Chronic Traumatic Encephalopathy is a progressive disease that results in a gradual decline in cognitive function. Victims of Chronic Traumatic Encephalopathy exhibit symptoms consistent with dementia, including confusion, memory loss, depression, and aggressive behavior. The hallmark indicator of Chronic Traumatic Encephalopathy on autopsy of the brain was the buildup of a plaque referred to as tau protein. While it was always understand that repeated concussions could result in the buildup of tau protein, it wasn’t until recently that researchers were able to identify the buildup of tau protein in individuals with only a single head injury. (Victoria E. Johnson, William Stewart, Douglas H. Smith. Widespread Tau and Amyloid-Beta Pathology Many Years After a Single Traumatic Brain Injury in Humans. Brain Pathology, 2011; DOI: 10.1111/j.1750-3639.2011.00513.x).

Alzheimer’s Disease is a progressive form of dementia. It is the most common type of dementia, resulting in confusion, anger outbursts, lack of long-term memory, and language deficits. The cost of Alzhiemer’s Disease on society is great. Because most Alzheimer’s patients will continually and progressively decline, at some point they will have to rely upon others for their care. While family members and loved ones usually try to provide care initially, the challenges of caring for an Alzheimer’s sufferer can take an incredible toll on every aspect of a caregiver’s life. What makes it additionally challenging and unrewarding is that, at some point, the Alzheimer’s sufferer will no longer have the long-term memory required to remember the identity of their caregiver. On autopsy it has been show that tau protein buildup is also a hallmark indicator of patients with Alzheimer’s Disease. Studies have shown that brain injury victims have an increased risk of developing Alzheimer’s Disease.

Parkinson’s Disease is a progressive disorder of the central nervous system with its origins in the midbrain. The initial symptoms of Parkinson’s Disease involve movement disorders, but later Parkinson’s Disease patients typically develop cognitive symptoms including dementia. Parkinson’s Disease, while typically idiopathic in origin, can follow traumatic brain injury that results in damage to the basal ganglia which can result in a dopamine production disruption. (Traumatic Brain Injury in Adult Rats Causes Progressive Nigrostriatal Dopaminergic Cell Loss and Enhanced Vulnerability to the Pesticide Paraquat Che Brown Hutson, Carlos R. Lazo, Farzad Mortazavi, Christopher C. Giza, David Hovda, and Marie-Francoise Chesselet Journal of Neurotrauma 2011 28:9, 1783-1801). Unfortunately, there is no lab test to definitively diagnose Parkinson’s Disease as of yet. Due to the degenerative nature of Parkinson’s Disease, patients and their loved ones face an enormous burden when dealing with long-term care for the Parkinson’s patient.

As if traumatic brain injury survivors did not have enough to deal with just attempting to recover from their injury, now studies have established that victims of TBI have an increased risk of developing early onset dementia, Chronic Traumatic Encephalopathy, Alzheimer’s Disease, and Parkinson’s Disease.

Headaches Attributed to Traumatic Brain Injury

The IHS further differentiates post-traumatic headache due to mild traumatic brain injury vs. moderate or severe traumatic brain injury.

The IHS classifies Post-Traumatic Headache Attributed to Mild TBI as the following:

• Headache within a week of the accident; AND
• Head Trauma with all of the following:

1. No loss of consciousness or loss of consciousness of less than 30 minutes
2. Glascow Coma Scale of greater than 12
3. Symptoms or signs consistent with concussion

Importantly, the IHS clarifies that mild head injury can result in a “complex of cognitive, behavioral and consciousness abnormalities,” despite the following:

• normal Glascow Coma Scale
• normal neurological examination
• normal neuroimaging (CT, MRI)
• normal EEG
• normal CSF examination
• normal vestibular function testing
• normal neuropsychological testing

The IHS classifies moderateTBI or severe TBI as the following:

• Headache within a week of regaining consciousness; AND
• Head Trauma with at least one of the following:

1. Loss of consciousness of more than 30 minutes
2. Glascow Coma Scale of less than 13
3. Post-Traumatic Amnesia of more than 48 hours
4. Abnormal neuroimaging (CT, MRI) demonstrating traumatic brain injury, i.e. lesion, diffuse axonal injury, subdural hematoma, skull fracture

As mentioned above, if the post-traumatic headache persists longer than 3 months it is considered chronic.

