Many psychiatric delusions appear to be associated with mild traumatic brain injury. Examples include content-specific personality changes, such as when the patient believes that family members are impostors or identical doubles. An extremely common delusion among domestic abusers and stalkers is pathological jealousy and preoccupation with another person.

Brain injury causes lesions that appear and change over time in the prefrontal cortex and its pathways to the older regions of the brain. This explains the wide spectrum of complex neurobehavioral complaints following MTBI: compulsive and explosive behavior, sensory anomalies, memory loss – as well as behavioral dis-inhibition, domestic violence, and alcohol intolerance.

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One of the biggest problems is the cognitive and neurological effects of repetitive head injuries (RHI). Almost every concussion causes some damage to the brain. Regardless of severity, a second brain injury can be life-threatening if experienced within hours or days of a first.

After one brain injury, you have a three-times greater risk for a second injury and an eight-times greater risk for subsequent injuries.

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If you are between the ages of 15 and 24 and drive a motor vehicle, ride a bicycle, or play sports, then you are at the top of the risk-list for head injury. Men are nearly twice as likely as women to injure their brains, but all of us are quite vulnerable.

Transportation accidents (cars, bikes, horses) account for nearly half of all traumatic brain injury, followed by falls (25%). Firearms (assaults and suicide) represent about 10%.

Falls are the most common cause of playground injuries and result in a higher proportion of severe injuries than either bicycle or motor vehicle crashes. Brain injuries account for 75% of children's deaths from falling off of playground equipment.
Traumatic brain injury is significantly underdiagnosed and has no cure, therefore prevention is crucial. Helmets, seat belts, air bags, and car seats have proven to reduce brain injury and death.

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Data from more than 2,300 hospitalized patients of all ages indicate that gender and age influence the outcome of serious brain injury. For children under ten years old, young girls were found to be four-times more likely to die from head injury than boys.

Hormones seem to play a role. Higher levels of testosterone in young men may offer protection by bulking up brain mass, just as it bulks up muscles. For young women, however, high levels of circulating estrogen could make them especially vulnerable to head injury.

In older individuals this injury "gender gap" is reversed. University of California, San Diego researcher Dr. Azadeh Farin said that "women in their 50s, 60s, or 70s are roughly twice as likely to survive traumatic brain injuries than men in the same age group."²

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Although young children with brain injury usually recover their mental abilities quite rapidly, they can have serious problems later. "These kids have incredible learning deficits even when the IQ returns to normal," said Dr. Sandra Bond Chapman, a University of Texas neurologist. She noted that 70% of children's brain injuries affect the frontal cortex.

Because growth in the brain's frontal regions continues throughout young adulthood, early injury there can damage formation of the protective myelin insulation around neurons . This can impair their ability to control emotions and inhibit inappropriate behavior. These kids have trouble responding to subtle social cues and planning difficult tasks.

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All concussions are cause for concern, but not all concussions are the same. Symptoms can include confusion, headache, concentration problems, mood swings, or sleep difficulties.

"Concussions are caused by a blow to the head," says Michael Goodman, M.D., a clinical assistant professor of Pediatrics and Neurology at Jefferson Medical College of Thomas Jefferson University, Philadelphia. "They can occur when a child falls and during any sport that can involve a collision of the head with another object – be it a head, a ball, or the ground."

To better help parents, teachers, and coaches evaluate the seriousness of a concussion, in 2000 a consensus group of medical and athletic associations developed guidelines to be implemented whenever there is a suspicion of a concussion.

The guidelines suggest that concussions should be graded on three levels. Dr. Goodman explains the three levels here.

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“With a GRADE 1 concussion, a child has a brief period of confusion and appears dazed without a loss of consciousness. During this time, for example, the child will respond inappropriately to an easy question. The symptoms disappear within 15 minutes.

At the first sign of a concussion, the child should be taken out of the game. He or she should be spoken to twice in a five-minute span to confirm that the child is not experiencing confusion.

This is a grade 1 concussion and if the child appears to be okay after five minutes, they can rejoin the game immediately.

But, if this scenario happens twice in a one-week period, the child should wait one week before resuming any sports.”

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“With a GRADE 2 concussion , the confusion can last from five minutes to an hour, but the child does not lose consciousness.

For a grade 2 concussion, the child should be spoken to in five-minute intervals until the child appears to be normal again.

