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Traumatic Brain Damage: What Did We Learn from the NFL and the NCAA? - Litigation News

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Litigation News

Posted on: Oct 4, 2019

By Dan Chamberlain, Cohen & Malad LLP

Among the 21,074 National Football League (NFL) retired players, a vast majority suffer brain damage as a result of practice and play. Almost 400,000 National College Athletic Association (NCAA) players suffer the same brain damage. By the time most NFL pros make it to the NFL, players have had up to 450,000 brain impacts in practice and play. 113 of 114 deceased players’ brains showed aggressive brain degeneration, also known as chronic traumatic encephalopathy.

There are roughly 3.5 million brain injuries each year in America. Some get better and others don’t. Previous research estimated that traumatic brain injury causes $80 billion in health care and vocational loss each year. Most recent research indicates that there is no longer a “miserable minority” of traumatic brain damage survivors. It is more likely than not that individuals that suffer a traumatic brain injury are going to suffer life-long impairments. The distinction between a mild traumatic brain injury (mTBI) and severe is now a moniker of little relevance. Brain damage is a serious medical condition.

Cognitive challenges associated with mTBI vary and change over time. Early in recovery, arousal, attention and concentration difficulties are prominent, as are memory-encoding problems. Later, difficulties with divided attention, memory, thought retrieval and executive functioning such as reasoning, planning, sequencing, decision-making and judgment may emerge.

Cognitive recovery evolves at a different pace for each person, with many interdependent factors affecting recovery. Some individuals with mTBI recover well and return to previous levels of functioning; others do not. Even after returning to routine activities, individuals with mTBI may experience reduced cognitive efficiency and inconsistency of performance.

mTBI survivors may have difficulty recognizing, assessing and managing novel, complex or stressful situations, making it difficult to monitor changes in their health or to reliably comply with medication or a medical treatment regimen. 

A traumatic brain injury is:

  1. An alteration of brain function, or
  2. Evidence of brain pathology, and 
  3. Caused by an external force

An alteration of brain function is defined as one or more of the following symptoms:

  1. Any period of loss of consciousness
  2. Any loss of memory of the events before or after the injury
  3. Neurologic deficits, including (but not limited to) weakness, loss of balance, change in vision, dyspraxia/plegia, sensory loss, aphasia, etc. 
  4. Any alteration in the mental state after injury

However, we need to recognize that clinical manifestations may be delayed. Clinical manifestations may be delayed by days, months, or years.

An mTBI, also known as a concussion, is a complex pathophysiological process induced by biomechanical forces to the head or to another part of the body that transmits to the head.  The injury produces an alteration of brain function that results in a wide range of neurological, physical, cognitive and neuropsychological impairments. These impairments can appear on an intermittent or persistent basis immediately or as many as ten or more years after injury.

Brain pathology may include visual, neuroradiologic, or laboratory confirmation of damage to the brain. A positive MRI, CT scan, or other diagnostic imaging technique is unnecessary if brain function was altered as a result of the incident. TBI is a risk factor for neurodegenerative disease. Also, there is a high comorbidity between TBI and psychiatric disorders which complicates recovery. Posttraumatic Stress Disorder may or may not accompany a TBI. Neither are mutually exclusive.

Brain pathology may also include biomarkers, TESLA 3 MRI, Diffuse Tensor Imaging, PET, SPECT, and neuropsychological examination. An mTBI protocol may include a TESLA 3 MRI with DTI, SWI and neuro quant to assess neuroanatomic/structural integrity as well as lab studies, including freeT4/TSH, B12, Folate, IGF-1, Testosterone (free and bound), vitamin D to rule out nutritional or endocrine contributors.

External force may include:

  1. The head struck by an object
  2. The head striking an object
  3. The brain undergoing an acceleration/deceleration movement without direct external trauma (i.e., coup/contra coup; diffuse axonal shearing; rotational tearing, another infarct, etc.)
  4. A foreign body penetrating the brain
  5. Forces generated from events such as a blast or explosion
  6. Or, other force yet to be defined

There is no such thing as a typical head injury or closed head injury. Damage to the brain is exactly that, brain damage. Brain damage typically does not get better and gets worse over time. It is a chronic ongoing disease process that degenerates the brain. While the brain damage survivor may look normal, many times, it is a different person/personality trapped in a body that used to work normally and function appropriately and no longer does so.

Scholarly, peer-reviewed literature prove that brain damage causes, in part, neurological insult to the motor, sensory and autonomic dysfunction as well as vestibular (balance) disturbances, visual perceptual (depth perception, visual figure-ground) and oculomotor deterioration (Impaired eye-tracking, eye-hand coordination), anosmia (loss of sense of smell), ageusia (loss of sense of taste and post-traumatic headache. Brain damage can cause lifelong chronic diseases, like:

  1. Parkinson’s
  2. Alzheimer’s
  3. ALS
  4. Dementia
  5. Chronic traumatic encephalopathy
  6. Epilepsy (1.5 times the normal risk)
  7. Central sleep apnea
  8. Pituitary hormonal dysfunction
  9. Atherosclerosis
  10. Fatigue
  11. Depression
  12. Decreased muscle mass
  13. Mood and behavioral changes 
  14. Hearing, smell and taste loss/impairment
  15. Impaired Cognition
  16. Sensitivity to light
  17. Short and long term memory loss
  18. A person with brain damage is more likely to have a second or more brain injury
  19. Vocational loss
  20. Survivor syndrome (post-traumatic stress disorder, survivor syndrome, family/caregiver dysfunction)  
  21. Behavior exacerbation/impulse control (i.e., gambling, drinking, sex, smoking, spending)

Brain damage is a cumulative ongoing disease syndrome. A loss of consciousness is not necessary to establish a traumatic brain injury. A practitioner that finds support in the Glasgow Coma Scale(GCS) as evidence against brain damage is misplaced. The GCS is a single classification system designed to speculate on the likelihood of death from traumatic brain injury.  Negative diagnostic imaging is an also unreliable tool and does not show microbleeds and infiltrates to the brain.

What did we learn?

  1. There is no need for a loss of consciousness to substantiate a TBI or brain damage.
  2. Clinical manifestations of TBI or brain damage may be delayed by hours, days, months, and years.
  3. Damaging forces to the brain are o-going and unknown at present. 
  4. Subtle damage to frontal lobe systems can prevent an mTBI survivor from effectively suppressing or consistently managing undesirable behavior, including suicide, and suicidal ideation.
  5. With any brain damage, there is a potential for life long chronic diseases.

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