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Table of Contents
Year : 2021  |  Volume : 4  |  Issue : 2  |  Page : 80-85

Vascular Parkinsonism and Parkinson’s disease: a prospective, clinico-radiological comparative study

1 Department of Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
2 Department of Radiodiagnosis, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India

Date of Submission09-Oct-2020
Date of Decision13-Mar-2021
Date of Acceptance19-May-2021
Date of Web Publication30-Aug-2021

Correspondence Address:
Dr. Deepika Joshi
Department of Neurology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AOMD.AOMD_53_20

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BACKGROUND: Vascular parkinsonism (VP) is an atypical Parkinsonian syndrome that is believed to have a temporal association with cerebrovascular disease. However, now it is evolving as a heterogeneous entity with no clear consensus on the definition and diagnostic criteria. AIM AND OBJECTIVES: This study aimed at evaluating the clinico-radiological profile of patients with VP and Parkinson’s disease (PD). MATERIALS AND METHODS: The present study was conducted at a tertiary care university hospital. A total of 80 patients, with a diagnosis of probable VP (40) and PD (40), were evaluated and compared with Unified Parkinson’s Disease Rating Scale (UPDRS) part III, gait scale, Mini-Mental State Examination (MMSE), Frontal Assessment Battery (FAB), and MRI brain. RESULTS: Significantly older age of onset (P = 0.005), higher vascular risk factors (P < 0.001), and motor scores in UPDRS part III (P < 0.001), gait scale (P < 0.001), and modified Hoehn and Yahr (P < 0.001) were seen in the VP as compared with the PD. On the cognitive scales, patients with VP scored significantly lower in MMSE (19.92 ± 6.0 vs. 24.90 ± 3.34; P < 0.001) and FAB (7.75 ± 4.27 vs. 11.22 ± 2.75; P < 0.001); on the modified Hachinski scale (7.77 ± 3.19 vs. 3.30 ± 1.97; P < 0.001), they scored higher compared with patients with PD. Periventricular ischemic changes, generalized brain atrophy, and multiple lacunar infarcts were the most common radiological abnormality found significantly more in patients with VP. CONCLUSION: An older age, worse cognitive scores and motor scores, and more profound periventricular and subcortical lesions on MRI favored VP.

Keywords: Acute parkinsonism, lower body parkinsonism, Parkinson’s disease, vascular parkinsonism

How to cite this article:
Rath S, Kumar A, Pathak A, Verma A, Singh VK, Chaurasia RN, Mishra VN, Joshi D. Vascular Parkinsonism and Parkinson’s disease: a prospective, clinico-radiological comparative study. Ann Mov Disord 2021;4:80-5

How to cite this URL:
Rath S, Kumar A, Pathak A, Verma A, Singh VK, Chaurasia RN, Mishra VN, Joshi D. Vascular Parkinsonism and Parkinson’s disease: a prospective, clinico-radiological comparative study. Ann Mov Disord [serial online] 2021 [cited 2023 Jan 29];4:80-5. Available from: https://www.aomd.in/text.asp?2021/4/2/80/324805

  Introduction Top

VP is a heterogeneous entity with varied clinical presentations posing real challenges in its diagnosis.[1],[2],[3] The very first recognition and description of this entity in 1929 were by Critchley, and he termed this “arteriosclerotic  Parkinsonism More Details.”[4],[5] In 1999, for the first time ever, Winikates and Jankovic propounded clinical criteria for the diagnosis of VP.[6] In 2004, Zijlmen et al. led a clinicopathological study that paved the way for the proposal of new and stringent diagnostic criteria that are in current use.[7] The criteria kept on evolving, with some authors focusing on clinical descriptors of VP: “pseudo-vascular parkinsonism” (neurodegenerative parkinsonism with nonspecific neuroimaging signal abnormalities), “vascular pseudo parkinsonism” (e.g., akinetic mutism due to bilateral mesial frontal strokes or apathetic depression from bilateral striatal lacunar strokes), or “pseudo-vascular pseudo parkinsonism” (e.g., higher-level gait disorders, including idiopathic normal pressure hydrocephalus [NPH]).[8] However, all these descriptive terms did not help to differentiate between the various clinical entities. In October 2015, the expert working group meeting for the first time during the 9th International Congress on Vascular Dementia, in Ljubljana, Slovenia, recognized the concept of VP as an entity and formulated the diagnostic criteria dividing VP into various subtypes.[9] They were: the “acute/subacute post-stroke VP” subtype presenting with (sub)acute onset of parkinsonism, which is typically asymmetric. The more frequent “insidious onset VP” subtype presents with progressive parkinsonism, lack/insufficiency of levodopa responsiveness, with more prominent postural instability and gait difficulties. Also included are a mixed shuffling-ataxic gait pattern, and upper motor neuron signs or incontinence. "Mixed idiopathic Parkinson's disease" or idiopathic Parkinson's disease with cerebrovascular disease (CVD), in which vascular lesions can further increase Parkinsonian symptoms, especially postural instability and gait difficulty.[9]

