Breaking News About TBI

Betacellulin Boosts Brain Tissue Repair After TBI

Administrator — Wed, 11 Jan 2012 04:00:05 +0000

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.

Improving Treatment Outcome for TBI by Healing Mitochondria

Administrator — Sun, 08 Jan 2012 16:31:57 +0000

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.

TBI SIGNIFICANTLY UPS RISK OF VIOLENT CRIME

Administrator — Thu, 05 Jan 2012 17:27:48 +0000

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.

CURING HORMONAL DEFICIENCY AFTER TBI

Administrator — Wed, 04 Jan 2012 19:45:19 +0000

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.

Treating TBI as a Chronic Disease

Administrator — Thu, 17 Nov 2011 15:05:21 +0000

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.

Adult Stem Cell Therapy for TBI Still on the Horizon

Administrator — Thu, 17 Nov 2011 01:57:57 +0000

In the Jan.-Feb 2009 issue of Disease Models & Mechanisms Dr. Peter A. Walker and colleagues summarized what we know so far about the use of progenitor cell therapies for traumatic brain injury. Due to evidence in rats that transplanation of embryonic stem cells grow tumors in the post-TBI brain and strict limits on the use of such cells, researchers have focused on adult stem cells. These cells congregate in certain areas of the adult human body, especially the bone marrow, the subventricular zone of the brain, the umbilicial cord and adipose (fat) tissue. There is preliminary evidence at this time that infusion of pluripotent adult stem cells into the brain post-TBI can protect damaged cells by supplying intact genetic material, producing neurotrophic growth factors, and by reducing inflammation. Much more clinical experimentation needs to be done, but researchers are hopeful that one day adult stem cells will become part of the acute treatment for TBI. Right now there is little physicians can due in the acute stage except monitor intracranial pressure; reduce IC pressure with drugs, shunts or both; and increase cerebral blood perfusion with drugs.

Can A New Blood Test Diagnose TBI In The Field?

Administrator — Fri, 11 Nov 2011 05:35:21 +0000

A study published by Dr. Linda Papa of Orlando, Florida, on November 10, 2011 in the Annals of Emergency Medicine found that patients with TBI had a significantly higher amount of an acidic protein in their blood than those without TBI. The protein at issue is called glial fibrillary acidic protein (GFAP). Dr. Papa said the test, which must be done within four hours after the injury, may be used someday in the field to diagnose TBI in wounded soldiers. She also said the test could help determine which patients with head trauma need or don’t need a head CT scan at a hospital.

Bedside EEG Test Shows Some TBI Patients Called Vegetative Are Aware

Administrator — Fri, 11 Nov 2011 05:17:19 +0000

In the November 10, 2011 issue of The Lancet Dr. Damian Cruse and colleagues describe an inexpensive, bedside technique for ascertaining if a person who appears to be in a vegetative state from severe TBI has awareness or not. The research team asked 16 severe TBI patients diagnosed as vegetative and 12 healthy controls to imagine moving their right fingers and toes while attached to a bedside EEG machine. Three of the TBI patients (19%) showed changes in their EEG consistent with being aware and generating mental imagery in compliance with the task similar to what the healthy controls did. This is a breakthrough since until now the only equipment available to make this kind of determination was a functional MRI machine which is too expensive for most facilities to acquire.

Mild TBI Disrupts Function of the Thalamus

Administrator — Thu, 10 Nov 2011 01:52:39 +0000

The July 2011 issue of the journal Radiology has an article by Yulin Ge, MD, of the Department of Radiology at NYU Langone Medical Center, and colleagues, regarding the effect of mild TBI on the thalamus. The thalamus is the part of the brain which receives sensory input from receptor areas for touch, hearing, sight, and taste, and relays them to appropriate areas of the brain for processing. It is also involved in regulation of consciousness, mood, and sleep. When the thalamus is at rest due to lack of sensory input it should be putting out relatively few signals and all the signals should be symmetrical. Dr. Ge used functional magnetic resonance imaging to compare the resting state of the thalamus in 17 normal controls vs. 24 patients with mild TBI. The fMRI scans showed that normal people displayed a normal thalamic resting state, whereas the patients with mild TBI had increased activation of the thalamus with asymmetrical outputs. Although there is no treatment for this problem as yet, this phenomenon could help explain why people with mild TBI show disrupted cognitive function, mood swings, psychiatric problems, and sleep disorders.

Brain Inflammation Secondary To TBI Can Be Limited

Administrator — Wed, 26 Oct 2011 13:35:32 +0000

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.