Handling the Traumatic Brain Injury Case
By: Keith Jackson
RILEY & JACKSON, P.C.
Alabama Law Weekly Tort/Workers’ Comp Conference
Birmingham, Alabama (2010)
With the various injuries a plaintiff may suffer, few are as medically complex as a traumatic brain injury (“TBI”). When a plaintiff presents with a TBI, regardless of whether the injury is mild or severe, the case potentially becomes much more complex because of the nature of TBIs. To evaluate and assess the damage component of a case involving a TBI, attorneys must ensure that they are prepared to handle the challenges of a complex medical presentation and a myriad of possible prognoses.
Our presentation will address numerous concepts with which practitioners who may be confronted with TBIs should be familiar. We will cover the basic (very basic) anatomy of the brain, the most common mechanisms of TBIs, the medical jargon associated with TBIs, and possible long-term prognoses. We will also touch upon how to depose the treating physicians and the areas of deposition inquiry about which a plaintiff should be prepared to testify or, for the defense attorneys, areas of damages that should be covered during the plaintiff’s deposition.
Basic Anatomy of the Brain
Put in the most basic terms, the anatomy of the major regions of the brain can fairly be divided into the cerebral hemispheres, diencephalon (thalamus and hypothalamus), brain stem, and cerebellum. Understanding the purposes of each of these sections of the brain and the ways in which a TBI to each area will manifest provides important insight into the nature of a specific TBI and its common underlying causes. Because most TBIs occur in the cerebral hemispheres, we will place most of our focus on that area during the presentation.
The cerebral hemispheres account for over 80% of total brain mass and are comprised of the cerebral cortex and various lobes. The cerebral cortex is a thin surface area that accounts for about 40% of total brain mass. The cortex is responsible for what we generally think of as conscious behavior.
Located within the cerebral hemispheres are the frontal lobes, parietal lobes, occipital lobes, and temporal lobes, which are depicted on the image attached as an addendum to this paper. Certain areas depicted on the image such as the central sulcus and sylvian fissure are beyond the scope of this presentation.
Understanding the basics of the brain’s anatomy is an important component of effective advocacy in a case involving a TBI. A well-prepared practitioner can understand the most likely origin of certain signs and symptoms of a TBI and can plan matters such as his or her discovery, physician discussions, and questioning of a treating physician or a plaintiff accordingly. In many instances, signs and symptoms of TBIs can be identified as likely originating in a specific area of the brain, thereby offering important insight into the nature of the TBI, where the original insult likely occurred, etc. For example, if a plaintiff suffered a mild concussion in a car wreck case but is complaining of signs and symptoms consistent with a hypoxic or anoxic injury, the attorney representing the plaintiff and the attorney defending the case should understand the distinction and plan their cases accordingly. In contrast, if a plaintiff involved in trauma is not at first diagnosed with a TBI but manifests memory problems following the trauma, this presents an area of damage that should be explored by the plaintiff’s attorney before the plaintiff is deposed. Toward the end of touching upon the functions served by major components of the brain that are generally susceptible to TBIs, we have included in our presentation a broad summary of the functions of these areas.
The frontal lobes handle planning, organizing, problem solving, selective attention, personality, and a variety of functions including behavior and emotions. The anterior of the frontal lobe is the prefrontal cortex, which must function properly to perform higher cognitive functions and is heavily involved in the determination of personality. The posterior of the frontal lobe consists of the premotor and motor areas. Nerve cells that produce movement are located in the motor areas. The premotor areas of the frontal lobe modify movements.
Injuries to the frontal lobe are common in front-head trauma such as MVAs, forward falls, and any high-energy contact to the front of the skull. These injuries may manifest as paralysis of various body parts, changes in personality, changes in social behavior, mood changes, and difficulty to express language. More eloquent presentations of a TBI to the frontal lobe can manifest as a loss of flexibility in cognitive thought, the overwhelming persistence of a single thought, an inability to focus on a given task, and the inability to formulate and execute movements necessary to complete complex tasks such as dressing a child, preparing dinner, or brewing a pot of coffee.
The parietal lobes are located near the top and rear of the skull and are heavily involved in controlling sensations such as touch, pressure, and determination of weight, size, and shape. An injury to one of the parietal lobes will often manifest as a marked decrease in fine motor skills. Victims of TBIs in this area of the brain will often experience significant difficulty with hand-to-eye coordination. They may often find it difficult to focus visually and to choose proper words for writing a sentence, reading, drawing, and solving mathematical equations.
The occipital lobes are at the rear of the skull, above the cerebellum. The occipital lobes process visual information and contain a significant number of crisscrossing optic fibers. This region not only processes images that are being received, but it is also responsible for aiding in visual recognition of shapes and colors. TBIs in this area will often lead to noticeable and permanent vision defects.
Distinguishing between a vision deficit caused by an injury to the occipital lobe and a vision deficit caused by a problem with a single eye is easily done by a physician who determines whether there is an entire field cut, meaning a vision deficit in both eyes. For example, the loss of right peripheral vision as a result of a TBI to the occipital lobe will typically have equal impact upon the right peripheral vision in both the right eye and the left eye. Injuries in this area can also cause recognition difficulties such as the inability to recognize words, colors, and objects, and these injuries may result in hallucinations.
The temporal lobes are at the side of the skull at approximately the level of the ears. The temporal lobes sort new information, may be heavily involved in short-term memory, and allow us to distinguish one smell or sound from another smell or sound. Injuries to these areas will often interfere with memory, both short-term and long-term. A person with a TBI to one of the temporal lobes can manifest the injury in a number of ways. For example, injuries to a temporal lobe can cause significant difficulty in understanding and processing the spoken word and in verbalizing information. These injuries can render a sufferer unable to categorize objects and to place appropriate selective attention to what he or she sees and hears. These injuries can also lead to aggressive behavior.
The cerebellum lies at the base of the skull and is important for motor control, but injuries to this area do not typically result in paralysis. Rather, the cerebellum is similar to a coordination center not unlike the U.S. Post Office. It receives information from the other areas of the brain, organizes that information, and redistributes it as motor activity that has been fine-tuned. Therefore, damage in this area is often dramatic and includes the inability to coordinate fine movements, walk, grab items, and make quick movements. Manifestations of these injuries also include dizziness and slurred speech.
