By Michael Maggiano, Esq.

In the simplest form and its most complex form, behavior is the response of an organism to a stimulus. Behavior is thus dependent upon two things: the ability to perceive a stimulus and the ability to respond to a stimulus.

What distinguishes us from the single-celled amoeba, is the complexity of the system that we have developed to perceive stimuli and to emit responses. What distinguishes us from the amoeba is our ability to identify small differences in complex stimuli and our ability to emit highly-complex differential responses of exquisite accuracy to these complex stimuli.

The sensitivity of our system to perceive minute differences in the stimuli and the ability of our system to generate highly-specific extremely accurate responses is dependent upon a gelatinous mass weighing at most, three pounds and occupying a volume somewhat larger than a softball, but certainly smaller than a football. This mass, which typically constitutes less than three per cent of our weight and less than five per cent of our volume, generates all of our thoughts, all of our emotions and every action we take, no matter how large or how small, no matter how gross or how fine, no matter how significant or how insignificant.

We are what we are, and who we are, because we have a brain. Its natural state resembles nothing so much as a soft wrinkled walnut. Yet despite this inauspicious appearance, the human brain can store more information than all the libraries in the world. It is also responsible for our most primitive urges, our loftiest ideals, the way we think, even the reason why, on occasion, we sometimes, do not think, but act instead. The workings of an organ capable of creating Hamlet, the Bill of Rights and Hiroshima remain deeply mysterious. How is it constructed? How did it develop? If we learn more about the brain, can we learn more about ourselves? Indeed, are we anything other than our brain?

None of us, no matter how alike we are, have the same brain. We are what we are as people, because each of our brains, although sharing certain characteristics with all other human brains, is unique. When we injure that brain, we change the character of who we are, not just for an instant, but forever.

Thus, when we talk about brain injury, we are really talking about events causing people to be different than they ever were and different than they might ever have been. Our job in the courtroom is to have six people who never thought very much about the brain, appreciate that if their brain was suddenly injured, they would go home irretrievably different, and, no matter how much time went by, no matter how hard they worked to get better, no matter how smart their treatment team, they would never again be the same. Our job is to have six people who never thought much about the brain and brain injuries, understand they would not be unique, if that happened, and similarly your client is not unique. Our job in the courtroom is to have six people understand that your client is one victim of what is a national epidemic.

This country screamed with outrage when fifty-seven thousand Americans died in ten years of combat in Vietnam and this country now stands by in silence as twice that number die each year of head injury. The only sound which can be consistently heard is the uninterrupted rhetoric of the insurance industry, which surely claims that Closed Head Injury is a fable born in the eyes and hearts and wallets of those of you attending this program. It is time to stay the lie and it is long past time that we rose up in anger and gave voice to those whose voices have been stilled forever. Head injury is not a myth, it is a national disaster and silence is a national disgrace.

The files that we carry to the courthouse and the docket numbers that they bear for the closed head injured victim are more than digits on a form. They represent the irreparable disruption of human life and incomprehensible pain, which that disruption brings to those whose lives have been so disrupted. Those of us who specialize in representing the injured, that is, those of us who specialize in representing people who are known as Plaintiffs are frequently pejoratively called advocates. Make no mistake about it, we trial lawyers who represent these victims and their families are proud to be advocates for those who cannot advocate for themselves.

Our advocacy is directed to finding ways to give voice to those who have lost their voice but our advocacy should also, in this age of No Fault insurance coverage, called PIP, be directed to assisting in the process of diagnosis and treatment with the ultimate goal of proper identification and treatment of those so injured. Who amongst us would not willingly trade one of our toys for just a little bit of hope, that we could find a way to reverse the seemingly permanent changes in the brains of the head injured. What is the price we put on the misery of a person who has lost the ability to function effectively in the world but who has not lost the ability to recognize the loss, who remembers vividly who he once was and recognizes sadly what he has now become – all through no fault of his own.

