Showing papers by "Klaus Seppi published in 2000"
TL;DR: This review focuses on depression in alpha-synucleinopathies, discussing epidemiological, pathophysiological and treatment aspects of this frequently disabling clinical feature which may occur in PD, DLB and MSA alike.
Abstract: Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) are increasingly recognized as alphasynucleinopathies, i.e. neurodegenerative disorders that share a common sub-cellular pathology characterized by alpha-synuclein abnormal aggregation. In the present review we focus on depression in alpha-synucleinopathies, discussing epidemiological, pathophysiological and treatment aspects of this frequently disabling clinical feature which may occur in PD, DLB and MSA alike.
18 citations
TL;DR: The clinical characteristics are progressive dementia, parkinsonian syndrome, fluctuations of cognitive functions, alertness, and attention, visual hallucinations, depression, REM sleep behavior disorder, adverse responses to standard neuroleptics doses, falls, syncopes, systematized delusions, and other modalities of hallucinations.
Abstract: Die Demenz mit Lewy-Korperchen (DLK) ist die zweithaufigste neuropathologisch diagnostizierte degenerative dementielle Erkrankung. Ihre klinischen Charakteristika sind progrediente Demenz, Parkinson-Symptome, Schwankungen der Hirnleistungen und Vigilanz, detaillierte wiedergegebene visuelle Halluzinationen, Depression, REM-Schlaf-Verhaltensstorungen, Uberempfindlichkeit auf die Dosen ublicher Neuroleptika, Sturze, Synkopen, systemisierter Wahn und Halluzinationen anderer Art. Die klinischen Kriterien haben eine hohe Spezifitat (95%) und eine deutlich geringere Sensitivitat. Die Erkrankung beginnt im Schnitt zwischen dem 60. und 68. Lebensjahr, betrifft Manner haufiger als Frauen und dauert 6–8 Jahre. Differenzialdiagnosen sind Demenz vom Alzheimer-Typ (DAT), Parkinson-Krankheit (PK), subkortikale arteriosklerotische Enzephalopathie, progressive supranukleare Parese, Multisystematrophie und bisweilen die Creutzfeldt-Jakob-Erkrankung. Der genetische Hintergrund der Erkrankung ist ungeklart. Bildgebende Diagnostik (Magnetresonanz-Imaging, Single-Photon-Emission-Tomographie) kann zur Differenzialdiagnose beitragen. Systematische Therapiestudien liegen noch nicht vor. Die Erkrankung wird mit L-Dopa, atypischen Neuroleptika, Azetylcholinesterase-Hemmern, blutdrucksteigernden Medikamenten, sowie zur Verbesserung der neurogenen Blasenstorungen mit peripheren Anticholinergika und α-Rezeptorenblockern behandelt.
17 citations
TL;DR: The findings indicate that beneficial protective effects of striatal grafts implanted into host striatum prior to excitotoxic insults are abolished in the presence of severe dopaminergic denervation.
15 citations
TL;DR: Evaluating embryonic neuronal grafts in a novel rat model of multiple system atrophy with the help of in vivo magnetic resonance imaging (MRI) and to correlate imaging with histological parameters obtained obtained obtained an excellent correlation between MRI and histological measurements.
10 citations
TL;DR: The clinical characteristics are progressive dementia, parkinsonian syndrome, fluctuations of cognitive functions, alertness, and attention, visual hallucinations, depression, REM sleep behavior disorder, adverse responses to standard neuroleptics doses, falls, syncopes, systematized delusions, and other modalities of hallucinations.
Abstract: Publisher Summary Dementia with Lewy bodies (DLB) represents the second most common cause of neurodegenerative dementia in the elderly after Alzheimer's disease (AD). Progressive cognitive decline with particular deficits of visuospatial ability as well as frontal executive function is accompanied by usually only mildly to moderately severe parkinsonism, which is often bilateral akinetic-rigid without the classical rest-tremor. Management of patients with DLB has to be based on a multidimensional approach taking into account the cognitive decline and dementia that form the core clinical syndrome, the characteristic hallucinations and visual delusions present in a majority of cases as well as dementia associated behavioral symptoms and depression. Patients with DLB have a pronounced cholinergic deficit and the treatment of DLB generally parallels that for AD. Currently there are no neuroprotective agents for DLB. Acetylcholinesterase (AChE) inhibitors, originally developed to treat AD, improve cognitive, neuropsychiatric and functional symptoms in DLB and PDD. Orthostatic hypotension may be a disabling feature of DLB that if present frequently exacerbates the disability arising from progressive motor disturbance.
9 citations
Journal Article•
TL;DR: Dementia with Lewy bodies is the second most frequent neuropathologically diagnosed degenerative dementing illness and is treated with L-dopa, atypical neuroleptics, acetylcholine esterase inhibitors, antihypotensive agents and peripheral anticholinergic and alpha-receptor-blocking medicaments to improve neurogenic bladder dysfunction.
3 citations
3 citations
01 Jan 2000
TL;DR: Immunohistochemical analysis in the double toxin double lesion MSA-SND model reveals characteristic changes with more than 90% loss of tyrosine hydroxylase positive neurons in the SNpc and more than 70% Loss of striatal cross-sectional surface area.
Abstract: L-DOPA unresponsive parkinsonism is widely considered the predominant motor disorder of multiple system atrophy (MSA). The neuropathological changes underlying MSA-associated parkinsonism are dominated by neuronal fall out in anatomically related nigral and striatal pathways including afferent projections arising from the caudolateral substantia nigra pars compacta (SNpc) and efferent striatopallidal projections originating in the dorsolateral posterior putamen (striatonigral degeneration SND). The characteristic lesion pattern of SND can be replicated in rats by a double toxin double lesion approach that requires sequential stereotaxic injections of a nigral (e.g. 6-hydroxydopamine; 6-OHDA) and a striatal neurotoxin (e.g. quinolinic acid; QA) into the medial forebrain bundle (MFB) and ipsilateral striatum, respectively (Wenning et al., 1996, 1999a). Immunohistochemical analysis in the double toxin double lesion MSA-SND model reveals characteristic changes with more than 90% loss of tyrosine hydroxylase positive (TH) neurons in the SNpc and more than 70% loss of striatal cross-sectional surface area. In addition to the double toxin double lesion model a single toxin double lesion approach has been proposed using mitochondrial respiratory chain (MRC) inhibitors such as 3-nitropropionic acid (3-NP) or l-methyl-4-phenyl-l,2,3,6 tetrahydropyridine (MPTP) (Wenning et al., 2000).