Types of MTBI | Varieties in Damage | Effects on Brain Function

What Happens to the Brain after an MTBI?


Traumatic brain injury is an acute injury to the central nervous system. Essentially there are two types of head injury: a closed head injury and an open head injury. In a closed head injury, the skull is not penetrated. The primary damage to the brain is the result of the direct acceleration impact on the skull from an external force. The force causes the brain to move around in the skull, resulting in both diffuse (widespread) and focal (localized) damage. In an open head injury, the skull is penetrated, resulting in damage to a specific area of the brain. In both types of injury, there is accompanying secondary damage to the brain resulting from swelling, hypoxia (oxygen deprivation), cellular damage, and chemical changes within the cells of the brain.

The consequences of an MTBI are multifaceted and often include altered physiological functions of cells, neurological and psychological impairments, medical difficulties, and other challenges that affect the individual with the MTBI, as well as their family, friends, community, and society in general. An MTBI often goes undiagnosed due in part to the urgent care needed for other, more pressing physical aspects of injury and trauma. The consequences of MTBI can affect an individual across a lifetime and often present new challenges as the individual enters various stages of life.

The literature on brain injuries supports the premise that interventions in mild to moderate cases of traumatic brain injury assist the healing process, resulting in a significant decrease in the number and intensity of symptoms and a more rapid return to work or school. Research is demonstrating that early interventions (including exercises like the ones in this book) may be more beneficial for mild head injuries than for more severe injuries. Unfortunately this is still not a universal belief in the medical community, and these types of interventions are often neglected. As technologies in imaging advance, we are better able to identify the correlation between the symptoms associated with brain injury and the actual parts of the brain that have been damaged. Imaging usually involves the use of either CAT (computerized axial tomography), MRI (magnetic resonance imaging), SPECT (single photon emission computerized tomography), or PET (positron emission tomography).

Direct Contact Force MTBI:

Impact or direct contact injuries result in specific damage to brain tissue within specific brain regions. Some damage to the brain results from the head directly striking an object, such as a dashboard or windshield. The portion of the brain that hits the object suffers damage. However, this is only part of the overall cause of brain damage from this type of injury. Acceleration/deceleration injuries also contribute to this overall injury. This type of injury is most commonly caused by auto accidents. Basically, the head is thrust forward until it comes to a sudden and dramatic stop after striking a stationary object. The brain continues in a forward motion until it strikes the front of the inner skull. This contact of the brain against the front of the skull results in frontotemporal lesions (bruising of the frontal and/or temporal lobes). This also causes shearing and tearing of brain tissue and neuron damage as the brain makes contact with rough bony ridges inside of the skull. The resulting brain deficits include difficulty with judgment, inflexibility in thinking, and poor memory, planning, organization, and concentration. Changes in personality and behaviors are also common as all of these skills are controlled by the frontal and temporal lobes. Damage to the subcortical connections between the lower area of the brain and the upper hemispheres also results in significant changes in brain function. Another direct contact force MTBI is the coup/countercoup injury. Essentially, this refers to blow/ counterblow damage. A moving object connects with the head and briefly dents the skull inward, causing the brain to bounce off the opposite side of the skull. The initial contact area is bruised as well as the area where the brain bounced. Impairment depends on where the blow occurs. Some resulting difficulties include personality changes, perceptual and sensory problems, difficulty with self-expression and balance, and motor difficulties.

Diffuse MTBI:

A diffuse MTBI results from a mild blow to the head that causes only momentary loss of consciousness and no observable disruption of nerve impulses. This is also known as a concussion. However, any time the brain suffers a violent force or movement, the soft, floating brain is slammed against the skull’s uneven and rough interior. The internal lower surface of the skull is a rough, bony structure that often damages the fragile tissues within the brain as it moves across the bone surface. The brain may even rotate during this process. This friction stretches and strains the brain’s threadlike nerve cells. The cells may even become torn either at the focal point or in other areas in a diffuse injury. Although the stretching and tearing of nerve fibers may seem relatively minor or microscopic, the impact on the brain’s neurological circuits is often subtle yet significant. It is now widely recognized that even a mild injury can result in significant physiological damage and cognitive deficits. This type of nerve damage often heals in time, but there can be long-term repercussions at the cellular level. Nerve impulses often fire at a slower rate and may become less consistent in their functioning. Diffuse damage from an MTBI often results in deficits in attention, slowed information processing, disrupted organization, and impoverished problem solving. Higher-order thinking may also suffer. Self-expression and communication skills may become less consistent, and abstract thinking may be impaired. This diffuse type of brain injury is often accompanied by damage from direct contact force. 

