Head Trauma and the Risk of Parkinson Disease

It has long been clear that patients with extensive head trauma have a greatly increased risk of subsequent neurodegenerative disease, especially tau-based traumatic encephalopathy in the frontotemporal dementia (FTD) spectrum. This is being appreciated as sadly too common in ex-boxers and American football players as well as others with repeated head trauma and concussions. There has also been quite a bit of evidence that some patients with these risks also develop other neurodegenerative diseases, eg, Parkinson disease. However, clear population associations have been difficult to dissect, making it challenging to determine true risks and to begin possible therapeutic interventions early in the process. One of the key questions for physicians in the community is to determine whether less significant head trauma in older patients has a clear association with the onset of Parkinson disease. A new study from Kristine Yaffe and colleagues presents data from a major effort to examine this question.

In this study the authors examined a very large cohort of patients (aged 55 and older) that presented to the ER from 2005-2006 either with traumatic brain injury (TBI) or other trauma without brain injury. They then examined the risk of these patients being diagnosed with Parkinson disease by the end of follow up in 2011, and compared the risks of these two cohorts, controlling for a large array of potentially confounding variables. The idea of comparing TBI vs non-TBI trauma patients is interesting and was designed to decrease the likelihood of “reverse causation” – the idea that a patient with early Parkinson disease might be more likely to fall and suffer trauma. Using this approach and controlling for variables, the authors found that TBI patients were 44% more likely to develop Parkinson disease in the ensuing several years.

The implications of this study are broad. Previous work has been a bit unclear about the degree of risk that brain trauma confers for Parkinson disease and this study helps to settle that question. In fact, this study should clear the way to studying particular groups of patients to determine whether those at increased risk of Parkinson disease after trauma have specific characteristics (genetic or environmental) that would allow them to be identified. This would open the way to prevention trials with neurotrophic or neuroprotective agents. The failure of these measures at this point may be due in part to their application only after patients begin to have overt signs of disease. By being able to identify those at increased risk after a defined event, it seems that a new era of preventive trials would have a better chance of being useful.