ADVOCATE April 2009 Issue
Journal of Consumers Attorneys Associations for Southern California
Mild Traumatic Brain Injury:
Very Real, Very Contentious
by Charles J. Furst, Ph.D. Los Angeles Neuropsychology Group
Most of the brain injuries that attorneys and doctors will see are
classified as mild. Mild traumatic brain injury (MTBI) accounts for
more than 80 percent of Closed head injuries. Nonetheless, the
specter of “brain damage” weighs heavily in forensic proceedings,
because of the popular, and largely correct, perception that brain
damage is permanent.
Moderate and sever brain injury are among the most disabling
conditions resulting from physical trauma, since the operations of
the brain underlie all of our behaviors, emotions and experience.
Other physical impairments can severely limit a person’s functioning in the world, but serious brain injuries can challenge the basis of who we believe we are in the world, our very identity. Traumatic brain injury (TBI) is a major public health problem and a leading cause of death and disability, especially among young people.
The prevalence of MTBI, together with the potentially large economic and social consequences of any permanent brain injury, makes MTBI on of the most contentious personal-injury claims in forensic settings. The debate tends to revolve around the issue of whether a specific person who has persistent cognitive and emotional dysfunction following an MTBI is suffering from permanent brain damage or some other temporary or treatable condition.
This debate is an old one, and despite considerable scientific advances over the past 20 years in our understanding of MTBI, it continues to be a recurrent bone of contention in personal-injury proceedings. Both sides of the debate are also represented in scientific treatments of the issue, with some viewing persistent MTBI symptoms as representing psychological injury or exaggeration for secondary gain (e.g., McCrea, M.A. Mild Traumatic Brain Injury and the Postconcussion Syndrome. N.Y.: (Oxford Univ. Press, 2008) and others allowing that at least some of these patients have an underlying subtle organic brain injury (e.g., Varney, N.R. & Roberts, R.J. The Evaluation and Treatment of Mild Traumatic Brain Injury, Erlbaum, 1999; Bigler, E.D. Arch. Clin. Nuropsychol., 2001, 16, 95-131).
In this article, I will try to describe the issues from the point of view of a neuropsychologist who has been on the front line of this battle over the years, and who has been privileged to be an “embedded observer” behind the lines on both sides. But first, I need to set the stage by describing the broader issues of determining damages in traumatic brain injury.
A primer of brain injury
In most brain injuries from closed head trauma, the underlying injury is the result of cerebral concussion, which literally means a forceful shaking or jolting of the brain. Since the brain substance is similar in consistency to Jell-O (or perhaps something like microscopic spider webs of electrical circuits suspended in Jell-O), it’s not hard to see how the structure and functioning of the brain can be disrupted by a concussion.
Concussion is produced by acceleration and deceleration forces acting on the brain, that produce stretch and compression of different parts of the brain, rotation of the brainstem, and cavitation (a force similar to a vacuum). In milder concussions, there is a temporary disruption of brain activity, with symptoms of headache, dizziness, and mental fogginess, and then complete recovery after a few days. In fact, concussion in popular usage has come to mean this milder type and is frequently synonymous with benign brain trauma. The technical or medical sense of the word encompasses also moderate and severe concussions, where there can be permanent brain damage.
MTBI is synonymous with a simple concussion with brief loss of consciousness (less than 20 minutes) or even no loss of consciousness, but with a report of being dazed or disoriented (athletes call it “getting one’s bell rung”). There is often a period of post-traumatic amnesia (less than 24 hours for MTBI), where a person may be awake — walking and talking and making sense — but with no subsequent memory of any events for a period of time. Head-injured patients may, for good reason, believe they were unconscious, and are surprised to have others describe conversations they had during this interval of time. Also, the definition of MTBI requires that there be no sign of intracranial abnormality (cerebral hemorrhage or contusion or brain swelling) on brain imaging, no seizures, and that the neurological exam be “non-focal” —i.e., not showing signs of hemiplegia, or other central nervous system motor or sensory deficit.
Table 1 shows common ways of evaluating the severity of a brain injury, based on parameters contemporaneous with the event. Not surprisingly, in general, the more severe the initial indicators of brain trauma, the worse the long-term outcome. Most patients in the severe category do not return to baseline levels of functioning. Because of cognitive and behavioral dysfunction, many are left with lifelong impairments in work, self-care, and the ability to maintain satisfying interpersonal relationships.