The real message of my monograph and this seminar is to bring home to you, the Advocate, that the overwhelming number of head injuries are mistakenly missed early on, and the patients with so-called minor head injuries have insult added to injury and neglect added to evolving pathology. Is it any wonder that the injured appear in our offices distraught, mistrustful and confused, certain that they must be nuts when in fact, they are twice injured; once by the injury to their brain, and then again by the disbelief of their doctors, friends, family and finally the judicial system.

It is important for us to understand the above and the consequences, namely, that our clients, are less apt to be forthright because of the expressions of disbelief directed at them, and they are less apt to be certain of your intentions and confident in your actions, simply because those professionals, with whom they most expect to be able to trust and confide in, abuse their trust and express disbelief in their shared confidences.

Your clients with head injuries do not choose to forget, yet in many cases their inability to remember is publicly represented to be an intentional attempt to obfuscate and conceal. Patients with head injuries do not elect to have difficulty reasoning and planning, but they have these difficulties and precisely for that reason, they are unable to respond appropriately to persons who would wrongly accuse them of intentionally misleading the system.

Patients with head injuries do not enjoy being unable to modulate their emotions and they do not enjoy being unable to conform their daily behavior to the expectations of the society around them. Ironically, the patients with head injuries are afraid to tell you that they cannot modulate their emotions and they are afraid, most of all, to tell you that they are afraid of themselves.

The language of the 1990’s so strongly tied to our technologies has made popular the notion of “wysiwyg” or what you see is what you get. Except within the context of technical jargon you rarely, if ever, see what you get and you rarely get what you see. Nowhere is this more true than in the field of closed-head injury.


Closed-head injury is an injury to a structure within a vault, which has not been opened. It is an injury, the presence of which is deduced from observations of changes in the way a person perceives stimuli and the way he or she responds to that stimuli. You might say that closed-head injury is the ultimate example of concealed damage. It is much like a claim for concealed damage made by receivers of shipments. These claims involve arguments, in which the shipper argues that the manufacturer is responsible for the damage and the manufacturer argues the shipper is responsible.

In simple words, the tortfeasor would have you believe that each closed-head injury arises not from the tort but from errors in our design or mistakes in our construction. The tortfeasors would have us all believe that the laws of the universe never apply to his or her particular accident and the tortfeasor would have us all believe that the gelatinous mass, which we call our brain, cannot be injured by the vective forces which clearly cause each accident and which wholly describe each accident.

What we see in our clients is what is characterized in ICD-9 Classification as a Post Concussion Syndrome. The condition relates to known changes in the brain as opposed to, for example, anxiety disorders. This injury adversely affects cognitive functions such as perception, thinking, remembering, synthesis, concentration and analysis.

Contrary to popular belief, closed-head injuries require neither that the head be impacted by an object, nor that the head impact an object. Such injury requires only that there be an energy transfer from some external force to the brain. Traumatic Brain Injury will occur where that force is of such magnitude that it will disrupt either the structure or the metabolic infrastructure of the brain cells upon which the force acts, independent of whether there is an impact by an external object to the cranial vault.

Since TBI presents such a formidable challenge to the Advocate, we must first learn the research in this field before we tackle the problem of marshaling the available evidence in our particular case. In a very literal sense, we must first use our brains to understand itself before we can venture forth to understand, and, ideally persuasively represent the traumatically brain injured.


Research has shown that organic damage to the brain may not show up on an MRI, CAT or EEG because these tests reveal structural damage. The damage involved may be due to excessive release of neurotransmitters. An EEG measures electrical functioning of various members of the brain, but not single cell testing. So we may see often the case of the Neurologist who finds no residual deficits on such testing – but the tests performed are really gross motor.

The modern age of understanding head injury began with Dr. Strich in 1956 and Dr. Oppenheimer in 1968. Dr. Strich was initially interested in developing ways to look separately at neurons and gleas. Neurons are the brain’s basic unit. The human brain has between ten billion and one hundred billion neurons. (No one really knows how many). Neurons communicate with each other through electrical and chemical messages. Dr. Strich examined the brains of the people who sustained severe head injury and noted that in these brains, there appear to be actual interruption of individual neurons as indicated by micro degeneration. This micro degeneration was noted to be associated with proliferation of adjacent glia to fill in the gap. It is essentially the same thing in brains of people who have sustained minor closed-head injuries. Dr. Oppenheimer and Dr. Strich both noted that these changes occurred in the absence of any observable injury or disruption to surrounding neurons. Somewhat later, another researcher (Ommaya) described what is now known to be a classic pattern of these injuries. Normally there exists a distribution gradient of this micro degeneration extending from the cortical mantel to the brain stem, which parallels the severity of the injury. Summarizing many authors and many studies, it is has been shown that the more severe the closed-head injury: (1) the greater the actual number of interrupted neurons; (2) the greater the density of interrupted neurons at any given site, and; (3) the closer to the brain stem are the locus of the sites of interruption.

