Eye Tracking Technology Diagnoses Traumatic Brain Injury

Uzma Samadani, MD, PhD, chief of neurosurgery, and colleagues at NYU Langone Hospital in New York have published a study showing the usefulness of eye tracking technology in diagnosing TBI. They used two groups of test subjects drawn from 169 veterans, some with abnormal eye movements and others with normal ones. They had both groups watch a music video or TV show for 220 seconds, during which a device scanned their eyes and a computer measured the ratio between vertical and horizontal eye movements. Patients with normal eye movements had a 1:1 ratio while patients with abnormal eye movements had abnormal ratios. The team found that abnormal ratios correlated with swelling in the brain near the site where cranial nerves controlled eye movement. Surgery to decompress the swelling cured the abnormal eye movement.

Keeping Brain Stem Cells Healthy While Aging

Stem cells in the subventricular area and hippocampus of the human brain can repair or replace brain cells damaged by traumatic brain injury. Unfortunately, as people age the amount and activity of their brain stem cells can dwindle. Can anything be done to keep a robust supply of neural stem cells while we age? The answer appears to be yes.

Researchers led by Dr. Robert K. Yu at the Medical College of Georgia at Georgia Regents University have discovered that the key ingredient in keeping stem cell populations high in the mouse brain is a ganglioside (a brain fat) attached to a sugar called lipid ganglioside GD3. In trials with mice they learned that this molecule has a remarkable capacity to boost the ability of brain stem cells to self-renew. In an earlier experiment in 2010 Dr. Simonetta Sipione at the University of Alberta, Canada, injected lipid ganglioside into the brains of mice with Huntington’s Disease and their symptoms improved.

Stopping Extra Brain Damage From Immune Cells After Head Injury

In October 2014 Dr Richard Tobin (a surgeon at Texas A&M University Health Center) and colleagues published their research in Acta Neuropathologica Communications on how to stop secondary brain damage from head trauma. They theorized that head trauma can disrupt the blood-brain barrier, activate immune cells known as T-cells, and allow T-cells into the brain where they kill brain cells that would have survived the blow to the head. They used a chemical process called CAP to stop activation of T-cells in one group of mice given head trauma. Compared with the control group (that was given head trauma without any CAP) the mice that got the T-cell activation blocker had significantly fewer and smaller brain lesions. This holds out the possibility of CAP treatment for humans with brain injuries from head trauma one day.

New Non-Invasive Device Measures Brain Health After TBI

On December 11, 2014 Tufts University announced the development and licensing of a new fiber-optic technology called CHS (coherent hemodynamics spectroscopy) to measure brain health after TBI, stroke or other brain trauma. The technology measures blood flow, blood volume, and oxygen consumption in the brain in real time in a non-invasive manner. It was invented by Tufts Professor of Biomedical Engineering Sergio Fantini. CHS works by attaching a fiber-optic device to the scalp which emits near infared light. Blood vessels in the brain absorb the light and then reflect it back to sensors. The data is interpreted by computer with the help of mathematical algorithms developed by Dr. Fantini to yield the desired information.

Help with PTSD after Brain Injury

Some people who sustain a traumatic brain injury (TBI) also suffer PTSD. Although it used to be believed that only conscious memory of trauma could cause PTSD, it is now clear that unremembered trauma can cause it. For example many war veterans who remember riding in a Humvee and then being rescued after a roadside bomb exploded (but who do not remember the explosion) have PTSD.

Current treatments for PTSD include individual and group psychotherapy, EMDR, and medications for anxiety/depression. Now a new possibility exists according to Michael T. Alkire, M.D., staff anesthesiologist at the Long Beach VA Healthcare System in California. Dr Alkire did a study on 12 patients with PTSD using a stellate ganglion block (SGB), a procedure in which a small amount of anesthetic is injected into a nerve junction between C7 and T1 in the spine. Although the SGB had only been used to treat regional pain syndromes in the past, Dr. Alkire was curious if it might help PTSD patients. What he found was very encouraging, which was that 75% of the patients demonstrated significant reduction of symptoms for 3 months with gradual fading of relief between months 4-6. If done by a trained anesthesiologist these injections are safe so they could be repeated.

Making Exercise Easier After TBI

People who sustain a TBI often experience a period of hospitalization, muscle disuse, and/or depressed mood that can be helped by exercise.  Physicians and physical therapists typically recommend daily walking at ever increasing distances, but this can pose challenges which include physical disability and lack of motivation. A new study in the journal Motivation and Emotion by Emily Balcetis and colleagues at NYU on the psychology of exercise demonstrates a way to stay motivated.

