scholarly journals A Comparative Study of the Behavioral Profile of the Behavioral Variant of Frontotemporal Dementia and Parkinson’s Disease Dementia

2020 ◽  
pp. 182-194
Author(s):  
Dinesh Saini ◽  
Adreesh Mukherjee ◽  
Arijit Roy ◽  
Atanu Biswas
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Frontotemporal Dementia ◽  
Severe Disease ◽  
Executive Dysfunction ◽  
Behavioral Symptoms ◽  
Parkinson’S Disease Dementia ◽  
Subcortical Dementia ◽  
Behavioral Profile ◽  
Cortical Dementia

<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.

scholarly journals Risk Factors for Psychosis in Parkinson’s Disease

2017 ◽  
Vol 13 (02) ◽  
pp. 78
Author(s):  
Matthew J Barrett ◽  
Keyword(s):  
Risk Factors ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Visual Processing ◽  
Severe Disease ◽  
Executive Dysfunction ◽  
Neuropsychiatric Symptom ◽  
Increased Risk ◽  
Common Manifestation ◽  
Gba Mutations

Psychosis is a characteristic neuropsychiatric symptom of Parkinson’s disease (PD) that is common and associated with worse outcomes. The purpose of this article is to review identified risk factors for visual hallucinations in PD, the most common manifestation of psychosis. With the possible exception of dopamine agonists, antiparkinsonian medications are only considered modifiers of psychosis in PD. Dementia in PD has consistently been shown to be associated with psychosis, and executive dysfunction and impairment in visual processing appear to play a role in its pathogenesis. The association of psychosis with disorders of sleep–wake dysregulation and autonomic dysfunction supports the involvement of brainstem dysfunction in PD psychosis. Despite many studies evaluating genetic risk factors for hallucinations, GBA mutations are the only variants consistently reported to be associated with an increased risk of hallucinations in PD. Lastly, psychosis in PD is associated with a more severe disease burden, both related and unrelated to PD pathology. Any explanatory model of psychosis in PD must incorporate pharmacological, neuroanatomic, pathological, and genetic factors before there can be a complete understanding of this common and disabling neuropsychiatric symptom.

scholarly journals Dementia with Lewy bodies and Parkinson’s disease dementia-two independent disorders or one clinical entity within a clinical spectrum of synucleinopathies?

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Ewa Papuć
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Features ◽  
Dementia With Lewy Bodies ◽  
Current Knowledge ◽  
Lewy Bodies ◽  
Executive Dysfunction ◽  
Clinical Entity ◽  
Parkinson’S Disease Dementia ◽  
Visual Spatial

AbstractIntroduction: Introduction: Both dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) are important dementia syndromes that overlap in their clinical features and clinical course, neuropathological abnormalities, and also therapeutic approach. Nevertheless it is still unclear whether DLB and PDD are two different disorders that require differentiation or are one clinical entity within a spectrum of Lewy body disease. Currently these disorders are mainly distinguished on the basis of the relative timing of the onset of symptoms of dementia and parkinsonism. The present paper presents current concepts on the pathogenesis of both disorders and their possible overlap.Material and methods: Online databases in the field of DLB and PDD were searched for to find potentially eligible articles. Only most recent articles published after the year 2000 were chosen.Results: The clinical features of DLB and PDD are similar and include dementia with hallucinations and cognitive fluctuations, as well as parkinsonian signs. Also cognitive deficits are similar in PDD and in DLB, with predominance of executive dysfunction, visual-spatial deficits and memory impairment. Neuropathological changes in both disorders involve the presence of Lewy bodies and Lewy neurites within brainstem, limbic and neocortex, as well as loss of midbrain dopamine cells, and loss of cholinergic neurons in the nuclei of ventral forebrain.Conclusions: Similarities in clinical manifestation, neuropsychological deficits and neuropathological abnormalities may suggest that both DLB and PDD are two different phenotypes of the same disorder. This review article presents current knowledge on similarities and differences between these two clinical entities and raises the question whether they require differentiation or not.