The importance of these observations cannot be overlooked; they suggest: (1) That the usual and customary pathways, the transmission of information from some point A to some point B within the brain, is either temporarily or permanently disrupted. When a brain cell is disrupted permanently, it breaks up and dies. Where there is such disruption, there results decreased ability in the brain to transmit information (2) The more severe the closed-head injury, the more likely it will result in neuronal interruption at the brain stem level, and, the less severe a closed head injury, the more likely that it will result in neuronal interruption at the brain level which controls thinking and; (3) Because some information within the brain can no longer be transmitted to and from sites remote from their locus of interruption, the effect of the interruption is widely felt within the brain, producing effects on cognition and other functioning at sites remote from the interruption.

Typically, in an acceleration/deceleration insult to the brain as occurs in a rear end impact, brain cells are stretched and may not go back to their normal state. Often, the speed of transmission of information is decreased in that the speed at which the information travels through the cell fibers is slowed due to the disruption caused by the trauma.

The more severe the head injury, the more likely it will result in neuronal interruption to the brain stem level. With this level of head injury, there is generally a loss of consciousness. The more severe the head injury, the more likely the disruption at the brain stem level.

The mere fact that these interruptions were noted to be visible and present only in those brains which have sustained injury, and never in uninjured brains gave rise to the great hope that these interruptions would provide a definitive marker of brain injury, which could be visualized in the living brain if only the technology caught up.

The advent of the CAT and the MRI has both helped and confused the issue. While these instruments provide an opportunity for an unbelievably-comprehensive view inside the living brain, they fall short of providing a certain marker of closed-head injury, not because the instruments do not work, but rather, because both MRI and CAT technology utilize averaging across a block of brain cells. Consequently neither technology has the resolution necessary to identify or locate interruptions of small numbers of axons in any given place. This is because the measured marker is averaged across so many cells that the injury is simply not visible. The consequences of this inadequacy, is that injuries which interfere with the physical integrity of neurons, located only in those layers of the brain which process integrative cognitive information, tend to be missed by these imaging techniques.

The uncritical acceptance of the requirement of MRI abnormalities as a necessary concomitant of closed-head injuries has resulted in the same erroneous belief which emerged from the early visualization capabilities developed by Madame Curie for bony structures. The uncritical reliance on CAT and MRI to define both the presence and extent of brain injury is unacceptable, both from the theoretical and a methodological perspective. Researchers, French and Dublin in a 1977 study, looked at CAT findings in a thousand consecutive known head injury patients. Ironically they are most remembered for demonstrating that thirteen per cent of alert, and clinically and neurologically intact patients with brain injuries, had abnormal CAT scans, whereas more importantly they demonstrated that more than fifty per cent of the patients in their sample, had clear and convincing evidence of clear neurological dysfunction with normal CAT scans.

Unfortunately, we do not know the hit and miss rate for MRI and CAT in minor closed-head injury. We do not know this because most minor closed-head injuries simply are not diagnosed early on.

The uncritical acceptance for the requirement that brain injuries be observable by the CAT or MRI and the use of this requirement in studies purporting to be validation studies of other diagnostic techniques ignores the vast majority of what is now known about the consequences of injury in closed-head trauma.


Essentially there are three major consequences of closed-head injury: structural interruption of conducting cells, interruption or disruption of transmission, and metabolic derangement. Structural interruption, as we have been talking about, speaks for itself – The nerve fiber is physically interrupted, it cannot respond normally to incoming information and it cannot provide accurate information to other cells upon which it acts.