The brainstem is located deep within the brain and structurally is continuous with the spinal cord. This is the nerve center of the brain as the nerve connections for motor and sensory functions from the brain to other areas of the body pass through this area. The brainstem also regulates heart rate, breathing patterns, alertness, and consciousness. Any serious brainstem injury can produce a coma. Other brainstem injuries may result in sleeping difficulties, dizziness, nausea, problems with balance, dysphagia, and a noticeable decrease in breathing capacity, which is important for speech.
How TBIs Occur
There are a number of potential causes for TBIs, but notable to attorneys is that motor vehicle accidents and falls are two of the top three leading causes, with the third being gunshot wounds. The mechanisms of injury are varied and complex and include open head injuries, closed head injuries, deceleration injuries, and chemical injuries. Other mechanisms of injury that are largely included by the medical community under the heading TBI, but that are beyond the scope of this presentation, include hypoxia or anoxia, tumors, infections, and strokes.
Open Head Injuries
Open head injuries occur just as their name describes, i.e., with trauma that fractures the skull and damages brain tissue or the surrounding membranes. Common causes are gunshot wounds, MVAs, falls, and any other mechanism whereby a blunt object strikes the skull with moderate to high force. For our purposes, we have focused on open head TBIs typically associated with MVAs and falls (such as workplace injuries) rather than high velocity injuries such as gunshot wounds.
With any open head TBI, the damage is usually, though not always, more focal than the damage typically seen with a closed head TBI. Open head TBIs will differ depending on the type of skull fracture suffered. There are four types of skull fracture: (1) Linear skull fracture; (2) depressed skull fracture; (3) basilar fracture; and (4) diastatic fracture. A linear skull fracture is simply a crack in the skull. This type of fracture does not penetrate the brain tissue. These fractures account for a high majority of open head injuries, are usually minor, and rarely require extensive treatment. The most common major complication of a linear skull fracture is leakage of cerebrospinal fluid, which may occur when the linear fracture extends into the sinus cavity.
Depressed skull fractures are usually caused by a severe blow to the head by a blunt object. The fracture appears just as its name describes, and broken skull fragments penetrate or compress brain tissue. These fractures can cause severe brain damage.
Diastatic fractures are almost always seen only in newborns and infants. This type of fracture occurs when the areas of the skull where the bones fuse together during childhood are widened by an external force. Also rare are basilar skull fractures, which are fractures at the base of the skull. These fractures can cause tears in the membranes holding the brain, which may cause leakage of cerebrospinal fluid from the nose and ears.
Not surprisingly, additional complications beyond the expected TBI can occur with open head injuries. These injuries can expose the brain to the outside environment. This leaves victims of open head injuries susceptible to infection, which itself can cause permanent brain damage or death. The most common type of infection resulting from open head injuries is meningitis, or infection of the membranes that surround the brain and spinal column. Caused by bacteria or viruses, meningitis is usually treated with aggressive antibiotics and drugs that reduce brain swelling. In addition to meningitis, open head injury can leave the brain vulnerable to other complications, including seizures, dementia, paralysis, coma, and death.
Simply put, any object that penetrates or fractures the skull or that comes into high energy contact with the skull can cause direct trauma to the brain in the form of an open head injury. It is very easy for a jury to envision how a displaced fracture of the skull could cause tissue damage. The practitioner has a somewhat more difficult task of explaining the injury to a jury when the direct trauma is caused by contact with an object that does not penetrate or fracture the skull, i.e., a closed head injury.
Closed Head Injuries
A closed head injury is any head injury that does not penetrate the skull. While there are a myriad of causes for closed head injuries, we generally see them in our practice as a result of a fall or MVA. They are also common in children who have bike accidents, swimming pool accidents, sports-related injuries, etc. The damage caused by a closed head injury tends to be diffuse, with the exception of contusions, whereas open head injuries typically cause more focal damage. Closed head injures include, but certainly are not limited to, concussions, brain contusions, diffuse axonal injuries (covered separately in deceleration TBIs), and hematomas.
The Mayo Clinic characterizes a concussion as any head injury that temporarily affects normal brain functions. Common signs and symptoms of a concussion include headache, dizziness, nausea, ringing in the ears, slurred speech, and vomiting. Secondary symptoms include drastic mood swings, sensitivity to light, and sleep pattern disturbances. Concussions are usually diagnosed promptly in cases that do not involve other serious injuries, and a plaintiff’s medical records will typically contain a diagnosis of concussion when the condition was present.
Brain contusions are bruises of the brain tissue. In some cases, brain contusions lead to hemorrhages, which are absorbed into the brain tissue. If blood is absorbed into the cerebrospinal fluid, it can cause permanent neurological damage. Brain contusions are generally localized, a characteristic that distinguishes them from concussions, which are more diffuse.
Contusions can be minor with very few symptoms and little or no damage to the brain. They can also be quite severe. People with severe contusions often spend some time unconscious following the injury, and they wake up confused, tired, emotional, or agitated. More severe contusions lead to swelling in the brain, which can cause additional brain damage. Other symptoms may include memory loss, attention problems, emotional disturbances, difficulty with motor coordination, numbness, and a loss of the ability to understand or express speech.
Hematomas are sometimes confused with contusions, but the two are very different injuries. Hematomas occur when the brain is forced against the inside of the skull, which causes a pool of blood either outside the blood vessels of the brain or between the skull and brain. The brain cannot drain this much fluid. Intracranial hematomas therefore can compress brain tissue. This may lead to unconsciousness, seizures, lethargy, or death.
The three types of intracranial hematomas are subdural, epidural, and intraparenchymal. Subdural hematomas occur when a vein ruptures between the brain and the membrane surrounding the brain, which is called the dura. The hematoma is below, or “sub”, the dura. An epidural hematoma is caused by a rupture between the dura mater and the skull. This hematoma is above, or “epi” in relation to, the dura. Intraparenchymal hematomas occur when blood collects within the brain tissue.