Headaches Attributed to Whiplash

Classification of post-traumatic headache resulting from whiplash requires the following:

• Headache within a week of the traumatic event; AND
• History of Whiplash defined as a sudden and significant acceleration/decleration of the neck with neck pain

As mentioned above, if the post-traumatic headache persists longer than 3 months it is considered chronic.

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Find more information on Post-Traumatic Headache or Post-Traumatic Migraine

A new study co-authored by the internationally renowned brain injury expert, Erin Bigler, Ph.D. of the Department of Psychology & Department of Neuroscience, Brigham Young University, Provo, Utah and the Department of Psychiatry and the Utah Brain Institute, University of Utah, Salt Lake City, Utah, has been able to objectively identify evidence of structural changes within the brain that account for memory deficits, which are so common following brain injury. The study also provides further support for the validity of the advanced imaging technique, MRI using diffusion tensor imaging (DTI), in evidencing organic changes within the brain.

The study, Diffusion Tensor Imaging of the Perforant Pathway Zone and Its Relation to Memory Function in Patients with Severe Traumatic Brain Injury, will be published in the peer-reviewed May 2011 edition of the Journal of Neurotrauma. The study focused on changes within the following three regions: 1) the Perforant Pathway; 2) Hippocampus; and 3) Temporal Lobe White and Gray Matter. The study utilized 14 severe traumatic brain injury survivors and were compared to imaging from a demographically comparable control group.

The imaging revealed several abnormalities in the brain injury survivors :

• Perforant Pathway Zone Bilaterally = Decreased Fractional Anisotropy (FA)
• Perforant Pathway Zone Bilaterally = Higher Apparent Diffusion Coefficient (ADC)
• Hippocampus Bilaterrally = Higher Apparent Diffusion Coefficient (ADC)
• Hippocampus Bilaterally = Decreased Volume
• Temporal Gray Matter = Decreased Volume

Memory deficits, specifically Consistent Long-Term Retrieval (CLTR) and Delayed Recall, were shown to be associated with the following:

• Perforant Pathway Zone Bilaterally = Higher Apparent Diffusion Coefficient (ADC)
• Left Hippocampus Apparent Diffusion Coefficient (ADC)
• Left Hippocampal Volume

Nonverbal Memory, immediate and delayed recall, was associated with the following:

• Perforant Pathway Zone Bilaterally = Higher Apparent Diffusion Coefficient (ADC)
• Left Hippocampal Volume
• Decreased Gray Matter Volume was associated with Immediate Recall
• Decreased White Matter Volume was associated with Immediate Recall Bilaterally and Delayed Recall, left

Our office has worked with many of the leading neuroradiologists that are capable of performing and interpreting Diffusion Tensor Imaging (DTI), the enhanced imaging technique utilized to prove evidence of brain damage.

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For more information contact an experienced Wisconsin TBI Attorney.

NFL-Great Terry Bradshaw

In a courageous effort to shed more light on the problem of the NFL concussions, Terry Bradshaw has come forward and disclosed that he is suffering the long-term consequences of repeated concussions. Bradshaw, always a brave competitor on the field, has now shown his bravery off the field by admitting that he is experiencing many common symptoms directly attributable to repeated concussions, including memory deficits, word-finding problems and eye-hand coordination problems. It took years before Bradshaw actually realized the permanent subtle deficits from the repeated mild traumatic brain injuries he sustained.

Bradshaw, now 62 years-old, has not played in the NFL for nearly 30 years. A 14 year quarterback for the Pittsburgh Steelers, Bradshaw sat out the first 14 games of the 1983 season following off-season arm surgery. Then, on December 10, 1983, he returned to play but left the game after hearing a pop in his elbow while throwing a touchdown pass. It would be his last NFL pass, as he subsequently retired.

