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Biomedical subjects

J B Aldenhoff

Publications and source records attributed to J B Aldenhoff.

At least 19 recordsLinked to original sources
PubMed2006

Improvement of cognitive functions in chronic schizophrenic patients by recombinant human erythropoietin.

Schizophrenia is increasingly recognized as a neurodevelopmental disease with an additional degenerative component, comprising cognitive decline and loss of cortical gray matter. We hypothesized that a neuroprotective/neurotrophic add-on strategy, recombinant human erythropoietin (rhEPO) in addition to stable antipsychotic medication, may be able to improve cognitive function even in chronic schizophrenic patients. Therefore, we designed a double-blind, placebo-controlled, randomized, multicenter, proof-of-principle (phase II) study. This study had a total duration of 2 years and an individual duration of 12 weeks with an additional safety visit at 16 weeks. Chronic schizophrenic men (N=39) with defined cognitive deficit (>or=1 s.d. below normal in the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)), stable medication and disease state, were treated for 3 months with a weekly short (15 min) intravenous infusion of 40,000 IU rhEPO (N=20) or placebo (N=19). Main outcome measure was schizophrenia-relevant cognitive function at week 12. The neuropsychological test set (RBANS subtests delayed memory, language-semantic fluency, attention and Wisconsin Card Sorting Test (WCST-64) - perseverative errors) was applied over 2 days at baseline, 2 weeks, 4 weeks and 12 weeks of study participation. Both placebo and rhEPO patients improved in all evaluated categories. Patients receiving rhEPO showed a significant improvement over placebo patients in schizophrenia-related cognitive performance (RBANS subtests, WCST-64), but no effects on psychopathology or social functioning. Also, a significant decline in serum levels of S100B, a glial damage marker, occurred upon rhEPO. The fact that rhEPO is the first compound to exert a selective and lasting beneficial effect on cognition should encourage new treatment strategies for schizophrenia.

Adult↗
PubMed2002

[Current standing of forensic psychotherapy in Germany].

Although treatment of inmates already has got a long tradition in Germany, forensic psychotherapy is - especially outside the so-called German "Massregelvollzug" - only at its beginnings, and consistent theories about delinquency and treatment programmes have not yet been established. While international studies show high prevalence of mental disorders in prisons (up to 60 - 70 %), in Germany even basic epidemiological data about the prevalence of mental disorders among inmates is still missing. Thus, the need for psychotherapy can only be roughly estimated. Ethical implications regarding the self-image, an ambivalent assignment for treatment (given by society) and a recent tightening of German law create a difficult framework for forensic psychotherapy, complicating the establishment as well as the evaluation of new treatment programmes, especially since many people still doubt the efficiency of forensic psychotherapy for delinquents despite convincing counter-evidence. It seems obvious that in Germany much research has to be done in the fields of epidemiology as well as in forensic psychotherapy in order to gain basic data and to be then able to provide effective psychotherapeutic treatment facilities aiming at the needs of mentally disturbed offenders.

Crime↗
PubMed2001

Polysomnographic findings in nights preceding a migraine attack.

Sleep recordings were performed in eight patients to analyse sleep alterations preceding migraine attacks. Polysomnographic recordings from nights before an attack were compared with nights without following migraine. We analysed standard sleep parameters and electroencephalogram (EEG) power spectra. The main findings preceding migraine attacks were a significant decrease in the number of arousals, a decrease in rapid eye movement (REM) density, a significant decrease of beta power in the slow wave sleep, and a decrease of alpha power during the first REM period. The results suggest a decrease in cortical activation during sleep preceding migraine attacks. According to the models of sleep regulation, alterations in the function of aminergic or cholinergic brainstem nuclei have to be discussed.

Electroencephalography↗
PubMed2001

[Zolpidem: the risk of tolerance and dependence according to case reports, systematic studies and recent molecularbiological data].

Our group as well as about 20 other publications report cases of dependence from zolpidem. Furthermore, there is epidemiological and polysomnographic evidence that there is a risk for tolerance and dependence for zolpidem although lower than in the case of benzodiazepines. Recent molecularbiological findings offer interesting data in this respect. Whereas in the recommended dose range zolpidem almost exclusively binds to the alpha(1) subunit of the GABA(A) receptor associated with sleep promotion, in higher doses it also binds the alpha(2), alpha(3) and alpha(5) subunits typically targeted by benzodiazepines and associated with anxiolytic effects. Moreover, because age, gender and alcohol were shown to significantly affect expression of these subunits in individual brain regions, dosage and duration of treatment with zolpidem as well as age, gender and additional consumption of alcohol, a history of abuse and dependence might play a role in the development of tolerance and dependence in individual patients.