The child should not resume playing but relax and stay away from sports for a full week.

If the symptoms do not disappear within a week, the child should be examined by a neurologist, who will likely recommend a neurological imaging test such as an MRI or CAT scan.”

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“With a GRADE 3 concussion , there is a loss of consciousness, even for a short time.

The most serious, a grade 3 concussion, requires that the child be brought immediately to a hospital emergency department where he or she will get a good neurological exam. If the results are normal – and the child was unconscious for only a brief time – the child can go home and resume sports in a week.

If the results of the exam are normal – but the child was out for a longer period of time – the child should refrain from sports for two weeks. If abnormal neurologic tests indicate a potential neurological problem, then the child should be given a CAT scan or MRI. “

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Dr. Goodman stresses that the three grade level descriptions are guidelines only, and that parents and children should heed the guidance of medical and athletic professionals during these situations.
He warns that anyone who sustains a concussion is at a greater risk for another. And, a person who gets a second concussion before the first one resolves is at risk for serious or, in some cases, catastrophic consequences.

But, he says, "kids and sports have been around for a long time. It is up to the adults who are involved in children's sports to keep a balance between safety and competition."
Dr. Goodman is clinical assistant professor of Pediatrics and Neurology at Jefferson Medical College of Thomas Jefferson University, Philadelphia.

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An injury to the head is just one way the brain can malfunction. Stress, disease, heavy metals, and poor nutrition can also diminish the brain's higher functions.

Nutritional supplements may be helpful in deterring violent and anti-social behavior. When vitamin and minerals were given to elementary school children with behavioral problems, it led to a reduction in the incidence of anti-social behavior.

The researchers said that "undiagnosed and untreated malnutrition may be impairing their brain function to such an extent that normal learning from discipline does not occur." ³

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Shaken Baby Syndrome is a closed head injury. An estimated 50,000 cases of this abuse occur each year in the United States. Twenty-five percent are fatal. But, the shaking doesn't even have to be very violent.

Researchers at the Royal London Hospital studied the brains of 37 babies less than a year old, who were suspected of dying from deliberate injuries. Three-quarters of the infants had died because of damage to a vital part of the spinal cord that controls breathing.

"We found an as yet unseen pathology focused on the craniocervical junction, the point where the brain meets the spinal cord," says neuropathologist Jennian Geddes. In very young babies, this area of their brain is uniquely vulnerable because their heads are relatively large and heavy, but their neck muscles are still weak.
"This is a type of damage that's not been reported before," Geddes said. It shows that you don't have to use a lot of force to injure a baby – just "vigorous unsupported movement of the head." ⁴

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An estimated 300,000 cases of traumatic brain injury occur each year from sports and recreation accidents. In a series of articles on TBI, the Journal of the American Medical Association (September 8, 1999) presented evidence linking sports-related concussions with lower scores on several tests of mental function.

Injuries associated with 10 different team sports (5 boys' and 5 girls') were surveyed at 235 U.S. high schools. From the data, more than 62,000 mild traumatic brain injuries are estimated to occur each year in these sports.

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One potential cause of mild traumatic brain injury that concerns researchers and parents is the heading of soccer balls – especially by children whose brains are still developing. Also, because younger girls are increasingly taking up the sport.

While little research has been done with children and adolescents, several studies have shown that adult soccer players have mental deficits measured in many parameters.

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A Norwegian study of active and former national soccer team players investigated the incidence of head injuries caused mainly by heading the ball. One-third of the players had central cerebral atrophy, and 81% had mild to severe deficits in attention, concentration, and memory. Players who headed the ball more frequently during competition had higher rates of cognitive loss. ⁵

In 1998, Dutch researchers showed that professional soccer players' performance on memory, planning, and visual-perceptual tasks declined as their number of concussions and frequency of heading the ball increased. ⁶ Amateur soccer players had similar results: performing significantly more poorly than control athletes on cognitive tests for attention, memory, and planning abilities. ⁷

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Although most sports-related head traumas come from contact with the ground, goalposts, or other players, heading soccer balls is an obvious factor – especially when practiced thousands of times during a season. A ball kicked at full force is estimated to hit a player's head with 175 pounds of force.

"No child under the age of 14 should head the ball," cautions Dr. Lyle Micheli, chair of the Sports Medicine Department at Children's Hospital in Boston.