Bradshaw admitted that he sustained multiple concussions over his 14 year career. He explained that back then, players, coaches, trainers, and owners simply referred to these concussions as “getting your bell rung.” Bradshaw would just inhale smelling salts and get back in the game. Oftentimes, in the huddle his teammates would have to call the play for Bradshaw because he was too disorientated.

Bradshaw explained that his cognitive deficits really hadn’t been a problem until last year. In a column on FoxSports.com, Bradshaw explained:

“Toward the end of last season on the FOX pregame show, maybe the last six weeks, I really started to forget things. That’s why I quit reciting statistics because I couldn’t remember them exactly and I stayed away from mentioning some players by name because I really wasn’t sure and I didn’t want to make a mistake. I’m on national TV in front of millions and I hate making mistakes. I told the people in Ruston that I suffered six concussions and numerous head injuries. I think that’s right, but I’m not really sure.”

Bradshaw also admitted that his personal struggle with the subtle cognitive deficits from the brain injuries has led to anxiety and depression, common consequences of brain injury. He stated:

“The memory loss made me jittery at times. It was driving me crazy that I couldn’t remember something that I studied the night before. All it did was trigger my anxiety and all of sudden everything would snowball on me. I know I have depression and it’s a horrible disease. This memory loss just made my depression worse.”

On behalf of all of my former, current and future brain injured clients, I would like to thank Mr. Bradshaw for his selfless act of coming forward with this story. He clearly has nothing to gain by sharing this information. You sir are a class act.

In the last blog entry we discussed how the insurance industry and some within the field of neuropsychology have conspired to create a fictitious defense to the existence of long-term problems associated with mild traumatic brain injury. Essentially they have created a Karl Rovian defense to mTBI. They took what was once common knowledge, ie that mTBI can result in long-term symptoms,  and they refuted the entire proposition, mainly by publishing flawed studies or by relying on simple works such as those authored by Michael McCrae.

McCrae’s premise is that the entire field of neuropsychology relied upon only two studies to establish the long-held belief that about 15% of mTBI’s result in long-term symptoms. McCrae then goes on to use flawed logic to refute these two studies, jumping to the conclusion that because these two studies were not valid, therefore the 15% number is actually less than 1%.

Any mild traumatic brain injury survivor with symptoms lasting longer than 6 months can tell you their symptoms are real and can be disabling. The common symptoms include the following:

• headaches
• dizziness
• nausea
• fatigue
• noise sensitivity
• irratibility
• sadness
• nervousness
• temper problems
• concentration deficits
• memory deficits
• difficulty reading
• sleep distrubance

Despite the prevalence of these symptoms in mild traumatic brain injury survivors, the insurance industry has persuaded a large segment of the field of neuropsychology to attempt to “prove” these ongoing symptoms are due to pre-existing depression, pre-existing anxiety or other pre-existing psychological issues. One of the most revealing claims made by this segment of the field of neuropsychology is that because these injuries cannot typically be shown with current imaging techniques, this means the injury is not real and is not organic. That argument is analogous to concluding that broken bones never existed prior to the advent of the X-ray.

Nevertheless, the neuropsychologists that are routinely hired by insurance company lawyers have gone to great lengths to establish some type of normative data to support their proposition that mild traumatic brain injuries cannot result in long-term symptoms. They have failed in their endeavors because each and every study can be easily refuted when closely scrutinized.

The adoption of the insurance industry’s agenda of denying that mild traumatic brain injury survivors could have injury-related symptoms by this segment of the field of neuropsychology is sure to create a huge cost to taxpayers through public benefit programs. Instead of holding the wrongdoers and their insurance companies responsible, we the tax payers will be paying for the ongoing care and treatment as well as the long-term disability benefits for these brain injury survivors that have permanent mTBI symptoms. While the lack of personal responsibility and accountabilility has the broadest impact to society, it is minor when compared to impact of this approach on the mild traumatic brain injury survivor.

Now more than ever it is critical that mild traumatic brain injury survivors retain an experienced, qualified brain injury attorney to advocate on their behalf. All too often, I am contacted by brain injury survivors after they retain an attorney and their attorney has completely bought into the insurance industry premise that mTBI’s cannot result in long-term consequences.

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Contact an experienced Wisconsin Brain Injury Attorney.