Head injury exists on a continuum that ranges from a bump on the head to death. At the most trivial end of the spectrum, we’ve all smacked our heads on something and wound up with a lump that disappears gradually without any lasting consequence. (See #1 & 2 below.) At the other end of the spectrum, tragically, TBI contributed to approximately 50,000 deaths (See # 9 below) in 2010 according to the Centers for Disease Control. Bound by those extremes, there are literally millions of Emergency Room visits, trips to primary care physicians and untreated head injuries that occur on playing fields, at work and during activities of normal daily living.
The most significant battles in traumatic brain injury lawsuits fall somewhere in the middle of the head injury spectrum, in cases classified as “mild” or “complicated mild” traumatic brain injury. (See # 4-6 above.)
As a trial lawyer who has devoted extraordinary amounts of time to representing clients with different levels of brain injury, I know that insurance companies and corporations that are often financially responsible for the injuries, damages and losses experienced by my clients will use fairly predictable techniques to undermine my clients’ claims. It is for that reason that much of my professional time is devoted to studying the contemporary scientific literature in the brain injury field. Several times a week, I receive notification of the “on-line” publication of peer-reviewed scientific articles from around the world. The notifications are transmitted with a “search term” that I have previously entered during scientific and medical research I have performed, and based upon the title of the new publication, I then decide whether or not to proceed to read the abstract for the article. From the abstract, I may purchase the full text of the article and then save it to my vast electronic library of journal articles.Today began with such a discovery as my attention was captured by the title: “From Phineas Gage and Monsieur Leborgne to H.M.: Revisiting Disconnection Syndromes”, de Schotten MT et al, Cerebral Cortex, 2015, 1–16 (open access). Two things stood out from the title alone. First, Phineas Gage holds a prominent place in traumatic brain injury lore. In 1848, Gage was a 25 year old railroad construction foreman who was using an explosive tamping rod to prepare for demolition. The explosive ignited, sending the iron bar through Gage’s left cheekbone and exiting through the top of his head. Not only did he survive, but Gage never even lost consciousness. However, he did experience severe personality and behavioral alterations consistent with the consequences of TBI. It was in this context that in 1979 I learned of Gage’s unwitting contribution to neuroscience. Then, traumatic brain injury cases were defended with the false claim that there “could be no brain injury if there was no loss of consciousness.” Gage’s history refuted that claim, and the myth that loss of consciousness is required for a TBI diagnosis is universally rejected.
The second thing that caught my attention was the reference to “Disconnection Syndrome,” and as I read the abstract, it became clear that the authors had engaged in a research project that sought to analyze old evidence from prominent cases involving brain injury and applied a probability analysis to demonstrate that the emotional, cognitive and behavioral changes in the subjects were consistent with the type of damage that occurs to white matter connections in the brain that help regulate emotion, behavior and cognition. Back in 1979, the MRI was about to explode on the scene. To that time, the most prominent diagnostic tool for brain injury, whether a stroke (hemorrhagic or ischemic), oxygen deprivation, or traumatic was the CT scan. However, the CT scan was useful only for identifying bleeding or bony fractures. It could not detect more subtle damage to gray matter or white matter. The MRI changed that. And over time, science has come to understand that damage to the brain is an evolving process – a cascade of cellular neuro-metabolic interactions that can cause damage to brain cells over an extended period that can last weeks, if not months. “The New Neurometabolic Cascade of Concussion”, Giza CC et al, Neurosurgery. 2014 October; 75(0 4): S24–S33 (Open Access). The damaging cascade can cause random disconnection among the previously normal integrated white matter circuits of the brain, in turn causing disruption of various physical and cognitive functions and/or emotional dysregulation.
In connection with litigating these cases, I have seen defense expert witnesses blame treating healthcare providers for causing an iatrogenic disability or illness because of a diagnosis of mTBI or post-concussion syndrome. The theory of an iatrogenic illness is that the treating healthcare provider has caused the patient to suffer or believe that he/she suffers from a physical and/or emotional injury. Some of these witnesses would have little work to do if not for the insurance defense work that they rely upon. Do you think they’re motivated to be untruthful or intellectually dishonest by secondary gain?
That is not to say that there is no room for disagreement when it comes to making a diagnosis of traumatic brain injury. And TBI can present an array of symptoms that are non-specific to brain injury. A non-specific symptom is a symptom that might exist because of another cause, for example, a headache in a head injury patient that also has a neck injury or concentration problems in a head injury patient being treated for pain from an orthopedic injury or chronic regional pain syndrome (“CRPS”.)
The most common examples of the physical, emotional, cognitive and behavioral symptoms of head injury follow:
Symptoms of a Concussion:
Table 7.2 Selected Signs and Symptoms of a Concussion Adapted from Sports Concussion Assessment Tool (SCAT2) and Halstead and Walter (2010):
|Headache||Feeling like “in a fog”||Irritability||Drowsiness|
|Nausea or vomiting||Difficulty concentrating||”Don’t feel right”||Sleep more than usual|
|Dizziness||Difficulty remembering||Sadness||Sleep less than usual|
|Loss of consciousness||Feels slowed down||Nervous or anxious||Har to fall asleep|
|Seizure or convulsion||Forgets recent events||More emotional|
|Neck pain||Confusion||”Pressure in head”|
|Sensitivity to light||Repeats questions|
|Sensitivity to noise||Answers slowly|
|Fatigue or low energy|
|stunned or dazed|
Note. Concussion should be suspected in the presence of any one or more of the above symptoms following some form of head injury.
It is not uncommon for head injury patients to have pre-existing depression, anxiety, or a history of substance abuse. These pre-injury factors present confounding issues that require careful consideration and analysis. The following flow chart presents a graphic that can help explain the inter-relationship of interacting issues that can confuse the diagnostic process.
Similarly, post-injury factors can complicate recovery, but are natural consequences of a TBI. The defense will always emphasize pre-existing problems without acknowledging that post-injury factors were produced by the injury. To be sure, it is well recognized in the scientific literature that many TBI patients continued to suffer from fatigue, balance problems and issues with cognition, communication, emotion, return to work and return to leisure activities long after suffering the injury.
See “Longitudinal follow-up of patients with traumatic brain injury: outcome at two, five, and ten years post-injury”, Ponsford GL et al, J Neurotrauma. 2014 Jan 1;31(1):64-77. Likewise, brain injury may produce stress and anxiety caused by the physical and emotional consequences of the injuries including loss of self-esteem; interpersonal losses; loss of employment and loss of independence. Post-injury factors superimposed upon pre-existing vulnerabilities can worsen the outcome following a TBI, but in many cases, the pre-existing vulnerabilities do not limit financial recovery, but instead help explain the failure to recover from the injuries.
By Stewart M. Casper. Posted August 26, 2015