C Lange-Asschenfeldt

Heinrich-Heine-Universität Düsseldorf, Düsseldorf, North Rhine-Westphalia, Germany

Are you C Lange-Asschenfeldt?

Claim your profile

Publications (9)7.15 Total impact

  • Article: [Psychopharmacotherapy in patients with cardiovascular diseases.]
    J Cordes, C Lange-Asschenfeldt, C Hiemke, K G Kahl
    [show abstract] [hide abstract]
    ABSTRACT: Increased cardiometabolic morbidity and increased overall mortality has been observed in patients with severe mental disorders. Therefore, cardiometabolic safety is an important issue in the treatment of patients with psychiatric disorders, in particular in patients with comorbid cardiometabolic diseases. Frequent adverse side effects include disturbances of lipid and glucose metabolism, body weight changes and alterations of the QTc interval. Dependent on the particular substance used and on factors concerning individual vulnerability, these side effects vary in relative frequency. Therefore, regular monitoring is recommended including ECG. Furthermore, interactions between different medicaments may occur, either leading to enhanced or decreased drug concentrations. Prior to psychopharmacological treatment, proper cardiological treatment is recommended. The management of cardiovascular risks under psychopharmacology requires interdisciplinary cooperation between the cardiologist, general practitioner and psychiatrist.
    Der Internist 10/2012; · 0.30 Impact Factor
  • Article: Antidepressive Therapie bei koronarer Herzkrankheit
    C. Lange-Asschenfeldt, F. Lederbogen
    [show abstract] [hide abstract]
    ABSTRACT: Die Depression gilt als unabhängiger Risikofaktor für die Entstehung der koronaren Herzkrankheit (KHK). Bei Patienten mit bestehender KHK ist ihr Vorliegen mit einem erhöhten Risiko für weitere kardiale Ereignisse und gesteigerte Mortalität verbunden. Bis zu 20% der Überlebenden eines akuten Myokardinfarktes erfüllen die diagnostischen Kriterien für eine Major-Depression, deren Anwesenheit mit einem 5fach erhöhten kardialen Mortalitätsrisiko innerhalb von 6Monaten einhergeht. Herzpatienten mit depressiver Komorbidität bedürfen einer intensiven Betreuung, um einerseits die affektive Erkrankung angemessen zu behandeln und andererseits das kardiale Risiko zu mindern. Die antidepressive Therapie sollte entsprechend den etablierten Leitlinien erfolgen; besonders ist darauf zu achten, unerwünschte kardiale Nebenwirkungen zu vermeiden. In dieser Übersicht beschreiben wir die pathophysiologische und prognostische Bedeutung von komorbider Depression und KHK und diskutieren Nutzen und Risiken verfügbarer Behandlungsoptionen, insbesondere verschiedener Klassen von Antidepressiva und Psychotherapie, unter Berücksichtigung neuerer Studienergebnisse. Depression is considered an independent risk factor for coronary artery disease (CAD) and other vascular conditions. Moreover, comorbid depressive disorder in CAD patients carries an increased risk of cardiac events and mortality. Among survivors of acute myocardial infarction, up to 20% meet diagnostic criteria for major depression, the presence of which carries a fivefold increased risk of cardiac death within 6 months. Heart patients with depressive comorbidity require particular care for both adequate treatment of their affective disorder and reduction of their cardiac risk. Antidepressant treatment must follow established guidelines; special care is needed to avoid cardiac side effects. In this review, we discuss the pathophysiological and prognostic significance of comorbid depression in CAD and weigh risks and benefits of available treatment options – particularly different drug classes and psychotherapy – in light of recent study results. SchlüsselwörterDepression–Kardiovaskuläres Risiko–Koronare Herzerkrankung–Mortalität–Antidepressiva KeywordsDepression–Cardiovascular risk–Coronary artery disease–Mortality–Antidepressive Agents
    Der Nervenarzt 05/2012; 82(5):657-666. · 0.68 Impact Factor
  • Article: [Antidepressant therapy in coronary artery disease].
    C Lange-Asschenfeldt, F Lederbogen
    [show abstract] [hide abstract]
    ABSTRACT: Depression is considered an independent risk factor for coronary artery disease (CAD) and other vascular conditions. Moreover, comorbid depressive disorder in CAD patients carries an increased risk of cardiac events and mortality. Among survivors of acute myocardial infarction, up to 20% meet diagnostic criteria for major depression, the presence of which carries a fivefold increased risk of cardiac death within 6 months. Heart patients with depressive comorbidity require particular care for both adequate treatment of their affective disorder and reduction of their cardiac risk. Antidepressant treatment must follow established guidelines; special care is needed to avoid cardiac side effects. In this review, we discuss the pathophysiological and prognostic significance of comorbid depression in CAD and weigh risks and benefits of available treatment options - particularly different drug classes and psychotherapy - in light of recent study results.
