Dear colleagues, I am Christoph Diener from the University of Essen in Germany. For the month of November, I have identified four interesting studies in neurology.
The first one was published in the European Heart Journal, and it addresses the question of whether, if you treat atrial fibrillation with anticoagulation, you can prevent the development of dementia. There are a number of studies which basically show that people with atrial fibrillation have an increased risk for dementia, and this is true for both Alzheimer disease and vascular dementia.
Investigators from Sweden looked at the national health registry and the drug prescription registry. They identified 444,106 patients who had atrial fibrillation. About half of them were anticoagulated and the other ones were not anticoagulated, for whatever reason. They found that in a period between 2006 and 2014, the risk of developing dementia was reduced by almost 30% in patients who were anticoagulated. This was true both for warfarin and for NOACs [novel oral anticoagulants]. This would indicate in a large sample of almost 450,000 patients with atrial fibrillation that anticoagulation can prevent the development of dementia.
The next study deals with secondary stroke prevention and smoking. This was a study which investigated pioglitazone in patients who had a TIA [transient ischemic attack] or stroke over a period of 5 years. This was called the IRIS trial. The investigators looked at patients who at baseline had the event—stroke or TIA—and smoked; then they looked at patients who quit smoking in the next 5 years. This percentage at the beginning was about 30%, and 42% of these patients stopped smoking. What they observed was a risk reduction of 35% for a recurrent stroke, myocardial infarction, and vascular death if people stopped smoking. The benefit was very clear for stroke and death. It was not significant for myocardial infarction.
Now, I would like to move to Parkinson's disease. There are a number of epidemiologic studies which would indicate that the consumption of caffeine can reduce the risk for Parkinson's disease. A publication in Neurology investigated whether caffeine given twice daily in a dose of 200 mg in a period of between 6 and 18 months has an impact on the symptoms of Parkinson's disease.
They randomized 120 patients to either caffeine twice daily or to placebo. The study could not show a benefit on the neurologic symptoms of Parkinson's disease, and there were no cognitive testing results in patients on caffeine. What the study does not answer is whether caffeine has a preventive effect on the cause of Parkinson's disease.
The last study was published in Annals of Neurology and investigated whether traumatic brain injury is a predictor of Parkinson's disease. The investigators identified almost 89,000 patients who had Parkinson's disease and 118,000 controls around the age of 65 years. They looked at the connection between traumatic brain injury in the past 5 years to the incidence of Parkinson's disease. They found that there was a 64% increase in the risk of developing Parkinson's disease if the traumatic brain injury was within the past 5 years. The risk increased with a shortening of the time interval between traumatic brain injury and Parkinson's disease.
Now, whether there is a causal relationship or whether the traumatic brain injury happened due to falls—because the patients already started having motor symptoms of Parkinson's disease—cannot be answered by this study. It also has no impact on patient handling because you cannot prevent traumatic brain injury or falls to prevent Parkinson's disease. At least it is an interesting study, indicating that head trauma and brain trauma might be risk factors for Parkinson's disease.
Ladies and gentlemen, here are two studies from the stroke field and two interesting studies from the Parkinson's disease field. I'm Christoph Diener, a neurologist from the Department of Neurology in Essen, Germany. Thank you for listening.
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Cite this: Four New Updates in Stroke and Parkinson Disease - Medscape - Dec 06, 2017.