ABSTRACT: Traumatic brain injuries (TBIs) have the potential to significantly disrupt a student’s cognitive, academic, social, emotional, behavioral, and physical functioning. It is important for educators to appreciate the array of difficulties students with TBI may experience in order to appropriately assess needs and create an educational plan that targets the needs. The purpose of this article is to provide an overview of the neuropsychological aspects of TBI and the implications these have on the role of educators. The author reviews the physical aspects of TBI, and summarizes the neuropsychological outcomes, with particular attention given to injury variables that impact assessment decisions. The author describes common challenges with the assessment of educational needs with emphasis placed on developing a hypothesis testing approach to information gathering and formal assessment.
Students who have sustained a traumatic brain injury (TBI) represent a diverse population that exhibit the full spectrum of educational needs. Brain injuries clearly carry with them the potential to significantly disrupt a student’s learning, and injuries affect aspects of social, emotional, behavioral, and physical functioning as well. Because of the diverse nature of TBI in children and adolescents, and because disciplines such as education and neuropsychology frequently do not interact closely, these students pose a unique and sometimes daunting challenge in the school setting. In this article, I provide an overview of the neuropsychological aspects of TBI and the implications these have for the role of educators. I provide an overview of the physical aspects of TBI and discuss variables, such as severity of injury and age at injury. I summarize the effects of TBI on various neuropsychological domains and address challenges associated with assessment of educational needs. Finally, I provide recommendations regarding assessment strategies as well as using information gathered during assessment to guide intervention decision making.
TBI sets in motion a cascade of pathophysiologic processes that continues for some time after the point of initial impact. The process of brain damage and the subsequent physiologic changes are a dynamic process that continues for some time following the actual traumatic injury (Bigler, 1997). It is important for educators working with students with TBI to have at least a cursory understanding of the physiological aspects of brain injury in order to better understand, predict, and plan for the student’s educational needs.
There are a number of ways to classify the physical sequelae of TBI. Injuries might be characterized as open/penetrating or closed, and resulting damage can be referred to as focal or diffuse. Focal effects of brain injuries include the primary point of contusion, tearing of surface vasculature, intracranial hemorrhage, and focal compression/laceration of brain tissue. Brain trauma can also result in diffuse physical damage that includes stretching and shearing of nerve fibers and blood vessels.
In an open head injury, there can be skull fracture and resultant tearing of the protective meninges surrounding the brain. This can result in focal compression and laceration of brain tissue, as well as destruction of brain vasculature. Focal effects of open/penetrating head injury can include the point of initial compression that results in contusion, and there can also be laceration of underlying brain tissue. Furthermore, any time the protective blood-brain barrier is disrupted, the brain is vulnerable to infection and toxic exposure.
In closed head injury, one mechanism for brain injury stemming from the physical forces associated with the trauma is the impact/compression of brain tissue inside the skull. At impact, momentum shifts the brain and can cause it to strike the interior of the skull. This creates a bruising (contusion) at the site of impact. The brain might then rebound and impact backward to injure a second site of contusion opposite the primary point of impact. The initial injury is referred to as the coup injury, whereas the injury opposite the point of impact is referred to as a contrecoup injury. Focal contusions are generally more likely to occur in the frontal and anterior temporal regions of the brain due to the bony extrusions of the cranium in those regions (Yeates, 2000). As the brain compresses and stretches, this energy can result in stretching and tearing of nerve fibers, particularly along the axon, which can result in more diffuse damage, which is in addition to focal damage caused by contusion.
If the impact causes the head to turn or twist, the force of impact can cause the brain to rotate inside the skull. At points of impact with the skull, this can again cause contusion, and these rotational forces can also stretch brain tissue to the point of rupture and shearing. Although contusion creates focal injury to the brain, axonal stretching and shearing results in more diffuse damage that can be degenerative in nature, cause metabolic changes within the brain, and ultimately result in cell death (Bigler, 1997). Stretching, shearing, and cellular degeneration are not always immediately visible on CT or MRI scans, because these occur at a cellular level that is currently beyond the resolution of these standard imaging techniques.
Neuropathology stemming from TBI can be categorized as primary or secondary. Primary injuries to the brain are directly related to the physical forces involved in the trauma, including acceleration-deceleration and rotational forces. Acceleration–deceleration occurs when the head is moving and then stops suddenly. For example, a fall in which the head strikes the ground or motor vehicle accident results in extremely rapid deceleration of the head and brain. A rotational injury occurs when the brain continues moving inside the skull in a nonlinear fashion after the head has stopped. For example, a side impact motor vehicle accident might result in angular acceleration-deceleration that causes the brain to twist inside the skull.
Secondary effects of the brain trauma include brain swelling, mass effects created by a hematoma, cerebral edema, and increased intracranial pressure. Any of these conditions create a situation in which oxygen is restricted from being delivered to brain tissue (hypoxia), which can lead to further damage or even death (Bruce, 1995). Seizure activity is another potential secondary effect of TBI, and children tend to be more likely to develop posttraumatic seizures compared to adults (Baron, Fennell, & Voeller, 1995).
From Preventing School Failure magazine. Heldref Publications. Reprinted with permission. www.heldref.org.