scholarly journals Impact of Progression of Parkinson's Disease and Various Other Factors on Generalized Anxiety Disorder

2018 ◽  
Vol 09 (03) ◽  
pp. 287-290 ◽  
Author(s):  
Abdul Qayyum Rana ◽  
Hamza Ansari ◽  
Abdul Rehman M. Qureshi ◽  
Eraad Rahman

ABSTRACT Objective: While much research has been conducted toward understanding the relationship between prevalence of Parkinson's disease (PD) and generalized anxiety, little has been done considering additional influential factors in the relationship by means of a large ethnically diverse sample. Our study strives to fulfill these deficits in the literature as we set out to determine the impact of progression of PD, age, gender, and Hoehn and Yahr (H and Y) staging of PD on generalized anxiety. Methods: A retrospective chart review analysis was performed on PD patients who were regularly examined in a community-based PD and movement disorders center from 2005 to 2010. Results: This study consisted of 310 patients with PD among whom 12% had generalized anxiety. Neither age nor gender was significant onset predictors at P = 0.05. The impact of progression of H and Y Stages 2–3 and 2–4 increased the odds of generalized anxiety disorder (GAD) prevalence though it was statistically insignificant at P = 0.05. Conclusions: Clinicians should not expect the risk of developing anxiety to depend on gender nor change as a function of age though it may increase with symptomatic progression of PD as outlined by H and Y. To the best of our knowledge, this is the largest and most ethnically diverse prevalence study with a focus on generalized anxiety and PD. Significant Outcomes and Limitations: The symptomatic progression of PD, but not age or gender, may be associated with an increased risk for GAD. This study lacked adjustment for potential confounders such as depression and PD medications.

2021 ◽  
pp. 000313482198903
Author(s):  
Mitsuru Ishizuka ◽  
Norisuke Shibuya ◽  
Kazutoshi Takagi ◽  
Hiroyuki Hachiya ◽  
Kazuma Tago ◽  
...  

Objective To explore the impact of appendectomy history on emergence of Parkinson’s disease (PD). Background Although there are several studies to investigate the relationship between appendectomy history and emergence of PD, the results are still controversial. Methods We performed a comprehensive electronic search of the literature (the Cochrane Library, PubMed, and the Web of Science) up to April 2020 to identify studies that had employed databases allowing comparison of emergence of PD between patients with and those without appendectomy history. To integrate the impact of appendectomy history on emergence of PD, a meta-analysis was performed using random-effects models to calculate the risk ratio (RR) and 95% confidence interval (CI) for the selected studies, and heterogeneity was analyzed using I2 statistics. Results Four studies involving a total of 6 080 710 patients were included in this meta-analysis. Among 1 470 613 patients with appendectomy history, 1845 (.13%) had emergences of PD during the observation period, whereas among 4 610 097 patients without appendectomy history, 6743 (.15%) had emergences of PD during the observation period. These results revealed that patients with appendectomy history and without appendectomy had almost the same emergence of PD (RR, 1.02; 95% CI, .87-1.20; P = .83; I2 = 87%). Conclusion This meta-analysis has demonstrated that there was no significant difference in emergence of PD between patients with and those without appendectomy history.


2021 ◽  
pp. 1-14
Author(s):  
Conor Fearon ◽  
Alfonso Fasano

Studies focusing on the relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), coronavirus disease 2019 (COVID-19), and Parkinson’s disease (PD) have provided conflicting results. We review the literature to investigate: 1) Are PD patients at higher risk for contracting COVID-19 and are there specific contributing factors to that risk? 2) How does COVID-19 affect PD symptoms? 3) How does COVID-19 present in PD patients? 4) What are the outcomes in PD patients who contract COVID-19? 5) What is the impact of COVID-19 on PD care? 6) Does COVID-19 increase the risk of developing PD? A literature search was performed from 1979 to 2020 using the terms: ‘Parkinson’s disease’ and ‘parkinsonism’ combined with: ‘COVID-19’; ‘SARS-CoV-2’ and ‘coronavirus’. It does not appear that PD is a specific risk factor for COVID-19. There is evidence for direct/indirect effects of SARS-CoV-2 on motor/non-motor symptoms of PD. Although many PD patients present with typical COVID-19 symptoms, some present atypically with isolated worsening of parkinsonian symptoms, requiring increased anti-PD therapy and having worse outcomes. Mortality data on PD patients with COVID-19 is inconclusive (ranging from 5.2%to 100%). Patients with advanced PD appear to be particularly vulnerable. Single cases of acute hypokinetic-rigid syndrome have been described but no other convincing data has been reported. The rapidity with which COVID-19 has swept across the globe has favored the proliferation of studies which lack scientific rigor and the PD literature has not been immune. A coordinated effort is required to assimilate data and answer these questions in larger PD cohorts.


