Kayle Sandberg-Lewis, MA, BCN

In April 2000, Betty, a 41-year-old female, was riding her bicycle when a car going 40 mph hit her. Although she lost consciousness for a short while, she was up and walking around by the time EMTs arrived. She complained of feeling dazed, having some hip pain, a slight headache and slight back pain. At the hospital, a CT scan was done, the results of which were negative. She was given Motrin and Vicodin and sent home.

Over the next several weeks, Betty returned to her physician’s office repeatedly, complaining of head pain and increasing mental fog. She was prescribed antidepressants. The following September, Betty’s left leg collapsed and she lost mobility in her left arm. Her primary care physician prescribed a course of physical therapy and acupuncture, and eventually sent her to a neuropsychologist to deal with her growing cognitive problems.

Increasingly, she was unable to process new information. For example, during this time, she changed apartments and although she could consistently get on the correct bus home and get off at the right stop, she repeatedly lost her way from that point, sometimes having to call friends for help.

About this time, a family member visited Betty and was alarmed by what she found. Instead of the woman who remembered minute details about every aspect of her busy life, there was a fuzzy thinker who needed to write down every detail to get through her day. She used a small spiral notebook, when she remembered she had it, and always returned it to her right hip pocket. The problem came when she needed to consult her notes – she forgot the notebook and the pocket. At that point, the entire extended family pressured Betty to move to Portland to live with family members until she could get back on her feet.

By the time Betty and her sister arrived in my office, it was August 2001 and Betty had been diagnosed with post-concussive syndrome – another term for Traumatic Brain Injury (TBI). Her chief complaint was that she could no longer learn. Known in her family as a voracious reader who “consumed” books, Betty’s family was perplexed that Betty could no longer track a 30-second television commercial. Betty was also known for her uncanny ability to remember names and faces. No more. Betty’s sister mentioned that although Betty had met the neighbors several times, she was unable to recognize either of them.

In addition to frequent headaches and body discomfort, Betty complained of a lack of energy. Her family characterized this as a loss of ambition.

Symptoms of TBI

This distinction is extremely important for the clinician to understand. Generally, the person with TBI is acutely aware of deficiencies, but often unable to communicate much more than a vague, “something’s not right.” On the other hand, close friends and family may be outspoken about what they see as increased confusion, forgetfulness and, perhaps, willful laziness or malingering. By the time cognitive deficits set in, it is not uncommon for the TBI survivor to have healed most, if not all, external signs of injury.

TBI is defined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain. It is a non-degenerative, non-congenital insult to the brain from an external mechanical force, resulting in cognitive, emotional, sensory and motor impairments that can lead to a variety of temporary or permanent disabilities (University of Minnesota, online posting).

On her second visit to my office, Betty expressed anger. She said she was feeling pressured by her family to “just get over it.”

It is not uncommon for TBI survivors – and, indirectly, their loved ones – to suffer from:

