The clinical and neuroimaging differences between vascular parkinsonism and Parkinson’s disease: a case-control study
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SUBMITTER: George P
PROVIDER: S-EPMC10845551 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe neuroanatomical substrates of Parkinson's disease (PD) with tremor-dominance (TD) and those with non-tremor dominance (nTD), postural instability and gait difficulty (PIGD), and akinetic-rigid (AR) are not fully differentiated. A better understanding of symptom specific pathoanatomical markers of PD subtypes may result in earlier diagnosis and more tailored treatment. Here, we aim to give an overview of the neuroimaging literature that compared PD motor subtypes.MethodsA systematic literature review on neuroimaging studies of PD subtypes was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Search terms submitted to the PubMed database included: "Parkinson's disease", "MRI" and "motor subtypes" (TD, nTD, PIGD, AR). The results are first discussed from macro to micro level of organization (i.e., (1) structural; (2) functional; and (3) molecular) and then by applied imaging methodology.FindingsSeveral neuroimaging methods including diffusion imaging and positron emission tomography (PET) distinguish specific PD motor subtypes well, although findings are mixed. Furthermore, our review demonstrates that nTD-PD patients have more severe neuroalterations compared to TD-PD patients. More specifically, nTD-PD patients have deficits within striato-thalamo-cortical (STC) circuitry and other thalamocortical projections related to cognitive and sensorimotor function, while TD-PD patients tend to have greater cerebello-thalamo-cortical (CTC) circuitry dysfunction.ConclusionsBased on the literature, STC and CTC circuitry deficits seem to be the key features of PD and the subtypes. Future research should make greater use of multimodal neuroimaging and techniques that have higher sensitivity in delineating subcortical structures involved in motor diseases.
| S-EPMC7853198 | biostudies-literature
Project description:BackgroundDifferential diagnosis between idiopathic normal pressure hydrocephalus (iNPH) associated with parkinsonism (iNPH-P) and Parkinson's disease (PD) may prove difficult when evaluating patients with early parkinsonism. The objective of this study was to evaluate differences in mobility during standardized tasks between iNPH-P and PD.MethodsWe selected 21 iNPH-P and 21 pharmacologically untreated PD patients. They all performed the instrumented Timed Up and Go test at the time of diagnosis.ResultsTurning tasks showed longer duration and lower speed in iNPH-P than in PD. Vertical variation in acceleration during the sit-to-stand phase was lower in iNPH-P patients, whereas the duration of the stand-to-sit phase was longer. On walking, iNPH-P showed smaller stride length and a longer gait cycle duration. In multivariate analysis adjusting for age and cognitive status as potential confounders, average angular speed on turning before sitting was the discriminating parameter between the two groups.ConclusionsPatients with iNPH-P showed specific abnormal mobility performances with respect to untreated PD, specifically during the turning-to-sitting transition.
| S-EPMC10026280 | biostudies-literature
Project description:IntroductionFor the diagnosis of Parkinson's disease (PD) and atypical parkinsonism (AP) using neuroimaging, structural measures have been largely employed since structural abnormalities are most noticeable in the diseases. Functional abnormalities have been known as well, though less clearly seen, and thus, the addition of functional measures to structural measures is expected to be more informative for the diagnosis. Here, we aimed to assess whether multimodal neuroimaging measures of structural and functional alterations could have potential for enhancing performance in diverse diagnostic classification problems.MethodsFor 77 patients with PD, 86 patients with AP comprising multiple system atrophy and progressive supranuclear palsy, and 53 healthy controls (HC), structural and functional MRI data were collected. Gray matter (GM) volume was acquired as a structural measure, and GM regional homogeneity and degree centrality were acquired as functional measures. The measures were used as predictors individually or in combination in support vector machine classifiers for different problems of distinguishing between HC and each diagnostic type and between different diagnostic types.ResultsIn statistical comparisons of the measures, structural alterations were extensively seen in all diagnostic types, whereas functional alterations were limited to specific diagnostic types. The addition of functional measures to the structural measure generally yielded statistically significant improvements to classification accuracy, compared to the use of the structural measure alone.ConclusionWe suggest the fusion of multimodal neuroimaging measures as an effective strategy that could generally cope with diverse prediction problems of clinical concerns.
| S-EPMC7667347 | biostudies-literature
Project description:Parkinson's disease (PD) is a common disorder in which the primary features can be related to dopamine deficiency. Changes on structural imaging are limited, but a wealth of abnormalities can be detected using positron emission tomography, single photon emission computed tomography, or functional magnetic resonance imaging to detect changes in neurochemical pathology or functional connectivity. The changes detected on these studies may reflect the disease process itself and/or compensatory responses to the disease, or they may arise in association with disease- and/or treatment-related complications. This review will focus mainly on neurochemical and metabolic studies and reviews various approaches to the assessment of dopaminergic function as well as the function of other neurotransmitters that may be affected in PD. A number of clinical applications are highlighted, including diagnostic utility, identification of preclinical disease, changes associated with motor and nonmotor complications of PD, and the effects of various therapeutic interventions.
