What Is A Brain Injury?
Effects On The Brain:
Common Symptoms of Brain Injury:
Proving a Brain Injury Occurred:
Epidemiology of Brain Injury:
Toxic Exposure:
Cognitive Disorders:
Perceptual Disorders:
Pain Disorder:
Depression:
Sleep Disorder:
Dreaming Disorder:
Headache:
Obesity:
Dizziness:
Imbalance:
Neuroendocrine Disturbances:
Epilepsy:
Behavioral Disorders:
Driving:
Recovery:
Psychological Considerations:
Substance Abuse:
Nutritional Support:
Effects on the Family:
Effects on Social Relationships:
Prevention of  Brain Injury:

WHAT IS A BRAIN INJURY?

The adult human brain weighs about 3 pounds, and has no pain fibers.  Neuropathologists have described its texture as being somewhat like jello. Most of its solids are composed of fats (especially the oily fats like Omega 3 which remain soft and flexible at body temperature). It contains 100 billion nerve cells or neurons plus another 200 billion support cells called glia (latin for glue). The brain is wrapped in 3 membranes (called meninges). Closest to the brain is the pia mater, then comes the arachnoid and farthest away is the dura. The dura is leathery in texture and firmly attached to the skull at a number of points. The meninges have pain fibers that can cause excruciating headache with such conditions as migraine and meningitis. Between the brain and the skull is a thin layer of cushioning liquid called CSF (cerebrospinal fluid) that is produced in the ventricles of the brain, circulates through and around the brain's membranes and is resorbed. CSF is a nutrient fluid for the brain. When CSF is blocked, the skull swells visibly causing hydrocephalus (water on the brain). The brain also contains its own blood supply with arteries (such as the carotid, vertebral and middle cerebral), veins (such as the jugular) and an incredibly fine mesh of arterioles and capillaries known as the "blood-brain barrier" because it screens out large, toxic molecules.

Trauma to the head sets the brain in motion inside the skull. Depending upon the degree and direction of the forces applied, the brain can be damaged in many different ways. These include surface contusions from coup-contre coup (an initial blow followed by a rebound against the opposite side of the skull), twisting from rotational force with stretch damage to fine structures like axons and capillaries and cavitation (sudden pressure differentials from rapid displacement of CSF with air bubble formation). The primary "mechanical" injury to brain structure is often followed by secondary damage arising from the brain's own chemical/metabolic response to injury. Secondary damage may come from excitatory release of toxins, reduction in cerebral blood flow (ischemia), reduction in glucose metabolism (hypoglycemia), apoptosis (programmed cell death), swelling and scar tissue formation. Depending upon the type of secondary damage, cells distant from the site of the trauma may die over a period of days, weeks, months or years, and this can be tracked with appropriate functional neuroimaging.
 

The specialized cells called neurons that do the processing work of the brain (such as thinking) are most highly concentrated in the outer layer or cortex (known as the gray matter). They also exist in isolated, dense clusters lying in the white matter such as the basal ganglia. The axonal projections from the neurons (long, hollow tubular structures) form the wiring or neural circuitry that links neuronal processing centers. These axonal "wires" called the white matter carry neural messages at incredible speeds of 1/10,000th of a second, because they are coated with a fatty substance called myelin that functions like insulation material. The neural message starts as an "action potential," a release of a miniscule electric charge down the axon that triggers the opening of pre-synaptic vessicles at the tip of the axon, causing chemical substances called "neurotransmitters" to flow across the gap between axon and dendrite and bind with matched receptor sites on nearby dendrites. For each axon there are typically anywhere from 100 to 10,000 dendrites arrayed to receive chemical messages . The precise alignment of these axon to dendrite connections or "synapses" is the product of genetic and environmental influences and incorporates what we have learned (both consciously and unconsciously) and what our central nervous system remembers.

The human brain is vulnerable to trauma both mechancially and chemically. Alteration of brain chemistry is most important, because that is what produces changes in how and what we perceive, remember, think, feel and do. Brain chemistry may be radically altered by microscopic damage to the brain that is not detectible structurally by MRI or CT. This is a huge problem both clinically and forensically, because physicians and lawyers who do not understand this, will likely judge victims of "mild" traumatic brain injury with negative results on MRI and CT as faking, exaggerating or over-reacting to a blow to the head. We can detect disturbances of normal brain chemistry today with functional imaging techniques including PET scans, fMRI and MRI spectroscopy. These show major disturbances of brain metabolism not just in mild tbi patients but in other patients whose brains look structurally normal on CT/MRI such as drug users and schizophrenics. Unfortunately these scans are expensive and hard to come by, partly due to health insurance restrictions and partly due to the scarcity of the scanning machines.

High speed impact to the skull is associated with a high degree of physical compression and torsion of brain tissue and physical battering of the brain against the skull wall, which results in grossly visible changes of brain structure. These include bleeding contusions to the brain surface, deep hemorrhagic lesions, epidural or subdural hematomas with compression of brain tissue and displacement or shift of brain structures over the mid-line with effacement of ventricular space. These changes to normal brain architecture are visible on CT or MRI. Lower speed impacts produce much more subtle damage. There may be no bleeding at all, or only micro-vascular bleeding too small to show up on CT scan. There may be perturbation of neuronal cell walls or stretch/twist damage to axons with disruption of normal exchange of nutrients, ions and neuro-transmitters. Sometimes there is only displacement of axon-dendrite connections or synapses. The fantastic complexity of the brain results in part from miniaturization. Each cubic millimeter of the human brain contains about two miles of neuroal wiring. Neither CT nor MRI can visualize what is going on in a space so small, so microscopic damage from "mild" tbi escapes them. We know its there from direct examination of superthing slices of brain tissue on autopsy of "mild" tbi patients who died from other causes.

So-called "mild" tbi, which makes up 80% of all cases of tbi, virtually never produces a visible lesion on CT or MRI. This is because the tissue damage occurs on the cellular level visible only under the microscope and is widely diffused, leaving blood vessels and major structures intact. In the clinical setting, the CT and MRI are still dominant, and the failure of mild tbi to appear on either, makes it a very underdiagnosed and undertreated malady. Quite a few victims of "mild" tbi lose their sense of smell (a condition called anosmia) because their olfactory nerve (Cranial Nerve I) is literally chewed up by being rubbed between the base of the frontal lobes and the rough bony shelf beneath it called the "cribiform plate." Yet this does not show up on conventional neuro-imaging. We know this happens, because of autopsy findings on such patients when they die of unrelated causes.

Depending on where the blow comes from the brain can be damaged on top, from the front, from the back, from below, from either side, or from a combination. Many brain injuries affect the frontal lobes. The frontal lobes which occupy 1/3rd the volume of the adult human brain, lie behind the forehead and the eyes. They are the control center for our "executive functions." When we are confronted with a stimulus (be it a driver running a stop sign, a job interview, an IRS audit or a first date) we use our frontal lobe circuits to evaluate the situation; consider our options in the context of social propriety, our immediate goals and desires, and the likely long term consequences; plan a response; issue commands to our muscles of speech and movement; monitor the result; and keep going or change our course of action depending on the feedback. Brain injury often affects the frontal lobes, because car accidents and falls tend to involve contact between the forehead and a hard surface, and the inner surface of the skull next to the frontal lobes contains a series of sharp, knife-like ridges. Frontal lobe injury not only interferes with planning, sequencing, execution and monitoring of everyday tasks, but tends to reduce motivation and interest in novelty, causing apathy. People with frontal lobe injury may know what to do, but cannot get it done due to a disconnect between acquired knowledge and skills, on the one side, and the capacity for action on the other. Action requires attention, memory and motivation.

From the outside the brain looks like a walnut, because the outer surface (known as the cortex or "gray matter") is highly wrinkled or convulated. It is densely packed with 6 identifiable layers of nerve cell "bodies" in a space just 1/8th of an inch thick.  The prune-like wrinkling of the cortex into gyri (ridges) and sulci (valleys) potentiates maximum brain surface area in the minimum space. The human cranium cannot expand, because any further size increase would make the infant's head too large to pass through the mother's pelvic outlet during the birth process. Inside the gray matter (cortex) is the white matter (parenchyma) which consists mainly of axons, the myelinated "wires" which enable brain cells in the cortex to transmit and receive messages from other brain cells. Within the white matter there are ventricles (which produce and circulate the cerebrospinal fluid) and various island-like clusters of cell bodies called nuclei, such as the basal ganglia which control automatic or subconscious movement. The brain is divided into a left (language dominant) hemisphere associated with math, science and logic; and a right (visuo-spatial) hemisphere associated with affect (emotional display), art, intuition, spirituality,   and religion. The two hemispheres are known collectively as the cerebrum. They are physically separated in front by the falx cerebri, but are connected and integrated deep within the brain by a fiber bridge called the corpus callosum which takes until age 3 to mature.

The exterior of the brain is vulnerable to focal contusions (bruises) from shaking or striking of the head, which bounces the brain against the inner walls of the hard skull. If the contact of brain against skull is hard enough the brain may swell up until it is crushed against the confines of the cranium, which will compress cerebral arteries and cause oxygen deprivation injury (anoxia) similar to stroke, unless the swelling is rapidly reversed by administration of mannitol or surgery. The interior of the brain is vulnerable to damage from stretching and tearing of axons, known as diffuse shear. Places in the brain where such shearing is particularly likely to occur when the head is forcibly rotated include the gray matter-white matter boundary and the corpus callosum. Severance of the corpus callosum creates "split brain" patients who may do opposite actions with their   hands (e.g. petting a cat with the right hand, and shooing it away with the left). When the twisting or torqueing of the brain causes rupture of blood vessels, an epidural, subdural or subarachnoid hemmorhage will result, depending upon where the vessels break. These bleeds may occur slowly or quickly, and may cause small, medium or large collections of blood, with characteristic shapes, depending on the specifics of the trauma. CT scan is excellent for detecting a bleed. A large bleed will lead to obvious disturbances of consciousness such as blank stare, slurred speech, dilated pupils, lethargy, etc., and will require a craniotomy to remove the clot or suction the liquid blood. Diffuse shear tends never to show up on CT scan, and only rarely on MRI. Diffuse shear is associated with "disconnection syndrome." This means brain circuits are compromised so that intact brain structures cease to do their jobs because they cannot communicate with each other and integrate their information into a coherent perception, action plan or command. Thus the functional consequences of a small lesion will go well beyond the size of the lesion if critical wiring pathways have been disrupted. 

The inner and outer portions of the brain have different densities. Trauma which rapidly jerks the head around and   which exerts rotational force on the brain, makes the inner and outer portions move at different velocities, and this can damage axons at the gray-white matter interface by mechanical stretch. Direct, blunt trauma (such as the head hitting a sidewalk or the B pillor inside a car) causes an initial contusion to the outside of the brain closer to the blow - the coup - followed by linear  acceleration of the brain into the opposite skull wall, where another contusion results called the contre coup. The same traumatic event (such as a car crash) can cause one or both types of damage. If the blow to the head is hard enough, the skull will cave inward and break into fragments which dig into the brain and cause bleeding. This is known as a depressed skull fracture, and is associated with an elevated risk of epilepsy. High speed car crashes (those at 60-80 mph) and other highly forcible impacts to the head, can send shock waves through the brain and so deform its inner structures, as to cause death, permanent vegetative state, hydrocephalus (ventricular blockage) or severe dementia. The smallest functional unit of the brain is the individual nerve cell or "neuron." Infants are born with over one hundred billion neurons. Neurons need a constant supply of oxygen and glucose to survive and remain vulnerable throughout the human lifespan to damage or death by traumatic events which cut off the supply of oxygen or glucose. These can range from cranio-cerebral traumas such as a mechanical blow to the head, heart attacks, near drownings,  toxic exposures, etc.

Most TBIs are "closed head," meaning the skull has not been openly penetrated by a knife, bullet or other object or been fractured into the brain tissue by collision with a hard, unyielding object. Brain injuries caused by a "missile" (such as a nail or metal fragment) tend to be focal and their damage confined narrowly to one or more specific functions, frequently detectable as "focal deficits" on a standard neurologic exam. Closed head brain injuries tend more towards being "diffuse" and involving more generalized or "global" disruption of brain function. Global disruption is rarely evident in a standard neurologic exam of mental status, motor control, reflexes and sensation, and more likely to be detected by neuropsychological evaluation of cognitive functioning. In its most severe form diffuse injury is obvious on MRI and fatal. In its milder and more common form diffuse injury is barely detectable or not detectable on MRI and its manifestations can be confused with depression, chronic fatigue, attention deficit disorder, somatiform disorder, hysteria or malingering. What is often called "mild traumatic brain injury," is in actuality a significant injury to the brain which has not been accompanied by obvious structural damage to anatomical landmarks.

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EFFECTS ON THE BRAIN:

The brain is "the fragile dwelling place of the soul." When the brain becomes injured by trauma, we expect to see, and do see, changes in how the person perceives, remembers, thinks, feels and relates to others. Injury to the brain changes the functioning of the individual and his identity. This should not be surprising, since the brain is so highly vulnerable to injury from trauma. It is a three pound mass of jelly-like consistency made up of one hundred  billion neurons and their interconnections. It is 90% water, and cannot be expected to retain its integrity in response to traumatic events such as car crashes, falls or criminal assaults in which the head is battered.

How rapidly and how completely a person recovers from brain injury, depends on a variety of factors including severity of initial injury, age, pre-morbid education, personality and temperament, presence or absence of complications such as chronic pain and/or post traumatic stress disorder, quality of treatment, quality of social support network, and many others. Every person has a different brain, so it is not surprising that 100 people will respond in 100 different ways to a head trauma of similar force, direction and impact point on their skulls. Our brains vary anatomically on account of genetics, age and gender. The unique developmental, educational, psychological, nutritional, toxic exposure and trauma history of each persons' brain affects how his brain is wired and how well or poorly it can adapt to a particular traumatic event. Over the past few years, Dr. Paul Thompson, a neurologist at the UCLA Lab of Neuroimaging, has been creating a whole brain 3D atlas of the brains of 1000s of "normal" individuals and inviduals with ALzheimer's Disease to help us better visualize the subtle differences. A by-product of this research is visual confirmation that every person's brain has a unique pattern of functional organization. This correlates with neurosurgery on epileptic and cancer patients in which mapping of the brain functions in an awake patient with an electric disrupter tool, shows the same unique layout of functions. In concrete terms, this means if you strike 100 people with a blunt instrument above and slightly behind the left ear with the same tool at the same level of force, you will be damaging different  brain circuits and disrupting different brain functions in each person, and each will respond differently. This is important, because in litigation the defense medical expert will often distort the truth by saying "most people struck in that part of the head show a different outcome than the plaintiff; therefore the plaintiff is faking his symptoms or they are the result of psychological stress not organic brain damage."

