Parkinson Disease: Jost W

Reichmann H, Jost W. · No affiliation provided · J Neurol. · Pubmed #16944350 No free full text.

This publication has no abstract.

Steiger M, Jost W, Grandas F, Van Camp G. · The Walton Centre for Neurology and Neurosurgery, Fazakerley, Liverpool, UK. · J Neural Transm. · Pubmed #19142570 No free full text.

Abstract: A literature review was conducted to assess risk of cardiac valve regurgitation (CVR) associated with use of ergot-derived and non-ergot dopamine agonists (DAs) in patients with Parkinson's disease (PD). Inclusion criteria: case-control/observational studies of >10 patients with PD treated with DAs, including a control group and assessment of incidence/risk of CVR. Of the 166 publications identified, 14 met all inclusion criteria and included 1,750 patients. In 11 of the studies, a significant increase in CVR frequency of any severity (at the aortic, mitral or tricuspid valve) in the ergot group vs. the non-ergot or control group was described. No study reported increased risk of CVR for non-ergot DAs, compared with controls. In the studies identified in the literature, the use of ergot-derived DAs (pergolide and cabergoline) in patients with PD was associated with increased risk of CVR. Increased risk of CVR was not associated with the use of non-ergot DAs.

Gerlach M, Hendrich A, Hueber R, Jost W, Winkler J, Woitalla D, Riederer P. · Universität Würzburg, Klinik und Poliklinik für Kinder- und Jugendpsychiatrie und Psychotherapie, Labor für Klinische Neurobiologie, Würzburg, Deutschland. · Neurodegener Dis. · Pubmed #18322371 No free full text.

Abstract: A biomarker (biological marker) is a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenetic processes or pharmacological responses to a therapeutic intervention. Expectations are high for the development of biomarkers since they make it possible to achieve a significant improvement in the diagnosis and classification of diseases like Parkinson's disease. As a surrogate marker for clinical studies, a biomarker can also be used to determine the efficacy of novel therapeutic interventions, such as neuroprotective strategies, and for monitoring the progress of the disease. Imaging techniques ((18)F-DOPA PET, (123)I-beta-CIT SPECT, MIBG scintigraphy, functional imaging), clinical tests (e.g. hyposmia, micrography, hyperechogenicity, apomorphine test), biochemical markers (e.g. alpha-synuclein and neuromelanin antibodies, oxidative and mitochondrial markers) and genetic tests for hereditary forms (PARK1 to PARK11) are evaluated for their suitability.

Naumann M, Jost W. · Department of Neurology, University of Würzburg, Würzburg, Germany. · Mov Disord. · Pubmed #15027066 No free full text.

Abstract: Botulinum neurotoxin serotype A (BoNT/A) has revolutionised the treatment of a variety of autonomic hypersecretory disorders. Several open and controlled studies indicate that BoNT/A is a safe and effective treatment for focal hyperhidrosis of the axillae and palms, for gustatory sweating, and for some other rare conditions associated with focal hyperhidrosis. There is class I evidence for the efficacy of botulinum toxin in axillary hyperhidrosis and class II evidence for palmar hyperhidrosis and gustatory sweating. BoNT/A has the potential to replace current invasive and surgical techniques and should at least be considered as a viable alternative. The results of pilot studies to treat sialorrhea are encouraging. However, the optimal dose, best mode of application, side effects, and duration of BoNT/A action in this condition remain uncertain. We need further formal clinical trials to evaluate risks and benefits of BoNT/A for palliative treatment in of sialorrhea in Parkinson's disease and in bulbar amyotrophic lateral sclerosis. Based on the few reports published, BoNT/A injections into the lacrimal gland for hyperlacrimation may be an elegant method to treat this sometimes disabling condition. Again, larger studies are needed to evaluate the risks and long-term benefits of this treatment option.

Castro-Caldas A, Delwaide P, Jost W, Merello M, Williams A, Lamberti P, Aguilar M, Del Signore S, Cesaro P, Anonymous00179. · Instituto de Ciências da Saúde, Universidade Católica Portuguesa, Lisboa, Portugal. · Mov Disord. · Pubmed #16267842 No free full text.

Abstract: Dopamine agonists have been recommended as early treatment for Parkinson's disease (PD), alone or combined with levodopa. Piribedil is a non-ergot selective D(2)/D(3) agonist with alpha(2) antagonist properties shown to be effective in the treatment of PD. This 12-month international, randomized, double-blind trial aimed to assess the efficacy of piribedil 150 mg versus bromocriptine 25 mg, in early combination with levodopa in Stage I to III PD patients. Motor efficacy was assessed using the Unified Parkinson's Disease Rating Scale (UPDRS III, Items 18-31) as improvement from baseline. Response rate was defined as a 30% improvement. Among the 425 randomly assigned patients, 178 were also included in a substudy on cognitive follow-up evaluated by a dysexecutive syndrome oriented battery. A relevant improvement in UPDRS III over the 12-month study duration was observed both in the piribedil and bromocriptine groups (-7.9 +/- 9.7 points from baseline versus -8.0 +/- 9.5; not significant [n.s.]) with a response rate of 58.4% and 55.3% (n.s.), respectively. Piribedil and bromocriptine resulted in similar improvement on all UPDRS III subscores. Piribedil patients required less levodopa dose increase than those on bromocriptine. Cognitive performance remained generally unchanged in both groups, with a significant effect of piribedil limited to the Wisconsin Card Sorting Test. An overall good tolerability of piribedil was observed. Early combination of piribedil 150 mg with levodopa resulted in significant long-term improvement of all motor symptoms in PD patients insufficiently controlled by levodopa alone. Taking into account both efficacy and acceptability in the long-term, piribedil proved in this bromocriptine controlled study to be an effective and safe treatment for PD.