    Der Nervenarzt 11/2010; 82(5):657-64; quiz 665-6. · 0.68 Impact Factor
  • Article: [Therapeutic options for weight management in schizophrenic patients treated with atypical antipsychotics].
    [show abstract] [hide abstract]
    ABSTRACT: Extensive, selective literature review of 2500 articles from the last years (up to December 2007) predominantly from Medline and Cochrane, using as search terms "antipsychotic or schizophrenia or individual drug names (amisulpride, aripiprazole, clozapine, olanzapine, quetiapine, risperidone, ziprasidone)" and the terms "BMI, weight gain, metabolic syndrome, diabetes, lipid(s), cholesterol, triglycerides" was conducted. Regardless of the advantages ascribed to atypical antipsychotics and the special effectiveness of clozapine in patients resistant to therapy and at risk for suicide, the probability of weight gain is considerably increased for some of these substances. Patients with schizophrenia have a considerably reduced life expectancy associated with an increased prevalence of cardiovascular risk factors. There is a lack of practical guidelines integrated into clinical psychiatric care for the management of cardiovascular risk factors. The monitoring of patients treated with atypics, which has been recommended in the APA/ADA Consensus Paper in light of these facts, is insufficiently established in clinical practice. A regular monitoring can convey self control and motivation to the patient. In the case of corresponding risk constellations further decisions regarding indication and therapy have to be considered. Especially patients with a high cardiovascular risk profile are highly recommended to participate in a weight-management program for prevention purposes. Such a special program should include elements of dietetic treatment and behaviour and exercise therapy. First controlled studies suggest an effective prevention of weight gain and metabolic changes when applying such a structured program. The practice oriented step by step concept presented here is meant to provide points of reference for the implementation of required medical and psychoeducative measures facilitating the management of weight and further cardiovascular risk factors in the context of psychiatric care in patients with schizophrenia.
    Fortschritte der Neurologie · Psychiatrie 11/2008; 76(12):703-14. · 0.74 Impact Factor
  • Article: Spatial performance in a complex maze is associated with persistent long-term potentiation enhancement in mouse hippocampal slices at early training stages.
    C Lange-Asschenfeldt, P Lohmann, M W Riepe
    [show abstract] [hide abstract]
    ABSTRACT: Long-term potentiation (LTP) and long-term depression (LTD) are principal reflections of synaptic plasticity that have been implicated in learning and memory. We have previously shown that spatial learning in a newly validated complex maze is accompanied by depression of hippocampal CA1 synaptic activity in hippocampal slices of trained mice ("behavioral LTD"). In the present study, we investigated whether behavioral LTD is accompanied by alterations of subsequent LTP induced by high-frequency stimulation (HFS). Moreover, we were interested in the time course of such alterations in relation to training stage. Animals underwent 1, 2, and 8 days of spatial training in the complex maze, respectively. Hippocampal slices were taken 24 h after the last training session. We found a simultaneous decrease of basal synaptic response and increase of HFS induced LTP magnitude compared with slices of untrained animals. Synaptic plasticity was not influenced by repeated running wheel exercise in an additional control group without spatial learning. The mentioned alterations occurred already after day 2 of maze exploration parallel to the most pronounced improvement of behavioral performance but did not change thereafter until day 8 despite further learning progress. They were also found when animals were trained for 2 days and kept at rest for a subsequent 6 days. In conclusion, spatial learning may be reflected by distinct and persistent measurable alterations of synaptic plasticity in hippocampal CA1 neurons at early training stages.