The brain circuits which get disrupted by trauma are composed of inter-connected neurons or brain cells. Neurons are nerve cells constructed to do the specialized work of the central nervous system. They consist of a cell body with a nucleus and cellular processes for the reception and transmission of nerve signals through chemical sustances called "neurotransmitters". Each neuron has a large collection of fernlike dendrites for message reception and one large tubular axon for signalling other neurons. Each dendrite has spines with pores called receptor sites. Molecules of neurotransmitter are released from pre-synaptic vessicles at the tip of the axon and flow across the gap between nerve cells (the synapse) where they "bind" with receptors on nearby dendrites. This signals the receiving cell to open up its pores and allow ion exchange with the extra-cellular environment. When this process works as designed, the influx of ions triggers a "depolarization" of the receiving nerve cell, which sends a mild electric current (or "action potential") pulsing down its axon, and triggering axonal release of more neurotransmitter. The human brain sends messages at 1/10,000th of a second largely because its axons are coated with a natural insulation material known as myelin.

Trauma disrupts the normal process of communication between neve cells by mechanical shaking and perturbation of cell membranes, mechanical striping away of myelin from axons, stetching of axons which triggers obstructive swellings to form in the axon and by triggering massive dumping of 1000s of time the normal quantities of neurotransmitters like glutamate. All these processes are destructive. Excess release of glutamate can cause nerve cells to literally explode. This happens when glutamate jams open nearby receptor sites and allows a toxic influx of calcium into nerve cells, shutting down their mitochondria, and depriving them of energy to work the sodium pumps to force sodium back out of the cell, resulting in extracellular water pouring in and bursting the cell like a balloon. 

When synapses are damaged and malfunction as a result of trauma, communication inside the brain is disturbed with evident consequences such as slowed thinking, forgeting of intentions or difficulty finding the right words to express oneself. Typically this occurs when external force on the head causes the brain to twist and bounce back and forth inside the hard, unyielding skull case. Although surface contusions to the gray matter may result, more often the damage is done by internal stretching and straining of the long axons, a form of microscopic damage not visible on MRI. Although a concussion causes an immediate episode of dazing or confusion (which may last just seconds or minutes), it generally takes 48 hours after the traumatic event for stetched axons to form obstructive swellings which block the flow of nutrients and gradually kill off the nerve cell or decrease its connections with other neurons that are no longer in physical communication.  A randomized kill off of   synaptic connections is much like a Florida hurricane ripping down phone lines in a helter-skelter manner. While the phone system as a whole is intact, some messages don't get through, others get delayed because of re-routing and others arrive in garbled fashion.

A person who suffers a concussion from closed head trauma will experience a momentary episode of dazing or confusion from twisting of the brain stem or an extra heavy discharge of neurotransmitters. This often clears by the time she is brought to the emegency room. Diffuse strain injury to axons produces no visible bleeding so the CT scan will be negative. Even if a CT scan could pick up microscopic damage to axons, it would not be visible in the ER right after the concussion, because the process of axonal destruction takes a good 48 hours to get going.   Thus an emergency room CT Scan will pick up bleeding in the brain from a depressed skull fracture, but cannot detect the damage done by mild brain injury because it has not happened yet. Due to poor training, many emergency room doctors equate a negative CT scan with complete absence of injury to the brain.

A great many victims of mild traumatic brain injury know intuitively that they are "different" following their accident, and that something is wrong with them, but never get properly diagnosed, treated, counseled, helped or rehabilitated. This happens so frequently because microscopic damage to axons is not detectible on standard neuroimaging techniques and does not produce any gross disturbances of reflexes (e.g. pupillary reflexes) that a neurologist would perceive as a significant abnormality of the central nerous system. Although PET scans can detect tiny disturbances of brain function, these tests are very expensive, and most insurers refuse to pay for them on the grounds of lack of "medical necessity." Fortunately many persons who suffer from the "milder" form of TBI (with no loss or only a minimal loss of consciousness and negative CT/MRI) eventually improve on their own, especially if they take time off work and get plenty of rest. For the ones who get better spontaneously, most show good improvement within three months post-accident and most, about 85%,  are symptom free within six to twelve months post -accident.

However, a minority of mild head injury, about 15%, show symptoms on a long term, even permanent basis. Typically, there is a mix of organic and psychological factors interacting to perpetuate their impairments on a chronic basis. It is now believed that at least some of these individuals have the APOE-e4 gene for Alzheimers Disease. It is also believed that other consequences of mild TBI may perpetuate symptoms, especially when untreated or undertreated. These include depression, anxiety disorder, panic disorder, post-traumatic stress disorder, substance abuse, pain disorder,  sleep disorder and   Rx medication side effects. Undoubtedly, the amount, the intensity and the complexity of life demands on the injured person play a role. Someone who was retired and sedentary before the brain injury will not experience the same level of complaints as someone who was a mother of 3 children or a full time breadwinner working as an accountant, software designer, attorney, engineer, physician, architect or equally challenging position. Persons of middle age ask a lot of themselves and become the most frustrated when they cannot function and meet their own demands. They also suffer from decreased neuronal reserve, i.e. they have fewer living brain cells than they did when they were children.
 

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COMMON SYMPTOMS OF BRAIN INJURY:

Severe and moderate traumatic brain injury, by definition, are immediately accompanied by a significant period of LOC (loss of consciousness) and PTA (post-traumatic amnesia). They do produce visible areas of damage on CT and MRI. Severe TBI (and to a lesser extent moderate TBI) may also be accompanied by temporary or permanent disorders of vision, speech, swallowing, movement and balance, which are so obvious as to be readily apparent to the untrained observor.  Mild brain injury is distinctly different. It frequently occurs with no detectible loss of consciousnes, and otherwise with just a brief period of LOC never exceeding 20 minutes. Mild TBI is marked at the accident scene by an episode of dazing or mental confusion with brief interruption of continuous memory, however slight. While severe and moderate TBI always result in admission to a hospital, at least half of all persons with mild TBI are not even brought to an emergency room. The National Institutes of Health concluded in a report published 9/8/99 in the New England Journal of Medicine that many cases of mild TBI go undiagnosed and untreated.

Mild brain injury and PCS (Post-concussion syndrome) share all of the following symptoms, which manifest themselves more or less completely and more or less intensely in different patients following closed head trauma: headache, floaters, hyper-sensitivity to light and/or noise, lightheadedness,   dizziness, blurry or dimmed vision, double vision, nausea, vomiting, poor short term memory, insomnia, fatigue, apathy, decreased libido, social withdrawal, irritability, sudden outbursts of anger and profanity, emotional liability, slowed thinking, having to re-read material over and over, inability to execute routine task sequences on automatic pilot, inability to learn new facts, disorganization, loss of ability to manage one’s paperwork and appointments, diminished attention span with easy distractibility and inability to maintain divided attention to two or more stimuli and a host of other symptoms. Are mild TBI and PCS the same thing? Some physicians say yes and others no. Because most if not all these symptoms are consistent with a variety of disorders, it is critical to go through differential diagnosis utilizing neuro-imaging; neuropsychological testing of post-morbid functioning;  careful estimation of pre-morbid functioning in the cognitive, emotional, behavioral, social and vocational areas; careful review of the type and amount of head trauma with attention to degree and duration of alteration of mental status; post-accident neuropsychological testing; and assessment of post-accident functioning from interviews with SOs (significant others, such as  the injured person’s spouse, parents, children, family doctor, employer and friends). If the review of these factors indicates the most likely explanation for the problems is mild TBI, then it is perfectly safe and correct for that patient to treat mild TBI and PCS as equivalent terms.

The brain is unimodal and heteromodal. Unimodal means it has columns or clusters of cells which perform a specific task in isolation from other areas, such as olfactory cells which only identify smells or cells in the primary visual cortex which only identify the edges, colors or textures of objects. This is also called parallel processing. Heteromodal means integrated activity of different brain areas, for example identifying a friend's face links simultaneous processing by the frontal lobes where the data is attended to and stored briefly while activating "face recognition" cells in the temporal lobe, the seat of that type of memory file; the parietal lobe (locating the face in a spatial context), the occipital lobe (processing the appearance of the face), limbic areas such as the amygdala which imbue recognition of the face with emotions, and so forth. If one type of circuit is damaged for integrated processing, then odd results occur, such as being able to see a face, but not recognize it and put a name on it, or being able to recognize who the face belongs to without being able to access any feelings about that person. Much of what we know about correlative neuro-anatomy comes from seeing what people can no longer do after a certain identified portion of their brain has been damaged. We also learn what the brain can still do without the missing part. This is where neuropsychological testing comes in. When a person complains of "poor memory" after a tbi, we cannot know which aspect of his memory is poor, and whether the poor quality relates to the tbi (rather than something else, say age), without testing. It is the testing which lets us know how poor the person's memory is vs. age matched controls without tbi, and which aspect of the memory is poor - verbal, visual, auditory, and whether the area of the brain displaying decreased function was likely exposed to the trauma. etc.

Researchers using PET and fMRI have begun to localize many brain functions to specific areas. When solving problems with a verbal strategy people tend to use Broca's area in the left postero-lateral frontal lobe, and when solving spatial problems with a visual strategy they tend to use the right superior parietal area, as was imaged with fMRI by a research team at Carnegie Mellon which just published its findings in the June 2000 issue of Cognitive Psychology. In the July 21, 200 issue of Science Dr. John Duncan and colleagues of the Medical Research Council in Cambridge, England, reported that the left dorso-lateral frontal lobe was activated by taking traditional IQ tests, and they dubbed that area the brain's "master problem solver" and the "seat of central intelligence for organizing and coordinating information from other parts of the brain." Whether this lofty claim is borne out, or not, it does point up that the brain has junction sites where different information streams come together. While massive trauma to both hemispheres of the brain is likely to cause a permanent vegetative state, most brain injuries cause partial damage, leaving some functions impaired and other spared. The functional outcome is not just a result of which areas were damaged, but how well the victim can compensate or make up for lost function by drawing upon spared areas of his brain and using them in adaptive ways. This is where neuropsychological assessment and tbi rehabilitation come together. The treatment team wants to know not only post-incident weaknesses in function, but pre-incident strengths and skills which can be called upon during recovery.

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PROVING A BRAIN INJURY OCCURRED

Most traumatic brain injuries are "mild," meaning they cause only a "mild" disturbance of consciousness when the injury is inflicted, which is manifested more by dazing, confusion or disorientation than by outright loss of consciousness. Neurologists, physiatrists and neuropsychologists  who treat patients with so called  "mild" brain injuries know that these people experience long term or even permanent ill effects, including insomnia, fatigue, dizziness, imbalance, irritability and decreases in the ability to concentrate, to remember new information, to organize complex information, to make decisions and alter decisions in a quick, adaptive manner to the rapidily changing circumstances at work or home. Yet, these "mild brain injuries" are frequently dismissed by primary care physicians, insurance adjusters and defense lawyers. Why? Because the people who have them are not in wheelchairs, because they look normal, dress normal, walk normal and talk normal, even if they can't remember what they did 5 minutes earlier. Still worse, their brain injuries do not show up on static neuroimaging such as CT and MRI. To make the invisible injury visible requires an experienced eye and a certain amount of ingenuity. 

Objectifying the "mild" brain injury, making it visible and proving it exists is the job of the neurolawyer. This job is comparatively easy when the injury involves blunt head trauma, coma and a positive CT scan which discloses a large intracranial hematoma. This job is much more challenging and difficult in cases of mild brain injury where the CT scans and MRIs come out completely negative and the client has sustained a transient alteration of consciousness at the accident scene but is coherent, oriented and alert when he gets to the emergency room. For this reason, neurolawyers utilize neuropsychological testing , SPECT scans and PET scans to bring out subtle abnormalities in brain function that are more characteristic of TBI than of pre-existing psychological problems, pre-existing learning disability, litigation stress or malingering. Neurolawyers also use non-medical evidence to contrast their client's quality of pre and post functioning, including records of school and job performance and testimony from family, friends, work colleagues, co-participants in sports and the client's priest, pastor, minister or rabbi.  In certain cases, sleep studies may even be used, to capture involuntary, night-time awakenings which the client does not remember, but which may be responsible for the tremendous fatigue he feels upon waking each day.

Some of the research which confirms organic brain damage from "minor" head injury without loss of consciousness is fascinating, but unlikely to be useful in Court, either because the research is too new and needs validation by other scientists or because it is so technical and so complex that jurors cannot relate to it. An ongoing research project at the UCLA Dept. of Radiology (reported in the May 2000 Journal of Neurotrauma) shows that victims of "mild" tbi have the very same abnormality of glucose metabolism (i.e. significant under-utilization of glucose) as patients in coma from severe tbi for a period of 6 months. MRI spectroscopy (which involves magnetizing protons in the solid parts of brain cells and then zapping them with a beam of electrons) has been used to show sub-cellular break down products associated with damged neuronal cell walls within days after "mild" tbi. Radioactive tracers have even been used to show how "mild" tbi caused mechanical damage to RNA in brain cells, which leads to cell death because the RNA can no longer instruct the DNA in the cell nucleus to make the proteins necessary for cell maintenance, such as rebuilding cell walls.

No matter how the neurolawyer proves his client's brain was injured by the trauma set in motion by the defendant's negligence, this is but part of his burden of proof. Proving how, and to what extent, the injury has adversely effected the client; whether the injury is temporary or permanent; what, if any, residual difficulties the client is likely to have 5, 10 or 15 years down the line and what type and amount of care are reasonably required to restore the client to pre-accident function are equally important. This is where experts come in from fields such as vocational economics, neurology, neuropsychiatry, neuropsychology, physiatry and tbi rehabilitation.