Dodel R, Csoti I, Ebersbach G, Fuchs G, Hahne M, Kuhn W, Oechsner M, Jost W, Reichmann H, Schulz JB. · Dept. of Neurology, Philipps-University Marburg, Marburg, Germany. · J Neurol. · Pubmed #18787881 No free full text.

Abstract: Parkinson's disease (PD) is characterized by its motor impairment. However, non-motor symptoms such as psychiatric disorders, autonomic disturbances and sleep disorders frequently complicate the course of the disease. In particular, psychiatric disturbances including cognitive impairment, depression and psychosis impact these patients considerably. Approximately 31 % of PD patients suffer from cognitive impairment and dementia. Currently, two different clinical presentations are distinguished in PD patients, who present with dementia: Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB), which are two different presentations of a single underlying disease process leading to the deposition of alpha-synuclein. Clinically, PDD is distinguished from DLB alone by the different temporal manifestations of extrapyramidal motor symptoms. Dementia is characterized by a subtle onset and progressive cognitive decline with a predominant dysexecutive syndrome, which can be accompanied by different behavioral symptoms such as hallucinations, depression, anxiety and sleep disorders. Dysregulation of different neurotransmitters has been associated with cognitive decline, but reduced cholinergic transmission is currently thought to be the pivotal mechanism in the development of cognitive dysfunction. Therefore, cholinesterase inhibitors are used in the treatment of dementia and accompanying behavioral symptoms in PDD and DLB. The occurrence of dementia impacts not only the patients themselves but also their care-givers and family.This article focuses on the clinical issues related to both disorders and is based on a meeting of experts which took place in April 2008 in Dresden.

Spiegel J, Hellwig D, Samnick S, Jost W, Möllers MO, Fassbender K, Kirsch CM, Dillmann U. · Department of Neurology, Saarland University, Homburg/Saar, Germany. · J Neural Transm. · Pubmed #16715205 No free full text.

Abstract: In idiopathic Parkinson's disease (PD), a tremor-dominant type (TDT), an akinetic-rigid type (ART), and a mixed type (MT) are distinguished. We compared cerebral [I-123]FP-CIT SPECT in the PD subtypes (67 patients Hoehn and Yahr stage 1:26 with ART, 19 with MT, 22 with TDT). We measured the ratios putamen/occipital lobe binding and caudate nucleus/occipital lobe binding. Parkinsonian motor symptoms were quantified by UPDRS motor scale. In both putamen and caudate nucleus contralateral to the clinically affected body side TDT patients showed a significantly higher FP-CIT uptake than ART or MT patients (ANOVA; p<0.01). Contralateral putamen and caudate nucleus FP-CIT uptake correlated significantly with severity of rigidity (p<0.01) and hypokinesia (p<0.01) but not with severity of resting or postural tremor (p>0.05). The missing correlation between striatal FP-CIT uptake and tremor suggests, that further systems besides the nigrostriatal dopaminergic system may contribute to generation of parkinsonian tremor.

Spiegel J, Hellwig D, Möllers MO, Behnke S, Jost W, Fassbender K, Samnick S, Dillmann U, Becker G, Kirsch CM. · Department of Neurology, Saarland University, Homburg/Saar, Germany. E-mail: · Brain. · Pubmed #16513685 links to  free full text

Abstract: Hyperechogenic signal of substantia nigra (SN) in transcranial sonography (TCS) and reduced striatal uptake in FP-CIT SPECT are common findings in idiopathic Parkinson's disease (PD). But so far it is unknown whether the extent of SN hyperechogenicity represents a correlate for the degeneration of presynaptic dopaminergic neurons in PD. We performed TCS and 123I-labelled N-(3-fluoropropyl)-2ss-carbomethoxy-3ss-(4-iodophenyl)nortropane ([123I]FP-CIT) SPECT in 53 patients with PD. Striatal FP-CIT uptake was quantified by measuring the striatal/posterior lobe binding of [123I]FP-CIT. SN echogenicity was quantified by planimetric measurement of the maximum extension of hyperechogenic signals. We found no correlation between striatal FP-CIT uptake and echogenicity of the SN, neither contralateral to the clinically more affected body side (r = +0.08, P = 0.57; Pearson's correlation) nor ipsilateral (r = +0.01; P = 0.92). Our data show that the extent of SN hyperechogenicity does not correlate with the degeneration of presynaptic dopaminergic nerve terminals. Obviously SN hyperechogenicity and degeneration of presynaptic dopaminergic nerve terminals exist independently from each other and may be based on different pathomechanisms.

Reichmann H, Jost W. · Dept. of Neurology, University of Dresden, Germany. · J Neurol. · Pubmed #18787875 No free full text.

This publication has no abstract.