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.

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.

Similarities of TBI and PTSD

While the moderate and severe forms of TBI are associated with blunt or penetrating head trauma and loss of consciousness, PTSD (an anxiety disorder) is associated with exposure to a terrifying, life-threatening danger that need not involve either head trauma or loss of consciousness. Yet the consequences of TBI and PTSD are remarkably similar. Both manifest as sleeplessness, anxiety, depression, and difficulties with memory and concentration. To further complicate matters some PTSD patients do suffer head trauma and some cannot remember if they did or not since the overwhelming fright they suffered has left them with only a patchwork of memory about the event, some of which is temporarily or permanently repressed.

So how do you differentiate TBI from PTSD and how do you treat a patient when you’re not sure? The advice from Dr. Lonser, an expert at the National Institutes of Neurological Disorders and Stroke, is not to waste time on diagnosis. The important thing is to treat the disabling behavioral symptoms. Whether the problems come from TBI or PTSD treatment should not depend on diagnostic labels. According to Micaela Cornis-Pop Ph.D., polytrauma/TBI coordinator with the U.S. Department of Veterans Affairs (VA) central office, “The mainstay of treatment [should be] symptom-specific intervention, such as managing headaches and improving sleep, and education.”

Caution issued against early withdrawal of Life Support for severe TBI

On 8/29/11 the Canadian Medical Association issued a caution against early withdrawal of life support for patients with severe TBI. They found that 70% of hospital deaths among patients with severe TBI came from withdrawal of life support within the first three days of admission to ICU. Yet withdrawing life support during that time frame based on low GCS (Glasgow Coma Scale) score could be a mistake because the low score could be due to the temporary effects of drugs or medicine and not the permanent effects of the brain injury.

Bedside EEG Test Shows Some TBI Patients Called Vegetative Are Aware

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.

Alzheimer’s Type Brain Degeneration Triggered By TBI

Douglas Smith, MD, Professor of Neurosurgery and Director of the Center for Brain Injury and Repair at Penn’s Perelman School of Medicine teamed up with neuropathologist William Stewart, MD, from the University of Glasgow, Scotland, to study the long term neuro-degenerative effects of a single TBI on the human brain. They used post-mortem examination of tissue slices of the brains of people who had sustained one non-fatal, moderate-to-severe TBI many years before death.

They concluded that just one moderate-to-severe TBI can initiate changes in brain tissue characteristic of Alzheimer’s disease involving the widespread appearance of tau tangles among axons and beta-amyloid plaques in brain cell bodies. These changes were visible in young and middle aged adults at an age long before the risk of Alzheimer’s disease is significant. Their study was published in the summer 2011 issue of Brain Pathology.