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EPIDEMIOLOGY:

Statistical data on the incidence of TBI has been collected by the 50 individual states, and by various agencies of the federal government, including the CDC (Centers for Disease Control). A new TBI occurs every 15 seconds in this country. The median rate of  annual TBIs across the country is 200 per every 100,000 persons, with individual variations by state and county. In the mid 1980s there were 2,000,000 new TBIs every year in the USA with 65,000 to 75,000 deaths and 500,000 hospitalizations. As of the late 1990s the national incidence rate dropped to 1.5 million new cases of TBI each year. These were associated with 50,000 deaths; 230,000 hospitalizations; 2,000 people in a permanent vegetative state; 5,000 people with seizure disorder; and 70,000 to 90,000 people living with significant long term or permanent disability. TBI is the leading killer and disabler of persons aged 1-44. The most hard hit group is males aged 15-24 (often from mixing alcohol with driving), followed by children (due to bicycle accidents and child abuse) and persons aged 75 plus (due to falls) . Males are twice as likely to sustain a TBI as females.  Half of all TBIs come from motor vehicle accidents, with the remainder due to firearms violence (20%), falls, bicycle accidents, contact sports injury and other assorted causes. Alcohol is associated with about half of all these incidents. Programs to curb drunk driving; programs to keep fatigued truck drivers off the highways; programs to increase helmet use by motorcycle riders and bicycle riders; programs to increase wearing of seatbelts in cars; developments of air bags; improved seat and headrest design; and longer "crumple zones" for head-on car collisions; have all contributed to a decrease in incidence of TBI.

In 1990 a neurologist named Goldstein published a now famous editorial in Annals of Neurology 27:327 calling Traumatic Brain Injury a "silent epidemic" due to a deafening lack of public attention and government funding of research and prevention efforts. Thanks to the concentrated efforts of the national brain injury association (www.bia.usa.org) and a host of individuals (including patient advocates, neurologists like James P. Kelly of Chicago, neurosurgeons like Randall Chestnut and others) we have come a long way. Two milestones were the enactment of the federal Traumatic Brain Injury Act in 1996, and the holding of the first ever National Insitututes of Health concensus conference on Rehabilitation of Persons with TBI in Bethesda, Maryland during  October 1998. As we move into a brand new century, we hope to sustain, and even increase, the momentum for new prevention efforts and increased spending on research, treatment, rehabilitation and cure. 

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TOXIC EXPOSURE:

The epidemiology of traumatic brain injury is fairly well known due to systematic data collection by state and county health departments and model TBI system centers; and due to data analysis by the federal Centers for Disease Control. This is not true of toxic exposure brain injuries. Public health officials remain under-informed about how these injuries occur, in what numbers, with what long term outcomes, and how to prevent them.
We are just beginning to recognize which workplace toxins cause
cognitive, memory, vision or balance problems; but for each one, the EPA and OSHA must wrestle with the quantity issue - what level of exposure is safe, and what level is unsafe. Perhaps the one exception is lead. It has been known for decades that lead exposure can cause irreversible brain damage, the most publicized example being children in "slum dwellings" who ate the paint chips peeling from the walls which contained lead and tasted sweet. Depending on how much they ate, these children had mild, moderate or severe cognitive impairments. In severe cases, the child would test out at the mentally retarded level. Lead was banned across the country as an ingredient in paint in 1978.

Yet the hazard remains in buildings built and painted before 1978, from water which flows through old lead pipes and sink faucets, the dust from deteriorated vinyl miniblinds and in soils near heavily traveled roads. One out of every 11 children in the U.S. has unsafe blood levels of lead. A good source of information about potential sources of lead poisoning and how to protect yourself and your children is the federal EPA. Landlords who do not give new tenants the EPA pamphlet on lead can be fined. If testing shows lead in the paint, the landlord must take reasonable measures to protect his tenants' children. Although scraping off all the old paint is typically not required, he could be required to cover the lead paint with wallpaper or new unleaded paint. The pamphlet can be ordered for free by calling the National Lead Information Clearinghouse at 800-424-4323. Today's renters should request landlords to perform lead tests. Concerned home buyers should pay for their own soil testing before they sign a contract to buy a house. If your faucets are lead, use a filter on them, and let the water run for a while to flush the pipe before letting anyone drink it. Parents of children at risk for lead exposure should have their childrens' blood tested. This is often covered by health insurance.

On 3/6/01 the strictest ever EPA lead regulations will go into effect. The final rules appear in the Jan. 5, 2001 Federal Register. One of them says that once an apartment or common area in an apartment is found to be a lead hazard, all other apartments or common areas are deemed to be a lead hazard without the need for specific proof. Another says that the presence of "any deteriorated lead-based paint" in dirt, soil or paint, constitutes a "hazard." The new regs will promote safety by imposing on affirmative obligation to assess and abate the lead hazard, and by defining the hazard in pro-consumer terms.

Brain injury from exposure to toxins other than lead has been documented in railway workers exposed to cleaning solvents. According to the Courier-Journal of Louisville, Kentucky, approximately 600 railway workers have been diagnosed with "toxic encephalopathy" from handling degreasing solvents such as trichloroethylene and perchloroethylene, resulting in many lawsuits. The suits claim workers were not given adequate respiratory protection or shop ventilation and were not warned they could develop decreased mental function. The Courrier-Journal reports that CSX has settled a significant number of claims, and claims are currently pending against Union Pacific, Norfolk Southern and Burlington Northern Sante Fe, as of June 2001.

COGNITIVE DISORDERS:

Following brain injury long term memories (e.g. of personal events like weddings and birthdays), knowledge of word meanings and general information (e.g. the names of U.S. Presidents) tend to be preserved, because it is "overlearned" material. Such material has been re-used so many times in the past, it has become stored in many different places and in many different ways in the brain's long term storage areas. What tends to most affected by brain injury is the capacity to attend to, recall and utilize newly presented or novel information. The cognitive processes most vulnerable to brain injury are alertness (readiness to receive new information), selectivity (the capacity to focus on the material at hand and ignore or shut out distractions), encoding (the retention of the new information) and speed (the rate of overall information processing). A group of Dutch scientists has established that people without a brain injury show electical brain activity in response to the expectation of learning something (an EEG pattern called the contingent negative varation, CNV, or "expectancy wave"), and that the CNV is decreased or absent in people with a TBI, suggestive of a "deficit in tonic alertness."

Persons with a TBI experience a "slowing of the central nervous system clock." They take longer to grasp new information, longer to retrieve it, longer to organize it and longer to apply it when forced to make choices or decisions. They have to work much harder to resist distraction and fatigue more easily. They are thown off by any increase in the number or intensity of distractions in their environment and by any increase in  the complexity or novelty of the information they are presented. They have difficulty making quick decisions and may become "flooded" (i.e. overwhelmed and confused) when forced to do so, especially when presented with a great many alternatives to choose from. A blow to the face which damages the frontal lobes is particularly like to cause these problems. Trauma to the frontal lobes which alters the function of the anterior cingulate gyrus has been shown by SPECT scans to make people freeze or develop a "mental block" to carrying out activity, according to Dr. Daniel Amen in Fairfield, California. When the injury is to the medial orbito-frontal cortex (the part of the brain which lies just over the olfactory nerve bundle, which processes our sense of smell), the person experiences difficulty separating out current, ongoing reality (what is happening here and now) from memories of past events which are irrelevant to the situation at hand. They fail to inhibit memory traces, which push their way into the person's consciousness at inappropriate times, making the person speak in non-sequitors, a process called "spontaneous confabulation." See, Journal of Neuroscience 8/1/00 20(15)5880-5884.

Another problem is loss of the analytic capacity to detect and correct errors, which requires the capacity to link errors to the defective actions which cause them and learn how to correct them. Neuroscientists have established that the anterior cingulate cortex in the medial frontal lobe and the lateral pre-frontal cortex work in tandem to monitor actions, detect errors and compensate for them. See, Gehring W. et al. "Pre-frontal cingulate interactions in action monitoring" Nature Neuroscience 5/2000 3(5): 516-520. Damage to either structure will impair those executive functions. Neurologist Antonio Damasio has demonstrated repeatedly that traumatic or stroke damage to a deeper brain structure (an almond shaped cluster of cells called the amygdala inside the dorso-medial temporal lobe) is associated with loss of "emotional intelligence." The amygdala appraises the emotional significance of actions and events in terms of helpful/harmful, threatening/non-threatening, useful/not useful, desirable/undesirable, etc. It is the emotional alarm in our head, which should ring when we are in danger, e.g. about to lose a lot of money at the gaming table or about to drive into a high crime area with no police. People with amygdalar damage make the same mistakes of judgment over and over, and fail to learn the error of their ways, because their emotional alarm fails to sound.

"Cognitive performance deficits" relate to how a person processes information, not how much he knows or how smart he is. A very smart, well read person with a TBI can test in the superior range on vocabulary but test in the impaired range on various tests of attention and short term memory. Slowing of the rate at which the brain   processes new information, or draws upon old information to solve new problems, is one of the most significant impairments of functioning caused by a TBI. This is more true today than ever before, because of the speed of information processing required of us in this age of Information Technology, marked by the Internet, Palm Pilots, Web TV, cell phones, 2 way audio-visual conferencing, PCs with pentium microprocessors, laptop computers, and other technological innovations which continuously accelerate the pace of information creation, information delivery and decisonmaking. Learning to manage your emotional response to reams of new information (taking a deep breathe, breaking it down into chunks and analyzing it step by step instead of hyperventilating and feeling doomed); role playing situations involving decisionmaking in a support group; using assistive technologies (e.g. tape recorder, notebook, day planner); and gradually boosting cognitive processing speed with computer-based cognitive therapy programs;  will surely help.

Not all "thinking" problems are caused directly by damage to the parts of the brain which analyze information. Some cognitive losses stem from insomnia. Others are attributable to traumatic impairment of vision, hearing or short term memory. Some result from temporary incapacitation by headache pain. Identifying these problems and working to fix them (through new glasses, vision therapy, a hearing aid, auditory therapy, etc.), would help increase your cognitive processing speed.  

A great deal of medical literature on "outcomes" from tbi stresses psychological and behavioral problems as the ones which last longest, and are most predictive of inability to return to work (e.g. being easily frustrated, rritable and socially inappropriate).  This is not always the case. I have represented clients with positive outlooks and good emotional self-control, who could not successfully return to their jobs on account of persistent cognitive limitations from their tbi, such as poor auditory retention or inability to multi-task. One recent study found that cognitive impairments were more likely than any other problems to keep mild tbi patients from successfully resuming work. See, Journal of Head Trauma Rehab 15(5): 1103-1112 Oct. 2000.

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PERCEPTUAL DISORDERS:
 

Cognition, the process of abstract thinking, requires acquisition of accurate data about persons and objects in the environment through perception and the capacity to encode and retrieve memories of prior perceptions and thoughts. Perceptual recognition and identification of persons and objects rests upon the 5 senses (sight, hearing, smell, taste and touch). Vision, hearing, smell and taste arise from brain processing of information fed by the cranial nerves of the head which are wired directly to the brain. Touch is mediated by the peripheral nerves and spinal cord. A tbi can disrupt one, some or all of the 5 senses.

Anosmia, the inability to smell, frequently accompanies frontal lobe injury, because the olfactory nerve bulbs which transmit smell data from the nose to the brain run directly under the medial frontal lobes. When the frontal lobes are subjected to traumatic forces which jerk them back and forth across a bony segment of skull called the cribiform plate, the olfactory bulbs get crushed or shredded. Anosmia produces inability to taste food, since taste is not merely a function of taste buds on the tongue but is largely a function of smells associated with foods. Studies of the brain show our sense of smell is structurally and functionally integrated with emotion and memory. Smells can trigger profound feelings and rekindle old memories in an instant, whether they be the smells of sex, of a morning walk in a pine forest or the smells of an old leather baseball glove. This is because the olfactory bulbs are wired to the piriform lobe of the cortex in the antero-medial temporal lobe, where axonal projections synapse with the amygdala (the part of the brain which appraises the emotional tone of situations) and entorhinal portion of the hippocampus (which plays the major role in preparation of episodic memories for long term storage, and retrieval of such memories from long term storage). The piriform lobe does not replicate individual smells in a point by point grid (as the visual cortex does for images), but "associates" with other parts of the brain to create a gestalt perception. J. Neuroscience 20(18): 6974-6982. Hence, destruction of the olfactory bulbs (with loss of input to the piriform) robs the victim, not just of the ability to identify select smells, but to remember and enjoy past experiences hooked up in time and space with those smells.

Blurry vision often follows trauma to the occipital lobes where the primary visual cortex fuses the separate visual streams transmitted through the optic nerves from the retinas of the left and right eyes. Problems with touch (such as numbness or hypersensitivity) accompany damage to the somato-sensory strip in the parietal lobes. Astereognosia, the inability to explore and discern the tactile properties of objects through exploration with the thumb and forefinger, follows damage to the superior parietal lobe. Problems with hearing accompany damage to the temporal lobe (where sounds are processed), to the auditory nerve which feeds sound data to the temporal lobe or to the hair cells in the inner ear. Balance is a systematic integration of sight, hearing and posture. Damage to any of these can produce dizziness or dysequilibrium.

Perceptual disorders are very consequential. They tend to cut the person off, to varying extents, from other people and the world around them. This partial black out of sensory information is isolating and leads to uncertainty and anxiety. Fortunately the perceptual distortions which accompany a tbi often improve with time as the brain or cranial nerve heals and as the person learns to compensate for the distortions. However, some perceptual deficits are permanent. Following a tbi, it is important to identify which of your 5 senses is "off," in what ways and by how much. Next, you should visit the appropriate specialist for testing. The starting place is the neurologist, ENT doctor or physiatrist. They in turn will refer patients for audiograms (hearing tests), neuro-ophthalmologic or neuro-optometric testing, smell testing and the like.

