consecutive sleep phase advance as a fast-acting therapy in depression: an open pilot trial in medicated and unmedicated patients.

OBJECTIVE: The authors' goal was to test the hypothesis that the antidepressant effect of total sleep deprivation can be maintained by initially avoiding sleep during a supposedly "critical" time period in the early morning. METHOD: They studied 33 inpatients with major depression, melancholic type, all of whom responded positively to total sleep deprivation. Twelve of the patients were men and 21 were women; their mean age was 46.7 years (SD = 13.7). After total sleep deprivation, the patients started a sleep schedule from 5:00 p.m. to 12:00 midnight, which then was shifted back by 1 hour each day until a sleep time of 11:00 p.m. to 6:00 a.m. was reached. RESULTS: Twenty (61%) of the 33 patients who responded to total sleep deprivation with an improved state of mood maintained this improvement during sleep phase advance therapy. Drug-free and medicated patients did not differ from each other. CONCLUSIONS: The rapid amelioration of mood observed with total sleep deprivation can be preserved with a succeeding phase shift of the sleep period.

Antidepressive Agents↗