Animals↗
PubMed2000

[Biological mechanisms in the psychotherapy of depression].

The question concerning biological changes during psychotherapy can be approached in the context of depressive disorders. In this sphere several clearly defined specific treatments are available with broad evidence for their effectiveness. Furthermore, detailed theories about the biological mechanisms in the context of depression are available. Important impulses for the understanding of the question focussed by this article were initiated by the research on placebos. Based on the evidence supplied by this research, the question can be discussed whether psychotherapy should be considered as a trigger for the self-healing tendencies of an organism.

Depressive Disorder↗
PubMed1999

The calcium response of human T lymphocytes is decreased in aging but increased in Alzheimer's dementia.

BACKGROUND: A significant increase in the [Ca2+]i response of single T lymphocytes to mitogenic stimulation with phytohemagglutinin is reported for 27 Alzheimer patients compared with 27 healthy gender- and age-matched control subjects, regardless of gender. METHODS: The [Ca2+]i signals of T lymphocytes were assessed using the Fura-2-AM method. RESULTS: In Alzheimer's disease (AD) the reaction pattern is similar to that seen in a group of 27 young healthy control subjects who exhibited a marked [Ca2+]i rise after stimulation. During normal aging the reaction pattern of T cells is significantly attenuated in comparison to that found in young subjects. In healthy control subjects differences in age-related changes in calcium homeostasis are highly significant among women, young women showing the most intense cell response. CONCLUSIONS: The elevation of [Ca2+]i appears to be a prerequisite for apoptosis, which is suggested to be involved in the neuronal death occurring in AD. An increased [Ca2+]i in AD is consistent with processes leading to neurodegeneration in AD.

Adult↗
PubMed1996

K+ currents of human T-lymphocytes are unaffected by Alzheimer's disease and amyloid beta protein.

Alterations of Ca2+ homeostasis have been reported for both fibroblasts and T-lymphocytes of patients with Alzheimer's disease (AD). Considering the importance of K+ conductances for the cellular Ca2+ regulation and the recently reported absence of a K+ channel in Alzheimer fibroblasts, we investigated K+ currents in T-lymphocytes of patients with AD. In addition, the finding that amyloid beta protein affects the Ca2+ signal of T-lymphocytes and the function of K+ channels in fibroblasts prompted us to study a possible influence of amyloid beta protein fragments on K+ channels of T-lymphocytes. Our data, obtained by means of the whole-cell patch-clamp configuration on freshly isolated T-lymphocytes, indicate that K+ channels of these cells do not present any functional deficit in AD, and amyloid beta protein does not mediate an alteration of their currents.

Alzheimer Disease↗
PubMed1995

Mitogen stimulated rise of intracellular calcium concentration in single T lymphocytes from patients with major depression is reduced.

1. The authors investigated the signal transduction in T-lymphocytes as a peripheral model for central neurons. 2. Intracellular free calcium concentration [Ca2+]i was measured using fura 2 in T-lymphocytes from 6 patients with major depression during and after depression and from 6 healthy controls. Patients were treated with interpersonal therapy (IPT) but not with psychotropic medication. 3. Phytohemagglutinin (PHA) triggers an oscillatory [Ca2+]i signal in human T-lymphocytes. This implies two mechanisms for [Ca2+]i regulation: inositol phophate (IP) mediated release from intracellular stores and [Ca2+]i influx from the extracellular medium. 4. PHA stimulates 49% of T cells from controls but only 17% of T cells from depressed patients. This finding explains previous results from cells in suspension indicating that [Ca2+]i signals after PHA-stimulation are reduced in cells from depressed patients. 5. Cells from depressed patients show less [Ca2+]i oscillations. Normal oscillation patterns are restored after clinical recovery from depression. 6. Thus altered [Ca2+]i oscillations in T-lymphocytes are a state phenomenon and may give us clues where to search for altered cellular mechanisms during depression.

Adult↗
PubMed1994

Cytosolic free [Ca2+] in single T-lymphocytes from depressed patients and healthy controls.