In the present study, we compared the clinical profile, with particular emphasis on the motor and cognitive impairments, along with the radiological abnormalities in patients with VP and PD for optimal patient diagnosis and prognosis.

  Materials and Methods Top


This is a single-center, prospective, cross-sectional, observational study in which a total of 80 consecutive patients who were attending the neurology department from August 2017 to December 2018 were enrolled. Out of them, 40 patients were diagnosed with VP and 40 patients were diagnosed with PD. All of them underwent detailed history, clinical examination with emphasis on motor and cognitive evaluation with brain imaging. VP was diagnosed based on Zijlmans et al’s (2004) criteria for probable VP.[7] PD was diagnosed based on the Queen Square Brain Bank for Neurological Disorders clinical criteria.[10] Inclusion criteria led to the enrolment of all patients fulfilling the criteria for probable VP: (a) clinical parkinsonism; (b) evidence of cerebrovascular disease; and (c) the two disorders must be related, by Zijlmans et al’s criteria.[7]

Exclusion criteria included the following:

  • Any alternative cause that significantly impaired gait or use of cognitive scales, and that might have posed challenges to the diagnosis

  • History of repeated head injury

  • Definite encephalitis

  • Neuroleptic treatment leading to parkinsonism

  • The inability of the patient to undergo neuroimaging

  • Family or patient’s refusal to give consent

  • Other Parkinson plus syndromes.

  • Of the initial 45 patients evaluated for VP, three patients were excluded based on orthopedic or rheumatological conditions that could have impaired gait and two patients were wheelchair-bound. The study was approved by the institutional ethical committee, number (EC/726).

    Variables, scales, and tests

    The following demographic and clinical data were studied: age, gender, educational status; vascular risk factors such as hypertension, diabetes mellitus, history of smoking, other modalities of tobacco use such as chewing, past cardiovascular and cerebrovascular events, clinical presentations, gait changes, tremor, postural instability, falls, urinary incontinence, pyramidal signs, cognitive decline, executive dysfunction, and freezing of gait (FOG) in “OFF” state (12-h withdrawal of levodopa in patients taking drugs) and in “ON” state (1h after the first daily dose of levodopa in patients taking drugs or 1h after 200 mg of levodopa in newly diagnosed patients).

    The onset of symptoms was categorized as: (a) acute onset within three months of stroke/transient ischemic attack, (b) insidious onset, and (c) insidious onset with acute deteriorations. Three categories were considered with regard to the clinical course: (a) progressive (worsening of symptoms—patients whose symptoms of motor and cognition worsened over one year); (b) stable; and (c) improvement—patients whose motor symptoms showed spontaneous improvement or with drugs. The cognitive assessment involved the application of the MMSE,[11] FAB,[12] Rosen’s Modification of Hachinski scale,[13],[14] UPDRS part III[15] and modified Hoehn and Yahr (H&Y) stage,[16] and gait scale for NPH,[17] all in “ON” and “OFF” states.

    An MRI brain was performed in all patients. An NCCT brain was done where MRI was contraindicated (patients with metal implants that were not MRI compatible).

    Patients were examined in the “OFF” state with UPDRS, modified H&Y, gait scale, and cognitive testing. Patients were examined again in the “ON” state with the aforementioned tests and scales. Response to levodopa was determined, and responders were patients who reached a percentage reduction exceeding 30% in part III of the UPDRS.

    Statistical analysis

    Descriptive analysis and comparison of continuous and categorical variables using SPSS V.16.0 software (Statistical Package for Social Sciences, IBM Corporation Software Group, USA) were undertaken. To compare categorical and continuous variables between the two groups, the likelihood ratio and Mann-Whitney tests were, respectively, used. The P values<0.05 were considered significant.

