Vascular parkinsonism: what makes it different?

Abstract

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.