Hematomas are potentially very serious and often require surgery and extensive recovery time. They can result in death or significant long-term medical complications in persons who survive them. They are a common presentation in falls, and there is a very good chance that a decedent who died as a result of a fall in a hospital or nursing home died of complications from an intracranial hematoma.
Although deceleration injuries are closed head injuries, we have addressed them separately because of the different mechanism of injury. The closed head injuries discussed above are directly caused by contact to head. Deceleration injuries present as diffuse axonal injuries.
Diffuse axonal injuries are self-defining, with diffuse simply indicating that the injury is spread over a wide area, and axonal referring to a portion of a nerve fiber. These injuries are the result of shearing forces that occur when the head is rapidly accelerated or decelerated, which obviously may happen in MVAs and falls.
The brain is no different from other organs in that it is vulnerable to movement injuries. For example, when a person is driving 70 mph on the interstate, his or her head is traveling the same speed. In a forceful collision, when the speed of the vehicle very quickly drops to zero and the driver’s face collides with the air-bag or steering wheel, the brain is vulnerable to a deceleration injury. Tissue slides over other tissue, resulting in an axonal injury, or an injury to the components of a nerve that allow one neuron to communicate with another. This is the result of isotropic stress.
Diffuse axonal injuries usually occur in the deeper white matter of the brain where the axons are subject to more stretching and therefore greater injury. Diffuse axonal injuries caused by isotropic stress often occur in conjunction with other injuries to the brain and are best understood in that context.
For example, in the MVA example above where a car traveling 70 mph is suddenly stopped with a resulting impact to the front of the skull, an injury may occur in the area of the brain that is closest to the impact. In our example, the injury would likely be to the outer part of the frontal lobe or the temporal lobes. This known as the coup injury, resulting from the primary impact, and the resulting damage would likely be one of the closed head injuries discussed above.
This type of blunt force trauma to the head may also cause a contrecoup injury from the secondary impact. This injury will appear directly opposite the side of trauma and generally occurs when a moving head strikes a stationary object. Another classic cause of such an injury in the litigation context is a fall injury. These injuries occur at impact when the brain opposite the point of impact is pulled away from the skull, thereby causing the injury in that location.
The force that passes between the point of initial contact (the coup injury) and the opposite side (the contrecoup injury) passes through the white matter of the brain. This displacement of energy, generally referred to as a “pulse”, moves through the brain at a very high speed, creating the shearing force that causes a diffuse axonal injury. There is a great deal of ongoing research into these types of injuries as men and women in service have returned from Iraq having suffered minor versions of this type of diffuse axonal injury from shell blasts caused when the pulse from the blast moves through the brain.
The other and likely more common type of diffuse axonal injury is caused by a whiplash motion. Severe sudden twisting of the brain can occur in any sudden acceleration or deceleration, even in the absence of a direct trauma to the skull. The axonal fibers are damaged by twisting or stretching that occurs with this type of injury. For whiplash severe enough to cause a diffuse axonal injury, a coma or at least temporary loss of consciousness generally results from the original injury.
We take for granted the fact that chemical injuries to certain organ systems are recognized as being very real, such as asbestosis and reactive airway disease. While attorneys today take that premise as a given, this truth was not always accepted in the medical or legal communities. Even today, with numerous chemical injuries not being an area subject to much controversy, the idea of chemical brain injuries can still draw skeptics to the discussion.
Chemical brain injuries are considered by many to be the overlooked TBI. Dr. Kaye Kilburn, a University of Southern California Professor of Medicine, authored a groundbreaking treatise in 1998 (republished since) on chemical brain injuries. He has participated in several studies that delve into the question of why chemical brain injuries do not garner more attention from researchers. Dr. Kilburn has posited the controversial yet evidence-based notion that conditions such as multiple chemical sensitivity (MCS), fibromyalgia, chronic fatigue syndrome, sick building syndrome, Gulf War syndrome, ADHD, and others may seem very different in their clinical presentations, but research has demonstrated they all may be induced by chemicals.
A reality of litigation over chemical brain injuries is that, in many cases, a myriad of possible causes may exist. Assume for example that a plaintiff claims an unusually high exposure to aluminum in a workplace accident caused her to suffer a chemical brain injury. Aluminum may be plentiful, but the human body has no use for it whatsoever. It can be toxic to us in certain quantities. Nonetheless, aluminum is contained in deodorant, vaccines, soft drink cans, baking powder, cake mixes, and numerous additives. Our plaintiff therefore will have to deal with the argument that her aluminum level documented by lab test could be from any number of sources.
For most litigators who do not specialize in toxic torts, chemical brain injury scenarios with which we are presented will often result from an acute and obvious toxic exposure rather than from a chronic exposure to lower levels of a toxic chemical, with one notable exception – heavy metals. While over 1,000 substances have been recognized as potentially having neurotoxic effects, metals such as lead garner a great deal of attention because of their effects on children. In our practice, which does not focus on toxic torts, we have been presented with several cases in which children had elevated levels of lead likely due to lead paint in rental homes. Mercury and manganese are also recognized as metals that cause brain damage. Other chemicals most likely to be the culprits in chemical brain injuries include pesticides, solvents, fuels, and carbon monoxide.
Neurotoxic chemicals can reach the brain via the blood following inhalation, ingestion, or through skin absorption. While severe acute exposure can result in death, paralysis, or other immediate complications with the central nervous system, less severe exposures can present more subtle symptoms and will require a more elegant neurological evaluation to determine the underlying cause of a plaintiff’s problems. Particularly in persons who work with or around neurotoxic chemicals, new onsets of any of the following symptoms deserve investigation: Impaired cognitive ability; memory problems; impaired balance; poor coordination; speech difficulties; sensory issues; tremor; chronic headaches; chronic pain; and intermittent impairment of consciousness.
Regardless of the type of TBI at issue, whether closed head, open head, deceleration, or chemical, the job of the prepared and experienced litigator is to ensure he or she explores all possible areas of causation and damages with the plaintiff and treating physicians. In many instances, plaintiffs may not be aware of their own neurological shortcomings, a topic that we address later in our presentation. To be an effective advocate for either the plaintiff or defendant in a TBI case, attorneys must be able to understand at least on a basic level the type of TBI at issue and how that particular TBI generally occurs.