    Neuroscience 07/2007; 147(2):318-24. · 3.38 Impact Factor
  • Article: [Autoimmune functional disorders of the thyroid during interferon-beta-1b treatment in patients with multiple sclerosis. Case report and literature review].
    C Lange-Asschenfeldt, S Boor, G J Kahaly, F Thömke
    [show abstract] [hide abstract]
    ABSTRACT: Occurrence of thyroid autoimmunity and dysfunction following interferon alpha treatment of viral hepatitis and other diseases are known adverse effects and have been ascribed to the cytokine's general immunomodulatory and -activating properties. However, in spite of its extensive application, there have been few reports of such incidents during interferon beta (IFN-beta-1a/b) therapy, which is considered the standard treatment of relapsing-remitting multiple sclerosis (MS), and prospective studies have been published only recently. Here we present the case of a 38-year-old woman with Graves' disease including massive thyroid-associated ophthalmopathy appearing de novo following IFN-beta-1b therapy for MS. A literature search revealed an 11% (5% clinically overt) overall incidence of de novo thyroid dysfunction in IFN-beta-treated MS patients, mostly autoimmune hyperthyroidism. (Large-scale comparative studies for IFN-beta-1a are not available at present). Specific treatment but not necessarily discontinuation of IFN-beta-1b therapy was required in most cases. Female gender, pre-existing thyroid autoimmunity, and family history of thyroid disorders are presumable risk factors for thyroid dysfunction de novo during IFN-beta-1b treatment.
    Der Nervenarzt 07/2004; 75(6):589-94. · 0.68 Impact Factor
  • Article: Autoimmune Funktionsstörungen der Schilddrüse unter Interferon-ß-1b-Therapie bei Patienten mit Multipler Sklerose
    C. Lange-Asschenfeldt, S. Boor, G. J. Kahaly, F. Thömke
    [show abstract] [hide abstract]
    ABSTRACT: Thyreoidale Autoimmunitt bzw. Schilddrsendysfunktion unter Interferon--Therapie der chronischen Hepatitis C oder anderer Erkrankungen sind bekannte Nebenwirkungen und werden allgemein immunmodulatorischen und -aktivierenden Eigenschaften des Zytokins zugeschrieben. Trotz weit verbreiteter Anwendung existieren jedoch wenig Berichte solcher Ereignisse unter Interferon(IFNB-1a/b)-Therapie, der derzeitigen Standardbehandlung der schubfrmigen Multiplen Sklerose (MS), Verlaufsuntersuchungen sind erst seit kurzem bekannt. Wir beschreiben hier den Fall einer 38-jhrigen Patientin mit unter IFNB-1b-Behandlung de novo aufgetretenem Morbus Basedow mit ausgeprgter endokriner Ophthalmopathie. Die Literaturdurchsicht ergab eine Inzidenz von Schilddrsenfunktionsstrungen de novo bei IFNB-1b-behandelten MS-Patienten von 11% (5% klinisch manifest), v.a. Hyperthyreosen (vergleichende Untersuchungen zu IFNB-1a stehen in grerem Umfang derzeit noch nicht zur Verfgung). Eine spezifische Behandlung wurde in den meisten Fllen erforderlich, jedoch nicht notwendigerweise ein Therapieabbruch. Weibliches Geschlecht, vorbestehende thyreoidale Autoimmunitt sowie positive Familienanamnese hinsichtlich Schilddrsenerkrankungen scheinen Risikofaktoren fr das Auftreten von Schilddrsenfunktionsstrungen de novo unter IFNB-1b-Therapie zu sein.Occurrence of thyroid autoimmunity and dysfunction following interferon treatment of viral hepatitis and other diseases are known adverse effects and have been ascribed to the cytokines general immunomodulatory and -activating properties. However, in spite of its extensive application, there have been few reports of such incidents during interferon (IFN--1a/b) therapy, which is considered the standard treatment of relapsing-remitting multiple sclerosis (MS), and prospective studies have been published only recently. Here we present the case of a 38-year-old woman with Graves disease including massive thyroid-associated ophthalmopathy appearing de novo following IFN--1b therapy for MS. A literature search revealed an 11% (5% clinically overt) overall incidence of de novo thyroid dysfunction in IFN--treated MS patients, mostly autoimmune hyperthyroidism. (Large-scale comparative studies for IFN--1a are not available at present). Specific treatment but not necessarily discontinuation of IFN--1b therapy was required in most cases. Female gender, pre-existing thyroid autoimmunity, and family history of thyroid disorders are presumable risk factors for thyroid dysfunction de novo during IFN--1b treatment.
    Der Nervenarzt 05/2004; 75(6):589-594. · 0.68 Impact Factor
  • Article: [18F]Fluoroethylflumazenil: a novel tracer for PET imaging of human benzodiazepine receptors.
    [show abstract] [hide abstract]