He argues that kids have not fully developed the musculoskeletal maturity or coordination to properly handle a header until they're about 14 years old. Micheli also points out that some kids in the U.S. use larger, professional-sized soccer balls, whereas in Europe most children gradually work up to the adult-sized ball.

According to the American Academy of Pediatrics Committee on Sports Medicine and Fitness: "Head and facial injuries account for 4.9% to 22% of soccer injuries, of which approximately 20% are concussions. . . Eye injuries are another subset of soccer-related head injuries."

Regarding heading, their recommendation was published in a policy statement in the March 2000 issue of Pediatrics.

"Researchers have expressed concern about cognitive deficits appearing in youth soccer participants after much shorter exposure time to heading the ball. . . The potential for permanent cognitive impairment from heading the ball needs to be explored further. Currently, there seems to be insufficient published data to support a recommendation that young soccer players completely refrain from heading the ball. However, adults who supervise participants in youth soccer should minimize the use of the technique of heading the ball until the potential for permanent cognitive impairment is further delineated."

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A University of North Carolina study found that football players who suffered one concussion were three times more likely than other players to suffer a second concussion in the same season. This suggests that the brain is more susceptible to injury when it has not had enough time to recover from a first injury.

"We believe recurrences are more likely because injured players are returning to practice and to games too quickly after blows to the head," said Dr. Kevin M. Guskiewicz, assistant professor of exercise and sport science "Many clinicians are not following the medical guidelines that players should be symptom-free for several days before returning." ⁸

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A 1999 study of college football players found that their learning disorders and reduced neuropsychological performance were independently associated with multiple concussions. Verbal learning and memory appeared to be the most sensitive components in athletes with concussions. ⁹

A survey of retired professional football players found that 60% had suffered at least one concussion during their amateur or professional careers, and 26% reported three or more concussions.

A survey of retired professional football players found that 60% had suffered at least one concussion during their amateur or professional careers, and 26% reported three or more concussions.

When compared to players who had no concussions, the group with one or more concussions reported significantly more neurological symptoms. These included problems with memory and concentration, confusion, speech or hearing difficulties, numbness or tingling in extremities, and headaches. ¹⁰

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A growing body of data suggests that those who suffer repetitive head injuries in sports may be at greater risk for neurodegenerative diseases later in life. The cumulative damage from successive concussions can increase the risk of premature senility, Alzheimer's disease , and Parkinson's disease, neurologists warn. ¹¹

According to researchers at the University of Pennsylvania School of Medicine, the brain has an increased vulnerability to severe, perhaps permanent, injury for at least a full day following a concussion.

In a study with mice, the effects of a second brain trauma within 24 hours seemed temporary. The mice returned to almost normal and did well on tests of cognitive and motor skills.

But, at about 56 days, there was "a measurable breakdown in motor skills and, subsequently, a breakdown in the cells of the brain," said Tracy K. McIntosh, Ph.D., the Director of the Penn Head Injury Center.

"Our findings represent the first real attempt to look at the science behind head injuries – and we were startled to see how permanent the damage can be," he said. This has serious implications for amateur and professional athletes, as well as victims of abuse and accidents, because permanent cognitive damage is not immediate. The effects of repetitive head injury may not be felt for months later.

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The link between head injury and the risk of Alzheimer's disease (AD) is indicated by data from the MIRAGE study (Multi-Institutional Research in Alzheimer Genetic Epidemiology). Patients with AD were nearly ten times more likely to have a history of head injury that resulted in loss of consciousness. The study suggests that "head injury with loss of consciousness and, to a lesser extent, head injury without loss of consciousness, increased the risk of AD." ¹³

Research led by Dr. Douglas H. Smith at the University of Pennsylvania supports previous epidemiological links between a single episode of brain trauma and the development of AD later in life. In animal studies, scientists induced brain injury without direct impact, similar to what humans often experience in automobile accidents. Analysis of damaged brain cells revealed extensive amyloid beta and tau accumulation, as well as plaque formation – all typical findings in Alzheimer's disease. These changes were evident as early as 3 to 10 days after the injury. ¹⁴

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Researchers at Penn's Center for Neurodegenerative Disease Research (CNDR) compared the brains of people with a genetic history of Alzheimer's disease with the brains of those with Dementia Pugilistica (DP), a memory disorder also known as Punch Drunk – or Boxer's – Syndrome.