The following table, which was prepared by Merck, summarizes various types of TBIs, the clinical presentation typically associated with the TBI, and the diagnostic tool utilized in confirming the TBI. This table may be used as a quick reference point when a TBI diagnosis is made or suspected in a plaintiff, but as with all cases involving a TBI, consultation with the treating physician is critical to understanding the TBI at issue.
|Common Types of Traumatic Brain Injury|
|Acute subdural hematoma||Typically, acute neurologic dysfunction, which may be focal, nonfocal, or both
Patients with small hematomas may have normal function
|CT: Hyperdensity in subdural space, classically crescent-shaped
Degree of midline shift important
|Basilar skull fracture||Leakage of CSF from the nose or ear
Blood behind the tympanic membrane (hemotympanum) or in the external ear
Ecchymosis behind the ear (Battle’s sign) or around the eye (raccoon eyes)
|CT: Usually visible|
|Brain contusion||Widely variable degrees of neurologic dysfunction or normal function||CT: Hyperdensities resulting from punctate hemorrhages of varied sizes|
|Concussion||Transient mental status alteration (e.g., loss of consciousness or memory) lasting < 6 hours||Based on clinical findings
CT or MRI: Clinical abnormalities not explained by lesions in brain parenchyma
|Chronic subdural hematoma||Gradual headache, somnolence, confusion, sometimes with focal deficits or seizures||CT: Hypodensity in subdural space (abnormality is isodense during subacute transition from hyperdense to hypodense)|
|Diffuse axonal injury||Loss of consciousness lasting > 6 hours but may not have focal deficits or motor posturing||Based on clinical findings
CT: At first, may be normal or show small hyperdensities in corpus callosum, centrum semiovale, basal ganglia, or brain stem. MRI: Often abnormal
|Epidural hematoma||Headache, impaired consciousness within hours, sometimes with a lucid interval
Herniation typically causing contralateral hemiparesis and ipsilateral pupillary dilation
|CT: Hyperdensity in epidural space, classically lenticular-shaped and located over the middle meningeal artery (temporal fossa) due to a temporal bone fracture|
|Subarachnoid hemorrhage||Typically, normal function
Occasionally, acute neurologic dysfunction
|CT: Hyperdensity within subarachnoid space on the surface of the brain; often outlining sulci|
Unraveling the Confusing TBI Language
We make no attempt to identify and define the universe of medical vernacular used in conjunction with the diagnosis and treatment of TBIs, but a familiarity with many of the more common words and phrases will be very helpful to any attorney meeting discussing a TBI with a treating physician or even with the plaintiff, who very likely will have learned a tremendous amount about his or her own injury by the time he or she is deposed. For the sake of brevity, we have simply defined below many of the more common words and phrases associated with TBIs by excerpting portions of an on-line TBI Glossary published by the Brain Injury Resource Center:
- Acuity – sharpness or quality of a sensation.
- ADL – activities of daily living. Routine activities carried out for personal hygiene and health such as eating, dressing, grooming, shaving, etc.
- Affect – the outward signs of individual emotions.
- Agnosia – failure to recognize familiar objects although the sensory mechanism is intact.
- Anomia – inability to recall names of objects.
- Anterograde Amnesia – inability to consolidate information about ongoing events
- Apraxia – inability to produce voluntary speech
- Ataxia – a problem of muscle coordination not due to apraxia, weakness, rigidity, spasticity or sensory loss. Caused by lesion of the cerebellum or basal ganglia. Can interfere with a person’s ability to walk, talk, eat and to perform other self care tasks.
- Cerebellum – the portion of the brain (located in the back) that helps coordinate movement.
- Cerebrospinal Fluid – a colorless solution similar to plasma protecting the brain and spinal cord from shock. CSF circulates through the subarachnoid space. For diagnosis purposes, a lumbar puncture (spinal tap) is used to draw CSF.
- Circumlocution – Use of other words to describe a specific word or idea which cannot be remembered.
- Clonus – A sustained series of rhythmic jerks following quick stretch of a muscle.
- Cognition – the mental process involved in knowing, thinking, learning and judging.
- Cognitive dissonance – individual awareness of inconsistencies in thoughts, feelings, rationale and opinions.
- Cognitive function -an intellectual process by which a person becomes aware of, perceives or understands ideas.
- Cognitive process -. The means by which an individual becomes aware of people, objects and situations in the environment and their subjective, symbolic meaning.
- Coma – a state of profound unconsciousness from which the person is incapable of any conscious action.
- Contracture – a pathologic, involuntary, irreversible shortening of a muscle.
- Contusion – a bruising of the neural tissues of the brain.
- Conversion disorder – a neurosis caused by the patient’s conscious or unconscious desire to escape or avoid some unpleasant situation or responsibility or, to obtain sympathy or some other secondary gain. The symptoms of TBI are sometimes mistakenly diagnosed as conversion disorder.
- Coup – a blow to the head at the site of impact.
- Contrecoup – injury to the brain resulting from a blow to the opposite side of the head.
- Diffuse axonal injury – a shearing injury of large nerve fibers (axons covered with myelin) in many areas of the brain.
- Diffuse brain injury – injury to cells in many areas of the brain rather than in one specific location.
- Diplopia – seeing two images of a single object; double vision.
- Dura mater – the outermost of three membranes protecting the brain and spinal cord.
- Edema – collection of fluid in the tissue causing swelling.
- Encephalography – non-invasive use of ultrasound waves to record echoes from brain tissue. Used to detect hematoma, tumor or ventricle problems.
- Frontal Lobe – front part of the brain; involved in planning, organizing, problem solving, selective attention, personality and a variety of higher cognitive functions.
- Glasgow Coma Scale – a standardized system used to assess the degree of brain impairment and to identify the seriousness of injury in relation to outcome.
- Hematoma – the collection of blood in tissues or a space following rupture of a blood vessel.
- Hemianopsia – visual field cut. Blindness for one half of the field of vision (both eyes).
