Fortschritte der Neurologie · Psychiatrie最新文献

{"title":"[Treatment with psychopharmaca during pregnancy - part I: as little as possible but as much as necessary].","authors":"A Rohde, V M Dorsch, C Schaefer","doi":"10.1055/s-0031-1299314","DOIUrl":"https://doi.org/10.1055/s-0031-1299314","url":null,"abstract":"Der Text soll dem Leser einen Überblick über die aktuelle Studienlage zu Embryound Fetotoxizität der bei psychischen Störungen verwendeten Psychopharmaka vermitteln. Der Leser soll in der Lage sein, bei der Nutzen-Risiko-Abwägung bezüglich der Gabe eines Psychopharmakons in der Schwangerschaft die relevanten Aspekte zu berücksichtigen und neben möglichen Einflüssen auf das Kind die mütterlichen Faktoren einzubeziehen.","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"227-40"},"PeriodicalIF":0.6,"publicationDate":"2012-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1299314","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39971979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Neuropsychopharmaca influence the intracellular pH value of central neurons].","authors":"U Bonnet,&nbsp;M Wiemann","doi":"10.1055/s-0031-1273231","DOIUrl":"https://doi.org/10.1055/s-0031-1273231","url":null,"abstract":"<p><p>The intracellular pH (pHi) of neurons is tightly regulated, mainly by membrane-bound transporters acting as acid extruders or acid loaders. Regulation of pHi helps to control neuronal excitability, as increased bioelectric activity moderately lowers pHi and, in the sense of a negative feedback loop, intracellular acidosis mostly reduces neuronal excitability. Moreover, a change of pHi widely influences complex cellular functions. With respect to neuropsychopharmaca, little is known about whether or not they may affect neuronal H ( + )-homeostasis. To this aim, we tested several antipsychotics, antidepressants, anticonvulsants, and lithium for effects on neuronal pHi, using guinea pig hippocampal slice preparations in which CA 3 pyramidal neurons were loaded with the pHi-sensitive dye BCECF-AM. All antipsychotics, most antidepressants and about half of the anticonvulsants tested so far elicited reversible changes of neuronal pHi when applied at therapeutic and supratherapeutic concentrations. Although these results await confirmatory in vivo experiments, we believe that the pHi activity of neuropsychopharmaca needs further attention, especially when therapeutic mechanisms or even harmful side effects are discussed.</p>","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"201-12"},"PeriodicalIF":0.6,"publicationDate":"2012-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1273231","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40097215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Psychiatry and psychopathology of people with intellectual disability].","authors":"C-W Wallesch","doi":"10.1055/s-0031-1299324","DOIUrl":"https://doi.org/10.1055/s-0031-1299324","url":null,"abstract":"","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"129"},"PeriodicalIF":0.6,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1299324","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40153821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Stimulant and non-stimulant medication in current and future therapy for ADHD].","authors":"A G Franke,&nbsp;A Konrad,&nbsp;K Lieb,&nbsp;M Huss","doi":"10.1055/s-0031-1273223","DOIUrl":"https://doi.org/10.1055/s-0031-1273223","url":null,"abstract":"! The current pharmacotherapy for attention-deficit hyperactivity disorder (ADHD) is mainly based on the stimulant methylphenidate and to a small extent on amphetamines which are not approved in Germany. The only approved non-stimulant so far is atomoxetin (Strattera ® ), a norepinephrine reuptake inhibitor. There is no approved pharmacotherapy for adults. The aim of the available medication is a reduction of impulsivity, hyperactivity, and attention deficits. Neu-robiological correlates of these effects are still not fully understood, however, a functional implication of dopaminergic and noradrenergic systems is known. To date there is no disease-modifying therapy. The currently available substances have limitations due to the short