• Anhedonia: Loss of sense of pleasure; inability to be moved by beauty.
• Adynamia: Apathy; dull or flat affect. Activity is difficult to self-initiate and the individual may appear unmotivated or lazy.
• Aphasia: Inability or difficulty expressing thoughts and understanding others. This may include problems identifying objects and their function as well as problems with reading, writing and ability to work with numbers. Problems with pragmatic language, decreased vocabulary and word substitution may occur. Speech therapy may be necessary to work with language problems.
• Apraxia: The person may have normal mobility and comprehension, yet be unable to perform basic tasks, such as answering the phone or coordinating the use of a knife and fork. This can appear as a consistent problem or be intermittent.
• Chronic pain: Head and neck pain are most common, but the entire body can become engulfed in chronic pain.
• Depression: There are many contributing factors, especially a profound sense of loss of self.
• Disinhibition: Increased impulsivity. Conversations may be disjointed and erratic with tangential interruptions – often speech volume as well as content is poorly regulated. People who once were known for their circumspect, sober behavior may, after TBI, act in unacceptable ways in social situations. Yes, a person can be both adynamic and disinhibited.
• Disrupted sexual functioning: Loss of libido or – due to disinhibition – inappropriate displays of sexual behaviors.
• Disrupted sleep patterns: “Pattern” may be a misnomer when it comes to TBI and sleep, because there often seems to be no rhyme or reason to how people experience sleep. For days on end they may be unable to sleep more than a few minutes at a time, while at other times they can sleep for what may seem like too many hours. They may be difficult to rouse, or unable to sleep through even the most mild disturbance.
• Disrupted appetite: Over- and under-eating can become issues. It often seems to have something to do with memory: The over-eater forgets he ate and the under-eater forgets to eat.
• Distractibility: Even for people who do not appear disinhibited, it can be very hard to sustain attention to track conversations or logical thought sequences.
• Emotional lability: Extreme mood swings may become predictable – generally to everyone other than the survivor.
• Flooding: Being overwhelmed by one’s emotions – even in situations that appear emotionally neutral. It can happen anywhere, anytime. Many TBI survivors describe it as “freezing.”
• Memory deficits: TBI survivors usually suffer from what my clients have called “blank spots” and “empty rooms.” One of the more intriguing memory problems TBI survivors have is remembering that they had a head injury. People, after telling me repeatedly they have had no head trauma, frequently suddenly remember some devastating incident when they were either knocked out or seriously injured but did not lose consciousness.
• Motor deficits: These include paralysis, poor balance, lower endurance, reduction in the ability to plan motor movements, delays in initiation, tremors, swallowing problems and poor coordination.
• Problems tracking time: Time can swell and expand or constrict dramatically. It usually means that survivors have difficulty maintaining a schedule or keeping appointments.
• Oppositional/defiant behavior: Frequently characterized as stubbornness. Families and friends complain about this often. I find it logical that a person will dig in when faced with the unknown. Without the capacity to track conversation or draw on memory or logic, one is unable to predict outcome, which increases anxiety. It becomes seemingly safer to just say no.
• Sensory distortions: There may be a loss of sense of taste and/or smell, or these senses may become extremely exaggerated, causing nausea or other discomfort. Vision may become permanently or sporadically compromised. Tinnitus may set in. There may also be tactile interference – either with increased sensitivity or numbness.
• Speech deficits: Speech might not be clear as a result of poor control of the speech muscles (lips, tongue, teeth, etc.) and poor breathing patterns.

According to the National Institute of Neurological Disorders and Stroke, TBI can cause a wide range of functional changes affecting thinking, sensation, language and/or emotions. It can also cause epilepsy and increase the risk for conditions such as Alzheimer’s disease, Parkinson’s disease and other brain disorders that become more prevalent with age (NINDS, 2002).

The Brain is a Raw Egg

Most people believe such severe damage must occur only in situations involving high speeds or with extreme impact. If only that was true. There are 2.55 million reported automobile rear-endings each year in the US. Two-thirds occur at speeds less than 30mph. Alan J. Watts, PhD, an expert in force analysis, shock physics and impact damage, reports that a rear-end collision of “only” 20mph generates 18Gs of force at 100 milliseconds after impact. This generates compression, torsion and shearing at the cellular level (quoted in Larsen, 2006). This cellular damage is known as diffuse axonal injury (DAI) and often occurs without loss of consciousness. And once the brain is injured, it is much more susceptible to further insult. After one TBI, the risk of incurring a second injury is three times greater; after a second TBI, the risk for a third injury is eight times greater (Osborn, 2000).

The living brain is the consistency of a raw egg – a giant raw egg made up of more than 100 billion neurons and perhaps 100 times that many glia. The design of the head and neck – basically a bowling ball filled with the above-mentioned raw egg, balanced on a segmented broom stick – is great for mobility and binocular vision, but it is not at all suited to rapid acceleration/deceleration. When the skull suddenly stops, the brain keeps moving, slamming into the interior wall of the skull. Due to the snapping back and forth of the neck during flexion/extension, this can happen several times very quickly. And due to the fact that the mass of gray matter is different than the mass of white matter, those layers move at different speeds, also causing DAI.