- Hemiplegia – paralysis of one side of the body as a result of injury to neurons carrying signals to muscles from the motor areas of the brain.
- Hemiparesis – weakness, paralysis or loss of movement on one side of the body.
- Hyperreflexia – Increased action of the reflexes.
- Hypoxia – lack of blood oxygen due to impaired lung function. Hypoxia can further damage oxygen sensitive nerve tissue in the brain.
- Intracranial Pressure (ICP) – cerebro-spinal fluid (CSF) pressure measured from a needle or bolt introduced into the CSF space surrounding the brain. It reflects the pressure inside of the skull.
- Ischemia – a reduction of blood flow that is thought to be a major cause of secondary injury to the brain or spinal cord after trauma.
- Mental Status Examinations (MSE) – standardized tests that evaluate verbal responses and behavioral reactions.
- Neurogenic Bladder – Any bladder disturbance due to an injury of the nervous system.
- Neuropsychological Assessment – an evaluation of the patient’s brain functions relating to behavior.
- Occipital Lobe – One of two lobes in the back of the brain that process visual information.
- Paraplegia – loss of function below the cervical spinal cord segments, wherein the upper body retains most function and sensation.
- Parietal Lobe – one of the two lobes of the brain located behind the frontal lobe at the top of the brain.
- Post-Concussion syndrome – a particular group of impairments that characterize the effects of injury on the brain and behavior.
- Post-Traumatic Amnesia – memory loss that can be caused by brain damage.
- Ptosis – drooping of a body part, such as the upper eyelid, from paralysis.
- Quadriplegia – loss of function of any injured or diseased cervical spinal cord segment, affecting all four body limbs.
- Retrograde Amnesia – inability to recall events prior to a TBI.
- Seizure – an uncontrolled discharge of nerve cells which may spread to other cells nearby or throughout the entire brain.
- Sequelae – residual symptoms frequently observed following recovery from a physical condition, treatment or injury.
- Spasticity – hyperactive muscles that move or jerk involuntarily.
- Subdural – beneath the dura covering the brain and spinal cord.
- Synapse – the specialized junction between a neuron and another neuron or muscle cell for transfer of information such as brain signals, sensory inputs, etc., along the nervous system.
- Temporal Lobe – one of two lobes on each side of the brain at about the level of the ears. These lobes allow a person to tell one smell from another and one sound from another. They also help in sorting out new information and are believed to be responsible for short-term memory.
- Ventricles (Brain) – four natural cavities in the brain which are filled with CSF.
Understanding Possible Long-Term Prognoses for TBI Patients
No two brain injuries are alike. There is no greater truth of which attorneys must be mindful when speaking with treating physicians about long-term prognoses for a plaintiff who suffered a TBI. Every case will be different.
Additionally, no discussion of TBIs, their severity, or their prognoses can occur without considering the use of the Glasgow Coma Scale (GCS). While the GCS is used by convention as an initial diagnostic tool when TBIs are present or suspected, its use is further reaching than that of an initial evaluation tool. It is an extremely tool in determining likely long-term prognoses, and it is sometimes used in conjunction with the Glasgow Outcome Scale, referenced below. As an introductory matter to understand the function and purposes of the GCS, the following table reflects the scoring methodology it uses:
A GCS score of less than 8 is typically regarded as a coma. A score of 3-8 is generally characterized as a severe TBI, with a score of 9-13 being moderate and 14-15 being mild. A score of 15 is the highest possible score, so some physicians have testified in our cases that a score of 15 indicates the absence of TBI.
The GCS is utilized not only for quantifying the severity of a TBI, but also for developing a prognosis, although it is not used as an independent tool. Both the severity and prognosis of a TBI are predicted more accurately by also considering diagnostic tests such as CT scans as well as other factors.
According to an article published in “Critical Care Medicine”, because hypoxia and hypotension can decrease the GCS, GCS values after resuscitation from cardiopulmonary insults are more specific for brain dysfunction than values determined before resuscitation. Similarly, sedating drugs can decrease GCS and are usually withheld if possible until after a full neurologic evaluation has occurred.
Although the GCS can provide meaningful information both as a diagnostic tool and for purposes of long-term prognosis, a myriad of symptoms may present following a TBI. Amnesia resulting from a TBI may persist. Post-concussion syndrome, which commonly follows a moderate or severe concussion, includes headache, dizziness, fatigue, difficulty concentrating, variable amnesia, depression, apathy, and anxiety. Symptoms of this condition usually resolve spontaneously over weeks to months. A range of cognitive and neuropsychiatric deficits can persist after severe and even moderate TBI, particularly if structural damage was significant. Other common problems include behavioral changes such as agitation, impulsivity, a lack of inhibition, a lack of motivation, emotional lability, sleep disturbances, and decreased intellectual function.
Late seizures, which are defined as seizures more than 7 days after the TBI, develop in a small percentage of TBI patients weeks, months, or even years later. Spastic motor impairment, gait and balance disturbances, ataxia, and sensory losses may also occur long-term.
Perhaps the most feared prognosis following a severe TBI is persistent vegetative state, commonly known as a coma. This generally results from a TBI that damages forebrain cognitive functions but not the brain stem. The capacity for self-awareness and other mental activity is missing, but autonomic and motor reflexes are preserved. Sleep-wake cycles are also normal. Few patients recover normal neurologic function when a persistent vegetative state lasts for 3 months after injury, and almost none recover after 6 months. A lingering medical curiosity is the fact that some patients may be comatose even in the absence of obvious abnormalities on CT scans or MRIs indicating damage causing the coma.
Following all but the most debilitating TBIs, neurologic function may continue to improve for a few years after the injury. Progress is generally the most rapid within the first six months after the injury. It is not correct, however, to say that almost everyone who suffers a TBI will get “better” to the extent “better” refers to a return to baseline prior to the injury.
According to a 2007 article published in the online Merck Manual, adults with severe TBI and who receive treatment have a mortality rate of 25-33%. Mortality is lower with higher GCS scores. Mortality rates are also lower in children 5 years or older, with less than a 10% mortality rate in this population with a GCS score of 5-7. Overall, children do better than adults with a comparable TBI.