      Results Top

    Thirty-six (90%) patients with VP were males with a mean age of 70.55 ± 10.50 years; four (10%) were females with a mean age of 59.50 ± 7.14 years. In the PD group, 24 (60%) patients were males with a mean age of 60.00 ± 6.61years, and 16 (40%) were females with a mean age of 65.41 ± 9.10 years. Patients with VP were older as compared with PD with P = 0.005. In the VP group, 55% were graduates and in the PD group, 45% were graduates. Vascular risk factors such as hypertension, diabetes mellitus, chronic kidney disease (CKD), ischemic heart disease (IHD), past history of stroke, and recurrent stroke were significantly more in patients with VP as compared with PD (P < 0.05).

    The onset of parkinsonism in PD was insidious and gradual, with a steadily progressive clinical course with excellent responsiveness to levodopa. In contrast, VP was either acute onset, insidious onset, or insidious onset with acute deterioration along with a rapidly progressive clinical course with poor responsiveness to levodopa. The most significant differentiating clinical features observed in patients with VP as compared with PD were postural instability with falls, urinary incontinence, pyramidal signs, pseudobulbar affect, and cognitive decline. Tremors were predominantly seen in patients with PD (P < 0.05). In the subgroup analysis of patients with VP, depending on the onset, data were analyzed after classifying patients into predominantly two groups: acute onset (12 [30%]) and insidious onset (28 [70%]) for ease of comparison. In the acute-onset group, hemi-parkinsonism, FOG, cognitive issues, pseudobulbar palsy, and bowel bladder involvement were found to be more prevalent; however, in the insidious onset group, lower body parkinsonism (LBP) and postural instability were the predominant features [Figure 1].
    Figure 1: Clinical features in the subtypes of VP (in percentage). BBI = bladder-bowel involvement, FOG = freezing of gait, VP = vascular parkinsonism

    Click here to view

    LBP was present in 85% of patients with VP and in none of the patients with PD. The FOG in the “OFF” state was present in 42.5% VP and in 20% PD (P = 0.06 for “OFF” state). Patients with VP had significantly higher UPDRS scale scores (part III) in both “OFF” and “ON” state (P < 0.001). The higher UPDRS scores in patients with VP were consistent with higher modified H&Y stages (P < 0.001). In the VP group, 90% had <30% change in the score after the levodopa challenge test as compared with the PD group, which showed changes >30% in almost 82.5% patients. Mean MMSE and FAB score in the VP group was lower compared with the PD group, whereas modified Hachinski scores were higher in the VP group, compared with the PD group and their differences were statistically significant (P < 0.001) for all parameters. The mean gait score (10-m walking test) was 28.85 ± 7.75 in the VP group as compared with the PD group (14.15 ± 6. 81; P < 0.001). [Table 1] shows the demographic and clinical profile, whereas [Table 2] depicts the scale scores.
    Table 1: Comparison of clinico-radiological profile between VP and PD

    Click here to view
    Table 2: Comparison between VP and PD on the basis of various scales along with “OFF” and “ON” state variations

    Click here to view


    Out of the 40 patients in the VP group; MRI could not be done in one patient, and in the rest (39 [100%]) MRIs were abnormal with infarcts seen in 35 (87.5%) and bleeding in four (10.2%). The most consistent finding was periventricular leukomalacia changes in 100%, generalized brain atrophy in 89.7%, subcortical white matter changes in 53.8%, and ventricular dilatation in 15.4%. Among the distribution of infarcts: The site most frequently affected was basal ganglia (53.8%), followed by brainstem (25%), thalamus (20.5%), and internal capsules in the VP group. In the PD group, MRI was available in 37 patients and it was abnormal in 20 (54.05%) patients. Generalized brain atrophy was the most common finding in 19 (51.35%), followed by periventricular white matter changes seen in 17 (45.94%), ventricular dilatation in three (8.01%), and subcortical white matter changes in one (2.70%) [Figure 2].
    Figure 2: Showing distribution of patients on the basis of neuroimaging findings in both VP and PD groups. BG = basal ganglia, IC = internal capsule, PD = Parkinson’s disease, PVL = periventricular leukomalacia, SCWM = subcortical white matter, VP = vascular parkinsonism