What can be done to increase function depends on the site and extent of the damage. For example, where head trauma has shaken and damaged hair cells in the inner ear, a cochlear implant can help by sending sound data directly to the auditory nerve bypassing the hair cells. Where cranio-facial trauma damages the retinas, implanted electrodes can stimulate the visual cortex at the back of the brain. However, if the deafness or blindness is "cortical," i.e. a result of damage to the areas of the brain which process and integrate sound or visual data, the deficits are harder to overcome, and require the patient to engage in systematic exercises to stimulate regrowth of cells. The leading agency of the federal government for research into perceptual disorders is the National Institute on Deafness and Other Communication Disorders or NIDCD, which has a website at http://www.nidcd.nih.gov

PAIN DISORDER:

The brain has no pain fibers (which is why patients undergoing epilepsy surgery are maintained in a conscious state and encouraged to verablize responses to questions about what they see, hear and feel during pre-surgical brain mapping). However, the very same trauma that produces the brain injury often damages other parts of the body which house pain fibers, such as the cranial nerves and spinal cord. Closed head trauma can also inflame the meninges (the membranes which cover the brain) and cause migraine headache pain by abnormal expansion of meningeal blood vessels. Trauma which violently jerks the neck or shoulder is known to cause stretch/strain damage to nerves in those areas, leaving scar tissue which sends pain signals along a cervical nerve root coming off the spinal cord in the neck or the brachial plexus in the shoulder region. Throbbing migrainous headache and burning neck or shoulder pain are not the only conditions that give rise to a CPD (chronic pain disorder).

CPD can result RSD (reflex sympathetic distrophy) or from limb loss. Phantom limb pain is constant and agonizing even years after the acute pain of the initial limb loss is long over. From application of MEG (magneto-encephalography) we know that the brain reorganizes its structure after limb loss, creating a zone of hyper-sensitivity which over-responds to the slightest touch of the portion of skin substituted for the lost limb. In some patients stroking of the skin on the face can trigger phantom limb pain. One theory put forward to explain this is that the brain abhors a sensory vacuum, and so when limb loss deprives the brain of input, it substitutes pain signals.

Traumatic loss of a limb is not the only trigger for reorganization of pain processing centers in the brain. We also know that chronic pain from chronic compression of a spinal nerve root can cause reorganization of the central nervous system with hypersensitivity. A recent study using SEP (somato-sensory evoked potential) showed that patients with chronic thumb pain in one hand from a C6 nerve root lesion, had undergone structural changes in their pain reception system (including thalamus, brainstem and dorsal horn of the spinal cord). These changes made the patients perceive pain with any type of sensory stimulation of the affected area, even gentle touch, and electrical measurement of their brains confirmed their abnormal brain response objectively. J. Neuroscience 12/15/00 20(24):9277-9283. This reasearch is very important, because it explains why a patient with CPD can continue to feel pain long after the visible effect of traumatic injury is gone (e.g. years after a herniated disc was surgically removed).

Treatment typically involves rest, pain medication (typically opiates), accupuncture, electrical devices to block pain signals such as TENS, psychotherapy and behavioral changes concerned with avoiding pain triggers. With severe, intractible pain, the patient is sometimes sent to a neurosurgeon for surgical removal of pain processing centers in the brain. A new avenue of promising research is the targeted delivery of a toxic substance (such as poison marine snail venom) to the cells in the spinal cord which relentlessly transmit pain signals. The mode of delivery is attach the toxin to substance P, a chemical messenger. CPD is often accompanied by insomnia and depression. It can block and defeat tbi rehabilitation if not brought under good control by a physician skilled in management of chronic pain such as a physiatrist (a doctor of physical medicine and rehabilitation).

Top pain medicine clinics with comprehensive pain management programs include Stanford Hospital in California, UC Medical Center in San Francisco, the Mayo Clinic in Rochester, Minn., the Cleveland Clinic, Johns Hopkins Hospital in Baltimore, Md and the Mensana Clinic in Stevenson, Md. Our Links page has links to some of these clinics and a link to a
comprehensive Pain Terns Glossary.

DEPRESSION:

Depression is extremely common following a TBI. It can, and often does, have an organic and psychogenic component. The organic compoment would include such things as physical damage to the left hemisphere of the brain; depletion of any of the monamine neurotransmitters (serotonin, dopamine or norepinephrine); insomnia with sleep debt and fatigue; lower ouput of of thyroid hormone; and overproduction of the stress hormone cortisol. Studies of stroke patients has revealed that damage to the left side of the brain is far more likely to trigger depression than damage to the right side. A 1988 study identified at least one factor behind this difference. The right side of the brain tends to keep serotonin at optimal levels in the brain following a brain attack, whereas the left side is less able to do so. Depletion of serotonin in non-brain damaged patients is associated with depression, irritability and increases in inter-personal violence or suicide, so this makes sense.

Neuropsychologists have observed the same response in TBI patients. People with tbi are under stress for a variety of reasons. They need to concentrate much harder to take in and remember new information, to shut out distractions and keep on task. They must also expend a great deal of extra energy to appear, or pass, as "normal." They don't sleep well which raises their level of stress hormones and blocks replenishment of "feel good" brain substances. They are understandably anxious about losing their spouse, friends, job and home. These and other "stressors" raises the level of cortisol in the bloodstream. This contributes to depression and poor memory by atrophy of the hippocampus. Older studies of war veterans with PTSD show hippocampal shrinkage. Much more recently, neurobiologists Barry Jaccobs, Henriettte van Praag and Fred Gage published a study in the July 2000 issue of the American Scientist in which they report that the dentate gyrus in the human hippocampus gives birth to 100s, possibly 1000s, of new "baby" neurons every day, which helps explain how humans can have a continuous, uninterrupted memory of their entire lives, when old hippocampal and other brain cells get retired every day - about 50,000 or so. They believe that hippocampal damage or suppression of hippocampal birthing of new cells explains poor memory and the depression which is so frequently linked to poor memory. There is some corroboration in reports of vigorous physical exercise stimulating birth of new brain cells in the rat hippocampus and improving the ability to rats to run mazes and remember the routes they took.

The psychogenic aspect refers to perceiving oneself as being impaired or disabled in the functions of everyday life, and then experiencing such negative emotional respones as shame, guilt, worry, fear, anxiety or dread. The American Medical Association's "Essential Guide to Depression," states that any random event which takes away a person's sense of having control over their life can precipitate depression, including not just a death in the family or loss of a job, but traumatic injury as well. Because of their obvious suffering, sadness, crankiness and impaired ability to function smoothly in social situations, TBI people are sometimes abandoned by friends, and this social isolation can compound the depression.To the extent depression drives a wedge between the person with the TBI and his spouse or children, the depression is also likely to worsen, as recognized in the AMA Guide.

Research shows that beginning about 3 months post-TBI, many patients who are then suffering from depression do not have identifiable structural damage to the left brain hemisphere damage, which means that  depression so long after the TBI has a  psychogenic component. Is psychogenic depression malingering? No. The depression is real and has real consequences, such as poor sleep, fatigue, over or under eating with significant weight loss or weight gain,  losing motivation, and dropping out of or curtailing vocational, social, sexual  and recreational activities. When depressed people respond well to anti-depressant medication and start sleeping well, their cognitive performance on testing goes up and they show improved brain metabolism in their frontal lobes on PET scans, as established by Dr. Helen Mayberg of the University of Texas Health Science Center in San Antonio. Litigation doctors who work for insurance companies like to separate out "organic brain problems" from "psychological troubles" arising from the mind, because this is way of linking the plaintiff's distress to something other than a TBI. Is this a fair distinction resting on contemporary neuroscientific knowledge?

Not really, because the brain that was violently shaken during the head trauma is the same brain which gives rise to and which "feels" the depression. As noted in a recent book on Functional Brain Imaging by Andrew Papanicolaou,  there is "not a single thought, decision, feeling, attitude or trait which does not depend on the brain." If depression following head trauma was faked for litigation, or resulted from the stress of litigation, one would expect the depression to show up only in head trauma patients who filed a lawsuit and to last only as long as the lawsuit . However, research shows that this type of depression strikes whether or not the person with the TBI has filed a lawsuit for damages, and that it long outlasts the monetary settlement of lawsuits. One such study appears at Journal of Psychiatry 1999; 156(3)374-378.

It is most unfortunate that in litigation for damages, the psychiatrists and psychologists who work for the insurance companies separate depression out from traumatic brain injury and phrase the debate in either/or terms, saying the plaintiff's problem is either TBI or depression, and for x reasons, the expert is convinced it is depression. This is a distortion of the medical literature which serves an economic purpose. PET scans of the brains of depressed vs. non-depressed persons are different. Depressed people (like schizophrenics) show decreased frontal lobe activation, whether the source of the depression is lifelong disorder or the recent consequence of a TBI. This result is not subject to voluntary control and cannot be faked. Autopsies of depressed suicide patients have shown structural abnormalities in serotonin receptors. See, Ernsberger's article at  Archives of Gen. Psychiatry (1990) 47:1038-1047. 

Depression tends to build on itself and worsen if not treated aggressively. Treatments include anti-depressant drugs, psychotherapy and behavior therapy (to change behaviors which may re-enforce depression). It is common for depression to become a bigger obstacle to recovery of employment and decent social functioning in the realm of marriage and family than cognitive deficits. There is no single bio-chemical cause of depression in all people, which is why some people respond well and some do not respond at all to the same anti-depressant, and why a psychiatrist may need to "try out" a patient on a variety of different anti-depressants until he hits the jackpot and gets good remission of the depression. Common anti-depressants include Elavil, Prozac,  Zoloft, Paxil   and Effexor, but there are many others. There are certain ways to predict whether a patient will respond or will not respond to anti-depressants. If the patient's depression is briefly relieved by alcohol he is likely to benefit from anti-depressants, because each drug activites the same neural circuitry. Using the PET scanner, Dr. Helen Mayberg has shown that a good clinical response to anti-depressant medication tends to occur only in patients who prior to treatment showed active  metabolism in part of the limbic system called the rostral anterior cingulate. She believes that the rostral anterior cingulate must be placed termporarily in a state of hypermetabolism to restore normal mood in a depressed patients, and that non-responders to anti-depressants are people who had weak metabolism in that part of their brain before and after the trial of medication.

Finally ATTITUDE matters. Clinical research shows that tbi survivors who engage in negative thinking all day long (e.g. blaming themselves for their injury, worrying about the future and wishing things were different) tend to be much more anxious and depressed than patients who focus on strategies of problem solving and positive outlook. See, Journal of Head Trauma Rehab. 15(6) 1256-1274) Dec. 2000 A good place to learn coping strategies that work is in a well run tbi support group.

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SLEEP DISORDER:

Although many people complain of headache, slowed cognitive processing and poor short term memory following a TBI, the one symptom that we see without fail in every survivor of a brain injury is sleep disorder. Why is this important? Lack of sleep causes lost cognitive sharpness with distinct decreases in attention, reaction time and working memory. In the April 2003 Journal of Sleep, Dr. Hans Van Dongen, Assistant Professor of Sleep at the Univ. of Pennsylvania, published a study showing that adults who get 6 continuous hours of sleep per night for two weeks perform as poorly on cognitive testing as people who were up for 48 straight hours. Typical clients of our office average 4-6 hours of highly fragmented sleep per night. You do not need an enormous brain lesion to have problems with concentration, irritability and memory, if your "mild" brain injury is disturbing your sleep-wake cycle.

Although there are some cases of hypersomnia (sleeping too much), it is far more typical to see insomnia with day time sleepiness. Why? Some physicians believe difficulties sleeping are due to depression (which tends to wake people up for the rest of the night around 2 or 3 am.) or anxiety (which makes it very hard to fall asleep in the first place) or both. Either mechanism would create a large sleep debt with oppressive day time fatigue. Other physicians  blame fatigue on cognitive impairments, which force the person with a TBI to expend extra energy to maintain  attention and to perform the mental work involved with retaining information, retrieving memories, making decisions, etc. The theory goes that people with a TBI must work many times harder to peform the same cognitive tasks as people without a TBI, and this extra effort wears the person with TBI down.

While there is some truth to all of these beliefs, if they were the only explanation, we would expect to see better, more refreshing sleep at night and a higher level of energy and alertness during the day in patients receiving appropriate treatment for those sequelae of a a TBI, such as anti-depressant medication, anti-anxiety medication and cognitive therapy. But we do not not. We might also expect correction of the problem from a sleep medication like Ambien (which quiets brain activity and relaxes the skeletal muscles), but we do not. Clinicians know that a planned, temporary period of sleep deprivation may jolt a depressed person out of his depressed mood and help him sleep, at least for a time. Unfortunately this remedy has not worked for persons with a TBI. To the contrary, sleep deprivation makes all their symptoms worse. 

Recent research into sleep disorders has shown that persons with a TBI experience highly disturbed and inefficient night-time sleep, and that (like sufferers of obstructive sleep apnea) they wake up 50 or more times a night. Such highly fragmented sleep accounts for why people with a TBI feel so exhausted and worn down all the time, as if they were suffering from chronic jet lag. While patients with obstuctive sleep apnea can be cured with weight loss, laser surgery on the throat, and other methods, there is little help available right now for TBI- induced insomnia.

A concensus as to the cause of the problem has begun to emerge. The sleep-wake cycle in the normal person conforms to the gradual, time sequenced release of pre-set quantities of certain neurotransmitters. The orchestration of neurotransmitter release for initiation and maintenance of sleep is done by the the suprachiasmatic nucleus (SCN) of the hypothalamus (which blocks histamine production and puts us into slow wave sleep), the pineal gland (which produces melatonin to signal the SCN to prepare the brain and body for sleep)and the PGO system (the pontine-lateral geniculate-occipital complex which activates dream or REM sleep in alteration with slow wave sleep). All 3 are affected by changes in light, and activated by the darkening associated with night. The 24 hour cycle of waking, slow wave sleep and REM sleep is controlled by the SCN, which obtains information about light conditions outside the body through the retinohypothalamic tract (RHT) and from intergeniculate leaflet fibers. The darkening of the light associated with the coming of night activates gastrin releasing peptide (GRP) which activates the SCN through BB2 receptors, see J. Neuroscience 7/15/2000. 20(14):5496. The dorsal raphe nuclei in the brainstem also pump serotonin to the SCN to help usher in sleep. During slow wave sleep the mind is calm.