Current imaging techniques generally do not show axonal injury. On the microscopic level, the axon may not be torn completely by the initial force, but the trauma still can produce focal alteration of the axoplasmic membrane, resulting in disruption of the action potential flowing down the axon. The axoplasmic membrane can swell and the axon then splits in two. A retraction ball forms, which is a pathologic hallmark of shearing injury. The axon then undergoes Wallerian degeneration – degeneration of the portion of the axon and the myelin sheath of a neuron distal to the site of injury. Dendritic restructuring may occur, with some regeneration possible in mild to moderate injury (Wasserman, online posting).

Use of Biofeedback

TBI survivors often turn to self medication, but because the brain is distorted in its functioning, the medications often have erratic or extreme effects. This, of course, may contribute to the tendency to re-injure oneself.

Once all this damage is done, how can a brain so traumatized be set right? Of course, we know that homeopathic remedies are priceless in their capacity to soothe and heal the brain. In addition, there is biofeedback.

Signals continually emanate from a living body as a byproduct of its functioning. As clinicians, we read these – for example, heart rate, breath rate and EEG – to assess physiological conditions. Biofeedback provides instruments by which the signals of physiological functions can be turned into information that is given back to the individual. That individual need not necessarily understand the information on a conscious level, which is why some forms of biofeedback, particularly neurofeedback (biofeedback for the brain) can work in training small children and animals.

Even in the naturopathic community, many people think of the brain as a primarily neurochemical organ. Medications are given with the intent of changing the EEG by influencing brain chemistry – neurotransmitters – which will change brain function and behavior.

For one with this mindset to embrace neurofeedback, it may require a paradigm shift. While medications can indirectly change the EEG, neurofeedback uses the EEG to change the EEG. This has been shown to have an effect on brain function, behavior and, ultimately, the need for medication. This is an electrochemical paradigm.

The brain is an electrical generator, capable of creating a spectrum of waveforms, each serving a purpose in our lives.

As indicated in Chart 1, the EEG we read on the surface is influenced by age and state. For example, delta waves – from about one-tenth to three cycles per second – are the signature waves of infants up to six months of age. They are also dominant during deep sleep in people of all ages. Stage-four sleep will be more than 50% delta waves (Thompson and Thompson, 2003). So when an older child or adult is awake but exhibits delta waves, it is a sign of cortical damage. While not all cortical damage is TBI, most brains with damage respond well to neurofeedback.

Information between neurons is relayed by neurotransmitters, while the information of the neuron is expressed in the electrical signal running down the axon. In the neurochemical approach, we are essentially changing the recipe for the soup that neurons live in. In the electrochemical approach, we are exploiting the signals that the neurons already make and, in the process, appear to affect the neurotransmitters released.

The way the brain learns is by generating new dendrites to catch those neurotransmitters. Our brains actually change shape as we learn, a phenomenon known as neural plasticity. The “beginner’s mind,” or the learning brain, has the most dendrites and is more able to recover from insult. When dendrites are not used over a period of time, the neuron, in an attempt to be efficient, will “shear” the dendrites. Unused dendrites are reabsorbed into the body of the neuron.

The signals we can access from sensor placements on the scalp are generated by the pyramidal cells in the cortex. Because of their alignment and synchronous firing, they create a current we can monitor. The firings of the cortical cells are influenced by subcortical structures, such as the thalamus and septum, and, through neurofeedback, the surface signals can be used to influence much deeper structures, including the brain stem where arousal levels are determined.

Two Methods of Neurofeedback

I use two methods of neurofeedback in my practice.

