Parkinsonism in Patients with Vascular Dementia: Clinical, Computed- and Positron Emission-Tomographic Findings

Abstract

Purpose: The present study investigates the vascular nature of parkinsonian features in patients with ‘probable’ vascular dementia. Patients and Methods: Forty patients with vascular dementia were studied with positron emission tomography (PET) using the steady state technique with ¹⁵O in order to assess regional cerebral blood flow (rCBF), regional oxygen extraction rate (rOER) and regional metabolic rate for oxygen (rCMRO₂) in different brain regions. The findings in 10 patients with (VaDP) were compared to 30 without parkinsonism (VaD). Results: The clinical and computed tomographic findings in the parkinsonian patients were similar to those described in the literature as probable vascular parkinsonism. The PET results showed decreased rCBF and rCMRO₂ in the frontal and parietal cortices and in the striatum of the VaDP compared to the VaD group. The decrease of rCBF and rCMRO₂ in frontal and parietal cortices is due to the more severe mental changes in the VaDP group. In the VaDP patients rCBF and rCMRO₂ were more decreased and rOER increased in the striatum contralateral to the most affected parkinsonian side. Conclusion: Our PET findings show that local ischemic changes in the striatum contribute to parkinsonism in vascular dementia patients.

Midbrain atrophy in subcortical ischemic vascular dementia

“…Vascular lesions or the hypometabolism of basal ganglia, disruption of sensorimotor integration by an impairment of long-loop reflexes traversing the white matter, and disruption by diffuse vascular lesions of the interconnecting fiber tracts between the basal ganglia and the motor cortex have been suggested as possible mechanisms of postural instability and gait disturbance in vascular Parkinsonism [1,5,33,34]. The tegmentum of the midbrain harbors important anatomical structures for posture and gait as well as for cognition and motor control.…”

“…Most of the studies on which this is based were designed in terms of making a differential diagnosis among PSP, Parkinson's disease and multiple systemic atrophy [28,35]. SIVD is usually diagnosed as vascular Parkinsonism when a patient presents with postural instability and gait disturbance [5,37]. Considering our observation of no difference in midbrain measurements between SIVD and PSP patients, an MRI measurement of the AP diameter of the midbrain alone without other clinical or radiological findings may not be sufficient to discriminate PSP from SIVD presenting as vascular Parkinsonism.…”

“…Vascular dementia is a heterogeneous clinical syndrome. Among the subtypes of vascular dementia, patients with subcortical ischemic vascular dementia (SIVD) usually present with postural instability, gait disturbance, and a varying degree of bradykinesia that is reminiscent of vascular Parkinsonism [5,29]. Moreover, a PSP-mimicking clinical syndrome was reported in cases of multiple cerebral infarction or Bingswanger's disease [8,23,36].…”

Stage-Specific Gender Differences in Cognitive and Neuropsychiatric Manifestations of Vascular Dementia

“…Furthermore, we adjusted for the use of anti-dementia and neuropsychiatric drugs and the parkinsonism, which may influence the neuropsychiatric symptoms. 22 P value <.05 was regarded as statistically significant.…”

Differential pattern of hand‐tapping compromise in vascular versus idiopathic parkinsonism: A study based on computerized movement analysis

“…The term “subcortical vascular encephalopathy” (SVE) is used here as the pathological basis of a movement disorder of patients with either multiple subcortical lacunar infarctions, diffuse white matter lesions, or both. Although both historical and more recent studies have stressed the importance of gait disturbances in patients with SVE who have been diagnosed with a “vascular” Parkinson syndrome,4–8 much less is known of the involvement of the hands and arms, which in clinical routine seem affected to a much lesser extent. In this sense, FitzGerald and Jankovic4 coined the term “lower body parkinsonism” when they clinically identified a series of 10 patients with a relatively severe gait disorder and “no or only minimal upper limb involvement,” who displayed the imaging characteristics of SVE.…”