JOB POSTING: POST DOCTORAL RESIDENT/PRE DOCTORAL INTERN (click here for more info)

Articles

Forensic Updates

How Much Do We Really Know About Traumatic Brain Injury?

Dr. Sam Goldstein

Complimentary Service of the Neurology, Learning and Behavior Center

HOW MUCH DO WE REALLY KNOW ABOUT TRAUMATIC BRAIN INJURY?

Perhaps no topic in forensic neuropsychology is as heatedly debated as the cause and effect relationship between Traumatic Brain Injury and an individual’s pre-trauma history, severity of and immediate response to trauma, physical findings, long-term sequelae and neuropsychological test data. Despite the publication each month of an increasing number of scientifically based, peer reviewed studies concerning the relationship of these variables and Traumatic Brain Injury, consensus remains elusive. On the one hand, although severity of immediate injury is still a popular marker to assess the validity of short and long term outcome, the field of clinical neuropsychology and neurology is increasingly recognizing that outcome is a complex process with severity of trauma representing only one variable contributing to and predicting ultimate outcome.

A recent study published in Developmental Medicine and Child Neurology (2001, Volume 43, 226-233) speaks very powerfully to this issue. A group of seventy-five children born very pre-term, were followed for nearly fifteen years. This group was divided between those with and without evidence of brain abnormality. Fifty-five percent of this group had evidence of brain abnormality. Both groups were compared to a control sample. Compared to a control sample of term adolescents, very pre-term participants had impairment only on a measure of word production. Measures of attention, memory, perceptual skill, visual motor and executive function were all within the normal range for the very pre-term children at fifteen years of age. Surprisingly, this was true whether or not they had evidence of brain abnormality based on Magnetic Resonance Imaging. In fact, these brain abnormalities were still evident at fifteen years of age. Furthermore, the pattern of results remained unaltered when comparisons were made between subgroups such as comparing those with and without white brain matter abnormalities or with and without ventricular enlargement.

An increasing body of research demonstrates that the young brain is primarily motor cortex. Certain parts of the brain are more likely to assume certain functions. However, if those parts are unable to assume those functions the “plasticity notion” appears to be accurate. Other parts of the brain take over. These findings suggest that the neuropsychological effects of pediatric trauma may improve through childhood. It is now well-accepted, however, that these types of injuries in the developed brain can and most often do lead to permanent impairments from which there may be minimal recovery.

The human brain contains 100 billion neurons and several times that number in supporting cells. Each neuron may connect to up to 500,000 others. In even a small slice of the brain there are billions of synapses. From a trauma standpoint any stretching, twisting or compression of the brain has the potential to alter the physical status for every one of these cells and each connection, not to mention the blood vessels that feed them. Moderate to severe physical forces can severe, rupture or fracture these structures. Even mild forces may stretch and strain them given the brain’s tenuous floating position within the skull. The absence of an evolutionary history during which time human beings were exposed to rapid acceleration – deceleration has left the brain and skull ill prepared for these forces. It is not surprising that even minor blows to the head result in, at the very least, short term physical and cognitive sequelae. Such sequelae can result in diffuse axonal injury with the physics of the trauma resulting in differing locations and severity of injury. Further, brief intense strain or rotational force can cause shearing injuries. Even a 5% stretching of the nerve fibers along the axon of a brain cell can result in disruption in the neuron’s function. Strain in excess of 20% has been demonstrated to produce immediate, irreversible damage.

More severe trauma can result in contusion as the brain strikes repeatedly against the inside of the skull, leading to vascular compromise and edema. As multiple researchers have scientifically demonstrated, however, the absence of physical findings does not equate with lack of impact or effect. In cases of most mild Traumatic Brain Injury, even those involving simple concussion, detectible abnormalities on traditional medical technology such as CT or MRI scan may not be observed. Yet, in reviewing the available literature in 1999 a National Institute of Health Consensus Development Panel concluded that concussion produces mild but persistent neurocognitive deficits. These include activities of daily living, cognitive efficiency, memory, attention and emotional regulation.