During intervals of dream sleep (known as REM or rapid eye movement sleep) brain secretion of acetylcholine (Ach) peaks and the mind becomes extremely active, but the muscles of the body are paralyzed by nitrous oxide emitted in the brainstem. Ach production peaks in the cholinergic neurons of the basal forebrain in response to release of neurotensin, which provokes burst-like discharges of Ach. Micro-injection of neurotensin into the basal forebrain of rats in slow wave sleep, provokes rapid rise in brain Ach with rapid onset of REM sleep. J. Neuroscience 11/15/00 20(222):8452-8461. Adults generally wake out of REM sleep in the morning. Waking at morning is produced by increases in histamine and cortisol production.

Brain trauma disturbs the normal cascade of neurotransmitter release, which causes frequent night-time awakenings known  as "sleep fragmentation." In a normal sleeper, the levels of norepinephrine, dopamine and serotonin gradually drop during the initial phase of sleep (slow wave) and fall to a virtually zero level during the second phase (rapid eye movement). During REM (the dream stage of sleep) brain levels of acetylcholine rises sharply. It is now believed that secretion of neuropeptides known as orexins (or hypocretins) from the prefornical area of the hypothalamus plays a significant role. People who lack type 2hypocretin (hrct2) are narcoleptic. When the sleeping fit strikes, they move suddenly and instantaneously from a state of wakeful alertness to REM sleep, no matter where they are or what they are doing. This corresponds to a light switch type shut off of neurons in the locus coeruleus of the brainstem which secrete norepinephrine. Injection of type 1 hypocretin (hrct1) activates the locus coeruleus and suppresses REM sleep. J. Neuroscience 10/15/00 20(20)7760-7765. Damage to the hrct producing area of the hypothalamus or the circuits linking it to the locus coeruleus of the brain stem, would appear to play a role in at least some sleep disturbances.

Studies of TBI patients in sleep labs shows them waking up for brief moments as many as 40-50 times a night, interrupting and shortening the periods of SWS (slow wave sleep) and REM (dream) sleep. This robs sleep of its restful, restorative character, leaving TBI people feeling tired, de-energized and out of sync with the rest of the world. Sleep researcher Eve Van Cauter, Phd at the University of Chicago has tracked the sleeping habits of a group of 149 men between the ages of 16 and 83 over a 14 year period. One of her principal discoveries is that HGH (human growth hormone) is secreted at its highest levels during SWS, and that as men age they get less slow wave sleep, secrete less HGH at night and lose muscle mass and muscle tone while gaining fat. Disturbance of SWS due to brain trauma would thus tend to speed up the natural aging of the body. Further, decreases in REM sleep from brain trauma cuts way back on dream time, when people consolidate their memories of newly learned facts and skills. Sleep research has established it is during the  REM phase of sleep that strengthening of new synaptic connections occur, and when REM is obstructed, people show reduced capacity to retain new information. 

College students and grad students who "cram" all night for an exam the next day, may pass the exam yet lose much of what they crammed into their brains. Does lack of sleep somehow prevent long term retention of the material? Yes, says a study in the December 2000 issue of Nature Neuroscience (Vol. 3 No. 12). Researcher Robert Stickgold took 24 Harvard students, had them learn some visual identification skills on computer, let 12 of them sleep the same night and kept the other 12 up. He then let all 24 sleep normally on 2nd and 3rd nights. On the 4th day he retested them. The 12 who got normal sleep the first night did much better and showed greater mastery of the new skill than the sleep deprived group. This is consistent with other studies, and tends to confirm the belief that the structural and chemical changes in the synaptic connections of the hippocampus and other parts of the brain necessary for long term storage of information requires adequate sleep, and that memory consolidation cannot take place without it. Electrical recordings of activity in the brains of songbirds, rats and humans suggests that part of the memory consolidation process involves re-living or replaying the day time event during sleep.

Can anything be done to promote better sleep in tbi patients? Some neurologists prescribe the anti-depressant Trazodone, either alone or with a dose of choral hydrate, to get insomniac patients to sleep at night following a TBI. Literature on effectiveness and safety of treatment is fairly sparse for TBI caused insomnia. Things are just the opposite with insomnia due to simple anxiety, for which Ambien is a great help in many cases. Researchers in England have found that use of lavendar as an "aromatherapy" is quite effective in getting hospital patients to fall asleep and remain asleep. So long as one is not allergic to lavender, it might be worth giving it a try. Some persons with insomnia have benefited from an intense dose of light from a sunlamp first thing in the morning upon waking, which appears to affect the SCN and reset the biological clock through "phase advance." If the insomnia is related more to "reactive anxiety" to having a tbi, than to neurotransmitter imbalance, medications such as Ativan or Buspar may help. These are effective anti-anxiety agents. Buspar is less sedating with regard to cognition.

Persons with insomnia and crushing fatigue following a TBI, should consider seeking evaluation and treatment at a sleep disorders clinic, where their disturbed sleep pattern can be documented and interpreted on the basis of night-time EEG tracings (EEB telemetry) and night-time filming of their sleep in a sleep lab. The "gold standard" for diagnosis of sleep disorders is called polysomnography, which combines measurements of brain waves (EEG), muscle tone (EMG) and eye movements (EOG). (brain waveSuch persons should also recognize that at least some of their day time difficulties with mental fuziness, slowed decision making, poor organization of time, poor memory, slowed movement, apathy, frustration and irritability, have to do with lack of healthy, restorative sleep. Finally, such persons in consultation with their neuropsychologist should reorganize their schedules to promote sleep and avoid activities like driving when they are most likely to be fatigued.

While sleep specialists cannot cure this problem, they can treach good "sleep hygiene" to mitigate the suffering that goes with not sleeping normally. This includes avoiding stimulants like coffee or cola and avoiding stimulating activities like intense exercise or computer games as bedtime nears. It includes having a regular sleep routine and regular bedtime and making sure to use one's bed for sleep and sex but not for eating, reading, etc. Having a chronic sleep disorder from a TBI is like living with permanent jet lag. You are awake while others sleeping, and you are dog tired while others are alert, active and energetic. This is a crucial problem which must be addressed much more vigorously in the diagnosis and care of persons with a TBI.

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DREAMING DISORDER : The amount, idea content, visual imagery and emotional tone of dreaming can be changed by trauma. The lives of patients with PTSD is much more influenced by dreams than "normal" people. PTSD patients have dreams with greater complexity, fright and anxiety, which they recall more vividly than other people, and to which they compulsively return each night, sometimes for months, years, even decades. Patients with TBI experience shortened, fragmented REM sleep and tend to have fewer dreams. If the TBI is severe enough it can wipe out the ability to dream by damaging structures or circuits in the medio-basal forebrain, medial temporal lobe, inferior parietal cortex or occipito-temporal cortex. Dreaming is associated with many positive functions including memory consolidation, problem solving and psychological integration of self. Disruption of dreaming by trauma can have a very negative impact on sufferers of TBI, which is often ignored or neglected in patient histories, and in diagnosis and treatment.
 

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HEADACHE: The traumatic event which causes the TBI generally causes headache of one or more kinds which can include muscular, cervicogenic and vascular. Muscular headache is associated with increased tension and spasm of the muscles in the scalp, neck and shoulders. Cervico-genic headache is associated with a pinched or stretched cervical nerve root. These headaches are potentially responsive to aspirin, Tylenol, anti-inflammatory medication, warm/cool compresses, physical therapy, accupuncture, nerve block injection to trigger points, and other treatments aimed at reducing the spasm and pain associated with muscle tightness. Behavioral change can help too. Instead of increasing activity at home or office when the tension headache starts, patients should slow down and rest. They should also avoid negative emotions and exposure to bright lights or loud noises, as these tend to trigger attacks of headache pain.

Vascular headache includes migraine, and much less commonly cluster headache. Migraine is an intense, throbbing headache often accompanied by hypersensitivity to light and sound, nausea, even vomiting. Classic migraine is preceded by preceded by a dazzling display of lights known as an aura. Other forms of migraine occur without aura, including post-traumatic migraine. Migraine headaches are sometimes accompanied by dizziness, blurry vision, allodynia (extreme pain reaction to the slightest touch of the skin), bloodshot and teary eyes, edema, and other unpleasant symptoms. They leave the sufferer spent, weak and sleepy - making sleep one of the few restoratives. These headaches require medications which constrict swollen intra-cranial blood vessels and quiet clusters of cells in the brain called "migraine generators" such as those found in the trigemino-vascular systems associated with the trigeminal nerve. Contemporary neurologic literature identifies overexcitation of the neurons in the trigeminal nerve as one important mechanism in generation of migraine. The trigeminal nerve (the 5th cranial nerve) arises at the base of the head and supplies the eyes, cheeks and jaw). The overexcited trigeminal precipitates rapid, dramatic swelling of blood vessels around the brain with release of inflammatory chemical substances (especially CGRP or calcitonin gene-related peptide) that perpetuate the vascular swelling and triggers excitatory changes in other neurons. During migraine the blood drained from the head by the jugular vein shows abnormal elevation of CGRP.

In head injury victims who develop migraine, the headache is often triggered by effortful visual or mental concentration. For such persons it literally hurts to think. The harder they concentrate on a task (such as reading) the more intense the headache until it evolves into a full blown migraine. Contrary to popular belief migraine is not a psychological disorder; it is most certainly a neurologic disorder. Migraine involves a "rolling tidal wave of pain." If appropriate medications are taken within 90 minutes of onset (especially the serotonin boosting "triptans" like Imitrex), the first wave can be stopped before excitation spreads to other migraine generators. If the headache is not stopped in time, the spread of the headache triggers odd sensations known as parasthesias (numbness and tingling in the head, face, jaw or tongue) and odd hypersensitivities (wherein light, sound or the touch of a comb on the hair, a breeze on the cheek or even the pressure of clothing can trigger agonizing pain). One client of our office suffered from unbearable scalp itch. If you are having these types of headaches after your head injury, it is imperative to tell your doctor. A scientific survey conducted for the National Headache Foundation presented in August 2000 showed that 52% of all migraine headache sufferers had not been diagnosed. See NHF HeadLines #115.
 

It is well established that a blow to the head can cause migraine of temporary or permanent duration, and this is recognized by the International Headache Society, which calls it post-traumatic migraine. A paradox recorded in the medical literature is that patients with mild head trauma tend to develop worse, more persistent headaches than patients with severe head trauma. Physicians retained by insurance companies to combat damage claims by victims of head injury say the opposite. Disregarding the medical literature, they say mild tbi produces only mild headaches and that any mild tbi patient who complains of frequent, severe headaches is either a malingerer seeking money or an exaggerator seeking attention and sympathy. These physicians are not in touch with the facts. Headache is the most common complaint following mild tbi and the one that its victims tend to complain about the longest. Even 4 years post-trauma some 20-25% still complain of headache. When the post-traumatic headache is the migraine type, extra damage to the brain can occur from abnormally high quantities of blood surging through the cerebral arteries for an extended period of time during migraine attacks. K. Michael Welch of the Kansas University Medical Center just told the International Headache Society in July 2001 that frequent migraine leads to deposition of iron particles in the brain tissue with gradual destruction of the periaqueductal gray matter, the part of the brain responsible for blocking or suppressing pain messages. He established this by using a form of MRI that maps iron concentration in the brain, and found it to be much higher in frequent migraine patients than in patients with episodic migraines or no migraines. The MRIs also showed erosion of the PAG in frequent migraineurs but not in the others. Once the PAG is damaged by iron, the patient will be susceptible to feeling severe pain at all times, not just during migraine. Therefore, says Welch, doctors must do all they can to prevent frequent recurrence of migraine. Depakote and Elavil have been used successfully in some patients to prevent migraines.

The most potent and fast acting migraine medications on the market today to stop or "abort" a migraine already in progress are known as triptans (the 5HT receptor agonists which mimic serotonin). These include Imitrex, Amerge and Maxalt. They work most effectively when taken rapidly after the first signs of headache onset, before the neurons in the occipital portion of the trigeminal nerve start an uncontrollable firing pattern that can take hours, even days to subside. These medications come in a fast dissolving pill that one can place under the tongue, like nitroglycerin for heart patients with angina. Since Imitrex is too strong for children, neurologists offer children Elavil (a tricyclic anti-depressant). The triptans stop or abort migraine headaches, which are already in progress.

Elavil is somewhat useful in headache prophylaxis, i.e. in preventing onset of new headaches. Still more useful in headache prevention are anti-convulsant medications such as Depakote, which blocks the enzyme that degrades GABA and thereby increases the supply of GABA in the brain, which places a neurochemical damper on spreading excitation.  A neurologist will prescribe Depakote only when migraines are not responsive to abortives such as the triptans or the migraines are occuring with extreme frequency. Depakote has bee shown to be safe and effective in large scale, double-blind, placebo controlled  studies. Although cognitive problems following a TBI are significant, sometimes the most persistent and most disabling problem associated with a TBI is migraine. Sometimes it is insomnia with fatigue. Unfortunately some persons are burdened on a chronic basis with migraine and insomnia. Such patients deserve a comprehensive neurologic work up and aggressive treatment.

In litigation situations where the plaintiff complains of migrainous headache pain, but is disbelieved by the insurance company, some doctors resort to CT or MRI scans. This is a waste of time and money. Migraine is not a permanent, structural abnormality but a transient condition involving sudden expansion of blood vessels, blood flow changes and inflammation. A recent review showed that CT studies are not helpful and are almost always negative, see   Headache  39:747-751 (Dec. 1999). If forensic proof of headache is needed, a SPECT scan showing blood flow changes or fMRI showing oxygenation changes in the blood would be a much higher yield choice.

Self-management of migraine is an essential part of living a better life. In his book Migraine, noted neurologist Oliver Sacks, M.D. points out that no matter how much tinkering your neurologist does with headache medication, your migraines will never be brought under lasting control without you taking the time to observe the patterns of your headaches - in particular what triggers them (e.g. red wine, fatigue) and what makes them better (e.g. rest). Chocoholics will be happy to learn there is no solid scientific proof that chocolate is a migraine trigger. However, in the Jan. 25, 2000 edition of Neurology, Dr. Werner Becker of the University of Calgary, Canada, published a study indicating that changes in weather patterns, especially the onset of "Chinooks" (warm, westerly, high speed winds), was a clear trigger for migraine in chronic migraine patients. Migraine affects at least 15 million Americans 75% of them women. It is a serious public health problem. Surveys the NHF (National Headache Foundation) reveal that many migraine sufferers do not seek medical help. Some are so resigned to having headaches it does not even occur to them that life could be different or that anyone could help. Some tried inappropriate treatments which failed and left them pessimistic about medical help. Others fear being perceived as "crazy" because of the odd nature of their symptoms.

