Vascular Parkinsonism: A Review of the Precision and Frequency of the Diagnosis

Foltynie, Thomas; Barker, Roger; Brayne, Carol

doi:10.1159/000048607

Cited by 47 publications

(23 citation statements)

References 29 publications

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“…Increased intracellular calcium concentration has also been shown in hypoxic venous endothelial cells, leading to activation of phospholipid A 2 and elevated prostaglandin synthesis [45,46]. Alteration of these cellular processes is thought to cause the release of inflammatory mediators [47]. Activation of venous endothelial cells by hypoxia also increases the release of β-fibroblast growth factors (bFGF) and prostaglandin F 2 α, which are known to stimulate smooth muscle cell migration and proliferation, a feature commonly observed in varicosities [6,46,48].…”

Section: Molecular Studiesmentioning

confidence: 99%

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

et al. 2010

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Venous hypoxia has long been postulated as a potential cause of varicosity formation. This article aimed to review the development of this hypothesis, including evidence supporting and controversies surrounding it. Vein wall oxygenation is achieved by oxygen diffusing from luminal blood and vasa vasorum. The whole media of varicosities is oxygenated by vasa vasorum as compared to only the outer two-thirds of media of normal veins. There was no evidence that differences exist between oxygen content of blood from varicose and non-varicose veins, although the former demonstrated larger fluctuations with postural changes. Studies using cell culture and ex vivo explants demonstrated that hypoxia activated leucocytes and endothelium which released mediators regulating vein wall remodelling similar to those observed in varicosities. Venoactive drugs may improve venous oxygenation, and inhibit hypoxia activation of leucocytes and endothelium. The evidence for hypoxia as a causative factor in varicosities remains inconclusive, mainly due to heterogeneity and poor design of published in vivostudies. However, molecular studies have shown that hypoxia was able to cause inflammatory changes and vein wall remodelling similar to those observed in varicosities. Further studies are needed to improve our understanding of the role of hypoxia and help identify potential therapeutic targets.

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Section: Molecular Studiesmentioning

confidence: 99%

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

et al. 2010

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“…B. in Anlehnung an die UK "brain bank criteria" [11]) definiertes VPS nach klinikopathologischen und epidemiologischen Studien nur ca. 3-6 aller Parkinson-Syndrome ausmacht [18]. Im Gegensatz hierzu stellen die mit subkortikaler arteriosklerotischer Enzephalopathie (SAE) assoziierten Gangstö-rungen, die bei Fehlen weiterer Kardinalsymptome nicht als VPS bezeichnet werden sollten, ein häufiges Phänomen des höheren Lebensalters dar [19,20,21].…”

Section: Häufigkeit Und Pathologieunclassified

Das vaskuläre Parkinson-Syndrom

Ebersbach

Poewe

2006

Nervenarzt

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The present review shows that vascular parkinsonian syndrome (VPS) fulfilling stringent diagnostic criteria for parkinsonism is a rare disease that cannot always be distinguished from neurodegenerative parkinsonism on clinical grounds. Thus VPS needs to be differentiated from other disturbances, which have distinct phenomenological and therapeutical features including isolated gait disturbances associated with subcortical arteriosclerotic encephalopathy and neurodegenerative parkinsonism complicated by comorbid vascular encephalopathy. Acute or subacute VPS is usually caused by contralateral infarctions involving the external globus pallidus, ventrolateral thalamus, and, less often, the substantia nigra. Chronic VPS with insidious onset is related to bilateral subcortical infarctions affecting thalamocortical projections. Differentiation from degenerative parkinsonism is difficult in cases of VPS that display a progressive course and response to levodopa.

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“…Approximately 3% to 6% of all cases of parkinsonism may have a vascular cause (Foltynie et al, 2002;De Rijk et al, 1997). In Spain, a prevalence of 2.5% of all patients with parkinsonism has been found (Benito-León et al, 2003).…”

Section: Vascular Pseudoparkinsonism (Vp)mentioning

confidence: 99%

123-I ioflupane (Datscan®) presynaptic nigrostriatal imaging in patients with movement disorders

Castrejón¹,

Vicente²,

Romera³

et al. 2005

Braz. arch. biol. technol.

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123-I Ioflupane (Datscan®) presynaptic imaging has been shown to have a significant utility in the assessment of patients with movement disorders 123-I Ioflupane SPECT is able to distinguish between Parkinson's disease (PD) and other forms of parkinsonism without degeneration of the nigrostriatal pathway, including a common movement disorder such as essential tremor, and to assess disease progression in PD and other neurodegenerative disordersinvolving the substantia nigra.

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Vascular Parkinsonism: A Review of the Precision and Frequency of the Diagnosis

Cited by 47 publications

References 29 publications

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

Das vaskuläre Parkinson-Syndrom

123-I ioflupane (Datscan®) presynaptic nigrostriatal imaging in patients with movement disorders

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