What has become known as the “traditional” method reads the EEG the brain is emanating. The practitioner determines which sites will be chosen – usually informed by neuroanatomy and neurophysiology to make placements situated on the scalp according to the 10-20 Electrode System of the International Federation in Electroencephalography and Clinical Neurophysiology – and what frequencies will be rewarded and/or inhibited. If there are particularly slow waves, faster waves may be encouraged or the slow waves may be inhibited or discouraged; or both. Because the brain is generating all signals all the time, it is simply a matter of monitoring the site, selecting an aspect of the spectrum to “feedback” and then conveying that information to the client in the form of tones, visual cues and/or tactile feedback. Most practitioners I know choose to be very generous with the reward signals, so the brain is hearing a lot of “yes!” To inhibit signals, most practitioners simply withhold rewards – meaning feedback is not given when there is not enough of a “yes!” and/or too much of a “no.” Negative feedback that would injure or discourage an individual is not used.

The other system I use, also with great success, is the Low Energy Neurofeedback System (LENS), which actually introduces a minute electromagnetic signal targeted to specific placements on the scalp. After taking generous data samples at a site, a pulse is administered for less than a second; it’s imperceptible to the client. The signal is smaller than that emitted by a battery-powered wristwatch. With this approach, a “map” of the brain is generated by following a modified 10/20 placement chart, sequentially placing a sensor on several of the scalp sites and reading the dominant frequencies and amplitudes of each site. The program’s software then sorts the sites, arranging them from most to least stable. Training then follows that path, working from stability to instability.

In truth, the two approaches have more commonalities than differences. Both require attaching sensors to the scalp with a thick conductive paste. Placements are chosen based on the individual’s presentation, although the method by which this is determined is different. Arguably, the most important commonality is that the results accumulate over time. On follow-up with clients who have not recently had neurofeedback, I am often told that the person’s functioning continues to improve. Clearly, this is not placebo, which generally wears off after about six weeks.

Why does such seemingly random and innocuous information matter to the brain? Even when injured, the brain, with its innate plasticity and trillions of redundant circuits, is a pattern-seeking learning device. I think of biofeedback as a way of holding up a mirror. Just as most of us need a mirror to get the spinach from between our teeth, the brain appreciates information about itself. With that information, it can heal itself.

Over the years, I have worked with hundreds of people whose brains have been injured through trauma, and can say with confidence that those people are often the first to respond to neurofeedback.

Results of One Patient’s Neurofeedback

So what happened to Betty? My initial recommendations involved addressing her breath patterns. It has been my observation that most trauma survivors have a “tucked” posture, which impedes breathing. With structural integration and use of biofeedback equipment that helped her see how her breathing patterns and cardiac activity interacted, she quickly developed better posture and was able to breathe more freely. Also, she experienced abdominal breathing to be analgesic and soothing to her underlying anxiety. I also suggested massage. Ashley Montague, social anthropologist, described the skin as “the surface of the brain.” There is no spot on the body that does not have neural connections to the brain. Safe, soothing touch can soothe the brain.

After our first session of neurofeedback, Betty started sleeping more – sometimes more than she wanted. Prior to the accident, she reported having been very active and never felt a need to sleep more than three or four hours per night. I attempted to convince her that her brain needed down time, but it was a difficult sell and she sometimes expressed dissatisfaction with her new sleep pattern.

On her third visit, she said, “After the accident, everything shut down. The EEG seems to be bringing everything back.” Even so, it was a slow process.