Avoidance of alcohol and stress, and getting lots of sleep can help reduce the frequency of migraine. TBI does not per se create a risk of alcohol abuse, except in persons who were abusing it before their injury. For those persons, rehab can include intervention to prevent relapse. Persons with a tbi face stress everyday associated with the frustration of forgetting what they just heard or read and from failing to perform tasks as quickly, efficiently or correctly as they once did. If they can learn techniques to lessen their levels of frustration and anger, this can help. Unfortunately, the insomnia which accompanies tbi is rarely responsive to medictions available at this time. Survivors of a tbi with insomnia and migraine face a difficult time, because they cannot get the sleep they need to "retune."

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OBESITY:

Following a TBI some persons develop "true hyperphagia" (uncontrollable increase in eating) due to a lesion of the ventro-medial hypothalamus or brain stem. In most cases, however, obesity is due to problems with behavior or mood or both. Impulsiveness and disinhibition lead to indiscriminate overeating. Depression, apathy,  reduced motivation or fatigue, lead to inactivity, which also produces weight gain. It is quite common for persons who have suffered a TBI to put on 25-35 extra pounds of fat. Extra fat and physical inactivity are associated with increased risk of high blood pressure, coronary artery disease, heart attacks, stroke, diabetes, colon cancer, gout and arthritis. Obesity from eating high-fat fast foods and not exercising must be a matter of concern for the patient, his family and his doctors, especially if the patient is smoking cigarettes or has other risk factors for circulatory disease. Obesity can contribute to depression by creating a poor self image and by limiting exercise which decreases blood circulation and lowers endorphin levels in the brain.  It is harder for persons with a TBI to lose weight on their own due to problems with apathy, poor memory and executive function disorder (disorganization).

There are no shortcuts to overcoming obesity. In the late 1990s the makers of mass, packaged snack foods (like chips, crackers and cookies) got FDA approval to insert "fat trapper" chemicals in their products. Their advertising says eat all you want, because these chemicals combine with dietary fats, trap them and cause them to be execreted whole without being broken down and released into the bloodstream. Unfortunately these food additives have side effects (like flatulence and rectal "leakage"). The popular chitosan supplements sold at health food stores as fat trappers appear not to work. In March 2001 a team of nutrition researchers led by Judith Davis at UC Davis in California released a study showing that fat content in the feces of men taking chitosan supplements and of men not taking them was identical over an extended period. Questions about fat trappers should be submitted to the obesity task force of the National Institute of Health in Bethesda, Md.

Health experts recommend the use of a structured weight loss and exercise program with external reminders and re-enforcement. Any such program should be customized to the individual's needs, based upon analysis of the cause of the problem (cognitive, behavioral, mood), the level of participation and degree of health risk. The medical literature on management of obesity associated with a TBI is relatively new, because it has taken a long time for doctors to recognize this problem and develop a clinical interest in it. New research has tied obesity with an increased risk of Alzheimer's Disease (AD), especially in people with the common genetic mutation known as the apoe-e4 gene. Anyone with that gene is now believed to be at 7-10 times the normal risk of developing AD solely as a result of having suffered a tbi. If the same person is also consuming a high fat diet, deficient in fruits and vegetables, and is smoking or not exercising, they are running a dangerously high combination risk of getting AD.

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DIZZINESS:

Following a TBI complaints of dizziness are very common for a period of days or weeks. Sometimes the dizziness lasts for months. Sometimes it never goes away. When physicians speak of "dizziness," they generally mean "positional vertigo" (having the room spin or tilt with a change in head position) rather than lightheadedness (from anxiety or low blood pressure) or dysequilibrium (postural abnormalities with imbalance). A blow to the head can cause dizziness by stretch injury to the vestibulo-cocchlear nerve; inflammation of the membraneous tissue of the labyrinth of the inner ear accompanied by hearing loss or nystagmus (called labyrinthine concussion); physical displacement of the calcified ear stones (otoliths) which sit atop the hair cells in the utricle of the inner ear, causing them to migrate into other parts of the ear; cerebellar damage; brainstem damage; or cervical injury (called cervical vertigo). Brainstem damage causing vertigo comes from diffuse axonal injury, which cannot be visualized on structural imaging. About one third of all migraine patients experience vertigo with their headaches. Post-traumatic migraine is no different, and our office has clients with PTM combined with vertigo.

With severe head trauma dizziness can arise from temporal bone fracture with bone or blood invading the ear canal. When blood gets inside the inner ear it can cause scarring with fluid blockage, a condition known as hydrops or post-traumatic Meniere's Syndrome that is accompanied by dizziness with noisses in the ear, fullness or hearing changes. Severe head trauma can cause perilymph fistula, a blow-out of the membrane between the inner and middle ear. Someone with this condition is likely to become dizzy upon hearing loud noise (Tullio's phenomenon). People with perilmph fistula can provoke dizziness by straining or blowing the nose. If the head trauma is severe enough it will trigger the death of hair cells in the cocchlea, and cause impairment of hearing in direct proportion to the number of hair cells killed (all the way from mild hearing loss to total deafness).

Diagnosis of post-traumatic vertigo is made by taking a histsory of onset and symptoms; by visual examination of the inner ear; by a pressure sensitivity test for perilymph fistula; by a hearing test (audiogram); by a tilt table test (to check cardiac output); caloric test (squirting ice water into the ear); by electronystagnogram, by platform posturography and other means. Persistent dizziness can be disabling. It is vital to tell your doctor about your dizziness and make sure you get tested if it does not go away. You can help your doctor diagnose the precise cause of your post-concussional dizziness by keeping a journal noting down which activities or events trigger it. For some patients only aerobics, jogging or other activities which jostle the head bring it on. For others the dizziness is relatively constant. Dizziness can also accompany post-traumatic headaches, especially post-traumatic migraine, which produces transient increases in the diameter of brain arteries with diminished blood flow and blood pressure. Treatment typically involved medication, changes in lifestyle (such as activity restrictions), physical therapy and more rarely surgery.

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IMBALANCE: Balance involves maintenance of a stable position at rest; stablizing voluntary movement; and reacting to external movements. Good balance means making immediate postural adjustments that shift the center of gravity to the center of support. TBI can impair balance while sitting, standing or walking to a mild, moderate or severe extent on a temporary or permanent basis. When severe, imbalance can reduce a patient's capacity to live alone and perform essential daily activities. Milder disturbances may limit sports, recreation and leisure. Patients with severe tbi almost always require balance and gait training during rehabilitation.
Patients with moderate or mild tbi have more subtle balance problems that may go undetected and untreated. Balance problems are more common following mild tbi in older patients, those over 50.

NEUROENDOCRINE DISTURBANCE:

The brain is home to the pituitary (the "master gland" of the endocrine system), the hypothalamus, the pineal and other structures which regulate mood, sleep, sex drive, aggression, hunger, thirst, blood pressure, metabolic rate, energy level, body temperature, and other basic physiological states, through production of or modulation of production of  hormones. When the brain is badly shaken or physically bounced off the bony walls inside the skull, These structures and their hormonal outputs are negatively affected, and the net result is that the body loses some of its homeostasis, its capacity to keep its vital systems in balance. Traumatic injury to the brain is accompanied by immediate, measurable hormonal changes, which can include some or all of the following: decreased  thyroid output (associated with slowed metabolism and depression), increased cortisol production (the stress hormone associated with agitation, anxiety, depression and insomnia ) and decreased testosterone (especially after severe TBI), which is associated with diminished libido. Cortisol is increased after mild and moderate TBI but decreased after severe TBI. Excess cortisol has been linked to depression in patients with Cushing's Diseaseand Post-Traumatic Stress Disorder.  The AMA's Essential Guide to Depression states that about 50% of all people with depression show abnormally high levels of cortisol.  This makes sense, because neuropsychologists note a surprising absence of depression in patients with severe TBI, yet cortisol is reduced below normal levels in those patients.

Low supplies of the neurotransmitter serotonin are associated with depression, anxiety, impulsive/aggressive conduct and suicide. Serotonin is produced primarily (but not exclusively) in clusters of nerve cells called the raphe nucleii distributed in structures at the back and base of the brain, i.e. the pons, midbrain and medulla. The rostral raphe nuclei in the upper pons deliver serotonin to the frontal lobes and limbic structures of the medial temporal lobes which regulate mood. It is believed that traumatic brain injury from a blow to the head can cause depression by shear-strain damage to the axonal connections which deliver serotonin from the rostral raphe nuclei to those areas. In the normal brain excess serotonin is cleared from the frontal lobes and limbic areas and brought back to the raphe nuclei at the back of the brain by SERT (the serotonin transporter system). Anti-depressant medications like Prozac and Zoloft (the SSRIs or selective serotonin reuptake inhibitors) improve depresssed mood by blocking SERT,  decreasing the reacquisition of serotonin and leaving more serotonin between synapses in the frontal and medial temporal lobes.

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EPILEPSY:

One very serious and tragic consequence of a TBI is post-traumatic epilepsy (PTE). Epilepsy is a disorder involving excessive excitation or insufficient inhibition of neuronal networks in the brain with resultant "storms" caused by massive, uncontrolled "firing" of neurons. Recent research shows a clear genetic predisposition in certain individuals, who would be at much higher risk of developing PTE from brain trauma. At this time two different mechanisms have been indentified as likely culprits in delayed onset of PTE following tbi. One is intracranial bleeding which bathes portions of the brain tissue in blood and deposits an iron compound from hemoglobin called hemosiderian which is toxic to the brain and may precipitate seizures after a latency period. The other mechanism is regrowth of neuronal networks in the place where "focal" brain damage killed off "inhibitory" brain cells (those which suppress uncontrolled firing). The new cells and connections are helpful in restoring lost movement, cognition or speech, but harmful in that they are hyperexcitable and likely to contribute to generation of seizures.  

Fortunately PTE occurs very rarely in association with mild TBI. The known risk factors for onset of PTE following a brain injury are: depressed skull fracture; bleeding in the brain; positive CT scan; craniotomy to remove a blood clot; abnormal reflexes on admission to the hospital; and a seizure within the first week of injury. When confronted with a hospital patient in the highest risk group for PTE, physicians will typically prescribe an anti-seizure medication such as phenytoin on a prophylatic basis to prevent seizures from ever starting. Disputes arise over how quickly to wean the patient off such medication, and whether to use the medication in tbi patients at moderate or low risk of PTE. Some physicians prefer rapid weaning; others are relaxed about leaving the patient on medication for 6-12 months.

Although the medical literature is in conflict, it appears that when patients in the highest risk group are given an anticonvulsant medication like phenytoin in the hospital on a prophylactic basis, many are spared from having a seizure. For patients who do not seize in the hospital the risk of developing PTE continues at an elevated level for 2 years, then gradually drops. At the end of the 5th year, their risk is no greater than anyone else, including people who never had a head injury. The diagnosis of epilepsy is made clinically on the basis of history and observation. EEG studies are of limited helpfulness. EEG measures only the electric output of neurons at the surface of the cortex, and not neurons deeps in the brain where any seizure focus would likely be found. Given the infrequency of seizures, most EEGs are administered in between seizures, and such EEGs have only a 50/50 chance of catching epileptiform wave activity. Thus a negative EEG can NEVER rule out epilepsy. To increase the liklihood of catching abnormal wave patterns, a physican can order 4 repeat EEGs; have the EEG performed after the patient has been sleep deprived and fallen asleep; have the EEG done while flashing lights in the patient's eyes; or pay for telemetry which is continuous 24 our per day EEG monitoring with a portable device over a period of 3 days.

Children are considerably more vulnerable to PTE from cranio-cerebral trauma, in part because their skulls are relatively soft, their brains do not fill their skulls and their brains are still developing.  PTE in children is much more likely to involve grand or petit mal seizures than PTE in adults. By far the most common form of PTE in adults is temporal lobe epilepsy (TLE) manifested by complex, partial seizure disorder. This disorder does not involve falling to the floor, flopping one's limbs and rolling one's eyes. It is far more subtle, and therefore diagnosis is frequently delayed for years or missed altogether. Complex, partial seizure disorder is associated with visual hallucinations (ranging from religious scenes to tunnel vision), olfactory hallucinations (smelling coffee or burnt rubber or tasting metal) and blanking (becoming mentally absent for short periods, often just 30-60 seconds). About 5-7% of TLE patients have intermittent explosive disorder (IED), which involves sudden, unpredictable violent rages. Studies of these patients show they sustained traumatic damage to a brain structure called the amygdala in their left temporal lobe at the time of hte brain injury.

People living with epilepsy can reduce the frequency of seizures by following certain health rules. They should not skip meals, drink alcohol, use street drugs, drink alot of coffee or cola, or start a new medication without consulting their epileptologist. They should get adequate rest and sleep, drink plenty of fluids, learn stress management/relaxation techniques and stay in close communication with their doctor. People with epilepsy, and their families, should also educate themselves as much as possible about the disorder. Organizations that teach the warning signs of an impending seizure, what to do for a person in seizure, when to seek emergency medical care, etc., are posted in the Links section of the Resources Page of this website. People with epilepsy who wish to purchase a medical alert bracelet should contact www.medicalert.org

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BEHAVIORAL DISORDERS:

These are problem behaviors which arise as a consequence of the TBI, especially with frontal lobe damage. Examples are apathy, loss of motivation, irritability, anger, aggressiveness, inappropriate laughing or crying, socially inappropriate speech which is obnoxious or offensive, loss of ability to keep up in normal conversation and loss of ability to take charge of a situation in a responsible and reliable way (e.g. to watch the children when the non-injured spouse goes shopping or to answer calls and take down information correctly at the office when a co-worker leaves). These kinds of problem behaviors can and do erode relationships to the point where the non-injured spouse will seek marital separation or dissolution or the employer will terminate the employment. These behaviors are often tolerated and excused early on after the TBI patient comes home or returns to work, but as these behaviors continue over time and disrupt the orderly flow of business in the home or workplace, they trigger greater annoyance and intolerance in others. To prevent irrevocable breakdown in important relationships, it is important to acknowledge these behaviors and get the patient into rehabilitation where a combination of counseling, education, drug therapy,  behavioral modification and group therapy can be employed to improve the behavioral picture and avoid a bad social or vocational outcome.