The majority of patients with mild TBI retain good neurologic function. With moderate or severe TBI, the prognosis is not as good, but there is a great deal of room for hope. The most commonly used scale to assess outcome in TBI patients is the Glasgow Outcome Scale. On this scale, the possible outcomes are:
- Good recovery (return to previous level of function)
- Moderate disability (capable of self-care)
- Severe disability (incapable of self-care)
- Vegetative (no cognitive function)
Over 50% of adults who suffer a severe TBI have a good recovery or moderate disability on the Glasgow Outcome Scale. The presence and duration of coma after a TBI are strong predictors of disability. For patients whose coma exceeds 24 hours, 50% have major persistent neurologic problems, and 2-6% remain in a persistent vegetative state at 6 months. Cognitive deficits, with impaired concentration, attention, and memory, and various personality changes, are a more common cause of disability in social relations and employment than are focal motor or sensory impairment, and it is this type of long-term deficit an alert attorney may notice in a client who is potentially unaware of his or her own neurological deficits.
To be certain, a person who suffers even a mild TBI and seeks treatment will usually have been diagnosed with a TBI and assessed and treated accordingly. The overwhelming number of plaintiffs with TBIs we have seen in our practice have been under appropriate physician care for their injuries and resulting deficits. In this situation, an understanding of the nature of TBIs and the specific TBI with which your client (or the opposing party) has been diagnosed will be adequate to begin case preparation in earnest with any eye toward establishing the presence of TBI and any long-term prognoses.
In limited instances, however, TBIs may have occurred without detection. It is not difficult to imagine this happening when the initial TBI is mild with no resulting clinical signs, or a mild TBI occurs in conjunction with other more urgent injuries. For example, in a catastrophic injury or high energy automobile collision, emergency room physicians may conduct a GCS, which in turn may reveal only a mild TBI or even a score of 15. The physicians may then appropriately address more serious and life-threatening injuries such as vertebral fractures, spinal cord injuries, lung injuries, long bone fractures, vascular injuries, etc. Clinically, the patient may not show any signs and symptoms of a TBI and may have no obvious abnormality revealed by CT scan or MRI.
We have seen instances in our practice, however, where neurological shortcomings present subtly as the patient goes through therapy and his or her recovery progresses. This is the type of TBI that may be overlooked even by the injured person. Understanding the long-term prognosis of various TBIs will allow an attorney representing such a person to detect possible neurological complications so that the client can then seek a referral for his or her physician for a neurological assessment.
Assume a plaintiff seriously injured in an accident suffered long bone fractures that required multiple surgeries. This plaintiff then makes a passing reference to memory problems during a meeting with her attorney and the plaintiff’s spouse. The GCS was 15, and the CT scans of the plaintiff’s head were largely normal. Based on what the attorney has heard about memory problems, however, the attorney should explore the issue further. A very similar occurrence happened in our practice when our client told us she and her husband were discussion her memory problems. She had forgotten whether she had taken a shower one day when in fact her hair was still wet from the shower she had just completed. After a neurological evaluation occurred a month or so later, our client had a diagnosis of anterograde amnesia, which is consistent with long-term complications from a mild TBI.
This type of neurological shortcoming is also discussed by Kara L. Swanson, a TBI sufferer, as told by her in the first person in her outstanding book, I’ll Carry the Fork! Recovering a Life After Brain Injury. Ms. Swanson relayed in her book that she was regularly forgetting whether she had used shampoo or conditioner while she was still in the shower. Although her TBI had previously been diagnosed and treated, much of her recovery and adjustment to her new life turned on small frustrations such as forgetting very recent actions. To address the particular issue with sequencing her shower activities, Ms. Swanson began taking the caps off all the bottles she used in the shower before beginning her shower. She would then replace the cap immediately after using a bottle, thereby showing herself whether the bottle had been used when she forgot a few minutes later where she was in her hygiene routine. We will discuss during our presentation many more aspects of Ms. Swanson’s book, which is the closest thing to a must-read there is for any attorney representing a TBI patient.
The only way to simplify the concept of long-term prognoses for TBI patients is to state the obvious. The more severe the TBI, the longer the recovery period will be. The longer the recovery period, the more likely it is that long-term effects of the TBI will persist. The brain works very hard to (a) begin functioning properly when swelling caused by a TBI is resolved, or (b) to compensate for areas that are permanently damaged. Even with such an elegant system of protections in place for recovery and compensation, any TBI at any level on the spectrum of severity may have permanent consequences.
Deposing the Treating Physician
From the perspective of a plaintiffs’ lawyer, unless the physician absolutely refuses to participate in any pre-deposition meetings, we never depose a physician who treated our TBI client without first meeting with the physician. Whether getting a meeting requires persistence, begging, or exorbitant payment akin to highway robbery, understanding the physician’s perspective of and opinions regarding a client’s TBI is critical to preparing for that physician’s deposition.
Obviously, most physicians who treat TBI patients will be specialists, at least those physicians involved in the care of the TBI. More serious TBI patients are routinely seen initially by trauma physicians who live and work in a world of controlled chaos. After the triage process, a neurosurgeon and/or neurologist will likely become involved in the TBI patient’s care. Often, the trauma physician, or a member of the trauma team, will be the admitting physician charged with overseeing the patient’s care and managing matters such as ventilator settings when required, arranging consultations, and monitoring recovery and course of treatment.
These specialties are demanding, both physically and mentally. Rarely do we encounter a trauma physician, a neurosurgeon, or a neurologist who considers meeting with an attorney anything other than a bothersome and perhaps unnecessary intrusion into the world of medicine and their busy schedules. One would think that, with the hourly rates these physicians customarily charge for these meetings, we would be greeted with a smile and a cup of coffee. That never happens. As a case in point, the most recent neurosurgeon with whom we met began the meeting with the kind introduction of “so, what do you want?”
To navigate these sometimes uncomfortable scenarios, we have found that the best approach is to be completely prepared and go directly to the point. When a physician realizes that the lawyer is also working very hard for the patient, the lawyer understands the basics of the injury, the lawyer has prepared for the meeting with a thorough review of the medical records so that the physician’s time is not wasted, and the lawyer is not trying to second guess the physician, the meetings often turn quickly toward a more positive tone. In other words, an attorney who knows the answer to the question of “what do you want” will be in a much better position to have a meaningful meeting with the physician.