By August 2004, we had completed 135 sessions. She only rarely had head pain, had consistently restful sleep and quit smoking – a pleasant side effect of the training. Over the span of our work together, she moved out of her sister’s home, enrolled in a community college and completed a certification course in a technical program. She applied for and received rehabilitation counseling through the state. After her class work was complete, she received a job offer on the East Coast. At the time of her departure, she was still unhappy with her condition, expressing regret over the person she would never be again. At the same time, she recognized her accomplishments and her improved health and physical well being. When she arrived in her new city, she transferred to that state’s rehab program, where they offered her counseling. She told them in no uncertain terms that she wanted more neurofeedback. When she asked if I knew the neurofeedback provider they had offered to assign her, I was thrilled. Dr. Angelo Bolea, a neuropsychologist, is a psychophysiology pioneer, having done neurofeedback since 1984. Betty’s progress since working with him has been nothing short of stunning. I recently received this e-mail from her:

“If it hadn’t been for you, Dr. Bolea and neurofeedback, I’d be a veggie. I swear, I’m NORMAL again. Well, normal for me … I can REMEMBER what I read!

“I would like to do something so that more people become aware of the benefits of neurofeedback. I’m working as an intern at NCI/NIH. Actually, the computer support team for NCI.

“And none of this would have been possible without you, Dr. Bolea and neurofeedback.”

Effects of TBI on the Gastrointestinal Tract

Most physicians, even the naturopathic variety, think of head injury as affecting the head, spine and extremities, but not the digestive tract … at least, not in any major way. My research has shown that GI effects are enormous and often devastating. As early as three hours after sustaining a brain injury, the following changes have been seen in the GI tract of rats (World, 2003):

• Shedding of enterocytes
• Splitting and fusion of villi
• Ulcer formation
• Attenuation of GI mucosa
• Blood vessel dilation in the villi
• Gastric/enteral bacterial overgrowth.

Other changes include gastric distention, delayed emptying and intestinal dilation (World, n.d.).

Effects of TBI on Nutrition and Nutritional Treatments

Patients with acute head injuries develop increased energy and protein expenditures, with rapid weight loss and protein (muscle) wasting. High levels of stress hormones cause a high risk of infections, loss of appetite, increased intestinal permeability and an attenuated intestinal lining. Early enteral or parenteral nutrition has been shown to improve the outcome in humans with acute TBI (Cochrane Database System, 2000). In fact, the time between head injury and recovery of the ability to take food by mouth had the most predictive value for brain recovery of any other parameter (Acta Neurochir, 2004). Pre-acidified feedings effectively eliminated and prevented bacterial infection of the stomach (Critical Care Med, 1992). Considering the fact that routine use of proton pump inhibitors is standard in most ICUs, it is likely that these patients are suffering from bacterial overgrowth.

A feeding formula containing glutamine and probiotics decreased the infection rate and reduced hospital stay (ICU) in brain injury patients (Clinical Science, 2004). Creatine-enhanced diets provide neuroprotection by preventing secondary brain injury (Neurochem Res., 2004). Secondary injury is the toxic effect of free radical generation in addition to the mechanical trauma of head injury. There is an increasing body of research to support and demonstrate this concept.

Zinc, alpha lipoic acid, N-acetyl cysteine and vitamin E are antioxidants that provide this protection. For example, prior zinc deficiency significantly alters brain response to TBI, increasing nerve cell death (Journal of Neurotrauma, 2001). Alpha-lipoic acid crosses the blood brain barrier and provides antioxidant protection, regenerating vitamins C and E and raising intracellular glutathione levels (Free Radic Biol Med, 1997). Administration of N-acetylcysteine (NAC) protects the brain, reduces inflammation and improves free radical protection, thereby reducing nerve cell death (Neurosci Res, 2004). Free radical scavengers have also been shown to prevent post-traumatic seizures (Acta Neurochir, 2005).

With regard to vitamin E, tocopherols improve cognitive function in mice following traumatic brain injury (Glia, 2006). Tocopherols also stimulate dramatic nerve proliferation, therefore “establishing vitamin E as the most potent, known microglial mitogen in vitro” (Neurology, 1985). In rats, vitamin E preserves fatty acid levels in the injured brain, thereby stabilizing membranes (Neurotrauma, 2003).

