Key Points
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Vascular changes in the brain can manifest as parkinsonism
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The predominant clinical feature in most cases of vascular parkinsonism (VP) is gait impairment, referred to as lower body parkinsonism
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As VP advances, patients develop cognitive impairment and incontinence
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The most prominent pathology observed by neuroimaging in patients with VP involves the white matter of the brain
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Patients with VP respond only slightly or not at all to dopaminergic medication
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Similar pathology and clinical features in VP and Binswanger disease suggest that they represent different manifestations along a disease spectrum
Abstract
Parkinson disease is a primary degenerative disease of the brain, but parkinsonism can also result from a variety of vascular disorders. Vascular parkinsonism (VP) most frequently presents as lower body parkinsonism, a condition that is accompanied by the development of white matter lesions (WMLs) and lacunes in the brain. Patients with lower body parkinsonism exhibit gait impairment and go on to develop urinary incontinence, abnormal pyramidal responses and cognitive decline. However, WMLs and lacunes are also common observations among elderly individuals who do not have parkinsonism, which causes difficulty in determining the pathogenetic mechanisms that lead to VP. In addition, imaging studies suggest that many pathological and clinical features are common to VP and Binswanger disease, a type of small vessel vascular dementia. This Review summarizes current understanding of the clinical characteristics of VP, as well as knowledge gained from neuroimaging and nuclear imaging of the pathological features of VP. The lack of current treatment options, and the emergence of new therapies such as cerebrospinal fluid drainage, are also discussed. Finally, consideration is given to whether the overlap between VP and Binswanger disease means that these two disorders should be considered as part of the same disease entity.
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Korczyn, A. Vascular parkinsonism—characteristics, pathogenesis and treatment. Nat Rev Neurol 11, 319–326 (2015). https://doi.org/10.1038/nrneurol.2015.61
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DOI: https://doi.org/10.1038/nrneurol.2015.61
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