scholarly journals Relationship Between Orthostatic Hypotension and Cognitive Functions in Multiple System Atrophy: A Longitudinal Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Sofia Cuoco ◽  
Immacolata Carotenuto ◽  
Arianna Cappiello ◽  
Sara Scannapieco ◽  
Maria Claudia Russillo ◽  
...  

Introduction: The aim of this study is to investigate the impact of orthostatic hypotension (OH) on cognitive functions in patients with multiple system atrophy (MSA) followed over time.Methods: Thirty-two MSA patients were enrolled and underwent a comprehensive neuropsychological battery; at baseline (T0) 15 out of 32 patients presented OH, assessed by means of orthostatic standing test. All patients underwent a follow-up (T1) evaluation 12 months after baseline. Thirteen out of 32 patients also underwent a second follow-up (T2) evaluation at 24 months. Changes over time on different neuropsychological tasks were compared between patients with and without OH by means of Mann-Whitney's U-test. Moreover, clinical categories of normal cognition, mild cognitive impairment, and dementia were determined, and changes at T1 and T2 in global cognitive status were compared between patients with and without OH.Results: At T0, patients with OH had better performance on words/non-words repetition task (p = 0.02) compared to patients without OH. Compared to patients without OH, patients with OH performed worse on semantic association task (p < 0.01) at T1 and on Stroop test-error effect (p = 0.04) at T2. The percentage of patients with worsened cognitive status at T1 was higher among patients with OH than among patients without OH (93 vs. 59%, p = 0.03). OH (β = −4.67, p = 0.01), education (β = 0.45, p = 0.02), age (β = 0.19, p = 0.03), and Montreal Cognitive Assessment battery (MOCA) score at T0 (β = −0.26, p = 0.04) were significant predictors of global cognitive status worsening at T1.Discussion: We found that global cognitive status worsened at 1-year follow-up in 93% of patients with OH, and OH, along with age, education, and MOCA score, predicted cognitive worsening over time. To clarify the relationship between OH and cognitive dysfunction in MSA, we suggest the use of clinical categories of normal cognition, mild cognitive impairment, and dementia in further longitudinal studies on MSA patients with and without OH.

Diagnostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 718
Author(s):  
Salvatore Mazzeo ◽  
Valentina Bessi ◽  
Silvia Bagnoli ◽  
Giulia Giacomucci ◽  
Juri Balestrini ◽  
...  

Background: Periodic circadian protein homolog 2 (PER2) has a role in the intracellular signaling pathways of long-term potentiation and has implications for synaptic plasticity. We aimed to assess the association of PER2 C111G polymorphism with cognitive functions in subjective cognitive decline (SCD). Methods: Forty-five SCD patients were included in this study. All participants underwent extensive neuropsychological investigation, analysis of apolipoprotein E (APOE) and PER2 genotypes, and neuropsychological follow-up every 12 or 24 months for a mean time of 9.87 ± 4.38 years. Results: Nine out of 45 patients (20%) were heterozygous carriers of the PER2 C111G polymorphism (G carriers), while 36 patients (80%) were not carriers of the G allele (G non-carriers). At baseline, G carriers had a higher language composite score compared to G non-carriers. During follow-up, 15 (34.88%) patients progressed to mild cognitive impairment (MCI). In this group, we found a significant interaction between PER2 G allele and follow-up time, as carriers of G allele showed greater worsening of executive function, visual-spatial ability, and language composite scores compared to G non-carriers. Conclusions: PER2 C111G polymorphism is associated with better language performance in SCD patients. Nevertheless, as patients progress to MCI, G allele carriers showed a greater worsening in cognitive performance compared to G non-carriers. The effect of PER2 C111G polymorphism depends on the global cognitive status of patients.


Neurology ◽  
2019 ◽  
Vol 92 (23) ◽  
pp. e2699-e2705
Author(s):  
Lisa Vermunt ◽  
Alegría J.L. van Paasen ◽  
Charlotte E. Teunissen ◽  
Philip Scheltens ◽  
Pieter Jelle Visser ◽  
...  

