Traumatic Brain Injury Blog

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TBI can trigger Pathology in the Gut-Brain Axis and Increase Infections

By on January 23, 2018 In Rehabilitation, Research
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Several of my traumatic brain injury (TBI) clients have been treated for gut issues – issues that were not present prior to their TBI. Insurers, of course, insist that this treatment cannot be related to the brain injury. The scientific literature indicates otherwise. Researchers at the University of Maryland School of Medicine recently found a two-way link between TBI and intestinal changes.

The findings indicate that this two way interaction may contribute to increased infections in TBI patients and may also worsen chronic brain damage.

Researchers have known for years that a TBI can have significant effects on the gastrointestinal tract. The Maryland study (based on research with mice) demonstrates that brain trauma can also make the colon more permeable, (“intestinal mucosal barrier dysfunction”) allowing harmful microbes to migrate to other parts of the body, causing infection. Intestinal mucosal barrier dysfunction has been implicated in numerous health conditions such as:

  • food allergies
  • microbial infections,
  • irritable bowel syndrome
  • inflammatory bowel disease
  • celiac disease, metabolic syndrome
  • non-alcoholic fatty liver disease
  • diabetes
  • septic shock

The “second brain” is in the gut

To appreciate the “gut-brain axis” studied by the Maryland researchers, it is important to understand the complex nervous system that exists in the gut. The gut features a mesh-like system of neurons that govern the function of the gastrointestinal tract, called the “enteric nervous system” (ENS). The ENS is sometimes called the “second brain.” It contains more than 100 million neurons, more than in either the spinal cord or peripheral nervous system. The ENS is one of the main divisions of the autonomic nervous system, capable of acting independent of the sympathetic and parasympathetic nervous systems, although it may be influenced by them.

The Maryland study offers further support for how the brain and ENS communicate with each other, with two way consequences. The researchers suggest that a key factor in the communication may be “enteric glial cells,” similar to brain “astroglial cells”; both of which are activated after a TBI. (“Glial cells” surround neurons and hold them in place, supply nutrients and oxygen to neurons and insulate one neuron from another.)

We know that activation of glial cells in the brain is associated with inflammation that contributes to delayed tissue damage in the brain. A similar process may be occurring in the gut.

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