What is the Medical Definition of 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 mechanically 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 pillar 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.

If you have suffered a serious head injury call (877)-833-1168 to find a Traumatic Brain Injury Attorney to fight for the compensation you deserve.