half-life of stimulants, the unknown pathomechanisms, and the use of stimulants in developing brains with possible long-term side-effects. Moreover, the abuse potential of stimulants is still controversially discussed. The recently developed Lisdexamfetamin and SPD-465 have stimulant effects, too. A number of different developmental substances in preclinical and clinical phases show other mechanisms: SPD-503 represents an α 2 A-adrenozeptoragonist, ABT-089 and ABT-418 have partial agonistic effects to the α 4 β 2 -subtype of nicotinic acetylcholinre-ceptors, CX-717, -1739, -1942 and -1796 are glutamatergic α -amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid (AMPA)-receptor agonists and PF-3654746 exhibits antagonistic properties to histaminergic","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"130-40"},"PeriodicalIF":0.6,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1273223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mild cognitive impairment and depressive symptoms in patients with Wilson's disease under long-term therapy].","authors":"P Günther,&nbsp;W Hermann","doi":"10.1055/s-0031-1282016","DOIUrl":"https://doi.org/10.1055/s-0031-1282016","url":null,"abstract":"<p><strong>Introduction: </strong>Wilson's disease is a rare autosomal recessive disorder of hepatic copper transport leading to a biliary excretion inhibition of copper. Overloading of the metal mainly in the liver and basal ganglia leads not only to hepatic but also to extrapyramidal motor as well as psychiatric clinical symptoms. Cognitive dysfunction is often reported and patients suffer from additional depressive symptoms.</p><p><strong>Methods: </strong>In this study, a cognitive impairment profile with SIDAM (SISCO) including mini-mental state, digit span and the trail making test was performed in 32 patients with Wilson's disease (24 patients with the neurological form, 8 patients with the non-neurological form) undergoing long-term medicamentous therapy. The extent of neurological impairment was assessed in a neurology score. The Beck depression inventory (BDI) was used for the detection of depressive symptoms. Results of cognitive testing and BDI score were correlated with the results of the clinical investigation.</p><p><strong>Results: </strong>Median results of MMSE, SIDAM, part of digit span and trail-making test are significantly worse in patients with the neurological form of Wilson's disease. There is no significant difference in median results of BDI, although the number of patients with a score suggesting a mild depressive disorder is higher in the group with the neurological form. The median result of SIDAM was 52 (45-55) in the neurological form and 54 (53-55) points in the non-neurological form. There is no statistical significance in the correlation to the severity of the neurological score.</p><p><strong>Conclusions: </strong>Depressive symptoms and cognitive impairment in Wilson's disease are frequently reported by patients who are on long-term treatment. In particular, the ability to concentrate and undertake executive functions are affected in the neurological form of Wilson's disease while functions of memory are less impaired. Since movement disorders often have improved with therapy, additional observation of cognitive function and depressive disorders seems to be useful. However, mild cognitive impairment occurs independently of the severity of the neurological symptoms.</p>","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"149-53"},"PeriodicalIF":0.6,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1282016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40153822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Botulinum toxin in clinical neurology].","authors":"J Wissel,&nbsp;F Kempf","doi":"10.1055/s-0031-1299095","DOIUrl":"https://doi.org/10.1055/s-0031-1299095","url":null,"abstract":"Mehr als 20 Jahre nach dem ersten Einsatz von Botulinum-Neurotoxin Typ A in der klinischen Neurologie stellt die Substanz heute bei der Behandlung einer Vielzahl von Erkrankungen die symptomatische Therapie der Wahl dar. Mit der chronischen Migräne und der neurogen überaktiven Blase stehen 2 weitere Zulassungen für BoNT-A in