In assessing neuro-behavioral disorders following a TBI the focus is generally on the inability of the brain injured patient to monitor his own behavior either through the eyes of others or from an objective standpoint of proper behavior in a given social situation or "script." Interestingly, recent research by neurologists at the University of Iowa College of Medicine and Salk Institute proves that a person with traumatic damage to their right parietal lobe will lose his ability to accurately sense the emotions that other people are feeling from seeing their facial expressions. See Journal of Neuroscience 4/1/2000 20(7):2683-2690. The lesion impairs his ability to generate an internal "somato-sensory representation" of how he would feel if he wore the same facial expression displayed by the other. Not being able to process the emotional cue given off by the facial expressions of others, the person with this type of brain injury cannot respond appropriately except by chance. Socially appropriate behavior not only requires an ability to monitor one's own behavior from an objective point of view and control one's own impulses, but the capacity to accurately perceive what other people are feeling from clues such as their facial expression, tone of voice, etc.

Any or all of these faculties can be impaired by a TBI, depending on where the damage occurs. Damage to the dorso-lateral portion of the frontal lobes is associated with apathy and loss of drives. Damage to the orbito-frontal area of the frontal lobes (located at the bottom of the frontal lobes towards the mid-line) is associated with inappropriate verbal and physical outbursts of anger. People with this sort of damage can be indentified through testing their sense of smell, since they generally have anosmia (lost sense of smell) due to damage to their olfactory nerve bundles attached to the bottom of their frontal lobes. A tbi which produces diffuse brain damage may lower serotonin output. Low serotonin levels are associated with inability to handle frustration or delay, anger, violence, homicide and suicide. Whereas a hemmorhagic contusion to the frontal lobes will be readily visible on CT, and will offer up a ready explanation for changed behavior, serotonin depletion from diffuse brain injury will not show up on standard neuro-imaging. More esoteric techniques like MRI spectroscopy must be used. Recent research confirms that stress evokes a response from cells in the dorsal raphe nucleus of the brain stem which secrete serotonin. J. Neuroscience 10/15/00 20(20):7728-7736. Adequate levels of serotonin enable a stressed person or animal to handle the situation. Inadequate serotonin secretion or delivery following stress will lead to the opposite, i.e. frustration, anger and rage.

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DRIVING:

Driving is often affected adversely by a TBI, even a "mild" one, because TBI is associated with visual impairments, slowed perception and reaction times, distractibility, poor memory, irritability and impaired judgment, amongst other deficits. Driving is important on a practical level for access to employment, education, medical services and social activities. It is also a symbol of independence and a source of self-esteem. Fear of losing their driving privilege, leads some people with a TBI to deny their driving skills are impaired or that they have been in a number of near-miss collision situations. Sometimes a family member will urge them to stop driving and will point out that they would rather have their loved one alive than let him risk death or injury by driving for some period of time after his TBI.

Statistics indicate that between 40-78% of persons with acquired brain damage will be re-licensed. A comprehensive review of driving and TBI in the June 2000 Journal of Head Trauma Rehabilitation at 15(3):895-908, indicates there is no clear, consistent match between mpairments of vision, cognition, motor skills or behavior which are diagnosed by paper and pencil tests in a doctor's office and actual fitness to drive in the real world. In the absence of a model which can predict fitness, or lack thereof, with a high degree of accuracy, it is best to have the person with TBI evaluated by a skilled specialist in what is called "adaptive driving." Physicians may overpredict or underpredict lack of fitness to drive and either unnecessarily deprive his patient of driving privileges or place the public at unnecessary risk of calamity. For persons living in northern California, one place they can go for a comprehensive evaluation of driving fitness after a tbi is the Occupational Therapy Department of the John Muir Hospital in Walnut Creek. Adaptive driving schools also exist, and are listed in the Yellow Pages. Anyone who feels unsure about their own capacity to drive safely while recovering from a TBI should err on the side of caution. At they very least they should get evaluated. Somtimes, only a few sessions are required to boost skills back to the safe range.

For anyone who is not sure if he can drive safely, it would be best to wait until the evaluation can be done. Meanwhile, TBI people who live in big cities can use public transportation, which can double as a form of therapy, because it requires working on memory, using maps,  looking for visual cues, making change, etc. People in rural areas do not have the same access to public transportation, but they can seek rides from friends or seek a driver through state agencies or volunteer organizations such as the Family Caregiver Alliance. There are also post-acute TBI treatment and rehab firms which provide in-home care visits.  One example in California is Rehab Without Walls located in San Jose at 1101 S. Winchester Blvd, Suite M-250. Remember that human beings lived and flourished for 99% of human history without cars. Foregoing driving for a while, will not ruin anyone. Once your doctor feels you have made sufficient recovery to consider driving again, you can get an adaptive driving evaluation through the occupational therapy departments of certain hospitals.

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RECOVERY:

If one defines recovery as complete restoration of the person to who he was before the TBI with all the same abilities and the same level of performance of daily activities, the likelihood of recovery decreases with as the severity of the TBI increases. For very severe TBI (e.g. patients with post-traumatic amnesia of one month or more) there is no chance of recovery in that sense of the word. For patients with very mild TBI, the odds of recovery in that sense of the word are fairly good, but without any guarantee. Physiatrists and other "rehabilitationists" who care for TBI patients in the post-acute setting, tend to use the terms "recovery" in a different sense. For them, recovery stands for the process by which the patient gains awareness of his deficits, works to improve them, accepts the permanence of the ones which fail to improve beyond a certain point, practices and masters new strategies of thinking and behaving to compensate for those deficits, readjusts personal goals to conform in a realistic manner to objective limitations of function, and learns to find pride and pleasure in achieving the new goals rather than making oneself sulky or angry at persistent failure to achieve pre-injury goasls which are now out of reach. With all that said, rehabilitationists strive always to keep hope alive while offering a realistic perspective. To deprive a TBI person of hope is to doom him to non-recovery. No one can know or predict in advance exactly how far a given patient will move beyond her early deficits.  Clinicians have published accounts of near miracles. Robust health, solid education and good attitude before the TBI certainly help as do the presence of loving, supportive and encouraging family or friends.

With regard to the rehabilitation process, for severe, and some cases of moderate brain injury, recovery will begin in the hospital, continue in a post-acute rehabilitation facility and then proceed on an out-patient basis with varying degrees of in-home assistance or follow-up home assessments. Cognitive therapy, occupational therapy, behavioral therapy and vocational rehabilitation with job coaching may be used. Persons with mild brain injury will have an assisted recovery only if a diagnosis is made. When the diagnosis is made the "assistance" may involve outpatient neuropsychological evaluation and counseling, anti-depressant medication, individual psychotherapy and sometimes family as well, support group meetings and medical care for problems like migraine, double vision, falling, insomnia, etc. Recovery tends to progress most quickly for the physical symptoms, more slowly for the deficits in thinking and slowest for behavioral problems like depression, irritability, lost impulse control, etc. Rules of thumb on recovery for mild brain injury indicate that many persons recover substantially within the first 3-6 months and most by 12 months. It is often stated little or no recovery can be expected beyond 18-24 months post-injury, and that approximately 10-15% of persons diagnosed with mild brain injury will have permanent problems (the "miserable minority").

These rules of thumb are statistical generalizations covering a highly diverse population and do not always predict what will happen to any one person. They are also more accurate for the obvious physical and cognitive impairments not the more subtle behavioral ones like changed personality. It has also been proven that some persons with brain injury do benefit positively from various forms of rehabilitation even 7-10 years after their injury. The duration and completeness of recovery will be affected by many variables including severity of initial injury, age, previous education, previous employment situation, existing psychological strengths or weaknesses, personality type and coping style, alcohol or drug abuse triggered by or exacerbated by the injuries, existence or non-existence of supportive family and friends, denial of deficits caused by organic damage to the brain or due unconscious refusal to acknowledge them, depression, and stress from job loss, debt, marital conflict, disputes over insurance benefits, tort litigation and other difficulties associated with the injuries.

One tragic statistic is that only 1 out of every 20 persons with a TBI receives truly comprehensive and adequate rehabilitation services. This can change only with increased education of the public, and advocacy by TBI organizations directed at government officials, HMO executives and other "gatekeepers" to medical services. One exception is the American Academy of Neurology, which fully grasps the tragedy of insuficient rehab services to persons with a TBI and other persons with chronic neurologic conditions. The AAN is spending its own money to promote patient advocacy efforts.

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PSYCHOLOGICAL CONSIDERATIONS:

Psychological considerations are of supreme importance in good recovery from brain injury. True restoration of the person means not just walking, talking and returning to work (of some type) but restoration of hope, purpose, goals and self-esteem. Brain injury is psychologically shattering because it reduces the survivor's control over his mind, body, moods and environment; and in doing so it challenges his core identity and forces him ultimately to give up or go through a healing process of denial, anger, grieving, acceptance and rebirth. The new life is one shaped around who he is, not who he was, around what he can still do, not what he used to do. The brain injured person needs help with his anger, rage, depression and apathy. Lithium for anger and anti-depressants for suicidal thoughts are not enough. An understanding and supportive psychotherapist is essential to guide the person through all the changes  post-injury and help him reach  the other side. When choosing a therapist, try to find someone with experience counseling brain injured people. Consumer satisfaction tends to be much higher with therapists who work direectly on the patient's cognitive and behavioral problems rather  than focusing on the "dynamics" of the therapist-patient relationship (See Harvard Mental Health Letter Feb. 2000).  Getting in touch with faith, spirituality or one's own "core" values can improve attitude and boost morale. Research on how people handle pain shows that positive thinking and hopefulness can stimulate the hypothalamus to instruct the pituitary to secrete natural pain blockers called endorphins, and bring about pain relief. Depression and pain re-enforce each other. One way to jump start a TBI patient is to get him into a TBI support group. This can bring open, honest talk  with, and emotional solidarity with, people in the same boat, and lessens the feelings of being isolated or being the only one to go through it. 

How doctors, family members, friends, employers and co-employees react to a brain injured person is important. When they show impatience, frustration and disappointment, and turn away, the injured person's tendency towards shame, avoidance and self-ostracism will be promoted. Counseling and education are not just for the injured person, but should be directed at significant others. The Law Office of Harvey A. Hyman is very sensitive to the psychological dimension of brain injury, the client’s need for psychotherapy by a qualified person (such as a clinical neuropsychologist) and anti-depressant medication and the importance of having the client’s family educated and counseled in how best to deal with their brain injured loved one at a time of maximum stress. Harvey Hyman is also sensitive to the pain, humiliation and anger felt by persons with mild brain injury when they are disbelieved and branded malingerers or hysterics by defense counsel and the defense experts in neurology and psychiatry.

In litigation the insurance company attorney will almost always question the persistence of symptoms, and suggest that psychological factors (not the brain injury) is the primary factor perpetuating the plaintiff's complaints. Older medical research suggests that most persons with "mild" tbi (equivalent to concussion with zero or minimal loss of consciousness) are symptom free in about 3 months, and only a minority of patients (around 10%) are still symptomatic from the brain injury at the end of 12 months post-injury. Newer research shows the % of patients with impairment or disability from a "mild" tbi at 12 months may be significantly higher. Until the newer research is duplicated and validated, cases will revolve around the organic vs. psychological explanations. Defense experts frequently point to pre-existing depression or psycho-somatic illness as a reason someone would unconsciously choose to feel ill and to "play the sick role" long after the organic cause of the illness was gone. They also blame doctors, attorneys and even tbi support groups for "iatrogenic causation," i.e. working to convince the patient he is worse off than he really is. This accusation can lead to bitter disputes. Sometimes the issue of organicity can be decided with a PET scan, which may show significant metabolic disturbances in the brain secondary to trauma in a person mistakenly labeled by the defense as a faker or hysteric. Sometimes the issue is more clouded, and consideration may be given to alternative explanations such as Post Traumatic Stress Disorder, Chronic Pain Disorder or other "co-morbid" disorders suffered along with the mild tbi. Sometimes what would have been a short lived concussion in one person, proves to be the "straw that broke the camel's back," because the victim had pre-existing burdens and could not shoulder the weight of the mild tbi. These may include learning disability, depressive disorder, anxiety disorder and others.

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SUBSTANCE ABUSE:

The anxiety, depression, social isolation, loneliness and tedium of rehab, which accompany a TBI, can push some survivors into excessive consumption of alcohol, prescription drugs or street drugs. So can chronic somatic pain from spinal or other injuries incurred from the traumatic event which caused the TBI. Substance abuse is an obstacle to full and meaningful participation in rehabilitation and can preclude reaping the benefits of rehab. It is crucial to identify the persons at highest risk of substance abuse post-TBI, to counsel them, monitor them and work with them to control the urge to use alcohol or drugs. The persons at highest risk are those persons who have a pre-injury history of addiction or abuse of substances. These same persons tend to have a genetic propensity to "crave" alcohol or drugs and a family history of abuse. The common denominator appears to be low serotonin production. Some people are born with a serotonin deficiency which produces a chronic, low level dissatisfaction with life known as dysthymia. While this condition can be effectively treated with drugs like Prozac or Zoloft, many people with the condition go undiagnosed and end up using alcohol to make themselves feel better. Alcohol abuse causes insomnia which further depletes serotonin. Other people actually create their own neurotransmitter deficiency. One brand new example is the use of the drug Ecstasy. A study in Neurology published on 7/25/00 indicates that autopsy of young ecstasy abusers shows a 50-80% reduction in expected levels of serotonin for age matched controls. We also know that heroin addicts who are tricked into buying a certain form of synthetic heroin destroy the part of the brain which produces dopamine, and they develop Parkinson's Disease. Persons who become euphoric with speed or cocaine, get extra secretion of dopamine, because there is an absence of serotonin to blunt excitatory glutamate transmission from the pre-frontal lobes to the dopamine producing area of the midbrain.