| S-EPMC3075732 | biostudies-literature
Project description:BackgroundMounting evidence has revealed an inverse association between cigarette smoking and the risk of Parkinson's disease (PD). Meanwhile, cigarette smoking has been found to be associated with cognitive impairment in PD patients. However, the neural mechanisms of the association between cigarette smoking and PD are not fully understood.ObjectiveThe aim of this study is to explore the neural mechanisms of the association between cigarette smoking and PD.MethodsA total of 129 PD patients and 69 controls were recruited from the Parkinson's Progression Markers Initiative (PPMI) cohort, including 39 PD patients with regular smoking history (PD-S), 90 PD patients without regular smoking history (PD-NS), 26 healthy controls with regular smoking history (HC-S), and 43 healthy controls without regular smoking history (HC-NS). Striatal dopamine transporter (DAT) binding and gray matter (GM) volume of the whole brain were compared among the four groups.ResultsPD patients showed significantly reduced striatal DAT binding compared with healthy controls, and HC-S showed significantly reduced striatal DAT binding compared with HC-NS. Moreover, smoking and PD showed a significant interaction effect in the left medial prefrontal cortex (mPFC). PD-S showed reduced GM volume in the left mPFC compared with PD-NS.ConclusionThe degeneration of dopaminergic neurons in PD results in a substantial reduction of the DAT and dopamine levels. Nicotine may act as a stimulant to inhibit the action of striatal DAT, increasing dopamine levels in the synaptic gap. The inverse alteration of dopamine levels between PD and nicotine addiction may be the reason for the inverse association between smoking and the risk of PD. In addition, the mPFC atrophy in PD-S may be associated with cognitive impairment.
| S-EPMC9019319 | biostudies-literature
Project description:IntroductionPredictive biomarkers of Parkinson's Disease progression are needed to expedite neuroprotective treatment development and facilitate prognoses for patients. This work uses measures derived from resting-state functional magnetic resonance imaging, including regional homogeneity (ReHo) and fractional amplitude of low frequency fluctuations (fALFF), to predict an individual's current and future severity over up to 4 years and to elucidate the most prognostic brain regions.MethodsReHo and fALFF are measured for 82 Parkinson's Disease subjects and used to train machine learning predictors of baseline clinical and future severity at 1 year, 2 years, and 4 years follow-up as measured by the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS). Predictive performance is measured with nested cross-validation, validated on an external dataset, and again validated through leave-one-site-out cross-validation. Important predictive features are identified.ResultsThe models explain up to 30.4% of the variance in current MDS-UPDRS scores, 55.8% of the variance in year 1 scores, and 47.1% of the variance in year 2 scores (p < 0.0001). For distinguishing high and low-severity individuals at each timepoint (MDS-UPDRS score above or below the median, respectively), the models achieve positive predictive values up to 79% and negative predictive values up to 80%. Higher ReHo and fALFF in several regions, including components of the default motor network, predicted lower severity across current and future timepoints.ConclusionThese results identify an accurate prognostic neuroimaging biomarker which may be used to better inform enrollment in trials of neuroprotective treatments and enable physicians to counsel their patients.
| S-EPMC8127393 | biostudies-literature
Project description:ObjectivesLife's essential 8 (LE8) is an emerging approach for accessing and quantifying cardiovascular health (CVH), but the effect on Parkinson's disease (PD) is still unclear. This study aimed to elucidate the association between LE8 metrics and PD in the US adults.MethodsData of 26,975 participants were extracted from the last 7 National Health and Nutrition Examination Survey (NHANES) cycles (2005-2018). The LE8 metrics were calculated according to the American Heart Association criterion, and participants were divided into 3 groups using tertile range. Multivariate logistic regression models were constructed to explore the association between LE8 metrics and PD. Sensitivity analysis was conducted to verify robustness. A nonlinear linkage was evaluated via restricted cubic spline (RCS). The stability of this effect was validated by subgroup analysis and interaction test.ResultsA total of 26,975 eligible participants (including 271 PD cases and 26,704 non-PD cases) were included in this study. The multivariate logistic regression models revealed a reverse association of continuous LE8 metrics with PD with ORs of 0.97 (unadjusted model [95% CI: 0.96-0.98, P < 0.01], partially adjusted model [95% CI: 0.97-0.98, P < 0.01], fully adjusted model [95% CI: 0.95-0.98, P < 0.01]). Compared to those of low group, the ORs for high group were 0.37 (95% CI: 0.27-0.50, P < 0.01) in unadjusted model, 0.51 (95% CI: 0.36-0.72, P < 0.01) in partially adjusted model, and 0.51 (95% CI: 0.32-0.81, P < 0.01) in fully adjusted model. The sensitivity analysis ensured the robustness of the observed LE8-PD association. A nonlinear relationship (P nonlinearity < 0.01) was observed via RCS analysis. The subgroup analysis showed that participants'gender might impact the strength of LE8 metrics-PD association (P interaction = 0.029).ConclusionsCVH, as delineated by LE8 metrics, was reversely associated with PD in the dose-response pattern, more pronounced in female compared to male. These findings highlight the potential of the LE8 metrics to guide targeted strategies for addressing gender-based CVH disparities, offering beneficial insights for the tertiary prevention of PD.
