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Vascular parkinsonism: what makes it different?
  1. Deepak Gupta1,
  2. Abraham Kuruvilla2
  1. 1Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
  2. 2Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India
  1. Correspondence to Deepak Gupta, Division of Neurology, Department of Medicine, Walter C Mackenzie Health Sciences Center, 8440–112 Street, University of Alberta, Edmonton, Alberta T6G 2B7, Canada; docdeepakgupta{at}


Vascular parkinsonism (VP) accounts for 2.5–5% of all cases of parkinsonism in various population based and clinical cohort studies. VP develops as a result of ischaemic cerebrovascular disease, so aetiologically it is classified as secondary parkinsonism. It has been variably referred to in the literature as arteriosclerotic parkinsonism, vascular pseudo-parkinsonism, and lower body parkinsonism. The most important consideration while making a diagnosis of VP should be to differentiate VP from Parkinson's disease (PD) because of prognostic and therapeutic implications. The salient clinical features in VP which differentiate it from PD are presentation with postural instability and falls rather than with upper limb rest tremor or bradykinesia; short shuffling parkinsonian gait in VP is accompanied by a wider base of stance and variable stride length (parkinsonian-ataxic gait), absence of festination, frequent occurrence of pyramidal signs, and early subcortical dementia. In a patient where the clinical features are suggestive of VP the clinical diagnosis can be supported by demonstration of diffuse white matter lesions and/or strategic subcortical infarcts in the MRI of the brain. The therapeutic options in VP are limited to levodopa, and a poor or non-sustained response to levodopa is another differentiating feature between VP and PD.

  • Stroke
  • Parkinson's disease

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  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.