Human lymphocytes are widely used as peripheral models for central neurones. Alterations in immune function have been reported in depressed patients, e.g. mitogen-induced proliferation is impaired during depression. One possible causative mechanism could be altered [Ca2+]i regulation. Phytohaemagglutinin (PHA)-induced rise of [Ca2+]i has been found to be diminished in lymphocyte suspensions from depressed patients (Ecker et al., this issue). We measured PHA-induced rise of [Ca2+]i in single Fura-2 AM-loaded T11+ lymphocytes of patients with major depression and controls to further analyse [Ca2+]i regulation in depression. The [Ca2+]i of resting lymphocytes was 57 +/- 2 nmol/l (mean +/- SEM). There was no difference in resting [Ca2+]i of resting lymphocytes of patients and controls. PHA evoked an increase of [Ca2+]i an 7 out of 14 cells from control subjects up to 400-500 nmol/l. In contrast, only 4 out of 13 cells from depressed patients showed an increase of [Ca2+]i up to 200 nmol/l. In a small fraction of cells from both groups the [Ca2+]i signal is oscillating. Our preliminary data confirm alteration of [Ca2+]i regulation in lymphocytes of depressed patients.

Adult↗
PubMed1994

Influence of the cholinesterase inhibitor galanthamine hydrobromide on normal sleep.

Evidence from animal experiments has suggested that the triggering and maintenance of rapid eye movement (REM) sleep is mainly under the control of cholinergic neurons in the brain stem. Correspondingly, studies in humans have demonstrated that the application of cholinergic agonists or cholinesterase inhibitors provokes an earlier onset of REM sleep. The present study investigated the influence of galanthamine hydrobromide, a reversible cholinesterase inhibitor, on REM sleep regulation in 18 healthy volunteers. After an adaptation night, the subjects were given two doses of galanthamine (10 mg and 15 mg) or placebo at 10 p.m. in a randomized double-blind design. Both doses of galanthamine shortened REM latency (with statistical significance depending on the definition of REM latency used), increased REM density, and reduced slow wave sleep mainly in the first non-REM cycle. Higher doses of galanthamine (15 mg) seem to be accompanied by unwanted side effects that warrant the application of a peripheral antidote. These results are comparable to those for other cholinomimetics and stress the usefulness of galanthamine for pharmacological challenge studies in healthy subjects and depressed patients.

Adult↗
PubMed1994

Functional properties of the brain during sleep under subchronic zopiclone administration in man.

Zopiclone, a non-benzodiazepine, has been shown to be efficient in the treatment of transient, short-term or chronic sleep disorders. Apart from its hypnotic effects zopiclone has anxiolytic, anticonvulsant and myorelaxant properties and is therefore hardly distinguishable from benzodiazepines. Dependence liability and discontinuation effects have been reported to be less pronounced. Therefore zopiclone seems to be a hypnotic drug which may cause fewer side effects than conventional benzodiazepines. From the electrophysiological point of view one requires from a hypnotic drug the induction of a physiological sleep pattern as well as no alterations of information processing by the brain. The aim of the present study was to investigate the subchronic effect of zopiclone medication on some functional properties of the sleep EEG in healthy subjects. In order to get better insight into the principles of information processing by the brain during sleep and its alterations under the influence of zopiclone we applied some tools from linear system theory to sleep EEG data. For this purpose we investigated late components of auditory and visual evoked potentials during different sleep stages and calculated from these the so-called amplitude-frequency characteristic of the brain. This function describes the relationship between an input and the output of the investigated system. The main advantage of this kind of analysis is that it enables one to detect functional differences during sleep stages. This information can hardly be obtained from conventional spectral analysis. As a result we could demonstrate that under subchronic zopiclone medication no quantitative or qualitative alterations of the functional sleep EEG properties concerning the transfer properties of the brain under auditory and visual stimulation were detectable.

Adult↗
PubMed1993

Estimation of the dimensionality of sleep-EEG data in schizophrenics.

Deterministic chaos could be regarded as a healthy flexibility of the human brain necessary for correct neuronal operations. Several investigations have demonstrated that in healthy subjects the dimensionality of REM sleep is much higher than that of slow wave sleep (SWS). We investigated the sleep-EEG of schizophrenic patients with methods from nonlinear system theory in order to estimate the dynamic properties of CNS. We hypothesized that schizophrenics would reveal alterations of their dynamic EEG features indicating impaired information processing. In 11 schizophrenic patients, the EEG's dimensionality during sleep stages II and REM was reduced. We suggest that such lower dimensional chaotic processes might be associated with an overloading of neuronal networks during sleep and therefore the psychopathology of schizophrenics might be due to impaired complexity of their EEG's dynamics.

