MEG Scanner Can Detect Mild/Moderate 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.

Cyclosporine Effectively Treats Severe TBI

NeuroVive Pharmaceutical, AB is a Swedish drug development company. Working with NeuroStat it has developed a mechanism for delivering drugs directly to the brain through the blood-brain-barrier which normally screens out large molecules. In recent tests NeuroVive has shown that cyclosporine A, a drug used to help organ transplant recipients avoid immune rejection, helps victims of severe traumatic brain injury by revving up the shocked mitochondria in their brain cells. Mitochondria are the part of cells that produce the vital energy needed for all cellular processes including cellular respiration, repair, and reproduction. NeuroVive continues to work on this new treatment, and it has just received a large grant from the Swedish government to use cyclosporine to treat acute stroke.

Seizures and Migraine Following TBI – Is There a Common Cause and a Common Method of Prevention?

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.

traumatic brain injury in sports

Brain Inflammation Secondary To TBI Can Be Limited

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.

Lithium Shows Promise as Treatment for Acute TBI

Lithium has been used for decades to treat mania. Psychiatrists believe that lithium controls mania in part by decreasing the activity of the excitatory neurotransmitter glutamate. Following TBI some brain cells release excessive quantities of glutamate which damages or kills other brain cells. Fengshan Yu and colleagues at NIH and the University of Health Sciences have explored the effect of lithium on acute TBI in mice. They devised an experiment in which some of the mice given a TBI under anesthesia were treated with lithium for 3 days and the others were treated with a placebo.

The key results of the study include: lithium chloride at 1.5 to 3.0 mEq/kg reduced brain lesion volume compared to control; lithium chloride reduced post-trauma related anxiety behavior during the outcome monitoring; lithium chloride reduced breakdown of the blood-brain barrier; and short-term and long-term motor coordination was better in the lithium group of mice. The researchers would like to try out lithium in a clinical study on human beings with TBI in the future. Their results were published in the Journal of Neurotrauma.

Treating TBI as a Chronic Disease

Steven Flanagan, M.D., Chairman of the Department of Rehabilitation Medicine at the NYU’s Rusk Medical Institute is an expert on rehabilitation of adult and child traumatic brain injuries. In December 2011 he will give a talk in Orlando, Florida, offering a rationale for treating TBI as a chronic disease with long-lasting medical problems requiring lifelong follow-up. Patients who suffer a TBI often exhaust the limited health care resources in the period soon after the initial injury – resulting in inadequate long-term care.

Curing Hormonal Deficiency after TBI

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.

TBI Significantly ups Risk of Violent Crime

The conclusion of a 35-year Swedish population study published in the December 27, 2011 online issue of PLOS Medicine was that TBI, but not epilepsy, increases the risk of violent crime. Researchers from the Centre for Violence Prevention at Sweden’s Karolinska Institute combined Swedish population registers from 1973 to 2009, and examined associations of epilepsy and traumatic brain injury with subsequent violent crime, defined as convictions for homicide, assault, robbery, arson, any sexual offense, or illegal threats or intimidation.

Each case was age and gender matched with 10 general-population controls. Cases were also compared with unaffected siblings to assess familial factors. After adjusting the numbers to account for confounding factors, the data showed that TBI significantly increased the risk of violent crime.

Improving Treatment Outcome for TBI by Healing Mitochondria

Mitchondria are the energy producing component of brain cells that fuel brain cell activity. Following TBI excessive release of the neurotransmitter glutamate can kill mitochondria by causing toxic influx of calcium into brain cells. A new treatment approach involving IV infusion of a drug called a mitochondria-uncoupler has been found to protect mitochondria from excessive glutamate. In one study adults with TBI showed 60% reduced mortality and improved brain function at 30 days following injury.

Dr. Jose Pineda at Washington University School of Medicine is using a drug to stimulate brain mitochondria in child patients with TBI and is seeing some remarkable results. Dr. Pineda was born in Guatamala where he studied biology before getting his medical degree. Before joining the faculty at W.U. he did laboratory and clinical studies on TBI at the McKnight Brain Institute of the University of Florida.

Betacellulin Boosts Brain Tissue Repair After TBI

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.