scholarly journals Autonomic dysfunction: A comparative study of patients with Alzheimer’s and frontotemporal dementia – A pilot study

2017 ◽  
Vol 08 (01) ◽  
pp. 084-088 ◽  
Author(s):  
Thomas Gregor Issac ◽  
Sadanandavalli Retnaswami Chandra ◽  
Neelesh Gupta ◽  
Malligurki Raghurama Rukmani ◽  
S. Deepika ◽  
...  

ABSTRACT Introduction: In frontotemporal dementia (FTD) and Alzheimer’s disease (AD), central autonomic structures get affected early. An insight into autonomic functions in these patients is likely to be of diagnostic importance and thus help in prognosticating and also probably explain unexplained sudden death in some of these patients. Objectives: The objective of this study is to identify autonomic dysfunction prevailing in patients. Then, if there is dysfunction, is the pattern same or different in these two conditions. And if different it will serve as an additional biomarker for specific diagnosis. Patients and Methods: There were 25 patients and 25 controls and six patients and three controls in AD and FTD groups, respectively. The participants who were recruited were assessed for heart rate variability and conventional cardiac autonomic function testing. The parameters were analyzed using LabChart version 7 software and compared with control population using appropriate statistical methods using SPSS version 22 software. Results: The mean overall total power was low in the FTD group (P < 0.001), and there was significant reduction in the standard deviation of normal-to-normal intervals and root mean square of successive differences (P < 0.001) with elevated sympathovagal balance in the FTD group (P = 0.04). Patients with AD also showed sympathetic dominance, but there was in addition parasympathetic suppression unlike in the FTD group. Conclusion: This study reveals autonomic dysfunction in patients with FTD and AD. Both conditions show sympathetic dominance, probably consecutive to the involvement of central autonomic regulatory structures as a shared domain. It remains to be confirmed if these findings are the cause or effect of neurodegeneration and might open up newer territories of research based on the causal role of neurotransmitters in these regions and thus lead to novel therapeutic options such as yoga. The presence of parasympathetic suppression in AD in addition helps differentiate these two conditions.

2021 ◽  
Author(s):  
Lysleine Alves Deus ◽  
Rodrigo Vanerson Passos Neves ◽  
Hugo de Luca Corrêa ◽  
Andrea Lucena Reis ◽  
Fernando Sousa Honorato ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ching-Feng Cheng ◽  
Terry B. J. Kuo ◽  
Wei-Nan Chen ◽  
Chao-Chieh Lin ◽  
Chih-Cheng Chen

Integration of sympathetic and parasympathetic outflow is essential in maintaining normal cardiac autonomic function. Recent studies demonstrate that acid-sensing ion channel 3 (ASIC3) is a sensitive acid sensor for cardiac ischemia and prolonged mild acidification can open ASIC3 and evoke a sustained inward current that fires action potentials in cardiac sensory neurons. However, the physiological role of ASIC3 in cardiac autonomic regulation is not known. In this study, we elucidate the role of ASIC3 in cardiac autonomic function usingAsic3−/−mice.Asic3−/−mice showed normal baseline heart rate and lower blood pressure as compared with their wild-type littermates. Heart rate variability analyses revealed imbalanced autonomic regulation, with decreased sympathetic function. Furthermore,Asic3−/−mice demonstrated a blunted response to isoproterenol-induced cardiac tachycardia and prolonged duration to recover to baseline heart rate. Moreover, quantitative RT-PCR analysis of gene expression in sensory ganglia and heart revealed that no gene compensation for muscarinic acetylcholines receptors and beta-adrenalin receptors were found inAsic3−/−mice. In summary, we unraveled an important role of ASIC3 in regulating cardiac autonomic function, whereby loss of ASIC3 alters the normal physiological response to ischemic stimuli, which reveals new implications for therapy in autonomic nervous system-related cardiovascular diseases.


2021 ◽  
Author(s):  
Lucia M Li ◽  
Ekawat Vichayanrat ◽  
Martina del Giovane ◽  
Helen HL Lai ◽  
Valeria Iodice

