View clinical trials related to Neurocognitive Function.
Filter by:Atrial fibrillation (AF) is the most common cardiac arrhythmia in the United States, and treatment by AF ablation is quickly becoming the favored definitive therapy. Nonetheless, AF ablation comes with some risk, including bleeds related to vascular access and myocardial damage, as well as the rare incidence of clinical stroke from blood clots that travel from the heart to the brain, termed "cerebrothromboemboli." In fact, cerebrothromboemboli without any symptoms have been detected by special imaging procedures called brain magnetic resonance imaging (MRI) in as many as 22% of cases.(1-6) There remains clinical equipoise amongst experts regarding balancing the risks and benefits of continued versus interrupted blood thinning, or "anticoagulation" during AF ablation as they pertain to risk of bleed and cerebrothromboemboli prevention, respectively, and the potentially more subtle sequelae of these apparently silent cerebrothromboemboli remain unknown. In fact, both interruption and continuation of anticoagulation during AF ablation are the standard of care. The investigators will perform the first randomized trial of uninterrupted versus interrupted anticoagulation in patients undergoing AF ablation to determine if it mitigates neurologic injury. The objective of this research is to investigate the effect of continued anticoagulation for AF ablation on cerebrothromboemboli, and the neurocognitive sequelae of embolic lesions, which to this point are considered subclinical. The investigators hypothesize that continued anticoagulation will both reduce cerebrothromboemboli and mitigate any potential decline in neurocognitive function post-procedurally. The investigators also hypothesize that the incidence of cerebrothromboemboli (CTE) by MRI will mediate that difference.
Previous researchers indicate that impaired cognitive flexibility was the primary factor distinguishing patients with from those without tardive dyskinesia (TD)1, and cognitive dysfunction correlates positively with the severity of TD2. Longitudinal data raised the possibility that the association between cognitive dysfunction and TD may reflect not organic vulnerability to but rather a state marker for this movement disorder as "tardive dementia"3. Atypical antipsychotic had been reported to alleviate the severity of TD4 and improved neurocognitive function separately5. But no researchers ever investigated the correlation of the two effects simultaneously. This randomized, single-blind and controlled study compared the effect of atypical antipsychotic on TD, neurocognitive function and associated factors for these changes.