Parkinson's Disease Dementia and Lewy Body Disease

2019 ◽  
Vol 39 (02) ◽  
pp. 274-282 ◽  
Author(s):  
Mine Sezgin ◽  
Basar Bilgic ◽  
Sule Tinaz ◽  
Murat Emre
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Body ◽  
Functional Neuroimaging ◽  
Neuropsychiatric Symptoms ◽  
Lewy Bodies ◽  
Lewy Body Disease ◽  
Behavioral Symptoms ◽  
Cognitive Symptoms ◽  
Parkinson’S Disease Dementia

AbstractDementia with Lewy bodies (DLB) and Parkinson's disease dementia (PD-D) are Lewy body-related neurodegenerative disorders sharing common clinical and neuropathological findings. The clinical features of both conditions include cognitive impairment, behavioral symptoms, autonomic dysfunction, sleep disorders, and parkinsonism. The cognitive profile of both disorders is characterized by particularly severe deficits in executive and visuospatial functions as well as attention. Clinical differentiation between DLB and PD-D is based on an arbitrary distinction between the time of onset of parkinsonism and cognitive symptoms; extrapyramidal symptoms precede dementia in PD-D, whereas it coincides with or follows dementia within 1 year in DLB. When the clinical picture is fully developed, DLB and PD-D are practically indistinguishable. Although the diagnosis is basically clinical, structural and functional neuroimaging as well as cerebrospinal fluid biomarkers may help the clinician in the diagnosis. Placebo-controlled randomized trials of the cholinesterase inhibitors have shown modest but significant benefits in cognition, global function, and neuropsychiatric symptoms in both disorders. Behavioral symptoms such as hallucinations and delusions should be treated with caution with antipsychotics, as they have the potential to worsen motor and cognitive symptoms.

scholarly journals Risk Factors for Psychosis in Parkinson’s Disease

US Neurology ◽  
2017 ◽  
Vol 13 (02) ◽  
pp. 78
Author(s):  
Matthew J Barrett ◽  
Keyword(s):  
Risk Factors ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Visual Processing ◽  
Severe Disease ◽  
Executive Dysfunction ◽  
Neuropsychiatric Symptom ◽  
Increased Risk ◽  
Common Manifestation ◽  
Gba Mutations

Psychosis is a characteristic neuropsychiatric symptom of Parkinson’s disease (PD) that is common and associated with worse outcomes. The purpose of this article is to review identified risk factors for visual hallucinations in PD, the most common manifestation of psychosis. With the possible exception of dopamine agonists, antiparkinsonian medications are only considered modifiers of psychosis in PD. Dementia in PD has consistently been shown to be associated with psychosis, and executive dysfunction and impairment in visual processing appear to play a role in its pathogenesis. The association of psychosis with disorders of sleep–wake dysregulation and autonomic dysfunction supports the involvement of brainstem dysfunction in PD psychosis. Despite many studies evaluating genetic risk factors for hallucinations, GBA mutations are the only variants consistently reported to be associated with an increased risk of hallucinations in PD. Lastly, psychosis in PD is associated with a more severe disease burden, both related and unrelated to PD pathology. Any explanatory model of psychosis in PD must incorporate pharmacological, neuroanatomic, pathological, and genetic factors before there can be a complete understanding of this common and disabling neuropsychiatric symptom.

scholarly journals Neuroinflammation and protein pathology in Parkinson’s disease dementia

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Antonina Kouli ◽  
Marta Camacho ◽  
Kieren Allinson ◽  
Caroline H. Williams-Gray
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
T Lymphocytes ◽  
Substantia Nigra ◽  
Amyloid Β ◽  
Brain Regions ◽  
Parkinson’S Disease Dementia ◽  
Activated Microglia ◽  
Cell Counts ◽  
The Brain

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.

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