Category: TBI

While MRI can detect brain swelling/compression and CT can detect brain bleeding, neither type of scanner can find small traumatic brain lesions involving torn axons. So many mild and some moderate traumatic brain injuries remain invisible. However, a team of researchers at UC San Diego is making use of a new high tech scanner called MEG (magneto-encephalography) that makes these invisible brain injuries visible. MEG pinpoints damaged areas of the brain by showing sites with low frequency brainwaves.

The researcher in charge of the ongoing research project is Mingxiong Huang, associate director of UC San Diego’s MEG Radiology Imaging Laboratory. In a June 1, 2011, interview he said MEG can also be used to diagnose PTSD.

Some of the soldiers returning from Iraq and Afghanistan with TBI are displaying the dual problem of seizures and migraine. Two University of Utah researchers (K.C. Brennan, M.D., assistant professor of Neurology, and Edward Dudek, Ph.D., professor and chair of the Department of Physiology) are teaming up with the Department of Defense to investigate this phenomenon. They suspect that seizures and migraine both arise from over-excitation of the brain due to TBI, and they are collaborating on a study to see if there is a common mechanism and a common method of preventing these very serious, long-term consequences of TBI.

Benjamin Cravatt, Ph.D., at the Scripps Research Institute and Daniel Nomura, Ph.D., at UC Berkeley have made an important discovery about how to block brain inflammation, something which can severely compound the initial damage done by a TBI. They learned that in the brain the production of arachidonic acid (which gets converted into the pro-inflammatory substances called prostaglandins) is controlled chiefly by the enzyme MAGL(monoacylglycerol lipase). MAGL uses the enzyme 2-AG to make arachidonic acid. 2-AG is a cannabinoid associated with pain reduction and pleasure production which mimics the effects of marijuana.

The research scientists showed that by blocking the activity of MAGL they could shrink of the pool of arachidonic acid and prostaglandins in mouse brains and effectively limit the amount of brain inflammation in mice. Brain inflammation (which occurs in Alzheimer’s and Parkinson’s diseases) is also a major problem following TBI, and limiting brain inflammation following TBI would prevent secondary damage. The researchers will continue studying the most effective ways to eliminate MAGL from the brain or to block its actions.

Mark Gordon, M.D. is an American physician who pioneered the recognition and treatment of hormonal deficiency caused by TBI. According to Dr. Gordon any TBI (mild, moderate or severe) can dysregulate a person’s hormones leading to increased risk of emotional instability, drug and alcohol abuse, depression, anxiety, mood swings, memory loss, fatigue, confusion, amnesia, poor cognition, learning disabilities, decreased communication skills, loss of muscle tone and loss of sex drive. Dr. Gordon sets out the medical proof of this assertion in his 2007 book The Clinical Application of Interventional Endocrinology.

In an article in the periodocal Life Extension in January 2012 he discusses how hormone replacement can be used to treat this problem. Dr. Gordon says he has improved depression using hormones in TBI survivors with serious depression who never responded to antidepressants no matter how many varieties they tried. Another pioneering expert in the field of hormonal treatment for TBI is Donald Stein, Ph.D., at Emory University School of Medicine who is the director of Emory’s Department of Emergency Medicine Brain Research Laboratory. Dr. Stein has been testing the use of progesterone.

In January 2012 Maria-Victoria Gomez-Gaviro and Dr Robin Lovell-Badgehave published an article in the Proceedings of the National Academy of Sciences about the potential for a cord blood protein called Betacellulin to boost brain tissue regneration following TBI. The human brain and mouse brain share niches filled with stem cells that can produce new brain cells (neuroblasts) to replace old ones that were killed off or new glial cells to form scar tissue to heal wounds to the brain.

Excessive scar tissue formation following TBI blocks new neurons from linking up their synapses and forming functional, connected systems. The scientists in this NIH-funded study found that giving mice Betacellulin following TBI caused significant, rapid proliferation of new brain cells, whereas using an antibody to suppress the activity of that protein led to a drop off of new brain cell production. The researchers will now seek permission to use Betacellulin on human beings.