Chapter 2

Understanding ABI from a Developmental Perspective

2.1 Myths About the Injured Brain
2.2 Causes of Acquired Brain Injury
2.3 Traumatic Brain Injury
2.4 Mild, Moderate, and Severe Injuries
2.5 Damage at Specific Stages During Child Development
2.6 Recovery and Long-Term Consequences

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2.1 - Myths About the Injured Brain

Myth:

All brain injuries are the same.

Fact:

No two brain injuries are alike. The brain is a unique and very complex organ and a brain injury is not like any other disease or injury. Recovery from a brain injury depends not only on the severity of the injury but also on the part of the brain involved. In addition, a decreased supply of oxygen, blood clots, tearing and shearing forces on the neurons, as well as swelling and bruising in the brain all play a part in determining the extent of an injury

Myth:

A brain injury will heal with time, and a good physical recovery indicates that the brain has completely healed.

Fact:

Once the nucleus (cell body) of a neuron is damaged, the neuron dies and a new one will not take its place. Damage to the brain is permanent. It is quite possible for a person with a severe brain injury to show no outward physical signs of a disability. Cognitive abilities such as memory, abstract thinking, attention, and judgment can all be seriously and permanently affected in the absence of physical injuries.

Myth:	A younger child will have a better outcome from a brain injury than an older student.
Fact:	Even though a young child's brain has more plasticity and a greater ability for other neurons to take on new function, the brain is less developed overall and the child has less pre-existing knowledge (including life experiences and skills) to help them adjust to the consequences associated with a brain injury.

 

2.2 - Causes of Acquired Brain Injury

Acquired Brain Injury (ABI) is any type of sudden injury that causes temporary or permanent damage to the brain. ABI can be divided into two categories:

• Traumatic: resulting from an external force applied to the head/brain (e.g., damage that is associated with some kind of trauma to the head, such as a concussion, a fall, or a motor vehicle collision is known as a traumatic brain injury.)
• Non-Traumatic: resulting from an internal source that inflicts injury to the brain (e.g., anoxia [near drowning], toxicity, infection, or cerebral vascular accident [stroke]).

The following chart provides examples of the most common causes of ABI.

Cause	Example
Traumatic
Blow to the head	- Motor vehicle accidents - Assault with an object - Shaken baby syndrome
Falling or tumbling	- Falling off a bicycle, tree, climbing equipment, or furniture - Sports injuries
Non-Traumatic
Anoxic injuries (lack of oxygen to the brain)	- Near drowning - Suffocation - Choking
Vascular injuries (disruption in blood supply to the brain)	- Stroke (blocked blood vessels in the brain) - Aneurysm (broken blood vessel in the brain)
Inhalation or ingestion of toxic substances	- Sniffing glue, paint, or carbon monoxide - Drug use
Infectious diseases	- Meningitis - Encephalitis

2.3 - Traumatic Brain Injury

Traumatic Brain Injuries (TBI) can also be divided into two main categories: open and closed. By knowing whether or not a person sustained an open-head injury versus a closed-head injury, some predictions about severity, outcome, and deficits can be made.

Open-Head Injuries	- The skull is penetrated. - Brain tissue becomes exposed to the outside environment. - Initially the person is susceptible to severe blood loss and infection. - Damage is usually focal (localized) in nature making deficits easier to predict and identify.
Closed-Head Injuries	- Skull remains intact. - Brain tissue is jolted around the inside of the skull. - The brain is bruised and swells (edema), blood vessels are ruptured, causing blood build-up (hematomas), both of which cause further damage. - Even through there may be only one initial point of impact, damage is global (diffuse) in nature, affecting many areas of the brain.