Abnormal tau proteins, which form fibrous tangles in the brains of AD sufferers, are identical to the abnormal tau proteins found in patients with DP. Although they share the same pathology, AD and DP lesions are generally found in different parts of the brain.

"Our findings suggest that brain injury can cause Boxer's Syndrome by activating mechanisms like the ones that cause tau lesions in Alzheimer's," says M. Luise Schmidt, Ph.D., a senior research investigator at the CNDR. "By extension, it also suggests that a head injury can increase susceptibility to Alzheimer's later in life."

Boxers, of course, participate in a sport that exposes them to repeated acts of brain trauma, but the researchers stressed the need for care and protection of the brain in any sporting activity. Even those who seem fine after a traumatic event may not realize the injury's full impact until years later. ¹⁵

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A study of myelin disorder in Alzheimer's disease indicated an increased amount of free radical destruction. The authors said, "The changes in myelin from humans with Alzheimer's disease are more pronounced than in normal aging. These changes might represent severe or accelerated aging."¹⁶

In a 1989 Swedish examination of the autopsied brains of people with Alzheimer's disease and vascular dementia, the neuroscientists determined "the myelin sheath is the primary lesion site." ¹⁷

A 1994 study by the same team at the University of Goteborg concluded that membrane fats selectively diminished in Alzheimer's brains indicate that demyelination is a primary event in late-onset form (type II) Alzheimer's disease.¹⁸

In the University of Pennsylvania animal study mentioned above, analysis of brain tissue revealed diffuse axonal pathology. The scientists concluded that this microscopic injury to the brain caused by trauma could be linked to the development of Alzheimer's disease many years after the injury.

Striking personality changes can result when the pathways between the prefrontal cortex and other regions of the brain are impaired – due to axonal shearing and the consequent free radical damage to the myelin sheath.

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An analysis of injured World War II veterans links serious head injury in early adulthood with Alzheimer’s disease in later life. The study by researchers at Duke University and the National Institute on Aging also suggests that the more severe the head injury, the greater the risk of developing AD.

While the findings do not demonstrate a direct cause-and-effect relationship between head injury in early life and the development of dementia, they show an association between the two that needs to be studied further. ¹⁹

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Children who experience early damage in the prefrontal cortex never completely develop social or moral reasoning. As adults, even on an intellectual level, they cannot refer to such behavior because they have little concept of it. In contrast, individuals with adult-acquired damage are usually aware of proper social and moral conduct, but are unable to apply such behaviors.

Neurology professor Dr. Antonio Damasio and colleagues at the University of Iowa College of Medicine reported on two cases of early brain damage to the prefrontal cortex. As adults, both patients showed the same two distinctive features: an almost total lack of guilt and an inability to plan for the future – but were normal in almost every other type of mental ability.

The patients had problems with violence and resembled "psychopathic individuals, who are characterized by high levels of aggression and antisocial behavior performed without guilt or empathy for their victims," commented Raymond Dolan of Institute of Neurology in London. Their brains were just not capable of acquiring social and moral knowledge even at a normal level. ²⁰

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Since the 1980s, scientists have correlated damage to the prefrontal cortex with psychopathic behavior and the inability to make morally and socially acceptable decisions. Unfortunately, this forehead region of the brain is often the site of injury.

Researchers at the University of Sweden have found the prefrontal cortex to be precisely the area of the brain that is impaired in murderers, rapists, and other violent criminals who repeatedly re-offend. At the November 1999 annual meeting of the Society for Neuroscience, Asa Bergvall presented findings on their study of violent offenders. The results were quite startling.

"The violent offenders are like the controls in every task but one, which taps prefrontal function," says Bergvall. "In that, it was as if they were retarded." They had an impaired ability to shift their attention in order to view the world in a different way – a function linked to the lateral prefrontal cortex. Other, higher order executive functions of their prefrontal cortex appeared to be unimpaired.

University of Southern California psychopathologist Adrian Raine has documented prefrontal damage in people with Antisocial Personality Disorder, which is characterized by irresponsibility and deceitfulness, lack of emotional depth and remorse. The antisocial men actually had 11-14% less brain tissue volume in their prefrontal cortexes, compared to normal males – a deficit of about two teaspoons' worth." ²¹

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The "amygdala" is a pair of small almond-shaped structures situated between the cerebral cortex and the limbic/emotional center of the brain. When this neural circuit for processing emotional information is damaged, the prefrontal cortex cannot interpret feedback from the limbic system.