Adult↗
PubMed1993

The influence of lorazepam medication upon the transfer properties of the brain during sleep in man.

In order to get better insight into the principles of information processing by the brain during sleep and its alterations under the influence of drugs we applied some tools from linear system theory to sleep EEG data. We investigated late components of auditory and visually evoked potentials (AEPs and VEPs) during different sleep stages and calculated from these the so-called amplitude-frequency characteristics (AFC). The main advantage of this analysis is that it enables one to detect functional differences during different sleep stages. This information can hardly be obtained by conventional spectral analysis. The result of our investigation was that the transfer properties of the brain during sleep were extremely different and that lorazepam medication not only resulted in quantitative alterations of the sleep profile but mainly in highly significant alterations of the functional properties of sleep.

Acoustic Stimulation↗
PubMed1992

Nimodipine in acute alcohol withdrawal state.

The effect of the calcium channel blocker, nimodipine, in acute alcohol withdrawal was investigated in a randomized, placebo controlled, double blind study. Thirty-two male patients with a history of alcohol dependence according to DSM-III criteria, but no other substance abuse, were included. A new rating instrument which fulfilled theoretical test criteria was applied to determine the severity of the alcohol withdrawal state. The patients received nimodipine or a placebo on four separate occasions (4 x 60 mg) and, in addition, clomethiazole, according to a standardized procedure. Our investigation has shown that, in the first 48-72 h of alcohol withdrawal, both groups consumed similar amounts of additional clomethiazole medication. Thus, no significant effect of nimodipine on the acute alcohol withdrawal state could be demonstrated. There was some tendency for nimodipine to ameliorate psychosensory dysfunction.

Acute Disease↗
PubMed1992

A nonlinear approach to brain function: deterministic chaos and sleep EEG.

In order to perform a nonlinear dimensional analysis of the sleep electroencephalogram (EEG), we applied an algorithm proposed by Grassberger and Procaccia to calculate the correlation dimension D2 of different sleep stages under Lorazepam medication versus placebo. This correlation dimension characterizes the dynamics of the sleep EEG and it estimates the degrees of freedom of the signal under study. We demonstrate that slow-wave sleep depicts a much smaller dimensionality than light or rapid eye movement (REM) sleep, and that Lorazepam does not alter the EEG's dimensionality except in stage II and REM.

Adult↗
PubMed1989

Computed tomography in depression: association between ventricular size and psychopathology.

The relationship between psychopathology and brain alterations, measured by computed tomography (CT), was investigated in 44 depressed patients. Comparisons of ventricle-brain ratio (VBR) between "endogenous" vs. "nonendogenous" subgroups, classified by six distinct diagnostic systems, revealed no significant differences. The VBR and the width of the third ventricle correlated significantly with scores on the Brief Psychiatric Rating Scale, the Global Assessment Scale, the Bech-Rafaelsen Melancholia Scale, the Rating for Emotional Blunting, and the Scale for the Assessment of Negative Symptoms, but not with scores on the Hamilton Rating Scale for Depression and the Hamilton Rating Scale for Anxiety. Item analyses of the Bech-Rafaelsen Melancholia Scale revealed that retardation-related items were most significantly correlated with ventricular size. The wider diameter of the third ventricle in psychotic patients was associated with higher scores on retardation in the psychotic subgroup, whereas the greater distances of both Sylvian fissures showed no relationship to psychomotor retardation. No significant correlations were found between CT values and anxiety, suicidal impulses, somatic complaints, and sleep disturbances.

Adult↗
PubMed1989

Imbalance of neuronal excitability as a cause of psychic disorder.

Electrical activity of neurons is characterized by an equilibrium between excitation and inhibition, maintained by negative feedback mechanisms at the cellular, synaptic and neurohumoral level. A central mechanism is the interaction between excitatory calcium currents and inhibitory potassium currents, linked by intracellular calcium concentration. These conductances are located in the somato-dendritic part of the neuron and fundamentally influence spontaneous activity and the processing of synaptic input. The electrical equilibrium is altered by different neuromodulators, such as biogenic amines, peptides, and steroids and by several drugs. Neuromodulatory desequilibration towards increased excitability may occur task-related in a transient way or in a cascade of desequilibrating and partially compensating mechanisms, producing distinct grades of functional impairment. Pharmacotherapeutic principles interfere with this process. It is postulated, that the imbalance between excitation and inhibition is a central factor in the origin of psychic disorder.

Animals↗