The mechanism of an open-head injury is fairly simplistic. An open wound in the brain, perhaps due to a gunshot or a knife, causes direct damage to the tissue. The mechanism of the closed-head injury is a little more complicated. When the head receives a blow, the brain is jolted inside the skull. If the blow is strong enough, the brain can “bang” against the inner wall of the skull, resulting in what is termed a “coup” injury. This can cause a contusion, or bruise, at this initial point of impact. It is then possible for the brain to rebound off the opposite side of the skull. This will cause yet another contusion on the opposite side of the brain, known as a “contracoup” injury. Depending on the force of the initial blow to the head, this rebounding effect on the brain can occur several times. With each back and forth motion of the rebounding effect, the brain is also being scraped back and forth across the bony, spike-like contours of the skull, causing bleeding and further tissue damage.

Secondary Factors

In addition to the more prominent localized injuries at the coup and contracoup injuries, the sudden starting and stopping motions of the head and brain (sometimes called acceleration and deceleration forces), as well as the rotational and shearing movements caused as the brain twists upon itself at the level of the brain stem, typically also result in a pattern of diffuse (widespread) damage to the neurons and blood vessels.

Hematomas

The brain is supplied with blood through an extensive network of arteries and blood vessels. When the brain has been impacted, many blood vessels may be ruptured. This causes excessive bleeding, leading to the formation of hematomas, or pools of blood on or in the brain.

Edema

Brain tissue is similar to other bodily tissues in that damaged tissue results in swelling or edema. Unfortunately, since the brain is encased inside the hard skull, there is very little room for the tissue to swell. Therefore, the swelling brain tissue becomes squished or compressed up against the inside of the skull, causing damage and cutting off local blood supply. Without blood supply, the neurons contained in the swelled tissue can die.

Disconnection of the Neural Pathways

The brain is an interconnected network of neurons that communicate with each other. Neurons pass information from one to another, both electrically and chemically, along fragile axonal fibres. Neurons don’t actually touch, so they need only to be knocked out of alignment and there will be a disruption in the signal transfer. Neurons thrive on being active and their survival depends on it. If one group of neurons becomes damaged and dies, then the neurons that they once communicated with will no longer receive information. Once those neurons are no longer receiving information from the damaged neurons, they can become inactive and die as well.

2.4 - Mild, Moderate, and Severe Injuries

As a means of standardization, professionals have devised 3 categories of ABI to help describe the severity of the injury. These three categories are Mild, Moderate, and Severe. The categories are principally determined by the degree of change in the individual’s level of consciousness and the extent of Post Traumatic Amnesia (PTA).

It is important to note that a person does not need to lose consciousness to sustain a brain injury.

In addition, it is important to note that the level of severity is not an entirely reliable predictor of outcomes.

The following chart highlights some of the possible symptoms of the three categories of ABI.

2.5 - Damage at Specific Stages During Child Development

• The developmental process of a child and of the brain involves the maturation of psychological and neurological systems within the brain, and if brain structures suddenly become damaged, the natural developmental process will be interrupted.
• Since certain skills and the level of maturation are dependent upon developmental stages, the impact that ABI has on an individual will vary according to chronological age. There are 5 peak maturation periods that occur during development: ages 1-6, 7-10, 11-13, 14-17, and 18-21.
• Often in children, skills that were acquired before the injury will be maintained, however, the ability to acquire new skills will be impeded, sometimes halting them in a certain developmental stage.
• Deficits that result from an injury occurring at an early age, may not emerge until the student is much older and at a developmental age where those skills are needed, (e.g., a student acquiring an injury to the frontal lobe at age 5 may not show deficits until age 12 or older when more sophisticated cognitive skills such as problem solving, judgment, and the ability to organize and prioritize are required.)

Potential Consequences of ABI: A Developmental Perspective

Age in Years	Normal Developmental Expectations	Possible Consequences that can Result after ABI
0-2	Behavioural Advances from forgetting about objects once out of sight, to actively searching for the item, to remembering and systematically searching previous location for the item. Uses only reflexive grasping initially and advances to being able to manipulate a crayon to scribble vigorously. Develops basic vocabulary and rudimentary sentence structure. Neurological Radial cells guide the formation of neuron connections. There is an increased rate of re-sorting and elimination of neurons (parsing).	Lack of neural sorting can result in disruption in all phases of development, including motor/physical, emotional, communication, and social. Poor coordination of limbs for gross motor control. Lack of precision with fine motor skills as in finger manipulation. Limits in receptive language.