The significance of the initial injury in closed-head injury, although certainly important by itself because of the disruption that it causes in the transmission of information, lies however primarily in the development of secondary events, such as edema , hemorrhage and swelling.

Recent studies, such as those of Frolich and his colleagues demonstrate that when highly-reproduceable focal cortical lesions are made in animals, there is a characteristic pattern of secondary damage which evolves and which can be treated and possibly prevented. That secondary damage includes progressive cortical hyperprofusion, with emphasis on the word progressive, edema and acute disruption of the blood brain barrier. Obviously, if actual neurons are interrupted and adjacent cells swallow the weak, then it can be expected that information in the nervous system will be negatively affected and that behavior will be altered. Neuropsychology measures cognitive disruption, which is the direct result of the structural alteration.

Experience has shown that closed-head injury is chiefly caused by abrupt rotational acceleration of the brain within the skull. This rotational force produces shearing strain on brain tissue and results in the tearing of axons therein. These injuries, referred to as Diffuse Axonal Injury, are microscopic and, therefore, not discernable by means of CAT Scan (Strich 1970; Ommaya and Gennarelli, 1974.) The greater the vector of rotational force, the deeper the shearing damage is likely to be. Damage is likely to proceed centripetally and outer cortical layers are more likely to be damaged than deeper brain regions. If brain stem signs are present, it is certain that higher brain levels have also been damaged.

Regardless of the site of impact on the skull, the more frequent loci of cerebral injury are the frontal and temporal folds. This observation appears to be attributable to the location of these regions in close proximity to bony protrusions of the interior of the skull and consequently increase the likelihood of contusions (Ommaya and Gennarelli, 1974.) Injury to these regions is likely to result in deficits in memory, concentration and abstract thinking.

Another consequence of brain injury is the disruption of the transmission processes in the absence of destruction of gross structure. Think for a moment of the number of different telephone numbers in this country. A good guess is that there may be as many as five hundred million different telephone numbers. Think what it would be like if exactly one half of these telephones are simultaneously picked up and each of these telephones then tried to call one of the remaining two hundred and fifty million numbers. If you have ever attempted to call home on either Mother’s Day or Christmas, you might be familiar with hearing, “all circuits are busy, please try your call again later”. I would suggest to you that Ma Bell’s task, regardless how complex its orders of magnitude, is easier than the task we assign our brain, with its one hundred billion neurons every moment of our entire lives.

The developing brain adds neurons at the rate of two hundred and fifty million per minute from conception to birth. It is easy to understand that if Ma Bell’s programmers goof and one of the major switching stations goes off line, our telephone system would be down. The system under those conditions goes down not because of interruption of individual lines, but rather because the intact individual lines have lost the ability to transmit to each other. It is easy to extend this analogy to our own personal network of one hundred billion lines and to understand the cascading effect that injury to the brain switching system can and does have. If injury happens fortuitously to injured synapses or other major neuronal switching stations, the connections between parts of the brain can be disrupted, even though each and every neuron is intact. This is what I mean by disruption of transmission as an effect of the trauma.

There was a study by Dr. Native which demonstrates the utility of consideration of alterations in transmissions. He tested the cortical potentials associated with simple goal directed forearm and finger movements in patients with post acute phase hemiplegia. The patients, as expected, showed reduced brain potentials for movements associated with their paretic limb, but more interestingly, they also showed reduced brain potentials to movements associated with the non-paretic limb. The study is important because it demonstrates that although there was no visualized injury to those brain centers, which control the non-paretic limb and no injury to the non-paretic limb, which could be measured on gross neurological examination, the damage to the area controlling the paretic limb appeared to have remote effects which produced changes of transmissions to the non-paretic limb. It would thus make perfectly good sense for these patients to exhibit bilateral motor deficits and bilateral inability to execute certain tasks; particularly, those tasks calling for speed of response. Absent these demonstrations by Dr. Native of the altered potentials, it is easy to see how both the medical and the legal community could conclude that the patient must be feigning the disability on the non-paretic side.

What this all means to you in your practice, simply put, is that representing the traumatically brain injured patient can be the most challenging but rewarding experience in your career.


