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Traumatic Brain Injury and Diffuse Axonal Injury (DAI) - a review by Cal Shipley, M.D.

DIFFUSE AXONAL INJURY (DAI)

DEFINITION

 

Traumatic brain injury (TBI), also called acquired brain injury or simply head injury, occurs when a sudden trauma causes damage to the brain. The damage can be focal (confined to one area of the brain) or diffuse (involving more than one area of the brain).

 

Concussion is the most common type of TBI. Technically, a concussion is a short loss of consciousness in response to a head injury, but in common language the term has come to mean any minor injury to the head or brain. Typically, there are no long term after effects on overall brain function from such injuries.

 

More severe forms of TBI occur in situations where the human head undergoes sudden changes in velocity, resulting in Diffuse Axonal Injury (DAI). Motor vehicle accidents (MVAs) are a frequent example of such situations. Severe TBI seen in MVAs arise as a result of acceleration-deceleration events of the brain within the skull, without skull fracture (so-called "closed head" trauma). This event usually occurs as vehicle occupants are thrown forward or sideways, resulting in collisions between the head and windshields, dashboards, etc. Brain injury in closed-head trauma may result from direct trauma to the peripheral margins of the cerebral hemispheres as they impact the skull, but the majority of severe brain injuries in acceleration-deceleration events result from DAI. While many such injuries involve physical impact of the head with some portion of the vehicle, it is the sudden acceleration-deceleration of the head, apart from impact, that results in DAI

 

DIFFUSE AXONAL INJURY (DAI)

 

Mechanism

 

DAI involves massive loss of neuronal function towards the central area of the brain, well away from any areas of direct trauma with the skull. Researchers were initially puzzled as to why such extensive damage occurred without direct trauma. The mechanism of DAI was subsequently discovered to occur as a result of rotational movement of the brain during acceleration-deceleration events. The key to understanding the injury lies in the varying densities of brain tissue. Grey matter (primarily the cerebral hemispheres) is less dense than white matter (i.e.- the brainstem and central brain structures). Due to different inertial characteristics based on these densities, as the brain rotates during acceleration-deceleration events, lower density tissues move more rapidly than those of greater density. This velocity difference causes shearing of neuronal axons which connect between the gray and white matter, and explains why DAI lesions are seen most frequently in the areas of the brain where white and gray matter meet (see specific affected areas below). The term "shear injury" may be used interchangeably with DAI. The magnitude of axonal injury in DIA is dependent on 3 factors: 1) the distance from the center of rotation, 2) the arc of the rotation, and 3) the duration and intensity of the force.

 

Typically, the process is widespread and bilateral, most frequently involving the frontal and temporal lobe white matter, corpus callosum (bridge between the cerebral hemispheres), and areas of the brainstem not involved with basic life functions (cardiac and respiratory). As a result, individuals suffering from DAI rarely die. There is almost no correlation between DAI and the presence or absence of skull fractures, or subarachnoid or subdural bleeding.

 

 

There appears to be two phases to the axonal injury in DAI. Primary injury, in which axons undergoing shear forces are stretched at the moment of impact, and then a secondary, or delayed phase, where strained axons undergo swelling and rupture as a result of biochemical changes related to the primary injury. It is currently thought that this delayed phase may take up to several weeks post-event to occur. The previously held theory that axons undergoing primary injury at the moment of impact are mechanically disrupted has largely been discredited in favor of the primary strain/ secondary rupture mechanism.

 

 

 

EFFECTS ON NEUROLOGICAL FUNCTION

 

The gray-white matter interface of the brain, where damage due to DAI most frequently occurs, consists of tens of millions of neurons interconnecting all of the various distinct functional areas of the brain - it’s like a highly sophisticated communications complex. DAI results in massive disruption of these interconnecting neurons and has a devastating effect on overall neurological function.

 

DAI results in an immediate loss of consciousness, and most individuals (>90%) remain in a persistent vegetative state. Essential cardiac and respiratory brain functions required for life are typically not affected by DAI, as these functions are located deep in the brainstem, away from the gray-white matter interface. As a result, DAI rarely causes death. The prognosis worsens in direct relationship to the number of lesions present.

 

Slightly less than 10% of individuals with DAI will regain consciousness. Improvement in neurological function in these individuals, if any, will occur within the first twelve months after injury. After this point, further resolution of deficits will be minimal to absent. Because DAI can affect virtually every higher brain function, deficits can consist of a broad range of cognitive problems.

 

Cognition is a term used to describe the processes of thinking, reasoning, problem solving, information processing, and memory. Most patients with severe DAI, if they recover consciousness, suffer from cognitive disabilities, including the loss of many higher-level mental skills. The most common cognitive impairment among severely head-injured patients is memory loss, characterized by some loss of specific memories and the partial inability to form or store new ones. Some of these patients may experience post-traumatic amnesia (PTA), either anterograde or retrograde. Anterograde PTA is impaired memory of events that happened after the DAI, while retrograde PTA is impaired memory of events that happened before the DAI.

 

Many patients with mild to moderate head injuries who experience cognitive deficits become easily confused or distracted and have problems with concentration and attention. They also have problems with higher level, so-called executive functions, such as planning, organizing, abstract reasoning, problem solving, and making judgments, which may make it difficult to resume pre-injury work-related activities. Many DAI patients have sensory problems, especially problems with vision. Patients may not be able to register what they are seeing or may be slow to recognize objects. Also, DAI patients often have difficulty with hand-eye coordination. Because of this, DAI patients may be prone to bumping into or dropping objects, or may seem generally unsteady. DAI patients may have difficulty driving a car, working complex machinery, or playing sports. Other sensory deficits may include problems with hearing, smell, taste, or touch.

