The following excerpts are derived from the book The Healing Power of Neurofeedback: The Revolutionary LENS Technique for Restoring Optimal Brain Function by Stephen Larsen
This book explores a much less invasive but highly effective technique of restoring brain function, explaining the innovative therapy that restores optimal functioning of the brain after physical or emotional trauma. It provides an alternative to the more invasive therapies of electroshock and drugs and includes extraordinary case histories that reveal the powerful results achieved.
TRAUMATIC BRAIN INJURY (TBI)
Most people are surprised to learn that a relatively low level of force is able to cause minimal brain dysfunction and that every mild insult succeeds the first one has a cumulative effect on a brain’s response to life’s demands. Slightly slower processing and reactions times are the first effects of a mild injury, even without a loss of consciousness.
An intact skull injury is considered a “closed head injury.” While sounding tame enough, closed head injuries can be quite serious, with wash and “contra-coup” syndrome, etc. Concussions are in levels, and clearly not all concussions are the same. The “dings” that occur in sports, the confusion following the blow to the head that made us see stars, the “mild” rear-ending that made your glasses fall off, all have varying degrees of consequence on the physical structure of the brain and its function. The effect of these incidents becomes cumulative until that seemingly inconsequential event that becomes the tipping point as it is followed by symptoms that interfere with memory, sleep, mood, pain, and the ability to get along with people.
A Clinical Definition of Brain Injury: An insult to the brain, not of degenerative or congenital nature, caused by an external physical force that may produce a diminished or altered state of consciousness, which results in an impairment of cognitive abilities or physical functioning. It can also result in the disturbance of behavioral or emotional functioning.
How Common Is Brain Injury? (“Surely It Hasn’t Happened to Me!”)
Each year 1.5 million people in the United States experience a traumatic brain injury. Fifty thousand die, and eighty thousand begin living with long-term disabilities. The remainder struggle with a puzzling array of cognitive problems, fatigue, mood problems, and difficulties in relating to others.
An eye-opening comparison with other illnesses shows the lack of public perception about the extent of TBI. In 1999, there were 176,300 of breast cancer, and 43,700 deaths from it. Incidence of breast cancer, multiple sclerosis, HIV/AIDS, and spinal cord injuries cases combined totaled 241,381. This number is a small fraction of the incidence of TBI; yet very little research money goes to finding treatments for TBI. There is no celebrity or poster person championing the cause of this problem, and most of us don’t recognize the importance of traumas that we’ve had.
Most people are unaware that they have had a brain injury. For example, in a retrospective study of Canadian Football League players in 1997, 44.8 percent of them experienced concussion symptoms, but only 18.8 percent realized that they had had a concussion. The following interactions demonstrate the point.
How Does the Brain Get Hurt?
There are more TBIs than ever, due to motor vehicle accidents and falls during sport-related activities—snowmobiles, skiing, sky diving, etc. Despite the use of helmets, TBIs from bike accidents and comparable sports are on the rise, probably because people, thinking they are protected, take more risks. If helmets are worn properly, they may protect against fracture, but they give no protection whatsoever against whiplash action. (Our fragile jellylike brain is not well suited to moving rapidly through space when sudden changes of speed and direction are introduced.) Dr. Muriel Lezak describes what happens inside the skull when there is a trauma while the body is in motion:
The key to the trauma pattern is rapid deceleration. What happens is that a driver or passenger riding in a car suddenly is hit or hits something and the car stops very rapidly. There may or may not be an impact of the head against anything. What is important is that the head that’s been going along . . . at 30, 40 or more miles per hour, suddenly comes to an instant halt. The skull is stopped against a windshield or seat headrest, or the car body. Unfortunately, the contents of the skull don’t stop moving because they too have been carried along at the rate of 30 or 40 miles an hour.
When the skull stops, the brain—which in its natural state is kind of a gelatinous mass that floats on a slender stalk in a liquid bath—has all of the momentum of its forward motion added to the sudden impact momentum. This sends shock waves through the brain, and sets up a rotary motion of the brain within the skull. It has been demonstrated that the brain ends up being bounced around onto the bony cage of the skull as it’s being forced back and forth with great rapidity. The force of the spin shears and snaps nerve fibers and tiny blood vessels. Knocking about within the skull cage bruises the vulnerable areas of the brain.
Diffuse damage to these areas causes attention deficits, slow thought processing, and diminished bilateral integration. Slow processing in head trauma patients can be understood when likening the brain to a most enormous, elaborate computer. This computer has billions of connections and programs that run its various parts and intermesh with each other. Then mild diffuse damage is created by someone coming along with a little hammer who knocks off a few connections here and a few connections there. When you turn on the machine, most of the programs would be slowed down, and as they become more complex, processing speed would become slower and slower. Destruction of any single connection would create something like a short circuit that would have to be bypassed and compensatory programs would have to be developed: all of this increases processing time… These patients frequently cannot do two things at once; they are easily distracted from what they do, and their every action involves slowed processing.’
A simple whiplash results in astounding activity inside the skull. There are 2.55 million reported automobile rear-endings each year in the United States. Two-thirds of them occur at speeds of less than thirty miles per hour. Most people think of whiplash as being a possible cause of neck or back pain, but what about the inside of our heavy heads? The G-forces generated by an accident occur in four phases:
In the first 100 milliseconds the car moves forward from under the passenger, the torso rises causing compression, torsion, and shearing at the cellular level in the brain.
At 200 milliseconds the head starts back, causing shearing and compression on a macro level. Between 200 and 300 microseconds after impact, the body starts forward even faster than it went backward, with the head always lagging behind.
The head moves forward as the seat goes back. In a collision of 20 mph, at 100 milliseconds there are 18 Gs generated in the skull; at 250 milliseconds there are 2.3 Gs, at 350 milliseconds the force is down to 1.7 Gs and, finally at 400 milliseconds, the G force is at 0.8. In less than the blink of an eye a cataclysmic event has occurred in the skull.
Fibers in the brain become swollen and varicose, leaving the neurons alive but dysfunctional. If the fibers rupture, more permanent damage occurs. In mild TBI the most common damage is called Grade One Diffuse Axonal Injury, and does not result in loss of consciousness. But the physical damage it refers to is also accompanied by neurochemical changes brought about by the damage done to the physical structure of neural cells. These changes result in “paralyzed, dysfunctional brain cells that create increased vulnerability to further injury.” There is a neurochemical and metabolic cascade that begins within the first hour of insult and continues for up to 10 days post-injury.
These metabolic changes create cells that are not necessarily irreversibly destroyed but are alive, although existing in a vulnerable state characterized by an increase in the demand for glucose (fuel) and a reduction in cerebral blood flow (CBF), or fuel delivery. Consequently, the neurovascular system is rendered unable to respond to demands for the energy required to return to normal neurochemical and ionic environments.