Carotid artery thickening and neurocirculatory abnormalities in de novo Parkinson disease

Kim, Joong‐Seok; Oh, Yoon‐Sang; Lee, Kwang Soo; Song, In‐Uk; Park, In-Seok; Yang, Dong-Won; Koo, Jaseong; Goldstein, David S.

doi:10.1007/s00702-014-1203-5

Cited by 12 publications

(21 citation statements)

References 32 publications

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“…Furthermore, orthostatic blood pressure changes and supine blood pressure [3] , and the presence of NH and nighttime SBP [4] , have been found to be positively correlated with the severity of white matter lesions. In addition, increased intima media thickness of the carotid artery has been associated with OH, SH, and supine and overnight blood pressure [5] .…”

Section: Discussionmentioning

confidence: 99%

“…Blood pressure abnormalities are common in Parkinson's disease (PD), and may manifest as orthostatic hypotension (OH), supine hypertension (SH), nocturnal hypertension (NH), or loss of nocturnal blood pressure dips (non-dipping), all of which frequently coexist [1] . In patients with PD, these blood pressure abnormalities are associated with cerebrovascular diseases, such as white matter hyperintensities [2] , [3] , [4] and carotid artery atherosclerosis [5] .…”

Section: Introductionmentioning

confidence: 99%

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Cerebral microbleeds and blood pressure abnormalities in Parkinson's disease

et al. 2018

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Blood pressure abnormalities are frequently observed in patients with Parkinson's disease (PD), and are associated with cerebrovascular diseases such as white matter hyperintensities and carotid atherosclerosis. We assessed the relationship between blood pressure abnormalities and cerebral microbleeds (CMBs), a marker of cerebral small vessel disease, in 128 patients with PD. We examined supine and orthostatic blood pressures and used 24-hour ambulatory blood pressure monitoring to assess the presence or absence of orthostatic hypotension (OH), supine hypertension (SH), nocturnal hypertension (NH), and loss of nocturnal blood pressure dips (non-dipping). CMBs were found in 13 (10.2%) patients, and the median number of CMBs was 1 (range: 1 to 10). Six of these patients had deep or infratentorial CMBs, six had strictly lobar CMBs, and one had mixed CMBs. Linear regression analysis indicated that presence of both OH and SH was independently associated with greater numbers of CMBs in deep or infratentorial regions, independent of age, sex, cardiovascular risk factors, and white matter hyperintensities. NH and non-dipping were not associated with CMBs in deep or infratentorial regions, and there was no association between blood pressure and CMBs in lobar regions. Our results suggest that the presence of both OH and SH may be related to deep or infratentorial CMBs in patients with PD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cerebral microbleeds and blood pressure abnormalities in Parkinson's disease

et al. 2018

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“…Cardiovascular autonomic dysfunctions are frequent in patients with PD, manifesting mainly as dizziness, faintness, orthostatic intolerance, and syncope. These abnormalities are also associated with cognitive impairments, white matter hyperintensity, carotid wall thickening, and mortality [ 1 , 5 , 19 - 21 ]. Cardiovascular autonomic dysfunction may result from myriad episodes of cerebral hypo- and hyper-perfusion, contributing to microvascular injury.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Autonomic Dysfunction in Mild and Advanced Parkinson’s Disease

Kim

Lee

et al. 2016

JMD

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ObjectiveThe purpose of the present study was to investigate cardiovascular autonomic dysfunction in patients with Parkinson’s disease (PD) with mild to severe stages of motor symptoms and to compare cardiovascular autonomic dysfunction between drug-naïve and dopaminergic drug-treated groups.MethodsThis study included 188 PD patients and 25 age-matched healthy controls who underwent head-up tilt-testing, 24-h ambulatory blood pressure (BP) monitoring and 24-h Holter monitoring. Autonomic function test results were evaluated among groups categorized by motor symptom severities (mild vs. moderate vs. severe) and treatment (drug-naïve or dopaminergic drug treatment).ResultsOrthostatic hypotension and supine hypertension were more frequent in patients with PD than in healthy controls. The frequencies of orthostatic hypotension, supine hypertension, nocturnal hypertension and non-dipping were not different among groups. Additionally, no significant differences were detected in supine BP, orthostatic BP change, nighttime BP, nocturnal BP dipping, or heart rate variabilities among groups.ConclusionsCardiovascular autonomic dysfunction is not confined to moderate to severe PD patients, and starts early in the course of the disease in a high proportion of PD patients. In addition, dopaminergic drug treatments do not affect cardiovascular autonomic function.

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“…Unlike motor symptoms, non-motor symptoms of PD are not improved by dopamine replacement therapy and seem to derive from the formation of Lewy bodies beyond midbrain dopaminergic neurons (Dickson et al, 2009). Cognitive impairment and dementia are the most disabling non-motor symptoms of PD, resulting from microvascular disease (Kim J.S. et al, 2014), deposition of Lewy bodies in neocortical and limbic areas, hyperphosphorylated tau-containing neurofibrillary tangles and formation of amyloid-beta-peptide plaques (Irwin et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

The Relevance of Insulin Action in the Dopaminergic System

et al. 2019

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The advances in medicine, together with lifestyle modifications, led to a rising life expectancy. Unfortunately, however, aging is accompanied by an alarming boost of age-associated chronic pathologies, including neurodegenerative and metabolic diseases. Interestingly, a non-negligible interplay between alterations of glucose homeostasis and brain dysfunction has clearly emerged. In particular, epidemiological studies have pointed out a possible association between Type 2 Diabetes (T2D) and Parkinson’s Disease (PD). Insulin resistance, one of the major hallmark for etiology of T2D, has a detrimental influence on PD, negatively affecting PD phenotype, accelerating its progression and worsening cognitive impairment. This review aims to provide an exhaustive analysis of the most recent evidences supporting the key role of insulin resistance in PD pathogenesis. It will focus on the relevance of insulin in the brain, working as pro-survival neurotrophic factor and as a master regulator of neuronal mitochondrial function and oxidative stress. Insulin action as a modulator of dopamine signaling and of alpha-synuclein degradation will be described in details, too. The intriguing idea that shared deregulated pathogenic pathways represent a link between PD and insulin resistance has clinical and therapeutic implications. Thus, ongoing studies about the promising healing potential of common antidiabetic drugs such as metformin, exenatide, DPP IV inhibitors, thiazolidinediones and bromocriptine, will be summarized and the rationale for their use to decelerate neurodegeneration will be critically assessed.

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Carotid artery thickening and neurocirculatory abnormalities in de novo Parkinson disease

Cited by 12 publications

References 32 publications

Cerebral microbleeds and blood pressure abnormalities in Parkinson's disease

Cerebral microbleeds and blood pressure abnormalities in Parkinson's disease

Cardiovascular Autonomic Dysfunction in Mild and Advanced Parkinson’s Disease

The Relevance of Insulin Action in the Dopaminergic System

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