However, the correlation between acute injury severity and long-term outcome is far from perfect. A small number of persons with severe brain injuries recover well enough to return to their former jobs and social roles (Masson, F., Maurette, P., & Salmi, L.R., et al., Brain Injury, 1996, 10, 487-497). Often they do this by learning strategies to compensate for memory or other cognitive problems.
Pathophysiology of brain injury
The pathophysiology of brain injury involves temporary and permanent changes in the brain. The first of these is a stretching or shearing of nerve fibers, as a result of mechanical forces acting on the brain during trauma. These acceleration/deceleration forces are the causes of closed brain trauma. Think of a brain traveling in an automobile at 50 mph rapidly decelerating, after the automobile strikes a stationary object and the skull strikes the dashboard. Or alternatively the acceleration on the brain when a person stopped in freeway traffic is rear-ended. These factors can cause concussive disruptions of brain cells and of chemical regulators in the brain. In more severe concussions, these forces cause contusions and hemorrhages in the brain.
The basic concussive injury is a stretching and shearing of nerve fibers, called axons. The injury is referred to as diffuse axonal injury, and this is the basic injury of concussions. Axons are the long fibers which a nerve cell, or neuron, uses to transmit information to other neurons downstream. Axons connect a neuron to others downstream at the synapse, where electrochemical interactions affect the firing of these other neurons. Tracts of axons serve in the brain as cables which transmit information. If an axon is sheared in two, the nerve cell eventually dies.
Diffuse axonal injury affects large areas of the brain and occurs at a microscopic level, and so it is rarely seen in neurodiagnostic images of the structure of the brain (CT and MRI scans).
In addition to diffuse axonal injury, there are a number of physiological and chemical changes that seem to reflect a general disruption of normal brain activity following concussion. This complex of transient changes in brain function, lasting from minutes to days, has been called the neurometabolic cascade. These include abnormalities in the supply of chemical transmitter substances which bridge the synapses and accomplish the transmission of nerve signals. These neurochemicals are important for normal emotional regulation as well as cognitive activities. The cascade affects the complex electrochemical processes by which nerve cells propagate their electrical signals.
In cases of more severe brain injuries, concussion, as described above, is the underlying brain damage, causing permanent changes in individual nerve cells, which eventually die off. Severe concussions affect large areas of the brain and can have devastating impact on attention, memory, and overall information-processing speed. Though the lesions are diffuse and usually microscopic, enough fiber tracts may be affected to show up in the connecting tracts of the brain, visualized as bright spots in certain types of MRI scans.
Superimposed on this in more severe cases can be focal brain damage. These are brain lesions which are localized and dense ― such as hemorrhagic contusions which can result in degeneration of neurons and the appearance of gaps in local areas of the brain which are visualized by conventional CT or MRI scans. Focal injuries in TBI come about from direct contusion to the brain matter, or from traumatic hemorrhages of torn blood vessels in the brain. Large blood clots compress the brain and require life-saving neurosurgery. Often the damage from hemorrhage is a result of ischemia, the disruption of blood supply to tissue, which then dies. As well, in cases of severe trauma, secondary brain damage can come about from swelling of the brain tissue in reaction to trauma, resulting in a squeezing within the cranial vault and further ischemic damage.
Evaluation and treatment
For Both clinical and medical-legal purposes it is essential to evaluate a patient for the long-term consequences of brain injury by several different and slightly overlapping specialties. A good starting point is a neurologist, who can evaluate the general health of the injured nervous system and its functioning. Neurologists can order and interpret brain scans looking for abnormalities in the brain’s structure (CT, MRI) and metabolic function (PET, SPECT). The neurologist can also evaluate and treat the complications of brain injury, such as post-traumatic seizures or endocrine abnormalities, and provide medical treatment for headaches and dizziness.
A neuropsychologist can evaluate changes in a person’s cognitive or mental abilities and in behavior. Neuropsychologists administer objective tests of memory, attention, problem-solving, sensory perception, planning, organization, and a long list of other types of cognitive ability. Neuropsychologists also evaluate a person’s psychological adjustment through interview, observation, and tests of personality. In this way, neuropsychological evaluations can categorize the various aspects of neuro-cognitive and behavioral change following brain trauma and make recommendations for rehabilitation treatment and symptom management.
In some cases, the complex behavioral difficulties that can arise from brain trauma are treatable by psychiatrists specializing in organic brain impairments ― neuropsychiatrists. These practitioners can frequently prescribe psychotropic medications which are useful in the management of organically-produced depressive symptoms, anxiety, fatigue, sleep disorders, emotional lability, and difficulties with impulse control. As well, neuropsychiatrists often provide psychotherapy support to patients and consultation to family members.
