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The concept of vascular parkinsonism (VP) has been highly controversial since the initial paper by Critchley in 1929. This review tentatively delineates the extent of the spectrum of VP. Much confusion has arisen owing to the lack of clear definitions of parkinsonism, “atypical parkinsonism” and “pseudoparkinsonism”, which we here attempt to define. Confusion has also arisen because incidental vascular lesions occurring in true idiopathic Parkinson's disease (IPD) are up to 10 times more common than parkinsonism due to cerebrovascular disease. VP is clinically heterogeneous. Most often VP is atypical and can be separated from IPD, on the basis of the presence of additional focal signs, and the absence of typical resting tremor in the upper limbs, of true akinesia (i. e.: with decrement and fatiguing of alternating movements), and of definite benefit from levodopa. Exceptionally, VP may mimic IPD or other degenerative diseases such as progressive supranuclear palsy or corticobasal degeneration. The lesions responsible for VP are mostly basal ganglia lacunes and/or subcortical white matter vasculopathy of the “Binswanger” type. Rarely, a single striatal infarct, striatal cribriform cavities or ischaemic changes in the substantia nigra have been described. Vascular “pseudo-parkinsonism” refers to isolated gait disorders called “lower body parkinsonism”, “frontal-type gait disorders” or “gait ignition failure” that are reminiscent of, but distinct from, that found in IPD. The pathophysiology of VP is poorly understood. Why some patients develop parkinsonism and others do not, despite the same apparent lesion load, remains a mystery.