Administration of niacin following TBI significantly reduced behavioral impairments in rats. These included sensorimotor performance and memory tests. B3 also reduced the size of the brain injury when given at 15 minutes and 24 hours after TBI (Brain Res Bull, 2006). Magnesium and riboflavin have also been shown to significantly improve recovery (additive effect) after TBI (Brain Res Bull, 2003). Magnesium therapy improves cognitive performance after brain injury in a dose-dependent manner (Brain Res Bull, 2003).

Botanical Interventions in TBI

Ginkgo biloba, an antioxidant/free radical scavenger, displays a variety of positive effects in TBI (Curr Drug Targets, 2000):

• Reverses losses nerve receptors
• Protects against neuronal death by preserving the brain’s blood supply
• Preserves function of the hippocampus
• Increases neuronal plasticity (nerve healing)
• Counteracts cognitive deficits after TBI or stress
• Improves energy production in the brain cells.

Maternal dietary supplementation with pomegranate juice was highly neuroprotective in an animal model of newborn brain injury – it decreased brain tissue loss by >60% compared to controls (Pediatr Res, 2005).

Hawthorn berry protected against brain damage in gerbils by decreasing free radical production and preventing neuronal damage in the hippocampus (J Neurochem, 2004).

TBI is different with every person and often inconsistent in its manifestations, but it is common for people to have difficulty in following directions and making well-informed decisions. They also often forget commitments and make bad business and personal choices, which may grow from increased difficulty in communicating with others. Consider TBI a possibility when dealing with your more inexplicable patients, and consider neurofeedback as a therapy.

Additional Reading

For additional reading on neurofeedback or TBI, I suggest:

Crimmins C: Where is the Mango Princess? A journey back from brain injury. New York, 2001, Vintage Books.

Larsen S: The Healing Power of Neurofeedback: The revolutionary LENS technique for restoring optimal brain function. Rochester, 2006, Healing Arts Press.

Osborn CL: Over My Head: A doctor’s own story of head injury from the inside looking out. Kansas City, 2000, Andrews McMeel Publishing.

Stoler DR and Hill BA: Coping With Mild Traumatic Brain Injury: A guide to living with the challenges associated with concussion/brain injury. New York, 1998, Avery.

Thompson M and Thompson L: The Neurofeedback Book: An introduction to basic concepts in applied psychophysiology. Wheat Ridge, 2003, Association for Applied Psychophysiology and Biofeedback.

References

University of Minnesota, PubH 6120 Injury Prevention. Available at http://enhs.umn.edu/6120/bicycle/index.html

National Institute of Neurological Disorders and Stroke. Traumatic brain injury: hope through research. Bethesda: National Institutes of Health; 2002 Feb. NIH Publication No. 02-158. Available at www.ninds.nih.gov/disorders/tbi/detail_tbi.htm

Larsen S: The Healing Power of Neurofeedback, Rochester, 2006, Healing Arts Press.

Osborn CL: Over My Head: A doctor’s own story of head injury from the inside looking out, Kansas City, 2000, Andrews McMeel Publishing.

Wasserman JR: Department of Diagnostic Radiology, Medical College of Pennsylvania-Hahnemann University Hospital. Available at www.emedicine.com/radio/topic216.htm

North American Brain Injury Society “Brain Injury Facts.” Available at North www.nabis.org/public/bfacts.shtml

Brain Injury Association of America: www.biausa.org/livingwithbi.htm

University of Minnesota, PubH 6120 Injury Prevention. Available at http://enhs.umn.edu/6120/bicycle/index.html

Thompson M and Thompson L: The Neurofeedback Book: An introduction to basic concepts in applied psychophysiology. Wheat Ridge, 2003, Association for Applied Psychophysiology and Biofeedback.

World J. Gastro, 2003 Dec;9(12):2776-81.

World J. Gastro, March;10(6):875-80.

Cochrane Database Syst. Rev. 2000;(3):CD001430

Acta Neurochir, 2004 May;146(5):457-62.

Crit Care Med 1992 Oct;20(10): 1388-94.

Clin Sci. 2004 Mar; 106(3):287-92.