A typical scenario may look something like this: Damage to frontal and temporal lobes from contact with rough surface of the inner skull Brain stem swelling and lower-brain damage.  Acceleration/deceleration forces cause diffuse shearing and stretching of neurons urface


Outcome and management of MTBI are determined by the severity, nature, and location of the injury. Brain damage may be primary, sustained at the time of impact, or secondary, the result of subsequent pathophysiologic processes (reactions of the body to injury).

Primary Damage
Primary damage to the brain from a traumatic brain injury can take many forms. These include:

  • alterations in cerebral blood flow
  • diffuse axonal injury (the stretching and tearing of brain tissue, causing short-circuiting
    throughout the brain)
  • intracranial lesions (specific damaged areas of the brain)
  • vestibular damage (disruption of the brain’s maintenance of the body’s equilibrium)
  • slowed information processing

There are many consequences of MTBI that result in damage to the brain and temporary or
permanent impairment in cognition. Rarely are the consequences limited to one set of symptoms or a
disability that affects only one part of a person’s life.

Secondary Damage:
Secondary factors exacerbating brain damage include:

  • neurotransmitter dysfunction (decrease in the brain’s release of chemicals)
  • intracranial hematoma (localized swelling)
  • cellular degeneration
  • decreased glucose uptake (diminished brain fuel)
  • a variety of pulmonary complications and hypoxia (oxygen deprivation)

The initial injuries combined with multiple secondary insults can result in a variety of symptoms. Diminished blood supply to the brain (ischemic damage) causes disturbance in the brain’s ability to function. Axons (brain fibers that transmit electrical impulses) in the cerebrum (cortical or higher areas of the brain) begin to die and eventually the various parts of the brain can no longer communicate with each other. This disconnection is called diffuse axonal injury. Diffuse axonal injury is the most common secondary result of an MTBI and manifests itself in subtle ways. Axonal damage can result from damage to a part of the neuronal cell.

The most common cause of diffuse axonal injury is motor vehicle accidents. The acceleration/ deceleration force of these accidents results in forceful forward and backward jarring of the head. When the head hits a stationary object, the brain is thrust forward and back in the bony calvarium (skull). The inertia of the impact causes the brain to slide and rotate within the skull, resulting in brain contusion (bruising) and the rupture of life-giving blood vessels.


MTBI can result in a multitude of neurological deficits and usually results in a combination of several. Any cognitive, sensory, motor, or autonomic function may be compromised. These impairments are referred to as functional, as they affect the way these processes function. Most of these complications are apparent within the first days or months following injury, depending on the severity of the initial trauma. Some long-term effects might include a variety of cognitive and movement disorders, seizures, headaches, visual deficits, and sleep disorders. Medical complications include, but are not limited to, cardiac and circulatory deficits, pulmonary complications, metabolic changes, nutritional concerns, gastrointestinal complications, musculoskeletal complaints, and dermatologic problems. The cognitive and emotional consequences of MTBI are equally diffuse. All of these consequences can occur singly or in combinations and are variable in terms of their effects on individuals. Furthermore, they change in severity and presentation (how they appear or manifest) over time. In combination, they produce myriad functional problems. Some of the most persistent problems include memory impairment and difficulties in attention and concentration. Deficits in language use and visual perception are common but often go unrecognized or aren’t taken seriously. Frontal lobe functions, such as judgment, planning, decision making, problem solving, cognitive flexibility (flexibility in thinking), abstract reasoning, insight, information processing, and organization are often affected to different degrees by an MTBI.

Cognitive deficits are complex in nature and can usually be further broken down and delineated. For example, there are different types of attention (like divided versus alternating attention), various stages of memory that can be affected (like retention versus recall memory deficits), expressive versus receptive language difficulties, and multiple components of complex information processing and sensory perception and processing. These systems are interconnected and thus a breakdown in one often results in a breakdown within the other systems. These deficits can further affect personal and professional social relationships, family dynamics and role functions, and employment and economic independence. These cognitive impairments are further exacerbated by factors such as the severity of injury, the age and general health of the individual, degree and stage of recovery, premorbid cognitive functioning (thinking abilities prior to the accident), and a whole array of genetic, psychological, and social considerations. Symptoms of postconcussive syndrome can be further exacerbated by stress (including post-traumatic stress disorder), depression, and anxiety.

Excerpts from the Mild Traumatic Brain Injury Workbook, Mason, D.J.; New Harbinger Publications

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