Deutschland kurz bevor. Trotz dieser Erfolgsstory für die Patienten mit entsprechenden Indikationen und die Hersteller der verfügbaren Produkte muss die derzeitige Zulassungssituation einschließlich dem Regressgebaren der Kostenträger als unbefriedigend gelöst beschrieben werden. Bei erhöhtem Zeitaufwand für das Erlernen und Durchführen einer BoNT-Behandlung und der geringen Honorierung im Bereich der ambulanten Medizin muss derzeit leider auch von einer insg. unbefriedigenden Situation für die beteiligten Leistungserbringer gesprochen werden. Dieser Artikel soll trotz der beschriebenen Hindernisse über den Stand der Kunst der Anwendung von BoNT in der klinischen Neurologie und benachbarter Gebiete informieren und dadurch helfen, die Versorgungssituation der Patienten mit BoNT-Indikation zu verbessern. Grundlagen ! Molekulare Mechanismen Botulinumtoxin (BoNT) ist ein Produkt des Bakteriums Clostridium botulinum, einem obligat anaeroben, grampositiven Stäbchen. Der klinische Effekt des Toxins besteht in der dosisabhängigen Denervierung cholinerger Synapsen in Muskeln und Drüsen. Die Struktur des Toxins ist gekennzeichnet durch das Neurotoxin, bestehend aus einer leichten und einer schweren Kette sowie einen nicht toxischen Proteinkomplex. Sieben verschiedene Botulinumtoxine sind bekannt; die Nomenklatur umfasst die Typen A– G. Zugelassen für den medizinischen Gebrauch sind 3 Präparate des Neurotoxins Typ A (Onabotulinumtoxin A=Onabotulinumtoxin A; Dysport® =Abotulinumtoxin A; Xeomin®= Incobotulinumtoxin A) und 1 Präparat des Neurotoxins Typ B (NeuroBloc® =Rimabotulinumtoxin B). Gemeinsam ist den verschiedenen Typen die Aufnahme in die Nervenendigung über die schwere Toxinkette und die Unterbrechung der Azetylcholinfreisetzung durch die leichte Toxinkette. BoNT-A und BoNT-B binden jeweils an unterschiedliche im Azetylcholinvesikel lokalisierte Rezeptoren: BoNT-A an SV2 und BoNT-B an Synaptotagmin [1]. Das intrazelluläre Substrat der leichten Kette ist je nach Toxintyp verschieden. BoNT-A spaltet das Enzym SNAP25, BoNT-B Syntaxin und führt damit zum vorübergehenden Sistieren der Azetylcholinausschüttung [1]. Als bakterielles Protein kann BoNT im menschlichen Körper immunogen wirken. Klinisch kann es hierdurch infolge der Injektion selten zu einer Reaktion mit grippeähnlichen Symptomen führen. Insbesondere kann eine Immunantwort durch Bildung von Toxinantikörpern und Neutralisierung des injizierten Toxinkomplexes zum Therapieversagen führen. Mit dem Maus-Diaphragma-Test steht ein Laborverfahren","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"167-78; quiz 179"},"PeriodicalIF":0.6,"publicationDate":"2012-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1299095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40153823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retrospective analysis of routine-MRI and correlation with aetiology of dementia, severity and neuropsychology in a memory-clinic population].","authors":"S Merkle,&nbsp;S Kreil,&nbsp;G Suttner,&nbsp;M Doelken,&nbsp;A Dörfler,&nbsp;T Richter-Schmidinger,&nbsp;J Kornhuber,&nbsp;M Weih","doi":"10.1055/s-0031-1281641","DOIUrl":"https://doi.org/10.1055/s-0031-1281641","url":null,"abstract":"<p><strong>Background: </strong>The contribution of potential treatable dementia aetiologies diagnosed using cerebral imaging varied considerably in previous studies and was not evaluated in a recent larger German sample of patients from a memory clinic.</p><p><strong>Material and methods: </strong>MRI images of 502 patients were retrospectively reassessed. Beside the proportion of potentially treatable dementia aetiology, the extent of whole brain atrophy (semiquantitative) and vascular white matter lesions were assessed.</p><p><strong>Results: </strong>Mean age of the patients was 63.7 ± 13.1 years; 49 % were female, mean MMST was 24.2 ± 5.5. In 74 % there was an agreement between the clinical dementia syndrome and MRI. 9 % (45 patients) had clearly discrepant imaging results, according to MRI criteria (21 × ischaemia, 20 × normal pressure hydrocephalus (NPH), 4 × intracerebral haemorrhage). These patients could not not be differentiated using age and MMST alone as clinical criteria. There was a significant correlation between global brain atrophy and MMST (r = -0.32; p < 0.001) and white matter lesion score (r = 0.28; p < 0.001).