Background and Objective: Survivors of moderate-severe traumatic brain injury (msTBI) frequently experience chronic, debilitating somatic symptoms, which are largely unexplained. The phenomenon of paroxysmal sympathetic hyperactivity, reflecting hyperacute autonomic dysfunction, is well-documented after msTBI. Limited animal and human studies, using experimental measures, have found evidence for autonomic dysfunction after msTBI. However, no studies have investigated the range and type of autonomic symptoms and autonomic dysfunction existing in msTBI. We set out to investigate the presence and type of subjective and objective autonomic dysfunction in msTBI. Methods: We conducted two cohort studies. Cohort 1 comprises msTBI patients prospectively recruited from a regional TBI outpatient clinic, in whom we assessed burden of autonomic symptoms using the Composite Autonomic Symptom Score (COMPASS31) autonomic symptom questionnaire. Cohort 2 comprises msTBI patients who had standard clinical autonomic function testing (supine/tilted catecholamine levels, head-up tilt, Valsalva manoeuvre, respiratory sinus arrhythmia assessment), retrospectively identified from the database of a regional clinical autonomic unit. Results: Cohort 1 comprises 29 msTBI patients (6 females, median age 40 years, range 19-76), with a median time since injury of 19 months (range 4-105). There was multi-domain symptom burden, with all but 3 patients reporting symptoms on the COMPASS31 questionnaire, and 17/29 reporting symptoms in 3+ domains. The most commonly reported symptoms were gastrointestinal (22/29), followed by orthostatic (17/19), pupillomotor (14/29), secretomotor (14/29), bladder (12/29) and, least commonly, vasomotor (6/29). Cohort 2 comprises 19 msTBI patients (7 females, median age 44 years, range 21-64), with a median time between injury and testing of 65 months (range: 2-416). The majority of patients (16/19) had orthostatic symptoms as part of the reason for referral. Clinical autonomic function testing revealed a broad spectrum of autonomic dysfunction: 4/19 had evidence of sympathetic dysfunction, 10/19 had evidence of parasympathetic dysfunction, of which 6 had evidence of mixed dysfunction. Discussion: Our results provide evidence for clinically relevant autonomic dysfunction after moderate-severe TBI, even at the chronic stage. Our study advocates for routine enquiry about potential autonomic symptoms in this population, and the utility of formal clinical autonomic testing in providing diagnoses.


2021 ◽  
Author(s):  
Myungshin Kim ◽  
Mi Yeon Kwon ◽  
HeeJeong Lee ◽  
Min Jeong Kim

Abstract Recent studies demonstrated a significant role of several microRNAs (miRs) in the development of leiomyoma. Here, we investigated miR expression profiles using microarray and found a significantly higher expression of miRs in leiomyoma than in adjacent myometrium. We also confirmed the upregulation of five selected miRs including miR-181a-5p, 127-3p, 28-3p, 30b-5p and let-7c-5p in cellular proliferation, extracellular matrix turnover, and angiogenesis by RT-qPCR. Interestingly, the miRs showed a higher expression in cases of large leiomyoma or in patients with a history of transfusion due to anemia. We then analyzed the expression of the miR target molecules including TGFBR2 and IGF2BP1 via immunohistochemistry. TGFBR2 and IGF2BP1 were positively stained in 81% and 62.5% of leiomyoma tissues but not in adjacent myometrium. Both were more frequently positive in patients with ≥ 6 cm leiomyoma and mass effect. The mean expression levels of miR-181a-5p, 127-3p, 28-3p, 30b-3p and let-7c-5p were higher in cases with TGFBR2 and IGF2BP1 positive leiomyoma. These results provide insight into the role of miRs in the development and progression of leiomyoma and underscore the need to validate their utility as diagnostic or therapeutic targets.


Author(s):  
Peter Hämmerle ◽  
Stefanie Aeschbacher ◽  
Anne Springer ◽  
Ceylan Eken ◽  
Michael Coslovsky ◽  
...  

Abstract Background Atrial fibrillation (AF) is associated with loss of cognition and dementia. Cardiac autonomic dysfunction has been linked to cognitive decline. We aimed to investigate if reduced cardiac autonomic function (CAF) is associated with cognitive impairment in AF patients. Methods Patients with paroxysmal, persistent and permanent AF were enrolled from a multicenter cohort study if they had AF (“AF group”) or sinus rhythm (“SR group”) on a baseline 5 min ECG recording. Parameters quantifying CAF (heart rate variability triangular index (HRVI), mean heart rate (MHR), RMSSD, SDNN, total power and power in the VLF, LF, HF ranges) were calculated. We used the Montreal Cognitive Assessment (MoCA) to assess global cognitive function. Results 1685 AF patients with a mean age of 73 ± 8 years, 29% females, were included. MoCA score was 24.5 ± 3.2 in the AF group (N = 710 patients) and 25.4 ± 3.2 in the SR group (N = 975 patients). After adjusting for multiple confounders, lower HRVI was associated with lower MoCA scores, both in the SR group [β = 0.049; 95% confidence interval (CI) 0.016–0.081; p = 0.003] and in the AF group (β = 0.068; 95% CI 0.020–0.116; p = 0.006). In the AF group, higher MHR was associated with a poorer performance in the MoCA (β =  − 0.008; 95% CI − 0.014 to − 0.002; p = 0.014). We found no convincing evidence of association for other CAF parameters with cognition. Conclusion Our data suggest that impaired CAF is associated with worse cognitive performance in patients with AF. Among standard HRV parameters, HRVI might be the most promising ECG index. Trial registration ClinicalTrials.gov Identifier: NCT02105844. Graphic abstract


2021 ◽  
Author(s):  
Ahsan Khan ◽  
Rehan Junejo ◽  
Neil Thomas ◽  
James Fisher ◽  
G. Lip

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