The important concept in marshalling the evidence and the witnesses, is to understand that intelligence is not a unitary concept, but rather a conglomerate of a number of abilities which when working in concert, allows a person to effectively interact with his or her environment. Thus, your role is important as the attorney to investigate the history of your client and obtain as much historical data as possible in terms of school records, physician records, military records, employment records, description of the accident and the observations of co-workers, family members and friends. Before and after data is extremely important in such cases.

In your Opening to the Jury you must nip the anticipated defense by answering it before it is ever raised. You protect the integrity of your expert and your witnesses by obtaining as much historically as possible – the good and the bad. Quite often the facts which the defense can use to confuse on Cross Exam when creatively brought out initially by you in Opening and in your Direct case will diffuse the potential damage.

On the issue of malingering, certain safeguards must be established and presented properly throughout your case. From a neuropsychological standpoint they are (1) Length of testing; (2) Cross testing; (3) The patient is not aware of what the tester is going to ask or have the patient do; (4) If the patient is trying to fake the test, usually all the test scores will be low as you see in malingering patients who randomly try to blow questions. In these cases there would be very poor internal consistency. The biggest check is the cross variety of tests performed by the capable clinical neuropsychologist as well as the experience of the tester.

I do not think there is a type of case that requires as much client management as in Closed Head Injury. You must become keenly aware of the needs and concerns of this type of client. Neuropsychologists have shared with me that they often see clients/patients who hurt themselves because of their anger and frustration with the system. They do not try as well as they could or should on testing not because they intentionally wish to fane injury or malinger, but simply because in their own way they are trying to prove a point. This is because they feel that no one believes their injury. Not their boss, not the IME doctors, perhaps not even their own doctors. Their spouses and children are frustrated with them and they are fearful that their attorneys may sell them short. With these fears they proceed to the neuropsychological testing and they feel that if they do not give optimal effort then the test will definitely show the problems they are experiencing.

What they do not understand, and, many lawyers do not understand, is that the tests in combination do, in fact, reveal even the subtle problems that your client is suffering cognitively. The neuropsychological examination takes anywhere from 5 to 7 hours. During this period, with the appropriate testing, the skilled examiner will be able to determine whether the patient is faking or exaggerating and when that happens, even if there is a real injury, the problem is now being imbedded in a psychogenic pattern and the organic injury will not be revealed. The test results found in such cases are clearly inconsistent with the nature of the injury, the results are outside of any anticipated reference ranges and an opportunity to prove real injury is lost. It is, therefore, very important that we spend time with our clients, review with them and the neuropsychologist what is to be done and why, and, of course, encourage the client to do his very best so that the subtle problems he is experiencing will be clearly identified and an appropriate remediation program can be established as part of the rehabilitation program which he must be eager to participate in. The jury will reward the stoic fighter. But, if he gives up on himself, the jury will give up on him in the jury room.


It is the art of Advocacy and your responsibility to establish early on, the skills and experience of the experts who you will be bringing before the Jury to demonstrate the reality of brain injury.

In the utilization of the neuropsychologist in such cases there has always been the fear of using the Ph.D., a non-medical person, to render a diagnosis. Therefore, you must bring out through the treating neurologist, neurosurgeon and/or psychiatrist, that the referral to the neuropsychologist was appropriate because it is only through the complex detailed testing of the trained neuropsychologist that the brain injury can be objectively and both quantitatively and qualitatively established. You can bring out, for example, during your Voir Dire of the various experts, that in medical school it is the neuropsychologist who trains and teaches the medical student in such areas. In presenting the testimony of the neuropsychologist, it is important that you describe at least one or two of the tests performed and their significance so that the Jury can appreciate the complexity and the detail of what was done as well as its reliability.

The use of the clinical Neuropsychologist and the effective use of before and after witnesses is most important in these cases to effectively and persuasively develop the mosaic of evidence necessary to establish causality and the degree of injury. Pre-morbid history is critical because you must diffuse the defense arguments that the deficits exhibited either in the work place, at home and/or upon neuropsychological testing are due not to the particular trauma, but either to prior or subsequent conditions. You must participate in obtaining the history by collecting as much data from the various spheres of your client’s life such as school records, health records, IQ scores, performance in vocational schools, work and skills exhibited in ones social life and activities of daily living. From each sphere of your client’s life you must bring a witness who will describe who this person was before so that the Jury may fully understand what he has now become. In so doing, we develop a marker of damage.