Uninhibited signals from the amygdala lead to free expression of emotions, and may manifest in violent and aggressive behavior, a common complaint following mild traumatic brain injury. The amygdala is responsible for emotional reactions that have to do with survival, including our ability to learn what is fearful to us.

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Like personal tectonic plates, the human braincase is composed of eight unique cranial bones. On either side of your skull, layers of material help protect your brain from normal wear and tear. On the outside are muscle, skin, and hair. On the inside, connective tissue and fibrous membranes do the cushioning. Within your skull, your gelatinous brain floats in a sea of cerebrospinal fluid that bathes and supports this precious organ, while acting as a shock absorber during rapid head movements.

Although the outer surface of the skull is smooth, parts of its inner surface are rough and jagged and can cause significant damage in acceleration/deceleration, or "closed head injuries." In this type of injury there may be no external damage, but because the head abruptly stops after being in motion, the brain rebounds back and forth against the skull's interior bony structures. This trauma initiates a cycle of biochemical events responsible for the major long-term deficits associated with brain injury.

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Unfortunately, the area of the head most vulnerable to injury is also where the most fragile and crucial region of the human brain is located. Behind your forehead lies your prefrontal cortex , the center of your higher-order "executive functions," as well as home to your social awareness and moral conscience.

Injury to the prefrontal cortex can affect your most human qualities: the ability to process information and solve problems; to concentrate, remember, and learn. Damage here can lead to personality changes that manifest in impulsive and socially inappropriate behavior, depression, and violence.

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The prefrontal cortex is the last to form the deep fissures that give the outer layer of the human brain its characteristic cauliflower-like appearance – and its vast array of higher functions. In the womb, this area is the slowest to develop. After birth, brain cells in the prefrontal cortex form connections more slowly than any other brain area, and levels of the key neurotransmitter dopamine rise very gradually.

The prefrontal cortex bestows humans with "executive functions," such as working memory and multi-tasking.

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The area above your eyes is sometimes called the "dashboard" of your brain. Like the dashboard of a car – where bundles of insulated electrical wires connect to the vehicle's other systems – your prefrontal cortex is integrated with regions deep in your brain by bundles of insulated nerve fibers.

Here, a subsystem in the prefrontal cortex (the orbitofrontal region) is supported by sharp-edged bony protrusions of the skull's interior. Although the protrusions do a good job of protecting the olfactory cranial nerve, they become a highly significant factor in brain injury during acceleration-deceleration forces to the brain.

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Source memory refers to remembering when or where something happened. Although persons with prefrontal cortex damage can recollect people, events, and facts, they may not be able to recall when the event happened or where they learned the fact. Their brains cannot access and integrate the diverse aspects of a stored memory.

Source memory is one of the slowest types of recall to develop in childhood, and the first to deteriorate with age. (This may be why young children can be so easily led astray by suggestive questioning.)

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Working memory is a simple term for the amazingly complex ability of your brain to temporarily hold and simultaneously compare present sense data with past images from its archives. Not just old factoids, these stored memories are reanimated and imbued with the emotions that originally created them.
Unfortunately, this higher brain function is quite vulnerable to injury.

Although many individuals with traumatic brain injury perform well on standard neuropsychological tests, they often exhibit significantly greater deficits on measures of executive function, including an impaired working memory.
Also, in patients with high blood pressure (hypertension) whose working memory was measurably impaired, brain scans showed a decrease in blood flow to the prefrontal (and parietal) region of the brain.

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What usually happens in brain injury at the cellular level is a combination of primary and secondary damage known as "axonal injury." Axons are the microscopic nerve fibers of neurons, the brain cells that communicate with each other. Axons form the long connecting nerve fibers of the neural networks throughout the brain.

After a closed head injury, the shifting and rotation of the brain inside the skull causes a shearing injury to the brain's complex circuitry. This axonal shearing can occur in localized areas or throughout the brain. The latter is called "diffuse axonal shear." Furthermore, the brain cells particularly important to learning and memory (cholinergic neurons), are apparently more vulnerable to trauma than other neurotransmitter systems.

