Traumatic Brain Injury Blog

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Neuroinflammation and TBI: Research Leads to Anti-inflammatory Lifestyle Strategies

By on November 16, 2015 In Rehabilitation, Research
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Neuroinflammation as a likely cause of persistent symptoms following traumatic brain injury (TBI), as well as increased risk of neurodegenerative complications, is leading to increased attention on anti-inflammatory strategies with diet, exercise, lifestyle and medication

Our May 28, 2015 blog post discussed the evidence offered by McMasters University researchers in support of their conclusion that the body’s immune response following injury can lead to unchecked, ultimately destructive neuroinflammation and that this likely underlies persistent symptoms following TBI as well as increased risk of neurodegenerative conditions such as chronic traumatic encephalopathy (CTE) and Alzheimers. The authors observed  similar neuroinflammatory processes in patients without a history of head injury, such as patients with serious infections, PTSD and Depression. They also noted that subtle genetic differences may explain differences in inflammatory responses between patients, leading to different long term outcomes. The October 2015 issue of Trends in Neuroscience includes a review by Ohio State neuroscientists with further support for this new paradigm for understanding the brain’s response to injury. See “Priming the Inflammatory Pump of the CNS after Traumatic Brain Injury.” 

As the authors explain,

“Mounting evidence indicates that neuroinflammatory processes progress after the initial head injury and worsen with time. Microglia contribute to this inflammation by maintaining a primed profile long after the acute effects of the injury have dissipated.”

This explains, the authors note, “vulnerability to a ‘second hit’ and subsequent neurophychiatric and neurodegenerative complications.”

The research described in these two articles explains not only why TBI can lead to psychiatric complications (like depression) and neurodegenerative complications (such as Alzheimers). It also helps to explain why certain pre-injury experiences, such as depression and anxiety, PTSD, migraines, and prior head injury – all conditions increasingly understood to be associated with neuroinflammation – increase vulnerability to more severe consequences following a TBI.

There is a growing body of literature that looks to hyperactive immune system responses and associated inflammation as an explanation for why both diet and chronic stress (such as the early life stress related to trauma) increases vulnerability to both brain disorders, such as depression and stroke, and other diseases such as heart disease and diabetes.

This research highlights why anti-inflammatory strategies related to diet, exercise, lifestyle and medication are important considerations for both TBI victims and individuals at increased risk of TBI.

Brain researchers at the University of California Geffen School of Medicine neurosurgery department reported several years ago that

“An increasing number of basic science studies indicate that environmental conditions and experiences encountered in the daily routine of individuals can dramatically affect the capacity of the brain to respond to challenges.”

The researchers identified the benefits of exercise and dietary factors such as omega-3 fatty acids and curcumin (tumeric) and the harm caused by diets rich in saturated fats.  See “The Influence of Diet and Physical Activity on Brain Repair and Neurosurgical Outcome.”  As discussed in earlier posts in this blog, researchers at the University of Buffalo have developed protocols to obtain the greatest benefit from exercise in brain injury recovery.

Recent research on diet has drawn particular attention to the benefits of curcumin (found in tumeric) in reducing the “ neuroinflammatory cascade”  that contributes to neuronal damage and behavioral impairment following TBI. The March 2014 issue of the Journal of Neuroinflammation, for example, reports that “post-injury, curcumin administration may improve patient outcome by reducing acute activation of microglia/macrophages and neuronal apoptosis.”  Researchers at the Salk Institute have reached similar findings.

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