ObjectiveTo identify potential predictors for outcome in individuals with mild cognitive impairment (MCI) who have reverted to normal cognition (NC).MethodsWe selected individuals with MCI, who reverted at follow-up to NC, with follow-up after reversion from Alzheimer's Disease Neuroimaging Initiative. Common clinical markers, Alzheimer disease (AD) biomarkers, and neurodegeneration imaging markers were used to compare MCI reverters based on subsequent clinical outcome (i.e., subsequent decline or stable reversion). For independent comparison, findings of the clinical Amsterdam Dementia Cohort are presented.ResultsSeventy-seven (10%) out of 757 individuals with MCI reverted to NC and 61 of these individuals had follow-up data available. After 3.2 ± 2.2 years, 16 (24%) progressed to MCI, and 3 (5%) to dementia. Those who declined were older and had a higher amyloid PET burden and higher CSF tau levels.ConclusionIn MCI reverters, abnormal biomarkers for AD pathology are associated with subsequent decline. AD biomarkers may aid in the prognosis of reverting MCI.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Gianmarco Borriello ◽  
Davide Viggiano ◽  
Giovambattista Capasso

Abstract Background and Aims Mild Cognitive Impairment (MCI) has been found to be highly prevalent amongst patients with Chronic Kidney Disease (CKD). In this cohort, the prevalence of MCI was estimated to be between 30% and 63%. Mild cognitive impairment is an intermediate state between normal aging and dementia. An individual suffering from MCI has difficulty in remembering, sustaining attention, or decision making which can negatively affect their daily lives. The aim of this study was to verify the role of different glomerular diseases diagnosed by kidney biopsy on the MCI through a retrospective study. Method We recruited 45 patients with bioptic diagnosis of the following glomerular diseases: Focal Segmental Glomerulo Sclerosis (FSGS), minimal change disease (MCD), membranous glomerular disease (MG), IgA nephropathy. The renal function was analyzed using clinical variables, while Cognitive functions using the MoCA test. Patients were divided into two groups based on 24h proteinuria. Results The MoCA score was directly correlated to the uric acid levels (R=0.13; p=0.03). The MoCa score in the group with higher proteinuria levels was significantly lower than those of the group with lower proteinuria levels (p = 0.03). Finally, the MoCA score in subjects with FSGS or MCD is significantly higher compared the other groups (p<0.05). Conclusion Our data suggest that serum uric acid and proteinuria in glomerular diseases influence cognitive functions. Interestingly, uric acid plays a neuroprotective role, as low levels of uric acid reduce the MoCA score. This result agrees with previous observations of a protective role of uric acid on dopamine neurons. Conversely, the extent proteinuria seems to negatively affect cognitive functions, suggesting a role of the endothelial dysfunction. Finally, glomerulopathies with a lower degree of inflammation (FSGS, MCD) have minor impact on cognitive functions.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S115-S115
Author(s):  
Carol Derby ◽  
Charles B Hall ◽  
Mindy Katz

Abstract Prior studies have shown that when standard diagnostic criteria are applied, the majority of individuals diagnosed with aMCI do not progress to clinical dementia, with a much larger proportion reverting to normal cognition. This suggests that a prospective confirmation of aMCI diagnosis may improve the specificity of the classification. We examined the rates of aMCI reversion using two definitions: one based on a single annual assessment, and one requiring a diagnosis over two consecutive annual assessments within the population based Einstein Aging Study Cohort. Using the definition that used a single annual assessment resulted in 224 incident aMCI cases in 5,321 person years of follow-up, for an incidence rate of 4.21 cases per 100 person years. Requiring the confirmatory diagnosis resulted in only 94 incident aMCI cases in 5736 person years of follow-up, for an incidence rate of 1.64 cases per 100 person years. 41% of the persons diagnosed with aMCI using the single annual assessment were cognitively normal at the next follow-up. Only 14% of the persons diagnosed with incident aMCI using the definition requiring later confirmation ever returned to being cognitively normal. When the aMCI definition that required confirmation was used, a dramatic reduction in the incidence rate of aMCI was observed in persons born after 1930, similar to what has been reported in the same cohort for dementia, but there was no such difference for the definition based on a single annual assessment.


2018 ◽  
Vol 45 (1-2) ◽  
pp. 66-78 ◽  
Author(s):  
Julius S. Ngwa ◽  
Thomas V. Fungwe ◽  
Oyonumo Ntekim ◽  
Joanne S. Allard ◽  
Sheree M. Johnson ◽  
...  