2010 ◽  
Vol 33 (2-3) ◽  
pp. 165-166 ◽  
Author(s):  
Dennis J. McFarland ◽  
Loretta S. Malta

AbstractIn the target article, Cramer et al. suggest that diagnostic classification is improved by modeling the relationship between manifest variables (i.e., symptoms) rather than modeling unobservable latent variables (i.e., diagnostic categories such as Generalized Anxiety Disorder). This commentary discusses whether symptoms represent manifest or latent variables and the implications of this distinction for diagnosis and treatment.


2018 ◽  
Vol 56 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Kiara Leonard ◽  
Amitai Abramovitch

AbstractBackground:Anxiety and worry are central symptoms of Generalized Anxiety Disorder (GAD) that have been theorized to negatively impact cognitive functions. However, most of the research has focused on threat-related or emotionally-charged stimuli, and a surprisingly small number of investigations examined ‘cold’ cognitive functions using classic neuropsychological tests. Such investigations are particularly important given that some theoretical models suggest compensatory mechanisms associated with anxiety that in certain circumstances may result in intact performance. The aim of the present study is to assess the neuropsychological profile associated with GAD, using a comprehensive neuropsychological battery.Methods:A sample of 23 college students meeting criteria for DSM-5 GAD and 20 control participants completed a psychometrically valid comprehensive computerized neuropsychological battery and clinical questionnaires.Results:The GAD sample presented with significantly elevated symptomatic rates of anxiety, worry, depression and stress. However, no significant differences were found on any neuropsychological outcome measures or domain indexes. Effect sizes were small, some of which favored the GAD sample.Conclusion:Despite substantial psychopathological burden, GAD exhibited intact cognitive functioning. These results support the Cognitive Control Theory of Anxiety, suggesting that elevated primary anxiety may not impact ‘cold’ cognitive functions in the absence of threat or substantial cognitive load. Given that this is one of the only studies employing a comprehensive neuropsychological battery in GAD, more research is needed in this population to replicate these results and to examine the impact of anxiety on cognitive functions at varying degrees of cognitive load in this population.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
M.A. Mychaskiw ◽  
J.M. Alvir ◽  
B.K. Herman ◽  
S. Pallanti ◽  
A. Joshi

Aims:To assess the impact of insomnia on quality of life (QoL) and functioning in patients with generalized anxiety disorder (GAD), and evaluate the efficacy of pregabalin and venlafaxine-XR in improving sleep and QoL.Methods:A double-blind trial in adults who met DSM-IV criteria for GAD, with a HAM-A total score ≥20,randomized to 8-weeks of flexible-dose treatment with pregabalin (300-600 mg/d, N=121), venlafaxine-XR (75-225 mg/d, N=125), or placebo (N=128).Results:At baseline, 64% of all subjects had insomnia (according to the Medical Outcomes Study Sleep scale [MOS]-Sleep Problems Index [SPI] criteria).While HAM-A total scores (minus the insomnia item) were similar for patients with and without baseline insomnia (25.7 vs. 25.0) those with reported significantly more impairment on the Quality of Life, Enjoyment, and Satisfaction Questionnaire (Q-LES-Q; 45.4 vs. 53.6; p< 0.0001) and Sheehan Disability Scale (SDS; 17.5 vs.14.3; p< 0.0001) than those without. At endpoint, there was a significantly greater mean improvement in MOS-sleep disturbance factor and MOS-SPI with pregabalin (-29.0 and -21.1, respectively) than venlafaxine-XR (-14.7 and -11.0) or placebo (-15.2 and -12.5; all p< 0.05). In more pregabalin (64%) than venlafaxine-XR (51%) or placebo (52%) subjects, abnormal baseline sleep had normalized by endpoint. Endpoint change in MOS-SPI significantly correlated with improvement in both Q-LES-Q and SDS-total scores (Spearman r-values, -0.48 and 0.46, respectively; both p< 0.0001; all subjects).Conclusion:Significantly greater impairment in QoL and functioning was observed in patients with high (vs. low) levels of insomnia. Pregabalin produced significantly greater improvement in insomnia than venlafaxine-XR or placebo.


2012 ◽  
Vol 29 (5) ◽  
pp. 386-391 ◽  
Author(s):  
Jennifer L. Francis ◽  
Ethan Moitra ◽  
Ingrid Dyck ◽  
Martin B. Keller

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