Note: None of the above “possible consequences” is, by itself, a reliable indication of an ABI.

Age in Years	Normal Developmental Expectations	Possible Consequences that can Result after ABI
3-5	Behavioural Formation of basic appropriate social interactions (e.g., share and play well with others). Expressive language formation. Learn basic aspects of personal care, (e.g., washing and dressing). Control over some emotional and behavioural expressions. Separates comfortably from parents for short periods of time and is able to be productive. Pre-operational thought and problem-solving skills begin to emerge for cause and effect relationships and comprehension. Neurological Time of rapid expansion of the connections between neurons, (e.g., ability to learn is accelerated).	Child may not play well with others and remain very self focused. Expressive language may remain very limited. May have difficulty understanding cause and effect relationships. May experience "temper tantrums" over relatively small issues and over time not appear to learn how to handle his/her emotions. May experience severe separation anxiety when away from parents. Long-term capacity for learning can be impaired after ABI since the brain has not developed adequate compensatory strategies.

Note: None of the above “possible consequences” is, by itself, a reliable indication of an ABI.

Age in Years	Normal Developmental Expectations	Possible Consequences that can Result after ABI
6-9	Behavioural Development of self-awareness begins and impact of one's actions on others is recognized. Development of concrete operations, (e.g., awareness of visual-spatial features in the environment, uses an empirical/experimental approach to discover relationships between objects and/or people) Neurological Most neurological development is complete with the exception of the frontal, hippocampal, and some temporal areas	One of the least devastating times for an injury to occur in terms of long-term prognostic outcome due to fact that much language learning has occurred, as well as some basic acquired skills in basic academic areas and social/emotional domains. Difficulties in impulsive control may present as distractibility and attention deficit and/or may be hyperactive in terms of not being able to inhibit movement and/or interactions. Difficulty with behavioural management problems, often considered a "difficult" child. Misunderstanding object relations, (e.g., can solve the world experimentally), therefore, gets very frustrated with outcomes s/he did not "predict." This can result in a child who "grows up" and appears lazy, unmotivated, detached, unresponsive, no "initiative." Lack of empathy, due to lack of alternative prospectives, returns to egocentric perspective. Inability to respond in expected manner to behaviour modification and consequences for actions due to decreased comprehension and/or perception of cause and effect relationships. Inability to understand/formulate alternative points of view. Disruption in moral understanding.

Note: None of the above “possible consequences” is, by itself, a reliable indication of an ABI.

Age in Years	Normal Developmental Expectations	Possible Consequences that can Result after ABI
10-15	Behavioural Learning appropriate social interactions with peers of opposite sex begins. More emphasis and expectations are placed on using executive cognitive functions, (e.g., memory, problem solving, sequencing, and judgment). Work well with others in group settings and/or with little supervision. Neurological Hormonal influences on the brain begin to occur. Connection between the two cerebral hemispheres becomes optimized. Increasingly complex neuron interconnections ease learning in areas such as reading, spelling, writing, math, and reasoning. Development is completed for hippocampal and temporal areas towards the end of this stage.	Inappropriate social interactions among peers. Student has problems with time management, attention, judgment, initiation, or processing speed. Low self-esteem. Does not work well with others or when there is little structure. Low self-control. Poor memory, with limited recognition and recall for post injury and recently experienced events. Interruption of pragmatic skills.

Note: None of the above “possible consequences” is, by itself, a reliable indication of an ABI.