</p><p><strong>Conclusion: </strong>In 9 % there was a clear discrepancy between MRI results and the clinical syndrome diagnosis in memory-clinic patients. As known from earlier studies and current German 3 rd generation guidelines, it is reasonable to perform MRI imaging in dementia to improve the aetiological and differential diagnoses and to detect a different aetiology that can be missed using the clinical dementia criteria alone.</p>","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"642-6"},"PeriodicalIF":0.6,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1281641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40125897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Progress in therapy and diagnostics of neuropsychiatric diseases].","authors":"P Falkai","doi":"10.1055/s-0031-1281819","DOIUrl":"https://doi.org/10.1055/s-0031-1281819","url":null,"abstract":"","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"631"},"PeriodicalIF":0.6,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1281819","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40125895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Deep brain stimulation in schizophrenia].","authors":"J Kuhn,&nbsp;M Bodatsch,&nbsp;V Sturm,&nbsp;D Lenartz,&nbsp;J Klosterkötter,&nbsp;P J Uhlhaas,&nbsp;C Winter,&nbsp;T O J Gründler","doi":"10.1055/s-0031-1281733","DOIUrl":"https://doi.org/10.1055/s-0031-1281733","url":null,"abstract":"<p><p>Deep brain stimulation (DBS) has successfully advanced our treatment options for putative therapy-resistant neuropsychiatric diseases. Building on this strong foundation, more and more mental disorders in the stadium of therapy-resistance are considered as possible indications for DBS. Especially, schizophrenia with its associated severe and difficult to treat symptoms is gaining attention. This attention demands critical questions regarding the assumed mechanisms of DBS and its possible influence on the supposed pathophysiology of schizophrenia. Here, we synoptically compare current approaches and theories of DBS and discuss the feasibility of DBS in schizophrenia as well as the transferability from other psychiatric disorders successfully treated with DBS. For this we consider recent advances in animal models of schizophrenic symptoms, results regarding the influence of DBS on dopaminergic transmission as well as data concerning neural oscillation and synchronisation. In conclusion, the use of DBS for some symptoms of schizophrenia seems to be a promising approach, but the lack of a comprehensive theory of the mechanisms of DBS as well as its impact on schizophrenia might hinder the use of DBS for schizophrenia at this point in time.</p>","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"632-41"},"PeriodicalIF":0.6,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1281733","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40125896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Metabolic myopathies - part II: disorders of the fat, purine, and oxidative energy metabolism].","authors":"J Finsterer","doi":"10.1055/s-0031-1281727","DOIUrl":"https://doi.org/10.1055/s-0031-1281727","url":null,"abstract":"Dieser Übersichtsartikel beschäftigt sich mit den metabolischen Myopathien. Im 1. Teil [1] wurden Myopathien, die durch Störung des Kohlehydratstoffwechsels bedingt sind, dargestellt [2]. Im 2. Teil wird ein kurzer Überblick über Ursache, Klinik, Diagnose und Therapie der wichtigsten metabolischen Myopathien, bedingt durch Störungen im Bereich des Fett-, Purinbzw. oxidativen Energiestoffwechsels, gegeben [3, 4]. Mitochondriale Myopathien werden dabei nur im Überblick behandelt, da eine ausführliche Behandlung dieses Themas den Rahmen dieser Monografie sprengen würde.","PeriodicalId":509563,"journal":{"name":"Fortschritte der Neurologie · Psychiatrie","volume":" ","pages":"668-7; quiz 679"},"PeriodicalIF":0.6,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0031-1281727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40125898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}