Background: It is increasingly evident that high blood pressure can promote reduction in global and regional brain volumes. While these effects may preferentially affect the hippocampus, reports are inconsistent. Methods: Using data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), we examined the relationships of hippocampal volume to pulse pressure (PPR) and systolic (SBP) and diastolic (DBP) blood pressure according to apolipoprotein (APOE) ɛ4 positivity and cognitive status. The ADNI data included 1,308 participants: Alzheimer disease (AD = 237), late mild cognitive impairment (LMCI = 454), early mild cognitive impairment (EMCI = 254), and cognitively normal (CN = 365), with up to 24 months of follow-up. Results: Higher quartiles of PPR were significantly associated with lower hippocampal volumes (Q1 vs. Q4, p = 0.034) in the CN and AD groups, but with increasing hippocampal volume (Q1, p = 0.008; Q2, p = 0.020; Q3, p = 0.017; Q4 = reference) in the MCI groups. In adjusted stratified analyses among non-APOE ɛ4 carriers, the effects in the CN (Q1 vs. Q4, p = 0.006) and EMCI groups (Q1, p = 0.002; Q2, p = 0.013; Q3, p = 0.002; Q4 = reference) remained statistically significant. Also, higher DBP was significantly associated with higher hippocampal volume (p = 0.002) while higher SBP was significantly associated with decreasing hippocampal volume in the EMCI group (p = 0.015). Conclusion: Changes in PPR, SBP, and DBP differentially influenced hippocampal volumes depending on the cognitive and APOE genotypic categories.


2010 ◽  
Vol 34 (1) ◽  
pp. 34-42 ◽  
Author(s):  
David S. Knopman ◽  
Rosebud O. Roberts ◽  
Yonas E. Geda ◽  
V. Shane Pankratz ◽  
Teresa J.H. Christianson ◽  
...  

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Pasquale Mone ◽  
Antonella Pansini ◽  
Giovambattista Capasso ◽  
Davide Viggiano

Abstract Background and Aims Mild Cognitive Impairment (MCI) is a common finding in chronic kidney disease (CKD) patients. Indeed, CKD represents a relevant risk factor for developing dementia and MCI. Cholinesterase inhibitors, such as rivastigmine, are among the few drugs approved for the treatment of dementia and MCI. Rivastigmine is also used to treat vascular dementia because it protects subcortical brain structures. Data are scanty regarding the use of rivastigmine in CKD patients with MCI and are much needed to guide the therapy for MCI in this cohort of patients. Method This retrospective case-control study compared the effects of rivastigmine on cognitive functions in MCI patients with CKD (stage III-IV; n= 20) and without CKD (n=21, control group), comparable for the extent of cognitive impairment (indexed by Montreal Cognitive Assessment, MoCA), age (range 18-65 years), gender, weight, and comorbidities. Patients under treatment with rivastigmine and with a baseline MoCA score available were included in the study. Exclusion criteria were ictus, psychiatric or other neurological conditions, heart failure, liver failure, severe obesity, anemia, electrolyte disorders, cancer, dialysis, and other severe comorbidities. Laboratory test data (glycemia, cholesterol, hemoglobin, proteinuria, creatinine) were used to characterize the two populations. MCI was defined as a MoCA score between 21-26. The cognitive screening was available at baseline (before treatment) and during a follow-up in a range of three-six months after the start of the treatment. CKD was defined by eGFR < 60 mL/min/1.73m2. Results The follow-up timing for cognitive screening was not statistically different between the two cohorts. The control group (MCI without CKD) showed a small, significant improvement in the MoCA score after treatment (baseline MoCA: 22.9±0.5, follow-up MoCA: 23.5±0.5, p=0.02, t-test for paired data). At variance, the MCI-CKD group showed a significant improvement in the MoCA score (baseline MoCA=23±0.4, follow-up MoCA=24.3±0.4, p<0.05). Accordingly, the extent of improvement of MoCA score after rivastigmine was inversely correlated to the eGFR (r = -0.23). Conclusion A significant improvement in MoCA score accompanied treatment with rivastigmine in the CKD group. More extensive population studies are needed to verify the greater efficacy of Acetylcholinesterase inhibitors in this population.


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