Neurochem Res. 2004 Feb:29(2):469-79.

J Neurotrauma, 2001 Apr;18(4):447-63 and  Nutr Neurosci. 2002 Oct;5(5):345-52.

Free Radic Biol Med. 1997;22(1-2):359-78 and Pharmacol Rep. 2005 Sep-Oct;57(5):570-7.

Neurosci Res. 2004 May;76(4);519-27.

Acta Neurochir Suppl. 2005;93:27-34.

Glia. 2006 Apr 15;53(6):669-74.

Neurology 1985 Jan;35(1):126-30.

Neurotrauma. 2003 Nov;20(11):1189-99.

Brain Res Bull. 2006 May;69(6):639-46.

Brain Res Bull. 2003 Apr;60(1-2):105-14.

Curr Drug Targets. 2000 Jul;1(1):25-58.

Pediatr Res. 2005 Jun;57(6):858-64.

J Neurochem. 2004 Jul;90(1):211-9.

 

Chart 1: Brainwaves and Activity

1-3Hz, Delta: Dreamless sleep; movement artifact; brain injury; learning disabilities. Dominant in infants.

4-8Hz, Theta: If entirely low, tuned out; sleepy – doorway to and from sleep. Internally focused – important in memory recall. Inspiration, but may be lost if not processed immediately. Dominant in young children.

8-12Hz, Alpha: Visualization, meditation. High µV alpha can correlate with chronic pain (migraine). Dominant in visual field of adults when eyes closed.

12-15Hz, Low Beta or SMR: Can be readiness state seen in peak performing athletes. When along sensory motor strip, is referred to as sensory motor rhythm. Tends to correlate with calm focus.

15-18Hz, Mid-Beta: Tends to correlate with problem solving. Aware of self and surroundings. Generally required for learning a new task. Alert, but not agitated.

18-23Hz, ~40Hz Gamma: Generally correlates with anxiety (though other Hz can, too). Present during cognitive activity – related to attention and “binding” information. Only Hz group found in every part of the brain.

 

TBI Statistics

The North American Brain Injury Society states that worldwide:

• Of all types of injury, those to the brain are among the most likely to result in death or permanent disability.
• Brain injury is the leading cause of death and disability worldwide.
• TBI is the leading cause of seizure disorders.
• The World Health Organization (WHO) adopted standards for the surveillance of central nervous system injury in 1993 (North American Brain Injury Society, online posting).
• Every 23 seconds, someone in the US suffers a TBI (BIAA, online posting).

According to NABIS, every year in the U.S. alone:

• 1.5 million Americans are treated and released from hospital emergency departments as a result of TBI. (The combined annual incidence of Multiple Sclerosis, HIV/AIDS and breast cancer is 230,381.) (University of Minnesota, online posting)
• 230,000 people are hospitalized and survive TBI.
• 80,000 people are estimated to be discharged from the hospital with some TBI-related disability.
• 50,000 people die from TBI.
• An estimated 5.3 million Americans are living today with disability related to TBI.
• The highest rate of injury occurs between the ages of 15-24 years, usually due to vehicular and sports-related accidents. Persons younger than the age of 5 or older than 75 are also at higher risk.

According to the CDC, 260,000 people are hospitalized with TBI annually. And what is the combined price tag in direct care and indirect costs to society? A “mere” $56 billion (University of Minnesota, online posting). The incidence of mild traumatic brain injury (MTBI) in hospital emergency rooms appears to have increased – almost doubling from 216 per 100,000 in 1991 (Sosin, Sniedzek and Thurman, 1996) to 392 per 100,000 in 1995-1996 (Guerrero, Thurman and Sniezek, 2000). In contrast, MTBI hospitalizations appear to have declined from 130 per 100,000 to 51 per 100,000 between 1980 and 1994 (Thurman and Guerrero, 1999). And, there are the unknown numbers who suffer from injuries that are never reported.