One of the key physicians who will be deposed in a TBI case is the rehabilitation physician. In cases where the TBI is moderate or severe, the obvious physiological shortcomings for which the plaintiff is in rehabilitation will be relatively clear. The mild TBI case presents a somewhat greater challenge for an attorney to present convincingly through physician testimony, however.
The American Congress of Rehabilitation Medicine has adopted a definition of mild TBI that attorneys should discuss with treating physicians and then discuss with the physicians during their depositions. A patient with mild traumatic brain injury is a person who has had a traumatically induced physiological disruption of brain function, as manifested by at least one of the following:
- Any period of loss of consciousness;
- any loss of memory for events immediately before or after the accident;
- any alteration in mental state at the time of the accident; and
- focal neurological deficits(s) that may or may not be transient;
but where the severity of the injury does not exceed the following:
- loss of consciousness of approximately 30 minutes or less;
- after 30 minutes, an initial Glasgow Coma Scale (GCS) of 13-15; and
- posttraumatic amnesia (PTA) not greater than 24 hours.
(Journal of Head Trauma Rehabilitation 86 (1993)).
This definition is helpful in establishing through rehabilitation physician testimony that patients with symptoms a juror may think are simply a normal part of trauma in fact meet an accepted definition of TBI. We have found that most trauma physicians, neurosurgeons, and neurologists in this area prefer to rely when possible, however, on the GCS and the associated definitions for mild, moderate, and severe TBI discussed above.
At the conclusion of the physician meeting, which in most cases will be the attorney’s only opportunity to speak with the treating physician face to face prior to the physician’s deposition, the attorney should have a firm grasp on a number of basic matters, such as (a) the patient’s initial presentation to the physician, including clinical signs and symptoms, how the physician became involved (e.g., front-line health care provider such as a trauma physician or by consultation ordered by the admitting physician), and the results of any prior objective tests, (b) the evaluation undertaken by the physician, including any diagnoses other than TBI that may have been on the differential diagnosis, (c) the approach the physician undertook either to determine the presence of TBI, to rule out other possible diagnoses on the differential, or both, (d) diagnoses at which the physician ultimately arrived, (e) treatment that was undertaken, and (f) long-term prognoses. Fully armed with this information, the attorney can structure the physician’s deposition for as seamless a presentation to the jury as possible.
Several different approaches and styles certainly work when deposing a treating physician, but in a TBI case, we have found that structuring the deposition in a certain order is helpful for the jury. Primarily, we like the physician to provide a good overview of our client’s TBI to the jury within the first 15-20 minutes of the physician’s deposition. We generally then spend approximately 30 minutes delving into the details, which we hopefully confirmed during the physician meeting.
TBIs are complex. Much of the focus in a physician’s deposition needs to be on ensuring that the physician conveys necessary information to the jury in an easily understandable fashion. For some physicians, this comes easily. For others, the attorney will have to follow up many answers with several more questions to define terms. The attorney should then ask a summarizing question in such a way so as to get the physician essentially to repeat the complicated answer while using terms easily understood by a jury. Underlying all of this is the need to ensure that causation is established and the medical necessity of the treatment is easily understood by a jury.
To accomplish the goals of keeping the jury’s attention while also getting out all of the testimony we need, we spend no more than a few minutes discussing the physician’s qualifications and explaining to the jury the scope of the physician’s specialty. In most cases, we then have the physician explain our client’s condition when the physician first saw him or her. Unless the physician’s scope of treatment was very narrow, we have the physician walk the jury through the entire course of treatment with a broad perspective. At the end of this part of the deposition, our goal is for the jury to understand that (a) the physician is a specialist who treats specific types of patients, (b) our client was one of those patients, and (c) our client underwent a critical course of treatment for serious injuries. The jury can then more easily follow the more complicated portion of the deposition, in which we have the physician elaborate on the portions of the assessment, treatment, diagnoses, and prognoses that we want highlighted for the jury.
In cases involving TBIs that are largely acknowledged by all parties to litigation, we have found one of the most effective lines of defense questioning is for the defense attorney to focus on the patient’s long-term prognoses. Most physicians will agree that considerable progress can be made by TBI victims over months and years. These physicians will further agree that the plaintiff may continue to make good and measurable progress long after the date of the physician’s deposition.
In response, the plaintiff’s attorney needs at his or her disposal the statistics and generally accepted facts regarding the recovery process for TBI patients. Most improvement is made in the first 6 months, as discussed above. After one year, improvement for most TBI patients will be nominal. Testifying physicians who treat TBI patients will be familiar with this information, a fact that should be confirmed during the physician meeting and before the deposition. By having this information readily available, the plaintiff’s attorney can neutralize some of the gains made by a defense lawyer on the issue of long-term prognoses and possible improvement.
In essence, the meaningful difference between deposing a physician who treated a TBI patient and a typical physician deposition in a trauma case not involving a TBI is the complexity of the information to be presented. Jurors can understand surgeries to repair fractures much more readily than anterograde amnesia resulting from a TBI. Phrases such as coup, contrecoup, and spasticity may be used conversationally by a neurosurgeon or neurologist, but they must be defined and explained for a juror much more thoroughly than the phrase compound fracture, for example. By becoming fully versed in the nuances of the particular TBI at issue, conducting a productive meeting with the physician prior to the deposition, and ordering the questions in a manner so as to facilitate a seamless and understandable presentation for the jury, attorneys for both the plaintiff and the defendant can convey to the jury every point they have determined is important in a clear and concise manner.
The Plaintiff’s Deposition
As most of us have heard stated at some point, most personal injury cases begin and end with the plaintiff. A jury will have an easier time believing the sometimes unusual symptoms a plaintiff with excellent credibility may have experienced after a TBI. A plaintiff with lower credibility may of course be seen by the same jury as a malingerer, even if that plaintiff’s symptoms are equally legitimate, an issue discussed below.