    Click here to view

      Discussion Top

    In our study, the patients in the VP group were significantly older as compared with the PD group, with the most discernable clinical features being LBP, a significant paucity of tremor, postural instability, falls, FOG, urinary incontinence, pyramidal signs, executive dysfunction, and the presence of significant cerebrovascular disease burden, which is similar to those described in other studies.[6],[18],[19],[20],[21] However, the disease onset in our patients with VP was insidious in 45%, acute in 30%, and insidious with acute deterioration in 25% patients, with lesser FOG and postural instability and falls, which differs from the previously reported series that reported a much higher frequency of acute onset and rapidly progressive symptoms, FOG, and postural instability in the VP group.[19],[20] There was a poor response to levodopa in the vast majority of the VP group with higher UPDRS III scores, which correlated significantly with worse performance on MMSE and FAB. Also, we found that there was a significant correlation between the worse gait score and the UPDRS III, MMSE, and FAB in this group. The neuroimaging abnormalities in the form of periventricular leukomalacia, subcortical white matter changes, and multiple infarcts were also significantly more in the VP group as compared with the PD group (P < 0.005). The MRI abnormalities also correlated significantly with worse scores on UPDRS III, gait score, MMSE, and FAB. These findings were consistent with previously reported studies showing that VP had significantly strong evidence of cerebrovascular disease as compared with PD.[6],[18],[19],[20],[21] In the VP group, the 10% of patients who showed >30% responsiveness in the levodopa challenge test probably belonged to the mixed pattern classification of the consensus criteria but, due to no availability of DAT SCAN, it was not possible to confirm the finding. LBP can be found in various other neurodegenerative parkinsonism and frontal lobe disorders. However, we have ruled out the other disorders by appropriate neuroimaging and by applying the validated diagnostic criteria for various entities.

    In contrast, the PD group had an insidious onset with slow progression, significantly more tremor (rest >> postural), good response to levodopa, with significantly lesser falls, FOG, and cognitive decline. They had a better gait score and performed significantly better on the MMSE and FAB. Also, they had significantly lesser cerebrovascular disease burden on MRI as compared with the VP group, with periventricular leukomalacia (42.5%) and subcortical white matter changes (2.5%) of patients.

    It is important to diagnose VP because of the different prognostic and therapeutic patient outcomes as compared with PD. Although various studies in the literature have addressed this issue, yet there is no clear consensus on its terminology and definitions. A more consistent nomenclature for the various subtypes of VP was recently proposed by the expert group,[9] wherein they divided VP into three groups: acute/subacute post-stroke VP, insidious VP, and mixed PD/CVD. However, this diagnostic approach needs to be validated in further longitudinal cross-sectional studies and compared with the neuropathological data. Also, incorporating novel vascular, neurotransmitter, and proteinopathy biomarkers into this diagnostic approach could help in solving the complex enigma for the exact substrate of insidious onset VP.

    There were a few limitations, such as, in some cases of overlap of clinical uncertainty between VP and other neurodegenerative parkinsonism, additional diagnostic testing for presynaptic dopamine and SPECT cardiac imaging using MIBG would be needed, which were not available at our institute. Due to the unavailability of DAT scanning, only clinical differentiation between patients with PD and VP was possible. Also, we were unable to assess the non-motor symptoms in the VP group, which would have been useful in this setting. Thus, the mixed variants could not be distinguished.

      Conclusion Top

    This is a first of its kind of study conducted at a tertiary care center in India. If vascular risk factors can be controlled, the question arises: Is VP a preventable disease? As is evident, VP has an older age of onset, LBP with the presence of florid pyramidal signs, cognitive decline, with the vast majority of patients having significant cerebrovascular burden. Treating physicians must keep these facts in mind when they are treating older individuals presenting with the features just mentioned.

    Declaration of patient consent

    The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

    Author contributions

    Shivani Rath, Anand Kumar: Planning and conception, data collection , writing of initial and final draft. Author 1 and 2 have contributed equally. Abhishek Pathak, Varun K. Singh, Rameshwar N. Chaurasia, Vijay N. Mishra: supervision, statistical analysis and final draft editing Ashish Verma: Interpretation of Neuroimaging abnormalities. Deepika Joshi: Planning, conception, supervision, statistical analysis, final draft editing and manuscript submission.

    Ethical compliance statement

    The study was approved by the Institute Ethical Committee of Banaras Hindu University.

    Conflicts of interest

    There are no conflicts of interest.

    Financial support and sponsorship


      References Top

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      [Figure 1], [Figure 2]

      [Table 1], [Table 2]


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