Starting out as a lawyer representing the injured twenty years ago, I began to notice mediocre results in the closed head injury case. First off, I should say looking back I could see that many cases simply were not recognized. “Your client just had a simple concussion, that’s all. The case is worth $1,500.00 to $3,000.00”. In twenty years, things haven’t changed much. A number of years back I began to wonder why we are all getting these compromised verdicts in these cases or very low offers. Why were these honest people who were genuinely injured receiving nominal sums for what I considered cases of considerable merit. It became clear that there were a number of perceptual problems in presenting these cases.

To understand this problem, we have to understand how jurors decide cases. I believe that jurors come to their verdicts not simply on the facts, but on their collective impression of the facts. The individual juror impressions are created by how each perceives the players in this drama we call the trial and how each perceives the message being conveyed as filtered through their own personal biases created by their individual prior life experiences. (This is why the Voir Dire becomes so important, especially in this type of case and especially today in an anti-lawyer and anti-lawsuit environment where the jurors are all Doubting Thomas’.

We have learned that the message in the courtroom is 7% verbal, 38% vocal and 55% non-verbal. We have also learned with regard to juror retention that the jurors retain 20% of what they hear, 40% of what they see, but 80% of what they see and hear. The art of the advocate requires that he utilize these basic facts of human communication in the perceptual problem of the closed head injury case which involves the presentation of abstract concepts to jurors who have not experienced such a problem. We are dealing with an inheritantly abstract matter which is not subject to simple concrete proof such as may be available to us in proofs of a bone fracture, herniated disc and other objective injuries. As a result of the perceptual problem, the defense, often and easily plays two tunes to the jury. (1) The causation defense: The tort feasor’s act was not the cause; (2) The malingering defense: Here the entire defense is the gentle character assassination of the Plaintiff.

Therefore, we must move from the objective to the subjective. With regard to the traumatic event itself, if we are fortunate enough to have physical evidence of a significant violent event, we must do all that we can to present visually the drama of the event itself in the courtroom. This, of course, can be done through photographs and videotapes of the scene and the resulting damage, to person and property; and now we even have computer simulations. If there are observable injuries such as contusions, ecchymosis, a nose or orbital fracture, through photographs and x-rays prepare demonstrative blow ups for trial.

Because of the natural human tendency to doubt whether a normal looking plaintiff suffered head injury; you must seek out witnesses ideally from each sphere of your client’s life to demonstrate the dramatic changes in him since the traumatic event.

In addition to each expert commenting on the sincerity and credibility of the Plaintiff during examinations, the use of before and after witnesses is very important in that none of the doctors knew the abilities of the Plaintiff before he or she found his way to their offices. Not having seen the Plaintiff before the trauma, your expert has basically only the word of the Plaintiff to rely upon, and to the extent that there is any corroboration, it is often only provided by relatives who are personally interested in the welfare of the Plaintiff and, therefore, the outcome of the case. Thus, you must go into the work-place, the neighborhood and his place of worship to find witnesses who will paint a word-picture of a damaged life.

Likewise, as we move from the objective to subjective in presenting the medical proofs, we move from the family physician to the neurologist, to the psychiatrist and then to the neuropsychologist. Through the family or treating physician, we establish what physical injuries there are and where you have them, you must emphasize them. (The police officer and EMT personnel may also be helpful, but you have to get to them early to preserve their testimony or they will quickly forget.) The family physician must also testify to the importance of psychiatric and psychological treatment and testing in such cases. You must describe the high esteem in which he holds the neurologist and/or psychiatrist who he referred his patient to. You must describe that the conditions he diagnosed or required a consult on were of such a nature as to be beyond his expertise as the family physician and required very specialized training and care.

