scholarly journals Lower Extremity Tremor Exacerbation due to Rivastigmine Administration for Treatment of Parkinson’s Disease Dementia

2018 ◽  
Vol 29 (2) ◽  
Author(s):  
Antonina Kouli ◽  
Marta Camacho ◽  
Kieren Allinson ◽  
Caroline H. Williams-Gray

AbstractParkinson’s disease dementia is neuropathologically characterized by aggregates of α-synuclein (Lewy bodies) in limbic and neocortical areas of the brain with additional involvement of Alzheimer’s disease-type pathology. Whilst immune activation is well-described in Parkinson’s disease (PD), how it links to protein aggregation and its role in PD dementia has not been explored. We hypothesized that neuroinflammatory processes are a critical contributor to the pathology of PDD. To address this hypothesis, we examined 7 brain regions at postmortem from 17 PD patients with no dementia (PDND), 11 patients with PD dementia (PDD), and 14 age and sex-matched neurologically healthy controls. Digital quantification after immunohistochemical staining showed a significant increase in the severity of α-synuclein pathology in the hippocampus, entorhinal and occipitotemporal cortex of PDD compared to PDND cases. In contrast, there was no difference in either tau or amyloid-β pathology between the groups in any of the examined regions. Importantly, we found an increase in activated microglia in the amygdala of demented PD brains compared to controls which correlated significantly with the extent of α-synuclein pathology in this region. Significant infiltration of CD4+ T lymphocytes into the brain parenchyma was commonly observed in PDND and PDD cases compared to controls, in both the substantia nigra and the amygdala. Amongst PDND/PDD cases, CD4+ T cell counts in the amygdala correlated with activated microglia, α-synuclein and tau pathology. Upregulation of the pro-inflammatory cytokine interleukin 1β was also evident in the substantia nigra as well as the frontal cortex in PDND/PDD versus controls with a concomitant upregulation in Toll-like receptor 4 (TLR4) in these regions, as well as the amygdala. The evidence presented in this study show an increased immune response in limbic and cortical brain regions, including increased microglial activation, infiltration of T lymphocytes, upregulation of pro-inflammatory cytokines and TLR gene expression, which has not been previously reported in the postmortem PDD brain.


2016 ◽  
Vol 10 (4) ◽  
pp. 339-343 ◽  
Author(s):  
Carlos Henrique Ferreira Camargo ◽  
Rafael Arthur Serpa ◽  
Thiago Matnei ◽  
Jivago Szpoganicz Sabatini ◽  
Hélio Afonso Ghizoni Teive

ABSTRACT Background: Apathy is one of the main neuropsychiatric symptoms in patients with Parkinson's disease (PD) and is associated with Parkinson's disease dementia (PDD). Objective: To identify the characteristics of apathy in individuals with PDD according to caregiver perception. Methods: Thirty-nine patients with PD according to MDS criteria for PDD were included. The following scales were used: the Hoehn and Yahr, the Unified Parkinson's Disease Rating Scale III, Scales for Outcomes in Parkinson's Disease-Cognition (SCOPA Cog), the Montgomery-Åsberg Depression Rating Scale (MADRS) and the Apathy Evaluation Scale (AES). Results: A total of 97.4% of the patients showed results consistent with apathy. Analysis of question 14 of the AES revealed no correlation with the total result of all the questions [r=-1293, r²=0.0167, 95%CI (-0.4274 to 0.1940), P=0.2162], however, there was a correlation of responses to the same question with depression data on the MADRS scale [r=-0.5213, r²=0.2718, 95%CI (-0.7186 to -0.2464), P=0.00033]. Conclusion: Apathy is a disorder associated with PDD. However, the scoring scheme of the AES questions can lead to different interpretations of caregiver responses, highlighting limitations of the tool for use in studies of PDD.


2008 ◽  
Vol 4 ◽  
pp. T173-T173
Author(s):  
Jina E. Swartz ◽  
Margaret L. Moline ◽  
Julian Gray ◽  
Gail Thomas ◽  
Mark Harre ◽  
...  

Author(s):  
Dinesh Saini ◽  
Adreesh Mukherjee ◽  
Arijit Roy ◽  
Atanu Biswas

<b><i>Background:</i></b> Executive dysfunction is the common thread between pure cortical dementia like the behavioral variant of frontotemporal dementia (bvFTD) and subcortical dementia like Parkinson’s disease dementia (PDD). Although there are clinical and cognitive features to differentiate cortical and subcortical dementia, the behavioral symptoms differentiating these 2 conditions are still not well known. <b><i>Objective:</i></b> To evaluate the behavioral profile of bvFTD and PDD and compare them to find out which behavioral symptoms can differentiate between the two. <b><i>Methods:</i></b> Twenty consecutive patients with bvFTD (&#x3e;1 year after diagnosis) and 20 PDD patients were recruited according to standard diagnostic criteria. Behavioral symptoms were collected from the reliable caregiver by means of a set of questionnaires and then compared between the 2 groups. <b><i>Results:</i></b> bvFTD patients had more severe disease and more behavioral symptoms than PDD. bvFTD patients were different from PDD patients due to their significantly greater: loss of basic emotion (<i>p</i> &#x3c; 0.001, odds ratio [OR] 44.33), loss of awareness of pain (<i>p</i> &#x3c; 0.001, OR 44.33), disinhibition (<i>p</i> &#x3c; 0.001, OR 35.29), utilization phenomenon (<i>p</i> = 0.008, OR 22.78), loss of taste discrimination (<i>p</i> &#x3c; 0.001, OR 17), neglect of hygiene (<i>p</i> = 0.001, OR 13.22), loss of embarrassment (<i>p</i> = 0.003, OR 10.52), wandering (<i>p</i> = 0.004, OR 9.33), pacing (<i>p</i> = 0.014, OR 9), selfishness (<i>p</i> = 0.014, OR 9), increased smoking (<i>p</i> = 0.014, OR 9), increased alcohol consumption (<i>p</i> = 0.031, OR 7.36), social avoidance (<i>p</i> = 0.012, OR 6.93), mutism (<i>p</i> = 0.041, OR 5.67), and failure to recognize objects (<i>p</i> = 0.027, OR 4.33). The bvFTD patients were also significantly less suspicious (<i>p</i> = 0.001, OR 0.0295), less inclined to have a false belief that people were in their home (<i>p</i> = 0.014, OR 0.11) and had fewer visual illusions/hallucinations (<i>p</i> = 0.004, OR 0.107) than PDD patients. <b><i>Conclusion:</i></b> Behavioral symptoms are helpful to distinguish bvFTD from PDD, and thus also cortical dementia with frontal-lobe dysfunction from subcortical dementia.


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