Balcetis did several experiments with two groups of walkers. One group was instructed to narrowly focus their attention on an object ahead of them as they walked toward it. The other group was instructed to let their attention wander naturally as they walked toward the same object. In all experiments those who “kept their eyes on the prize” did better. Why? When walking, staying focused on a specific target ahead can make the distance to it appear shorter and help people walk there faster. Balcetis said, “People are less interested in exercise if physical activity seems daunting, which can happen when distances to be walked appear quite long…..These findings indicate that narrowly focusing visual attention on a specific target, like a building a few blocks ahead, rather than looking around your surroundings, makes that distance appear shorter, helps you walk faster, and also makes exercising seem easier.”

Consequences of Insomnia After TBI

One of the most common effects of a traumatic brain injury is insomnia. Insomnia is not your friend. It has been linked with obesity, depression, memory loss, stroke, and other adverse conditions. How does insomnia affect the brain? Christian Benedict at the Department of Neuroscience, Uppsala University, Sweden, did a study involving a group of healthy young men. He had half sleep a normal 8 hours at night, while the other half was kept sleep deprived. In the morning he checked their blood. In the sleep deprived group he found a significant increase in two molecules (NSE and S-110B) that should stay in the brain. Their presence in the peripheral blood supply outside the brain indicates some degree of brain damage. While one night of sleep deprivation is not a big deal, if insomnia goes on for weeks or months this would place a great deal of stress on the brain.

People with a TBI who are suffering from insomnia should not ignore it, but should make a concerted effort to seek out a treatment that works. Depending on individual differences a person could benefit from one or more sleep remedies such as prescription sleep medication, melatonin, smelling a fragrance, using white noise, making your bedroom extra dark or coming up with a sleep hygiene program. Certain things to be avoided in the evening are caffeinated beverages and upsetting materials on the TV news, magazines or books. Reduce rather than increase your level of stimulation. Stretching and slow, deep breathing while imagining waves washing gently upon a beautiful beach can help.

Effective Treatment for Pill Resistant Depression

After TBI many people experience persistent depression even after trying anti-depressant medication. Transcranial magnetic stimulation (TMS) is a modality that can help relieve pill resistant depression without causing the tiny seizures or memory dysfunction associated with electroconvulsant therapy. TMS treatments are administered by placing a small device on the patient’s scalp while she sits in a chair in an office. Typically treatments are administered over a 25 day course. Multiple studies have shown that TMS reduces depression without showing how.

On 9/25/14 researchers Connor Liston and Marc Dubin from the Weill Cornell Medical College in New York published a study that sheds light on how TMS works. Using functional MRI they found that prior to treatment depressed patients had hyper-connectivity between the subgenual cingulate cortex and a part of the medial prefrontal cortex of the brain. After treatment connectivity between the neurons in these areas was reduced back to normal and the patients were less depressed. The patients who benefited most from TMS were the ones with the greatest pre-treatment hyperconnectivity.


How Concussions Cause Dementia

Neuroscience has already established that concussions can trigger the build up of sticky tau protein in the brain that causes the same destructive effects of Alzheimer’s disease. How does this happen? The answer comes from research published in the December 2014 issue of the Journal of Neuroscience by Maiken Nedergaard, M.D., D.M.Sc., co-director of the University of Rochester Center for Translational Neuromedicine. Dr. Nedergaard says that the brain has its own separate system for waste removal called the glymphatic system which utilizes very fine structures to carry cerebro-spinal fluid bearing waste products away from the brain. These structures are fragile and vulnerable to brain trauma from blows to the head. When they become damaged they stop removing waste products from the brain, including the sticky tau protein that gums up brain cells.

Loss of Empathy After Severe TBI

Families, employers, and physicians of people with a severe TBI often notice dramatic personality changes. One of the most common changes they see is that the person becomes egocentric, self-centred, and insensitive to the needs of others. Why does this occur? Neuroscientists have traced it to a loss of responsiveness to the emotions of others. Testing done by researchers at at the University of New South Wales, Australia, that was published in the May 2011 issue of Elsevier’s Cortex helps us understand what is going on physiologically.

When an uninjured person sees the face of another person in distress she mimicks the distressed person’s facial expression and experiences emotional empathy. When she sees an angry face her facial muscles contort to mimick the angry person’s face and her sweat glands make sweat. But when a person with a severe TBI sees these two faces there is neither mimicking, nor sweating when he sees the angry face. This tells researchers that severe TBI can damage the neuronal circuits necessary for emotional responsiveness, including empathy in response to another’s distress and fear/alarm in response to someone else’s anger.