frontal damage (the olfactory nerve passes between the bony cribiform plate and the orbitofrontal cortex) and, where present, is usually associated with very poor long-term social and vocational outcomes.21 It is generally accepted that, although the
prognosis is favorable for the majority of MTBI patients, a significant minority of pa- tients develops a chronic, often-debilitating constellation of signs and symptoms known as “chronic post-concussive syndrome.”22 Most of the patients exhibiting these long term disabilities (including many athletes as discussed above) do not exhibit any focal signs of brain injury. Autopsy studies tell us that in most cases, the injury to the brain is microscopic, at the cellular level.
Proving MTBI
Since even the most powerful diagnos- tic imaging is not capable of examining the brain cells of living patients, we are left try- ing to infer the injury from its footprints, ei- ther chemical (as in the case of some of the newer advanced imaging techniques) or cognitive (for example, the pattern of cog- nitive deficits associated with brain injuries as understood by the field of neuropsychol- ogy). These inferential methods are fraught with potential problems. Neuropsycholo- gists have developed refined tests for de- termining if a patient is demonstrating the full “effort” necessary for testing to pro- duce valid results, but unfortunately there are many reasons why patients may be un- able to give full effort other than malinger- ing, as discussed in Murial Lezak’s leading text on neuropsychological evaluation.23 When this occurs, however, the inferential tool of neuropsychology becomes essen- tially useless as a tool for proving the injury. The CDC findings reflect the prevailing understanding that brain trauma initiates a metabolic process that can have destruc- tive consequences over a course of time— in other words, that the delay in certain symptoms is normal and not a justified ba- sis, standing alone, to question credibility. This has been well understood for years. For example, a respected learned treatise, Greenfield’s Neuropathology, describes this process as follows:
The delayed consequences of the pri- mary injury have only recently begun to be understood. These are various events that have been triggered by the primary injury and include neurobio- logical processes involving cellular dys- function such as free radical formation, receptor mediated mechanisms, calci- um and inflammation mediated dam- age. In various combinations, and in various severities, the resultant cellular dysfunction defines the nature and ex- tent of the primary injury, the outcome
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of which may not become apparent for several days or even weeks after the in- jury.24
In many cases, the most persuasive proof must necessarily come from “before” and “after” fact witnesses. Many cases have been won based not on the science, but on the testimony of exceptionally credible be- fore and after witnesses—either indepen- dent witnesses like a respected employer, clergy, or leader of a non-profit the victim was actively involved with, or less indepen- dent witnesses like a young child who in- nocently talks about how mommy or daddy are different.
Another potentially useful method to “authenticate” a brain injury is through a qualified biomechanical analysis of both the acceleration/deceleration and rotational forces involved in the accident and a com- parison of those forces to tolerance data available from public agencies. If persua- sive evidence can be offered that the forces exceeded the tolerance of the typical hu- man brain, the “differential diagnosis” of brain injury becomes more persuasive. Brain injury is different in one critical way
from other serious injuries like orthopedic injuries. For reasons that are still not fully understood, there is tremendous variability in the way different brains respond to trau- ma and recover from trauma. This makes it much harder to predict what will happen in any individual case. Some expectations have changed radically over time, based on evolving research. For example, it used to be thought that the brains of young chil- dren are especially malleable and would therefore recover from trauma easier than adults. Recent research demonstrates that it is exactly the opposite: young children may be particularly susceptible to perma- nent consequences, especially in the area of social dysfunction.25
Current researchers,
like Dr. Thomas McAllister at Dartmouth, are looking at factors such as genetics to try to understand this variability. The attention now being given to trau- matic brain injury, including MTBI, makes it less challenging to bring brain injury claims. It is now much more generally understood that someone who looks fine and can walk and talk can in fact have a disabling condi- tion caused by injury to the brain. The at- tention being given to TBI has also accel- erated research on better methods of di- agnosis and treatment. Imaging technolo- gy is increasingly effective at detecting the “footprints” of brain injury. For example, on March 2, 2012, the Journal of Neurosurgery published very exciting research regarding a new, powerful tool developed at the Uni- versity of Pittsburgh Medical Center for vi- sualizing the footprints of microscopic brain damage called “high definition fiber track- ing.” This technology promises to be even
THE VERMONT BAR JOURNAL • SPRING 2012 15
Proving a “Mild” Traumatic Brain Injury
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