The neurologist must become the teacher in the courtroom through the use of charts and other demonstrative evidence. He must bring the reality of closed head injury to the eyes and minds of the jurors. Throughout the mosaic of testimony, credibility is key. Time must be spent with your experts and you should workshop your direct examination so that you take the complex and break it down to it’s simplest and most digestible form. If your first witness is your psychiatrist or psychologist, I believe you have made a mistake because you are really presenting critical facts on causation at a time when the jurors have not yet come to the place of mental acceptance that they need to be at when such evidence is presented. The evidence indeed, must be built from the objective to the subjective. Before we get to the psychiatrist and neuropsychological opinions the jurors must have the short course on the anatomy and physiology of the brain and the biomechanics of trauma.

As we move from the objective to the subjective, the original treating physician, the neurologist and the psychiatrist, as the case may be in the chain of referring physicians, all should explain that it is the psychologist who was trained in administering the sophisticated tests needed and in interpreting them so as to provide more clearly an objective basis upon which to make a proper diagnosis. Each physician must explain that the more accurate the diagnosis, the more effective the subsequent treatment plan, therefore, the importance of appropriate clinical neuropsychological testing. The experts should explain that when the psychological tests are considered in conjunction with the expert’s clinical impressions, together they provide a comprehensive map of the Plaintiff’s mind, permitting reasoned conclusions and predictions.

In the representation of the traumatically brain injured, what you see is not always what you get and what you get is not always what you see. Our task in the courtroom is to bring our vision of our client to the Jury in such a way and in such a form and with such words that the six people in the Jury box can understand how it is, that we came to view this head-injured victim, our client, as we do.


Then why did God Plague us with the power to think? Mr. Brady, why do you deny the one faculty which lifts man above all other creatures on the earth: the power of his brain to reason. What other merit have we? The elephant is larger, the horse is stronger and swifter, the butterfly more beautiful, the mosquito more prolific, even the simple sponge is more durable! (Wheeling on BRADY) Or does a sponge think?

I don’t know. I’m a man, not a sponge.

(There are a few snickers at this; the crowd seems to be slipping away from BRADY and aligning itself more and more with DRUMMOND.)

Do you think a sponge thinks?

If the Lord wishes a sponge to think, it thinks.

Does a man have the same privileges that a sponge does?

Of course.

(Roaring, for the first time: stretching his arm towards CATES)

This man wishes to be accorded the same privilege as a sponge! He wishes to think!

(There is some applause. The sound of it strikes BRADY exactly as if he had been slapped in the face.)


The following is a list of journal articles that will prove helpful in understanding the clinical and forensic aspects involved. Each article further cites many other treatises and research data that will be of assistance in understanding your case, communicating with your experts, seeking additional experts, cross examining the defense experts and in appreciating the physical and psychological dilemma of your client.

• 1. Barth J.T., Gideon D.A. et al, Forensic Aspects of Mild Head Trauma. Journal of Head Trauma Rehabilitation 1986:1(2):63-70.
• 2. Alves W.M., Coloban A.R.T. et al. Understanding Post Traumatic Symptoms After Minor Head Injury. Journal of Head Trauma Rehabilitation 1986:1(2):1-12.
• 3. Gennarelli T.A. Mechanics and Pathopsychology of Cerebral Concussion Journal of Head Trauma Rehabilitation 1986:1(2) 23-29.
• 4. Rimel, R.W., Giordani B. et al. Disability Caused by Minor Head Injury. Neurosurgery, 1981, Vol. 9 No. 3 pp. 323-346.
• 5. Binder L.M., Persisting Symptoms after Mild Head Injury: A Review of the Post Concussive Syndrome. Journal of Clinical and Experimental Neuropsychology, 1986: Vol. 28 No. 4, pp. 323-346.
• 6. Sbordone R.J., Purisch A.D., Clinical Neuropsychology: Medico-Legal Applications. Trauma 1987, Vol. 28 No. 5 pp. 49-106.
• 7. Houts M., Krueger J. Presenting the Medical Evidence: Pre Trial Discovery to Probe for a Possible Malingering Plaintiff. Trauma, 1987, Vol. 28 No. 5 pp. 5-47. Matthew Bender, Publ.