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Axonal shear is a microscopic tear along the myelin sheath surrounding the nerve fiber that is often followed by microswelling and the formation of scar tissue. According to Kit W. Harrison, Ph.D., at the Houston Behavioral Health Associates:

"First, the nerve fiber itself may be damaged and begin to swell. The swelling usually acutely reduces functioning of that cell but some neurocognitive functions may be restored soon after as swelling reduces. The process of scarring, however, follows and can take weeks, months, or even years, to complete. As the axon scars over, fewer and fewer impulses can be carried through the tough scar tissue, and the axon may begin to necrotize (die) and lose connectivity function over time. This accounts for a number of symptoms which could worsen with time."

For the past decade, Drs. Maxwell and Graham at the Institute of Biomedical and Life Sciences, University of Glasgow, Scotland have focused on the effect of brain injury at the level of the axon. They have concluded that "two different mechanisms of injury may be occurring in non-impact injury to the head. The first is shearing of axons and sealing of fragmented axonal membranes within 60 minutes. A second mechanism occurs in other fibres where perturbation of the axon results in axonal swelling and disconnection at a minimum of 2 hours after injury." ²²

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Researchers at the University of Pennsylvania Medical Center have determined that after brain trauma one of the initial events triggering long-term problems includes a massive flood of electrically-charged calcium atoms that enter axons.

"It appears that that the physical motions of trauma literally tears open proteins that act as gates on the axon membrane," explains Douglas Smith, MD, an associate professor in the Penn Department of Neurosurgery. "We have now found that it is the rapid flow of sodium ions through the damaged gates that triggers a subsequent inflow of calcium ions."

By evaluating therapies that block the sodium channels, Smith is convinced that the damage can be slowed down and eventually even stopped. ²³

Hours, even months, can go by after a head injury before progressive damage to the axons becomes so severe that the neurons can no longer function.

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Myelin is a fatty substance that coats and protects the axons. A myelin sheath insulates these individual axons and is crucial to the speed and accuracy of its electrochemical impulse. If the myelin sheath is structurally damaged, then its electrophysiological properties are disrupted, and the electrochemical impulse will become abnormal and uncoordinated down the length of the axon. Consequently the information being conveyed by these nerve fibers will be scrambled or cut off.

Most significantly, "myelination" of the prefrontal cortex is especially slow – not beginning until the ninth prenatal month, and continuing as late as the mid-twenties. That's why brain injury at an early age can be the most devastating.

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A key factor in recovery time is the extent of damage to the white matter, the myelinated neuronal axons that serve as cables linking the different areas of the brain. When they are injured, then vital connections needed to allocate functions elsewhere are lost.

"The involvement of white matter tracts portends slower and reduced recovery," said Dr. Keith Thulborn, director of MR research at the University of Illinois. "This may reflect reduced capacity to redistribute workload when the connectivity through white matter is disrupted."

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Children suffer 50,000 bicycle-related brain injuries in the U.S. each year, and more than 400 of them die as a result. Helmets are the single most important way to prevent a serious head injury in a bike crash. Bicyclists who wear helmets can reduce the severity of brain injuries by as much as 85%, however half of all bike riders still do not regularly wear a helmet.

According to the Consumer Product Safety Commission, the rate of head injuries caused by bicycle accidents actually increased by 51% during the 1990s – even as ridership declined and helmet use became more widespread.

Factors that account for this include more aggressive riders, more traffic, and fewer safe places to ride.

But don't be complacent. Helmets do not prevent accidents. To be effective, they must be worn correctly.

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In the rough and tumble sport of rugby – whose players do not wear helmets – as many as 25% of injuries appear to involve the brain trauma of concussion.

A quarter of playing days lost from rugby involved such head injuries. ²⁴

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Helmets would also prevent brain damage in water and winter sports. Head injuries account for 29% of all jet-ski injuries and 15% of sledding accidents. They are the leading cause of death and serious injury among skiers and snowboarders, mostly from collisions with a tree. Many of these head injuries could be prevented if helmets were worn.

Motorcycle riding has 16 times the death rate per mile compared to automobiles. Riders without helmets are 10 times more likely to need brain surgery due to head injury. A 1997 report by the National Highway Traffic Safety Administration showed that helmets do not restrict hearing, nor do motorcyclists have trouble compensating for any restriction of vision. When motorcyclists wear helmets, death is reduced by 38%.

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