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.

Brain Injury Support Groups Facilitate Re-Learning

TBI support groups are invaluable psychologically because so many people living with TBI feel isolated and misunderstood until they have the opportunity to meet regularly with others in their shoes. That’s when they get the understanding and social support they have been craving. But TBI support groups can do even more. If they are run by a speech-language pathologist they can help each group member improve his or her communication skills including pragmatics (the ability to use speech appropriately in a social context to productively interact with others). Support groups can also help with community re-integration by doing fundraisers or volunteer work in the community. The vast potential of support groups has yet to be tapped.

Reducing Headache without Drugs in People with TBI

Dr. Ron Stram, a specialist in integrative medicine in Albany, N.Y., has developed a handheld device for treating migraines and nerve pain in patients who have sustained head injuries such as soldiers exposed to blast forces in Iraq or Afghanistan. The device emits changing frequencies of electric current through the skin and teaches the nerves to handle many different kinds of stimulation. This has the effect of reducing the hypersensitivity of the nerves along with the frequency of migraines or nerve pain.

TBI Decreases Facial Affect Recognition

A major problem for some survivors of TBI is recognizing what emotions other people are experiencing based on their facial expressions. This impairs work and social relationships. A meta-analysis published in the summer 2011 issue of Neuropsychology examined the magnitude of facial affect recognition difficulties after TBI. Effect sizes were calculated from 13 studies that compared adults with moderate to severe TBI to matched healthy controls on static measures of facial affect recognition. The studies collectively presented data from 296 adults with TBI and 296 matched controls and results showed that between 13% and 39% of people with moderate to severe TBI have significant difficulties with facial affect recognition depending on the cut-off criterion used.

Mild TBI Disrupts Function of the Thalamus

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.

Omega-3 Supplements reduce Risk of Dementia Post-TBI

In the Feb. 2011 issue of Neurosurgery James Mills, M.D. and colleagues published research showing that giving rats Omega-3 supplements consisting of DHA (docosahexaenoic acid) for 30 days prior to TBI reduced the amount of beta-amyloid precursor protein (APP) in the axons of the rats’ brains. Hight amounts of APP are associated with Alzheimer’s Disease which can be triggered by TBI. The rats which received the highest pre-TBI dose of DHA had the least amount of APP following TBI and also did the best on water maze tests of memory post-TBI.

Doctor examining a brain CT scan

Brainscope device for on-field Diagnosis of MTBI

BrainScope is a new EEG device designed to detect concussions in athletes on the field. A concussion is a mild traumatic brain injury. BrainScope consists of a headband with 8 electrodes placed over the forehead and temples. The device sends EEG data to a handheld computer for processing. The mini-computer lets a physician know if the athlete’s EEGs are within normal parameters. A study in 2010 showed the device can detect EEG abnormalities consistent with concussion. Starting in the summer of 2011 Dr. Jeffrey Bazarian with the University of Rochester Medical Center will be testing BrainScope to see if it can be used to discern which players may have a brain bleed and need to get a head CT scan.

TBI Increases the Risk of Parkinson’s Disease

Researchers at the UCLA Department of Neurobiology led by Dr. Marie-Francoise Chesselet demonstrated in 2012 that inducing a moderate TBI in rats caused the rats to lose 30% of their dopamine-producing neurons within a 26 week period following the TBI. This made the rats vulnerable to developing Parkinson’s Disease (PD).

The researchers found that exposing the brain injured rats to the neurotoxic pesticide paraquat led them to lose 30% of their dopamine producing neurons in just 13 weeks. They concluded that TBI alone is a risk factor for delayed onset of PD, and that it renders the brain more vulnerable to developing PD following separate brain insults.