Cognitive rehabilitation specialists can help the patient with cognitive problems to learn compensatory strategies for overcoming these problems in everyday settings. For more severely injured patients, this is accomplished within a comprehensive post-actute rehabilitation program, often based in an outpatient hospital setting. Cognitive rehabilitation therapists tend to be speech therapists and occupational therapists with specialized experience, and some of them offer services in the home-and-community setting.
MTBI and persistent post-concussive syndrome
Now we return to the MTBI debate. Table 2 presents one commonly accepted way of defining an MTBI.
Following a mild concussion, a person may report a longer period in which they have headaches, dizziness, disorientation, ringing in the ears, and difficulty concentrating. The great majority of persons who sustain MTBI recover within weeks to months, with no permanent symptoms (Gulf War and Health, Volume 7: Long-term consequences of Traumatic Brain Injury. Washington, National Academies Press, 2008). A small percentage, less than five percent, do not.
This group, with persistent post-concussive syndrome, is frequently called the “miserable minority” in neurological and neuropsychological discussions, because they are often seen as very miserable indeed. They may have intractable headache pain, unusual sensitivity to light and noises, difficulty tolerating frustration, emotional lability, and difficulty concentrating and remembering.
There is a long history of debate in medical and scientific circles on the organic versus psychological basis of persistent symptoms following MTBI. The condition has gone by various names, post-concussive syndrome, mild closed head injury, mild traumatic brain injury (MTBI) ― the latter being the most common designation in recent years. These are patients who are usually released from emergency rooms with little or no information on potential cognitive and emotional problems lasting more than a few days. This situation in and of itself can be very stressful, because the acute symptoms of concussion often challenge the very foundations of a sense of competency in the world. No wonder most of these patients are also depressed!
In MTBI mood disorders can have organic causes as well, since traumatic injury causes dysfunction in the brain centers that regulate emotion.
Many “post-concussion” symptoms can occur with head injury where there is no concussion, or be related to injuries to parts of the head outside of the bran. Headaches can come from muscle contraction, common in neck injuries. Dizziness can occur from a concussion-like injury to the inner ear. Emotional difficulties are common following all kinds of physical trauma. In fact, it is found that a large number of “post-concussion” symptoms are common among persons in general medical treatment who never sustained head trauma (Lees-Haley, P.R., Fox, D.D. & Courtney, J.C., Arch. Clin. Neuropsychol., 2001, 16, 689-695).
The scientific pendulum has swung back and forth over the years between organic versus psychological explanations of these conditions. An early view, when it was generally believed that simple concussion was benign and reversible, was that persistent post-concussion syndrome (PPCS) represented an “accident neurosis” ― a purely psychological condition. Twenty years ago, many of us were impressed with emerging evidence that there are indeed pathophysiological changes in the brain following simple concussion, and that earlier views that these patients were simply suffering from accident neuroses were incorrect (Furst, C.J., Advocate, 1984, 11(4), 12-16).
Since then, several well-controlled outcome studies have been published showing an expectation of complete recovery of cognitive abilities in patients followed prospectively (“Prospective” refers to selecting patient subjects from the time of emergency room admission; retrospective studies of patients with persistent cognitive problems may suffer from bias in selecting the study sample.) As well, there has emerged a new field of sports neuropsychology, which enables cognitive tests to be administered to athletes, such as football players, before they sustain their first concussion, and follow them up with serial testing after a concussion.
It is true that most patients with persistent MTBI symptoms have a large number of psychological problems, and many have pre-accident psychological conditions or vulnerabilities. There is a high co-morbidity of reactive psychological disorders involving anxiety and depression in this group of patients. Both anxiety and depression can produce attention deficits and inefficiency in memory, problem-solving, and other cognitive activities. Also, many patients may not appreciate their degree of normalcy in cognitive functioning as they recover. If a patient becomes sensitized to his or her alarming memory problems (which may have had an organic basis in the weeks following MTBI) that person may later misjudge normal memory lapses (when they recover) and mis-attribute these lapses when they occur (Gunstad, J. & Suhr, A., J. Int. Neuropsychol. Soc., 2001, 7, 323-333; Lees-Haley, P.R., Williams, C.W., Zasher, N.D., et al., Brain Injury, 1997, 11, 791-799).