Of what relevance is this to attorneys litigating mild to moderate traumatic brain injury cases, particularly those presenting with an absence of immediate or long-term physical findings such as those seen on x-rays, CT’s or MRI’s? First, data generated by neuroimaging tools is complimentary to data generated by a thorough neuropsychological assessment. Though a number of years ago the American Academy of Neurology suggested that neuropsychological assessment data should be considered secondary to the neurology exam and physical findings, emerging research trends contradict this point of view. As the study I cited in the beginning of this update points out, it is equally likely to find individuals with neuroimaging based impairments absent significant neuropsychological findings and vice versa.

Second, the concept of dose response may not be accurate. That is, the greater the neuroimaging and related findings the greater the expected neuropsychological impairment and vice versa may not be true. Forensic neuropsychologists pointing to physical findings in a neurology exam or for that matter neuroimaging data as the determination of severity of current impairment may be on shaky ground absent confirming neuropsychological test data and reports of daily functioning.

Third, the absence of confirming neuroimaging and for that matter neuropsychological test data cannot be used to exclusively determine that daily functional impairments may not be the consequence of a Traumatic Brain Injury. To best understand this phenomena, forensic neuropsychologists must be willing to carefully and patiently develop an understanding of an individual’s pre-trauma history and functioning. An emerging body of literature suggests that just as there may be “thin skull plaintiffs”, there are also “thin psyche” or “thin frontal lobe”, etc., plaintiffs as well. Some individuals, pre-trauma, given their emotional, psychiatric, behavioral or neurocognitive histories, will be less capable and competent to deal with even mild impairments that may be much better tolerated by the general population. Further, some of these individuals may appear “brain damaged” following a trauma, when in fact their presentation is psychological as opposed to neurological in etiology.

As with any scientific field, common sense is a valuable ally. Belief too may be a valuable ally in the absence of fact. However, as we as a scientific field generate increasing data concerning the forces that affect outcome of the diagnosis and treatment of Traumatic Brain Injury, belief must be replaced by fact, proven theory and sound scientific practice.

Related research:

Anderson, S.W., Bechara, A., Damasio, H., et al. (1999). Impairment of social and moral behavior related to early damage in human pre-frontal cortex. Nature Neuroscience, 2, 1032-1037.

Berry, H. (2000). Chronic whiplash syndrome as a functional disorder. Archives of Neurology, 57, 592-594.

Bigler, E.D. (1999). Neuroimaging in pediatric traumatic head injury: Diagnostic consideration and relationships to neurobehavioral outcome. Journal of Head Trauma Rehabilitation, 14, 70-87.

Bigler, E.D. (2001). The lesions in traumatic brain injury: Implications for clinical neuropsychology. Archives of Clinical Neuropsychology, 16, 95-131.

Bigler, E.D., & Snyder, J. (1995). Neuropsychological outcome in quantitative neuroimaging in mild head injury. Archives of Clinical Neuropsychology, 10, 159-174.

Cicerone, K.D., & Kalmar, K. (1997). Does premorbid depression influence post-concussive symptoms and neuropsychological functioning? Brain Injury, 11, 643-648.

Colantonio, A., Dawson, D.R., & McLellan, B.A. (1998). Head injury in young adults: Long-term outcome. Archives of Physical Medicine, 79, 550-558.

Johnson, S.C., Bigler, E.D., Burr, R.B., & Blatter, D.D. (1994). White matter atrophy, ventricular dilatation and intellectual functioning following traumatic brain injury. Neuropsychology, 8, 307-315.

NIH Consensus Development Pattern and Rehabilitation of Persons with Traumatic Brain Injury (1999). Rehabilitation of persons with traumatic brain injury. Journal of the American Medical Association, 282, 974-983.

Rushe, T.M., Rifkin, L., Stewart, A.L., et al. (2001). Neuropsychological outcome at adolescence of very pre-term birth and it’s relation to brain structure. Developmental Medicine in Child Neurology, 43, 226-233.

Ursano, R.J., Fullterton, C.S., Epstein, R.S., et al. (1999). Acute and chronic post traumatic stress disorder in motor vehicle accident victims. American Journal of Psychiatry, 156, 589-595.

The Neurology, Learning and Behavior Center provides clinical and forensic assessment, case management, trial consultation, and treatment services for children and adults with brain injury and dysfunction, Attention-Deficit Hyperactivity Disorder, language disorders, learning disability, developmental delay, Autism, emotional disorders and adjustment problems. The Center is dedicated to the provision of treatment services.