Long Term Consequences of Traumatic Brain Injury (TBI)

An interesting article appears in the journal PLOS ONE looking at the consequences of traumatic brain injury (TBI) using rate models. The researchers used rat models and found that overtime TBI results in progressive brain deterioration characterized by elevated inflammation and suppressed cell regeneration. Long-term neurological deficits from TBI related to inflammation may cause more severe secondary injuries and even predispose people to neurodegenerative diseases later in life.

Traumatic brain injuries are important to study since troops in the U.S. military have increasingly suffered TBI from improvised explosive devices.

One of the coauthors from the journal article (Dr. Paul R. Sanberg) says

“Progressive injury to hippocampal, cortical and thalamic regions contributes to long-term cognitive damage post-TBI. Both military and civilian patients have shown functional and cognitive deficits resulting from TBI.”

In the study researchers looked at different parts of the brain in the rat such as the hippocampus, corpus callosum white matter, thalamus, and dorsal striatum. The researchers found that neuroinflammation after TBI causes cell death that hinders the brain’s ability to regenerate.

After looking at the rats brains eight weeks after trauma the researchers found

“a significant up-regulation of activated microglia cells, not only in the area of direct trauma, but also in adjacent as well as distant areas.”

Microglia cells are responsible for the main form of immune defense in the central nervous system and make up 20% percent of the glial cell population located in the brain.

The researchers concluded though that intervention in the chronic stage of TBI could potentially help prevent further deterioration.

Source: Sandra A. Acosta, and et. al. “Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model. PLoS ONE, vol. 8, issue, e53376, 2013.

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