 

Speech is often slow, slurred, and garbled. Some may have problems with intonation or inflection, called prosodic dysfunction. An important aspect of speech, inflection conveys emotional meaning and is necessary for certain aspects of language, such as irony. Affected individuals may lose a previous ability to speak a foreign language. These language deficits can lead to miscommunication, confusion, and frustration for the patient as well as those interacting with him or her.

 

Most DAI patients have emotional or behavioral problems that fit under the broad category of psychiatric health. Family members of DAI patients often find that personality changes and behavioral problems are the most difficult disabilities to handle. Psychiatric problems that may surface include depression, apathy, anxiety, irritability, anger, paranoia, confusion, frustration, agitation, insomnia or other sleep problems, and mood swings.

 

Problem behaviors may include aggression and violence, impulsivity, disinhibition, "acting out", noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, egocentrism, inappropriate sexual activity, and alcohol or drug abuse/addiction. Some patients' personality problems may be so severe that they are diagnosed with borderline personality disorder, a psychiatric condition characterized by many of the problems mentioned above. Sometimes DAI patients suffer from developmental stagnation, meaning that they fail to mature emotionally, socially, or psychologically after the trauma. This is a serious problem for children and young adults who suffer from a DAI. Attitudes and behaviors that are appropriate for a child or teenager become inappropriate in adulthood. Many DAI patients who show psychiatric or behavioral problems can be helped with medication and psychotherapy.

 

 

 

DIAGNOSIS

 

Virtually all individuals who are rendered unconscious by a closed head acceleration-deceleration event will suffer some degree of DAI. Those who regain consciousness will manifest disorders of cognition

and personality to variable degrees, and recovery from these disorders will be equally variable. In depth evaluation by appropriately trained neuro-psychiatrists is probably the most effective means of determining the breadth and extent of neurological deficits in a particular afflicted individual. Imaging studies of the brain have been used to chart DAI, particularly when medical-legal proceedings take place post-injury. Juries in such cases tend to be more impressed by lesions that can be seen on brain scans than by lengthy verbal expositions by neuro-psychiatrists. There are, however, distinct limitations to the use of currently available brain imaging in DAI. The sensitivity of imaging studies in detecting the full extent of DAI may be low, particularly in the early post-injury period. There may also be a very poor correlation between findings on imaging studies and actual neurological deficits. In the first several weeks post-injury, deficits tend to be greater than lesions on imaging studies would suggest, whereas at 12 months, the relationship is often inverted. Imaging one year out may show extensive brain atrophy in individuals whose deficits have actually improved due to re-assignment of brain functions from damaged to healthy areas.

 

 

 

DIFFUSE AXONAL INJURY (DAI)

PLAIN FILM RADIOGRAPHS

 

No specific findings related to DAI can be seen on plain film xrays.

 

 

CT SCANS

 

50-80% of individuals with DAI have a normal CT scan when performed immediately post-injury. In those cases where CT scan is positive, small hemorrhages may be seen at the gray-white matter junction, within the corpus callosum, and in the brainstem. Small focal areas of low density on CT, corresponding to edema in areas of shear injury may also be seen. CT scan may also be helpful in demonstrating areas of atrophy 12-24 months post injury.

 

Specific criteria for detecting DAI in the immediate post injury period have been suggested by Wang et al (1998) as follows:

 

-Single or multiple small intra-parenchymal hemorrhages less than 2cm in diameter in the cerebral hemispheres

 

-Intraventricular hemorrhage

 

-Hemorrhage within the corpus callosum

 

-Small focal areas of hemorrhage (<2cm in diameter) adjacent to the third ventricle

 

-Brainstem hemorrhage

 

 

MRI

 

Individuals in whom clinical symptoms exceed injury noted on CT scan should have MRI imaging performed. Compared to CT, Magnetic Resonance Imaging (MRI) tends to be a more sensitive modality for detecting DAI, particularly in the immediate post-injury period. There are several techniques for the application of MRI imaging of human tissue. These techniques are named and categorized according to how specific portions of the magnetic data are emphasized (weighted) by the computer in creating the final image:

 

"T1-weighted" images are sensitive to hemorrhage within areas of shear.

 

"T2-weighted" and "diffusion-weighted" images are sensitive to non-hemorrhagic areas of axonal injury.

 

"Gradient-echo" images have a very high sensitivity to changes associated with DAI in both the early and late post-injury periods, and are the current mainstay for detection of shear injury

 

 

NUCLEAR MEDICINE

 

Nuclear medicine imaging is not currently being used to assess individuals with possible DAI, however, iodine-123 single-photo emission (PET Scan) studies have demonstrated abnormal brain function in areas that MRI studies have missed. This and several other developing imaging technologies show promise for the future.

 

 

PROGNOSIS

 

90% of individuals with DAI remain in a persistent vegetative state indefinitely, and may remain so for decades. Of the 10% who regain consciousness, the majority will sustain permanent and far-reaching functional deficits as reviewed above. Only a small percentage of these individuals will attain near-normal neurological function. What improvement occurs does so within the first 12 months after the injury. Significant improvement occurring more than one year after injury is rare.

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