    ABSTRACT: 5-(2'-[18F]Fluoroethyl)flumazenil ([18F]FEF) is a fluorine-18 labelled positron emission tomography (PET) tracer for central benzodiazepine receptors. Compared with the established [11C]flumazenil, it has the advantage of the longer half-life of the fluorine-18 label. After optimisation of its synthesis and determination of its in vitro receptor affinities, we performed first PET studies in humans. PET studies in seven healthy human volunteers were performed on a Siemens ECAT EXACT whole-body scanner after injection of 100-280 MBq [L8F]FEF. In two subjects, a second PET scan was conducted after pretreatment with unlabelled flumazenil (1 mg or 2.5 mg i.v., 3 min before tracer injection). A third subject was studied both with [18F]FEF and with [11C]flumazenil. Brain radioactivity was measured for 60-90 min p.i. and analysed with a region of interest-oriented approach and on a voxelwise basis with spectral analysis. Plasma radioactivity was determined from arterial blood samples and metabolites were determined by high-performance liquid chromatography. In human brain, maximum radioactivity accumulation was observed 4 +/- 2 min p.i., with a fast clearance kinetics resulting in 50% and 20% of maximal activities at about 10 and 30 min, respectively. [18F]FEF uptake followed the known central benzodiazepine receptor distribution in the human brain (occipital cortex >temporal cortex >cerebellum >thalamus >pons). Pretreatment with unlabelled flumazenil resulted in reduced tracer uptake in all brain areas except for receptor-free reference regions like the pons. Parametric images of distribution volume and binding potential generated on a voxelwise basis revealed two- to three-fold lower in vivo receptor binding of [18F]FEF compared with [11C]flumazenil, while relative uptake of [18F]FEF was higher in the cerebellum, most likely owing to its relatively higher affinity for benzodiazepine receptors containing the alpha6 subunit. Metabolism of [18F]FEF was very rapid. Polar metabolites represented about 50%-60% of total plasma radioactivity at 5 min and 80%-90% at 20 min p.i. Although [11C]flumazenil has some advantages over [18F]FEF (higher affinity, slower metabolism, slower kinetics), our results indicate that [18F]FEF is a suitable PET ligand for quantitative assessment of central benzodiazepine receptors, which can be used independently of an on-site cyclotron.
    European Journal of Nuclear Medicine 10/2001; 28(10):1463-70.
  • Article: Spatial performance in a complex maze is associated with persistent long-term potentiation enhancement in mouse hippocampal slices at early training stages
    C. Lange-Asschenfeldt, P. Lohmann, M.W. Riepe
    [show abstract] [hide abstract]
    ABSTRACT: Long-term potentiation (LTP) and long-term depression (LTD) are principal reflections of synaptic plasticity that have been implicated in learning and memory. We have previously shown that spatial learning in a newly validated complex maze is accompanied by depression of hippocampal CA1 synaptic activity in hippocampal slices of trained mice (“behavioral LTD”). In the present study, we investigated whether behavioral LTD is accompanied by alterations of subsequent LTP induced by high-frequency stimulation (HFS). Moreover, we were interested in the time course of such alterations in relation to training stage. Animals underwent 1, 2, and 8 days of spatial training in the complex maze, respectively. Hippocampal slices were taken 24 h after the last training session. We found a simultaneous decrease of basal synaptic response and increase of HFS induced LTP magnitude compared with slices of untrained animals. Synaptic plasticity was not influenced by repeated running wheel exercise in an additional control group without spatial learning. The mentioned alterations occurred already after day 2 of maze exploration parallel to the most pronounced improvement of behavioral performance but did not change thereafter until day 8 despite further learning progress. They were also found when animals were trained for 2 days and kept at rest for a subsequent 6 days. In conclusion, spatial learning may be reflected by distinct and persistent measurable alterations of synaptic plasticity in hippocampal CA1 neurons at early training stages.
    Neuroscience.

Institutions

  • 2007–2010
    • Heinrich-Heine-Universität Düsseldorf
      • Klinik und Poliklinik für Psychiatrie und Psychotherapie der HHU, Rheinische Kliniken Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2004
    • Johannes Gutenberg-Universität Mainz
      • Klinik und Poliklinik für Neurologie
      Mainz, Rhineland-Palatinate, Germany