Category: TBI

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.

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.

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.

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.

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.

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.