| S-EPMC11786534 | biostudies-literature
Project description:The possible relationship between essential tremor (ET) and Parkinson's disease (PD) has been controversial since the first description of PD. However, there is increasing evidence suggesting an overlap between these two disorders. The aim of this review is to examine the relationship between PD and ET, focusing on clinical, epidemiologic, genetic, neuroimaging, and neuropathological data, and the presence of cardinal parkinsonism symptoms in ET. We conducted a PubMed search for articles published between 1966 and November 2011 regarding the relationship between ET and PD and the presence of postural tremor in PD patients; the presence of rest tremor, rigidity, and slowed movements in ET patients is reviewed. Clinical series, follow-up studies of ET patients, and case-control and genetic epidemiological studies indicate that ET is associated with increased risk for PD. Some neuroimaging studies and neuropathological reports suggest an association between the two diseases. ET patients show high prevalence of rest tremor, and at least seven studies described slowed movements (possibly related to cerebellar dysfunction and/or bradykinesia) in patients with ET. There is reasonable epidemiological and clinical evidence to support a link between ET and PD, although it is not clear what factors predict ET patient risk for developing PD or, more rarely, of PD patients developing ET. Future multicentric and multidisciplinary studies including epidemiological, clinical, neuroimaging, genetic, and neuropathological assessments are required to understand these associations.
| S-EPMC3572635 | biostudies-literature
Project description:BackgroundDrug-induced parkinsonism (DIP) is common, but diagnosis is challenging. Although dopamine transporter imaging is useful, the cost and inconvenience are problematic, and an easily accessible screening technique is needed. We aimed to determine whether optical coherence tomography (OCT) findings could differentiate DIP from Parkinson's disease (PD).MethodsWe investigated 97 de novo PD patients and 27 DIP patients using OCT and [18F] N-(3-fluoropropyl)-2b-carbon ethoxy-3b-(4-iodophenyl) nortropane (FP-CIT) positron emission tomography. We compared peripapillary retinal nerve fiber layer thickness (pRNFLT) and macular retinal thickness (mRT) between PD and DIP patients as well as interocular differences in the pRNFLT and the mRT. Asymmetric index (%) for retinal thickness (AIRT) was calculated to measure the interocular differences between pRNFLT and mRT. The correlation between AIRT and total striatal specific/non-specific binding ratio asymmetry index (SNBRAI) was investigated in PD and DIP patients.ResultsNo significant differences in pRNFLT and mRT values were observed between PD and DIP patients (all P values > 0.090). The mean SNBRAI was significantly higher in PD than in DIP (P = 0.008) patients; however, AIRT did not differ between PD and DIP patients in pRNFLT and mRT (all P values > 0.100). SNBRAI did not correlate with AIRT of pRNFL or mRT in PD and DIP patients (all P values > 0.060).ConclusionOur study showed no benefit of retinal thickness and interocular asymmetry measurements using OCT for distinguishing PD from DIP in the early stages. Additional investigations are needed for confirmation.
| S-EPMC10027544 | biostudies-literature
Project description:This article reviews was to review genes where putative or confirmed pathogenic mutations causing Parkinson's disease or Parkinsonism have been identified since 2012, and summarizes the clinical and pathological picture of the associated disease subtypes.Newly reported genes for dominant Parkinson's disease are DNAJC13, CHCHD2, and TMEM230. However, the evidence for a disease-causing role is not conclusive, and further genetic and functional studies are warranted. RIC3 mutations have been reported from one family but not yet encountered in other patients. New genes for autosomal recessive disease include SYNJ1, DNAJC6, VPS13C, and PTRHD1. Deletions of a region on chromosome 22 (22q11.2del) are also associated with early-onset PD, but the mode of inheritance and the underlying causative gene remain unclear. PODXL mutations were reported in autosomal recessive PD, but their roles remain to be confirmed. Mutations in RAB39B cause an X-linked Parkinsonian disorder. Mutations in the new dominant PD genes have generally been found in medium- to late-onset Parkinson's disease. Many mutations in the new recessive and X-chromosomal genes cause severe atypical juvenile Parkinsonism, but less devastating mutations in these genes may cause PD.
| S-EPMC5522513 | biostudies-other