One  tip off or red flag to the clinician should be the role of alcohol in the occurrence of the injury or presence of high blood alcohol content at the time of injury. Astute clinicians who are on the look out for a history of substance abuse can then guage the potential for relapse under the stresses of the TBI, and guard against it. Statistics show that relapse can be prevented and that substance abuse can be eliminated or controlled in rehab, and after, when the treaters are aggressive in dealing with it. Ignoring a pre-injury history of addiction, and failing to be pro-active, are the surest ways of promoting a return to substance abuse during the rehab process. Since excessive consumption of alcohol sedates and slows the activity of brain cells, impairs new learning (skill acquisition) and blunts regeneration of damaged neural circuitry in the brain, it is imperative to use the rehab process to stop such abuse. Preventing relapse will maximize the survivor's chances of good recovery of brain function. Treatments include 12 step groups, individual psychotherapy, drugs like buspar or sinequan which decrease anxiety by activating the GABA circuits in the amygdala, drugs like Prozac or Zoloft which eliminate the craving for euphoria by increasing serotonin and drugs like Naltexone which block activation of the reward center (and resultant euphoria) that accompanies drinking. Heavy alcohol intake is bad for anyone, because it burns up glucose needed for mental activity and leads to a protein deficient diet with undersupply of important neurotransmitters. Hypoglycemia and neurotransmitter deficiency hit TBI patients harder, because they are working with less. Further, alcohol can trigger epileptic seizures.

NUTRITIONAL SUPPORT:

There are no "magic bullets" in the fireld of nutrition that will cure a TBI. However, proper attention to good nutrition can help TBI people ride out rough spots in their day more smoothly. High protein foods in the morning (like a soy protein/banana milk shake, yogurt or cottage cheese) will furnish tryptophans and other slow burning proteins for focused mental energy during the day. A bowl of hot oatmeal with fruit and milk will provide a good mix of proteins, carbs and fat. Sprinkling some wheat germ in your protein shake or on your oatmeal will extend the benefits. Some fats in the diet are needed to supply fatty acids for daily maintenance of myelin sheathing of axons, neuronal cell membranes and other brain structures. A little fresh butter on your oatmeal or a low fat fruit scone is fine. Don't skip coffee. It not only produces mental sharpness but for headache sufferers, it helps by increasing the ability of the stomach to absorb aspirin or acetaminophen, and speeds relief. A crunchy green leaf salad stocked with veggies for lunch is a good natural source of vitamins, minerals and roughage for the health of the bowels. A hard boiled egg or a little mound of tuna will provide protein to slow the consumption of carbs and feed the brain with neurotransmitters for alertness and concentration. A turkey sandwich on whole wheat bread with mustard is fine, and the carbs will burn more slowly than with white bread. Drink plenty of water to prevent dehydration, flush out toxins and keep the kidneys healthy.  Complex  carbohydrate foods like pasta for dinner will supply brain chemicals such as serotonin for relaxation and improved sleep. Covering the pasta with fresh chopped tomato is a rich source of beta carotene for the immune system. Making a side dish of steamed spinach with lemon juice or flash sauteeing a dark green leaf veggie with garlic and tossing it into the pasta is equally good. While sweets for dessert release feel-good endorphins for a momentary feeling of euphoria, the extra sugar can race your brain when your goal is sleep, and too much sweets leads to obesity and heart disease.

Some general rules are don't skip meals, because hypoglycemia is bad for the brain and will cause "sugar crash." To combat a feeling of depletion in the afternoon, don't go for the donut. Eat like an athelete instead - have some dried fruit, a whole grain fruit bar or some trail mix. Stoking the immune system with Vitamin C is also a good idea, since TBI tends to compromise the immune system.  This can be done in the morning with a 4- 8 oz. glass of orange juice plus a 500 mg. chewable OJ tablet. Studies show this regime of taking Vitamin C also protects against stroke and heart disease. By eating in this way, you will promote better health, stabilize your mood and keep your mental energy up. Remember that "eating" is different from getting nutrition through pills or powders at the health food store. Although some nutritional supplements are harmless, and may be good for you in small doses, some supplements are actually or potentially harmful. The Wellness Letter of the UCSF Medical Center recently reported that freeze dried, blue green algae from Upper Klamath Lake, Oregon, marketed as Aphanizomenon may be injurious to your brain, because it is harvested from lake water with populations of  other algaes which contain neuro-toxic substances called microcystins. Take special care to check out the toxicity research on any nutritional supplement before you start consuming it. The Wellness Letter quotes Dr. Verro Tyler (a nationally respected expert on herbs) as saying you are much better off eating a carrot than ingesting Aphanizomenon. Does good nutrition substitute completely for medication, psychotherapy, speech therapy, cognitive remediation and other forms of therapy? Of course not, but it is a nice complement to them and is a way of taking care of yourself. In addition to eating well, try very hard to get at least 30 minutes of exercise at least 4 days a week, even if that exercise is limited to a brisk walk. Wheelchair bound people can work out their upper bodies on Cybex machines or similar machines at the YMCA or a fitness center. Exercise stimulates immune function, promotes heart heatlh and increases blood flow to all parts of the body including the brain. It also releases brain endorphins, which put people in a more positive frame of mind.  

EFFECTS ON THE FAMILY:

A TBI occuring to one member of a family has immediate and long term emotional, social and financial consequences to the family as a whole. A severe TBI to one member will stress the family, test it and change it forever. Some families are devastated and fall apart.  Others pull closer and become stronger in the face of challenge and adversity. The perpsective of the family on TBI will always be different from that of the treating doctors. The family has an open-ended horizon and wants to know what comes next, and how do we deal with it? Doctors seek closure. They  are concerned with the survival, stabilization and discharge of the patient from the hospital, so they can move onto the next trauma victim. How much a family should be told at the hospital depends in part upon how much information they want and are ready to handle at that moment. While a few doctors may dump too much negative news, too fast, most err on the side of not disclosing enough and failing to the give the family a detailed roadmap of what lies ahead. In general doctors will meet with the family just before discharge and impart generic "information" about TBI along with a prognosis based on group statistics rather than an individualized study of the patient. Many families are in "denial" about just how impaired their loved one is when he first comes home or at least naive about what is likely to happen. Very understandably they are thankful he survived, excited to get him back home at last and eager to celebrate every little sign of progress to reassure themselves things will be OK. Statistical studies show the average family does better coping the first year than it does the 5th year out. Between the lst and the 5th year, progess in recovery slows, and the family comes to understand that certain cognitive and behavioral problems are not going to go away, and that their injured member will remain dependent on them.  During this extended time frame, the family becomes socially isolated because of the huge demands of caregiving and lack of opportunity to socialize with friends. Very often the caregiving spouse experiences clinically significant distress, anxiety, tension and depression, which merits psychological intervention, even medication, for the caregiver.  Caregiver burnout and family deterioration are likely to result in the absence of outside support. How could any family know at the outset how difficult this would be or prepared to meet all the objective and subjective burdens? This is not their fault. There are no courses in high school or college for this, and it is certainly not common knowledge. What can be done to make things easier, and bring hope and help to these families?

Certain types of outside supports have proven valuable in keeping the family afloat. Respite care involves a paid helper or volunteer watching the injured family member, while the caretaker gets to refresh herself with an activity of her choice, be it extra sleep, a movie, a walk in the park or having coffee with a friend. Social skills training to the family member with the TBI is very useful. To the extent he learned things like how to take turns in conversation and how to avoid stressful social situations which cause overload, he can leave the house more to be with others. Job training will improve his self-confidence and self-esteem and provide chances to socialize. Recreational outtings will put some fun back into his life and increase his sense of being part of the community again. Having the injured family member and caregivers participate in a TBI support group is very helpful. This is a place to share common experiences and feel less alone, to learn new coping skills and strategies and become more informed.

The neuro-rehabilitation literature establishes that the skills learned during in-patient rehab are not easily retained or easily transferred to the home enviornment; and that a great deal of practice, repetition and reenforcement are needed. To make rehab work there must be a direct extension of rehab into the home. Ideally there should be frequent, open-ended communication between treating doctors and family members after the patient was discharged from care. Families find hospital consultations to be of limited value when the doctor is lecturing to or "talking at" them, rather than listening empathetically to their concerns and seeking ways to support them in their role as lifelong caretakers. What most families says they want is for the doctor to visit the house, see for himself what is going wrong in the actual home environment and coach the whole family on new strategies. What do families have to deal with? Examples include: an adult child who is always late because he constantly loses his keys, wallet or glasses; a parent who cannot be taken to a restaurant or movie theatre because he uses profanity in a loud, booming voice or laughs loudly and uncontrollably at things only he finds funny; a family member who keep touching and poking other people during conversation, who will not stop no matter how annoyed or upset people get at him; or one who seems always to take too much or too little of his prescription medication, getting himself sick in the process, no matter how hard the family tries to devise a system for proper medication use. These burdens are great but can be handled with the right mixture of patience, humor and a strong belief system, be it religion, the value of self-reliance or other. Organizations including TBI support groups, the state brain injury association and caregivers' alliances should be contacted and asked for assistance. If there is a personal injury claim, then the attorney representing the brain injured loved one, can also be a source of informational guidance, physician referral, social service referral and emotional support. If workers compensation or the HMO is willing to pay for the services of a case manager, this is a great help, because a certified case manager has access to huge web of services, and knows how to access them at lowest cost. There is no doubt that the survival and well being of the family are linked with the survival and well being of the family member with TBI. If they become overwhelmed and burnt out, the TBI survivor suffers and so do the other children, whose emotional development can be harmed. But if they get the help they need and grow into their new roles, everyone will make it.

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EFFECTS ON SOCIAL RELATIONSHIPS:

Following a TBI friends seem to disappear. It is very typical for survivors of a TBI to experience social isolation and loneliness. What factors are involved? It begins with a lengthy period of hospitalization and rehab when the injured person is out of the social loop, allowing the social caravan to move on without him. More dedicated friends will make an effort to call or come over for a visit, but the brain injured person is no longer the same outgoing, funny and witty person they once knew. He is often depressed. He may suffer from conversational slowness,  word finding difficulty, perseveration (repetition of ideas or words), poor memory of what was already said, loss of affect or emotional blunting, or emotional lability (pathological laughing or  crying). During long conversational pauses some visitors feel awkward. There is often acute emotional discomfort in the social visitor who may feel guilt that he is healthy and unimpaired, while his friend is having so much difficulty. Often friends censor what they will say and become hyper-cautious, out of an exaggerated fear of saying anything inadvertently to offend or wound their injured comrade. Some friends even withdraw because being around someone with a brain injure evokes a fear in them of their own vulnerability to injury, disability or death. When a spouse, lover or friend leaves for good, they usually say something to themselves like "I feel bad about this, but he is not the same person I chose to be with." Obviously this is not fair to the person with the TBI, because he did not chose to become brain injured and he needs love and social support to help him recover his capacity for self-acceptance, self-esteem and feeling joy again in everyday life. Very often a TBI person is left dependent on his own immediate family for a social life, which places great burdens on his family. It would be best for the TBI survivor and his immediate family if the injured person could hold onto good friends or make new good friends. What advice do people with a TBI give on this point? Most will say don't judge me, don't feel sorry for me, don't patronize me, just accept me as I am now... accept me for who I am today, forget who I used to be. When taken to heart this advice can make a big difference and pave the way for true acceptance and true friendship in the present.

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PREVENTION OF BRAIN INJURY:

Because traumatic brain injury is not reversible or curable, at  our current level of medical knowledge and skill, prevention is still  the best way to avoid the disabling effects of a TBI. Remarkably adults still ride in cars without wearing their seatbelts, and they still forget or neglect to properly fasten infant car seats. A tragic example from the newspapers is the needless death of Kansas CIty Chiefs linebacker Derrick Thomas 2/8/2000. He suffered head injuries and severance of his cervical spinal cord from a car accident,  because he chose not to  wear his seatbelt  while driving with friends at night in bad weather. On 1/30/2000 the national BIA reported that 30% of children still ride unrestrained in cars, and that 85% of infant car seats are not properly fastened. A new TBI occurs every 15 seconds in our country. Each day one child dies and 50 others sustain permanent brain injuries from bicycle accidents. Nationally the rate of helmet wearing by child cyclists is very low. This is not acceptable.

However, there are some bright spots. In Seattle, WA, physicians Abe Bergman and Fred Rivara developed a program for subsidized production of safer bike helmets  with instruction on proper usage for school age children, and reduced the rate of TBIs from childhood cycling accidents by two-thirds. BMW has just begun selling a car with improved seat and headrest deisign to lower the incidence of TBI in rear-end auto crashes.
NHTSA is taking steps to reduce the incidence of tbi. One example is collecting and releasing data concerning the relative risk that a given automobile will "roll over" in an accident along with an easy to understand ranking scale. Another, is its recommendation that all states enact laws to require child safety seats for all children lighter than 80 pounds. As of August 2000 California was moving to enact a law requiring car safety seats for children younger than 6 or lighter than 60 pounds.

Here in California, as a result of lobbying by our state brain injury assocation, the legislature enacted a helmet law effective 1/1/92 requiring all motorcycle riders to wear a helmet. In 1991 there were 512 deaths and 16,910 injuries from motorcycle crashes in California. Although motorcyclists made up just 4.2% of licensed drivers, they accounted for 11.3% of all motor vehicle fatalities and 17.5% of all severe injuries, and most of them did not carry medical insurance, so taxpayers footed the huge health care bills to treat their catastrophic head injuries. As a result of that law, and police enforcement, fatalities from motorcycle accidents dropped 30% and injuries dropped 20% in 1992, and have continued to decline since then. Consequently total medical care costs for injured motorcyclists dropped by $35 million (a 35% reduction) in 1993. See, "Putting a Lid on Injury Costs: The Economic Impact of the California Motorcycle Helmet Law." by Wendy Max, Phd et al. in Journ. of Trauma, Injury, Infection and Critical Care Vol. 45, Issue 3 (Sept. 1998). Yet, every year Harley Davidson finances a sophisticated lobbying effort to repeal that law, and every year the Brain Injury Association of California Board of Directors must drive to Sacramento and counter-lobby legislators to block repeal, and save the law. Traffic fines for non-compliance with the motor cycle helmet law have raised over $1 million per year for public funding of TBI rehab services to persons who cannot afford it. 

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