Age in Years	Normal Developmental Expectations	Possible Consequences that can Result after ABI
16-25	Behavioural Young adulthood phase of adolescent application and exercise of formal cognitive thought (e.g., consideration of multiple variables influencing prediction and outcome). Flexibility in cognitive thought enhanced (e.g., being able to shift and test hypotheses rapidly and effectively based on feedback from the environment). Increased sophistication of being able to adapt and predict alternative perspectives (e.g., how things affect others, how others learn, how other outcomes may occur and how others will react to those outcomes). Increased reliance on, and identification with peers in social choices, judgment and modelling of behaviour; increased social interactions and contact; increased independence from familial support and judgment. Social-personal relations and learning emphasized (e.g., sexuality, intimacy). Neurological Frontal lobe development is completed. Completion of neural myelination (e.g. insulation of the neural axons) takes place, thus increasing efficiency and communication within the neural systems	Apparent lack of interest and lethargy, "attitude," lack of drive. Awkward and/or inappropriate social-personal expression. Inability to inhibit instinctual drives in order to permit concentration in academic as opposed to social priorities. Perseveration of thought, (e.g., being "stuck" on a particular item, idea, and/or concern). Lack of attention to detail, will overlook and/or not detect objects, items, facts, or variables that are relevant to decision making and/or action. Limited emotional control, may appear depressed, angry, volatile. Lack of insight, limited social judgment and decision making. Disruption in organizational skills (e.g., planning, sequencing predicting, anticipating) and other "executive" functions. Brain region "specific" disorders (e.g., parietal injury - spatial disruption, temporal - language disruption, occipital - disruption in vision).

Note: None of the above “possible consequences” is, by itself, a reliable indication of an ABI.

Difficulties of Diagnosing

An ABI is usually diagnosed by the treating physicians in the hospital emergency department, or by the family doctor. However, in the midst of other injuries (physical or life-threatening), a traumatic brain injury can easily be overlooked. In addition, more subtle or mild brain injuries may not be detectable during a basic neurological exam or even on extensive medical scans (CAT or MRI).

Many students who suffer a mild brain injury return to school without a proper diagnosis or follow-up. Worse yet is the fact that the family may, for a variety of reasons, fail to inform the school of the student’s ABI. Even if they do inform the educator, there is no obligation to enter that information in the permanent school records. In cases when the student appears to totally recover from the symptoms of the ABI as well as any physical injuries, the ABI is often totally forgotten by students and parents. The deficits resulting in ABI may manifest themselves several years post-injury when the student reaches a development stage which places new cognitive demands on them.

2.6 - Recovery and Long-Term Consequences

The unparalleled complexity of the brain makes it very difficult to determine the extent of the brain injury or the prognosis for recovery. There are many factors influencing the recovery process:

• Characteristics of the injury — The severity and extent of damage, the specific areas of the brain that are injured, and the nature of the injury (focal or diffuse) all have a role in the student’s outcome.
  
  
• Physical recovery of the brain — There is some degree of spontaneous physical recovery following an ABI. Swelling decreases, normal blood flow is restored, and, since some reorganization of neural networks is possible, the brain can compensate for some types of impaired function.
  
  
• The individual child — Characteristics of the student, including age and developmental stage at the time of the injury, his/her personality traits, pre-existing skills and knowledge, his/her history of learning or developmental difficulties, and specific organization of the brain can all impact recovery positively or negatively.
  
  
• The environment — Informed and supportive family, friends, supportive school and community with ready access to quality medical care and rehabilitation tailored specifically to the student’s individual needs are critical factors that will allow the achievement of the student’s full potential for recovery.

The speed and extent of recovery is variable. The greatest recovery and functional improvement is expected within the first 2 years post-injury and typically there is no long-term prognosis given until that time. Most of the spontaneous physical recovery of the brain is expected to occur within 1 year post-injury, and generally gains occur more slowly after that time. In addition, some consequences of an ABI may not be noticeable until the child reaches a later developmental stage due to the fact that the injured part of the brain is not yet heavily relied upon. The younger the child is at the time of injury, the greater the impact will be on new learning, development, and long-term outcome.

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