Vascular parkinsonism

Abstract

Parkinsonism can be the result of several disorders affecting the brain. In idiopathic Parkinson’s disease, a loss of 60-70 % of the nearly 450,000 dopamine-producing neurons of the human substantia nigra pars compacta, and related decrease of the dopamine level at the striatum, must occur before parkinsonian symptoms will be clinically detectable. However, parkinsonism can result from lesions outside the nigra, and these can be caused by inflammatory, toxic, and vascular mechanisms. Critchley (Brain 52:23-83, 1929) coined the term arteriosclerotic parkinsonism, consisting of “rigidity, fixed facies, and short-stepping gait” with the absence of rest tremor. This syndrome, now known as lower body parkinsonism (LBP), is considered to be the most frequent form of vascular parkinsonism. LBP is most commonly accompanied by cerebral white matter lesions (WMLs), frequently accompanied by lacunar infarcts, either in the white matter or the basal ganglia, as well as by ventricular dilatation. In other cases, small intracerebral hemorrhages or ischemic strokes in the brain stem or elsewhere can lead to clinical syndromes which include hemiparkinsonism. In addition to age, risk factors for WMLs are mainly cardiovascular ones. The clinical correlates of WMLs may include, in addition to LBP, nonspecific gait disturbances, cognitive impairment, depression, and urinary incontinence. Although the same MRI features can occur in normal elderly people, they are predictive of future appearance of gait impairment and cognitive decline.