Because the focus of this presentation is TBIs, we have foregone a discussion of generally preparing a plaintiff for deposition or taking the plaintiff’s deposition in a PI case. We have instead focused on the area of general damages unique to TBIs and questions regarding mechanism of injury that any plaintiff who recalls the injury should be asked.
One of the first issues we sometimes have to address when preparing a TBI plaintiff for deposition is that the plaintiff is not always aware of all of his or her symptoms, particularly when the TBI is mild or on the low end of moderate. Confusion, memory lapses, mood swings, and personality changes are not always as apparent to the sufferer as those around the sufferer. Preparing a plaintiff to discuss his or her damages when the plaintiff is not necessarily aware of all of the damages can be a challenge.
We address this contingency at our first client meeting. At that meeting, we ask the spouse or other appropriate family member to begin preparing a journal for our purposes to use as the plaintiff’s attorney. Because we have our eye toward the spouse or family member ultimately being able to offer supporting testimony on damages, however, we give the necessary advice to ensure that the journal would be a useful tool for a jury if we elect to publish it to opposing counsel. We hope the journal will contain incidents of TBI symptoms as they manifest in daily life, be they slight or severe. This ongoing journal not only helps the plaintiff become and remain aware of his or her issues, it also presents the plaintiff’s attorney with the opportunity at the appropriate time to remove the cloak of protection afforded by the work product doctrine so that the journal can be used either to buttress the plaintiff’s testimony or to fill in any gaps.
Both when preparing the TBI plaintiff for deposition and when deposing the plaintiff, attorneys for either party should fully explore certain issues of long-term symptoms that may not necessarily be included in the medical records, including:
- Memory impairment, such as trouble finding the correct word to speak, walking out the door to run an errand and then forgetting the destination, etc.; and
- Impairment of executive functions, such as planning, priority setting, problem solving, etc. According to Schapiro & Saachetti, “Neuropsychological Sequelae of Minor Head Trauma”, in Minor Head Trauma 88, “[s]ubtle deficits involving initiation and planning often become manifested in problems with organization. Executives and others involved in administrative duties may appear less organized. . . . Difficulties with initiation and planning typically have been associated with frontal lobe dysfunction.”
Rehabilitation physicians will focus on physiological rehabilitation. A neuropsychologist is best equipped to discuss the long-term outlook for these types of symptoms, but the plaintiff needs to be able to discuss the symptoms when possible. A plaintiff’s attorney certainly does not want a client to omit these symptoms inadvertently, and a defense attorney does not want to hear them for the first time at trial because he or she neglected to ask a specific question.
Other areas of long-term damages inquiry for which the plaintiff should be prepared, and about which the plaintiff should be asked during deposition, include the following:
- Divided Attention and Problems with Multi-Tasking (e.g., preparing a meal while helping children with homework);
- Sensitivity to Light;
- Sensitivity to Noise;
- Cognitive Fatigue, which will be more notable at the end of the day;
- Balance Impairment;
- Inadequate Impulse Control; and
- Tinnitus (ringing in the ears).
An effective defense attorney will fish the entire pond of relevant inquiry during a TBI plaintiff’s deposition looking for an opportunity that will benefit his or her client’s position. An effective plaintiff’s attorney will have already determined beginning with the first meeting with the potential client what the answers are to these areas of inquiry and will factor that information into the determination of whether to accept representation.
As discussed above, certain TBIs are generally associated with specific mechanisms of injury. Therefore, the plaintiff should be asked (and should be prepared to discuss) the mechanism of injury to the extent possible. Several basic questions to ask include the following:
- Did the plaintiff strike his or her head on an object? If so, what was it and where was the point of contact? While TBIs can certainly occur in the absence of a blow to the head, the question still must be asked as it is relevant to the type of TBI claimed;
- When a plaintiff cannot recall the answer, both the plaintiff’s attorney during deposition preparation (actually during the initial client interview) and the defense attorney should comprehensively review the records for any indication of direct head trauma, such as bruising, redness, etc.; and
- What was the direction of impact? This will determine the likely area of both the coup and any contrecoup injury.
In cases where the attorney for either party suspects that the claimed TBI is inconsistent with the forces applied, factors such as the weight and speed of the vehicles involved in an MVA should be established. The plaintiff may, of course, be able to offer insight into his or her speed at the time of impact. For a workplace fall, in contrast, the precise location from which the plaintiff fell, the motion of the plaintiff’s body during the fall, and the material that struck plaintiff’s head should be determined to the extent possible. This will be very useful information for any biomechanical expert that may become involved.
Finally, the TBI plaintiff must be deposed when appropriate on the issue of malingering. This is particularly true when the injury is a mild TBI. Malingering is an accepted psychiatric diagnosis and is defined by the American Psychiatric Association as the “intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives such as avoiding military duty, avoiding work, [or] obtaining financial compensation . . . “.
Malingering can particularly be an issue, legitimate or otherwise, in a mild TBI case because there will often be a discrepancy between the TBI patient’s claimed symptoms and the objective findings. The problem for the plaintiff’s attorney, and the opportunity for the defense counsel, is that jurors often hesitate to acknowledge a significant injury in the absence of objective physical manifestations such as broken bones and deep cuts. Because TBIs can be subtle, it is very important that the plaintiff’s attorney carefully screen TBI cases to ensure that any allegation of malingering can be effectively refuted. It is equally important that the defense attorney know as much as possible about the mechanism and nature of the injury and the claimed long-term damages.
TBI cases cannot effectively be prosecuted or defended if they are approached as a traditional PI case. TBI case preparation and defense take an inordinate amount of time, energy, and expense. Even an experienced personal injury attorney will be thrust into a world where the language is unique to the injury, the objective tests often present false negatives, long-term damages are at best only partially understood, and key components of the case that are usually established by the injured person may present a challenge because the injured person quite literally cannot recall any of the key components.
Thorough study, preparation, and consultation is critical to effective advocacy in the field of TBIs. Whether representing the plaintiff or defendant, attorneys should strive to learn the vernacular and become familiar with the nuances of TBIs before delving into this complex, expensive, and often frustrating field of litigation.