There also are a number of patients with persistent MTBI symptoms who have a somatoform disorder ― a psychiatric condition where emotional conflict is expressed by preoccupation with physical symptoms, or exacerbation of theses symptoms through psychological or psychophysiological channels. There has even recently been proposed a new diagnosis to encompass patients with somatoform cognitive dysfunction ― called cogniform disorder (Delis, D.C. & Wetter, S.R., Arch. Clin. Neuropsychol., 2007,22,589-604).
Recovery from brain injury
Most brain lesions ― both diffuse and focal ― are permanent, as most brain neurons do not regenerate. Yet, people do gradually experience some recovery. In the initial weeks and months, there is a gradual return of function in brain neurons and circuits only temporarily affected. Brain swelling goes down, dead tissues are reabsorbed, metabolism and general brain chemistry normalize. Longer-term recovery from permanent brain damage is believed to rely on two main factors: (1) the brain’s ability to recruit what may be excess or redundant neurons to learn the functions of the damaged neurons and substitute, in some sense, for them; and (2) compensatory strategies learned by the person, both consciously and neurologically (e.g., speech therapy or cognitive rehabilitation therapy).
Vulnerability of the brain is a factor in some patients with persistent symptoms. Persons with history of prior concussions in many cases do much worse if they receive subsequent (even mild) concussions. This has led to the notion of brain reserve capacity, which describes the finding that people who are younger, healthier, and smarter recover better from brain injury and are more resistant to dementing diseases than people who are older, less intellectually endowed or who have brains compromised by disease or previous compromise, such as birth trauma, history of childhood learning disability, history of alcohol abuse, or familial tendencies towards Alzheimer’s dementia (Stern, Y. Cognitive Reserve: Theory and Applications. Philadelphia: Taylor & Francis, 2007). This type of vulnerability may underlie the persistent-post-concussion syndromes of some persons following MTBI.
Although most mild concussions are not thought to produce permanent cellular damage, there are some facts which suggest that there may indeed be subtle undetected changes in the brain. It is well-known that concussions accumulate in the brain. Even in cases where recovery is complete, it can be shown that a second or third mild concussion has more severe and prolonged effects on cognitive function than if it had not occurred (Gronwall, D. & Wrightson, P., Lancet, 1975, ii, 995997). This is a fact known by most sports fans. Consider the number of star quarterbacks who had to retire early because of repeated concussions on the field.
Also, when the brains are examined of persons who have died following MTBI (from causes other than brain injury), it is found that there are markers of cell disruption, even in milder concussions (Oppenheimer, D.R., J. Neurol. Neurosurg., Psychiat., 1968,31,299-306; Bigler, E.D., J. Int. Neuropsychol. Soc.,2004, 10, 794-806). Experimental research also shows axonal shearing if the brains of animals are subjected to acceleration/deceleration forces greater than a certain threshold (McCrea, 2007, ibid., Ch. 5).
We are born with over 100 billion neurons in our brains (a figure so large you couldn’t count up to it in a lifetime). We lose brain cells throughout life. Some estimates are hundreds of neurons lost per day of normal living. Perhaps another hundred for each beer we drink. And yet, even though we don’t grow many cells to replace them, we manage to function well enough, at least, into old age. (Consider the average age of Supreme Court justices ― although arguably they have mastered compensatory strategies for failing memory, as do most of us). It is this surfeit of redundant computational elements in our brains which enables us to endure the ravages of time and trauma.
The resolution of the debate over the organic basis for persistent symptoms following MTBI may come as a result of new brain-imaging technologies. CT and MRI imaging look at the macroscopic structure of the brain, and miss abnormalities of microstructure. New variants of MRI ― Diffusion Tensor Imaging (DTI) and Magnetic Transfer Imaging (MTI) ― have increased sensitivity to detecting microscopic structural changes. Other new techniques look at function of different brain regions. These include PET and SPECT scans, which have been around for a while, as well as functional MRI (fMRI) which is the basis of much ground-breaking scientific research on how the brain works. Although these techniques are not generally used as clinical tools for diagnosing traumatic brain injury and may result in a Frye or Daubert challenge (see Mardirossian, G. & Barrett, J.M., CAOC Forum, Oct. 1999, 8-13), they show promise for answering the thorny questions, clinical and forensic, about MTBI.
Charles J. Furst, Ph.D. is a board-certified clinical neuropsychologist in West Los Angeles. Dr. Furst was, for many years, the neuropsychologist at the award-winning New Pathways brain-injury rehabilitation program at Daniel Freeman Memorial Hospital. He has held academic appointments at Dartmouth College and UCLA, and is the author of a number of peer-reviewed articles and a book on the brain and cognition.